Cardiac Study Guide
Cardiac Study Guide
Cardiac Study Guide
AUTONOMIC NERVOUS SYSTEM PHARMACOLOGY When does the coronary arteries receive their blood flow?
PNS (Peripheral Nervous System)
1) Somatic Division: Cranial/Spinal motor nerves that innervate skeletal muscle (Vol/consc)
2) Autonomic Nervous System: Cranial/Spinal nerves that innervate (cardiac/smooth/glands) What is collateral blood flow?
(involuntary/unconscious control)
Parasympathetic Nervous System The left coronary artery begins as one main artery. What are the two
C III, VII, IX, and X (S2-S4 arteries that it branches into?
Preganglionic=Long________Post ganglionic short (message to one site cardiac/smooth/gland)
Cholinergic Nerves (ACH) (act on Muscarinic receptors) if they inhibit called anticholinergic) What do the two feed?
ONE body system at a time. REST & DIGEST or FEED & BREED
HR, protects retina, BP, Empties bowel/bladder, GI motility, absorption of nutrients. The Right Coronary Artery in 90% of the population becomes the
Sympathetic Nervous System posterior descending coronary artery. What does it feed? What are
Thoracolumbar Division the branches?
T1-L3
What does RIBLAT stand for?
Preganglionic=short____Postganglionic=long (Global response Cardiac/Smooth/Glands)
Adrenergic (ACH from PRE and Norepinephrine from POST)
What does it mean to be RIGHT or LEFT sided dominant?
ALL systems respond FIGHT or FLIGHT
HR, BP, Blood shunted to skeletal muscles, Blood Glucose, Pupils dilate, Epineprine
What does a Swan Ganz catheter measure?
MOST MAJOR BODY SYS. & GLANDS RECEIVE A NERVE FROM EACH but BLOOD
VESSELS ARE NOT PNS INNERVATED
What does the wedge pressure measure?
One system dominates at a time.
When one Autonomic Nervous System is blocked, the other will work.
What is an ejection fraction? What is the normal ejection fraction?
Medications are made to stimulate or block a system or receptor site
NEUROTRANSMITTERS
What is SVO2? What is the normal value when your body is at rest?
ACH:
DOPAMINE: most turns into norepinephrine, (Fine motor movement/emotions) What three effector organs does the Sympathetic NS stimulate?
EPINEPHRINE: made from norepinephrine in the adrenal medulla adrenaline-adrenergic fibers
NOREPINEPHRINE: Excitatory What system is responsible for involuntary muscle movement?
SEROTONIN: Sleep, Behavior, and Consciousness
GABA: feeling of panic/anxiety (amygdala releases GABA to inhibit this response) The adrenergic nervous system is another name for the SNS
Tranquilizing, calming effect on emotion. (inhibitory) Benzodiazepines for these patients)
ONE OF THREE THINGS OCCUR
Neurotransmitter released, attaches, and you have a RESPONSE. The cholinergic nervous system is another name for the PSNS
Passes back to pre-synaptic neuron for RE-UPTAKE
Extra may be destroyed by Monoamine Oxidase MAO There are specific neurotransmitters responsible for carrying on the
ACH is released and binds with cholinergic receptor sitesaction occursACE inactivates message in the SNS
extra no further actions occur.
ALPHA 1 Receptors: Smooth Muscles of the arterial system (Vasoconstrict when stimulated) FILL TANK
BETA 1 Receptors: one heart Rate, Conduction, & Contraction of cardiac cells and tissue There are specific neurotransmitters responsible for carrying on the
BETA 2 Receptors: two lungs Smooth muscles specifically at bronchiole/vasc. level. Dilation when message in the PSNS
stimulated
DOPAMINERGIC Receptors: renal arterioles, vasodilate GFR/Urinary output. sodium excretion What happens to the messengers when they dont all bind to
Inotrope/contractility--------Chronotrope/rate-------Dromotrope/conductivity effector organs receptor sites?
