Cardiology DR - Ahmed Mowafy
Cardiology DR - Ahmed Mowafy
Cardiology DR - Ahmed Mowafy
Internal Medicine
Cardiology
Second edition
By :
Dr. Ahmad M.Mowafy
اخ ْذَنا إِنت رَّبَنا الَ تُؤ ِ
َ ت َو َعمَْيهَا َما ا ْكتَ َسَب ْ َ ف المّهُ َن ْفساً إِالَّ ُو ْس َعهَا لَهَا َما َك َسَب ْالَ ُي َكمِّ ُ
ين ِمن قَْبمَِنا َرَّبَنا َوالَ َِّ
ص اًر َك َما َح َمْمتَهُ َعمَى الذ َ
ِ
طأَْنا َرَّبَنا َوالَ تَ ْحم ْل َعمَْيَنا إِ ْ َّن ِس َينا أ َْو أ ْ
َخ َ
انص ْرَنا َعمَى اغ ِف ْر لََنا َو ْار َح ْمَنا أ َ
َنت َم ْوالََنا فَ ُ ف َعَّنا َو ْ تُ َح ِّمْمَنا َما الَ طَاقَةَ لََنا بِ ِه َو ْ
اع ُ
ِ
اْل َ ْوِ اْل َكاف ِر َ
ين
صد ا العظي
سورة البقرة (آية)286
Preface
- First and foremost, thanks are due to ALLAH, to whom I relate
any success in achieving any work in my life.
Prof. Dr. Hossam Mowafy ; Head of critical care unit, Kasr El Ainy.
Ahmad Mowafy
Index
www.incapsuleseries.com
In Capsule Series Cardiology
Cardiology scheme
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Investigations : 4 items
1- X ray :
o Chamber enlargement .
o Pulmonary congestion in left sided diseases.
o Pleural effusion .
2- ECG :
o Chamber enlargement .
o Detect the cause .
you have to know ECG changes of the following diseases :
- angina - MI - dry pericarditis .
3- Echo :
o Chamber enlargement .
o Detect the cause .
o Paradoxical movement of the myocardium.
4- Catheterization :
o Chamber enlargement .
o Detect the cause .
But :
In myocardial infarction add : cardiac enzymes.
In infective endocarditis add : blood culture .
In pulmonary embolism add : pulmonary angiography
In dissecting aorta add : CT & MRI .
Treatment :
1- Treatment of the cause.
2- Treatment of precipitating factors : e.g. hyperlipidemia :
- statins : 20 - 80 mg/d SE: myositis .
- Fenofibrate : 300 mg/d - Omega 3 ( fish oil ) .
3- Specific treatment : unfortunately it differs according to the disease !!!!
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Heart Failure
Definition:
It is a clinical syndrome in which the heart can’t maintain adequate cardiac
output to meet the metabolic needs of the body despite a normal ventricular
filling.
Classification:
1- Left sided Right sided Both (congestive HF)
Etiology:
I- Left – sided heart failure :
Diastolic heart failure: In this type of HF, the decrease in COP is due
to inadequate ventricular filling, not impaired systolic contraction.
Clinical Picture:
І- Left sided heart failure: Scheme + cardiac signs
1- Manifestations of LCOP : 7 items
1- CNS : Dizziness, headache, syncope .
2-CVS : Ischemic heart disease.
3-Kidney : Oliguria .
4-Skin : Cold, peripheral cyanosis .
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5-Skletal muscle : fatigue , intermittent claudication .
6-Blood pressure: low systolic blood pressure.
7-Pulse : Weak.
2- Manifestations of pulmonary congestion: 7 items
1-Dyspnea: Exertional , orthopnea, paroxysmal nocturnal dyspnea or
dyspnea at rest .
2- Exertional Cough .
3-Recurrent chest infections.
4-Hemoptysis.
5-Pleural effusion.
6-Pulmonary edema .
7-Bilatera basal crepitation.
3-Features of the cause: Ischemic heart diseases , Systemic hypertension.
4-Cardiac signs:
a- Left ventricular enlargement .
b- Tachycardia.
c- Pulsus alternans: alternating strong & weak beats ( In advanced stage )
d- Gallop on the apex: due to flabby ventricle.
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5-Liver: enlarged , soft, tender.
6-GIT: dyspepsia, malabsorption may lead to cardiac cachexia.
7-Pleural effusion.
3-Features of the cause: e.g. - LSHF .
- Pulmonary hypertension .
4-Cardiav Signs: ( the same as left – pulsus alternans )
Differential Diagnosis :
LSHF RSHF
-Causes of dyspnea &orthopnea. -Pericardial effusion
-COPD
-Obesity
-Liver cirrhosis
Investigations:
1- X ray:
o Chamber enlargement .
o Pulmonary congestion in LSHF.
o Pleural effusion
2-ECG:
o Detect the cause e.g. MI
o Chamber enlargement.
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stroke volume
Ejection fraction = (n = 50%)
End diastolic volume
4-cardiac catheterization:
o Chamber enlargement .
o Detect the cause .
5-BNP ( B natriuretic peptide ) : (if normal, HF is unlikely)
3-Sedation: as diazepam.
4- Diuretics:
Aim:
a. They increase salt & water excretion blood Volume So,
decrease the work of the heart .
b. Edema & visceral congestion .
Types:
ị- Loop diuretics:
-act on Loop of henle ( reabsorption of Na, H2O, K, Cl)
-e.g.
- Furosemide ( Lasix ) : 40-160 mg/d (oral, IV, IM).
- Bumetanide ( Burinex )
ị ị- Thiazides:
-act on distal tubules ( reabsorption of Na, H2O, K, Cl)
-e.g.
- Hydrochlorothiazide: 25-100 mg/d
- Chlorothalidone.
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6- Inotropic agents:
- Digitalis .
- Dopamine .
- Dobutamine .
- Milrinone: phospho diastrase inhibitors, used in emergency .
Digitalis
Action:
o Contractility of the ventricles .
o Excitability .
o Conductivity .
o HR : by direct action & vagal stimulation .
o On ECG: sagging depression of ST segment .
Mechanism of action : ( contractility )
Inhibition of Na - K ATPase (Na pump) intracellular Na intracellular
Ca increase muscle contraction by sliding of actin & myosin .
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Contraindications:
o Absolute contraindications :
- Digitals toxicity .
- Ventricular tachycardia (VT).
o Relative contraindications :
- Partial heart block .
- Peptic ulcer .
Administration :
o Digitalization : (to reach optimum therapeutic level )
2 tablets daily for 5 days (oral).
o Maintenance dose : (compensates for daily urinary excretion )
0.5 – 1 tablets daily (oral)
Preparations :
o Digoxin (Lanoxin):excreted mainly by the kidney (tab=0.25mg , amp=0.5mg )
o Digitoxin : metabolized mainly in the liver (digitoxine hepatic).
o Ouabain (IV) .
DIGITALIS TOXICITY :
o Precipitating factors:
Old age. Renal failure.
Hypercalcemia. Hypokalemia.
Drugs : quinidine. Thyroid disorders.
o Clinical picture:
Non cardiac :
GIT : Anorexia , nausea, vomiting (1STsymptom)
Neurological: Psychosis , yellow vision .
Gynecomasteia .
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o Treatment :
Stop digitalis.
Stop diuretics.
Give K.
Digitalis antibodies (Digibind).
Anti-arrhythmic drugs (e.g. phenytoin , lidocaine ) .
o To avoid toxicity :
Decrease the dose.
Drug holiday.
Routine estimation of serum level of digitalis(N=0.5-2ng/ml).
7-β-blockers :
Historically , β blockers were contraindicated in HF due to their -ve
inotropic effect.
Recently : β blockers are indicated in HF because they were found to :
Reduce mortality & improve the prognosis.
Prevent arrhythmia.
Decrease blood pressure.
e.g.
Metoprolol ( 2nd generation β1 blocker )
Carvedilol (3rd generation β blocker).
Start with low doses with gradual increase .
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8- Aminophylline :
Action :
Bronchodilator . Vasodilator .
Diuretic effect . +ve inotropic .
Administration :
Oral , suppositories , IV.
IV injection must be very slowly to avoid arrhythmia .
9- Oxygen therapy :
Especially in acute pulmonary edema , MI & hypoxic cor pulmonale
Clinical picture :
Severe dyspnea at rest & orthopnea.
Sense of impending death.
Sweating & irritability.
Cyanosis.
Crepitation .
Cough with frothy pink sputum.
Differential Diagnosis :
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Treatment :
5) Vasodilators (IV):
Na nitroprusside IV infusion (0.5 – 5 mg / kg/ min)
Nitroglaycrin IV infusion (S/E: tolerance).
6) Inotropics :
- Dobutamine (β receptor agonist): +ve inotropic & vasodilatation (inodilator)
- Milrinone (phosphodiesterase inhibitor): inodilator.
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ETIOLOGY :
Diagnostic error : the case may be pericardial effusion rather
heart failure .
Improper management : Inadequate salt restriction .
Discontinuation of treatment .
presence of a precipitating factor :e.g. infection .
presence of the cause : uncontrolled hypertension , AS .
Terminal cases of heart failure .
TREATMENT :
Reassess the cause.
Removal of mechanical factor : valve replacement .
Removal of precipitating factor.
Proper management :
Strict bed rest.
Salt & even fluid restriction.
Proper doses.
For terminal cases :
IV Lasix , morphine , dobutamine , nitrate may be used .
Mechanical ventilation .
Cardiac transplantation .
I know not with what weapons World War III will be fought, but World War IV will be
fought with sticks and stones.
Albert Einstein
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Etiology :
MS AS MR AR
1. Rheumatic ( The most common )
2. Congenital.
3. Relative (functional)
4- Infective endocarditis.
5- Surgical.
4- Carey Coomb murmur 4- Calcification. 6- Mitral prolapse. 6- Syphilis.
5-Austin Flint murmur. 5- IHSS. 7- Papillary muscle 7- Dissecting aorta.
dysfunction.
Hemodynamics :
The Lung
o Left atrial pressure :
LV
LA
RA
RV
o Pulmonary congestion.
o Pulmonary hypertension.
o RSHF. ( late ) 4 3 2 1
o LSHF ( late ) in all except MS.
In general, any stenosis lead to pressure overload on the upstream cardiac chamber
whereas regurgitant lesions cause volume overload.
Clinical picture :
Clinical picture of hemodynamics plus :
MS 4 Stages. ( LAP , P congestion , P HTN , RSHF )
AS Syncope.
Any Aorta ( AS , AR ) Angina.
Any regurge (AR , MR ) Palpitation , general throbbing.
AR Peripheral signs of AR ( 9 signs )
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Cardiac examination :
Inspection & palpation :
- Apex :
o MS Slapping apex.
o AS Sustained apex.
o AR , MR hyperdynamic apex.
- Pulsation in the 2nd left intercostals space : by appearance of Pulmonary hypertension.
- Signs of ventricular enlargement ( late). ( no LVE in MS ).
Percussion : Dullness in the 2nd left intercostals space in a stage of pulmonary HTN.
Auscultation :
i. Normal heart sounds:
o S1 : in MS , in MR.
o S2 : pulmonary component may be accentuated due to pulmonary HTN (late)
ii. Additional sounds :
o Ejection click ( due to P. HTN )
o Gallop ( due to heart failure )
o Opening snap : in MS.
iii. Murmur : A M - A M
o Ejection Systolic : AS .
o Pan systolic : MR .
o Early diastolic : AR .
o Mid diastolic : MS .
Complications : 12
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6. LA enlargement compression on :
Lung dyspnea & cough.
Esophagus dysphagia.
Left recurrent laryngeal nerve hoarseness of voice.
