PHYSIOLOGY

CARDIOVASCULAR

AfTe1Te1fTeeh.com
Table of Contents
Anatomy & physiology 1 Normal sinus rhythm 47
Lymphatic anatomy & physiology 8 ECG Rate and rhythm 47
Normal heart sounds 12 ECG Intervals 48
Abnormal heart sounds 13 ECG axis 49
ECG transition 49
Blood pressure regulation 23 ECG cardiac hypertrophy
Baroreceptors 23 and enlargement 51
Chemoreceptors 25 ECG myocardial infarction and ischemia 52
Renin-angiotensin
aldosterone system 27 Hemodynamics 54
Blood pressure, flow and resistance 54
Cardiac cycle 29 Pressure in the cvs system 55
Measuring cardiac output – Fick Resistance to blood flow 59
principle 29 Laminar flow and Reynolds number 61
Cardiac and vascular Compliance of blood vessels 62
function curve 29
Altering cardiac & Normal variations 64
vascular function curves 30 CVS changes during exercise 64
Pressure volume loops 31 CVS changes during hemorrhage 65
Changes in pressure CVS changes during postural change 67
volume loops 33
Cardiac work 34 Specific circulations 70
Cardiac preload 35 Cerebral circulation 70
Cardiac afterload 36 Coronary circulation 71
Law of Laplace 37 Control of blood flow circulation 72
Frank-Starling relationship 38 Micro-circulation and Starling forces 73
Stroke volume, ejection
fraction & cardiac output 38 Thermoregulation 75
Cardiovascular temperature homeostasis 75
Cardiac Electrophysiology 39
Action potential in pacemaker cells 39
Action potential in myocytes 40
Electrical conduction in heart 41
Cardiac conduction velocity 41
Excitability and refractory periods 42
Cardiac excitation contraction coupling 42
Cardiac length tension 44
Cardiac contractility 4$

ECG 46
ECG Basics 46
 NOTES

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1111111 CARDIOVASCULARANATOMY & PHYSIOLOGY
NOTES

CARDIOVASCULAR ANATOMY &

PHYSIOLOGY
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CARDIOVASCULARSYSTEM , Sits on top of diaphragm (main

• Cardia-. cardi-, cardio- breathing muscle)
O Heart, which pumps blood , Behind sternum (breast bone)
• Vascular: blood vessels (carry blood to , In front of vertebral column
body, return it to heart) , Between lungs
• Delivers oxygen, nutrients to organs, , Enclosed, protected by ribs
tissues , Right. left sides separated by muscular
• Removes waste (carbon dioxide, other septum
cellular respiration by-products) from
organs. tissues Heart wall layers
• Epicardium: covers surface of heart. great
vessels (AKA visceral pericardium)
MORPHOLOGY
• Myocardium: muscular middle layer
• Size: about size of person's first (correlated
, Cardiac muscle cells: striated branching
with person's size)
cells with many mitochondria,
• Shape: blunt cone-shaped
intercalated disks for synchronous
• Position: slightly shifted to left side contraction
• Location , Cardiac myocytes: striated, branching
O Lies in mediastinum in thoracic cavity cells with fibrous cardiac skeleton

lEFT
"'MIDDLE of
THORAX SIDE
RIIS
ST£RNUM
lUNGS

VERT£81tAl
COlUMN

Figure 14.1 Heart location relative to other thoracic structures.

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(supports muscle tissue, crisscrossing , Serous pericardium: simple squamous
connective tissue collagen fibers); epithelium layer
coronary vessels (lie on outside of heart, , Parietal pericardium: lines fibrous
penetrate into myocardium to bring pericardium
blood to that layer) , Visceral pericardium (epicardiumJ:
• Endocardium: innermost layer covers outer surface of heart
O Made of thin epithelial layer, underlying , Cells of parietal, visceral pericardium
connective tissue secrete protein-rich fluid (pericardia I
O Lines heart chamber, valve fluid) ---'> fills space between layers
• Pericardium: double-layered sac (lubricant for heart, prevents friction)
surrounding heart
O Fibrous pericardium: outer layer; tough
fibrous connective tissue anchors heart
within mediastinum

CORONARY VESSELS
!. ENDOCARDIUM t. EPICARDIUM
*ENOOTHEUUM
.I.

CARDIAC.
MUSCLE C..ELL
CONNECTIVE
TISSUE
"'COLLAGEN
• SUPPORTS MUSCLE
a, MYOCARDIUM

Figure 14.2 Heart wall layers, from superficial to deep.

SEROUS PERICARDIUM
SAC. of FLUID
,--PARIETAL LAYER

------ .i,,r- FIBROUS PERIC..ARDIUM

_ ..
~ ---PROTEIN-RIC..H FLUID
SURFACE of VISCERAL
l HEART LAYER J
I
EPIC..ARDIUM

Figure 14.3 Layers of the pericardium (the double-layered sac surrounding the heart.)

2
Atrioventricular valves ventricle - pulmonary valve - pulmonary
• Separate atria from ventricles trunk - pulmonary arteries - pulmonary
• Tricuspid valve arterioles - pulmonary capillaries - alveoli
O Three cusps with chordae tendinae • Blood collects oxygen from alveoli, removes
(tether valve to papillary muscle) carbon dioxide
O Prevents blood backflow into right • Oxygenated blood travels through
atrium (right ventricle contracts - pulmonary venules - pulmonary veins -
papillary muscles contract, keep chordae left atrium - bicuspid/mitral valve - left
tendineae taut) ventricle - aortic valve - aorta - organs,
tissues
• Bicuspid I mitral valve
• Deoxygenated blood returns to heart
O Two cusps: anterior, posterior leaflet
O Both have chordae tendineae tethered
to papillary muscles in left ventricle SYSTEMIC VS. PULMONARY
O Prevents blood backflow back into left CIRCULATION
atrium • Pulmonary, systemic circulation both pump
same amount of blood
Semilunar valves
• Located where two major arteries leave Pulmonary circulation
ventricles • Low pressure system
• Pulmonary valve • Right side of heart pumps deoxygenated
O Three half-moon shaped cusps blood through pulmonary circulation to
collect oxygen
O Prevents blood backflow into right
ventricle 'Right atrium - right ventricle -
pulmonary arteries - lungs
• Aortic valve
O Three cusps Systemic circulation
O Prevents blood backflow into left • High pressure system
ventricle • Left side of heart pumps oxygenated blood
to systemic circulation
Blood flow physiology
' Pulmonary veins - left atrium - left
• Deoxygenated blood enters right side of
ventricle - aorta - body
heart via superior, inferior vena cava (veins)
' Left ventricle three times thicker than
• Coronary sinus (tiny right atrium opening)
right ventricle (l systemic circulation
collects blood from coronary vessels -
resistance)
right atrium - tricuspid valve - right

SEMllUNARVALVES
PULMONARY VALVE.

AORTIC VALVE.

CHOROAE. TE.NOINE.AE.
ATRIOVENTRIC.UlARVALVES
- - PAPILLARY MUSCLE.
TRICUSPIO VALVE.

81CUSPIO/MITRAL VALVE.-~~~~:::::~~

Figure 14.4 The four heart valves. The chordae tendineae and papillary muscles attached to the
atrioventricular valves prevent blood backflow into the atria.

3
 14. SOOY~(-------,

5. PULMONARY VALVE
13.AORTA

t s· PULMONARY ARTERIES-~
.~

1. LUNGS
-""""""" i. PULMONARY VEINS ( /
"\. LEFT ATRIUM
a. RIGHT ATRIUM
10. MITRAL/BICUSPIO VALVE
3. TRICUSPIO VALVE
11. LEFT VENTRICLE

...I~.....,-1:t. AORTIC VALVE

Figure 14.5 Blood flow physiology starting with the superior and inferior vena cavae bringing
deoxygenated blood from the body to the right atrium of the heart.

VENTRICULAR SYSTOLE VS. of four heart chambers

DIASTOLE • 15% (750ml/0.2gal) in systemic arteries
, 15% to brain
Systole
, 5% nourishes heart
• Ventricular contraction/atrial relaxation
, 25% to kidneys
• Occurs during Sl sound
, 25% to GI organs
O Aortic, pulmonic valves open ----. blood
pushed into aorta, pulmonary arteries , 25% to skeletal muscles
• Systolic blood pressure , 5% to skin
O Arterial pressure when ventricles • 5% (250ml/0.07gal) in systemic capillaries
squeeze out blood under high pressure • 65% (3.25L/0.86gal) in systemic veins
O Peripheral pulse felt • Numbers can change (e.g. exercise)

Diastole
• Ventricular relaxation/atrial contraction
BLOOD FLOW TERMINOLOGY
• Occurs during S2 sound Preload
O Tricuspid, mitral valves open ----. blood • Amount of blood in left ventricle before
fills ventricles contraction
• Diastolic blood pressure • Determined by filling pressure (end diastolic
O Ventricles fill with more blood (lower pressure)
pressure) • "Volume work" of heart

Afterload
BLOOD DISTRIBUTION
• Resistance (load) left ventricle needs
• Average adult: 5L/1.32gal total blood to push against to eject blood during
volume (not cardiac output) contraction
• 10% of total volume (approx. • "Tension work" of heart
500ml/0.13gal) in pulmonary arteries,
• Components include
capillaries, pulmonic circulatory veins
, Amount of blood in systemic circulation
• 5% of total volume (250ml/0.07gal) in one

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O Degree of arterial vessel wall Venous return
constriction (for left side of heart, main • Blood-flow from veins back to atria
afterload source is systemic arterial
resistance; for right side of heart, main Ejection fraction (EF)
afterload source is pulmonary arterial • Percentage of blood leaving heart during
pressure) each contraction
• EF = (stroke volumeend diastolic volume) *
Stroke volume (SV)
100
• Blood volume (in liters) pumped by heart
per contraction Frank-Starling Mechanism
• Determined by amount of blood filling • Ventricular contraction strength related to
ventricle, compliance of ventricular amount of ventricular myocardial stretch
myocardium • Maximum contraction force achieved
when myocardial actin, myosin fibers are
Cardiac output (CO)
stretched about 2-2.5 times normal resting
• Blood volume pumped by heart per minute length
(L/min)
• CO= SV * heart rate
BLOOD VESSEL LAYERS ("TUNICS")
• Example
O SV = 70ml ejected per contraction Tunica intima (interna)
o HR= 70bpm • Innermost layer
° CO = 70 * 70 = 4900ml/min = 4.9L/min

A. ADULT .., S LITERS oJ BLOOD

15%(0.?5 l) ~ 10%(0.5 l)
ARTERIES ( PVLMONARY
G1RC..ULAT10N

SYSTEMIC, 5%(0.~5 l) -{ •
GIRC..ULATION CAPILLARIES ( 1 •

,5% (S.~5 l) ~
VEINS

HEART

B. SYSTEMIC. ARTERIAL BLOOD DISTRIBUTION

Figure 14.6 A: Total blood volume distribution in an average adult. B: Systemic arterial blood
distribution.
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• Endothelial cells create slick surface for Types
smooth blood flow • "Elastic" arteries (conducting arteries)
• Receives nutrients from blood in lumen , Lots of elastin in tunica externa, media
• Only one cell thick , Stretchy; allows arteries to expand,
O Larger vessels may have subendothelial recoil during systole, diastole
basement membrane layer (supports , Absorbs pressure
endothelial cells) , Largest arteries closest to heart (aorta,
main branches of aorta, pulmonary
Tunica media
arteries) have most elastic in walls
• Middle layer
• Muscular arteries (distributing arteries)
• Mostly made of smooth muscle cells, elastin
, Carry blood to organs, distant body
protein sheets
parts
• Receives nutrients from blood in lumen
, Thick muscular layer
Tunica externa • Arterioles (smallest arteries)
• Outermost layer , Artery branches when they reach
• Made of loosely woven fibers of collagen, organs, tissues
elastic , Major systemic vascular resistance
O Protects, reinforces blood vessel; regulators
anchors it in place , Bulky tunica media (thick smooth
• Vaso vasorum ("vessels of the vessels") muscle layer)
O Tunica externa blood vessels are very , Regulate blood flow to organs, tissues
large, need own blood supply , Contract (vasoconstriction) in response
to hormones/autonomic nervous system,
! blood/j systemic resistance
ARTERIES
, Vasodilate (relax) I blood flow to
Key features organs/tissues, ! systemic resistance
• High pressure, thicker than veins, no valves , Ability to contract/dilate provides
thermoregulation

VEINS
Key features
• Low pressure
1. Tut..11£..A ItJTIM~ • Cannot tolerate high pressure but are
distensible e- adapts to different volumes,
a. i\ltJIC.A ~E.DIA pressures
• Have valves (folds in tunica interna)
3. TUNIC.A £)(TflltJA
to resist gravity, keep blood flowing
unidirectionally heart

Types
• Venules: small veins that connect to
capillaries

CAPILLARIES
• Only one cell thick (flat endothelial cells)
• Oxygen, carbon dioxide, nutrients,
Figure 14.7 The three layers, or "tunics," of a metabolic waste easily exchanged between
blood vessel.
tissues; circulation through capillary wall by
diffusion

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• Fluid moves out of vessel, into interstitial Key features
space (space between blood vessels, cells) • Moves large amounts of water, substances
O Water-soluble substances (ions) cross in same direction through fenestrated
capillary wall through clefts, between capillaries
endothelial cells, through large pores in • Material movement
fenestrated capillary walls • Faster transport method
O Lipid-soluble molecules (oxygen, • Regulates blood, interstitial volume
carbon dioxide) dissolve, diffuse across
• Filtration, reabsorption
endothelial cell membranes
• Continuous fluid mixing between plasma,
interstitial fluid
BULi( FLOW
• Passive water, nutrient movement across Types
capillary wall down concentration gradient • Filtration: bulk flow when moving from
blood to interstitium
• Reabsorption: bulk flow when moving from
interstitium to blood

Other characteristics
• Kidney: major site of bulk flow where
waste products are filtered out, nutrients
reabsorbed
• Fluid filters out of capillaries into interstitial
space (net filtration) at arteriolar end,
reabsorbed (net reabsorption) at venous
end
A\?T~IZIOLE. , Hydrostatic interstitial fluid pressure
draws fluid into capillary
, Hydrostatic capillary pressure pushes
fluid out of capillary
, Colloid interstitial fluid pressure pushes
fluid out of capillary
, Colloid capillary pressure draws fluid
into capillary

MICROCIRCULATION
• Microcirculation: arterioles + capillaries +
venules
• Arteriole blood flow through capillary bed,
to venule (nutrient, waste, fluid exchange)
, Capillary beds composed of vascular
shunt (vessel connects arteriole, venule
M£.TA AftfflllOLf. V~tJULE. to capillaries), actual capillaries

'-------~
r \ , Terminal arteriole - metarteriole -
thoroughfare channel - postcapillary
venule
, Precapillary sphincter: valve regulates
blood flow into capillary
, Various chemicals, hormones,
Figure 14.8 Key features of different blood vasomotor nerve fibers regulate amount
vessel types. of blood entering capillary bed

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 LYMPHATIC ANATOMY &
PHYSIOLOGY
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LYMPHATIC SYSTEM • Carries particles away from inflammation
sites/injury towards bloodstream, stopping
Function first through lymph nodes that filter out
• Fluid balance harmful substances
O Returns leaked interstitial fluid, plasma • Overlapping endothelial cells create valves;
proteins to blood, heart via lymphatic prevent backflow, infectious spread
vessels • Lacteals: specialized lymphatic capillaries
O Lymph: name of interstitial fluid when in found in small intestine villi
lymph vessels , Carry absorbed fats into blood
OLymphedema: lymph dysfunctional/ , Chyle: fat-containing lymph
absent (lymph node removal in cancer)
- edema forms Larger lymphatics
• Immunity • Capillaries - collecting vessels - trunks -
• Fat absorption ducts - angle of jugular, subclavian veins;
right lymphatic duct empties into right
Lymphatic capillaries angle, thoracic into left
• Collect interstitial fluid leaked by capillaries • Collecting vessels have more valves, more
• Found in all tissues (except bone, teeth, anastomoses than veins
marrow) , Superficial collecting vessels follow
O Microscopic dead-ended vessels unlike veins
blood capillaries, helps fluid remain , Deep collecting vessels follow arteries
inside • Lymphatic trunks
O Usually found next to blood capillaries , Paired: lumbar, bronchomediastinal,
• Lymph moves via breathing, muscle subclavian, jugular
contractions, arterial pulsation in tight , Singular: intestinal
tissues

LYr\f~A1'lC.
C.A PlllAth( ~

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Figure 14.9 Lymphatic vessels collect interstitial fluid (which is then called lymph) and return
it to the veins. Lymphatic capillaries have minivalves that open when pressure in the interstitial
space is higher than in the capillary and shut when pressure in the interstitial space is lower.
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Figure 14.10 Lymphatic system structures and their locations in the body.