SYMPATHOMIMETICS NUR 272 PHARMACOLOGY VASODILATORS (LETS BRING IT DOWN)
Mimics the SNS CALCIUM CHANNEL BLOCKERS (DIPINE) NITROGLYCERIN 3
Produces similar effects to neurotransmitters blocks inward movement of Ca into cardiac/smooth Dilates venous beds in low doses
May be Alpha, Beta, or both cells preload=HR
DOPAMINE Cardiac Muscle (Negative Inotropes Dilates arteriole beds high doses afterload
Pressor first used for Hypotension Conduction (Negative Chronotropes/Dromotropes for Coronary artery vasodilator/cerebral ( HA)
Titrated to keep SBP >90-100 automaticity) Can develop tolerance with long term use
Monitor MAP (action dose related Vascular Smooth Muscle: vasodilator 10-20mcg/min starting dose, up to 200mcg/min
5mcg/kg/min (Dopaminergic dose, vasodilates renal Side Effects: Constipation, headache, edema, Vital signs both arms, higher of the two pressures
arterioles GFR/urinary output/promotes Na excretion) hypotension, drowsiness, dizziness, and nausea Remove old patches, not over bone
>5mcg/kg/min= dromotrope/chronotrope SBP NORVASC (Amlodipine) NITROPRUSSIDE (nipride, nitropress)
>10mcg/kg/min= vasoconstriction, monitor peripheral peripheral vascular resistance binds to vascular smooth muscle causing
circulation, and maintain CVP 8-10 for hydration Cardiac output ( preload) vasodilation by interfering with Ca influx
EPINEPHRINE PROCARDIA (Nifedipine) preload/afterload
Stimulates BETA 1, Force of contraction, HR due to afterload Immediate onset, 2 minute 1/2life
increased membrane depolarization of pacemaker cells. Myocardial oxygen demand Used in Hypertensive crisis
cardiac output CARDIZEM (Diltiazem) Creates cyanide ion when binded to HgB, can
1:10,000 Cardiac arrest 1mg IVP Effective against fast dysrhythmias (AFIB) create toxic levels of cyanide. (lower rate, shorter
1:1,000 0.5ml SQ (anaphylaxis ventricular rate with A-FIB/A-FLUTTER period of time for excretion) (use extreme caution
LEVOPHED (Norepinephrine) Dilates coronary arteries w/ Prinzmetals Angina in renal failure)
potent inotrope at </= 2mcg/min OR 2-10mcg/min afterload & Myocardial Oxygen Demand 0.5-4mcg/min (protect from light)
ALPHA1 ACE INHIBITORS (PRILS) Side effects: Hypotension, seizures, bradycardia,
May need low doses of dopamine (renal protectant) Blocks the Angiotensin I converting enzyme (ACE) flushing, blurred vision, agitation, ICP
Monitor for reflex bradycardia Angiotensin II is a vasoconstrictor, also causes NICARDIPINE (Cardene)
Potential for CO due to peripheral vascoconstriction ( aldosterone release (Na & H2O) anti-hypertensive
preload) Blocks conversion from Angiotensin III Usually given for patients not responsible to
vascular resistance to renal beds by 55% Popular with CHF crowd, reducing remodeling labetalol.
Monitor renal function/distal circulation May cause hyperkalemia w/ renal function _________________________________________________
DOBUTAMINE (monitor creatine level) (Angio edema)
Beta 1 Agonist (facilitates action) vascular inflammation and helps with plaque stab. CARDIAC GLYCOSIDES
Ionotrope effect BETA BLOCKERS (LOL-Little Old Lady) (typically not 1st for DIGOXIN
HR with higher doses, can cause dysrhythmias HTN) + inotrope, -chronotrope/dromotrope
Potential cause of BP due to mild Beta 2 effects on blood Role with ischemic heart disease to myocardial Check apical heart rate
vessels. oxygen demand. CHF/Atrial Fibrillation/other tachycardias
Role with certain dysrhythmias due to stimulation Can be VERY TOXIC 0.5-2.0ng/ml
of beta 1 receptors Can cause hypokalemia
Used to treat HTN Hold for HR < 60BPM
_________________________________________________________ There are non-specific beta blockers Adverse affects: Nausea/loss of appetite,
ARB (ANGIOTENSIN II BLOCKER) (SARTAN) NORMODYNE (Labetalol) vomiting/diarrhea, dizziness, blurred vision,
No big difference between the ACE Inhibitors Beta1/Beta2 blockade yellow or green halos, difficult breathing.
