BNB - Heart Failure

Elevated jugular venous pressure

A sign of heart failure. Place the patient at a 45 degree angle. Look for height of the waves and then compare it to the height of the sternum. Normal is 6-8. If it is much higher than than that it is a sign of heart failure. Pushing on the liver causes a greater increase.

Metolazone

A thiazide like diuretic. It inhibits Na-Cl reabsorption. Can be given with loop diuretics to give a vigorous kick. Knocking out both major channels of Na absorption gives it a boost.

A patient has dyspnea and an end diastolic volume of 200 cc and an end systolic volume of 150 cc. Which is the most likely causes of the dyspnea? A. Systolic heart failure B. Diastolic heart failure C. Restrictive cardiomyopathy D. Cardiac tamponade

A. Stroke volume is end diastolic minus end systolic. 50 cc in this patient. LVEF is equal to stroke volume divided by end diastolic volume. For this patient that would be 25%. This is less than the standard 55% and at less than 40% would be categorized as systolic heart failure.

82 year old man presents for evaluation of abdominal distension and leg swelling. He was treated for chronic hepatitis C ten years ago. For the past month, he has had fatigue and dyspnea on exertion. Exam reveals clear lungs. There is a 2/6 holosystolic mumur at the left sternal border that increases with inspiration. JVP is increased. Abdomen is distended and liver is palpable. Lower extremities show 2+ edema. ECG is within normal limits. Echocardiography shows normal LV function with increased left ventricular wall thickness. Which of the following is the most likely diagnosis? A. Restrictive cardiomyopathy B. Ischemic cardiomyopathy C. Pulmonary embolism D. Portal hypertension E. Mitral regurgitation.

A. The patient has clinical features consistent with restrictive cardiomyopathy and senile amyloidosis. Echocardiography shows increased LV wall thickness in the setting of a normal ECG. Restrictive cardiomyopathy and constrictive pericarditis often have prominent right heart failure symptoms. In ischemic the LVEF would be reduced. Massive pulmonary embolism can lead to right heart failure. Chest pain would usually be present though, and sinus tachycardia would be seen on ECG. Portal hypertension occurs in liver cirrhosis and may cause abdominal distensiot and ascites. Elevated JVP should not be present and is the key to distinguishing portal hypertension from right heart failure.

Heart failure hormones

ANP BNP

Heart failure sounds

Abnormal heart sounds S3 is associated with high left atrial pressure S4 is associated with stiff left ventricle (diastolic heart failure) Displaced apical impulse - enlarged heart causes this impulse to move.

RAAS

Activated by decreased cardiac ouput as seen in heart failure. Causes increased peripheral vascular resistance and retention of sodium and water.

Sympathetic nervous system

Activated by decreased cardiac output. Causes increased peripheral vascular resistance as a response

Vasdilators

Afterload reduction ACE inhibitors, Hydralazine Relieve symptoms

A patient has dyspnea, rales, and an elevated jugular venous pressure. Their end diastolic volume is 100 cc and end systolic volume is 40cc. Which of the following is the most likely cause of this patient's dyspnea? A. Ischemic cardiomyopathy B. Diastolic heart failure C. Takotsubu cardiomyopathy D. Peri-partum cardiomyopathy

B. Stroke volume is EDV minus ESV. For this patient that is 60 cc. LVEF is equal to SV/EDV. 60% in this paient. This patient has a normal LVEF which is consistent with diastolic heart failure.

Tachycardia mediated

Constant, rapid heart rate for weeks/months. Leads to depression of systolic function. Reversible if you treat the arrhtyhmia

All forms of heart failure lead to

Decreased cardiac output

Physiologic responses to heart failure.

Decreased cardiac output activates: - Sympathetic nervous system - Renin-angiotensin-aldosterone system Activated by decreased cardiac ouput as seen in heart failure. They cause increased peripheral vascular resistance and retention of sodium and water.