• Ducts , Found in larger organs (lymph nodes)/

O Upper right lymphatic drains right arm; individually (mucosa)
right thorax; right side of head, neck
O Thoracic duct drains into cisterna chyli LYMPHOID ORGANS
(a dilation created to gather all lymph
drained from body area that's not Spleen
covered by upper right lymphatic duct) • Largest lymphoid tissue in body
• Located below left side of diaphragm
LYMPHOID CELLS • Blood supplied by splenic artery; blood
• Lymphocytes: T subtype activate immune leaves spleen via splenic vein
response; B subtype - plasma cells, , Capsules with projections into organ.
produce antibodies form splenic trabeculae
• Macrophages: important in T cell activation, • Function
phagocytosis , Macrophages remove foreign particles,
• Dendrocytes: return to nodes from pathogens from blood
inflammation sites to present antigens , Red blood cell turnover
• Reticular cells: similar to fibroblasts; create , Compound storage (e.g. iron)
mesh to contain other immune cells , Platelet/monocyte storage
, Blood reservoir: stores about
LYMPHOID TISSUES 300mU0.08gal
• Reticular connective tissue , Fetal erythrocyte production
• Composition: macrophage-embedded • Histology
reticular fibers , White pulp: lymphocyte, macrophage
• Loose islands that surround central arteries
O Diffuse lymphoid tissue , Red pulp: composed mostly of red
O Venules enter. filters blood blood cells. macrophages; macrophages
remove old red blood cells, platelets;
° Found in all organs
splenic cords (reticular tissues running
• Dense between venous sinusoids)
° Follicles/nodules

O Mostly contain germinal centers

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3. ANTIBODY

LYMPH
~~ DRAINS inlo
LYMPH NODES

Figure 14.11 In lymph nodes, dendritic cells present pieces of pathogens they come across to B
cells. If a dendritic cell presents something foreign to a B cell, the B cell turns into a plasma cell
and starts secreting antibodies, which flow into the lymph and exit the lymph node.

Figure 14.12 Spleen location, histology.

Lymph nodes • Kidney-shaped formations

• Hundreds scattered throughout body, often , Built like tiny spleens, 1-25cm/0.4-9.8in
grouped along lymphatic vessels long
O Superficial, deep , Covered by capsule with trabeculae,
O Many found in inguinal, axillary, cervical extend inward; trabeculae divide nodes
regions sectionally
• Function • Cortex
O Lymph filtration, immune system , Subcapsular sinus, lymphoid follicle,
activation germinal center
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• Medulla Appendix
O Medullary cord, medullary sinus • Worm-like large bowel extension
• Lymph flows through afferent lymphatic • Contains numerous lymphoid follicles
vessels - enters node through hilum - • Fights intestinal infections
subcapsular sinus - cortex - medullary
sinus - exiting via efferent lymphatic
vessels in hilum
° Fewer efferent vessels than afferent
vessels, slows traffic down - allows
node to filter lymphatic fluid
• Swollen painful nodes indicate
inflammation, painless nodes may indicate
cancer

Thymus
• Located between sternum, aorta in
mediastinum
• Two lobes, many lobules composed of
cortex, medulla
° Cortex: T lymphocyte maturation site
(immature T lymphocytes move from
bone marrow to thymus for maturation)
O Medulla: contains some mature T
lymphocytes, macrophages, cell-clusters Figure 14.13 Thymus location.
called thymic corpuscles (corpuscles
contain special T lymphocytes
thought to be involved in preventing
autoimmune disease)
• Lymphocyte production site in fetal life
__......._ -
O Active in neonatal, early life; atrophies
with age

Bone marrow
• 8 cells: made, mature in bone marrow
• T cells: made in bone marrow, mature in
thymus

Mucosa-associated lymphoid tissue (MALT)

• Lymphoid tissue that is associated with
mucosal membranes
• Tonsils: lymphoid-tissue ring around
pharynx
Figure 14.14 Tubal, pharyngeal (adenoid),
O Have crypts (epithelial invaginations)
palatine, and lingual tonsils create a
which trap bacteria
lymphoid-tissue ring around pharynx.
O Palatine: paired tonsils on each side
of pharynx (largest tonsils, most often
inflamed)
O Lingual: near base of tongue
O Pharyngeal: near nasal cavity (called
adenoid when inflamed)
O Tubal: near Eustachian tube
• Peyer's patches: small bowel MALT

11
 NORMAL HEART SOUNDS
osms.i"l/ n0Tmo.l-hec11·-l-sounds
HEART SOUNDS 51 heart sound
• "Lub": low-pitched sound
Causes
• Marks beginning of systole/end of diastole
• Opening I closing cardiac valves
• Early ventricular contraction (systole) --->
• Blood movement: into chambers, through
ventricular pressure rises above atrial
pathological constrictions, through
pressure---> atrioventricular valves close-«
pathological openings
Sl
• 51: mitral, tricuspid closure
WHERE ARE THEY HEARD? , Intensity predominantly determined by
• By auscultating specific points individual mitral valve component, loudest at apex
sounds can be isolated • Sl (lub) louder, more resonant than 52
O These points are not directly above (dub)
their respective valves, but are where • Sl displays negligible variation during
valve sounds are best heard; however, breathing
they generally map a representation of
different heart chambers 52 heart sound
• Knowing normal heart size, auscultation • "Dub": higher-pitched sound
locations allows for enlarged (diseased) • Marks end of systole/beginning of diastole
heart detection • 52: semilunar valves (aortic, pulmonic) snap
shut at beginning of ventricular relaxation
Optimal auscultation sites
(diastole) ---> short, sharp sound
• Aortic valve sounds: 2nd intercostal, right
• Best heard at Erb's point, 3rd intercostal
sternal margin
space on left, medial to midclavicular line
• Pulmonary valve sounds: 2nd intercostal
• Splits on expiration
space, left sternal margin
, During expiration S2 split into earlier
• Tricuspid valve sounds: 4t5th intercostal, left
aortic component; later, softer pulmonic
sternal margin
component (A2 P2). Lower intrathoracic
• Mitral valve sounds: 5th intercostal space,
pressure during inspiration ---> f right
midclavicular line (apex)
r
ventricular preload ---> right ventricular
systole duration ---> delays P2
NORMAL HEART SOUNDS , ! left ventricular preload during
• Two sounds for each beat inspiration ---> shorter ventricular systole,
O Lub (Sl), dub (S2) earlier A2
• Factors affecting intensity , A2, P2 splitting during inspiration
O Intervening tissue, fluid presence, usually about 40ms
quantity , A2, P2 intensity roughly proportional
O Mitral valve closure speed (mitral valve to respective systemic. pulmonary
circulation pressures
contraction strength)
, P2 best heard over pulmonic area

12
 Fl~ST HEAR.T SOUND (s1)

HITlAL UAUIE.

SECO~D HE~RT SOUNI) {S2)

Aomc VALVE

PULHONAlY V~
Figure 14.15 Valves that close to produce Sl and S2 sounds and optimal auscultation sites.

ABNORMAL HEART SOUNDS

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ABNORMAL S1 drift towards each other before onset of
systole
Loud 51
, Shorter PR interval - less time to drift
• As left ventricle fills, pressure increases closure - wider closure distance -
• As left atrium empties, pressure increases louder Sl
as it empties against increasingly pressure- , Short PR interval - incomplete
loaded ventricle; as atrium approaches ventricular emptying - higher
empty, pressure begins to decrease ventricular filling pressure - ventricular
• Differential diagnosis: short PR interval, pressure crosses critical atrioventricular
mild mitral stenosis, hyperdynamic states valve closing threshold while atrial
• Short PR interval (< 120ms) pressures are still high - load snap
O Normally atrioventricular valve leaflets

13
• Mild mitral stenosis ventricle
O Significant force required to close
stenotic mitral valve-« large ABNORMALsa
atrioventricular pressure gradient
required Split52
O Slam shut with increased force, • Physiological S2 splitting
producing loud sound , Expiration: Sl A2P2 (no split)
• Hyperdynamic states , Inspiration: Sl A2 .... P2 (40ms split)
O Shortened diastole ----. large amount of • Wide split
ongoing flow across valve during systole
, Detection: splitting during expiration
----. leaflets wide apart, pressure remains
, Expiration: Sl A2 .. P2 (slight split)
high
, Inspiration: Sl A2 P2 (wide split)
O Results in forceful atrioventricular valve
closure , Differential diagnosis: right bundle
branch block, left ventricle preexcitation,
Soft51 pulmonary hypertension, massive
• Differential diagnosis: long PR intervals, pulmonary embolism, severe mitral
severe mitral stenosis, left bundle branch regurgitation, constrictive pericarditis
block, chronic obstructive pulmonary • Fixed split
disease (COPD), obesity, pericardia! , Splitting during both expiration,
effusion inspiration; does not lengthen during
• Long PR intervals (> 200ms) inspiration
O Atrium empties fully----. low pressure , Expiration: Sl A2 .. P2 (slight split)
----. low ventricular pressure required , Inspiration: Sl A2 .. P2 (slight split)
to close atrioventricular valves ----. , Differential diagnosis: atrial septal
valves close when ventricle is in early defect, severe right ventricular failure
acceleration phase (low pressures) ----.
• Reversed split
soft sound
, Split during expiration, but not
• Severe mitral stenosis
inspiration
O Leaflets too stiff, fixed to change
, Expiration: Sl P2 .... A2 (moderate split)
position
, Inspiration: Sl P2A2
Variable 51 , Differential diagnosis: left bundle branch
• Auscultatory alternans block, right ventricle preexcitation, aortic
O When observed with severe left stenosis/AR
ventricular dysfunction, correlate of
Abnormal single 52 variants
pulsus alternans
• Loud P2
• Differential diagnosis: atrioventricular
dissociation, atrial fibrillation, large , Expiration: Sl A2P2
pericardia I effusion, severe left ventricular , Inspiration: Sl A2 .... P2!
dysfunction , Diagnosis: pulmonary hypertension
• Left ventricular outflow obstruction
Split51
, Absent A2
• Sl usually a single sound
, Expiration: Sl P2
O Near-simultaneous mitral, tricuspid
, Inspiration: Sl P2
valve closures; soft intensity of tricuspid
valve closure , Diagnosis: severe aortic valve disease
• Splitting usually from tricuspid valve closure • Fused A2/P2
being delayed relative to mitral valve , Expiration: Sl A2P2
closure , Inspiration: Sl A2P2
• Differential diagnosis: right bundle , Differential diagnosis: ventricular septal
branch block, left-sided preexcitation, defect with Eisenmenger's syndrome,
idioventricular rhythm arising from left single ventricle
14
ADDED HEART SOUNDS • Auscultatory summary: SL. S2.S3 ... Sl

53 heart sound 54 heart sound

• S3 (ventricular gallop) • S4 (atrial gallop): low pitched late diastolic
O Low-pitched early diastolic sound (pre-systolic) sound, best heard in mitral/
O Best heard in mitral/apex region apex region, left lateral decubitus position
O Left lateral decubitus position • Associated with hypertension, left
ventricular hypertrophy, ischaemic
• Associated with volume overload
cardiomyopathy
conditions
• Pressure overload: thought to be caused by
• Early diastolic sound, produced in rapid
atrial contraction into stiff I non-compliant
filling phase - excessive volume filling
ventricle
ventricle in short period - rapid filling -
chordae tendineae tensing - S3 sound • Chronic heart contraction effort against
increased pressure - hypertrophy - stiff
• Children/adolescents: may be normal
ventricle (concentric hypertrophy)
• Middle aged/elderly person: usually
• Always pathological
pathological
• Auscultatory summary: S4.Sl...S2 ... S4.Sl
O Over 40 years old: indicative of left
ventricular failure

A. NORHAL ''LUS" ''DUB''

DIASTOLE: SYSTOLE DIASTOLE:

St St

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8.S3
I 11
''LU8"

OIASTOL[ SYSTOLE

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11 I
C. S'-1 "TA'' ''LUB" ''DUB''

OIASTOL[ SYSTOLE DIASTOL[

SL'+ St St • STIFF
; • HVPE~TeOPH1£()

\\

Figure 14.16 Linear representation of A: normal (Sl, S2), 8: S3, and C: S4 heart sounds.
15
Summation gallop • Location
• Superimposition of atrial, ventricular gallops , Location on chest wall where murmur is
during tachycardia best heard
• Heart rate I - diastole shortens more than • Radiation
systole - S3, S4 brought closer together , Location where murmur is audible
until they merge despite not lying directly over heart
, Generally radiate in same direction as
HEART MURMURS turbulent blood is flowing
, Aortic stenosis: carotid arteries
Key features
, Tricuspid regurgitation: anterior right
• Blood flow silent when laminar, thorax
uninterrupted
, Mitral regurgitation: left axilla
• Turbulent flow may generate abnormal
• Shape
sounds (AKA "heart murmurs")
, How sound intensity changes from
• Murmurs can be auscultated with
onset to completion
stethoscope
, Shape determined by pattern of
Causes pressure gradient driving turbulent flow,
• May be normal in young children, some loudest segment occurring at time of
elderly individuals greatest gradient (moment of highest
velocity)
• ! blood viscosity (e.g. anaemia)
, Three basic shapes: crescendo-
• ! diameter of vessel, valve, orifice (e.g.
decrescendo, uniform (holosystolic when
valvular stenosis, coarctation of aorta,
occurring during systole), decrescendo
ventricular septal defect)
, Crescendo-decrescendo, uniform
• j blood velocity through normal structures
generally systolic; decrescendo murmurs
(e.g. hyperdynamic states-sepsis,
generally diastolic
hyperthyroid)
• Regurgitation across incompetent valve
(e.g. valvular regurgitation)
C~tSCENDO - OECfESCENDO MURMUR
Describing heart murmurs
l~I
• Specific language used to describe
murmurs in diagnostic workup DIASTOLE: DIASTOLE:
• Timing: refers to timing relative to cardiac S~STOLE
cycle S1 S1
O Systolic "flow murmurs": aortic,
pulmonic stenosis; mitral, tricuspid t>ECRESlEUDO HURHUi
regurgitation; ventricular septal defect;

°
aortic outflow tract obstruction
Diastolic: aortic, pulmonic regurgitation;
mitral, tricuspid stenosis
Continuous murmurs are least common,
IS1
SYSTOLE I
S1
~··
DIASTOLE I
·1

51
generally seen in children with
congenital heart disease (e.g. patent UNlfORH HURHUR
ductus arteriosus, cervical venous hum) CLICK
O Occasionally may have two related
murmurs, one systolic, one diastolic;
gives impression of continuous murmur
(e.g. concurrent aortic stenosis, aortic
I ~"·- I
51 S1

regurgitation) Figure 14.17 Three basic heart murmur

shapes: crescendo-decrescendo,
decrescendo, uniform/holosystolic.