Irbesartan (Avapro) Alpha 1 blockade as well _________________________________________________
Losartan (Cozaar) Used for hypertensive crises LASIX (Last six hrs)
Olmesartan (Benicar) BETA 1 SELECTIVE (cardioselective) HCTX (last up to 12hrs)
Valsartan (Diovan) LOPRESSOR (Metoprolol) ZAROXOLYN (thiazide diuretic)
Lower dose, primarily B1 antagonist lasts up to 24hrs
_________________________________________________________ Higher doses aslo B2 receptor blocker works better with patients with creatinine
ALPHA ONE BLOCKERS Toprol XL-extended release levels
blocks norepinephrine from vascoconstricting vessels Atenolol (Tenormin) Can diurese patients with GFR <20ml/min
Doxazosin (Cardura) _________________________________________________
Esmolol (Brevibloc)
Prazosin (Minipress) CARE AND COMFORT
NON-SELECTIVE
Terazosin (Hytrin) Administer through CVAD, use pump
Nadolol (Corgard)
Alfuzaosin (Uroxatral If placed peripherally (Phentolamine/Regitine)
Propranolol (Inderal)
_________________________________________________________ can be given for infiltrate (physician can give)
Sotalol (Betapace)
ADENOSINE Perform double checks with another RN
Timolol (Timoptic)
Natural neurotransmitter in your body Add current weights to pumps
Coreg (with alpha blocker)
Acts as a sedative LABEL LABEL AND LABEL
Two problems with Beta Blockers: Diabetics (signs of
6, 12, 12 mg life, 10 seconds give close to the heart AC
hypoglycemia were blocked and reactive airway disease due to
bronchoconstriction)
NUR 272-RF-11
THE ELECTROCARDIOGRAM BASIC CARDIAC ELECTROPHYSIOLOGY FIVE RULES FOR BASIC INTERPRETATION
Recording of Electrical Activity in the heart. Special pathways exist w/I the myocardium Is there a P wave for every QRS complex?
Gives only the ELECTRICAL activity within the heart Automaticity (Pacemaker cells only) What is the PR interval? 4
Does not reflect MECHANICAL activity. Excitability: ability to charge What is the QRS interval?
Isoelectric Line: Flat line denoting no electrical activity, heart at rest. Conductivity: Ability to transmit the electrical charge Is the rhythm regular or irregular?
P Wave: Refractoriness: Inability to prematurely depolarize What is the ventricular and atrial rate?
Atrial Depolarization (Toilet bowl theory) USE OF COUMADIN:
From the SA node Contractility: It either does or does not. Low risk emboli= ASA
Typically upright Polarization: (Gear Up) Resting membrane potential Moderate risk emboli= ASA or COUMADIN
PR Interval: outside is +, and inside it is Great risk of emboli=COUMADIN
Onset of P wave ends onset of QRS complex Depolarization: (Trigger): Ions move across the INR 2-3
0.12-0.20 seconds membrane changing the apposing charge===action Risks: Cardiac Failure, DM, Age, HTN, and
Conduction through the atria>AV Junction potential Stroke.
Can potentially be wide (medications, conditions) Repolarization (Re-charge): Ions move back in to Risk of Fall vs. benefits.
QRS Complex position, cell becomes negative again. APICAL-RADIAL PULSE DEFICIT
Q wave: 1st negative deflection following P Refractory Period: (absolute)Myocardial cell will not Apical pulse might differ from radial rate.