Heart failure diagnosis

Diagnosed by looking at the signs and symptoms. Elevated BNP level is helpful Heart catheterization - definitive diagnosis, but usually not necessary. You would measure increased LVEDP (left heart congestion), increased RA or RVEDP (right heart congestion).

Acute exarbations

Dietary indiscretion - High salt intake Poor medicine compliance

Nitrates

Used to treat acute heart failure. Predominant mechanism is venous dilation. Bigger veins hold more blood. Takes blood away from LV Lowers LVEDV (preload), and LA pressure. Less pulmonary edema and improved dyspnea

Loop diuretics

Used to treat acute heart failure. The major ones are Furosemide, bumetanide, torsemide. Inhibit Na-K-Cl pump. Result in salt water excretion. Relieve congestion.

ANP and BNP

Do the opposite of RAAS but they aren't as strong as RAAS. Can't counteract the RAAS. BNP

Clinical features of restrictive heart disease

Dyspnea Prominent right heart failure. The right ventricle is very sensitive to impaired filling. Markedly elevated JVP. Lower extremity edema Liver congestion May lead to cirrohsis ('nutmeg liver').

Left heart failure symptoms

Dyspnea on extertion Paroxysmal nocturnal dyspnea (wake up SOB) Orthopnea (cant breathe lying flat)

LVEDP and pulmonary effects

Elevated LVEDP leads to elevated LA pressure. The mitral valve closes earlier and the LA is more full than it usually is. When one chamber fails it starts to affect the previous chamber. Elevated LA pressure leads to pulmonary effects: Dyspnea and pulmonary edema.

Cause of restrictive heart disease in children

Endocardial fibroelastosis

Chronic heart failure

Euvolemic Clear lungs No pitting edema JVP flat

Diastolic heart failure

Exact cause unknown Many cases have concentric hypertrophy Associated with: advanced age, diabetes, hypertension. AKA: heart failure with preserved ejection fraction, HFpEF, diastolic dysfunction

Heart failure pathophysiology

Failing chambers lead to increased pressures. Pressures rise in cardiac chambers.

Sarcoidosis

Granuloma formation Usually involves the lungs.

Nitrate side effects

Headache Flushing Hypotension All are dilator effects

What heart failure is associated with restrictive heart disease?

Heart cannot relax and fill. Severe diastolic heart failure ensues.

High output heart failure

Heart in overdrive Severe anemia, thyroid disease, thiamine b1 deficiency (beriberi), A-V fistulas Exact mechanism unclear: may be due to decreased LV filling time The only heart failure where cardiac output is high. Heart failure symptoms with high cardiac output.

Most common cause of R heart failure

L heart failure.

Nonischemic cardiomyopathy

May follow upper respiratory infection Many associated viruses (coxackie is the most common). Virus enter myocytes

Forward failure signs

More rare Low flow signs/symptoms Loss of appetite Weight loss Confusion Cool extremities Narrow pulse pressure - the difference between the systolic and diastolic pressure are very small. Seen in very low cardiac output

Familial nonischemic cardiomyopathy

Mutations: often sarcomere proteins, beta myosin heavy chain, alpha myosin heavy chain, troponin Many are AD X linked and AR also seen

Systolic Heart failure most common cause

Myocardial infarctions Myocytes are replaced by scar tissue. Ischemic cariomyopathy

NSAIDs and heart failure

NSAIDs are contraindicated Inhibit cyclooxygenase (COX). This decreases prostoglandins. Prostaglandins maintain renal perfusion. Without them there is more salt/water retention.

Dietary indiscretion and heart failure

Na+ intake leads to Increased plasma osmolarity leads to Increased ADH leads to Increased water retention leads to Increased blood volume. NOrmally this is managed with the RAAS system, but

Combination that is helpful in black patients

Nitrate plus hydralazine

Chemotherapy induced cardiomyopathy

Nonischemic cardiomyopathy Usually follows treatment with anthracylcines: doxyrubin

Classic image finding of restrictive heart disease

Normal left ventricular function/size Massive bi-atrial enlargement.