16
• Pitch , ! intrathoracic pressure - j pulmonary
O High pressure gradients - high pitched venous return to right heart - j right
murmurs (e.g. mitral regurgitation, heart stroke volume - right sided
ventricular septal defect) murmurs - t intensity
O Large volume of blood-flow across , Dilation of pulmonary vascular system
low pressure gradients - low pitched - ! pulmonary venous return to left
murmurs (e.g. mitral stenosis) side of heart - ! left heart stroke
O If both high pressure, high flow volume - left side murmurs - !
(severe aortic stenosis), both high, low intensity
pitches are produced simultaneously • Expiration
- subjectively unpleasant/"harsh" , j intrathoracic pressure - ! venous
sounding murmur return to right heart - ! right ventricle
• Intensity stroke volume - ! intensity of right
O Murmur loudness graded on scale from sided murmurs
I-VI , j pulmonary venous return to left side
O Dependent on blood velocity generating - I left ventricle stroke volume - left
murmur; acoustic properties of sided murmur - t intensity
intervening tissue; hearing; examiner • Valsalva maneuver
experience; stethoscope used, ambient , Forceful exhalation against closed glottis
noise presence , ! venous return to heart - ! left
O I: barely audible ventricular volume - I cardiac output
O II: faint, but certainly present , Murmurs of hypertrophic obstructive
O Ill: easily, immediately heard cardiomyopathy, occasionally mitral
O IV: associated with thrill (palpable valve prolapse - t intensity
vibration over involved heart valve) , All other systolic murmurs - ! intensity
O V: heard with only edge of stethoscope • Isometric handgrip
touching chest wall , Squeeze two objects (such as rolled
O VI: heard without stethoscope (or towels) with both hands
without it making direct contact with , Do not simultaneously Valsalva
chest wall) , If unconscious. simulate by transient
• Quality arterial occlusion (BP cuffs applied
O Subjective, attempt to describe timbre, to both upper arms, inflated to 20-
depends on how many different base 40mmHg above systolic blood pressure
frequencies of sound are generated, for 20 seconds)
relative amplitude of various harmonics ' j venous return, l sympathetic tone -
O Mitral regurgitation: blowing/musical j heart rate, systemic venous return
O Mitral stenosis: rumbling - l cardiac output - murmurs from
mitral regurgitation, aortic regurgitation,
O Aortic stenosis: harsh
ventricular septa I defect - t intensity
O Aortic regurgitation: blowing
, Murmur from hypertrophic obstructive
O Still's murmur (benign childhood): cardiomyopathy - ! intensity
musical
, Murmur from aortic stenosis - most
O Patent ductus arteriosus: machine-like commonly unchanged
Diagnostic maneuvers (dynamic • Leg elevation
auscultation) 'Lying supine, both legs raised 45°
• Some maneuvers may elicit characteristic ' j venous return - f left ventricular
intensity/timing changes (changes in volume
hemodynamics during maneuvers) , Murmur from hypertrophic obstructive
• Dynamic auscultation: listening for subtle cardiomyopathy - ! intensity
changes during physical maneuvers , Murmurs from aortic stenosis. mitral
• Inspiration regurgitation may - t intensity

17
• Muller's maneuver , Radiates to neck/carotids (murmur
O Nares closed, forcibly suck on incentive occurs in aorta, these are its first
spirometer/air-filled syringe for 10 branches)
seconds (conceptual opposite of , Auscultatory summary: Sl. Ejection
Va Isa Iva) click. Crescendo-decrescendo murmur.
0 I venous return-« ! left ventricular S2
volume e- ! systemic venous resistance • Pulmonic stenosis
murmur from hypertrophic obstructive , Pulmonary valve auscultation site: 2nd
rnvopathv -e j intensity intercostal space, left sternal margin
O Murmur from aortic stenosis may---'> I , Sl, closing of tricuspid valve, during
intensity systole
• Squatting to standing , Heart contracts against closed pulmonic
O Abruptly stand up after 30 seconds of valve c- pressure builds during systole,
squatting forcing open stenotic pulmonic valve e-
0 I venous return-« ! left ventricular valve pops open ---'> ejection click
volume , Flow rate increases as heart contracts
O Murmur from hypertrophic obstructive more forcefully to empty right ventricle
cardlomvopathv-« j intensity ---'> murmur gets louder as flow across
O Murmur from aortic stenosis may---'> I partially open valve lncreases=-.
intensity chamber empties---'> pressure, flow
diminishing ---'> ! murmur intensity
• Standing to squatting
, Radiates to neck/carotids, back
° From standing upright, squat down
, Auscultatory summary: Sl. Ejection
O If unable to squat, examiner can
click. Crescendo-decrescendo murmur.
passively bend knees up towards
S2
abdomen to mimic maneuver
• Mitral regurgitation
O j venous return-e j left ventricular
volume , Mitral valve auscultation site: 5th
intercostal space, midclavicular line/apex
O Murmur from hypertrophic obstructive
, Holo-/pansystolic murmur (occurs for
cardiornvopathv -e ! intensity
systole duration)
O Murmur from aortic stenosis may - j
intensity , Normal Sl as mitral valve closes e-
in mitral regurgitation, valve cannot
O Murmur from aortic regurgitation ---'> T
completely close ---'> pressure builds in
intensity
left ventricle (with closed aortic valve)
Systolic murmurs ---'> blood forced back through partially
closed mitral valve e- murmur occurs
• Aortic stenosis
along with Sl as long as pressures
O Aortic valve auscultation site: 2nd
remain high enough
intercostal, right sternal margin
, Aortic valve will open to redirect
O Sl, closing of mitral valve, during
majority of blood ---'> left ventricle
systole---'> heart contracts against closed
continues contracting ---'> continuously
stenotic aortic valve---'> pressure must
raised pressures ---'> blood continuously
rise during systole to force open stenotic
flowing through partially closed mitral
aortic valve c- valve pops open ---'>
valve (whole of systole)
produces ejection click
, As heart continues to contract, pressure
° Followed by j flow as heart contracts
j, but atrium becomes more compliant.
more forcefully to empty left ventricle Even though blood-flow across partially
---'> murmur intensity l as flow across
closed valve may l, pressure in atrium
partially open valve j
does not significantly increase
° Chamber begins to empty---'> pressure,
, Left ventricle pressure notably higher
flow diminish ---'> ! murmur intensity
than left atrium ---'> sound does not

18
 change throughout murmur mitral regurgitation may follow
O Referred to as "flat" murmur because , Auscultatory summary: Sl. Mid systolic
intensity does not change click with late systolic murmur. S2
O Radiates to axilla due to direction of
Diastolic murmurs
regurgitant jet
• Aortic regurgitation
O Auscultatory summary: Sl. Flat
murmur. S2 , Aortic regurgitation auscultation site:
left parasternal border
• Tricuspid regurgitation
, Blood flows back through incompletely
O Tricuspid valve auscultation site: 4/5th
closed aortic valve
intercostal, left sternal margin
, Occurs between S2, Sl
O Holo-/pansystolic murmur
, S2, aortic valve closure e- mitral valve
O Normal Sl occurs due to tricuspid
opens, heart in diastole ---'> blood enters
valve closure e- pulmonic valve closed,
left ventricle through regurgitant valve,
pressure rises in right ventricle
through normal filling via mitral valve
O In tricuspid regurgitation, valve cannot
, Initially, low pressure in ventricle
completely close ---'> pressure builds in
(compared to systemic blood pressure
right ventricle c- blood forced back out
forcing blood through regurgitant valve)
through partially closed tricuspid valve
---'> ventricle fills ---'> as pressure mounts,
---'> murmur is continuous as long as
less flow through regurgitant valve-»
pressures remain high enough
decrescendo murmur
O Pulmonic valve opens to redirect blood
, Early diastolic decrescendo murmur
---'> left ventricle maintains contraction
(thus raises pressure) ---'> blood , Auscultatory summary: Sl. S2. Early
continues flowing through partially diastolic decrescendo murmur. Sl
closed tricuspid valve (through whole • Pulmonic regurgitation
systole) , Pulmonic regurgitation auscultation
O Arium becomes more compliant as it fills site: upper left parasternal border
---'> atrium pressure does not significantly , Blood flows back through incompletely
increase closed pulmonic valve
O Right ventricle pressure notably higher , Occurs between S2, Sl
than that of right atrium ---'> murmur , S2 aortic valve closure ---'> tricuspid valve
sound does not change throughout opens, heart in dlastole e- incomplete
murmur pulmonic valve closure-» right ventricle
O Referred to as "flat" murmur (intensity fills via incompletely closed pulmonic
does not change) valve as well as tricuspid valve
O Auscultatory summary: Sl. flat murmur. , Initially---'> low ventricle pressure allows
S2 for high flow through regurgitant
• Mitral valve prolapse valve e- pressure rises, ! flow through
O Mitral valve auscultation site: 5th regurgitant valve---'> decrescendo
intercostal space. midclavicular line/apex murmur
O Mitral valve billows into left atrium ---'> , Early diastolic decrescendo murmur
clicking sound (unlike aortic stenosis, , Auscultatory summary: Sl. S2. Early
not associated with ejection of blood, diastolic decrescendo murmur. Sl
non-ejection click, mid-late systolic) • Mitral stenosis
O Ventricle contracts ---'> mitral valve , Mitral valve auscultation site: 5th
closure-» Sl---'> pressure rises e- intercostal space, midclavicular line/apex
mitral valve accelerates into left atrium , Mitral valve can't open efficiently
---'> stops abruptly (chordae tendineae , S2 ---'> aortic valve closure ---'>
restraint) ---'> rapid tensing ---'> click
milliseconds later. mitral valve should
O Often associated with mitral open (fill ventricle during diastole), only
regurgitation ---'> after click murmur of small opening occurs

19
 afratafreeh.com exclusive

SVSTOLIC HURHURS

DIASTOLE: DIASTOLE:
SYSTOLE
S1 S1

STENOS IS AORTIC VALUE STEAIOSIS

L AORTIC. Of' PULHONIC VALV£

~~

PUU10NARY VALVE STEAIOSIS

RE&UiG.ITATION
L HITRAL or TRICUSPII> VALVE TilCUSPID VALVE
REGiUf&ITATION

HITlRL VALVE
REGiUfG.ITATION

HITRAL VALVE PROLAPSE VENTRAL SEPTAL DEFECT

- i. f S£V£~£ ENOUGH ~ * HOLOSYSTOLIC HugHUR
MITRAL REG.URGITATIOII
~IUH

~RICLE
c.
~
r
Figure 14.18 Causes of systolic murmurs.

20
 o Beginning of diastole, highest flow of
blood comes from left atrium to left DIACiTOLIC HURHURS
ventricle (rapid filling), fills more blood
''LUB" ''DUB''
at beginning of diastole (beginning due
'"WHOOSl1''
to highest pressure difference) ----> most
intense phase of murmur DIASTOLE: SVSTOLE DIASTOLE:
o Aortic valve closure e- mitral valve
opens, due to stenotic leaflets, they 51 S1
can only open slightly----> chordae
tendineae snap as limit is reached Figure 14.19 Diastolic murmurs are heard as
(similar to ejection snap) ----> opening a "whoosh" after S2.
snap from stenotic leaflets shooting
open (milliseconds after S2) ---->
highest intensity of murmur thereafter Murmur Identification
----> murmur diminishes as pressure • Detect murmur?
equalises , Yes/no
o End of diastole atrium contracts to • Identify phase?
force remaining blood into left ventricle
, Systoliddiastolic: Sl -systole- S2
----> atrial kick sound (presystolic
-diastole- Sl (in tachycardia, feel pulse
accentuation at end of murmur)
----, tapping ----> ejection phase, therefore
o Auscultatory summary: Sl. S2. Opening Sl)
snap. Decrescendo mid diastolic rumble.
• Which valves normally open/which valves
Atrial kick. Sl
normally closed
• Tricuspid stenosis
, Systole, aortic and pulmonic, open
o Tricuspid valve auscultation site: 4/51h (mitral and tricuspid, closed)
intercostal space, left sternal margin
, If systolic murmur, either open valves
o Tricuspid valve can't open efficiently stenotidclosed valves regurgitant (1/4
o S2----> pulmonic valve closure v- choice)
milliseconds later, tricuspid valve should , Diastole, mitral and tricuspid, open
open (fill ventricle during diastole), only (aortic and pulmonic, closed) (1/4
small opening occurs choice)
o Beginning of diastole, high flow of • To choose between four resultant options
blood comes from right atrium to right auscultate over respective areas, employ
ventricle (rapid filling), fills more blood maneuvers as required
at beginning of diastole (due to highest
pressure difference) ----> most intense
murmur phase MISCELLANEOUS HEART SOUNDS
o Pulmonic valve closure v- tricuspid • Mechanical valve clicks
valve opens (due to stenotic leaflets, , Distinctly audible, harsh, metallic sound
they can only open slightly) ----> chordae • Pericardia! knock
tendineae snap as limit is reached , Sound occasionally heard in constrictive
(similar to ejection snap) ----> opening pericarditis; similar in acoustics, timing
snap from stenotic leaflets shooting to S3
open (milliseconds after S2) ----> highest
• Tumor plop
murmur intensity thereafter----> murmur
, Rare low-pitched early diastolic sound,
diminishes as pressures equalise
occasionally heard in atrial myxoma
o End of diastole atrium contracts to
presence
force remaining blood into left ventricle
, Occurs when relatively mobile tumour
----> atrial kick sound (presystolic
accentuation at end of murmur) moves in front of mitral valve during
diastole e- functional mitral stenosis
o Auscultatory summary: Sl. S2. Opening
along with low pitched diastolic
snap. Decrescendo mid diastolic rumble.
rumbling murmur
Atrial kick. Sl
21
NOTES

:,~ NOTES
lJ 8lOOD PRESSURE REGULATION
REGULATION OF ARTERIAL using a sphygmomanometer
PRESSURE l.Wrap blood pressure cuff around upper
• Must be maintained at a constant level of arm just above elbow
-lOOmmHg 2.Rapidly inflate cuff until pressure in it
• Changes in blood pressure activate exceeds systolic pressure (up to around
baroreceptors and/or chemoreceptors 180mmHg) to stop blood flow
(fast response) and renin-angiotensin- 3.Press lightly with the stethoscope bell over
aldosterone system (slow response), the brachia I artery just below edge of cuff
causing a series of events that eventually 4.Reduce cuff pressure slowly and listen
bring blood pressure back to normal with stethoscope for sounds in the brachia!
(discussed later) artery while simultaneously observing the
• Central mechanisms regulating blood mercury gauge
pressure are cardiac output, peripheral , The first tapping sound (Korotkoff
resistance, and blood volume sound) represents systolic pressure
Cardiac output and peripheral resistance , When the tapping sound disappears, it
relate to blood pressure represents diastolic pressure
• P0 = cardiac output x TPR
O P. = mean arterial pressure HOMEOSTATIC IMBALANCES IN
° Cardiac output= cardiac output (ml/ BLOOD PRESSURE
min)
Normal blood pressure in adults
O TPR = total peripheral resistance
• Affected by age, weight, sex and race
(mmHg/mL/min)
• Systolic pressure: 90-120mmHg
• Mean arterial pressure varies directly
with cardiac output and total peripheral • Diastolic pressure: 60-80mmHg
pressure, can be changed by altering one
Hypertension
or both
• Chronically elevated blood pressure
• Blood pressure varies directly with blood
, Systolic pressure: > 140mmHg
volume because cardiac output depends on
blood volume , Diastolic pressure: > 90mmHg
° Cardiac output is equal to stroke volume
Hypotension
(ml/min) times heart rate (beats/min)
• Low blood pressure
O Normal is 5-5.5L/min
, Systolic pressure: <90mmHg
• P. is regulated by two mechanisms
, Diastolic pressure: <60mmHg
O Baroreceptor reflex: neurally mediated
• Often normal variation
(short-term, fast response)
• Acute hypotension
O Renin-angiotensin-aldosterone system:
hormonally mediated (long-term, slow , Can be a sign of circulatory shock
response) • Orthostatic hypotension
, Temporary drop in blood pressure
caused by rapidly standing up from a
MEASURING BLOOD PRESSURE
sitting or lying position
• Auscultatory method: an indirect method
, Common in the elderly
of measuring pressure by listening to
Korotkoff sounds in the brachia I artery • Chronic hypotension
, Often a sign of an underlying condition
22
 BARORECEPTORS
osms.i-l/\,o.roreeep-lors
BARORECEPTOR REFLEX INTEGRATED FUNCTION OF
• Short term, fast neural response to change BARORECEPTORS
in blood pressure
Response to increased P0
• Alters peripheral resistance and cardiac
• I firing rate: carotid sinus nerve
output
(glossopharyngeal nerve, CN IX), aortic
• Mediated by baroreceptor cells arch nerve afferent fibers (vagus nerve, CN
o Specialized nerve endings called X)
mechanoreceptors, located in aortic arch • Glossopharyngeal, vagus nerve fibers
and carotid sinus; sensitive to pressure synapse in nucleus tractus solitarius
or stretching of medulla, (transmits blood pressure
o Most sensitive to rapid pressure information)
changes • Nucleus tractus solitarius governs
• Carotid sinus baroreceptors: responsive to coordinated response series; returns P.
both decreases and increases in pressure down to normal levels
• Aortic arch baroreceptors: predominantly , j parasympathetic outflow to heart
responsive to increases in pressure , ! sympathetic outflow to heart, blood
• Change in blood pressure activates reflex vessels
arc • Decrease in sympathetic activity
o Baroreceptors - afferent neurons , Complements increase in
- brain stem centers - processing parasympathetic activity - decrease in
information and generating response - heart rate
efferent neurons - changes in the heart
, Decrease in cardiac contractility
and blood vessels
, Decreased heart rate + decreased
o Increase of blood pressure - stretching
cardiac contractility - decrease in
of baroreceptors - depolarizing
cardiac output- decrease of P. (P. =
receptor potential (higher rate action
cardiac output x TPR)
potential)
, Arteriolar vasodilation - decrease in
o Decrease of blood pressure -
TPR - decrease of P. ( P. = cardiac
decreased stretch of baroreceptors -
output x TPR)
hyperpolarizing potential {lower rate
action potential) • Vasodilation of veins - increased
compliance of veins - increased
• Sensitivity can be altered as a result of
unstressed volume - decreased
some diseases
stressed volume - reduction in P.
• Chronic hypertension: result is adaptation
• Once P reduced back to the set-point
of baroreceptors
pressure (i.e .. 100 mmHg), activity of the
o Baroreceptors are adjusted to monitor
baroreceptors and the cardiovascular
pressure changes at higher setpoint brainstem centers return to baseline level
• Atherosclerosis: carotid sinus syndrome
o Baroreceptors are more sensitive; even
light pressure on the carotid sinus can
cause extreme bradycardia

23
 8RAINSTEM PAMSYMPATHe:TjC.
OUTFLOW TRAC.T

MEDULLA S'{MPATHETIC. _1,,.:::;;;:::,.,;;;;t;~7-

OBLONGATA NUCLEUS NERVE FIBERS
TRAC.TUS
SOLITAP.IUS

(
t
'
ARTERIAL
~LOSSOPHAR~NGEAL
,._. (I')(.) CRANIALNE.RVE. BARORE.C£PTORS

Figure 15.1 Locations of arterial baroreceptors and pathways that transmit their signals.