R wave: 1st positive after the P wave respond. (toilet bowel) QRS complex>>>>>peak of T What is conducted might not be felt in the
S wave: 1st negative deflection after the R wave wave (relative) some cells have repolarized and have periphery.
Ventricular Depolarization the potential to be stimulated. (downslope of T wave
Q-T Interval
Beginning of QRS complex to end of T wave CONDUCTION SYSTEM
Denotes ventricular activity PACEMAKER SITES (From 1 of 3 sites)
0.36-0.44 Altered by: MI, Acidosis, Electrolytes Abnormalities,
Hypoxia, Age, Drugs, Altered pathways, Pericarditis,
varies with HR
Electrocution
ST Segment
Atria (SA Node 60-100)
between end of QRS and beginning of T wave
Posterior wall, right atrium
Point where QRS complex meets the ST segment is J point
Early repolarization of ventricles Natural Pacemaker
T Wave Right Coronary Artery supplies blood
Rounded and upright AV Junction (AV node 40-60)
Ventricular Repolarization AV node & Bundle of His
Typically follows direction of QRS complex Gatekeeper, electrical link between
U Wave: atria/ventricles
follows T wave when seen Right Coronary Artery supplies blood
May represent repolarization of Purkinje fibers Right and Left Bundle Branches
Easier to see with slower rates, < 2 mm Right-R Ventricle
Left-L Ventricle
COUNT THE RATE Conducts the electrical impulses down to
ventricles
Ventricles (Purkinje Fibers (20-40)
Spreads impulses received from bundles to
ventricular walls.
0.08-0.12 seconds to occur
Ectopic Pacemaker (Ectopic beat)
Impulses created outside the normal conductive
pathway.
Creates ectopic beat (not from SA node)
SEE BELOW CARDIAC
**** LOOK AT THE QRS COMPLEX**********
Narrow: Atria or AV Junction
RHYTHM STRIPS
Wide: Artificial Pacemaker, Bundle or Ventricular in nature
Does it have P waves?
SUPRAVENTRICULAR TACYCARDIA SINUS RHYTHM w/ THIRD DEGREE AV BLOCK
NORMAL SINUS RHYTHM (PR intervals differentGate is closed 5
SINUS TACHYCARDIA
NORMAL SINUS RHYTHM w/ FIRST DEGREE AV
BLOCK (<0.12) ATRIAL FLUTTER (One site)
ASYSTOLE
ISCHEMIA vs. INJURY & INFARCTION ACUTE CORONARY SYNDROMES WHATS IT FEELS LIKE?
unstable lesions lead to infarction Coronary Perfusion: Pressure sensation, squeezing, substernal or
Result from blockages in coronary artery Heart Rate (too fast or too slow can CO)
epigastric pain.
6
Rupture of lesions release substances causing platelet Aortic Pressure (Can be too high or low>>>>>CO Dull ache, does not increase with deep breath
aggregation, thrombin generation & vasoconstriction. Metabolic Activity (Metabolic Acidosis affects, Elephant sitting on my chest.
Acidosis develops and depresses myocardial contractility. contractility. Nausea, indigestion, weakness, upper back pain,
Collateral circulation??? Is it present (age of patient) Collateral Circulation: If it isnt present, suddent and fatigue
Cellular acidosis cardiac death. Hearts way to preserving itself SIGNS AND SYMPTOMS
Decreased myocardial contraction ( CO) Diameter of the vessel: leads to pressure. Diaphoresis, Cool/mottled skin, palpitations
Electrolyte imbalances ( K, Mg, lead to Torsades) CO can lead to an MI Nausea/vomiting, dysrhythmias, L/R HF
Impulse conduction complications (BBB) Oxygen to the tissues: Altered mental status.