7. Pulmonary congestion hemoptysis & recurrent chest infections.
8. Pulmonary infection.
9. Pulmonary embolism ( secondary to DVT )
10. RSHF.
11. LSHF except in MS.
12. Complications of surgery ( artificial valves ) :
Mechanical dysfunction. Thromboembolism.
Infective endocarditis. Hemolytic anemia.
Investigations :
X ray :
Chamber enlargement. Pulmonary congestion.
ECG :
Chamber enlargement e.g. LA P mitrale ( m shaped P wave )
Pulmonary hypertension P pulmonale ( Peaked P wave )
Echo & Doppler echo : ( The most important )
Chamber enlargement .
Detect the severity of the valve lesion.
Catheterization & angiography :
Detect the severity.
Chamber enlargement.
Treatment :
Medical :
1- Prophylaxis against IE & rheumatic activity.
2- Treatment of complications e.g. HF , AF , infections …
Surgical :
1- Balloon dilatation ( Percutaneous balloon valvuloplasty) for stenosis especially pure MS.
2- Valvotomy ( commissurotomy) : for stenosis.
3- Valve replacement : Tissue or synthetic valves .
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Mitral stenosis
Anatomy of Mitral valve :
Site : between the LA & LV .
Surface area : 4 - 5 cm2 , if < 1 cm2 tight MS.
Shape of mitral orifice : rounded or oval during
diastole & slit like during systole.
Axis : downward , forward & to the left.
Components:
– Fibrous ring.
– 2 cusps ( anteromedial & posterolateral )
– 2 papillary muscles : arise from the ventricle, to control the cusps movement.
– Chordae tendinae : arise from papillary muscles to both cusps.
Etiology :
1- Rheumatic heart disease : the commonest cause (99% ), more common in female (Ms).
Occurs years after the original attack & usually associated with multi valvular lesions.
2- Congenital : Lutembacher’s syndrome ( ASD + MS ) ?
3- Relative :
o Carrey coomb’s murmur : in acute stage of rheumatic fever due to :
edema of the cusps transient narrowing of the mitral valve.
o Austin-Flint murmur : murmur of MS in sever AR ( The regurged blood during
diastole interferes with the opening of mitral valve ).
o Conditions of blood flow through the mitral valve : VSD , PDA , MR.
Hemodynamics : 4 stages
1- LA Pressure with dilatation
2- back pressure on pulmonary vein The Lung
LV
LA
RA
RV
PA PV
( pulmonary congestion )
3- Pulmonary hypertension 4 3 2 1
4- RSHF
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Clinical picture :
Stage I : asymptomatic ( just of LA pressure )
Stage II : manifestations of pulmonary congestion : dyspnea , ….( p edema not common )
Stage III : manifestations of pulmonary hypertension : LCOP , Malar flush , giant (a) wave
Stage IV : manifestations of RSHF : LCOP, systemic congestion.
Cardiac examinations :
Inspection & palpation :
o Slapping apex : weak impulse (due to LV filling) with palpable S1 (due to accentuated S1)
o Apical diastolic thrill.
o Stage III : Pulsation & systolic thrill in the 2nd left intercostals space with palpable S2 .
Percussion : Stage III : Dullness in the 2nd left intercostals space .
Auscultation :
Normal heart sounds :
Accentuated S1 :
o The stenotic valve has to open as wide as possible to overcome this stenosis ,
leading to closure of mitral cusps from lower position S1 .
o The more the accentuated S1 , the more the stenosis.
o Causes of weak S1 in a case of MS : Calcification & Associated MR.
S2 : normal , may be accentuated in stage III ( pulmonary hypertension )
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Additional sounds :
1. Opening snap :
o Sharp snapping sound following S2 due to sudden opening of rigid cusps.
o The closer the snap to S2 , the more the stenosis.
o Calcification causes disappearance of opening snap.
2. Ejection click : in stage III ( Pulmonary hypertension )
3. Gallop on tricuspid area : in stage IV ( RSHF )
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Investigation :
X ray :
o LA enlargement ( lateral view with barium )
o Pulmonary congestion.
o Dilated pulmonary artery.
o RVE.
o Calcification of mitral valve.
ECG :
o LA enlargement ( P mitrale : m shaped P wave )
o Pulmonary hypertension ( P pulmonale : peaked P wave )
o RVE.
Echo & echo Doppler :
o Chamber enlargement . o Valve lesion. o Calcification.
Catheterization & angiography:
o Chamber enlargement.
o Mitral stenosis index = COP/LAP x 100 = 5/5 x 100 = 100% ( < 25 % is tight MS )
Treatment :
Medical :
1- Prophylaxis against IE & rheumatic activity.
2- Treatment of complications e.g. HF , AF , infections …
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Mitral Regurge
Etiology :
o Rheumatic ( the commonest ) o Surgical.
o Congenital. o Mitral valve prolapse.
o Infective endocarditis. o Papillary muscle dysfunction.
o Functional ( relative ) : dilatation of mitral ring due to dilatation of LV e.g. LSHF , AR.
Hemodynamics :
During systole : A part of blood regurgitates from LV to LA leading to LA dilatation .
During diastole : blood flow through the mitral valve volume load on LV LV
enlargement then failure.
In acute MR : as in myocardial infarction & IE , the LA has no time to dilate and
accommodate the regurgitant blood great of LAP rapid pulmonary
congestion then pulmonary edema & can lead to cardiogenic shock.
Clinical picture :
1- Asymptomatic for many years in mild cases.
2- Palpitation & general throbbing due to LV volume overload.
3- Manifestations of LSHF ( late )
4- Manifestations of pulmonary congestion then pulmonary hypertension RSHF later.
5- Acute pulmonary edema in a case of acute MR.
Cardiac examination :
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Additional sounds:
o With HF Gallop.
o With pulmonary hypertension Ejection click.
Murmur :
- Murmur of MR :
Site : best heard at the apex.
Character : blowing.
Relation to respiration & position : with expiration & in left lateral position.
Propagation : to axilla ( except in posterior leaflet regurge radiate to the base of heart)
Timing : Pansystolic murmur. ( plateau )
- Relative MS : mid diastolic murmur due to excess blood flow across the mitral valve.
Investigations :
– X ray & ECG : Chamber enlargement e.g. LA , LV .
– Echo : - Chamber enlargement - Valve lesion.
– Catheterization : - Chamber enlargement - Valve lesion .
Treatment :
o Medical : see scheme .
o Surgical : valve replacement or mitral valve repair.
Mitral valve prolapse
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Aortic Stenosis
Anatomy :
o 3 semilunar cusps attached to a fibrous valve ring .
o In about 1 % of individuals , only 2 cusps are present ( Bicuspid aortic valve ).
Etiology :
1- Rheumatic fever.
2- Congenital : it may be valvular , subvalvular or supravalvular.
3- Calcifications.
4- Hypertrophic cardiomyopathy : ( Idiopathic Hypertrophic Subaortic Stenosis - IHSS )
5- Relative :
o blood flow across the aortic valve : AR.
o Dilatation of aorta : Hypertension , atherosclerosis .
Hemodynamics :
During systole , there is obstruction of LV outflow results in :
o LCOP.
o Pressure overload on LV leading to LV hypertrophy then failure.
Clinical picture :
Asymptomatic in mild cases. Manifestations of LCOP.
Syncope : especially Exertional due to low fixed COP.
Angina : Due to :
o LCOP coronary blood flow.
o LV hypertrophy O2 demand.
o Associated atherosclerosis or AR.
Manifestations of LSHF.
Cardiac examinations :
LVE.
Sustained apex : ( forcible ,sustained apex )
Systolic thrill over 2nd right intercostal space ( A1 ) & propagated to apex & neck.
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Auscultation :
Weak S2 with closed , single or paradoxical splitting ( delayed aortic component )
Additional sounds :
o Ejection click due to opening of rigid aortic cusps , disappears with calcification.
o gallop due to LSHF.
o S4 : due to pressure overload on the LV.
Murmur :
- Murmur of AS :
Site : maximum over A1 area ( 2nd right intercostal space ).
Character : Harsh but may be soft in relative AS.
Relation to respiration & position : with expiration & with leaning forward.
Propagation : neck (carotid arteries ) & apex.
Timing : Ejection ( mid ) systolic murmur ( diamond shaped , crescendo decrescendo)
- Murmur of functional MR ( due to dilated LV ) : pansystolic murmur on the apex .
Investigation :
– X ray :
o LVE.
o Post stenotic dilatation ( in valvular type )
o Pulmonary congestion.
o Calcification.
– ECG : LVE.
– Echo : Detects the severity of valve lesion ( < 0.8 cm2 severe AS )
chamber enlargement.
– Catheterization : Detects the severity (it can measure the pressure gradient across aortic valve)
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Treatment :
Aortic Regurge
Etiology :
1- Rheumatic fever.
2- Congenital.
3- Infective endocarditis.
4- Surgical.
5- Dilatation of the ascending aorta :
o Syphilis. o Aortic dissection.
o Marfan syndrome. o Ankylosing spondylitis.
o Severe hypertension.
Hemodynamics :
During diastole : regurgitation of blood from the aorta to the LV leading to :
Volume overload on the LV LVE the failure.
coronary blood flow Angina.
blood in LV LV contraction stroke volume systolic pressure .
This high systolic BP is compensated by peripheral VD which ( together with
regurgitation ) will decrease the diastolic BP. So in AR :
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Clinical picture :
1- Asymptomatic in mild cases.
2- General throbbing : due to arterial pulsation.
3- Palpitation : due to forcible LV contraction.
4- Angina : there are 2 types
Classic angina : due to :
o Diastolic BP coronary blood flow.
o LVE O2 demand.
Angina of Lewis : Nocturnal , prolonged angina & associated with autonomic
disturbances (sweating , tachycardia)
5- Manifestations of LSHF : Pulmonary congestion & LCOP.
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Cardiac examination :
LVE . Hyperdynamic apex.
No thrill over the aortic area in isolated AR.
Auscultation :
Investigations :
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Treatment :
Medical : As scheme.
Surgical : Valve replacement in severe organic cases with LV dysfunction.
Rheumatic AR Syphilitic AR
Age 20 - 40 years > 40 years
History Of rheumatic fever Of syphilis
Valvular lesion yes no
Angina Less common. More common.
S2 Usually normal
Murmur (maximum intensity) Over A2 Over A1
X ray Calcification Aortic aneurysm.
Tricuspid Stenosis
Etiology :
It’s usually rheumatic in origin & usually associated with mitral or aortic valve diseases.
Clinical picture:
- Symptoms of LCOP. - Symptoms of systemic congestion.
- Symptoms of associated lesions e.g. MS
NB : TS symptoms of MS due to restriction of pulmonary flow.
General signs :
- LCOP. - Systemic congestion.
- Neck vein : Giant (a) wave.
Cardiac sign :
- RA & RV enlargement.
- mid diastolic presystolic murmur at lower left sternal border, increases by inspiration.
Investigation :
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Tricuspid Regurge
Cardiac signs :
RA & RV enlargement
Systolic thrill over tricuspid area.
Murmur :
- Pansystolic murmur. - Increased by inspiration.
- Maximum over tricuspid area & propagated to the apex but not to the axilla.
Investigations :
- X ray & ECG : RA & RV enlargement.
- Echo & catheterization : Diagnostic.
Treatment :
- Treatment of RSHF . - Valve replacement.
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DD of systolic murmurs :
1. AS
2. PS
3. MR
4. TR.
5. VSD
6. PDA
7. Coarctation of aorta
DD of diastolic murmurs :
1. AR
2. PR
3. MS
4. TS
5. PDA
6. Coarctation of aorta
Over the apex :
o MS : either organic or relative.
o Propagated from other area : AR , PR
Over the base :
o AR , PR , PDA
o coarctation of aorta ( due to collaterals )
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Anatomy :
- There is an abnormal opening between the two atria, producing left to right shunt.