CARDIOPULMONARY (LOW , ANP causes generalized vasodilation

PRESSURE)BARORECEPTORS , This vasodilatation in the kidney
• Located in the vena cava, pulmonary increases glomerular filtration rate
arteries and atria which results in increased Na2• and H20
• These baroreceptors are volume receptors - filtration and excretion - decreased
they detect changes in blood volume blood volume
• Increased blood volume and subsequent • Decreased secretion in ADH
increases in venous and atrial pressure are , Decreased water reabsorption in the
detected by cardiopulmonary baroreceptors collecting ducts - decreased blood
which generates several responses volume
• Increase of heart rate (Bainbridge reflex)
Cardiopulmonary baroreceptors responses
, Increased cardiac output - increased
• Secretion of atrial natriuretic peptide (ANP).
renal perfusion - increased Na· and
a polypeptide hormone secreted by the
H20 excretion
myocytes in the atrial wall

24
 GARl>IOPULMONAR'I BARORECEPTORS

PULMONARY
ARTERIES
I ; ;)!PULMONARY
' VEINS
',
C..ARDIOVASC..ULAR
RIG.HT "'--
vAG.USNERVE CENTERS
ATRIUM {
f--_ t HEAP.T RATE
&. t (C,0)
RIG.HT
VENTRICLE

Figure 15.2 Locations of cardiopulmonary baroreceptors and pathway that transmits their signals.

CHEMORECEPTORS
osmsJl/ ehemoY-eeep-loY-s
CHEMORECEPTOR REFLEX , Decrease of p02 causes an increase
• Blood pressure regulation pathway that in ventilation which decreases the
involves chemoreceptors for 02 in the aortic parasympathetic outflow to heart-» r
and carotid bodies heart rate----> I cardiac output
• Central and peripheral chemoreceptors
CENTRAL CHEMORECEPTORS
PERIPHERAL CHEMORECEPTORS • Located in the medulla
• Located in carotid bodies (near common • Most sensitive: C02, pH
carotid artery bifurcation, in aortic bodies • Less sensitive: 02
along aortic arch) • Reflex arc
• Very sensitive partial pressure of 02 , Decrease in brain blood flow---->
decreases increased pC02, decreased pH ---->
O Also sensitive to partial pressure of C02 chemoreceptors (afferent neurons)
increases (pC02), pH decreases increase firing of action potential
• Reflex arc (hyperpolarization potential) ----> efferent
O Decreased p02 ----> chemoreceptors neurons ----> increased sympathetic
(afferent neurons) increase firing of outftow -» arterial vasoconstriction in
action potential (hyperpolarization skeletal muscle, renal and splanchnic
potential) ----> efferent neurons----> circulation ----> increased total peripheral
increased sympathetic outflow ----> pressure
arterial vasoconstriction in skeletal
muscle, renal and splanchnic circulation
----> increased total peripheral pressure
• These chemoreceptors are also involved in
control of breathing

25
 CHE.MORE.C£PTORS
L P£RIPH£RAL
PAMSVMPATHETIG
OUTFLOW TRAC.T
SRAINSTE.M

RESPIRATOP.V SVMPATHETIC. _1.:::::::),._;;;t;:";;19-

C.£NTERS N£ R VE FIBERS

GiLOSSO-
PHARVNGi£AL UX)

AORTIC, 80DY

Figure 15.3 Locations of peripheral chemoreceptors and locations in the brainstem to which
they transmit their signals.

t PC.0.2
!pH \

C.E.NTRAL
C.HE.MOREC,f.PTORS ---..____
------:)~ VASOMOTOR
C,E.NT£R
~
ARTERIOLAR 1 V£NOUS
CONSTRICTION
!
t TOTAL PERIPHERAL
ReSJSTANC.£ ITPll
!
t 8LOOO PRESSURE IIPl

Figure 15.4 Central chemoreceptors are located in the medulla of the brainstem and are most
sensitive to changes in C02 and pH levels.

26
 RENIN-ANGIOTENSIN
ALDOSTERONE SYSTEM
osmsJl/ Y-enin-o.ngio-lensin_o.ldos-leY-one_s14s-lem

• Hormonally mediated, slow regulation of , Stimulates the synthesis and secretion

blood pressure of aldosterone in the glomerulosa cells
• Regulates P0 by regulating blood volume of the adrenal gland
, Aldosterone causes Na· reabsorption to
Direct renal mechanism increase in principal cells of renal distal
• Increase of P a causes increased filtration tubule, collecting duct
rate in the tubules , Increased Na- concentration -
• In this situation, the kidney cannot reabsorb increased osmolarity - increased ECF
filtrate fast enough - more fluid leaves the and blood volume
body in urine - blood volume and blood • Angiotensin II
pressure drops
, Stimulates Na·- H· exchange -
Indirect renal mechanism increased Na· reabsorption

• Renin-angiotensin aldosterone system , Stimulates antidiuretic hormone (ADH)

secretion
• Decrease of P and/or decrease of Na-
•
concentration causes decrease in kidney , Acts on hypothalamus (stimulates thirst,
perfusion which in turn causes a series of water intake)
events , Causes vasoconstriction of the arterioles
• Cells of the macula densa sense the change - increased total peripheral resistance
in blood volume/osmolarity and in turn (TPR)
stimulate renin production
Antidiuretic hormone (ADH)
O Renin is an enzyme secreted
• Hormone produced in hypothalamus,
by juxtaglomerular cells of the
secreted by pituitary gland's posterior lobe
juxtaglomerular apparatus of the
• Stimulated by low blood volume, increase
nephron
of serum osmolarity and angiotensin II
O Renal sympathetic nerves and beta-1
• Receptors for ADH
agonists also cause renin production
• Vl receptors: vasoconstriction of arterioles
• Renin converts angiotensinogen to
angiotensin I • V2 receptors: increase water reabsorption
by principal cells of the renal collecting duct
• Angiotensin-converting enzyme (ACE) in
the lungs and kidneys converts angiotensin
I to angiotensin II

27
 RENAL CORPUSCLE

AFF~T AltTE.(101.t

:J'V'ltTAC:,LOME.R\11.AR
c.tu.«i.
\

Figure 15.5 Macula densa cells are chemoreceptors located in the distal convoluted tubule.
When they sense a ! in P. and/or Na-. Cl, they stimulate renin production by nearby
juxtaglomerular cells. Renin initiates angiotensin II activation, which acts in multiple areas to
increase blood pressure.

E.F'F'tfUNT
Aitru,o~
C..ONSTRI,~
M~~THAl'II
AFF~fC£:NT
Lf6F'R
P~OtlMAL
TV&VI.E.
IU.AS~Oli:C!>S
MO!lf. N~•
L 1'·Hl\rit
l. t blooc.lprer.!.11~
A~£:NAL
,o~Ti"
0~1,,tot-1~
AN610T~N~IN ll
L Rttow, No•, ... tO

Figure 15.6 RAAS system summary.

28
 NOTES

MEASURING CARDIAC OUTPUT

I
FICI( PRINCIPLE
osms.i"l/Fiek-pTineiple
• Model used to measure cardiac output (CO) • 250mUminute = total 02 consumption
O Output of left, right ventricles equal (70kg, biologically-male individual);
during normal cardiac function pulmonary venous 02 content= 0.20/ml;
• Steady state: rate of 02 consumption = pulmonary arterial 02 content= 0.15/ml
amount of 02 leaving lungs via pulmonary
vein - amount of 02 returning via Cardiac Output=
pulmonary arteries x CO 250ml/min = 5000mL/min
0.20ml - 0.15ml
• Pulmonary blood flow of right heart= CO
of left heart: used to calculate CO
• Also measures blood flow to individual
Cardiac Output = organs
-----=-02consumption , Renal blood flow = renal 02
(02] pulmonary vein - (02] pulmonary artery consumption I renal arterial 02 - renal
venous 02

CARDIAC & VASCULAR FUNCTION

CURVES
osms.it/ ee1Tdie1e-e1nd-ve1seule1T-fune-lion-eu rvss
• Curves depicting functional connections independent variable; CO, dependent
between vascular system. right atrial variable
pressure, and CO , j venous retum-e- j RA pressure ----. l
LV end-diastolic volume (EDV)/preload,
CARDIAC FUNCTION CURVE (CO myocardial fiber stretch ----. j CO
CURVE) , LV CO (Umin)= LVvenous return/
• Plot of relationship between left ventricle preload (RA pressure in mmHg)
(LV) CO, right atrial (RA) pressure , Relationship remains intact with steady
state of venous return
• Based on Frank-Starling relationship
describing CO dependence on preload , RA pressure 4mmHg----. curve levels off
O Preload (determined by RA pressure). at maximum 9L/min

29
 VASCULAR FUNCTION CURVE Mean systemic pressure (MSP)
• Plot of relationship between venous return, • Pressure equal throughout vasculature
RA pressure • Influenced by blood volume, distribution

I • Independent
O

O
of Frank-Starling

pressure dependent variable

relationship
Venous return independent variable;

Venous return, RA pressure: inverse

relationship
• j RA pressure ----. ! pressure gradient
RA Total peripheral resistance (TPR)
• Primarily determined by pressure in
arterioles; determines slope of curve
• ! TPR (! arteriolar resistance) ----. j flow
from arterial to venous clrcufatton=-. j
venous return-« clockwise rotation of
between systemic arteries, RA ----. ! venous
curve
return to RA; CO
• I TPR (i arteriolar resistance) ----. ! flow
from arterial to venous circulatton-« !
venous return-« counterclockwise rotation
of curve

ALTERING CARDIAC & VASCULAR

FUNCTION CURVES
osms.i"l/ o.1-leTlng-eo.Tdlo.e-vo.seulo.T-fune-llon-euTves
• Curves combinec -e changes in CO to right, (3) no change in TPR
visualized, cardiovascular parameters • ! circulating volume (e.g. hemorrhage)
altered , Opposite effect
• Curves can be displaced by changes in • Changes in venous compliance are similar
blood volume, inotropy, TPR to blood volume changes
, ! venous compliance ----. changes similar
INOTROPIC AGENTS to i circulating volume
• Alters cardiac curve , j venous compliance ----. changes similar
• Positive inotropic agents (e.g. digoxin) at to! circulating volume
any level of RA pressure
O l contractility, stroke volume (SV), CO TOTAL PERIPHERAL RESISTANCE
----. (1) cardiac curve shifts upward, (2) • Alters both curves due to changes in
vascular function curve not affected, (3) afterload (cardiac curve), venous return
x-intercept (steady state) shifts upward, (vascular curve)
to left
• l TPR----. j arterial pressure----. j afterload
• Negative inotropic agents (e.g. beta- ----. ! CO----. (1) downward shift of cardiac
blockers) curve, (2) counterclockwise rotation of
O Opposite effect vascular curve, (3) ! venous return, (4) RA
pressure unchanged, !Ii {depending on
BLOOD VOLUME cardiac, venous curve alteration), (5) curves
intersect at altered steady state
• Alters vascular curve
• ! TPR (arteriolar dilation)
• j circulating volume (e.g. blood transfusion)
, Opposite effect
O l MSP----. (1) curves intersect at j
CO, RA pressure, (2) parallel shift of
x-intercept (steady state), vascular curve

30
 PRESSURE-VOLUME LOOPS
osmsJl/ pTessuTe-volume_loops

• Graphs represent pressure, volume

changes in LV during one heartbeat (one
Ventricular ejection
• Pressure in left ventricle > aortic pressure
I
cardiac cycle/"stroke work") ----. aortic valve opens----. blood ejected
• Pressure in left ventricle on y axis, volume
of left ventricle on x axis lsovolumic relaxation
• Ventricle starts relaxing ----. aortic pressure >
LV pressure ----. aortic valve closes
FOUR PHASES
• End of systole
Ventricular filling during diastole • ESV = 70ml
• At end of this phase:
O Mitral valve closed STROkE VOLUME (SV)
O Left ventricle filled (EDV); relaxed, • STROKE VOLUME (SV)
distended • Amount of blood pumped by ventricles in
o EDV = 140ml one contraction
• SV = EDV - ESV
lsovolumic contraction
• Systole begins (ventricular contraction)
• No changes to ventricular volume (mitral, STROkE WORk (SW)
aortic valve closed) • Work of ventricles to eject a volume of
• Pressure builds blood (i.e. to eject SV)
• Represented by area inside of loop

-----~
H
11nolie8P
PULSE
RESSURE
Dio.nolie SP
------- H~~~SlA~--1• ( ST~OKE:)
!!?
l ~DP
e!
a.. ~·
3 ·- I

LV Vol1.1m~ End- End-

STROKE
s11nolie dto.slolle
VOLUME
volume volume
I I I

Figure 16.1 Measurements that can be obtained from the pressure-volume loop graph. Pulse
pressure is measured in mm Hg and reflects the throbbing pulsation felt in an artery during
systole. Pulse pressure= systolic blood pressure - diastolic blood pressure. Stroke volume is
measured in ml and is blood volume ejected by left ventricle during every heartbeat. Stroke
volume = end-diastolic volume - end systolic volume.

31
I
@ EJ"ECTION @ ISOVOLUMETRIC CONTRACTION

C) Mih-o.1 valve opens

C) Mth-o.l valve closes
() AoT'tle valve opens
ON~
HlARTl!.~AT O Aodlc valve closes
( SiltOl<f:)

e,J

1
3'-------------+-------~

DIASTOLE

@ISOVOLUMETRIC RELAXATION @ RELAXATION

M1TltAL MITltAL
VAl..\/t. VA~Vt.

Figure 16.2 The four phases of the pressure-volume loop and the condition of the heart during
each phase.

32
 CHANGES IN PRESSURE-VOLUME
LOOPS
osms.i"l/eho.nges_in_pTessuTe-volume_loops I
• Cardiac parameters change----> volume- (ESV) ----> ! SV----> loop narrower, taller
pressure loops change (smaller SV, higher pressure; stroke work
• j preload (i EDV) ----> t strength of remains relatively stable)
contraction ----> j stroke volurne c- larger • t contractility----> blood under t pressure
loop ----> longer ejection phase ----> left ventricular
• j afterload ----> t ventricular pressure during pressure = aortic pressure ----> t SV, stroke
isovolumetric contraction ----> j less blood work, ! ejection fraction (EF), EDV----> loop
leaves ventricle ----> t end-systolic volume widens

A. NORMAL PRESSURE-VOLUME LOOP B. INCREASED PRELOAD

T
I
I
I
: ;tftOKE: ;tftOKE:
\ WORK WORK
I I
I
I lAl6t.tt
I ~
I
j
·.=-- ---
I1 --
---
-------1 3..._ ...... i--------~
LV Ve>l1.1rn& LV Vol1.1rn&
f.1110
$'(,; TOL.IC..
'vOL.UMt:

C. 1NCREASED AFTERLOAD D. INCREASED CONTRACTILITY

£.~P -----

;tftOKE: ;tftOKE:
WORK- WORK
RemQ,ns. I
~lCl\:1~ly LAl6E.tt
s.lobh. ~

- j
3.__~--~~~ ..... ~~--~--.