Dysrhythmias (biggest complication) Oxygen has to get in RIGHT SIDED HEART FAILURE
ISCHEMIA Got to have Hemoglobin to carry it. JVD, Peripheral edema, Hepatomegaly
Pump Abdominal pain, loss of appetite, CVP
Ability to unload O2 Increased abdominal girth
STABLE vs. UNSTABLE ANGINA ANGINAL EQUIVALENTS
STABLE Shortness of breath
Predictable. Fatigue
Usually activity related Pallor/Palpitations
Cold/stressed Anxiety, Nausea and vomiting
ST segment depression >/= 1mm below the isoelectric line
Rest and Nitroglycerin Diaphoresis, lightheadedness
in 2 leads
Pain is easily relieved Impending doom, weakness
Can lead to Infarction
UNSTABLE Indigestion/heartburn
Also note K levels
Take a nitro and it continues
Patient rests and the pain continues
INJURY/INFARCTION
The pain is unpredictable or becomes more frequent
PRINZMETALS (Variant)
Spasm or lesion
Does not usually occur with activity or stress
Usually occurs with some degree of stenosis or
fibrous plaque.
Can be secondary to recreational drugs.
ST segment elevation >/= 1mm above the isoelectric line in ACUTE CORONARY SYNDROMES CAUSED BY
2 leads. Rupture of atherosclerotic plaque (activation of
May see T-wave inversion SNS/Catecholamine release)
May see Q-waves Vasospasm
PATHOLOGICAL Q-WAVES Obstruction of plaque or re-stenosis
Inflammation of coronary artery
Increased oxygen demand.
INFLAMMATORY CHANGES
Lipid Core (fibrous cap) seperates the clotting factors
in the blood. (thicker it is the better)
< 20 minutes, subendocardial injury (small not through the Inflammatory cells and macrophages erode protective
muscle completely, NO Q wave present) cap and it ruptures.
> 1-6hrs, transmural infarction noted (large completely Contact with blood in the lumen
through the muscle Q WAVE PRESENT, possibly inverted Platelet aggregation and thrombin then generated
T wave) (re-modeling of the ventricle, HF, Aneurysm, THROMBOSIS-----then ACS
rupture) Lactic acid causes the pain CO
EMERGENT PACEMAKER YOU SEE (BRADYCARDIA)
Hemodynamically significant bradycardia
Bradycardia unresponsive to drugs.
I ISUPREL
D DOPAMINE
E EPINEPHRINE
A ATROPINE
DIAGNOSTIC TESTING AND LAB RESULTS MEDICAL MANAGEMENT OF THE MI BETA BLOCKERS
EKG (but be careful with it..) PATIENT Be CAREFUL 7
Electrolytes, CBC w/ diff, CPK w/ isoenzymes ACUTE MANAGEMENT Contraindications
CXR to rule out aortic dissection prior to lytics MONA (morphine, oxygen, nitro, and asprin) ** O2 Heart failure
CPK w/ Isoenzymes (MB%) FIRST Elderly
MB% > 5% indicative of MI Beta blockers Hypotension
Levels q8hrs X 3 Fibrinolytics HR > 110, <60
Elevated up to 72hrs post MI Arrhythmics May be added a few days post MI
(elevate with, injections, cardioversion, trauma, Diuretics********monitor renal status******* VENTRICULAR DYSRHYTHMIAS
rhabdomyolysis, CPR, debrillated) ACE Inhibitors Short Term (No treatment needed)
Troponin I (T) (proteins of actin/myosin unit released with Heart failure risks and overall mortality Long Term (Persist 48 post MI, consider ICD)
cardiac damage/measured in blood) Anticoagulants MEDICATIONS THAT INDUCE HYPOTENSION
Should be O LMW Heparin (lovenox) POST MI
Peaks in 24hrs (elevated 7-14 days post MI IV Heparin Thrombolytics (bleeding site)
renal failure, cardiac surgery, shock, myocarditis, Coumadin (LV impairment or A-fib) Beta Blockers
heart failure(BNP, normal EKG and no chest pain), Statins (works in liver) Ace Inhibitors (monitor creatinine)
cardiac contusion, cardioversion Zetia (decreased amount of absorbtion in the GI Nitrates
Myoglobin tract specifically the small bowel) Calcium Channel Blockers
Unreliable (muscle damage, peaks early) Vytorin(statin/zetia together) Digoxin (PRE-MI)
Stress Testing (on or off treadmill) Antiplatelet aggregates CORONARY ARTERY BYPASS GRAFTING (CABG)
ECHO (Detect wall abnormalities/valvular problems) EF % Stool Softners LIMA, Mammary artery more durable
Computed Tomography Angiography (X-rays taken PLAVIX Saphenous vein
following dye injection, takes about 20 minutes, Synergistic w/ ASA Secondary prevention (STOP smoking and
overestimate size of occlusion) risk of bleeding CONTROL diabetes)
PCI (Percutaneous Coronary Intervention) Avoid use of PPIs (Protonix) (different metabolism Mediastinal chest tubes
BMS: Bare Metal Stent (no medication, 20% and difficult to deal with side effects. Epicardial pacemaker placed.