Takotsub/Apical ballooning

Stress induced cardiomyopathy Occurs after severe emotional distress Markedly reduced LVEF Increased CK, MB, troponin. Looks like an anterior MI (but no coronary disease) Usually resolve after 4-6 weeks. Apical ballooning - the apex doesn't contract, so it looks like it balloons when the rest of the heart contracts

ECG of systolic and diastolic heart failure

Systolic - ejection fraction is reduced. Diastolic - EF is normal Both have signs and symptoms of heart failure, but they are occurring for different reasons.

Dilated cardiomyopathy

Systolic heart failure with LV cavity dilation Eccentric hypertrophy Volume overload response Myocytes become strange and elongated. Walls don't get thicker they get thinner and longer. Sarcomeres are being added in series.

Inspiration and restrictive heart cardiomyopathy

The RV is receiving blood from the venous system. When a patient breathes in it creates a negative pressure that draws blood towards the lung. The RV can't take this extra blood though and it gets backed up leading to Kussmail's sign, increased JVP on inspiration.

Classic signs of restrictive heart disease

Thickened myocardium with low voltage on EKG. You would normally expect large QRS spikes. The heart is thickened not by myocytes though, but with amyloid. Classic finding in amyloidosis and Fabry disease.

A 78 year old man presents with dyspnea. He has been short of breath and fatigued for the past three days. It is difficult for him to breathe when lying flat so he has been sleeping in the recliner. He has noticed swelling of his ankles. On physical exam, there are bilateral rales and an elevatd jugular venous pressure. A prominent S3 is heard. Lower extremities show 2+ pitting edema. The primary causes of this man's condition is abnormal fucntion of which structure? A. Left ventricle B. Right ventricle C. Left atrium D. Aorta

This patient has heart failure by abnormal function of the left ventricle. There is evidence of right ventricle failure as well. Howevere, the right ventricle is not the primary causes of the condition.

Acute heart failure edema

Congested/Swollen Pulmonary edema Increased JVP Need care in a hospital

Peri-partum

A nonischemic cardiomyopathy Lat in preganncy or early post pregnancy Exact cause unknown Women often advised to avoid future pregnancies.

Pulmonary chain of events.

Increased pulmonary capillary pressure leads to increased PA pressure leads to increased RV pressure leads to increased RA pressure leads to increased venous pressure. Now we start to see systemic effects.

Acute exacerbation causes (non dietary)

Infection/trauma/surgery Ischemia NSAIDs

Acute heart failure drugs

1. Loop diuretics 2. Metalazone (a thiazide like diuretic) 3. Nitrates 4. Vasodilators (ACEIs, Hydralazine, etc.)

A 30 year old woman presents with fatigue, dyspnea and lower extremity swelling. She recently recovered from an upper respiratory illness. Chest x ray shows increased vascular makings consistent with pulmonary edema. On exam, the JVP is 12 cm (normal is 8). and there is 2+ pitting lower extremity edema. Compared to a normal patient, which of the following changes are expected for her ANP, Angiotensin II, and aldosterone levels?

All will be increased. In heart failure, left atrial pressure rises. This streches atrial myocytes, triggering the release of ANP. Reduce cardiac output in heart failure activates the renin-angiotensin-aldosterone system. Levels of angiotensin II and aldosterone will be increased.

Amyloidosis

Amyloid protein deposits in the heart. Various forms (primary, secondary, etc.). You'll see apple green bioforingence.

Milrinone

An inotorpe Phosphodiesterase 3 inhbitior. This raises cAMP and increases contracility. Increases inotropy, vasodilation and hypotension. Reserved for critically ill patients

LA and pulmonary capillaries

As the LA pressure rises it backs up to the pulmonary system all the way to pulmonary capillaries which start pushing more fluid out into the lungs.

