Pathophys Of Heart Failure I, Ii

Front 1

End diastolic pressure is aka

Back 1

preload

Front 2

What is the physical stretching of cardiac muscle that permits optimum overlap of thick and thin filaments and allows the development of tension?

Back 2

preload

Front 3

Alteration in developed tension at a set length or set preload

Back 3

contractility

Front 4

What is the length-tension curve?

Back 4

Length is on the x axis, tension is on the y axis.

Tells the amount of tension that is developed for a given length/preload.

Front 5

What does muscle obtained from a failing heart show on the length tension curve?

Back 5

It is shifted down and to the right. That means for a given length (preload), it's not able to generate as much tension.

Front 6

the "load" that the heart must eject blood against.

Back 6

afterload

Front 7

A(n) (decrease, increase) in afterload decreases the velocity of fiber shortening

Back 7

increase

Front 8

The interaction between afterload and preload is utilized in the treatment of heart failure, in which ______ drugs are used to augment stroke volume by decreasing afterload, and at the same time, reduce ventricular preload.

Back 8

vasodilator

Front 9

The greater the afterload, the (more, less) the sarcomere shortening

Back 9

Less

Front 10

What are the 3 mechanisms by which tension developed by cardiac muscle can be altered?

Back 10

1) Change in preload

2) Change in afterload

3) Change in contractility

Front 11

What are the 2 main peripheral vascular determinants of cardiac function?

Back 11

1) Venomotor changes that normally alter ventricular loaded end diastolic fiber length

2) Arterial resistance changes that alter left ventricular ejection by regulating aortic impedance.

Front 12

What is an indirect but accurate measurement of preload?

Back 12

pulmonary capillary wedge pressure.

Front 13

Left atrial pressure =

Back 13

pulmonary capillary wedge pressure.

Front 14

What types of things reduce preload?

Back 14

diuretic, venodilation, enhancing ejection fraction, increased ventricular stiffness.

They affect the relative or absolute change in intravascular volume.

Front 15

what is major mechanism in decompensated patient with heart failure to decrease preload?

Back 15

Increase in intravascular volume (leads to edema)

Front 16

Two major determinants of afterload

Back 16

1) Systolic pressure

2) Ventricular radius

Front 17

What are the three major determinants of myocardial oxygen demand?

Back 17

1) myocardial contractility

2) tension development

3) heart rate

Front 18

What is the MOST major determinant of myocardial oxygen demand?

Back 18

Tension development

Front 19

Which uses more energy - isometric or isotonic contraction?

Back 19

Isometric (2-3 times more)

Front 20

T/F An increase in afterload results in an increase in myocardial oxygen demand

Back 20

T

Front 21

The number one cause of heart failure is ______

Back 21

coronary artery disease (CAD) presenting as ischemic cardiomyopathy.

Front 22

What is the Frank-Starling mechanism (or Starling's Law of the heart)?

Back 22

The ability of the heart to change force of contraction in response to changes in venous return.

Front 23

(Diastolic, systolic) dysfunction results from a loss of intrinsic inotropy (contractility), most likely due to alterations in signal transduction mechanisms responsible for regulating inotropy.

Back 23

systolic

Front 24

What are the two main classes of drugs used to improve heart function in heart failure?

Back 24

Therapeutic interventions to improve cardiac function in heart failure include the use of cardiostimulatory drugs (e.g., beta-agonists and digitalis) that stimulate heart rate and contractility, and vasodilator drugs that reduce ventricular afterload and thereby enhance stroke volume.

Front 25

What is the net effect of Neurohumoral responses? (these include activation of sympathetic nerves and the renin-angiotensin system, and increased release of antidiuretic hormone (vasopressin) and atrial natriuretic peptide.)

Back 25

They act to increase blood pressure (arterial and venous) and increase volume.

Front 26

How can activation of sympathetic nerves and the renin-angiotensin system, and increased release of antidiuretic hormone (vasopressin) and atrial natriuretic peptide be harmful in heart failure?

Back 26

They act to increase blood pressure (arterial and venous) and increase volume, so they increase afterload and preload to the point that edema may occur.

Front 27

Why are beta blockers beneficial in heart failure?

Back 27

they block the effects of excessive sympathetic activation on the heart.

Front 28

What is the rational behind using Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone receptor antagonists to treat heart failure?

Back 28

They block the RAA system from increasing volume and thus increasing afterload and preload.

Front 29

What is the primary method the body uses to compensate for the reduction in cardiac output when heart failure starts?

Back 29

Activation of sympathetic ns. and RAA system in order to <b> increase systemic vascular resistance.</b>

Front 30

What mechanisms increase blood volume in order to increase the venous return to the heart in the body's attempt to increase CO via the Frank Starling mech?

Back 30

1) Decreased renal perfusion --> retention of fluid.

2) RAA - contribute to retention of fluid.

3) increase in renal reabsorption of sodium and water

Front 31

A patient with congestive heart failure can be characterized as having a decrease in CO at the expense of an increase in what?

Back 31

TPR and intravascular volume overload.

Front 32

What is the most common cause of CHF in younger patients?

Back 32

Dilated cardiomyopathy.

There are MANY causes for this.