High ASD ( ostium secondum ) : the most common.
Low ASD ( ostium premium ) : may be associated with Mitral valve disease
( Lutembacher’s syndrome ) . MCQ
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Hemodynamics :
As the pressure in LA is higher than in RA , blood is shunted from LA RA RV ( causing
RVE ) PA ( causing its dilatation ) Lung ( blood flow
through pulmonary arterioles causing lung plethora & then
pulmonary hypertension ) The blood from lung comes back
to LA & the cycle is repeated .
- Notice that blood passing from LA to LV will be less than
normal LCOP.
So, in ASD there are :
Lung plethora.
LCOP. Notice that O2 level is high in the RV & PA (N :75%)
RVE.
Clinical picture :
Symptoms :
1- Asymptomatic in mild cases or in early life.
2- Symptoms of hemodynamics :
Symptoms of lung plethora : Exertional dyspnea , recurrent chest infection…
Symptoms of LCOP .
3- Symptoms of complication.
4- Symptoms of other congenital anomalies.
Signs :
1- No signs in mild cases.
2- Signs of hemodynamics :
Signs of lung plethora.
Signs of LCOP.
3- Signs of complication.
4- Neck vein : No giant (a) wave inspite of pulmonary hypertension ?
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Cardiac examination :
1- RVE.
2- Auscultation :
i. S2 : Accentuated , wide fixed splitting S2
- Accentuated & Wide splitting : due to pulmonary hypertension.
- Fixed : because the VR to the RA during inspiration is compensated by blood
shunted from LA to RA .
ii. Murmur :
No murmur of ASD itself because of low pressure gradients between the 2 atria.
Murmur of relative TS & PS may be heard.
Complication :
1- RSHF.
2- Paradoxical embolism e.g. stroke.
3- Eisenmenger’s syndrome: cyanosis with shunt reversal.
4- Infective endocarditis : rare due to low pressure gradient.
5- Arrhythmia : AF
Investigations :
X ray : RVE , dilated pulmonary artery , lung plethora.
ECG : RBBB in most cases , RVE.
Echo : RVE , detect the defect.
Catheterization :
Detect the defect : the catheter may pass through ASD.
pressure in the right side of the heart.
O2 level in RA in comparison to superior & inferior vena cava.
Treatment :
Closure of the defect : must be done before reversal of the shunt.
Treatment of complications.
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Pulmonary Stenosis ( PS )
Anatomy :
Valvular : the most common type (80 % ) .
Subvalvular ( Infundibular ). Supravalvular : rare.
Hemodynamics :
PS the resistance ( afterload ) against the RV leading to :
LCOP. RVE then failure.
Clinical picture :
Symptoms :
Asymptomatic in mild cases.
Symptoms of hemodynamics : LCOP , RSHF.
Signs :
General :
Signs of LCOP. Signs of RSHF. Giant (a) wave.
Cardiac :
RVE.
Systolic thrill on pulmonary area.
Auscultation :
- S2 : weak pulmonary component of S2 with wide splitting.
- Additional sounds : Ejection click in valvular type , S4 on tricuspid area.
- Murmur : ejection systolic murmur on pulmonary area.
Complications :
RSHF. Infective endocarditis.
TB due to lung oligemia.
Investigations :
X ray : RVE , Lung oligemia , Post stenotic dilatation in valvular type.
ECG : P pulmonale , RVE. Echo : Diagnostic.
Catheterization: Diagnostic .
detects the pressure gradient across the pulmonary valve : if >50 severe PS.
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Treatment :
Prophylaxis against infective endocardits Treatment of RSHF.
Surgical : in severe PS
- Valvular type : valvotomy or replacement.
- Subvalvular type : resection of infundibulum.
Anatomy :
- Persistence of ductus arteriosus between the
left pulmonary artery & the aorta just distal to
the left subclavian artery.
- PDA is normal during fetal life & it closes soon
or shortly after birth.
- PDA is common in premature babies ,
particularly female infants.
Hemodynamics :
- The aortic pressure (120/80 mmHg) is higher than pulmonary pressure (20/10 mmHg) in both
systole & diastole so the blood is shunted from aorta to PA in both systole & diastole
leading to :
blood flow to pulmonary arteries (lung plethora) blood flow to LA to LV causing LVE(
later failure) to the aorta causing high COP & high systolic BP.
- The escape of blood from the aorta to the PA causes low diastolic BP.
(high SBP & low DBP hyperdynamic circulation )
- Later on , pulmonary hypertension & reversal of the shunt occur ( Eisenmenger’s syndrome ).
Clinical picture :
Symptoms :
1- No symptoms in mild cases.
2- Symptoms of hemodynamics :
Symptoms of lung plethora.
Symptoms of hyperdynamic circulation : palpitation & general throbbing.
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3- Symptoms of complications.
4- Symptoms of other congenital anomalies.
Signs :
1- No signs in mild cases .
2- Signs of hemodynamics :
Signs of lung plethora.
Signs of hyperdynamic circulation : the same as peripheral signs of AR. (9)
3- Signs of complications.
4- Neck vein : Giant (a) wave due to pulmonary hypertension.
Cardiac examination :
1. LVE.
2. Continuous thrill over left infraclavicular area ( site of DA).
3. Auscultation :
S2 : Accentuated, reversed splitting S2 ( due to delayed evacuation of LV ).
Murmur : Continuous "machinery " murmur over left infraclavicular area.
DD of continuous murmur :
1- Arterio-venous fistula.
2- PDA.
3- Coarctation of aorta.
4- Double mitral ( combined MS & MR ).
Complications :
1- LSHF.
2- Paradoxical embolism e.g. stroke.
3- Infective endocarditis.
4- Eisenmenger’s syndrome differential cyanosis ( cyanosis only in LL ) because
the reversed cyanotic blood enter aorta distal to subclavian artery.
5- Arrhythmia.
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Investigation :
X ray : - Dilatation of aorta , PA , LA & LV. - Lung plethora.
ECG : LVE.
Echo : show chamber dilatation.
Catheterization :
Detect the defect : the catheter may pass through PDA.
Pulmonary pressure.
O2 level in PA in comparison to RV.
Treatment :
Medical :
Prophylaxis against infective endocarditis.
Treatment of complications
Medical closure of the duct : Indomethacin.
Surgical : Closure of the duct.
Coarctation of aorta
Anatomy :
- Congenital narrowing of a part of aorta usually distal to the left subclavian artery.
- Associated congenital anomalies :
Bicuspid aortic valve ( AS , AR ) , PDA , VSD , Congenital aneurism of Circle of Willis ,
Turner’s syndrome.
Hemodynamics :
Narrowing of a part of aorta causes :
o BP in the proximal part ( before the
narrowing)
o BP in the distal part ( after the
narrowing )
o Development of collaterals between
the proximal & distal part.
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Clinical picture :
Symptoms :
1- Asymptomatic in mild cases.
2- Symptoms of hemodynamics :
BP in the upper half Symptoms of hypertension e.g. headache , epistaxis ..
BP in the lower half Fatigue & Intermittent claudication of the LL.
Collaterals Pain around left shoulder.
3- Symptoms of complications.
4- Symptoms of other congenital anomalies e.g. AS , AR , PDA ….
Signs :
1- No signs in mild cases.
2- Signs of hemodynamics :
BP in arms, prominent carotid pulsation.
BP in legs , weak pulsations of LL e.g. dorsalis pedis.
Collaterals may be seen in interscapular area ( Suzman’s sign ).
3- Signs of complications.
4- Signs of other congenital anomalies.
Cardiac examination :
1. LV hypertrophy.
2. Auscultation :
Accentuated S2
Murmurs:
o Ejection systolic murmur due to :
Coarctation itself ( below left infraclavicular area ) , Associated AS ,Hypertension.
o Early diastolic murmur due to associated AR.
o Continuous murmur over the collaterals.
Complications :
1- Complications of hypertension e.g. cerebral hemorrhage …..
2- Heart failure.
3- Infective endocarditis.
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Investigations :
1- X ray :
LVE.
Rosler’s sign : Rib notching due to erosion by collaterals.
2- ECG : LVE .
3- Echo : LVE , can detect the coarctation .
4- Catheterization & aortography : can detect the site & severity of the coarctation.
Treatment :
Medical : prophylaxis against IE & treatment of the complications.
Surgical repair : in early childhood to avoid persistent hypertension.
Anatomy :
- There is an abnormal opening between the two ventricles, producing left to right shunt.
- It’s the most common congenital heart disease.
- There are 2 types :
o Big membranous type : occurs in the membranous part of the interventricular septum.
o Small muscular type (Roger’s disease) : occurs in muscular part of interventricular septum ,
it’s hemodynamically insignificant & more than 90% of cases close spontaneously.
Hemodynamics :
- The pressure in LV is 120 / 0 mmHg.
- The pressure in RV is 25 / 0 mmHg.
So , the blood is shunted from LV to RV
during systole only leading to :
- The shunted blood to the RV causes RVE
blood flow to pulmonary arteries
(lung plethora & pulmonary hypertension)
blood flow to LA to LV causing LVE
( later failure) Pulmonary artery
- Notice that blood passing from LV to aorta will be less than normal LCOP.
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So, in VSD there are :
Lung plethora.
Biventricular enlargement.
LCOP.
Clinical picture :
Symptoms :
1. Asymptomatic in mild cases & in Roger’s disease.
2. Symptoms of hemodynamics :
Symptoms of lung plethora : Exertional dyspnea ,recurrent chest infection…
Symptoms of LCOP.
3. Symptoms of the complications.
4. Symptoms of other congenital anomalies.
Signs :
1. No signs in mild cases.
2. Signs of hemodynamics : Lung plethora & LCOP.
3. Signs of complications.
4. Neck vein : Giant (a) wave.
Cardiac examination :
1. Biventricular enlargement with hyperdynamic apex.
2. Auscultation :
S2 : Accentuated pulmonary component , wide splitting.
Murmur :
- Harsh pansystolic murmur with thrill over the 3rd,4th intercostals spaces.
- Ejection systolic murmur of pulmonary hypertension.
- Mid diastolic murmur of relative MS ( blood flow across the mitral valve )
Complication :
1- HF.
2- Infective endocarditis.
3- Paradoxical embolism.
4- Eisenmenger’s syndrome : usually at 2nd - 3rd decade.
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Investigations :
1. X ray : Biventricular enlargement , lung plethora.
2. ECG : Biventricular enlargement.
3. Echo : Biventricular enlargement , diagnosis of anomaly.
4. Catheterization :
Detect the defect : the catheter may pass through VSD.
pressure in the RV & PA.
O2 level in RV in comparison to RA.
Treatment :
Prophylaxis against IE & treatment of complications.
Surgical closure of large defect.
Tetralogy of Fallot ( F4 )
Anatomy : Slight deviation of the upper part of interventricular septum to the right leading to:
1- PS ( subvalvular )
2- Mild RVE.
3- VSD ( not significant )
4- Overriding of Aorta.
Hemodynamics :
1- PS : deoxygenated blood passes to
aorta p.oligemia ¢ral cyanosis.
2- Mild RVE : because RV has 2 ways:
stenosed PA & wide aorta.
3- Overriding of aorta : it receives blood
from both ventricles central
cyanosis.
4- VSD : not significant ( silent ) despite
big VSD because the pressures in both
ventricles are equal.
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Clinical picture :
Symptoms :
1- Central cyanosis since birth or shortly after.
2- Central dyspnea. ( hypoxia respiratory center )
3- Clubbing.
4- Cyanotic spell : ( cyanosis with exertion)
Exertion sympathetic stimulation spasm of subvalvular tissue ( infandibulum )
of the RV sever PS deoxygenated blood flow to aorta cyanosis.