ANP

Atrial natriuretic peptide When atrial myocytes are stretched due to pressure and volume increase they release ANP. ANP is a counter to the RAAS system, but is not as strong. It is a vasodilator (fights angiotensin II). Constricts renal efferents/dilates afferents Increases diuresis (opposite of aldosterone). Again not as strong.

An 82 year old woman with diabetes and hypertension presents with dyspnea. She has no history of cardiac disease. She has been extremely tired for the past week. She gets short of breath while walking. On exam she has bilateral rales. JVP is 14 cm. There is 1+ pitting edema. BP is 160/90. Echocardiography shows a left ventricular ejection fraction of 60% with increased ventricular wall thickness. The left atrium is dilated. Which of the following is the most likely cause of this woman's condition? A. Decreased afterload B. Decreased compliance C. Decreased contractility D. Decreased preload

B. The patient has the symptoms of acute heart failure. In patients with diastolic heart failure, the primary problem is a decrease in left ventricular compliance.

Blood pressure and heart failure

BP is often high (due to the TPR increase as a result of decreased cardiac output). However it may be low if the cardiac output is very small. BP = CO x TPR End stage heart failure is usually hypotensive.

Heart failure cells

Biopsy of lung tissue will find heart failure cells. Hemosiderin (iron) laden macrophages RBCs are being pushed out of the capillaries and engulfed by the macrophages. Leads to the brown pigment (hemosiderin) in the macrophages.

BNP

Brain natriuretic peptide Released in the ventricles (first discovered in the brain but not released there). This is counter of ANP which is released in the atria. Both ANP and BNP rise with volume/pressure overload. Both conter RAAAS BNP sometimes used for diagnosis in dyspnea. BNP is an important marker in diagnosing if dyspnea is heart failure induced.

A 67 year old man has a routine CBC. Results show elevated WBC with 62% eosinophils (normal is 6%). He drops out of follow up. Two years later he presents to an ER with dyspnea and fatigue. JVP is elevated and rises on inspiration. Edema, distended abdomen. Which of the following is the most likely cause of this patient's presentation? A. Decreased LV contractility B. Incrased LV afterload C. Decreased LV compliance D. Decrease LV preload E. LV thrombus formation

C The question describes a case of hypereosinophilic syndrome with cardiac involvement (Loffler's endocarditis). Hypereosinophilia has many causes. Regardless of cause, eosinophils may infiltrate many organs including the brain, skin, or GI. Cardiac involvement leads to a restrictive cardiomyopathy. Endocardial biopsy will demonstrate presence of eosinophils. Restrictive cardiomyopathy is characterized by impaired ventricular filling and decreased ventricular compliance.

A four month old male infant is brought in for evaluation of respiratory distress. The mother states that the child has been breathing irregularly for several days. He has not been feeding. Today she noted a gray discoloration of the skin and brought the baby to the hospital. Diffuse rales are heard bilaterally. There are no murmurs. Despite resuscitative measures, the baby dies. At autopsy, a 2 mm yellow-white tissue layer is found covering the left ventricle and portions of the left atrium. Which of the following is the cause of death? A. Ischemia B. Congenital malformation C. Impaired left ventricular filling D. Beta-myosin heavy chain gene mutation.

C. This describes a case of endocardail fibroelastosis, a rare cardiac disorder in children. In EFE, diffuse thickening of left ventricular endocardium occurs due to proliferation of fibrous and elastic tissue. EFE is considered a form of restrictive cardiomyopathy (RCM) because fibrous tissue in the LV cavity impairs left ventricular relaxation and filling.

Hemochromatosis

Cause of restrictive heart disease Caused by iron excess. Commonly causes dilated cardiomyopathy, but will rarely cause restrictive instead.