reocclusion rate) Altered effects in some, doesnt always work COCAINE
DES: Drug eluded Stent (with medication Sirolimus- NITROGLYCERIN Premature Atherosclerosis
RAPAMUNE immunosupressant) Need IV for Nitro virgin (give Nitro if VS ok LVH due to Hypertension
CRP (C-reactive protein) released by the liver due to Give 3Sl 5 minutes apart Coronary artery vasoconstriction
inflammation Take BPs both arms and use higher of two O2 demand, thrombus formation
<1.0 Low RISK Repeat B/P in between each NTG BASIC CARE AND COMFORT
1.0-3.0mg/L= Average RISK EKG before and after pain relief RELIEVE THE PAIN, THIS IS PRIORITY
>3.0mg/L= high risk for MI NTG drip for unrelieved pain and consider morphine. Oxygen and pulse ox
elevated in: aged, increased body mass, HTN, and Tobacco smoke. THROMBOLYTIC ENZYMES (ASE) Monitor for dysrhythmias
REVIEW QUESTIONS GO AHEAD QUIZ YOURSELF! Break up the clotting mechanisms Monitor Neurological status (lytic therapy-signs
Differentiate the anginas alteplase recombinant (Activase) of bleeding)
Typically, what does an inverted T wave mean? anistreplase (Eminase) Monitor labs, vital signs and lung sounds.
Typically, what does ST segment depression mean? reteplase recombinant (Retavase) Emotional support.
Typically, what does ST segment elevation mean? streptokinase (Streptase)
Cold patient (bradycardia, a-fib, pressure
With an MI, what could be your EKG changes?
tenecteplase recombinant (TNKase) fluctuations)
Differentiate between a non-Q wave and a Q wave MI
urokinase (Abbokinase) Re-warming ( o2 demand) thorazine, morphine,
What does acidosis do to heart muscle?
TISSUE PLASMINOGEN ACTIVATOR (TPa) and valium
What is an anginal equivalent?
Most frequently used CHEST TUBE (No more than 70ml/hr, monitor
Name some common ones
What is different about women? Bleeding, anaphylaxis for TAMPONADE (chest tube drainage STOPS)
Differentiate between the cardiac markers Used for all clots. Disturbed Thought Process (clots, sleep
What does IDEA stand for? GLYCOPROTEIN IIb/IIIa Inhibitors disruption or CO????)
Name the drugs Inhibitors of platelet aggregation Monitor for infection, FEED patient, anemia,
What are the drugs used acutely for a patient with for acute episodes of unstable angina or MI/ patient depression
unstable angina or MI? going for angioplasty with or w/o stenting
What is the FIRST one used? ReoPro, Integrilin, Aggrastat
Name the categories of drugs used for maintenance post Given IVP or through infusion
MI understand their mechanism of action for their use Monitor for bleeding/thrombocytopenia
What are some complications post MI? ANTI-PLATELET AGGREGATES
How would we manage them? * Aspirin and Plavix
Be able to discuss the labs that need to be closely
monitored post MI
ACUTE DECREASE IN CARDIAC OUTPUT ACUTE HEART FAILURE PATHOPHYSIOLOGY
(Mechanisms that would typically HELP in a CO situation can OXYGEN GETS TO THE TISSUES: YOU HAVE TO THINK CELLULAR LEVEL 8
COMPLICATE things. Have Oxygen? 1. HYDROSTATIC PRESSURE ,
Chronic heart failure patients have no reserve, this quickly Hemoglobin to carry it. which passes the ONCOTIC pressure. (fluids start
tips the scale for them and they decompensate quickly. Pump to get oxygen to the tissues. to shift)
Activation of SNS can complication the situation (SEE Hemoglobin to unload the oxygen to the tissues. 2. VASOCONSTRICTION secondary to hypoxia.