C/P :
1. Cyanosis 2. Convulsion 3. Cardiac arrest
4. Squatting position kinking of femoral artery resistance of the aorta
blood flow from RV to aorta more blood to the lung cyanosis& dyspnea
Signs :
1- Central cyanosis 2- Clubbing 3- Stunted (delayed ) growth.
4- Neck vein : dominant (a) wave.
Cardiac examination :
1. Slight RVE (may be absent )
2. Auscultation :
S2 : Accentuated(due to aortic flow), Single(pulmonary component is very weak to be heard)
Murmur :
o Ejection systolic murmur of PS.
o No murmur of VSD because it is not significant ( silent VSD ).
Complication :
1- Polycythemia due to hypoxia.
2- Pulmonary TB due to lung oligemia.
3- Paradoxical embolism.
4- Cyanotic spell.
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Investigations :
1- X ray : Boot shaped heart : narrow base with elevated apex.
Pulmonary oligemia.
2- ECG : RVE.
3- Echo :diagnostic.
4- Catheterization : diagnostic.
Treatment :
1- Treatment of cyanotic spell : Squatting position , O2 , blocker.
2- Prophylaxis against infective endocarditis.
3- Blalock Taussig operation : acquired PDA.
4- Surgical total correction.
Triology of Fallot ( F3 )
1. PS ( valvular )
2. Marked RVE.
3. ASD.
Eisenmenger’s syndrome
Definition :
It is a condition in which a left-to-right shunt in the heart causes pulmonary hypertension,
which in turn ,causes increased pressure in the right side of the heart and reversal of the
shunt into a right-to-left shunt.
Etiology :
VSD.
PDA.
ASD.
Eisenmenger complex was applied to patients with reversal of shunt in a case of VSD
by Dr. Victor Eisenmenger in 1897 but the definition was extended by Dr. Paul Wood
to include shunts at any level VSD, ASD, PDA ,..
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Clinical picture :
1- History of congenital heart disease : VSD , PDA , ASD.
2- Pulmonary infection & hemoptysis.
3- C/P of pulmonary hypertension .
4- C/P of RSHF.
5- Decrease of the original murmur of the shunt due to low pressure gradient.
Treatment :
Prevention is best.
Closure of the defect is contraindicated as it increases the pressure in the right
side of the heart.
Symptomatic treatment e.g. HF. Heart lung transplantation.
The position of the aorta & the PA are reversed, this leads to separate 2 circuits :
The aorta arises from the RV ,so most of the blood returning to the heart from the
body is pumped back out through the aorta without going to the lung central
cyanosis.
The PA arises from the LV ,so the blood returning from the lungs goes back to the
lungs again.
To maintain life , an associated ASD , VSD , PDA ,PS should exist.
Treatment : Keep the PDA by Prostaglandin E1 , surgical correction.
Dextrocardia
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Angina Pectoris
Definition :
It is a clinical syndrome of chest pain due to imbalance between oxygen
supply & demands of the myocardium.
Etiology :
I. Decreased myocardial oxygen supply :
1) Decrease in quantity :
a) Coronary artery disease :
Atherosclerosis. ( most common cause )
Arteritis : polyarteritis nodosa , SLE .
Coronary spasm .
Coronary embolism .
Coronary osteial stenosis of syphilis .
Congenital anomalies .
b) As a part of LCOP : AS , LSHF .
2) Decrease in quality :
Anemia.
Hypoxia.
II. Increased myocardial oxygen demand :
Ventricular hypertrophy .
Tachycardia .
Risk factors for atherosclerosis:
Non modifiable :
Age .
Sex : male > female .
+ve family history .
Modifiable :
Hypertension : cause endothelial damage.
Hyperglycemia
Hyperlipidemia especially LDL .
Hyperuricemia .
Sedentary life style .
Smoking.
Stress & type A personality .
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Clinical picture :
6) Relieving factors :
- Rest, but occasionally the pain disappears with continued exercise ( walk through angina)
- Sublingual nitrates.
7) Association :
- Sweating - Dizziness - Dyspnea :may occur due to LVF .
- Fear of death ( angor animi ) - Eructation at the end of the attack.
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Types of Angina :
1) Stable angina: (typical)
o The pain is relatively constant as regard to severity, precipitating factors & relief.
o Same amount of exercise always reproduces the pain & relieved by rest.
2) Unstable angina : ( is considered intermediate syndrome between stable angina & MI)
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Investigation :
1- ECG :
A) Resting ECG :
In between the attacks :
usually normal.
ECG of old MI .
During the attack:
ST segment : depressed. ( more than 1mm )
T wave : Inverted .
B) Exercise ECG : ( in between the attacks only )
- The patient is exercises on a treadmill & ECG changes & vital signs are recorded.
- Stress test can be done with dobutamine in patients unable to do exertion.
- Stress test is considered +ve when : one or more of these changes are present :
Symptom : Typical anginal pain during the test.
Sign : Fall in blood pressure (10 mmHg or more) suggests ischemia
ECG : Depressed ST segment > 1mm .
NB : Exercise test can be misleading as there are :
False negative test : So normal test doesn’t exclude IHD .
False positive test :especially in patients with left ventricular hypertrophy.
Stress test is contraindicated in :
- Acute attacks. - Severe AS.
- Severe hypertension. - Congestive heart failure.
- Orthopedic problems.
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2- Echo & dobutamine Echo : may show abnormal motion of the myocardium .
Treatment : 4
1- Control of risk factors :
Reassurance & sedation. No smoking.
Treatment of hyperlipidemia. Control of hypertension.
Control of diabetes. Weight loss.
Change of life style ( regular exercise program ).
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Side effects :
Headache.
Hypotension.
Tolerance : so start with minimal effective dose with nitrate free interval periods.
ii. β blockers :
Action :
Reduce oxygen demand since they reduce heart rate, blood pressure & contractility.
Preparation :
Propranolol ( indral ) : non selective β blocker .
Atenolol (ateno), Metoprolol (betaloc) , Bisoprolol (concor) : Selective β blockers.
Carvedilol ( cardilol ) : β blocker with an arteriolar vasodilating action.
Side effects :
Lung : Bronchospasm.
Heart : Bradycardia , Heart block.
Depression , Impotence.
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iv. Antiplatelet :
Aspirin : 75 mg single dose : it improves the prognosis.
Clopidogrel ( plavix ) :expensive.
3- Coronary revascularization :
Indications :
Angina not responding to medical treatment.
Post infarction angina to improve the prognosis.
Techniques :
1- PTCA ( Percutaneous Transluminal Coronary Angioplasty ):
Introduction of balloon or stent to dilate the stenotic artery( balloon-tipped catheter)
Indication of PTCA :
Stenosis of one or two vessels only ( except left main coronary artery )
2- CABG ( Coronary Artery Bypass Graft ) :
Grafting a piece of saphenous vein or internal mammary artery between the aorta &
the coronary artery distal to any obstruction.
Indication of CABG :
Stenosis of 3 or more vessels.
Stenosis of left main coronary artery.
4- Treatment of anginal attack :
Complete rest.
Nitroglycerine (0.5 mg) or isosorbide dinitrate (5mg) sublingually & repeated up to 3
times successively with interval of 3 minutes.
NB : If the patient is not relieved after the use of 2-3 tablets ,the patient should be immediately
transferred to hospital & evaluated for the possibility of myocardial infarction.
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Myocardial infarction
Definition :
Ischemic necrosis of part of the cardiac muscle due to sudden , persistent & complete
cessation of its blood supply.
Etiology :
Thrombosis on top of atherosclerosis. ♫♫
Coronary embolism ( rare ).
Severe coronary spasm.
Pathology :
Site:
1- Occlusion of the left anterior descending artery anterior infarction.
2- Occlusion of the circumflex artery lateral infarction.
3- Occlusion of the right coronary artery inferior infarction.
Types :
Transmural infarction ( ST elevation myocardial infarction - STEMI ) : infarction of full
thickness of the ventricular wall.
Subendocardial infarction ( Non ST elevation myocardial infarction -NSTEMI ) :
Transient or incomplete vessel occlusion.
Clinical picture : Pain and/or complications
I. Chest pain: Similar to angina but :
More severe, it may be severe enough to be described as the worst pain the patient has ever felt.
Radiates more : may below epigastric area but never below umbilicus.
More prolonged : up to several hours.
Unrelated to precipitating factors : may at rest.
Not relieved by rest or sublingual nitrate.
Associations: like angina & may also associated with complications.
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o Elderly.
o Diabetic neuropathy.
o Patient under anesthesia.
o Transplanted heart ( denervated ).
Rupture of the ventricular free wall blood fills the pericardium cardiac tamponade.
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Blood pressure :
o Hypertension : sympathetic stimulation .
o Hypotension : LVF , shock .
Cardiac auscultation :
o S1 : weak.
o S2 : reversed splitting.
o S3 : due to LVF.
o S4 : due to decreased myocardial compliance.
o Murmur : of MR , VSD .
o Pericardial rub : Dry pericarditis.
Congested neck vein : in right ventricular infarction.
Differential Diagnosis :
Causes of acute chest pain :
o Ischemic heart diseases : Angina , MI. o Pneumothorax.
o Pulmonary embolism. o Acute dry pericarditis.
o Aortic dissection. o Cardiac neurosis.
o Esophageal spasm , Perforating peptic ulcer , Cholecystitis.
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Investigations:
1- Cardiac enzymes :
Cardiac enzymes are released into blood from necrotic heart muscle after an acute MI.
Marker Initial rise Return to normal Notes
Creatine phosphokinase 4-8 h 2-4 days Non specific because it
( CPK ) may rise in damaged
skeletal muscles or brain.
CPK-MB 4-8 h 2-4 days It’s isoenzyme of CPK ,
specific to cardiac muscle
Lactic dehydrogenase 10 h 1-2 weeks Not specific .
( LDH )
Troponin ( cTnT , cTnI ) 2-6 h 1 week Most sensitive & specific
markers of myocardial
damage .
2- ECG :
In transmural infarction ( ST Elevation MI ):
1. Convex elevation of ST segment .
2. T wave :
Tall (hyperacute) in the first few minutes after vessel occlusion (the earliest change)
later on : Inverted T wave ( representing sever ischemia )
3. Finally, pathological Q waves occur, representing significant myocardial necrosis
& replacement by scar tissue.
NB: The ECG may be normal during the first few hours of infarction .
In old MI : The only residual change is the pathological Q wave.
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3- Echocardiography :
Ventricular wall motion abnormalities.
Complications : MR , myocardial aneurysm.
5- Coronary angiography :
reveals which vessels have been affected and the extent of damage.
Treatment : 3
I. Pre hospital :
1- Rapid transfer to hospital is a must ( Time lost is lives lost ) .
2- Oxygen inhalation.
3- Analgesics for pain Morphine 5 - 10 mg IV
4- For ventricular arrhythmias Lidocaine 50 – 100 mg IV ??
5- For heart block Atropine 0.5 – 1 mg IV .
NB : ACE Inhibitors are vasodilator that reduce cardiac work & decrease myocardial energy requirement .
ACE Inhibitors also have inhibitory effect on the cardiac remodeling.
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Rheumatic fever
Definition:
Diffuse inflammatory disease typically caused by an abnormal immune response to
upper respiratory tract infection with group A - hemolytic streptococci .
Etiology : There are 2 theories
1- Antigenic similarity :
The antigen of streptococci is similar to the antigens of heart & connective tissue so,
antibodies produced against streptococci can react with cardiac muscle & other CT .
2- Altered antigenicity :
Streptococci or its toxins may change the character of the connective tissue making
it abnormal to the body so acting as an antigen of auto antibodies against it.
Pathology :
I- Site : ( Rheumatic fever bites the heart & licks the joints )
1- Joints : synovial membrane .
