Mitral Valve Stenosis  decreased cross sectional area of the valve

 dec. blood flow from left atrium to left ventricle

 progressively can cause left atrial distension, pulmonary venous congestion, CHF
 common complication of rheumatic fever and slowly progressive
 Mitral valve stenosis → obstruction of blood flow into the left ventricle (LV)
→ limited diastolic filling of the LV (↓ end-diastolic LV volume)
→ decreased stroke volume → decreased cardiac output (forward heart failure)
 Mitral valve stenosis → increase in left atrial pressure → backup of blood
into lungs → increased pulmonary capillary pressure → cardiogenic
pulmonary edema → pulmonary hypertension → backward heart failure and right
ventricular hypertrophy
 Loud S1 sound, late rumbling diastolic murmur, opening snap after S2
 Classically seen as the left atrial pressure increases (Wiggers diagram)

Mitral Valve Prolapse  Midsystolic click --> stretching of chordae tendon
 late systolic crescendo murmur
 murmur heard at the apex or mitral area
 structural defect of the mitral valve where the mitral valve leaflets bulge into the left atrium
during systole
 most common cause of mitral regurgitation
 Marfan, Ehlers Danlos, acute rheumatic disease and infective endocarditis (bacterial )
 deposition of glycosaminoglycans on mitral valve
Hypertrophic  Left Sternal Border
Cardiomyopathy  Genetic condition
Pericardial effusion  acute or chronic accumulation of fluid in the pericardial space could be either blood or
serous
 usually asymptomatic initially
Cardiac tamponade  decreased pulse pressure
 Classic presentation: jugular venous distention (dec. systemic venous return), hypotension
(dec. cardiac output), muffled heart sounds, pulsus paradoxus ( massive dec. in systolic BP
during inspiration).
 pericardial fluid collection (e.g., bloody or serous) → ↑ pressure in the pericardial
space → compression of the heart (especially of the right ventricle due to its thinner wall)
→ interventricular septum shift toward the left ventricle chamber → ↓ systemic venous
return (preload) → ↓ ventricular diastolic filling → ↓ stroke volume (and
venous congestion) → ↓ cardiac output and equal end-diastolic pressures in all 4 chambers
Ventral Septal Defect  holosytolic, harsh sounding machine murmur
Mitral/Tricuspid  holosytolic, blowing murmur
Regurgitation
Atrial Fibrillation  Missing P waves
 Can lead to stroke
 Palpitations and lightheadedness
 can lead to a decreased preload as a result of uncoordinated atrial contraction
 tachycardia (shortens the duration of diastole)
 ireggularly, ireggular rr Interval, narrow qrs, missing p waves
Aortic Regurgitation
Aortic Valve Stenosis
Aortic stiffening
Atrial Fibrillation
Atrial Flutter
Hypertrophic cardiomyopathy
Wolf Parkinson White Syndrome (WPW)
Pericardial effusion
Isolated systolic hypertension
Causes of reduced renal artery blood flow
Primary hyperaldosteronism
Orthostatic hypotension
 blood comes into the left ventricle during
isovolumetric relaxation when the left ventricle
trying to decrease pressure
 Widened pulse pressure (classically seen on Wiggers
diagram)
 Causes: bicuspid aortic valve, endocarditis, aortic
root dilation, rheumatic fear (BEAR)
 Diastolic decrescendo murmur
 elevated LVEDV
 this is volume issue!
 Large left ventricular pressure in order to open up
against a stiff aortic valve (Wiggers diagram)
 pulse pressure is decreased
 pain radiates to carotids
 concentric left ventricular hypertrophy
 increased afterload
 this is pressure issue!
 Increased pulse pressure --> age related
 irregularly, irregular
 missing P waves
 4: 1 sawtooth pattern
 dec preload makes the obstruction worse (Valsava or
standing up)
 inc afterload makes intensity LESS
 a congenital condition characterized by intermittent
tachycardias and signs of ventricular
preexcitation on ECG, both of which arise from
an accessory pathway known as the bundle of Kent
 connects atria and ventricle bypassing AV node ->
ventricular pre-excitation
 shortened PR interval, widened
 inflammatory cells and mediators penetrate and
cause pleuritic chest pain
 decrease in arterial compliance and increased
stiffness, patients usually older than 60, widened
pulse pressure
 renal artery stenosis, external compression of renal
arteries (tumor or cyst), atherosclerosis, and
fibromuscular dysplasia --> (stenosis of small and
medium sized arteries in young patients)
 most common cause of secondary hypertension,
systolic and diastolic blood pressure are both
elevated, resistant hypertension and hypokalemia
 due to decrease in baroreceptor sensitivity
  characterized by autonomic dysfunction
 dizziness and syncope after standing up
Heart block  electrical impulses from the SA node are not
conducted to the ventricles
 spontaneous depolarization of other nodal cells -->
escape rhythms
 the site of the ectopic pacemakers can be determined
by the QRS complex shape ( normal, narrow QRS
complex includes everything from SA node to the
bundle of his, bundle branch and purkinje is a wide
QRS complex)

