 Functional(reversible with Preload /LVEDV decreasing drugs as diuretics)MR(due to excessive

ventricular dilation by increased preload in abscence of valvular lesion)>Bibasilar Crackles (due

to high venous P/pulm.edema)at lung bases+Orthopnea/dyspnea+S3 gallop(shows increased
left ventricular filling rate in Mid diastole)+Holosystolic murmur over cardiac apex
 MC anatomical abnormality producing MR>Myxomatous degen.of mitral valve/Mitral valve
Prolapse/MVP
 Afterload reduction would reduce MR due to any cause because it decreases intraventricular P
required to generate a stroke volume.
 Mitral annular/fibrous ring calcification usually does not result in valvular disease and is seen in
older. may lead to stenosis.
 Diastolic dysfunction(by ventricular stiffness/hypertrophy)>elevated LVEDP+ Normal LVEDV and
LVEF(ejection fraction>50%)+Left shift of P_V curve (shows decreased distensibility)....when
LVEDP continues to rise>pressure is transmitted back to left atrium,Pulmonary
system>pulm.hypertension/edema>Exertional dyspnea
 In contrast Systolic HF>elevated LVEDP and LVEDV+decreased LVEF(<50%)+progressive chamber
dilation
 Q6 GALLOPS........murmur in expiration>Left heart abnorm(as blood from lungs returns to left
atria to ventricles........during inhalation>Right heart abno.(as venous return increases during
inhalation)
 Pulsus paradoxus/KUSMMAUL SIGN>Pericardial disease as Cardiac temponade or in
asthma,copd,constrictive pericarditis(not MR)...these diseases increase excessively venous
return resulting in BOWING of septum to left(instead of expansion of right ventricle only in
pericardial space)>decreased stroke volume>FALL IN BP >10mmhg during
INSPIRATION(increases venous return)
 pulsus paradoxus is detected by KORTOCOFF SOUNDS. the difference when first kortocoff
sound becomes audible and when they are heard throughout the respiratory cycle quantifies
the pulsus paradoxus using BP aparatus.
 pulsus parvus et tardus>due to LV outflow tract obstruction(as by valvular stenosis)..It is
palpable as slow rising, low amplitude pulse due to diminished stroke volume(pulsus parvus)and
prolonged LV ejection time(pulsus Tardus)
 pts with chronic MR> have a BOUNDING PULSE with brisk upstroke due to Increased LV
ejection volumes
 Mitral stenosis>Low amplitude pulse due to diminished stroke volume
 MI/ischemia>Hypotension by reduced CO.
 peripheral arterial disease>diminished affected extemities pulses
 dyspnea,tachypnea,prolonged expiration,bilateral wheezing in abscence of Heart/pericardium
disease+pulsus paradoxus> ACUTE COPD/asthma...treat with beta agonists
 Coronary steal phenomenon(tested during exercise because coronary vessels are already
dilated)> Adenosine/Dipyridamole(coronary arteries vasodilators) cause generalized coronary
artery vasodilation>reduction of flow to ischemic areas of myocardium>detection of such areas.
 Note:normally arterioles in ischemic areas are maximally dilated by local mediators...exogenous
coronary artery vasodilators dilate dont cause further dilation of arterioles in ischemic areas but
they cause dilation in non ischemic areas so blood is diverted to theses areas and it reduces
blood flow to ischemic areas causing exacerbation of ischemia.
 Q10..............AUDIO
 Atrial contraction accounts for 20% of blood that enters from atria to ventricle,....80% is by
PASSIVE pressure difference b/w atria and ventricle.Atrial contarction)left) is esp.imp in pts of
Aortic stenosis with high bp(leads to LVH>reduced compliance),otherwise such pts in case of
atrial fibrillation may develop severe HYpotension and Tacchycardia.+pum.edema >dyspnea
 Atrial contraction occurs in late ventricular diastole
 Ventricular filling/ventricular EDV shows PRELOAD and its rate shows rate of Preload filling
 OS.................? q15
 Beck triad(low arterial pressure on inspiration/pulsus paradoxus if >10mmhg+Distended
Jugular veins+MUFFLED heart sounds)>is pathognomic of CARDIAC TEMPONADE.Lungs are
CLEAR to auscultation.Loss of palpable pulse on inspiration also occurs.
 Triad of (Pleuritic chest pain+pericardial fricion rub+history of upper respiratory tract
infection)>ACUTE FIBRINOUS PERICARDITIS
 Constrictive pericarditis is a CHRONIC process and requires MONTHS to YEARS to develoo
cardiac temponade.
 RALES on auscul.> show pulmonary edema
 AP TB ka mreez hai>2245 (aortic,pulmonary valves, ..tricuspid and
biscuspid/mitral valves)numbers show intercostal space.Only Aortic valve
closure sound is heard on RIGHT border of sternum.5th space is called
mitral area as mitral valve closure sound is heard here.S1>mitral/tricuspid
closure and S2>pulm/aortic valve closure
 MVP and HCM murmurs are the only murmurs that increase upon
decreasing venous return e.g by standing/valslva.they can b distinguished
by MID SYSTOLIC CLICK which is diagnostic of MVP.
 IN CHF>COMPENSATORY MECHANISMS START A VICIOUS
CYCLE>RESULTS IN INCREASED ARTERIOLAR RESISTANCE>heart
has to pump with more force aginst increased afterload>less
perfusion then again more arteriolar constriction by Angiotensin
system
 In Conn synd:
 Hypokalemia can b exacerbated by Increased sodium
intake/Diuretics as they cause increased distal tubule delivery of
 sodium so more aldosterone is produced to reabsorb that causes
more H and K secretion causing hypokalemia(muscle weakness
and cramps and arrythmias)/metabolic alkalosis
 somatostatin decreases Insulin more than glucagon so in
SOMATOSTATINOMAS,the net result is HYPERGLYCEMIA
 vasopressin is potentiator of CRH so increases ACTH but there is
no feedback loop b/w them.