Figure 16.3 Changes in stroke work as a result of increased preload (B). afterload (C), and
contractility (DJ represented on pressure-volume loop graphs.
33
 CARDIAC WORI(

I osms.i"l/ eo.Tdio.e-woTlc
• Work heart performs as blood moves from
venous to arterial circulation during cardiac
ventricular pressure< aortic pressure----.
aortic valve closes (S2); causes dicrotic
cycle notch on aortic pressure curve
• All valves closed
PHASES OF CARDIAC WORI( • Ventricular volume
, Constant
Atrial systole
• Complete ventricular repolarization
• Begins when atria, ventricles in diastole
• ECG
• Atrioventricular (AV) valves open----. passive
, Twave ends
ventricular filling
• Atrial depolarization ----. atria contract (atrial Rapid ventricular filling
kick during systole)----. completes ventricular • Ventricular diastole continues v- ventricular
filling (EDV) pressure< atrial pressure----. AV valves
• Venous pulse: "a" wave (t atrial pressure) open
• ECG • Passive ventricular filling (ventricles
O P wave, PR interval relaxed, compliant)
• S3 (normal in children) produced by rapid
lsovolumetricventricular contraction filling
• Ventricular contraction begins (ventricular
systole) ----. ventricular pressure > atrial Reduced ventricular filling (diastasis)
pressure----. AV valves close (Sl); semilunar • Ventricular diastole continues; ventricles
valves closed relaxed
• ECG • Mitral valve open
n QRS complex • Changes in heart rate (HR) alter length of
diastasis
Rapid ventricular ejection
• Ventricular systole continues ----. left
ventricular pressure> aortic pressure ----.
TYPES OF CARDIAC WORI(
aortic valve forced open ----. blood ejected Internal work
(SV) (blood also ejected into pulmonary
• Pressure work: within the ventricle to
vasculature via pulmonic valve)
prepare for ejection
• l aortic pressure
• Quantified by multiplying isovolumic
• Atrial filling begins contraction time by ventricular wall stress
• ECG • Accounts for 90% of cardiac work
, ST segment
External work
Reduced ventricular ejection • Volume work: ejecting blood against
• !ventricular ejection velocity arterial resistance; product of pressure
• t atrial pressure developed during ejection, SV
• Ventricular repolarization begins • Represented by area contained in pressure-
• ECG volume loop
, Twave • Accounts for 10% of cardiac work

lsovolumetricventricular relaxation Myocardial oxygen consumption

• Ventricles relaxed (ventricular diastole); • Pressure work> volume work

34
• Aortic stenosis - ii pressure work - ii • Pressure work: LV (aortic pressure
oxygen consumption, ! CO lOOmmHg) > RV (pulmonary pressure
• Strenuous exercise - j volume work - j 15mmHg)
t CO

I
oxygen consumption, , j systemic pressure (e.g. hypertension)
- I LV pressure work - ventricular
LV and right ventricle (RV) wall hypertrophy
• Volume work: CO LV = RV CO , Law of Laplace for sphere (e.g. heart):
thickness of heart wall increases -
greater pressure produced

CARDIAC PRELOAD
osms.i"l/ ee1Tclie1e- Teloe1cl
• EDV: volume load created by blood Atrial contraction
entering ventricles at end of diastole before • Early ventricular diastole - ventricles
contraction relaxed, passively fill with blood from atria
• Establishes sarcomere length. ventricular via open AV valves - late ventricular
stretch as ventricles fill (length-tension diastole atrial systole (atrial kick) -
relationship) additional blood into ventricles
• Accounts for 20% of ventricular preload
FACTORS AFFECTING PRELOAD Resistance from valves
Venous pressure • Stenotic mitral, tricuspid valves create
• Includes blood volume, rate of venous inflow resistance - ! filling - ! preload
return to RA • Stenotic pulmonic, aortic valves create
• j blood volume. venous return - j preload outflow resistance - ! emptying - I
preload
Ventricular compliance
HR
• Flexibility: ability to yield when pressure
applied • Normal heart rate allows adequate time for
ventricles to fill
• Compliant, "stretchy" ventricles - j preload
• Tachyarrhythmias - ! filling time - !
• Noncompliant, stiff ventricles - ! preload
preload

35
 CARDIAC AFTERLOAD

I osmsJl/ eo.Tdio.e-o.f-leTloo.d
• Amount of resistance ventricles must
overcome during systole
FACTORS AFFECTING AFTERLOAD
LV
• Establishes degree, speed of sarcomere
shortening, ventricular wall stress (force- • Systemic vascular resistance (SVR)
velocity relationship) • Aortic pressure
• j afterload - I velocity of sarcomere RV
shortening
• Pulmonary pressure
• ! afterload - t velocity of sarcomere
shortening Resistance from valves
• Stenotic pulmonic, aortic valves create
outflow resistance - t afterload

LAW OF LAPLACE
osms.it/lo.w-of-Lo. plo.ee
• Describes pressure-volume relationships of •T=Elu
spheres h
• Blood vessels , T = wall tension
0 > radius of artery= > pressure on , P = pressure
arterial wall , r = radius of ventricle
• Heart , h = ventricular wall thickness
O Wall tension produced by myocardial • Dilation of heart muscle increases tension
fibers when ejecting blood depends on that must be developed within heart wall to
thickness of sphere (heart wall) eject same amount of blood per beat
• Laplace's formula: tension on myocardial • Myocytes of dilated left ventricle have
fibers in heart wall= pressure within greater load (tension)
ventricle x volume in ventricle (radius) I wall
, Must produce greater tension to
thickness
overcome aortic pressure, eject blood -
! co

36
 FRANl(-STARLING RELATIONSHIP
osmsJl:/FTe1nlc-S-l:e1Tling_Tele1-l:ionshi
• Loading ventricle with blood during
diastole, stretching cardiac muscle - force
I
of contraction during systole
• Length-tension relationship
O Amount of tension (force of muscle
contraction during systole) - depends
on resting length of sarcomere -
depends on amount of blood that fills
ventricles during diastole (EDV)
O Length of sarcomere determines
amount of overlap between actin,
VENTRICULAREND-DIASTOLIC.
myosin filaments, amount of myosin
: VOLUME(EDV) I
heads that bind to actin at cross-bridge _,.,,,.,-- ,~ ,' .' ' ..........
formation 1' : ,· ....

O
Low EDV - ! sarcomere stretching -
! myosin heads bind to actin - weak ·~·~E~
contraction during systole - ! SV A. Low EDV 8. Mid.-ro.nge C.. High EDV
O Too much sarcomere stretching EDV
prevents optimal overlap between actin,
myosin - ! force of contraction - ! SV Figure 16.4 Graphical representation of the
• Allows intrinsic control of heart = venous Frank-Starling relationship and sarcomere
return with SV length at low, mid-range, and high EDVs.
A mid-range EDV (B), where the volume
• Extrinsic control through sympathetic
of blood returning to the ventricles is
stimulation, hormones (e.g. epinephrine),
increasing but is not too large (C), allows for
medications (e.g. digoxin) - j contractility
best myosin-actin binding - j strength of
(positive inotropy), SV
contractions - j stroke volume.
• Negative inotropic agents (e.g beta-
blockers) - ! contractility - ! SV

END-DIASTOLIC.VOLUME

Figure 16.5 Graphical representation of

positive and negative inotropic effects on the
Frank-Starling relationship.

37
 STROl(E VOLUME, EJ"ECTION
FRACTION, & CARDIAC OUTPUT
I osms.i"l/s-lToke-volume-ejee-lion-f Taelion-eaTdiae-ou-lpu-l

sv
• Volume of blood (ml) ejected from ventricle
with each contraction
• Calculated as difference between volume
of blood before ejection/EDV, after ejection
(ESV)
• EDV (120ml) - ESV (50ml) = 70ml
• SV affected by preload, afterload, inotropy

EF
• Fraction of EDV ejected with each
contraction
• SV (70)/EDV (120) = 58 (EF)
• Average = 50-65%

C,Q
• Volume of blood ejected by ventricles per
minute
• SV (120) x HR (70) = 4900ml/min

38
 NOTES

ACTION POTENTIALS IN
PACEMAl(ER CELLS
osmsJl/po.eemo.keT-eell-o.e-lion-po-le n-lio.ls

Pacemaker cells
• Groups of cardiac muscle cells with ability
to spontaneously create action potential
(automaticity) and comprise intrinsic
conduction system
• Directly influenced by sympathetic and
parasympathetic nervous systems
• Comprise about 1 % of heart cells
• Differ in speed of spontaneous
depolarization
• Cells with fastest rate of depolarization at
any given time determine heart rhythm
O Remaining/slower cells called latent Figure 17.1 Locations of pacemaker cells
pacemakers within the heart.

SA node
• Primary pacemaker cells located in wall of Action potentials in pacemaker cells
right atrium
• Rapid electrical changes across membrane
• Rate: 60-lOObpm of pacemaker cells
O Usually determines normal heart rhythm • Conducted to rest of heart
Latent pacemaker cells Action potential phases
• AV node • Phase 4: sodium moves into cell through
O Located at base of right atrium, near funny channels (open in response to
septum hyperpolarization); slowly depolarizes cell
O Rate: 40-60bpm until threshold potential met
• Bundle of His , Responsible for instability of resting
O Divides into right and left bundle membrane potential
branches, travels through septum • Phase 0: strong inward calcium current;
between ventricles responsible for rapid depolarization
O Rate: 20-40bpm • Phase 3: strong potassium current moves
• Purkinje fibers out of cell; responsible for repolarization
O Spread throughout ventricles , Phases 1, 2 absent in pacemaker cells
----> no plateau
O Rate: 20-40bpm

39
 afratafreeh.com exclusive

~
>
E
.....'.:1~10-1------,---~~
tr o------
~
~
1~-s-"c;o-----',I'
I
I

Tl~E.

Figure 17.2 Graph depicting the action

potential of a pacemaker cell.

ACTION POTENTIALS IN
MYOCYTES
osms.il/ m14oe14le-cidion-polenlicils

Myocytes , Phase 3: calcium current moving into

• Receive signal from from pacemaker cells cell stops; potassium current moving
causing them to contract out of cell continues; repolarization
continues
• Able to depolarize, spread action potentials
, Phase 4: potassium current moving
• Action potential phases:
O Phase O (depolarization
out of cell approaches equilibrium
phase): rapid
between inside, outside of cell; sodium,
influx of sodium into cell (inward
calcium current moving into cell balance
current); responsible for rapid
outward potassium current; resting
depolarization
membrane potential achieved
O Phase 1: sodium current stops,
potassium slowly flows out of cell;
depolarization stops, re-polarization
starts
O Phase 2: calcium current moves into cell,
balances potassium current moving out
of cell; charge balance between inside,
outside of cell creates plateau

40
 ELECTRICAL CONDUCTION
IN THE HEART
osMs.i-l/heo.T-l-elee-lTieo.1-eondue-lion

• Transmission of electrical signals across , These structures responsible for

heart cells leads to rhythmic myocardial electrical conduction, spontaneous
contraction depolarization; do not generate
• Intercalated discs connect cells and allow contractile force
myocardium to act as syncytium
° Contain desmosomes (holds cells
together) and gap junctions (areas of
low resistance to electrical flow)
• Cardiac action potential: sequential flow of
electrons across ion channels in cardiac cell
membranes, resulting in electrical activation
of myocardial cells
O Depolarization: cation movement into
cell, producing positive cell charge
relative to outside
O Polarization: anion movement into cell,
producing negative cell charge relative
to outside
• Pathway of electrical conduction
O Sinoatrial node (SA node) - atrial Figure 17.3 Desmosomes and gap junctions
internodal fibers - atrioventricular node present at intercalated discs allow the
(AV node) - bundle of His - Purkinje myocardium to act as a syncytium.
fibers - ventricular myocytes

CARDIAC CONDUCTION VELOCITY

osmsJl/ eo.TcJ.io.e-eoncJ.ue-lion-veloei-l14
• Speed at which depolarization wave • Rapid conduction through Purkinje fibers
spreads among myocardial cells ensures adequate blood ejection
O Measured in meters per second (mis) , Speed: 2-4m/s
• Each myocardial structure has a different
Velocity depends on two factors
conduction speed related to its purpose
O Slowest:
• Amount of ions going into cell during action
AV node
potential
° Fastest: Purkinje fibers
, More ions - faster depolarization -
• AV delay: slow conduction through AV
faster spread
node ensures adequate ventricular filling
, Fewer ions - slower depolarization -
O Speed: 0.01-0.05m/s
slower spread
O Blood flows from atria to ventricles
41
• Interconnectedness of myocardial , Fewer gap junctions ----> fewer
conduction cells interconnected cells=-. increased
O More gap junctions ----> more resistance to ion flow between cells
interconnected cells v- less resistance to
ion flow between cells

AV tJOOE.
ATIZ,IA ~0.1-0.S M/S Vf.tJlllU.~S
N lto11fS,v --+ '°'J
--+ ~ -vlM/S"'
~ ALLOWS AT~IPI Tl~E.

I I ti> C.O~TfZAC.T

~ If<--~ --lOO""s-~)I J
M:~,-------------1'2.0 N\S -------------

Figure 17.4 Conduction speeds of different myocardial structures.

EXCITABILITY & REFRACTORY

PERIODS

Refractory period Excitability

• Time in which myocardial cell cannot be • Ability of myocardial cells to depolarize in
depolarized response to incoming depolarizing current
• Absolute refractory period: no stimulus, no • Supranormal period:< normal stimulus
matter its size, can depolarize cell may produce action potential large enough
O Phases 0, 1; part of phase 2 to be conducted
• Effective refractory period: large stimulus , Resting membrane potential has not yet
can generate action potential been achieved
O However, too weak to be conducted , Membrane potential closer to threshold
than normal, refractory periods over
• Relative refractory period: large stimulus
can generate action potential
O Big enough to be conducted

42
 CARDIAC EXCITATION-
CONTRACTION COUPLING
osms.i'l/ e<11"di<1e_exeit<1tion-eont1"<1etion_eoupling

• Plateau in action potential of myocyte

membrane allows influx of calcium,
stimulating muscle contraction
° Calcium enters cell via L-type voltage
T-TUS\JLE
gated channels SARCOPLASMIC
O Higher intracellular Ca2- triggers
release of more Ca2- from sarcoplasmic RETICULUM
reticulum through ryanodine receptors
(AKA calcium-induced release)
O Released Ca2• attaches to troponin C
---'> tropomyosin moves---'> actin-myosin
cross bridges ---'> contraction
• Cross bridges last as long as Ca2• occupies
troponin
O Tension is proportional to intracellular
Ca2• concentration
• Intracellular Ca2• removed by two
mechanisms that induce relaxation, keep
Ca2- from damaging cell contents
Figure 17.5 Depolarization of a
° Ca2• ATPase uses ATP energy, Na·/ cardiomyocyte by calcium-induced calcium
Ca2• ATP exchanger uses Na· inward release.
current to remove Ca2• from cell through
sarcolemmal membrane, remove Na·
through Na·/K· ATPase
° Ca2• ATPase removes Ca2• into
sarcoplasmic reticulum; calsequestrin
2 inside sarcoplasmic reticulum binds
Ca2+, keeping it inside

43
 CARDIAC LENGTH TENSION
osms.i"l/ eo.Tclio.e-lenglh-tension
• Degree filament overlap correlates to • I resting tension: small changes produce t
tension tension
O Lmax = 2.2 µmis maximal tension • Frank-Starling basis; t fiber length ---->
O In shorter/longer cells, tension will be stronger contraction
decreased , Preload = LV end-diastolic volume (L), if
• j L----> t Ca2• sensitivity of troponin C----> j t means ventricular fiber length f
Ca2• release from sarcoplasmic reticulum , Afterload = aortic pressure; if preload j
• Can extend to ventricle length/tension ----> afterload tension and pressure I
relationship curve
° Cardiac muscle < elastic than skeletal;
only ascending curve demonstrates its
contraction

CARDIAC CONTRACTILITY

• Positive inotropes: l force of myocardial faster, systole shorter; Frank-Starling

contraction effective
• Negative inotropes: ! force of myocardial , Na-/K· ATPase phosphorylation;
contraction increases relaxation due to secondary
• Proportional to Ca2• concentration channel activations
O Proportional to Ca2• released , Troponin I phosphorylation; Ca2• binds
O Depends on storage, current size less troponin C ----> effect on excitation
contraction coupling, prolongs filling,
higher ejection fraction
WHAT AFFECTS INOTROPISM? -
AUTONOMIC NERVOUS SYSTEM Parasympathetic
• Negative inotropic effects: ! contractility on
Sympathetic atria via muscarinic receptors
• Positive inotropic effects: j contractility • Acidosis also has negative inotropic effect
• Causes faster relaxation, faster refill, ----> ! contractility
increased heart rate (HR) • Gk (type of G;), adenylyl cyclase couple,
• Increased tension development rate resulting in
0 (31 receptor is G, coupled, activates , Decreased Ca2• plateau current
adenylyl cyclase----> cAMP produced , ACh increases lkACh
O pKA activated ----> phosphorylation ----> j , ----> ! action potential duration ----> ! Ca2•
sarcolemmal Ca2- channel activity----> j current-» ! AP width
contraction
• Phosphodiesterase metabolises cAMP,
O Phospholamban phosphorylation; stops inhibit phosphodiesterase, increase
sarcoplasmic Ca2- ATPase inhibition, contractility IP3 stimulates Ca release in
decreasing time of IC Ca2+, making HR SR, increases force of contraction
44
Heart rate (HR) WHAT AFFECTS INOTROPISM? -
• HR increases contractility DRUGS
• Diastole affected more than systole Cardiac glycosides
• Ca can't be removed as quickly as it • Digoxin, digitoxin, ouabain; congestive
accumulates - new equilibrium heart failure treatment
Of action potentials/time: increased total , Inhibit Na•/K- ATPase; + inotropic, i
trigger Ca2+, increased inward current
intracellular Na• changes Na/Ca -
O t Ca2• influx - j stores; phospholamban decreases exchange - intracellular
phosphorylated, thus inhibited calcium increases - increases tension
• Positive staircase effect/Bowditch , Nifedipine also acts on Ca2- by blocking
staircase/Treppe phenomenon ryanodine receptors
O On first, beat still no extra Ca2•
Beta adrenergics
o Afterward, Ca2• accumulates until max
Ca2• storage achieved • lsoproterenol, norepinephrine, epinephrine,
dopamine, dobutamine
• Postextrasystolic potentiation
o Same effect as positive staircase , l cAMP - j contractility
o Extrasystole < powerful, but creates
one more chance for calcium entry
O Because the voltage channels are open
more, postextrasystolic beat has higher
tension than extrasystolic

45
NOTES

ECG BASICS
osmsJl:/EC,G-\>o.sies
• ECG traces provide information on heart's O PR segment: end of P wave to
electrical activity, rate, rhythm beginning of QRS complex; signifies AV
, Depolarization waves moving towards nodal delay
electrode ----> positive deflection • QRS complex: ventricular depolarization
, Depolarization waves moving away • T wave: ventricular repolarization
from electrode----> negative deflection • QT interval: time from start of Q wave to
• 12 lead ECG (EKG) records heart electrical end of T wave; represents time taken for
activity during heartbeat ventricular depolarization, repolarization
, Six limb leads (I, II, Ill, AVR, AVL, AVF) • U wave: sometimes seen after T wave
, Six chest leads (Vl-V6) (not shown), represents purkinje fiber
• P wave: atrial depolarization repolarization

, PR interval: beginning of atrial

contraction to beginning of ventricular RECORDING ECGs
contraction (time for impulse to reach • Recorded on lmm graph paper (lOmm =
ventricles form sinus node) lmV)

l'l.-LE.AD
EC.~

Figure 18.1 Lead placement in the coronal and transverse plane.

