Robbins pg 365-368

Question 1

When does the CV become functional during development?

Answer 1

It is the first organ system to become fully functional
in utero (at approximately 8 weeks of gestation)

Question 2

Although a host of diseases can affect the cardiovascular
system, the pathophysiologic pathways that result in a
“broken” heart distill down to six principal mechanisms:

Answer 2

1) Failure of the pump (aka systolic dysfunction)
2) Obstruction of flow
3) Regurgitant flow
4) Shunted flow
5) Disorders of cardiac conduction
6) Rupture of the heart of major vessel

Question 3

What is systolic dysfunction?

Answer 3

In the most common situation, the cardiac muscle contracts weakly and the chambers cannot empty properly

Question 4

What is diastolic dysfunction?

Answer 4

the muscle cannot relax sufficiently to permit

ventricular filling, resulting in diastolic dysfunction.

Question 5

Heart failure generally is referred to as _____

Answer 5

congestive heart failure (CHF).

Question 6

Most cases of heart failure are due to what?

Answer 6

systolic dysfunction—inadequate myocardial contractile function,
characteristically a consequence of ischemic heart disease or hypertension.

Question 7

What things can cause diastolic dysfunction?

Answer 7

left ventricular hypertrophy, myocardial fibrosis, amyloid deposition, or constrictive
pericarditis.

Indeed, heart failure in elderly persons, diabetic patients, and women may be more commonly
attributable to diastolic dysfunction

Various studies suggest that 40–60% of cases of CHF may be due to diastolic dysfunction.

Question 8

In CHF, the failing heart can no longer efficiently pump

the blood delivered to it by the venous circulation. What is the result?

Answer 8

The result is an increased end-diastolic ventricular volume, leading to increased end-diastolic pressures and, finally, elevated venous pressures.

Thus, inadequate cardiac output—called forward failure—is almost always accompanied by increased congestion of the venous circulation— that is, backward failure.

Question 9

What is the impact of backward failure in CHF?

Answer 9

As a consequence, although the root
problem in CHF typically is deficient cardiac function, virtually every other organ is eventually affected by some
combination of forward and backward failure.

Question 10

The cardiovascular system attempts to compensate for
reduced myocardial contractility or increased hemodynamic
burden through several homeostatic mechanisms:

Answer 10

• The Frank-Starling mechanism
• Activation of neurohumoral systems
• Myocardial structural changes

Question 11

What is the frank starling mechanism?

Answer 11

Increased end-diastolic
filling volumes dilate the heart and cause increased cardiac myofiber stretching; these lengthened fibers contract more forcibly, thereby increasing CO.

If the dilated ventricle is able to maintain cardiac output by this means, the patient is said to be in compensated heart failure. However, ventricular dilation comes at the expense of increased wall tension and amplifies the oxygen requirements of an already-compromised myocardium.

With time, the failing muscle is no longer able to propel sufficient blood to meet the needs of the body, and the patient develops decompensated heart failure

Question 12

What things are involved in activation of neurohumoral systems?

Answer 12

Release of NOR by
the ANS increases HR and augments myocardial contractility and vascular resistance.

Activation of the renin
system augments water and salt retention (augmenting
circulatory volume) and increases vascular tone.

Release of atrial natriuretic peptide acts to balance the renin-angiotensin-aldosterone system through diuresis
and vascular smooth muscle relaxation.

Question 13

What kind of changes take place in the myocardium in CHF or any situation where a pressure overload exists in the atrium/ventricles?

Answer 13

Cardiac myocytes cannot proliferate, yet can adapt to increased workloads by assembling increased
numbers of sarcomeres, a change that is accompanied by myocyte enlargement (hypertrophy)

Question 14

How are new sarcomeres assembled in pressure overload situations (e.g., HTN or valvular stenosis)?

Answer 14

New sarcomeres tend to be added parallel to the long axis of the myocytes, adjacent to existing sarcomeres. The growing muscle fiber diameter thus results in concentric hypertrophy— the ventricular wall
thickness increases without an increase in the size of the chamber.

Question 15

What happens in volume overload states (e.g., valvular regurgitation
or shunts)?