2- Heart : Pancarditis .
3- CNS .
4- Skin & subcutaneous tissue .
5- Small blood vessels .
6- Serous membrane . ( Pleura , Peritoneum , Pericardium )
II- Types : There are 2 types
1- Exudative lesion :
Affecting mainly the serous membrane .
Heals mostly without scaring or deformity .
2- Proliferative lesion : formation of Aschoff nodules
Affects mainly the heart & the skin .
Heals by fibrosis .
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Predisposing factors :
Clinical picture :
Latent period : 1- 3 weeks
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5- ERythema marginatum :
- No need to say that if arthritis is taken as a major criteria , don’t consider arthralagia as a minor criteria.
- Also if carditis is taken as a major criteria , don’t consider prolonged PR interval as a minor criteria.
Complications :
Acute complications : i. Heart failure ii. Arrhythmia & heart block .
Chronic complications = Complications of valvular heart diseases .
Differential diagnosis :
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Treatment :
Prophylactic :
For 5 years after the last attack or till age of 25 ( which is longer) & may for ever.
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Curative :
4- Anti-inflammatory drugs :
Congestive heart failure : Digitalis , Dilator , Diuretic. Unlike normal heart failure,
rheumatic heart failure responds well to cortisone.
Chorea : Chlorpromazine , Haloperidol.
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Infective endocarditis
Etiology :
The development of infective endocarditis requires combination of 2 factors :
I. Infection.
II. Underlying cardiac disease.
I- Infection : ( any organism but commonly bacteria )
a) Gram +ve cocci :
o Strept. viridans (the most common organism): e.g. tooth extraction.
o Strept. foecalis : e.g. GIT procedures.
o Staph. aureus :e.g. cardiac catheterization.
Types:
Sub acute IE : most common & requires combinations of the 2 factors (infection & cardiac lesion).
Acute IE : affecting the healthy endocardium ,usually occurs in the right side of the heart in addicts.
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Pathology :
Vegetations are formed over the valvular & mural endocardium causing valvular
damage.(The organism in the center surrounded by fibrin & platelets) Vegetation may
detach leading to embolization.
Notice that this vegetation is big , friable & septic.
Also the myocardium may contain foci of inflammation.
Clinical picture :
Manifestations of the disease are due to :
Toxemia.
Embolization.
Immune complexes.
Face :
i. Fever ( usually low grade & prolonged ).
Any prolonged unexplained fever in cardiac patient is considered & treated as
infective endocarditis until proved otherwise.
ii. Pallor & toxic facies.
iii. Eye :
Subcojunctival hemorrhage . ( Toxemia )
Roth spots (area of retinal hemorrhage with pale center)
Sudden blindness : due to embolism of the central retinal artery.
Upper & lower limbs :
i. Clubbing : It occurs with long standing cases .
ii. Splinter hemorrhage : longitudinal hemorrhage under the nails due to rupture
capillaries (toxemia)
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iii. Osler’s nodule : Small , painful , intracutaneous in the pulps of fingers & toes.( due
to toxic endothelial hyperplasia of the capillary .
iv. Janeway’s nodule : Small painless patches on the palms .
v. Abnormalities of the redial pulse :
Tachycardia : due to fever .
Absent pulse : due to embolization of brachial artery.
Spleen :
Kidney :
CNS :
Lung :
Infection : pneumonia.
Infarction : due to pulmonary embolism in right sided endocarditis .(rare)
B) Cardiac manifestations :
1- Features of the underlying cardiac disease which already existed before IE.
2- Precipitation of heart failure.
3- New murmurs due to perforated cusps or rupture of chordae tendineae.
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Investigations :
1- Blood culture : for organism ( the most important investigation )
It is +ve in most cases ( 90 % )
At least 3 samples are taken during fever & cultured under aerobic & anaerobic
conditions.
The result are observed from 3 days up to 3 weeks.
Negative culture may be seen in :
o Antibiotic treatment before taking the blood sample .
o Some organisms e.g. fungi .
Treatment :
I- Prophylactic :
a) Correction of the underlying cardiac lesion e.g. closure of VSD.
b) Prevention of infection : Antibiotics
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II- Curative :
a) Medical treatment :
1- Antibiotics :
o Once infective endocarditis is suspected , the patient must rest in bed & blood
samples are taken for culture & sensitivity test .
o Treatment with antibiotics must start immediately without waiting for the result of
blood culture.
o Strong antibiotics in large doses are given parenterally for at least 4-6 weeks.
o Start with : ( even before the result of blood culture )
Penicillin G : 24 million units/day IV. plus
Gentamycin 80 mg /8h IM.
o Resistant cases should be treated according to the result of blood culture e.g. :
For Strept. viridans : penicillin G + gentamycin as before
For Staphyloccoci : ox , clox , diclox acillin . or vancomycin 1gm/12h IV.
For pseudomonas : ceftazidime 2g /8h or carbinicillin .
For fungal infections : Amphotericin B .
mycotic aneurysm .
b) Surgical treatment :
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Etiology :
1- Idiopathic : most probably viral.
4- Irradiation .
5- Immunological : SLE , RA .
Clinical picture :
1- General symptoms : FHMA ( fever, headache , malaise , anorexia )
2- Local symptoms : Pain .
3- Signs : Pericardial rub .
4- Features of the cause .
The characteristics of the pain :
Site : pericardial.
Character : sever stitching .
Radiation : may radiate to the shoulders .
Duration : continuous .
Increased by : movement & respiration .
Decreased by : sitting & leaning forward .
Associated with : pleurisy .
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Investigations:
DD of elevated ST segment
Acute pericarditis Myocardial infarction Prinzmetal angina
Concave elevation convex flat
In all leads In some leads In some leads
Pathological Q :absent May present absent
Cardiac enzymes : normal elevated normal
Treatment :
Pericardial effusion
Etiology : according to the fluid in the pericardial sac
Exudate (seropericardium) : cell , protein content > 3gm% & specific gravity >1018
It’s due to capillary permeability .
Produced by all causes of dry pericarditis .
TB is the most common cause of pericardial effusion .
NB : Hemorrhagic effusion : exudate with excessive RBCs e.g. malignancy , MI , TB , CRF.
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Transudate ( hydropericardium ): low cell & protein content < 3gm% & specific gravity<1018
The same causes of generalized edema :
o Heart failure hydrostatic pressure .
o Liver cirrhosis, Nephrotic syndrome , Malnutrition hypoproteinemia.
Hemodynamics :
- The effusion results in compression of the heart so interferes with cardiac relaxation &
limit ventricular filling .
- It affects right side of the heart more than left side due to high pressure in the left side.
Clinical picture :
Symptoms : 2 hemodynamic + 2 P
1- Symptoms of systemic congestion .
2- Symptoms of LCOP .
3- Pain : dull aching pain due to stretch of parietal pericardium .
4- Pressure manifestations :
o On lung : dyspnea , improved by sitting up & leaning forward .
o On esophagus : dysphagia .
o On left recurrent laryngeal nerve : hoarseness of voice .
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Signs : 2 hemodynamic + 2 P
1- Signs of systemic congestion :
i - Neck vein :
o Congested neck vein .
o Kussmaul’s sign : inspiratory filling of neck vein due to failure of the heart to
accept the increased VR during inspiration .
o Friedreich’s sign : Rapid deep Y wave . ( Y wave = atrial emptying )
ii – Enlarged tender liver .
iii – Ascites before edema LL ( ascites precox ) due to :
o Kinking of hepatic vein .
o Obstruction of lymphatics passing through central tendon of
diaphragm causes accumulation of lymph in peritoneum .
2- Signs of LCOP : cold hand , pallor , los systolic blood pressure , weak pulse .
3- Prayer’s position .
4- Pulsus pardoxus : exaggerated inspiratory fall in systolic BP ( >10 mmHg ).
Normally , there is slight fall in systolic BP during inspiration ( < 10 mmHg )
Notice that Pulsus paradoxus is an exaggerated of the normal & not a paradox .
Explanation :
Normally : During inspiration :
i - VR to the right side of the heart COP .
ii – Expansion of the lung taking part of COP of the right ventricle.
So, the net result is : normal or Minimal of COP .
In pericardial effusion : During inspiration :
i - VR but the compression of the right side of the heart prevents the proper
filling of ventricle no COP.
ii – Expansion of the lung taking part of COP of the right ventricle .
So, the net result is massive COP .
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Cardiac examination :
Complications :
1- Cardiac tamponade .
2- Constrictive pericarditis .
Investigations :
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Echo : The most important for diagnosis of pericardial effusion & for detection of
severity
Catheterization : Not needed any more after echo .
Aspiration ( pericardiocentesis ) : may needed for diagnosis of the cause by analysis
of the pericardial fluid .
DD of pericardial effusion :
Treatment :
Cardiac tamponade
It’s a severest form of pericardial effusion.
Etiology :
The same as pericardial effusion .
But , the most common causes are :
Idiopathic.
CRF.
Neoplastic.
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Clinical picture :
- The same as pericardial effusion Plus
- Beck’s triad : 3D
Decrease of systolic BP .
Distended Jugular vein .
Diminished heart sounds ( quite heart ) .
Investigations & treatment : The same as pericardial effusion .
Constrictive pericarditis
Etiology :
Hemodynamics :
Clinical picture :
Symptoms :
Similar to pericardial effusion but :
o Without or with minimal pressure manifestations.
o AF in 30 % of cases.
Signs :
Similar to pericardial effusion but with no special decubitus ( no prayer’s position)
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Cardiac signs :
o Weak or absent apical pulsation.
o Pericardial knock : High pitched early diastolic sound due to sudden halting of the
relaxing ventricles by rigid pericardium.
Investigations :
o X ray : Calcification.
o ECG : Low voltage , Flat or inverted T wave .
o Echo : Pericardial thickening , calcification , exclude the effusion.
o CT & MRI : Highly diagnostic.
Treatment :
Adhesive pericarditis
o Adhesions between the pericardium & the surrounding mediastinal strictures &
chest wall.
o It occurs as a late complication of rheumatic fever or may be due to an extension of
inflammation from neighbor strictures.
A doctor must work eighteen hours a day and seven days a week. If you cannot console
yourself to this, get out of the profession.
Martin H. Fischer
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Systemic hypertension
Definition:
140 130
- Persistent elevation of arterial BP greater than /90 mmHg & above /80 mmHg in
the patients with diabetes or renal disease .
Types:
1- Isolated systolic hypertension :
systolic BP without diastolic BP .
Etiology :
o Atherosclerosis : aortic compliance .
o stroke volume : hyperdynamic circulation , AR , PDA .
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4- Multifactorial theory :
Stress sympathetic renal ischemia rennin aldosterone BP .
5- Hyperinsulinemia due to peripheral insulin resistance .
6- Decreased atrial natriuretic peptide ( ANP )
7- Barroreceptors resetting .
2- Endocrinal :
o Pituitary : Acromegaly ( endothelial hyperplasia , Na & water retention )
o Thyroid : - Hypothyroidism.
- Hyperthyroidism isolated systolic hypertension .
o Parathyroid : Hyperparathyroidism .
o DM .
o SRG : - Conn’s syndrome : never sever HTN ,muscle weakness &hypokalemia
- Cushing syndrome . - Pheochromocytoma : paroxysmal HTN.
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3- CNS :
o ICT .
o Lesions of the medulla .
4- Vascular :
o Polyarteritis nodosa .
o Polycythemia .
o Coarctation of the aorta .
5- Iatrogenic :
o Contraceptive pills .
o Cortisone .
o Catecholamine .
o Calcium .
Clinical picture:
Symptoms :
1- Asymptomatic in most cases .
2- May discovered accidentally .
3- Headache after information .
4- Headache is usually occipital .