46
 O x-axis= time (lmm = 0.04s) O Electrodes placed on shoulders,
O y- axis = voltage (lOmm = lmV) abdomen to record limb leads
• Limb leads: I, II, Ill, AVR, AVL, AVF • Chest leads (precordial): Vl -V6
O Bipolar leads: I, II, Ill O Septal leads: Vl,V2
O Unipolar leads: AVR, AVL, AVF O Lateral leads: V5,V6
(augmented voltage for right arm, left O Anterior leads: V3,V 4
arm, left foot O Six chest leads provide six viewpoints of
O Lateral leads: I, aVL, V5, V6 cardiac activity, in horizontal plane
O Inferior leads: 11, 111, AVF
O Six limb leads provide six viewpoints of
cardiac activity, in frontal plane

ECG NORMAL SINUS RHYTHM

osms.i"l/ECG-no,-mo.l-sinus-,-h14-lhm
• P waves precede QRS complexes in 1:1 • P waves
relationship , Upright in leads I, 11, AVF
• SA node (sinus node), dominant centre of , Amplitude< 2.5mm in limb leads
automaticity , Sinus arrhythmia: can be normal if
O Normal sinus rhythm 50-90bpm sinus rate varies with respiratory cycle,
• Constant RR interval relatively mild/abnormal if sinus rate
• Predictable recurring wave pattern varies unpredictably.very dramatic
(P-waves, QRS, T waves)

ECG RATE & RHYTHM

RATE DETERMINATION , Locate R wave peak on large block line

• Box method: measure R-R interval by large as "start"
boxes , Count subsequent number of complete
O ECG grid: thick lines 5mm apart (0.20s); R waves in 10s strip (total strip)
thin lines lmm (0.04s) • To calculate heart rate
O Locate R wave peak on thick line as , Count number of QRS complexes across
"start" entire recording, multiply by six for heart
O Label blocks (thick lines): 300; 150; rate; used to estimate heart rate during
100; 75; 60; 50 irregular rhythms
O Locate next R wave peak to estimate
heart rate
• Fast heart rates: use fine division within
boxes for more accurate estimates
• Slow heart rates: use 2.5s marks at top of
trace paper
47
 SIC, SOX SMALL SOX
0.:1.s O.Olls

1
I-;
~
1----i
3
I I
'f
I I
s
'300 'oprn ISO 'opM 100 ',,p"" 1'£, 'opM

Figure 18.2 The Box method measures distance between R-R intervals to calculate the heart
rate.

ECG INTERVALS
osmsJl/EC,G-in-leTve1ls
PR INTERVAL & SEGMENT O QTc interval corrected for heart rate;
• Normal interval 0.12-0.20s 0.35-0.44s for normal heart rate
= Measure duration(s) from start of P to (60-lOObpm)
start of Q O Long QTc (> 500ms) - prone to rapid,
• Normal segment: usually isoelectric, may potentially fatal ventricular rhythm
be displaced

QllS COMPLEX
QRS INTERVAL ( ~ <100ms
• Normal QRS: <0.10-0.12s (slight variation
between references)
, Measured from start of Q to end of S
• QRS amplitude (voltage): wide range of
normal limits
, Low voltage: < 5mm limb leads, <
QT INTERVAL
lOmm chest leads <IIIIOm, (mPn)
(460m~(women)1
, Increased voltage can indicate left
®';01,pm
ventricular hypertrophy, right ventricular
hypertrophy, may be normal Figure 18.3 An ECG interval includes a
, Narrow(< 0.12s) I wide(> 0.12s) segment and one or more waves and should
be completed within a specific amount of
QT INTERVAL time to be considered healthy.
• Normal QT< 50% RR interval, only for
normal heart rates
• Measure QT from start of Q to end of T
• Measure RR interval as time between R-R

48
 ECG AXIS
osms.i"l/ECG-e1xis
• Mean direction (vector) of ventricular
depolarization wavefront oVR oVL
O Mean QRS vector normally downward -1so· -!o·
from AV node through stronger left I
+110··--...;::,,,ii,::;...:;.._-o·
ventricle
• Normal axis range -30° to +90° of frontal
plane
• Limb leads indicate vector deviation in
frontal plane
O Divided into four quadrants Figure 18.4 The green shows a normal
range. The red bottom left quadrant would
indicate right ventricular hypertrophy while
the top right would indicate left ventricular
hypertrophy.

ECG TRANSITION
osms.i-l/ECG--lTe1nsi-lion
• Chest leads provide information on vector ABNORMAL RATES & RHYTHMS
rotation in horizontal plane • Conventionally defined, sinus bradycardia
O Normal: gradual transition of QRS <60bpm
through leads Vl-V6 , True normal adult resting heart rate is
O QRS complex switches from 50-90bpm
predominantly negative to positive • Sinus tachycardia > lOObpm
either between V2, V3 or between V3, • If SA node fails. other latent ectopic
V4 pacemakers capable of automaticity
, Atria, AV junction, His bundle, bundle
R WAVE PROGRESSION branches can set heart rate
• Early: tall R wave in Vl, V2 , Each foci has unique rate (atrial foci
• Delayed R: transition point between V4, 60-80bpm; junctional foci 40-60bpm;
V5/between V5, V6 ventricular foci 20-40bpm)
OR amplitude> S; no progression through , Overdrive suppression: mechanism
V5,V6 by which only foci/node with highest
firing frequency rate conducts impulses.
• Reverse: decreasing amplitude
suppresses other pacemaker sites

ASSESSMENT FOR NORMAL Heart blocks

REGULAR RHYTHM • Sinus block
• Is there a P before every QRS complex? , SA node temporarily ceases to conduct
• Is there a QRS after every P? impulse; usually resumes, may cause
• Are the P waves normal? escape rhythm

49
• AV block , Broad QRS < 120ms
° First degree: prolonged PR interval > , Dominant S wave in Vl
0.2s , Absence of Q waves, broad monophasic
O Second degree: some P waves R wave in lateral leads
conducted to ventricles, followed by • Left anterior fascicular block
QRS complex while some not , Impulses conducted to left ventricle via
O Third degree: atria, ventricles beat left posterior fascicle
asynchronously with no conduction , Left axis deviation
through AV node (complete dissociation
, Increased R wave peak time in aVL
between P, QRS complexes)
, Small Q waves, tall R waves in leads 1,
Bundle branch blocks aVL
• Left bundle branch block (LBBB) , Small R waves, deep S waves in leads
O Activation of left ventricle delayed II, 111, aVF
causing left ventricle to contract later , Increased QRS voltage in limb leads
than right ventricle , Prolonged R wave peak time in aVL >
O Broad QRS < 120ms 45ms
O Secondary R wave (R') in leads Vl-3 • Left posterior fascicular block
O Slurred S wave in lateral leads (I, avL. , Impulses conducted to left ventricle via
V5-6) left anterior fascicle
O Secondary repolarization abnormalities , Right axis deviation
in right precordial leads (ST depression, , Increased R wave peak time in aVF
T wave inversions) , Small R waves with deep S waves in
• Right bundle branch block (RBBB) leads I, aVL
O Activation of right ventricle delayed , Small Q waves with tall R waves in
causing right ventricle to contract later leads II, Ill, aVF
than left ventricle , Increased QRS voltage in limb leads

QRS TRANSITION ZONE

Figure 18.5 The QRS transition zone usually occurs in the V3 and V4 lead. Vl and V2 are
mostly positive while V5 and V6 are mostly negative.

50
 ECG CARDIAC HYPERTROPHY &
ENLARGEMENT
osms.it/EC,G-ee1rdie1e-h14pertroph14-enle1rgement
ATRIAL DILATION/ENLARGEMENT • Sum of S wave depth in Vl + R wave
• Biphasic P waves > one small box in lead height in either V5N6 > 35mm
Vl • Possible left axis deviation
• Initial component of wave larger • Left ventricular 'strain pattern'
O Right atrial enlargement , Downsloping ST segments, T wave
• Terminal component of wave larger inversions in lateral leads
O Left atrial enlargement
• Amplitude of P wave in any limb lead >
2.5mm
O Probable right atrial enlargement

RIGHT VENTRICULAR
HYPERTROPHY
• Vl-V6 all consisting of small r waves, deep
S waves (no R wave transition)
• Tall R wave in Vl that progressively
shortens across to V6 (reverse R wave
transition)
• Possible right axis deviation

Figure 18.6 Hypertrophy is an enlargement

LEFT VENTRICULAR of the muscle wall while an increase in
HYPERTROPHY volume is known as dilation.
• Deep S wave in lead Vl
• Tall R wave in V5 and/or V6

V1: Biphasic P,
II & V1: Big P
II: Double-Humped

V1: Big R; Vl: Huge S;

VS: Big S VS & V6: Huge R

51
 ECG MYOCARDIAL INFARCTION &
ISCHEMIA
osms.i"l/EC,G-eo.rdio.e-info.retion-isehemio.
MYOCARDIAL INFARCTION NECROSIS
• Complete/partial blockage in coronary artery • Pathologic Q wave; > 0.04s, amplitude cZ
causing myocardial damage - V4mm the R wave height
• ST elevation Mis (STEMls): complete artery , Non-pathological q waves < 0.04s
blockage considered normal
O ST elevation present on ECG; emergency • Ignore AVR lead; record leads with Q
• Non-ST elevation Mis (NSTEM/s): partial (pathological), q (physiological) waves; ST
artery blockage depression/elevation; inverted T waves
O ST elevations not present on ECG • Anterior left ventricular infarction (q in V5,
O Less emergent than STEMI V6)
, Chest leads anterior location; Q waves in
leads Vl, V2, V3 N4
ISCHEMIA • Posterior infarction
• Inverted T waves; slight to deep; most
, Large R in leads Vl, V2; possible Qin V6
pronounced in chest leads
, Mirror test: invert, examine reflection for
• Angina: transient T wave inversion; may
vQ, ST elevation in leads Vl, V2
occur without infarction
• Lateral infarction: Qin leads I, AVL
• Inverted T wave in any leads V2-V6 are
abnormal • Inferior infarction: Qin leads II, 111, AVF
O Suggest ischemia, variety of other
pathologies
• Acute or recent infarction: elevated ST
segment (slight to extensive)
O One of the earliest ECG signs of
infarction
O Returns to baseline over time
• Restricted coronary blood flow: flat
depressed ST segment
O Suggests subendocardial infarction; any
ST depression

52
 Unstable angina;
Stable angina; NSTEMI;
ST Depressions ST Depresssions;
T wave Inversion

STEMI;
Unstable angina;
T wave inversions;
NSTEMI;
Hyperacute T waves;
ST Depresssions;
ST elevation;
T wave Inversion
Pathologic Q waves

53
NOTES

BLOOD PRESSURE, BLOOD FLOW, &

RESISTANCE
osmsJl/\,lood-pY-essu Y-e-\>lood-flow-Y-esis-lo.nee
PRESSURE(P) • Using the equation for area (A) of a circle,
• Force over area ----> blood pressure is force (d/2)2 x n, we get (2 I 2)2 x ;r = 3.14cm2
of blood over blood vessel surface area • Since cardiac output= blood ffow -»
convert Umin to cm3/s----> 1000cm3 in a L.
60 seconds in a minute, multiplying those
BLOOD FLOW (Q) equals 83cm3/sec
• Volume (cm3) blood flow through vessel
• Rearranging formula, velocity equals flow
over period of seconds (s)
rate divided by area, equals about 26cm/s,
• E.g. Q = 83cm3/s about lkm/hr
Determined by two factors
• ~p = Pressure gradient
(mmHg); difference TOTAL PERIPHERALRESISTANCE
in pressure between two blood vessel ends (TPR)
• R = Resistance (mm Hg/ml per min) • Resistance of entire systemic vasculature
o Q=~P/R , Can be measured by substituting
• Q directly proportional to pressure gradient cardiac output for flow (Q). pressure
O Increased pressure gradient----> difference between aorta. vena cava for
increased blood flow .0.P
• Resistance within an organ
• Q inversely proportional to resistance
, Can be measured by substituting
O Increased resistance ----> decreased blood
flow organ blood flow for flow (Q). pressure
difference in pressure between organ
artery, vein for .0.P
BLOOD FLOW VELOCITY(v)
• Major mechanism for changing blood flow
is changing resistance
• Blood flow velocity (v) is distance (cm)
traveled in certain amount of time (s)

54
 PRESSURES IN THE
CARDIOVASCULAR SYSTEM
osmsJl/ eo:rcliovo.seulo.T-s14stem- ressurss
• Blood pressure highest in large arteries • For person with normal blood pressure of
(e.g. brachia! artery), about 120/SOmmHg 120/SOmmHg
, MAP= .% 120 + % 80 = 93mmHg
SYSTOLIC BLOOD PRESSURE • Diastole lasts longer than systole; roughly
• First/top number equal to diastolic pressure plus one-third
pulse pressure
• Pressure in aorta caused by ventricular
contraction . . pulse pressure
i\l!AP = Diastolic pressure+~~~--
• During systole, heart contracts ----> transfers 3
kinetic energy (140mmHg) to blood ---->
• For person with normal blood pressure of
aortic elastic walls stretched, where some
120/SOmmHg
kinetic energy stored as elastic energy of
120mmHu
walls (form of potential energy) ----> blood i\l!AP = 80mmHg + ° 93mmHg
3
pressure drops to 120mmHg (systolic
pressure) • MAP demonstrated using relationship of
blood flow, blood pressure, resistance,
applying the following equation
DIASTOLIC, BLOOD PRESSURE • Q=llP/R ----> P; - P1 = Q x R
• Second/bottom number ' P; = mean arterial pressure (MAP)
• Pressure caused by recoil of arteries during O P1= central venous pressure (CVP)
diastole
, Q = blood flow, equals cardiac output
• During diastole, heart relaxes, aortic valves (CO)
close-» kinetic energy drops to 50mmHg
, R = resistance; combined resistance
----> potential energy of stretched aortic
of all of blood vessels of systemic
walls adds to kinetic energy again when
circulation equals systemic vascular
walls recoil=- pressure rises to 60mmHg
resistance (SVR)
(diastolic pressure) ----> allows blood to move
forward • Applying this equals the following
, MAP - CVP = CO x SVR
• Pulse pressure: difference between
systolic, diastolic pressure • CVP is a small number, usually ignored;
equation simplified
Mean arterialpressure(MAPIP.) , MAP = CO x SVR
• Average blood pressure during cardiac • Based on this relationship ----> increased
cycle including systolic, diastolic blood resistance will cause increased blood
pressure pressure
• MAP, pulse pressure decline with distance
from heart

MAP measuredin two ways

• Diastole lasts longer than systole, therefore
MAP is equal to one third systolic pressure
plus two thirds diastolic pressure
O MAP = .% systolic pressure + % diastolic
pressure

55
 AORTA

A~T6fW>L~S ~
CAPllLA!lt f;~

(.Boov)
Figure 19.1 Visualization of MAP equation components.