Answer 15

The new sarcomeres are added in series
with existing sarcomeres, so that the muscle fiber length increases. Consequently, the ventricle tends to dilate, and the resulting wall thickness can be increased, normal, or decreased; thus, heart weight— rather than wall thickness—is the best measure of hypertrophy in volume-overloaded hearts.

Question 16

Compensatory hypertrophy comes at a cost to the myocyte. What is it?

Answer 16

The oxygen requirements of hypertrophic myocardium are amplified owing to increased myocardial cell mass. Because
the myocardial capillary bed does not expand in step with the increased myocardial oxygen demands, the myocardium becomes vulnerable to ischemic injury.

Question 17

What else occurs with hypertrophy?

Answer 17

Hypertrophy also typically is associated with altered patterns of gene expression reminiscent of the fetal myocytes, such as changes in the dominant form of myosin heavy chain produced.

Altered gene expression may contribute to changes in myocyte function that lead to increases in heart rate and force of contraction, both of which improve cardiac output,
but which also lead to higher cardiac oxygen consumption.

Question 18

In the face of ischemia and chronic increases in workload, other untoward changes also eventually supervene,
including:

Answer 18

myocyte apoptosis, cytoskeletal alterations, and increased ECM deposition.

Question 19

T or F. Pathologic compensatory cardiac hypertrophy is correlated
with increased mortality

Answer 19

T, cardiac hypertrophy

is an independent risk factor for sudden cardiac death.

Question 20

Is the volume-loaded hypertrophy induced by regular aerobic exercise (physiologic hypertrophy) correlated with increased mortality?

Answer 20

No, this is typically
accompanied by an increase in capillary density, with decreased resting heart rate and blood pressure.

These physiologic adaptations reduce overall CV morbidity and mortality.

In comparison, static exercise (e.g., weight lifting) is associated with pressure hypertrophy and may not have the same beneficial effects.

Question 21

The most common causes of left-sided cardiac failure are what?

Answer 21

• ischemic heart disease (IHD),
• systemic HTN,
• mitral or aortic valve disease, and
• primary diseases of the myocardium (e.g., amyloidosis).

The morphologic and clinical effects of left-sided CHF stem from diminished systemic perfusion and the elevated back-pressures within the pulmonary
circulation.

Question 22

What is usually the
earliest and most significant symptom of left-sided heart
failure?

Answer 22

Dyspnea (shortness of breath) on exertion

Cough also is common as a consequence of fluid
transudation into air spaces.

Question 23

What does dyspnea progress to typically in light-side heart failure?

Answer 23

As failure progresses, patients experience dyspnea when recumbent (orthopnea)

Question 24

Why does orthopnea occur?

Answer 24

because the supine position increases venous return from the lower extremities and also elevates the diaphragm.

Question 25

How is orthopnea typically relieved?

Answer 25

Orthopnea typically is relieved by sitting or standing, so patients usually sleep in a semiseated position.

Question 26

What is Paroxysmal

nocturnal dyspnea?

Answer 26

A particularly dramatic form of breathlessness,

awakening patients from sleep with extreme dyspnea bordering on feelings of suffocation.

Question 27

What are some other manifestations of left ventricular failure?

Answer 27

an enlarged heart (cardiomegaly), tachycardia, a third heart sound (S3), and fine rales at the lung bases, caused by the opening of edematous pulmonary alveoli.

Question 28

What happens with progressive ventricular dilation in left side ventricular failure?

Answer 28

With progressive
ventricular dilation, the papillary muscles are
displaced outwards, causing mitral regurgitation and a
systolic murmur.

Subsequent chronic dilation of the left
atrium can cause atrial fibrillation, manifested by an “irregularly irregular” heartbeat

Question 29

What does a fib cause?

Answer 29

Such uncoordinated, chaotic atrial contractions reduce the ventricular stroke volume and also can cause stasis. The stagnant blood is prone to form thrombi (particularly in the atrial appendage) that can shed emboli and cause strokes and manifestations of
infarction in other organs.

Question 30

What does the diminished CO from left ventricular failure cause?

Answer 30

decreased renal perfusion that in turn triggers renin release increasing intravascular
volume and pressures.

Question 31

What is a major downside of increasing intravascular volume and pressure via renin release in left ventricular failure?

