Congestive Heart Failure (CHF)

Question 1

Generally describe the condition of CHF

Answer 1

The heart is unable to pump blood at the rate sufficient to meet the metabolic demands of the tissues or can only do so at an elevated filling pressures.

Question 2

How can CHF occur?

Answer 2

Most often insidiously via chronic work overload (i.e. HTN or valvular diseases) or ischemic myocardial disease (following MI). Can also happen acutely via fluid overload, acute valvular dysfunction or a large MI.

Question 3

What is the concept of the Frank-Sterling mechanism and how does this explain why during CHF the body tries to compensate with more fluid retention?

Answer 3

Frank sterling mechanism states (in this case it applies to myocytes) that when a muscle is stretched (up to a point) with increased volume, more of the sarcomeres become involved and cross-bridges, and therefore the heart will contract with more force, and the body accomplishes this by having more fluid retention to increase pre-load.

Question 4

What is “ventricular remodeling?”

Answer 4

Molecular, cellular and structural changes of the heart, such as cardiac hypertrophy.

Question 5

How does the body attempt to compensate for CHF in terms of neuroendocrine?

Answer 5

NorEpi is released by adrenergic nerves (to increase heart rate and contractility, and vascular resistance), activation of the RAS system and release of atrial natriuretic peptide (the latter two adjust filling volumes and pressures).

Question 6

Most frequent cause of heart failure?

Answer 6

Systolic dysfunction, progressive deterioration of contractile function of the heart, due to ischemic injure, pressure/volume overload or dilated cardiomyopathy.

Question 7

What is “diastolic dysfunction?”

Answer 7

Ventricles fails to fill appropriately during diastole, i.e. massive left ventricular hypertrophy, fibrosis, amyloid deposition, or constrictive pericarditis.

Question 8

What are two causes of cardiac hypertrophy?

Answer 8

Increased mechanical work due to pressure/volume overload, or activation of ß adrenergic receptors.

Question 9

Histologically how do hypertrophied myocytes look?

Answer 9

Large nucleus w/ increased mitochondria, the nucleus is larger due to more DNA but no division.

Question 10

What is “pressure overload hypertrophy” and what causes it?

Answer 10

Increase of ventricle size due to concentric bands of muscle being made and increased thickness, this happens in response to HTN or valvular disease which would increase the pressure in the ventricles.

Question 11

How do volume overload hypertrophy differ from pressure overload?

Answer 11

Characterized by ventricular dilation due to myocytes growing in series rather than increase in ventricular muscle thickness where myocytes increases in cross sectional area. In fact the wall can be thicker, thinner or normal in ventricular hypertrophy thus we must measure heart weight rather than heart thickness.

Question 12

Why is ventricular hypertrophy a bad thing, shouldnt a larger heart be more powerful?

Answer 12

Increased size doesn’t correlate with increased capillary supply, so basically we have a bigger mass that needs more nutrients but the same amount of supply that it had when the heart was much smaller –> muscles get exhausted and increased possibilities of ischemia.

Question 13

How is fibrosis involved in hypertrophy?

Answer 13

Along with hypertrophy, fibrosis is accompanied.

Question 14

What happens at a genetic level with prolonged hemodynamic overload?

Answer 14

Shift in genetic expression to that seen in fetal cardiac development (where we have fetal forms of ß myosin heavy chains).

Question 15

How is gene expression appeared to be altered?

Answer 15

Changes in the expression of miRNA (non coding RNA that inhibit the expression of certain proteins in mRNA).

Question 16

Which miRNA is associated with cardiac hypertrophy? Prevention of cardiac hypertrophy?

Answer 16

downregulation of miR-208 and upregulation of miR-195 = cardiac hypertrophy. Overexpression of miR-195 will lead to hypertrophy, overexpression of miR-208 is protective.

Question 17

What kind of cardiac hypertrophy is associated with aerobic exercise?

Answer 17

Volume overload hypertrophy w/ increased capillary supply, aka physiologic hypertrophy. This is also accompanied by descreased HR and BP.

Question 18

Is weight lifting good for the heart?

Answer 18

Evidently not… it is associated with pressure-overload hypertrophy and thus deleterous effects.

Question 19

What is “forward failure” and “backwards failure?”

Answer 19

The inability of the heart to deliver enough blood to cause tissue perfusion is forward failure, and the pooling of blood in the venous system is called backwards failure (which can cause pulmonary/peripheral edema).

Question 20

What are the 4 main causes of left sided heart failure? What do these generally have in common?

Answer 20

Ischemic heart disease, HTN, aortic and mitral valve disease and myocardial diseases. Generally occurs from pulmonary circulation congestion, stasis of blood in left chamber, and hypoperfusion of tissues leading to organ dysfunction.

Question 21

How does the atria suffer from impaired ventricular function?

Answer 21

Causes dilation of the left atria and increases risk of a fib, resulting in stasis of blood esp in the atrial appendage.

Question 22

What is a common site of thrombus formation in the atria if blood is static?

Answer 22

The atrial appendage.

Question 23

What causes the Kerley B lines noted in the chest x-rays?