A 72 year old man with diabetes and hypertension presents with dyspnea. He has no history of cardiac disease. He has been extremely tired for the past week. He gets easily short of breath when walking. On exam he has bilateral rales. Jugular venous pressure is 14 cm. There is 1+ pitting edema. Blood pressure is 160/90. Echocardiography shows a left ventricular ejection fraction of 30%. Which of the following is the primary cause of this man's condition? A. Increased afterload B. Decreased compliance C. Decreased contractility D. Decreased preload

C. This patient has the signs and symptoms of acute heart failure. His echocardiogram shows a reduced LVEF consistent with systolic heart failure. In patients with systolic heart failure, the primary problem is a decrease in left ventricular contractility.

A patient presents with fatigue, dyspnea, and lower extremity swelling. Chest x ray shows increased vascular markings consistent with pulmonary edema. Which of the following is the cause of pulmonary edema? A. Decreased capillary oncotic pressure B. Increased capillary permeability C. Increased capillary hydrostatic pressure D. Decreased left atrial pressure. E. Decreased left ventricular end diastolic pressure.

C. Two forces control the movement of fluid out of capillaries: hydrostatic pressure and oncotic pressure. Hydrostatic pressure drives fluid out of capillaries into tissue beds. Oncotic pressure is a form of osmotic pressure exerted by proteins like albumin. These proteins tend to draw fluid into the capillary and limit fluid movement out. The question describes heart failure. In heart failure, left atrial pressure rises. This pressure is transmitted to the pulmonary veins and capillaries. This increases capillary hydrostatic pressure and drives fluid into tissue beds causing pulmonary edema.

Post radiation cardiomyopthy

Can cause restrictive heart failure. Causes inflammation of the heart acutely. Fibroblast recruitment occurs and ECM deposition. Pericarditis may occur acutely after radiation therapy. Long tern there can be chronic pericarditis, coronary artery disease, valvular disease and restrictive cardiomyopathy due to fibrous tissue accumulation.

A 5 year old girl is brought in for evaluation to a medical mission in rural China. The child lives on a remote far and eats a diet of mostly rice. The girl's mother states that the child has been lethargic for several weeks. In addition, her ankles have become swollen. The girl feels like sleeping all the time. She becomes easily breathless with exertion. On exam her jugular venous pressure is 12 (normal <8). Bilateral rales are present. There is 2+ pitting edema. Which of the following is expected for cardiac output and left atrial pressure in this child?

Cardiac output - increased Left atrial pressure - increased This child's history is consistent with high output heart failure from thiamine deficiency. Thiamine (B1) is a co-factor in cellular metabolism. Deficiency can lead to neurologic symptoms including neuritis and muscle weakness (dry beriberi). The exact mechanisms of high output are not well understood. Cardiac output rises and SVR is low. Despite the high output, left atrial pressure rises leading to typical heart failure findings like pulmonary edema and systemic backflow symptoms.

Peripheral resistance in heart failure

Cardiac output fall Body vasoconstricts Angiotensin and sympathetic nervous system work to raise the TPR.

Sodium/water retention

Cardiac output falls The effective circulating volume of the body falls. This activates RAAS, SNS and ADH. These conspire to increase sodium and H2O. Total body water rises, but the circulating volume drops. Most of the water is sitting in the lungs and the lower extremities, not circulating.

Chest x ray with heart failure

Chest shows congestion The lung fields are white due to increased fluid.

Alcohol cardiomyopathy

Chronic consumption of alcohol can cause cardiomyopathy. Believed to be due to toxic metabolites. Can recover with cessation of alcohol

Lung findings

Class findings is rales Fluid filled alveoli pop open with inspiration.

Nitrates plus Hydralazine

Combination therapy for acute and chronic HF Studied in systolic heart failure. Reduction in preload (nitrates) and afterload (hydralzine). Acute effect: improves symptoms Chronic effect: Lowers mortality Largely replaced by ACE inhibitors today, but studies suggest that this therapy is beneficial in black patients.