5- Blurring of vision , tinnitus , epistaxis , nausea & vomiting .
6- Complications of HTN may be the first presentation .
Signs :
Blood pressure : persistent elevation > 140/90 mmHg .
Signs of left ventricular hypertrophy .
Auscultation :
o Accentuated S2 . o Closed splitting S2 .
o S4 . o Ejection click .
o Ejection systolic murmur : due to relative AS .
o Early diastolic murmur : due to relative AR .
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Hypertensive urgency:
Rapid rise of BP > 220/120 mmHg & not associated with target organ damage e.g.
renal failure , heart failure .
Hypertensive emergency:
Rapid rise of BP > 220/120 mmHg & associated with target organ damage .
Malignant HTN : Hypertensive emergency with development of papilloedema .
Accelerated HTN : Similar to malignant HTN without papilloedema .
Complications :
1- Cardiac :
o LSHF : due to pressure overload .
o Ischemic heart disease : due to atherosclerosis & hypertrophy .
o Bernheim effect : ( signs of RSHF )
Hypertrophy oh LV may cause bulging of the septum in th RV leading to
slight impairment of the filling of RV signs of RSHF .
2- Cerebral :
o Cerebral atherosclerosis .
o Cerebral ischemia & thrombosis ( infarction )
o Cerebral hemorrhage ( stroke )
o Hypertensive encephalopathy :
As a result of acute rise of BP , the cerebral blood vessels are no longer able
to maintain the necessary degree of constriction ( failure of auto regulation )
& they begin to dilate cerebral blood flow ICT , brain edema , coma &
convulsion may occur .
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3- Renal :
o Renal failure .
o Hematuria & proteinuria .
4- Retinal : 4 grades
o Grade I : Thickening of retinal arterioles ( silver wire appearance ).
o Grade II : Kinking of retinal veins .
o Grade III : Hemorrhage & exudates .
o Grade IV : Papilloedema .
5- Vascular :
o Atherosclerosis .
o Aortic dissection .
Investigations :
Treatment :
140
The target BP is lower than /90 mmHg , unless the patient has diabetes or renal
130
disease, in which case the target would be lower than /80 mmHg.
A) Lines of treatment :
I – Non pharmacological ( lifestyle modification ) .
II – Pharmacological :
Treatment of associated risk factors e.g. hyperlipidemia
Treatment of the cause : in a case of secondary hypertension .
Antihypertensive drugs
B) Choice of treatment.
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A) Lines of treatment :
I – Non pharmacological ( lifestyle modifications ):
o Lose weight if overweight .
o Reduce salt intake .
o Reduce dietary fat intake .
o Stop smoking .
o Regular exercise .
o Avoid stressful condition as possible ( meditation ) .
Value :
May normalize BP in prehypertension or in mild cases without any drug.
Facilitate BP control by antihypertensive drugs.
Control of risk factors .
II - Antihypertensive drugs :
1. Diuretics
2. Sympathetic blockers
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blockers :
Mechanism of action :
Is still questionable .
contractility , HR COP .
renin release .
Preparation :
Propranolol ( indral ) : non selective β blocker .
Atenolol (ateno) , Metoprolol (betaloc) , Bisoprolol (concor) : Selective β1 blockers.
Carvedilol (cardilol) ,Labetalol : Combined β & blockers ( blockers with vasodilation)
Side effects :
Lung : Bronchospasm.
Heart : Bradycardia , Heart block.
Depression , Impotence.
CVS uses of blockers : Hypertension Angina Heart failure
Arrhythmia F4 Mitral valve prolapse.
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3. Vasodilators
Na nitroprusside : (Nipride)
These drugs inhibit the angiotensin converting enzyme which converts angiotensin I into
angiotensin II , These drugs also diminish the rate of bradykinin inactivation .
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VD .
Decreased angiotensin II
secretion of aldosterone retension of Na.
Losartan (CozAAr )
Valsartan ( Tareg )
S/E : Similar to ACE inhibitors but no cough .
B) Choice of treatment :
Non pharmacological measures ( lifestyle modification) should be initiated
in all hypertensive patients & those with prehypertension .
The selection of a specific antihypertensive drug should take into
consideration comorbid conditions associated with hypertension as well as
the patient’s personal, response & financial .
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NB : The use of lower doses of 2 or more drugs may lower BP with fewer adverse effects
than the use of higher dose of a single agent .
2- Hypertensive crisis:
The aim of treatment is to lower the BP rapidly to terminate ongoing target
organ damage (TOD ).
It is unwise to lower the BP too quickly as it may lead to organ hypoperfusion .
Avoid initial reduction in BP more than 25 % & remember that the patients
with chronic hypertension may not tolerate a normal BP so , be judicious
when lowering the BP .
i. Rapid acting antihypertensive drugs :
Na nitroprusside ( Nipride ) : 0.5 – 2 g/kg/min ( infusion ) .
Nitroglycerine : 10 – 100 g/kg/min.
Diazoxide : 100 – 300 mg rapidly IV .
Hydralazine : 20 mg IV .
Labetalol : 20 mg IV every 10 minutes until control of BP ( maximum 200 mg)
Fenoldopam : is a new dopamine receptor agonist .
Lasix may be used with one of the above agents .
ii. Specific treatment :
a) Hypertensive encephalopathy : add
Anticonvulsant : Diazepam IV .
Cerebral dehydrating measures : 25 % Mannitol infusion with lasix .
b) Treatment of the target organ damage ( TOD ) :
Cerebral stroke , acute LSHF & renal failure .
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NB : Hypokalemic hypertension :
1- Conn’s syndrome . 2- Cushing syndrome .
3- Renal artery stenosis . 4- Iatrogenic : Diuretics .
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Aortic dissection
(Dissecting aortic aneurysm)
Definition:
It is a tear of the inner wall of the aorta ( intima ) ,
creating a false lumen for blood flow longitudinally
along the media of the aorta.
- It is most often seen in men 50 to 70 years old.
Etiology :
o Hypertension .
o Marfan syndrome.
o Atherosclerosis.
o Iatrogenic : catheterization.
Classification :
Type I - Originates in ascending aorta, propagates at least to the aortic arch.
Type II – Originates in and is confined to the ascending aorta.
Type III – Originates in descending aorta.
Clinical picture :
1- Chest pain : The main symptom
o Acute onset , Severe sharp tearing pain , radiating to the back.
o The condition must be differentiated from other causes of acute chest pain
especially MI by the following criteria :
i. Patients usually have no previous attacks of similar pain.
ii. The pain is usually of maximal intensity from the start.
iii. Associated AR or unequal pulse.
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Investigations :
o X ray :Mediastinal widening.
o ECG : to exclude other causes of acute chest pain e.g. MI.
o Trans Esophageal Echo (TEE) , Aortography , CT : diagnostic.
o MRI : gold standard for final diagnosis.
Treatment :
1- Control of hypertension : blocker ( Esmolol ) with Nitroprusside.
2- Surgical correction :
o Acute dissection in ascending aorta is a surgical emergency.
o Prognosis without surgery is very poor.
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Cardiomyopathy
Definition:
Dilated cardiomyopathy
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o Endocinal : DM , Acromegaly .
o Nurological : Freidreich’s ataxia , Duchenne myopathy , myotonia atrophica . MCQ
Clinical picture :
o Congestive heart failure.( LSHF , RSHF )
o Arrhythmia.
o Thromboembolism.
Investigations :
o X ray , ECG , Echo : show dilated heart.
o Biopsy : for amyloidosis or sarcoidosis.
Treatment :
o Treatment of HF : ACEI , blocker , Diuretic & heart transplant in refractory cases.
o Treatment of arrhythmia .
o Treatment of thromboembolism : anticoagulant.
Hypertrophic cardiomyopathy
Clinical picture :
o Diastolic dysfunction : Pulmonary congestion & LCOP.
o Manifestations of AS : Angina , Syncope.
o Sudden death : usually associated with sports most probably due to ventricular
arrhythmias.
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General signs :
o Giant (a) wave if there is right ventricular outflow tract obstruction.
o Jerky ( bifid ) carotid pulse.
Cardiac examination :
o Double apical impulse : due to palpable atrial systole ( S4 ).
o Paradoxical splitting of S2
o No click as obstruction is subvalvular and not valvular.
o Left parasternal late ejection systolic murmur.
o Associated MR is common : apical pansystolic murmur.
o The murmur of HCM , contrary to valvular AS , decreases by leg raising or squatting
because of venous return which fills the ventricle and so decrease obstruction.
Investigations :
o X ray : No cardiomegaly , pulmonary congestion.
o ECG : Left ventricular hypertrophy , deep wide Q wave , arrhythmias.
o Echo : Ventricular hypertrophy , mitral systolic anterior motion ( SAM )
Treatment :
o Amiodarone for arrhythmias.
o blockers : contractility & outflow obstruction.
o Ca Channel blockers : contractility & outflow obstruction.
o Avoid digitalis & other inotropics outflow obstruction .
o Surgical resection of hypertrophied septum.
Restrictive cardiomyopathy
Etiology :
o Idiopathic endomyocardial fibrosis.
o Infiltration : Amyloidosis , Sarcoidosis , Hemochromatosis. ♫♫
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Clinical picture :
- Similar to constrictive pericarditis ( IF RV is involved )
o Systemic congestion.
o LCOP.
o AF.
- Pulmonary congestion if LV is involved.
Cardiac signs :
o Signs of RVE : Late & mild.
o Murmur of mitral & tricuspid regurge : due to involvement of the papillary muscles
by fibrosis.
o No pericardial knock.
Investigations :
o X ray : No or mild RVE , no calcification ( to differentiate it from constrictive
pericarditis )
o ECG : Low voltage.
o Echo : Diastolic dysfunction.
o Endomyocardial biopsy : Diagnostic.
Treatment :
o Treatment of the cause e.g. Hemochromatosis.
o Symptomatic treatment : HF , Arrhythmias , Thromboembolism.
o Cardiac transplant in refractory cases.
Medicine cannot, except over a short period, increase the population of the world.
Bertrand Russell
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Pulmonary hypertension
Definition:
35
Elevation of the pulmonary arterial pressure above /17 mmHg.
Etiology :
Primary pulmonary hypertension (PPH) :
Very rare ( represents less than 1 % of all cases of pulmonary hypertension ).
Etiology is unknown , occurs more commonly in middle aged female with repeated
pregnancies.
May be due to repeated thromboembolism , pulmonary vasculitis.
Secondary pulmonary hypertension :
1- Hyperdynamic pulmonary hypertension :
Due to increased pulmonary arterial blood flow :
Hyperdynamic circulation.
Congenital heart diseases : ASD , VSD , PDA .
2- Passive pulmonary hypertension :
Due to pulmonary congestion : Mitral valve disease . LSHF .
3- Vasoconstrictive ( reactive ) Pulmonary hypertension :
Due to reflex VC of pulmonary arteriole in response to :
Long standing pulmonary congestion.
Long standing hyperdynamic pulmonary hypertension .
Hypoxia : COPD .
4- Obstructive pulmonary hypertension :
Long standing vasoconstrictive pulmonary hypertension Irreversible VC of
pulmonary arterioles.
5- Acute obstructive pulmonary hypertension :
Massive pulmonary embolism .
Clinical picture :
1- C/P of the cause .
2- Right ventricular enlargement .
3- RSHF .
4- Signs of pulmonary hypertension :
General : Giant “a” wave . ( no giant “a” wave in ASD ?? )
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Cardiac :
Inspection : Pulsation in the 2nd left intercostals space .
Palpation : Diastolic shock ( palpable accentuated pulmonary component of S2 )
Percussion : Dullness in the 2nd left intercostals space .