Answer 23

Caused by perivascular and interstitial edema esp in the interlobar septa –> creates an image of the kerley B lines in chest x ray, which are horizontal lines seen at the base of the lungs.

Question 24

What are “heart failure cells” and what do they indicate?

Answer 24

These are hemosiderin laden macrophages; RBC seems into the pulmonary edema fluid and macrophages eat them, but store the hemoglobin in the form of hemosiderin. This indicates previous episodes of pulmonary edema if seen.

Question 25

What are clinical manifestations of left sided heart failure?

Answer 25

Cough and dyspnea (first in exercise and later at rest) seen initially, and later as disease progresses to more pulmonary edema pt’s get orthopnea and paroxymal nocternal dyspnea

Question 26

What is “paroxymal nocternal dyspnea?”

Answer 26

Dyspnea so bad that it feels like suffocation that occurs at night.

Question 27

What causes thrombus and thromboembolic strokes risk in CHF?

Answer 27

LV dysfunction often leads to a fib which causes stasis of blood –> thrombus –> increased risk of strokes and thromboembolic events.

Question 28

Why does CHF activate RAS? Why is this a problem?

Answer 28

Less renal perfusion due to decreased stroke volume from the heart, which induces an activation of renin and the RAS cascade, increase fluid retention and contribute to/exacerbate pleural edema.

Question 29

Besides activating the RAS pathway, what else does CHF cause the kidney to do?

Answer 29

If hypoperfusion of the kidney is severe enough, it will lead to pre-renal azotemia.

Question 30

How is the brain affected by left sided heart failure?

Answer 30

In severe cases pts get cerebral hypoxia which gives rise to hypoxic encephalopathy, and this can progress into stupor or coma.

Question 31

Left sided heart failure can be divided into systolic and diastolic failure, what are they?

Answer 31

Systolic failure is caused by whatever damage that produces decreased cardiac output by the LV. Diastolic failure is when cardiac output is ok at rest, but the LV is very stiff so the heart is unable to accomidate for exercise because LV will be unable to fill up and thus pump out sufficient blood.

Question 32

What is “flash pulmonary edema”?

Answer 32

In diastolic failure where the LV is quite stiff, any increase in LV backs blood up in the LA and into the pulmonary circuit –> rapid pulmonary edema onset, emergency.

Question 33

Who are more prone for diastolic failure?

Answer 33

Women over the age of 65, reason for female unknown.

Question 34

What causes diastolic failure?

Answer 34

HTN, DM, obesity, bilateral renal artery stenosis, fibrosis, restrictive cardiomypoathies and pericarditis. Also the heart stiffens with age naturally anyway.

Question 35

What is the most common cause of right sided heart failure?

Answer 35

Left sided heart failure which puts more strain on the right side, and eventually that also fails, thus everything that causes LS HF also causes RS HF.

Question 36

What is “Cor Pulmonale?”

Answer 36

RS HF unassociated with the left side, this is due to parenchymal diseases of the lungs, or secondary to disorders that messes with pulmonary vasculature, pulmonary embolus, chronic causes of hypoxia. All of this has pulmonary HTN in common.

Question 37

What is a common feature of all the etiologies that causes right sided HF?

Answer 37

Pulmonary HTN as a result of Right side of the heart dilation and hypertrophy.

Question 38

How does right sided heart failure differ from the left?

Answer 38

Pulmonary congestion is minimal, but the engorgement of systemic and portal venous system is pronounced.

Question 39

How can RS heart failure lead to “Nutmeg Liver?”

Answer 39

Fluid will back up in the portal and hepatic vessels from the lungs, causing congestion around the central veins of hepatic lobules making the center red-brown and the periphery more pale and fatty –> produces the nutmeg like appearance.

Question 40

What is cardiac sclerosis and cardiac cirrhosis?

Answer 40

In the case of RS HF esp in conjunction with LS HF, central areas of the liver becomes fibrotic causing the sclerosis, and in extreme cases the cardiac cirrhosis.

Question 41

What is pulmonary edema and pleural effusions associated with?

Answer 41

Left sided heart failure, LSHF.

Question 42

What are consequences of intense pleural edema?

Answer 42

There can be so much fluid that corresponding lung fails to inflate, causing atelactesis. Fluid can also seep into the peritoneal space and produce ascites.

Question 43

What kind of edema is the hallmark of RS HF?

Answer 43

Edema of the peripheral and dependent portions of the body (ankle and periorbital edema). If hospitalized bedridden pt, presacral edema might predominate. Anasarca can also occur.

Question 44

What are pedal, periorbital, presacral and generalized edema (anasarca) associated with?

Answer 44

Right Sided heart failure RSHF.

Question 45

What are clinical features of RSHF?

Answer 45

HSM, peripheral and periorbital edema, pleural effussions and ascites.

Question 46

Which sided heart failure affects the kidneys more?

Answer 46

Right sided, leading to more fluid retention and azotemia than LSHF.

Question 47

What do pharmacologic tx of CHF try to do?

Answer 47

Deal with the excess fluids (via diuretics), try t block the renin (ACEi), and lower adrenergic tone to deal with the NorEpi (Beta 1 adrenergic blockers)