Loeffler's syndrome

Hypereosinophilic syndomre. Usually affects Skin and lungs, but one potential effect is restrictive heart disease.

Loop diuretic side effects

Hypokalemia, volume depletion (renal problems, hypotension).

Loop diruetics are better as IV/PO

IV is better. Patients have swollen guts usually.

Heart Failure

Impaired ability of the heart to pump blood. Hallmark: low cardiac output

Occasionally right failure occurs in isolation

In these cases there will be High pulmonary artery, right ventricular, and right atrial pressure. Usually secondary to a lung process (seen in pulmonary hypertension, COPD)

Inotropes

Increase contractility. Only useful in systolic heart failure. All activate B1 Some activate B2 (vasodilation and hypotension)

Right heart failure symptoms

Increased JVP Lower extremity edema Liver congestion

Lower extremity pitting edema

Increased capillary hydrostatic pressure. Fluid leak from capillaries perfuses the tissue. Gravity pulls the fluid to the lower extremities.

A 64 year old man presents with fatigue, dyspnea and LE edema. JVP is 12 (normal <8). Urinarlysis demostrates proteinuria. He is also noted to have a large tongue. An abdominal fat bad biopsy shows a pink, waxy substance. Congo red stains show green birefringece under polarized light. Which findings are most likely in this patients for LVEF, LV size, and left atrial pressure?

LVEF - normal LV size - normal LAP - increased The patient has classic findings of primary amyloidosis. This disorder is caused by a clonal proliferation of plasma cells which produce light chains that deposit in tissues forming amyloid. The kidney is commonly involved and proteinuria is one of the classic features. Tongue enlargement and apple green birefringence of stains are also classic. Amyloidosis is the classic example of an infiltrative disorder that causes restrictive cardiomyopathy. This is a diastolic heart failure, so the ejection fraction is preserved. The wall thickness of the ventricle is increased, but the left ventricular size (volume) is usually normal. LAP is high as indicated by his pulmonary edema.

LVEF and heart disease

LVEF = normal Left ventricular volume = normal (not dialted) Restricted filling occurs though and you'll see increased atrial pressure. The atria become dilated.

Left ventricular failure

Leads to increased LV pressure. LV systolic pressure depends on contractility LVEDP is always high in left heart failure. In systolic, less blood pumped out leads to more left behind leads more pressure. In diastolic there is a stiff ventricle and thus higher pressure. Either way the LVEDP rises.

Fabry disease

Lyposomal storage disease Cause of restrictive heart disease.

Rhythm disturbances

MI disrupts electrical activity. Ventricular tachycardia, and AV block can occur.

Acute heart failure therapy

Often treated in the hospital. Goal: symptom relief. Contrast with chronic HF: this is all about reducing mortality and hospitalizations. Often same therapies for both diastolic and systolic heart failure. In both cases the lungs are congested and the goal is removing fluid.

A 50 year old man presents with new onset dyspnea, fatigue and lower extremity swelling. He finds it difficult to lie flat and has been sleeping uncomfortably in his recliner. Pulse is 110/min. Blood pressure is 150/80 mm Hg. Jugular venous pressure is 12 cm (normal is <8). Bilateral rales are heard. Lower extremities show 2+ edema. Which of the following is true of the systemic capillaries of this patient regarding oncotic pressure and hydrostatic pressure?

Oncotic pressure - no change Hydrostatic pressure - increased Two forces control the movement of fluid out of capillaries: hydrostatic pressure and oncotic pressure. Hydrostatic pressure drives fluid out of capillaries into tissue beds. Oncotic pressure is a form of osmotic pressure exerted by proteins like albumin. These proteins tend to draw fluid into the capillary and limit fluid movement out. The question describes the classic features of heart failure. In the setting of heart failure, the elevated right atrial pressure is transmitted backwards to the systemic veins and capillaries. This increases capillary hydrostatic pressure and drives fluid into tissue beds causing edema. New onset heart failure doesn't alter albumin levels. Capillary oncotic pressure would be unchanged, but no as influential as it would be with a normal hydrostatic pressure.