Auscultation :
o Accentuated S2 .
o Wide splitting S2 .
o S4 .
o Ejection click .
o Ejection systolic murmur : due to relative PS .
o Early diastolic murmur : due to relative PR .
Investigations :
X ray :
o Dilated pulmonary artery .
o RVE .
ECG :
o Peaked P wave ( P pulmonale ) .
Echo :
o Detection of the cause .
o Estimation of the pulmonary artery pressure .
o RVE .
Catheterization :
o Detection of the cause .
o Estimation of the pulmonary artery pressure .
o RVE .
Treatment :
Treatment of the cause .
Treatment of RSHF .
Drugs : ( limited benefit )
o ACE inhibitors , Anticoagulants .
o PGI2 . ( potent systemic & pulmonary vasodilator )
o Ca channel blockers .
o Diuretics .
Heart lung transplantation : is the chief therapeutic option .
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Pulmonary embolism
Old age .
Clinical picture :
Unfortunately, there are no clinical or laboratory findings that will confirm or
exclude the diagnosis of pulmonary embolism .
The clinical picture of pulmonary embolism is not specific , so successful
management of pulmonary embolism requires a combination of clinical
suspicion & appropriate use of diagnostic tools .
The clinical presentations are ranging from asymptomatic to sudden death
depending on the size of the embolus .
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1- Small sized emboli :
3- Acute massive pulmonary embolism : occlusion > 60% of the vascular bed
i. Acute dyspnea .
ii. Acute chest pain : ( similar to angina pain ) due to :
o Distension of the pulmonary artery .
o Reflex coronary spasm .
iii. Sudden appearance of pulmonary hypertension .
iv. Acute right sided heart failure . ( see HF )
v. Shock : It is an obstructive shock in which there is marked of blood flow to
the lung blood flow to left atrium COP shock .
vi. Sudden death : may be the first manifestation if occlusion involves more
than 80% of the vascular bed .
vii. Finding suggestive for DVT : Tenderness , swelling , redness of the LL .
unfortunately, DVT of the leg is often clinically silent .
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Differential diagnosis :
Causes of acute dyspnea with acute chest pain :
1- Pulmonary embolism .
2- Myocardial infarction .
3- Pericardial effusion .
4- Acute pulmonary edema ( acute heart failure ) .
5- Pneumonia .
6- Tension pneumothorax .
7- Bronchial asthma .
Clinical & Lab findings in patients with suspected pulmonary embolism : Not to memorize
Dyspnea 37 % 75 %
Tachycardia 47 % 86 %
Hemoptysis 32 % 67 %
Hypoxemia 34 % 70 %
+ve predictive value : It expresses the likelihood that a PE is present when the finding is present.
-ve predictive value : It expresses the likelihood that a PE is not present when the finding is also not present .
rd
The ICU Book , 3 edition 2007 Paul Marino
Investigations :
1- Chest x ray :
o Normal in most cases .
o Elevated cupola of the diaphragm.
o Pleural effusion .
o Pulmonary infarction : wedge shaped opacity .
o Dilated pulmonary artery with decreased pulmonary vasculature (Westermark sign)
o Hypoxia with a normal x ray should raise the possibility of PE .
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2- ECG :
o May be normal .
o Sinus tachycardia & atrial fibrillation .
o S1 Q3 T3 pattern ( S wave in lead I , Q wave in lead III & an inverted T in lead III )
o The most important value is to exclude MI as a cause of dyspnea & chest pain.
II- Curative :
1- Hospitalization in CCU .
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2- Anticoagulants :
Heparin :
Mechanism of action : activation of antithrombin III .
5000 – 10000 units IV as a loading dose then ,1000 units /h (infusion)
Duration : for about one week or till clinical improvement .
Follow up: by estimation of PTT, should be maintained twice the normal
Antidote : protamine sulphate IV .
4- Pulmonary embolectomy :
Is used for those with massive PE when thrombolysis is contraindicated.
5- Symptomatic treatment :
Pain : Analgesics e.g. pethidine ( avoid morphine )
Dyspnea : Oxygen inhalation & mechanical ventilation in severe cases .
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7- Inferior vena caval filters : e.g. Greenfield filter
Meshlike filter can be placed in the inferior vena cava to trap emboli &
prevent them from traveling to the lungs .
Should be considered when anticoagulants are contraindicated .
Cor pulmonale
Definition :
Cor pulmonale is right ventricular enlargement with or without failure resulting from
pulmonary disease after exclusion of LSHF & congenital heart diseases .
Pulmonary disease Pulmonary HTN RV enlargement RSHF
Etiology :
1- Acute cor pulmonale :
o Acute massive pulmonary embolism .
o Acute massive lung collapse .
o Tension pneumothorax .
2- Subacute cor pulmonale :
o Recurrent small pulmonary embolization.
o Lumphangitis carcinomatosis of the lung .
3- Chronic cor pulmonale :
o Parenchymal lung diseases : COPD , IPF .
o Pulmonary vascular diseases : Bilharziasis , primary pulmonary hypertension .
o Thoracic wall diseases : kyphoscoliosis , Pickwickian syndrome .
Clinical picture , investigations , treatment : 4
i. Of the cause : Bilhrziasis : see GIT book p 50 , COPD : see chest .
ii. Of pulmonary hypertension .
iii. Of RV enlargement : may be masked by emphysema in a case of COPD .
iv. Of RSHF .
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Arrhythmias
Definition:
Arrhythmia is an abnormality of the cardiac rhythm or rate .
The conducting system of the heart :
Under normal condition ,the pacemaker of the heart is Sinoatrial node(SAN)
The cardiac impulses arises from SAN in a rate ( 60 – 90
beats/min)
The impulse spreads through the walls of the atria causing them
to contract.
Next ,the impulse reaches the AV node ,in which there is a delay
of conduction to allow the atria to contract before the ventricles.
Then the impulse reaches bundle of Hiss in the interventricular
septum , then along the 2 bundle branches (left & right) & finally
Purkinje fibers to terminate in the ventricular myocardium causing ventricular contraction.
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Arrhythmia scheme
I- Etiology of any arrhythmia : 7
Tachyarrhythmia Bradyarrhythmia
1- Myocarditis.
2- Ischemic heart disease ( Myocardial infarction ).
3- Rheumatic heart disease .
4- Congenital heart disease .
5- Digitalis.
6- Sympathomimetics . 6- Sympatholytics
7- Thyrotoxicosis . 7- Hypothyroidism .
Exceptions :
Sinus ( tachy or brady ) arrhythmias : Physiological & pathological causes .
Atrial flutter or Atrial fibrillation : begin the etiology by : MS & thyrotoxicosis.
Symptoms of tachyarrhythmias :
1- Asymptomatic .
2- palpitation :
o Onset :
o Offset :
o Duration of the disease : short in serious arrhythmias e.g. VT,CHB.
3- Manifestations of LCOP .
4- Precipitation of HF & angina.
5- Features of the cause e.g. : MI , Rheumatic heart disease, digitalis toxicity ……
Symptoms of bradyarrhythmias :
The same but no precipitation of angina .
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Exceptions :
Atrial fibrillation ( AF ) : add thromboembolism.
Ventricular tachycardia ( VT ) : add Sudden death .
Complete heart block : add Syncope , Sudden death .
Signs :
simply: any arrhythmia contain this word , ventricular , in its name no effect
( no parasympathetic supply )
d) Respiratory sinus arrhythmia: -ve in all arrhythmias except in both sinus tachy
& bradyarrhythmias .
Simply, it is –ve in any arrhythmia except when arrhythmia contains this word , sinus ,
it is +ve .
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III- Investigations :
1- ECG :
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Albert Einstein
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Sinus tachycardia
Definition :
It is a condition in which the SAN discharges impulses faster than normal (>100 / min)
Etiology :
o Physiological : Exercise , Emotions , Excessive coffee .
o Pathological : Hypotension,Hyperdynamic circulation, Hyperthermia , Heart failure
o Pharmacological : Adrenaline , Atropine .
Clinical Picture :
Symptoms :
o The same as scheme .
o Onset & offset : gradual.
o Duration of the disease is usually long as the condition is mostly physiological.
Signs :
1- Radial pulse :
o Rate : > 100 /min but usually less than 160 / min.
o Rhythm : regular.
o Response to carotid sinus massage : gradual HR
o Respiratory sinus arrhythmia : +ve.
3- Auscultation : Accentuated S1 .
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ECG :
o Rhythm : regular.
o Rate : 100 – 160 / min.
o P waves : are normal & each P wave is followed by normal QRS .
Notice that the heart neglects the SAN & follows the focus
Etiology :
o Physiological : excessive coffee , smoking .
o Pathological : the same as scheme .
Symptoms :
o The same as scheme.
o Sudden onset & offset.
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2- Neck vein :
Atrial tachycardia : Normal rapid waves .
Nodal tachycardia : Cannon A waves .
3- Auscultation : Accentuated S1 .
ECG :
o P wave : - In atrial tachycardia : deformed.
- In nodal tachycardia : absent or inverted.
o QRS : rapid , regular with normal shape.
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Atrial Flutter
Definition :
It is a condition in which there is an abnormal focus in the atrium that discharges
rapid regular impulses ( 250 – 350 /min ) , but due to physiological block of AVN ,
not all atrial impulses are conducted to the ventricles – only ½ , ⅓ , ¼ , …of the atrial
impulses will pass to the ventricles .
Notice that not all atrial impulses are conducted to the ventricles
The same as scheme but begin with : Mitral stenosis & thyrotoxicosis . ♫♫
Clinical picture :
Symptoms :
o The same as scheme.
o Sudden onset & offset .
o Duration of the disease : Short , it is a transient arrhythmia between normal
sinus rhythm & atrial fibrillation .
Signs :
1- Radial pulse:
o Rate : Variable according the degree of AV conduction , 150 , 100, 75 beats/m.
o Rhythm : regular .
o Response to carotid massage : HR in mathematical pattern due to↑ AV
block from 2:1 to 3:1 to 4:1 So, HR from 150 to 100 to 75 beats/min .
o Respiratory sinus arrhythmia : -ve ( SAN is not the pacemaker )
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2- Neck vein : number of A waves is double, triple or quadriple the pulse rate accord-
ing to the degree of AVN conduction .
3- Auscultation : Accentuated S1 .
o P waves : abnormal ,replaced by multiple small flutter (f) waves before each QRS
o QRS : normal , regular , at a rate of ½ , ⅓ or ¼ the atrial rate according to AVN
conduction.
Treatment :
1- Drugs : to control the ventricular rate ( AVN conduction )
β blockers , Ca channel blocker ( verapamil ) or digitalis .
2- DC cardioversion : if the patient is hemodynamically unstable.
Ventricular tachycardia
Definition :
It is a paroxysmal condition in which there is abnormal focus in the ventricle that
discharge impulses more than SAN ( 150 – 250 / min ).
- Since the focus is in the ventricle & there is no retrograde conduction in the AVN, So
ventricles will follow the ectopic focus & atria will follow the SAN ( AV dissociation )
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Clinical picture :
Symptoms :
o The same as scheme.
o Sudden onset & offset .
o Duration of the disease : short history because it is a serious condition.
o Duration of the attack :
Sustained VT : more than 30 seconds ( hemodynamically unstable)
Non sustained VT : less than 30 seconds .
o Sudden death : if converted to ventricular fibrillation .
Signs :
1- Redial pulse :
o Rate : 150 – 250 / min ( uncountable ).
o Rhythm : regular .
o Response to carotid massage : no effect (no parasympathetic supply to ventricles)
o Respiratory sinus arrhythmia : -ve .
2- Neck vein :
o Occasional cannon A wave ( because occasionally the atria & ventricles may
contract together).
3- Auscultation : Variable S1 , occasionally cannon sounds.