BELOW---THINK ABOUT WHAT IT HAPPENING HEART FAILURE 3. FLUID shifts from capillary beds in to the
WITH THE PATIENT) Hearts inability to generate an adequate cardiac ALVEOLI in the lungs. (red blood cells too)
PHYSIOLOGICAL RESPONSES TO CARDIAC OUTPUT output. 4. GAS exchange.
CO (due to infection, hypovolemia, dysrhythmias) Cardiac Output is compromised: HEMODYNAMICS
1. Sympathetic ALPHA 1 Vascoconstriction Afterload: HTN PAWP >25mmHg)
BETA 1 Heart Rate Preload: Lasix (fluid is held) CVP
BETA 2 Bronchodilation Heart rate: too fast vs. too slow (a-fib 20%) Dysrhythmias
2. Chemoreceptors Respiratory Rate Contractility: ability to pump AMI EKG Changes (is this why their in Acute CHF)
3. Renin Aldosterone System--- Vasoconstriction/ LEFT SIDED (pulmonary edema) SIGNS AND SYMPTOMS
Aldosterone (H2o-Na) Left Ventricular issue (MI, HTN A-Fib) Dyspnea and Tachypnea
4. Antidiuretic Hormone (ADH)--- Keeps H2O only Hypertention hypotention/cardiogenic
RIGHT SIDED (systemic edema/periphery)
CARDIOGENIC SHOCK OCCURS WHEN THE BP DROPS shock
Acute pulmonary Diseases
BELOW 90 and THE BODY CAN NO LONGER COMPENSATE Crackles/wheezes
Effect of Left sided failure
Right Ventricular infarct. Fatigue
LETS REVIEW SOME SHALL WE?????? Restlesness, CP, Tachycardia
SYSTOLIC HEART FAILURE
Low ejection fraction (<50%) Pale, Cool, Clammy Skin
* There are very specific signs/symptoms of right sided
Think decrease CO LABS
heart failure.
Weakness, fatigue, exercise tolerance BNP
There are very specific signs/symptoms of acute left
DIASTOLIC HEART FAILURE B-Type (brain) natriuretic peptide
sided heart failure.
Need to know those compensatory mechanisms and Ejection fraction is normal Hormone secreted by the ventricles in response to
how it causes decompensation in acute heart failure TOO much stretch
CAUSES OF HEART FAILURE
What does a BNP tell you about your patients Cardiogenic: MI, Acute Heart Failure, Acute HTN, New A-fib or Higher it is the worse it is
ventricles? Do we always pay attention to the exact change in rate (GOAL IS TO HEART FUNCTION) Can decrease with proper management
number? Non Cardiogenic: Heroin, ARDS, or Sepsis (GOAL IS TO Helps differentiate COPD vs. CHF
Identify, by labs and diagnostics, that a client is in TREAT CAUSE) FOLLOW TRENDS
acute heart failure. < 100 no heart failure
What are the treatment goals for a patient in acute 100-300 heart failure present
heart failure? >300= mild heart failure
What classes of medications would be most likely >600= moderate heart failure
ordered for a patient admitted with acute heart failure? > 900= severe heart failure
Why is Natrecor ordered for a patient? ABGs
List the responsibilities of the nurse during an acute Respiratory alkalosis (early) followed by
episode of heart failure. respiratory acidosis
Basic care and comfort! CXR, electrolytes, LFTs, Thyroid function,
12EKG