PRESSURE GRADIENT • Pulse pressure lower in aorta than in large

• Pressure gradient pressure difference arteries - because pressure from blood
between two ends of blood vessel travels faster than blood itself; pressure
O Gradient from aorta to arteriole ends waves bounce off branch points in arteries
which increases pressure even more
• Pressures in different parts of
cardiovascular system not equal, keeps • Systolic pressure higher in large arteries
blood moving than aorta, blood keeps moving forward
• Blood flow generated by heart pumping • Diastolic pressure is lower than in large
action, moves along pressure gradient arteries - mean arterial pressure mostly
from high pressure areas (arteries) to low affected by diastolic pressure - mean
pressure areas (veins) arterial pressure is higher in aorta - driving
force for blood flow
• Fluctuations on arterial side
' For example: aortic systolic pressure
1. Blood ejected into aorta - pressure
is 115mmHg; diastolic pressure is
rises
85mmHg - Mean arterial pressure is
2. Small amount of blood backflows into
95mmHg; large artery systolic pressure
ventricles
is 120mmHg; diastolic pressure is
3. Valves close - pressure drops 80mmHg - mean arterial pressure is
4. Dicrotic notch/incisura pressure drop 93mmHg
followed by small pressure increase as a
result of valve recoiling
5. Aorta settles, heart relaxes - pressure
drops

56
 DIC.IZOTtC. tJOTC.H
(ltJC.ISV~~)

d)£
c --
® ®f" -
~
tw.
::,/"'
Vt ,n
Q) 1(f
<I\ :t.
.... f
Qt !
®
=
a_'-'
~
A~n1t16S V~1~S
®~
Figure 19.2 The five stages of fluctuation in arterial pulse pressure.

SYSTEMIC CIRCULATION Veins

• Mean pressure in aorta results from two • Systolic pressure drops even further -
factors 4mmHg in vena cava, 2mmHg in right
O Blood volume (cardiac output) atrium
° Compliance (low compliance - high , Venous pressure too low to promote
pressure) venous return to heart
• Pressure remains high in large arteries • Factors that facilitate venous return
because of high elastic recoil , Muscular pump: as muscles contract,
relax they compress surrounding veins,
Small arteries force blood towards heart
• Pressure decreases; biggest pressure drop , Respiratory pump: during inhalation,
is in arterioles (30mmHg) abdominal pressure increases, forces
O Occurs because arterioles develop high blood in local veins forward
resistance to flow , Sympathetic vasoconstriction: as
smooth muscle in veins contracts, blood
Capillaries
pushed towards heart
• Pressure drops for 30mmHg to lOmmHg
• Two causes for pressure drop
° Fluid filtration in capillaries
PULMONARY CIRCULATION
• Right ventricle - lungs - left atrium
O Increase frictional resistance
• Pulmonary arteries: systolic pressure
• Pressure drop is less than in arterioles
25mmHg; diastolic pressure 8mmHg
O Many capillaries running in parallel -
, Mean arterial pressure - 25 (Ya) + 8 (%)
reduces total resistance (total resistance
for vessels in parallel is less than
= 14mmHg
resistance in any individual vessel) • Capillaries: pressure drops to lOmmHg
• Pulmonary vein: pressure drops to 8mmHg
• Left atrium: pressure drops to 2-5mmHg

57
 LARGE ·1NC.REASING RADII
AORTA ARTERIES •HIGH COMPLIANCE
,-"---,, ,-"--,

ARTERIOLES
~
CAPILLARIES
~VENULES
,....J>--.,
LARGE VEINS
,...---... ,....-_
VENA C.AVAE

ARTERIES VEINS

Figure 19.3 Visualizing pressures throughout the systemic cardiovascular system.

c;'tSTE.M IC. P\JL.MON"it"t

C.l~UJLATION
C.I IZC.v LAT I ON

~~P-= ('h)lS-+ (2/?;i

: !It""""~

2.5

U'Vllo\OtJ~tt~)
AflUlllf.S

Figure 19.4 Visualizing pressures in the pulmonary circulation.

58
 RESISTANCE TO BLOOD FLOW
osms.i"l/ Tesis-lo.nee--lo-\>lood-flow
RESISTANCE Series resistance
• Opposition to flow - amount friction as • Sequential flow from one vessel to next
blood passes through blood vessels • Illustrated by arrangement of blood vessels
• Determined by within an organ
o Blood viscosity • Major artery - smaller arteries - arterioles
O Total length blood vessels - capillaries - venules - veins
O Diameter blood vessels • Total resistance of system arranged
in series is equal to sum of individual
Poiseuille Equation resistances
• Describes relationship between resistance,
blood vessel diameter, blood viscosity
• Blood flow at each part of system
8r]l
R=- is identical but pressure decreases
itr' progressively (greatest decrease in
o R = resistance arterioles)
o rJ = blood viscosity Parallel resistance
O I = length of blood vessel
• Simultaneous flow through each parallel
O r4 = radius (diameter) blood vessel vessel
raised to fourth power • Illustrated by arrangement of arteries
Points expressed by Poiseuille equation branching off aorta

• Resistance to blood flow is directly • Cardiac output - aorta - branching -

proportional to blood viscosity, blood vessel cerebral, coronary, renal system etc. -
length capillaries - venules - veins - vena cava
- right atrium
• Resistance to flow is inversely proportional
• Total resistance less than any individual
to radius to fourth power (r') - when
radius decreases, resistance increases by resistance
fourth power - e.g radius decreases by 1 1 1 1 1 1
one half, resistance increases 16-fold -=-+-+-+-+-+ ...
R,cra/ s, R, R3 R, R;
, Numbered subscripts represent
SERIES& PARALLELRESISTANCE cerebral, renal, coronary, other systems
• Resistance also depends on blood vessel • Blood flow in each system is only small
arrangement - series/parallel portion of total blood flow - no pressure
lost in major arteries (remains same as in
aorta)

59
 afratafreeh.com exclusive

....... 1-t, .... ;,.

L,tc.r

OroTl'L

Figure 19.5 Calculating the total resistance for this system involves finding the total parallel
resistance first and then adding R1, RParalleJ' and R5. The total blood flow in series, Q. is equal
across all parts of the system. Individual vessels in the parallel system have different Qs, since
the blood flow is split between each of the vessels, but they add up to Q-otar

60
 LAMINAR FLOW &
REYNOLDS NUMBER
osms.i"l/lo.mino.T-flow-o.nd-Re14nolds-num\,eT
LAMINAR FLOW • Since velocity depends on diameter
• Smooth blood flow through blood vessels , v = 4Q /Jrd2
- blood velocity highest in center, lowest , Decrease in diameter (e.g. thrombus,
towards blood vessel walls - zero at walls atherosclerotic plaque) - velocity
increases - Reynolds number
TURBULENT FLOW increases
• Laminar flow disrupted; blood flows axially, • Values of Reynolds number
radially - kinetic energy wasted - more , lf « 2000 - laminar flow
energy needed to drive blood , If> 2000 - increased likelihood of
turbulent flow
Reynolds Number
, If> 3000 - turbulent flow
• Determines whether flow likely to be
laminar/turbulent
SHEAR
N = pdv • Friction between blood, vessel walls
R Tl
, Highest at vessel wall, lowest in center
O NR = Reynolds number - difference in blood flow velocity
o p = blood density • Difference in velocity is parabolic - moving
O d = blood vessel diameter away from walls velocity increases quickly,
near middle change in velocity low
O v = blood flow velocity
• Shear inhibits red blood cell aggregation,
o 1J = blood viscosity
lowers viscosity
• As viscosity decreases (e.g. anemia),
Reynolds number increases
• As velocity increases (e.g. increased cardiac
output), Reynolds number increases

Re:: yol-1
11
.--~~~~~~--_.JL-~~~~~~~-
( ~
LAMINAR TURBULENT
c; SHE~il ~
< :l.000 > 3000

Figure 19.6 Reynolds number is a way to predict whether a fluid is going to be laminar (smooth)
or turbulent. Differences in velocity across a blood vessel cause shear.
61
 COMPLIANCE OF BLOOD VESSELS
osms.i"l/eomplio.nee-of-\,lood-vessels
COMPLIANCE ( C) ELASTANCE (E)
• AKA capacitance/distensibility: ability of • Inverse of compliance
blood vessels to distend, hold an amount of , Blood vessel ability to recoil back after
blood with pressure changes distension
• C=V/P • E=P/V
° C = compliance of blood vessel (ml/ , E = elastance of blood vessel (mmHg/
mm Hg) ml)
O V = volume of blood (ml) ,P = pressure (mmHg)
o P = pressure (mmHg) , V = volume of blood (ml)
• High volume, low pressure----. high
compliance (veins); low volume, high During systole
pressure ----. low compliance (arteries) • Heart contracts ----. transfers kinetic energy
• Arteriosclerosls-« low cornpllance c- low (140mmHg) to blood-« stretches aortic
ability to hold an amount of blood at same elastic wall, where some kinetic energy
pressure ----. blood backs up in veins stored as elastic energy of walls (form of
potential energy) ----. blood pressure drops
O Arteries also become less compliant
to 120mmHg (systolic pressure)
with age
O If compliance decreases in veins During diastole
(venoconstriction) ----. volume decreases • Heart relaxes, aortic valves close ----. kinetic
(shift from veins to arteries) energy drops to 50mmHg----. potential
energy of stretched aortic walls adds to
kinetic energy again when walls recoil

COMPUANCE - C = V (ml) ----. pressure rises to 60mmHg (diastolic

pressure) ----. allows blood to move forward
P (mmHg) during diastole
• Pulse pressure: 120mmHg - 60mmHg =
60mmHg
• Elastance buffers, dampens pulse pressure
----. Windkessel effect
• Without elastic properties, blood pressure
would be 140/50mmHg with pulse
pressure 90mmHg

PRESSURE

Figure 19.7 The same pressure will expand

the volumes of vessels differently depending
on their compliance.

62
 WINDICESSEl EFFECT

WITHOUT ElASTIC. ARTERIES

It
l(INETIC ENERGY POTENTIAL ENERGY
I
ICE + PRESSURE _ E - TOTAL -
ENERGY ENERGY

HEART \k 1' 1' 1' 1' 1'

SYSTOLE CONTRACTS
• • • • • 1llOmmH9
LAORTA, SOmmH9 ~ P.P = C,Q

DIASTOLE l .... r
RELAXES __ t_:l IT
~ J
~
DAMPENED
WITH ElASTIC. ARTERIES
l(INETIC ENERGY
I
POTENTIAL ENERGY
(
i
~
ICE +PRESSURE+ ELASTIC. E -TOTAL -
ENERGY :
r ENERGY

.,. .,. .,.

ENERGY

SYSTOLE
rl HEART
CONTRACTS

VOLUME
t~OmmH9 y P.P = GO
C.OmmH9

l ...., HELD AORTA~

! i 4 J ~
DIASTOLE
RELAXES
~ :. : I ! I

l
t
!
l
t
i
1
1
~
! IT
l
T T
(_RECOILS

Figure 19.8 Windkessel effect: elastance dampens pulse pressure by lowering systolic pressure
and increasing diastolic pressure.

Systole: aorta's walls stretch with high pressure contractions and store some energy as elastic
energy. Since the total energy is the same as it would be without elastic arteries, there must be
less kinetic energy and pressure energy to make room for the elastic energy - lower systolic
blood pressure.

Diastole: elastic walls recoil, releasing the stored elastic energy and converting it to pressure
energy and kinetic energy - more pressure energy.

63
NOTES
.,,.
,. NOTES
'-,-
• Physiological
NORMAL VARIATIONS
adaptations within
cardiovascular system in response to
changes such as hemorrhage, exercise,
postural changes

CARDIOVASCULAR CHANGES
DURING EXERCISE
osmsJl/eo:rcliovo.seulo.T-eho.nges-exeTeise
• Involves central nervous system (CNS),
local mechanisms
° CNS responses: changes in autonomic
nervous system (ANS) due to inputs
from cerebral motor cortex
O Local responses: exercise causes j
blood flow, 02 delivery to skeletal
muscles tr
• Exercise results in j sympathetic (151
receptors), ! parasympathetic activity to t
heart - j cardiac output due to j heart rate
+ j stroke volume i
• Muscle changes also occur (increased stroke
O i metabolites (lactate, potassium, volume)
adenosine) are produced - metabolites
stimulate local vasodilation - j blood ti
flow - ! overall total peripheral
resistance (TPR) t

OVERALL RESPONSETO EXERCISE i

{slight)
• Central command: l cardiac output (CO),
vasoconstriction in some vascular beds
(excludes exercising skeletal muscle,
cerebral, coronary circulations)
O j CO - j heart rate, contractility
ti
(increased tissue
O
j contractility - j stroke volume - j
02 composition)
pulse pressure
O j CO due to l venous return
(sympathetic vein constriction,
squeezing action of skeletal muscle on
veins) 64
 ( EXERCISE )

l
--~~~~~--I-~~~~~~--i
r c.ENTR.AL c.OMMANo , LOCAL RESPONSE

t SYMPAlllETIC. OVTFtOW t VASODILATOR

+ PARASYMPATHETIC. METABOLITES
OUTFLOW (HEART RATE ONLY)

l 1 i
t HEART RATE
f C.ONTR.AC.T1LITY
[ CONSTRICTION of ARTERIOLES
(SPLANCIINIC. & RENAL)
I C.ONSTR.IC.TION of VEINS
+ UNSTRESSEO VOLUME
DILATION of SICELETALMUSCLE
ARTERIOLES
f CARDIAC. OUTPUT t VENOUS RETURN PPR

CONSTRICTION of VEINS
+ VNSTRESSEO VOLUME
t VENOUS RETURN

Figure 20.1 Flowchart showing cardiovascular response to exercise.

CARDIOVASCULAR CHANGES
DURING HEMORRHAGE
osmsJl/ eo:rdiovo.seulo.T-eho.nges-hemoTTho.ge
• Blood loss ----> ! arterial pressure----> , Kidney secretes renin from renal
compensatory responses to restore arterial juxtaglomerular cells e- j angiotensin I
pressure production ----> converted to angiotensin
O Response mediated by baroreceptor II (causes arteriolar vasoconstriction,
reflex. renin-angiotensin-aldosterone stimulates aldosterone secretion)
system (RAAS), vascular actions • Capillary changes favor fluid reabsorption
, j sympathetic outflow to blood
Decrease in arterial pressure
vessels, angiotensin II----> arteriolar
• Hemorrhage ----> ! total blood volume ----> vasoconstriction ----> ! capillary
! venous return to heart.} right atrial hydrostatic pressure (P)--> restricts
pressure ----> ! cardiac output----> ! P. as a filtration out of capillaries, favors
product of cardiac output, TPR absorption
Return of arterial pressure
• Baroreceptors in carotid sinus detect ! P. OTHER RESPONSES IN
----> relay information to medulla via carotid HEMORRHAGE
sinus nerve ----> j sympathetic outflow to • Hypoxemia (! arterial P0J carotid, aortic
heart, blood vessels; ! parasympathetic bodies chemoreceptors sense ! P02 ----> j
outflow to heart----> j heart rate, j sympathetic outflow to blood vessels ----> j
contractility, j TPR. constriction of veins vasoconstriction, TPR. P.
• ! mean arterial pressure----> ! perfusion to • Cerebral ischemia: local j Pcoz
kidney----> response via RAAS
65
• ! blood volume - ! return of blood to heart
- detection by atria volume receptors
- ADH secretion to maintain adequate
blood pressure - water reabsorption
by renal collecting ducts - arteriolar
vasoconstriction

t
!
(produces increased
venous return)

i
(secreted from
adrenal medulla)

i
(stimulated by
decreased
blood volume)

66
 ( HEMORRHAGE - l Po. )

i------f---i
BAROREC.EPTOR RENIN- C.APILLARIES
REFLEX ANGIOTENSIN 11-
ALDOSTERONE

t SYMPATHETIC.
OUTFLOW t
ANGIOTENSIN II i
f HEART RATE C.ONSTRIC,TlON of VEINS C.ONSTRIC,TION of
f C.ONTRAC.TILITY l UNSTRESSED VOLUME ARTERIOLES
f C.ARDIAC. t VENOUS RETURN f TPR
OUTPUT
f BLOOD
VOLUME
fNo.·
REABSORPTION

t BLOOD
VOLUME

Figure 20.2 Flowchart showing cardiovascular responses to hemorrhage.

CARDIOVASCULAR CHANGES
DURING POSTURAL CHANGE
osms.i"l/ ee1rdlove1seule1r-ehe1nges- os-lure1I
• Standing up quickly--. lightheadedness, into interstitial fluid, ! intravascular
sometimes fainting (due to delayed volume
constriction of lower extremity blood , Severe ! blood pressure----. syncope
vessels ----. orthostatic hypotension)
0 ! in systolic blood pressure > 20mmHg/ Response of baroreceptor reflex
diastolic blood pressure> lOmmHg • Responsible for homeostatic blood pressure
within three minutes of standing maintenance
• Initiating event: pooling of blood in • Carotid sinus baroreceptors detect ! P.----.
extremities sends information to medullary vasomotor
O Moving from supine to standing center e- inactivates medulla vagal
position: blood pools in veins of lower neurons, activates sympathetic neurons
extrernities e- ! venous return to heart, ----. j sympathetic outflow to heart, blood
! cardiac output----. ! mean arterial vessels, ! parasympathetic outflow to heart
pressure to normalize P.
O Venous poolinq-» j hydrostatic • l systemic vascular resistance, cardiac
pressure in leg vetns=- j fluid filtration output act in negative feedback mechanism
to maintain P.
67
 ! (toward normal)

! l
(decreased venous return) (toward normal)

! l
(decreased stroke volume) (toward normal)

i
!
(pooling of blood in l
(toward normal)
lower extremities)

68
 POOLING of BLOOD In VEINS

I SARORECPTOR REFLEX I

,
I t SYMPATHETIC OUTFLOW I

,
'
t HEART RATE
f CONTRACTILITY
f CARDIAC OUTPUT
CONSTRICTION of
ARTERIOLES
f TPR
'
CONSTRICTION of VEINS
i UNSTRESSED VOLUME
t VENOUS RETURN

Figure 20.3 Flowchart showing cardiovascular response to postural change.