ECG :
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Treatment :
During the attack :
If the patient is hemodynamically unstable :
Immediate cardioversion ( start at 100 J & repeat if needed & add 100 J to each successive shock.)
o Amiodarone .
o Lidocaine.
o β blockers .
o Implantable Cardioverter defibrillator (ICD) : in resistant cases.
Torsades de points : ( French for twisting of the points )
- It is a multifocal VT characterized by QRS complexes that change in amplitude & appear to be
twisting around the isoelectric line of the ECG & associated with prolonged QT interval.
- AE :
Antiarrhythmic drugs & electrolyte disorders (hypokalemia, hypommagnesemia , hypocalcemia)
- Treatment : Mg & ventricular pacing may be needed.
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DD of regular tachycardia :
Sinus tachycardia PSVT Atrial flutter VT
Pharmacological:2A Pathological:scheme
Complaint (palpitation)
Gradual onset Acute onset Acute onset Acute onset
(transient) (serious)
Radial pulse:
Rate 100 – 160 /m 150 – 250 /m Variable(150,100,..) 150 – 250 /m
Rhythm Regular Regular Regular Regular
Response to carotid +ve ( gradual ) +ve ( sudden ) +ve (mathematical ) - ve
massage +ve -ve -ve -ve
Respiratory sinus
arrhythmia
Neck vein Rapid & normal Atrial :rapid ,normal Multiple a wave : Normal with
Nodal : cannon 2,3,4 time the radial occasional
rate cannon
S1 ↑ ↑ ↑ variable
Nodal: absent P
wave
Treatment
ttt of the cause Vagal stimulation drugs: B, C, D Cardioversion
Cardioversion Lidocaine.
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Sinus bradycardia
Definition :
It is a condition in which the SAN discharges impulses by a rate less than 60 / min
Etiology :
o Physiological : During sleep , Athletes .
o Pathological : Obstructive jaundice , Hypothyroidism.
o Pharmacological : β blockers , Ca channel blockers , Digitalis .
Clinical picture:
Symptoms : usually asymptomatic
3- Auscultation : Weak S1 .
ECG :
o Rhythm : regular.
o Rate : < 60/min.
o P waves : are normal & each P wave is followed by normal QRS .
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Definition :
- It is a condition in which the heart is controlled by the AVN .
- Here , the impulses reach the atria & ventricles in the same time .
Etiology : The same as scheme ( the most common causes are digitalis & MI )
Clinical picture :
Symptoms :
o The same as scheme.
o Sudden onset & offset .
o Duration of the disease : usually short history except if congenital .
Signs :
1- Radial pulse :
o Rate : slow (40 – 50 /min) .
o Rhythm : regular.
o Response to exercise or atropine : gradual ↑ HR .
o Respiratory sinus arrhythmia : -ve . ( SAN is not the pacemaker )
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ECG :
o P waves : Inverted & come approximately at the same time with QRS so may
be absent
o QRS : Slow , regular with normal shape .
Treatment :
o Treatment of the cause.
o Atropine.
o Artificial pacemaker may be needed in severe cases.
Heart block
Types :
Sino atrial block : failure of impulse to conduct between the SAN & the atria.
AV block : failure of impulse to conduct between the atria & the ventricles.
Bundle branch block (BBB) : either in left or right bundles .
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o The AVN transmits one impulse for each 2 ,3, 4 or more atrial impulses .
o This block may be fixed ( e.g. 2:1 all the time ) or variable ( irregular ).
Notice that the atria are controlled by SAN & the ventricles are controlled by idioventricular rhythm.
(Atrio ventricular dissociation)
- Idioventricular rhythm may originate anywhere from AVN to the bundle branches
or purkinje fibers. ( The closer the origin to AVN , the faster the rate )
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Clinical picture :
Symptoms :
o The same as scheme. Plus 2S
o Sudden death.
Signs :
1- Redial pulse :
o Rate : 30-40 /min.
o Rhythm : regular.
o Response to atropine : -ve ( ventricular escape phenomenon).
o Respiratory sinus arrhythmia : -ve .
2- Neck vein : normal with occasional cannon A waves.
3- Auscultation : Variable S1 with occasional sounds.
ECG :
Treatment :
o Treatment of the cause.
o Atropine.
o Artificial pacemaker : the treatment of choice.
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In one word :
Atrial fibrillation
Definition :
It is a condition in which there are rapid irregular impulses (400-600/min) arise
from the atria by multiple ectopic foci ( so the atria don’t contract effectively ) &
due to physiological delay at AVN , not all impulses are conducted to the ventricles.
Notice that there are multiple foci ending in ineffective atrial contraction
Etiology :
o Mitral stenosis & thyrotoxicosis . ♫♫
o Constrictive pericarditis & Cardiac surgery.
o Lone AF (idiopathic) : especially in elderly.
o Other causes : like scheme.
Clinical picture :
Symptoms :
o The same as scheme .
o Palpitation : rapid , irregular & may be paroxysmal or sustained.
o Duration of the disease : may be long .
(the patients may accommodate for a new rhythm & palpitation disappears)
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If the radial pulse becomes regular & slow in a case of AF : CHB is suspected.
If the radial pulse become regular & rapid in a case of AF : VT is suspected.
ECG :
Treatment :
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Indication :
Recent onset of AF.
No history of recent embolism.
No significant left atrial enlargement.
Precautions :
Anticoagulant must be given at least 2 weeks before reversion to
decrease the risk of embolization.
Discontinuation of digitalis before electrical cardioversion is a must.
NB: - In some cases atrial fibrillation is better treated by anticoagulant therapy &
control of ventricular rate without any trial to return to sinus rhythm.
- Recurrent AF is treated by long use of propafenone, flacinide or amioda-
rone.
It is an ectopic impulses arising from the atria , AVN or ventricles before the ex-
pected next beat causing what is called premature beat.
- Premature beats occur during relative refractory period (RRP)
Notice that the premature beat is followed by compensatory pause & forceful contraction
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Etiology :
o Physiological : Emotions , smoking or excessive coffee.
o Pathological : The same as scheme.
Clinical picture :
Symptoms :
o Asymptomatic in most cases.
o Occasional irregular palpitation .
Signs :
1- Redial pulse :
o Rate : normal , tachy or bradycardia.
o Rhythm : Occasional irregularity.
Pulse deficit : < 10 / min.
o Response to exercise : The irregularity disappears due to in diastolic
period.
ECG :
ventricular premature beats are wide bizarre QRS not preceded by P wave & fol-
lowed by compensatory pause.
Treatment :
1- Reassurance .
2- Treatment of the cause.
3- In chronic stable cases : Amiodarone, β blocker, Ca channel blocker or qunidine.
4- Lidocaine (IV) in emergency cases.
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Treatment of arrhythmias
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Qunidine :
Allergy & hypotension .
Cinchonism ( headache, vomiting , tinnitus & blurring of vision ).
Digitalis toxicity .
Lidocaine : 3m
Mental confusion.
Myocardial depression.
Muscle twitching.
Amiodarone : due to its tendency to accumulate in body tissue it may lead to:
CNS : Dizziness, depression , tremors.
Corneal deposits.
Thyroid dysfunctions ( hyper or hypo thyroidism )
Pulmonary fibrosis.
Elevation of hepatic enzymes.
Constipation.
Skin pigmentation.
I have not failed. I've just found 10,000 ways that won't work.
Thomas Edison
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5 Hs :
o Hypovolemia
o Hypoxia.
o Hydrogen ions ( acidosis )
o Hyperkalemia & Hypokalemia.( Hyper more common )
o Hypothermia.
5 Ts :
o Toxins : CO , Cyanide .
o Tamponade. ( I mean cardiac tamponade )
o Tension pneumothorax.
o Thrombosis of coronary artery.
o Thrombosis of pulmonary artery.
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Definition :
Awareness or difficulty of breathing.
Etiology :
CVS : Any left sided heart disease lung congestion.
LSHF , MS , MR , AS , AR , myocardial infarction …….
Chest : All chest diseases
o Chest wall : obesity , Kyphoscoliosis …
o Bronchial : COPD , bronchial asthma ….
o Pleural : pleurisy , pleural effusion ….
o Pulmonary circulation diseases : pulmonary embolism , pulmonary hypertension.
CNS :
Increased ICT of respiratory center.
Abdominal : of intra abdominal pressure.
Pregnancy , Ascites , HSM ….
Metabolic : Any acidosis
DKA , Lactic acidosis , Uremic acidosis …
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Orthopnea :
- Dyspnea on lying flat , partially relieved by sitting.
- This occurs due to :
- No one can blame me when I say that orthopnea is not specific to cardiac diseases , It
also may occur due to chest or abdominal causes.
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Hemoptysis
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Syncope
Definition :
Sudden, transient loss of consciousness due to cerebral ischemia followed by spontaneous
recovery.
Causes :
1- Vasomotor syncope :
i- Vaso vagal attack : bad sight , bad smell , exposure to fear…..
ii- Carotid sinus syndrome : shaving , carotid sinus massage.
2- Orthostatic syncope : ( postural hypotension )
Autonomic neuropathy as in DM.
Adisson’s disease.
Antihypertensive drugs : blockers , methyl dopa .
Weakness of the muscles of the lower limbs.
3- Cardiac :
A) Exertional : AS , LSHF .
B) At rest : CHB , VT.
C) Positional ( syncope in certain position ) : Left atrial myxoma.
D) Acute decrease of VR e.g.hemorrhage.
E) Hypoxia : as in F4 ( Cyanotic spell )
4- Cerebral :
Transient ischemic attack (TIA).
Hypertensive encephalopathy. Cerebral embolism.
5- Situational :
Cough syncope :
Severe cough intrathoracic pressure VR cerebral blood flow syncope.
Micturation syncope : occurs in old men with BPH.
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Shock
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Hemodynamic changes in shock :
CO SVR CVP
Hypovolemic
Cardiogenic
Obstructive
Distributive Septic , Neurogenic
Clinical picture:
General manifestations common to all types of shock :
1. Hypotension ( systolic < 100 mmHg , mean BP < 60 mmHg )
2. Tachycardia > 100/m ( sympathetic ) , except in Neurogenic shock.
3. Tachypnea. ( due to metabolic acidosis & pulmonary congestion )
4. Oliguria ( < 30 ml/h ).
5. Drowsiness , confusion .
6. Cold extremities except in early distributive shock.
7. Multi organ failure ( MOF ).
Specific manifestations :
1- Hypovolemic shock :
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o It is classified according to the percentage of blood loss into 4 classes :
- Class I : up to 15 % - Class II : 15 - 30 %
2- Cardiogenic shock :
3- Obstructive shock :
4- Distributive shock :
Septic shock :
Anaphylactic shock :
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Investigations :
Laboratory :
Imaging :
Treatment :
General measures :
o Monitoring of hemodynamics : CVP , CO , SVR.
o Trendelenburg position . ( legs up , head down )
o Patent airway.
o Oxygen therapy.
o IV fluid therapy in noncardiogenic shock patients.
Hypovolemic shock :
o Identify source of volume depletion.
o Blood transfusion in a cases of bleeding.
Cardiogenic shock :
o Treatment of the cause e.g. MI
o Dopamine , Dobutamine .
o Mechanical assist devices : Intra aortic balloon counterpulsation.
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Obstructive shock: relief of the obstruction is life saving
o If cardiac tamponade is present, urgent pericardiocentesis is essential.
o Tension pneumothorax must be treated with needle thoracostomy.
o Massive pulmonary embolism requires urgent thrombolysis or surgical removal.
Anaphylactic shock :
o Adrenaline .
o Hydrocortisone IV
o Antihistaminic.
Septic shock :
o Treatment of infection by antibiotics .
o Vasopressor as Adrenaline.
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Cardiac parameters
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Mean ( MAP ) : 70 - 105 mmHg.
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