Answer 31

These compensatory effects exacerbate the pulmonary edema.

Question 32

What happens in extended reduction in renal perfusion?

Answer 32

prerenal azotemia may supervene, with impaired excretion of nitrogenous wastes and increasing metabolic derangement.

Question 33

In severe CHF, diminished cerebral perfusion can manifest as what?

Answer 33

hypoxic encephalopathy with irritability, diminished cognition, and
restlessness that can progress to stupor and coma.

Question 34

What is right heart failure typically caused by?

Answer 34

Right heart failure usually is the consequence of left-sided heart failure, since any pressure increase in the pulmonary circulation inevitably produces an increased burden on the right side of the heart.

Question 35

Other causes of right heart failure?

Answer 35

severe pulmonary hypertension, resulting in right-sided heart pathology termed for pulmonale

or primary pulmonic or tricuspid valve disease

or congenital heart disease, such as with left-to-right shunts causing chronic volume and pressure overloads

Question 36

What happens in cor pulmonate?

Answer 36

In cor pulmonale,
myocardial hypertrophy and dilation generally are confined to the right ventricle and atrium, although bulging of
the ventricular septum to the left can cause left ventricular dysfunction.

Question 37

How does right heart failure manifest?

Answer 37

differ from those of left-sided heart failure in that engorgement of the systemic and portal
venous systems typically is pronounced and pulmonary congestion is minimal.

Question 38

Morphology of right heart failure.

Answer 38

• The liver usually is increased in size and weight (congestive hepatomegaly). A cut section displays prominent passive congestion, a pattern referred to as nutmeg liver
• Right-sided heart failure also leads to elevated pressure in the portal vein and its tributaries (portal hypertension), with vascular congestion producing a tense, enlarged spleen
  (congestive splenomegaly).
• Chronic passive congestion of the bowel wall with edema can be severe enough to
  interfere with absorption of nutrients and medications.

Question 39

Effect of right heart failure on the pleural, pericardial, and peritoneal spaces?

Answer 39

Systemic venous congestion due to right heart failure can lead to
transudates (effusions) in the pleural and pericardial spaces, but usually does not cause pulmonary parenchymal edema.

Question 40

When are pleural effusions most pronounced in right heart failure?

Answer 40

when there is increase in pulmonary venous as well as systemic venous pressures, as occurs in combined right and left heart failure.

Question 41

Large (e.g., 1 L or more) pleural effusions can cause what?

Answer 41

atelectasis, and, very uncommonly, substantial pericardial effusions (greater than 500 mL) can limit cardiac filling and cause cardiac failure (due to tamponade).

Question 42

How can right heart failure cause ascites?

Answer 42

A combination of hepatic congestion (with or without diminished albumin synthesis) and portal HTN leads to peritoneal transudates (ascites)

The effusions into the various body cavities typically are serous, with a low protein content, and lack inflammatory cells.

Question 43

Peripheral edema of dependent portions of the body, especially ___ and _____ edema, is a hallmark of right heart failure.

Answer 43

ankle (pedal) and pretibial

In chronically bedridden patients, the edema may be primarily presacral. In particularly severe cases, generalized massive edema (anasarca) may be seen.

Question 44

What are the clinical features of right heart failure?

Answer 44

• very few respiratory
  symptoms.

Instead, the clinical manifestations are related to systemic and portal venous congestion, including hepatic and splenic enlargement, peripheral edema, pleural effusion, and ascites.

Question 45

T or F. Venous congestion and hypoxia of the kidneys and brain due to right heart failure can produce deficits comparable to those caused by the hypo perfusion caused by left heart failure.

Answer 45

T. As congestive heart failure progresses, patients may become frankly cyanotic and acidotic, as a consequence of
decreased tissue perfusion resulting from both diminished
forward flow and increasing retrograde congestion.

Question 46

Note about LHF

Answer 46

In LHF- the capillaries in the lungs will burst and rbcs will enter the alveoli and macrophages will come in and eat the red cells, releasing iron. So with LHF, you will have a lot of iron (stains Prussian-blue) (called heart failure cells- hemosiderin laden macrophages)

Question 47

Shane is….

Answer 47

Gggggaaaayyyyyy