69
NOTES

NOTES
I SPECIFIC, CIRCULATIONS

CEREBRAL CIRCULATION
osmsJl/eeTe bTo.1-eiTeulo.-lion
• Cerebral circulation: managed almost Anterior segment
entirely by local (intrinsic) control • Supplied by internal carotid arteries
(autoregulation; active, reactive hyperemia) • Enter skull in carotid canal, branch out
O
t pC02 (tW, !PH) - arteriolar , Ophthalmic arteries: supply eyes, orbits,
vasodilation - l blood flow - C02 forehead, nose
removal (most vasoactive metabolites
, Anterior cerebral artery: medial part of
too big to cross blood-brain barrier -
frontal, parietal lobes; anastomoses with
do not affect cerebral tissue
counterpart via anterior communicating
O Hyperventilation works by artery (part of circle of Willis)
same mechanism - ! pC02 -
, Middle cerebral artery: supplies lateral
vasoconstriction (used to reduce
sides of temporal, parietal, frontal lobes
swelling in situations of cerebral edema)
Posterior segment
CEREBRAL BLOOD SUPPLY • Supplied by vertebral arteries
SEGMENTATION • Enter skull through foramen magnum,
• Cerebral blood supply separated into branch out
anterior, posterior segments , Right, left vertebral arteries fuse in
• Anterior, posterior circulatory segments skull - basilar artery which supplies
join via arterial posterior communicating brainstem, cerebellum, pons
arteries, form circle of Willis , Posterior cerebral arteries: supply
O Back-up circulation in case of blood occipital lobes, inferior parts of temporal
vessel occlusion lobes

70
 CORONARY CIRCULATION
osms.i"l/ eoTone1T14-eiTeule1-l:ion
• Coronary arteries: blood vessels delivering CORONARY CIRCULATION CONTROL
oxygenated blood to heart (myocardium) • Coronary circulation managed primarily
• Cardiac veins: blood vessels retrieving by local (intrinsic) control, secondarily by
deoxygenated blood from heart sympathetic nervous system
• I oxygen demand - I blood flow
CORONARY ARTERIES • Active hyperemia via local (intrinsic) control
triggers
• Two coronary arteries emerge from base of
aorta, surround heart in coronary sulcus , Hypoxia - build-up of metabolites
ADP, AMP - degraded to adenosine
Left coronary artery (potent vasodilator) - binds to coronary
• Two branches; supplies left atrium. left vascular smooth muscle - ! calcium
ventricle, interventricular septum influx into cells - vasodilation - j
° Circumflex artery: supplies left atrium, blood flow, oxygen delivery
posterior wall of left ventricle • Other intrinsic control of vascular tone
O Anterior interventricular artery: supplies provided by endothelial factors
interventricular septum, anterior walls of , Endothelium-derived nitric oxide:
ventricles relaxes arterial smooth muscle
, Prostacyclin: vasodilator
Right coronary artery
, Endothelium-derived hyperpolarizing
• Two branches; supplies right atrium, right factor (EDHF): vasodilator
ventricle, part of left ventricle, electrical
, Endothelin 1: vasoconstrictor
conduction system
• Reactive hyperemia
O Right marginal artery: supplies lateral
, Brief arterial occlusion period during
right side of heart, superficial parts of
ventricle systole - ! blood flow - j 02 debt -
vasodilation during diastole - l blood
O Posterior interventricular artery:
flow - 02 demands are met
supplies interventricular septum.
posterior walls of ventricles

71
 CONTROL OF BLOOD FLOW
CIRCULATION
osms.tl/\>lood-flow
• Blood flow regulation • Metabolic hypothesis for autoregulation,
O Intrinsic (local): humoral, myogenic active, reactive hyperemia
control ' 02 distribution changes in response to
O Extrinsic (systemic): hormonal, neural 02 consumption via altering arteriolar
resistance
' i metabolism - l vasodilating
LOCAL (INTRINSIC) BLOOD FLOW metabolites (C02, H-. K+, lactate,
CONTROL adenosine) - arteriole vasodilation
Mechanisms - ! resistance - j blood flow, 02
distribution
• Humoral: mediated by vasoactive
substances , Certain tissues more susceptible
O Histamine,
to certain metabolites (coronary
nitric oxide (arteriole dilation)
clrculation=Po.; adenosine; cerebral
O Endothelin, serotonin
circulation-PC02)
• Autoregulation: maintains constant blood
flow via direct control of arterial resistance
O Present in organs such as kidneys, brain,
NEURAL & HORMONAL (EXTRINSIC)
heart, skeletal muscle (e.g. ! coronary
CONTROL
artery pressure - compensatory • Neural: sympathetic nervous system acts
arteriole vasodilation - ! vessel on vascular smooth muscle
resistance - constant blood flow) , al: vasoconstriction - skin, intestines
• Active hyperemia: I blood flow directed to , {32: vasodilation - lungs, skeletal
organ/tissue associated with l metabolic muscles
activity (e.g. l blood flow in active skeletal • Hormonal: vasopressin released from
muscle) anterior pituitary - vasoconstriction
• Reactive hyperemia: temporary j blood
flow following ischemia (! blood flow) in
organ (e.g. arterial occlusion - ! blood flow
- I 02 debt - vasodilation. l blood flow)
• Myogenic hypothesis for autoregulation
° Focus on arteriolar resistance: vascular
smooth muscle contracts upon
stretching (l wall tension) and vice versa
O
l blood flow - arteriole stretching -
contraction - l resistance - constant
blood flow
0
! blood flow - ! arteriole stretching -
relaxation - ! resistance - constant
blood flow
O Explained by law of Laplace: l pressure
(P) + ! radius (r) - tension (T) remains
constant (T =P x r)

72
 MICROCIRCULATION &
STARLING FORCES
osms.i"l/mieroeireulo.-lion-s-le1rling-forees
• Microcirculation: vascular network involving • Vesicular transport: large molecule
capillaries, lymphatic vessels exchange (proteins) via pinocytic vesicles
(caveolae)
Capillaries O In some tissues (kidney, intestine)
• Vessels: thin walls lined with endothelial proteins pass through capillary
cells fenestrations
• Arterioles ----> metarterioles----> capillaries----> • Osmosis: if capillary wall has aqueous
venules v- veins pores, pressure gradient across membrane,
O Metarterioles end in precapillary driven by Starling forces
sphlncters=- smooth muscle ring
controls blood flow/capillary exchange
rate by constricting/relaxing
STARLING FORCES
• Capillary filtration/absorption depend on
° Capillary blood flow regulated by
Starling forces: hydrostatic, colloid osmotic
intrinsic (local), extrinsic (systemic)
(oncotic) pressure
control
, Filtration: fluid movement from
capillaries----> interstitium
CAPILLARY EXCHANGE , Absorption: fluid movement from
• Capillaries: exchange sites for nutrients, interstitium ----> capillaries
waste, fluids between interstitial, vascular
space Hydrostatic pressure
O Afferent blood: capillaries----> interstitial • Pressure exerted by fluid against capillary
space ----> tissue wall
O Efferent blood: tissue ----> interstitial • Capillary hydrostatic pressure (Pc)
space----> capillaries ° Favors filtration: tends to move fluid out
of capillaries
Capillary exchange types
O Blood pressure ! throughout capillary
• Simple diffusion: substance exchange beds ----> arterial (37mmHg) > venous
through lipid bilayer/between capillary
(17mmHg) pressure
wall's epithelial cells
• Interstitial fluid hydrostatic pressure (PJ
O Depends on driving force (partial
, Opposes filtration: pressure exerted
pressure gradient), available diffusion
outside capillary wall
area
O Driving force: substances
, Tends to move fluid into capillary
move across
their own partial pressure gradient , Contains very little fluid----> P considered
(towards ! concentration area) zero, slightly positive/sliqhtlv negative
(lmmHg)
O Lipid soluble substances (02, C02) pass
through lipid bilayer Colloid osmotic pressure (oncotic pressure)
O Water soluble substances (ions, glucose, • Pressure gradient: large non-diffusible
amino acids) pass between endothelial molecules (e.g. plasma proteins)
cells through fluid-filled intercellular
, Capillary oncotic pressure (rt)
clefts/fenestrations
(25mmHg): created by plasma proteins
(primarily albumin; reflection coefficient
= 1.0); opposes filtration
73
 O Interstitial oncotic pressure (re) LYMPH
(OmmHg): contains very little protein; • Lymphatic capillaries drain excess fluid +
favors filtration some proteins from interstitial space into
venous system
Flow direction
, Lymphatic capillaries - lymphatic
• Arterial end of capillary
vessels - thoracic duct/right lymphatic
OBlood pressure's outward driving force > duct - subclavian vein
inwardly directed oncotic pressure force
, One way valves - unidirectional flow
- fluid moves out of vessel
• Venous end of capillary Edema
O Oncotic pressure inward driving force > • Abnormal buildup of fluid in interstitial
outwardly directed hydrostatic pressure space
- fluid moves into vessel • Causes
• Most fluid leaving capillary at arterial end , Imbalance of Starling forces
reenters capillary before leaving venous , l hydrostatic capillary pressure (i
end volume-e.g. heart failure; obstruction;
• Fluid remaining in interstitial space e.g. thrombosis)
recovered by lymphatic vessels , ! oncotic capillary
pressure (!
• Fluid movement through capillary wall is plasma protein -e.g. liver failure,
dependent on Starling force malnourishment, nephrotic syndrome
, l capillary permeability (burns/
Starling equation
inflammation)
• Jv = Kf [( Pc - P) - (rec - r9]
, Impaired drainage (immobility; lack of/
o J = fluid movement (mUmin)
v irradiated lymphatic nodes; parasitic
° K1 = hydraulic conductance (wall to infections of lymphatic nodes-e.g.
water permeability; depends on tissue, filariasis)
wall structure-e.g. fenestrated, non-
fenestrated)

74
 NOTES

NOTES
BODY TEMPERATURE REGULATION

BODY TEMPERATURE REGULATION

(THERMOREGULATION)

NORMAL BODY TEMPERATURE production

▪ 37 ± 0.5 °C (98.6 ± 0.9 °F) ▫ Piloerection (goosebumps) → heat
▪ Hypothalamic thermoregulatory center acts trapping
as a thermostat ▪ Thyroid hormones released from
▫ Sets temperature set-point hypothalamus → ↑ metabolic rate → ↑ heat
▪ Thermoreceptors production
▫ Peripheral (in skin) → sense surface ▪ Non-shivering thermogenesis using brown
temperature adipose tissue
▫ Central (in the body core—e.g. ▫ Activation of primary motor center for
hypothalamus itself) → sense core shivering in the posterior hypothalamus
temperature → skeletal muscle contraction →
shivering → ↑ heat production
▪ Temperature variations activate
thermoreceptors → thermoreceptors ▫ Behavioral changes (adding garments,
inform hypothalamus → hypothalamus tightening the arms across the chest,
activates heat regulation mechanisms → moving around)
temperature returns to baseline
Heat dissipation
▪ Body region variations
▪ Inhibition of sympathetic activity in skin
▫ Core: higher temperature, more stable blood vessels → blood goes to skin → ↑
▫ Skin: lower temperature, more variable heat loss
▪ Core temperature varies with throughout ▪ Activation of sympathetic cholinergic fibers
the day innervating sweat glands → ↑ sweating →
▫ Lower during sleep ↑ heat loss
▫ Higher when awake ▪ Behavioral changes (removing garments,
reducing movements, fanning air over
body)
BODY TEMPERATURE
MAINTENANCE Fever
▪ Body temperature maintained by balancing ▪ Body temperature elevation due to change
heat-generation, heat loss in hypothalamic set-point
Heat generation ▪ Pyrogens act on hypothalamus →
hypothalamus releases prostaglandins
▪ Activation of sympathetic nervous system
→ hypothalamic set-point temperature
▫ Vasoconstriction of skin arterioles → increases → heat-generating mechanisms
blood bypasses skin → ↓ heat loss kicks in → body temperature rises and
▫ Adrenal glands release catecholamines reaches new baseline temperature
(epinephrine, norepinephrine) → ▫ Aspirin reduces fever by inhibiting
increased metabolic rate → ↑ heat prostaglandins production
75

OSMOSIS.ORG 157
 ▪ Benefits of fever ▫ Depolarizing muscle relaxants:
▫ Inhibit bacterial growth by making Succinylcholine, Decamethonium
growing conditions less favorable ▪ Potentially fatal
▫ Increase efficiency of immune cells ▪ Treatment
▫ Dantrolene (skeletal muscle relaxant)
HYPERTHERMIA
▪ Elevation of body temperature without HYPOTHERMIA
change in hypothalamic set-point ▪ Abnormally low temperature
▪ Normal mechanisms of thermoregulation ▫ Diagnosis: core temperature <
are overwhelmed by various factors 35°C/95°F
▫ Excessive environmental temperature ▪ Compensatory mechanisms responding to
▫ Impaired ability to dissipate heat cold stress are overwhelmed
▫ Excessive heat production ▪ ↓ core body temperature → ↓↓ metabolic
rate → myocardial irritability, cold diuresis
Heat exhaustion (↓ renal blood flow, water resorption)
▪ Excessive sweating → significant water ▫ Progressive oliguria as ↓ core
and electrolyte loss → ↓ blood volume → ↓ temperature → ↓ intravascular volume,
arterial pressure ↑ hematocrit, central nervous system
depression
Heat stroke
▪ Hyperthermia > 40°C/105.1°F Risk factors
▪ Potentially fatal ▪ Prolonged cold exposure
▪ Causes ▫ E.g. inadequate clothing/shelter, cold
▫ High environmental temperature water immersion
▫ Periods of intense physical activity ▪ Impaired thermoregulation
▪ Risk factors ▫ E.g. hypothalamic dysfunction,
▫ Susceptible individuals: infants, children metabolic derangement
(higher metabolic rate; ineffective ▪ ↑ heat loss
sweating; physical, psychological ▫ Multisystem trauma, shock, spinal cord
limitations); elderly (pre-existing transection
conditions; physical, psychological ▪ Iatrogenic
limitations)
▫ Cold IV fluid administration, inadequate
▫ Medications: ones that inhibit heat- operating room warming
dissipating mechanisms (beta blockers,
▪ ↑ risk populations
diuretics)
▫ Older adults (↓ physiologic reserve, ↓
Malignant hyperthermia sensory perception, chronic medical
▪ Genetic alteration of ryanodine receptor 1 conditions)
(RYR1) in the muscle cells ▫ Children (↑ body surface area to
▪ Normally: cell depolarization → RYR1 body mass ratio, ↓ glycogen stores,
activation → calcium release from young infants unable to use shivering
sarcoplasmic reticulum into cytoplasm → thermogenesis)
muscle contraction
Complications
▪ In malignant hyperthermia: cell
▪ Cardiac arrhythmias, myocardial infarction,
depolarization → RYR1 hyperactivation →
pulmonary edema, pulmonary embolism,
excessive calcium release → inappropriate
lactic acidosis, disseminated intravascular
muscle contraction, ↑↑ metabolic rate →
coagulation (DIC), coma, death
excessive heat production
▪ Triggered by drugs Signs & symptoms
▫ Anesthetic gas: Alothane, Sevoflurane, ▪ Mild hypothermia
Desflurane ▫ Core temperature 32–35°C/90–95°F
76

158 OSMOSIS.ORG
 Chapter 22 Body Temperature Regulation

▫ Shivering, tachypnea, tachycardia,

confusion
▪ Moderate hypothermia
▫ Core temperature 28–32°C/82–90°F
▫ ↓ shivering and muscle rigidity,
hypoventilation, bradycardia, ↓ cardiac
output, lethargy, arrhythmias, loss of
pupillary reflexes
▪ Severe hypothermia
▫ Core temperature < 28ºC/82°F
▫ Apnea, ↓ cardiac activity → ventricular
arrhythmias → asystole, coma, loss of
ocular reflexes, ↓↓ metabolic rate

Rewarming treatment
▪ Warmed blankets/forced warm-air system;
heated, humidified oxygen; warmed
crystalloid IV fluid; pleural, peritoneal lavage
using warm saline solution; vasopressors
▪ Extracorporeal blood rewarming
▫ Venovenous rewarming, hemodialysis,
continuous arteriovenous rewarming
(CAVR), cardiopulmonary bypass (CPB),
extracorporeal membrane oxygenation
(ECMO)

77

OSMOSIS.ORG 159