Heart failure and lying flat

Physiologic effects of lying flat: increased venous return redistribution of blood volume from lower extremities and splanchnic beds to lungs. Little effect in normal individuals but worsening of pulmonary congestion in heart failure patients.

Concentric hypertrophy

Pressure overload response Chronic elevated pressure in ventricle as seen in chronic hypertension, or aortic stenosis. Decreased wall compliance (stiff ventricle). Often seen in diastolic heart failure. Increased myocyte size. Sarcomres are added in parallel instead of in series.

Pressure volume loop of diastolic heart failure

Problem of LV compliance and lusitropy. Cardiac output goes down The problem is in diastole Fall in LV compliance and lusitropy means the ventricle has become stiff and resistant to filling with blood. Can't get blood in. A decrease in compliance shifts the relationship up and to the left. Greater pressure per volume. Small decrease in stroke volume. EDV goes down due to decreased filling. The LVEDP is greatly increased (it's due to the stiff ventricle, not the volume though).

Pressure volume loop of systolic heart failure

Problem of contractility Cardiac output is decreased. Systole is the problem. Decreased contractility means systole isn't able to get normal amount of blood out. Stroke volume goes down SV = EDV - ESV ESV is increased (due to the contractility decrease) EDV rises too. Higher ESV has VR added to it. LVEDP increases. As we move to the right in volume, we move up in pressure as well. Changes in contractility shift down and to the right.

Heart failure model

Pump drains water from a pipe fed tank. If the pump fails, the water in the tank rises as the pipe is still feeding it but not as much is going out. Eventually the tank overflows. Pump - heart Water - blood Tank - Lungs and veins

Nesiritide

Recombinant BNP Vasodilator Decreased afterload, incrased CO. Expensive and clinical trials showed it wasn't worth shit. Used rarely

Hallmark of left heart failure

Rise in LVEDP. Less blood pumped out leads to more left behind leads more pressure. In diastolic there is a stiff ventricle and thus higher pressure. Either way raised LVEDP.

Systolic and Diastolic

Same signs/symptoms: dyspnea, orthopnea, paroxysmal nocturnal dyspnea. Rales, JVP, pitting edema Low flow symptoms are found in systolic only: cool extremities, cachexia (weight loss), confusion.

Nutmeg liver

Seen in right heart failure. Particularly common in restrictive cardiomyopathy.

Frank Starling curve

Shows relationship between preload and stroke volume. A fall in contractility shifts the curve down and to the right. This means that for any preload you will get a lower than normal stroke volume.

Restrictive Heart Disease

Something infiltrates the myocardium. Granulomas (sarcoidosis) Amyloid protein (amyloidosis) Heart cannot relax and fill.

A 62 year old woman presents with fatigue, dyspnea, and lower extremity swelling. Two weeks ago, she had an anterior ST-elevation myocardial infarction. She was treated with placement of a drug eluting stent. After stent placement, her left ventricular ejection fraction was estimated at 30% (normal is 55%). Chest x ray shows increased vascular markings consistent with pulmonary edema. On exam, the JVP is 14 cm (normal <8) and there is 2+ pitting lower extremity edema. Compared to before the onset of her current condition, which of the following changes are expected for body weight and sympathetic nervous system activity?

Weight - increased SNS activity - increased Question describes many classic features of heart failure. Heart failure activates the sympathetic nervous system and RAAS. Both of these lead to retention of sodium and water by the kidneys. This expands the total body water and increases weight.

Kussmaul's sign

When the patient inspires there is a rise in JVP. Seen in restrictive heart disease. Normally inspiration lowers JVP. With restricive cardiomyopathy the ventricle can't accept the extra venous return and gets backed up.