Paroxysmal Supraventricular Tachycardia  intermittent palpitations, light headedness, dyspnea,
 narrow complex tachycardia, without p waves
 treatment: carotid massage --> used to treat this by
acting glossopharyngeal nerve to decrease heart rate
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Prerenal Azotemia  Prerenal acute kidney injury occurs as there is

decreased renal perfusion
 BUN/Creatine >20 Bun is reabsorbed creatine is not
and reabsorption increases with hypovolemia
 Decreased blood supply to kidneys (due
to hypovolemia, hypotension, or
renal vasoconstriction) → failure of renal vascular
autoregulation to maintain renal perfusion →
decreased GFR → activation of renin-angiotensin
system → increased aldosterone release
→ increased reabsorption of Na+, H2O →
increased urine osmolality → secretion
of antidiuretic hormone → increased reabsorption
of H2O and urea
 Creatinine is still secreted in the proximal tubules, so
the blood BUN:creatinine ratio increases.

Nephrotic Syndrome  Charge barrier of the glomerular filtration barrier is
 lost --> leads to albumineria, hyperlipedemia,
hypoproteinemia, generalized edema
 Loss of oncotic pressure and you will have tons of
edema everywhere
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Maneuvers:

Carotid sinus massage stimulates baroreceptors, which transmits a signal to the medulla oblongata via CN IX. The
efferent signals from the medulla to the myocardium are conducted via the vagus nerve (parasympathetic supply),
which results in↓ AV nodal conduction, ↓ heart rate, ↓ contractility, and vasodilation (↓ blood pressure). This
patient's symptoms are caused by AV nodal re-entry; slowing AV nodal conduction terminates the arrhythmia.

Pharm:

Voltage-gated potassium channels are the target of class III antiarrhythmic

drugs like sotalol, amiodarone, dofetilide, and ibutilide. The markedly
prolonged repolarization on the action potential curve here indicates potassium channel
inhibition, which normally functions to restore resting cardiac myocyte membrane polarity. This
effect prolongs the overall action potential and the effective refractory period, which explains
the effectiveness of these drugs in treating tachyarrhythmias such as atrial fibrillation, atrial
flutter, and ventricular tachycardias.
Nitroglycerin
 Exogenous supply of nitric oxide (NO) through nitrate → activation of guanylyl cyclase → ↑ cyclic
guanosine monophosphate (cGMP) → activation of protein kinase G
o Increases SERCA activity → ↓ intracellular calcium → ↓ recruitment of contractile units
→ vasodilation
 o Increases myosin light chain phosphatase activity → ↓ phosphorylated myosin → smooth
muscle relaxation → vasodilation
 Peripheral vasodilation
 Decreased preload through venous dilation (venous
pooling) → reduces myocardial wall
tension → improved myocardial perfusion
 Decreased afterload → reduces contraction
effort → ↓ myocardial oxygen demand 
 Greater vasodilatory effect on veins than arteries (except for sodium
nitroprusside) 
 Coronary dilation → improved myocardial perfusion 
 In patients with atherosclerotic CAD, arterioles are already dilated
to maximize cardiac blood flow (due to flow-limiting stenosis) →
difficult to dilate coronary vessels further → limited effect of
nitrates
 Anginal pain relief: ↓ preload through venous pooling → ↓ heart size → ↓ oxygen demand → ↓ pain

Peak of the coronary flow is when the difference between aortic pressure and ventricular pressure is the greatest (in
diasole).

Heart Failure Overview

Physiologic manifestiations
 inc hydrostatic pressure in the lungs --> edema --> makes the lungs stiffer --> reduces compliance
 inc pulmonary venous congestion --> pulm vascular resistance

Clinical manifestations
 exertional dyspnea indicative of left sided heart failure
 orthopnea
 crackles hypotension
 pulmonary edema --> left sided
The compensation mechanisms are meant to maintain the cardiac output when stroke volume is reduced. 
 Increased adrenergic activity : increase in heart rate, blood pressure, and ventricular contractility
 Increase of renin-angiotensin-aldosterone system activity (RAAS): activated following decrease in
renal perfusion secondary to reduction of stroke volume and cardiac output 
o ↑ Angiotensin II secretion results in:
 Peripheral vasoconstriction → ↑ systemic blood pressure → ↑ afterload
 Vasoconstriction of the efferent arterioles  → ↓ net renal blood flow and ↑
intraglomerular pressure → maintained GFR
o ↑ Aldosterone secretion → ↑ renal Na+ and H2O resorption → ↑ preload 
 Secretion of brain natriuretic peptide (BNP)
o Definition: ventricular myocyte hormone released in response to increased ventricular
filling and stretching
o Mechanism of action: ↑ intracellular smooth
muscle cGMP → vasodilation → hypotension and decreased pulmonary capillary wedge
pressure