Front 33

Most common causes of dilated cardiomyopathy in the US.

Back 33

Alcohol

Adriamycin

Hypertension

Sarcoid

Genetic defects

Front 34

Valvular heart disease that causes CHF in older people is primarily _____ while in younger people is primarily ______.

Back 34

Calcified aortic stenosis; Mitral valve syndrome

Front 35

When does the left ventricle "burn out" in corrected congenital heart disease?

Back 35

third or fourth decade

Front 36

What is the final common pathway in heart failure?

Back 36

A loss of contractile myocytes and a progressive weakening of the pump. This results in a decrease in cardiac output and stroke volume.

Front 37

What does the decrease in cardiac output activate as a "compensatory" mechanism?

Back 37

Called compensatory, but is really pathophysiologic.

Actiates the neurohumoral storm.

Front 38

Short term regulation of arterial pressure

Back 38

Aorta baroreceptor system; Carotid sinus system ---> Decrease in CO activates <b> sympathetic nervous system</b>

Front 39

How is the sympathetic nervous system's reaction to decreased CO pathophysiologic in heart failure?

Back 39

It releases NE which causes
1) Increase in HR

2) Attempt to increase contractility (obviously it can't do too much bc the heart is failing)

3) Increases TPR

Front 40

T/F In decompensated CHF, circulating NE levels are high

Back 40

T

Front 41

What physical findings in decompensated CHF is NE responsible for?

Back 41

Resting tachycardia

Cold, clammy skin

Sweating (diaphoresis)

Front 42

Intermediate-term regulation of arterial pressure

Back 42

Renin-Angiotensin system.

Decreased CO --> Decreased Renal blood flow ---> Renin release --> AI converted to A2 by ACE --> Volume retention

Front 43

How does Angiotensin II affect the brain?

Back 43

It drives thirst response in hypothalamus.

Patients with CHF are always thirsty.

Stimulates posterior pituitary to release ADH.

Front 44

What is beta natriuretic peptide?

Back 44

polypeptide secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells

Front 45

When is beta natriuretic peptide released and what does it do?

Back 45

Released when the heart is volume overloaded (ie., in CHF).

Attempts to cause systemic and pulmonary arterial vasodilation and salt-wasting.

Unfortunately it is overwhelmed by the actions of angiotensin II and other neurohormones.

Front 46

Since beta natriuretic peptide doesn't actually cause a natriuresis or diuresis in heart failure, what is it useful for?

Back 46

Diagnosis. Presence of this in the presence of volume overload strongly suggests heart failure.

Front 47

What is left ventricular afterload reduction?

Back 47

It's using pharmacology to decrease TPR and inhibit the neurohormonal storm, thus decreasing afterload and increasing CO in heart failure.

It's been the guiding light in development of successful treatment for CHF.

Front 48

_________ is a cofactor for fibrosis formation

Back 48

Aldosterone. It promotes fibrosis in the myocardium!

Front 49

What is the mechanism of sudden death in advanced heart failure?

Back 49

Increased wall tension, stretching of the conduction system ---> VT ---> VF --> death

Front 50

How is the overuse of diuretics related to sudden death in heart disease?

Back 50

Diuretics cause hypokalemia and hypomagnesemia.

This promotes arrhythmia generation. Ventricular fibrillation rapidly leads to death.

Front 51

Chief complaints in CHF

Back 51

Fatigue, shortness of breath, dyspnea on exertion

Front 52

PE findings in CHF

Back 52

Resting tachycardia

Narrow pulse pressure.

JVP distension

Enlarged liver

Lateral displacement of apical impulse

Front 53

What is cause of narrow pulse pressure in CHF?

Back 53

Increased sympathetic drive with decreased CO

Front 54

What are ECG findings in CHF?

Back 54

Sinus tach; evidence of old MI (possibly); LV hypertrophy (with htn); right or left bundle branch blocks

Front 55

What are CXR findings in CHF?

Back 55

Cardiomegaly with pulmonary venous htn and LA and LV enlargement

Front 56

What is the best/most essential dx test in CHF?

Back 56

echocardiogram.

Quantitates the degree of LV dysfunction, chamber size, chamber enlargement, chamber volumes, and regurgitant lesions.

Front 57

What is the cause of the “pseudodesert” or “pseudohemorrage” in CHF that leads to the reduction in arterial pressure?

Back 57

Reduced stroke volume and cardiac output.

Front 58

Persistently positive plasma troponin - what does it mean?

Back 58

It's a poor prognostic sign.

It means that there is calcium load and apoptotic programs have been increased.

Front 59

What hormone causes myocyte hypertrophy and apoptosis?

Back 59

Angiotensin II

Front 60

Increasing atrial stretch thru volume overload can cause what?

Back 60

Atrial arrhythmias/atrial fibrillation.

Front 61

What kind of prognostic sign is persistently elevated endogenous natriuretic peptides?

Back 61

failure to normalize natriuretic peptide plasma levels a poor prognostic sign

Front 62

What synergistic factors predispose to life-threatening arrhythmias in CHF?

Back 62

1) Arrhythmogenic substrates: infarcts, areas of fibrosis; slowed conduction; favor reentrant arrhythmias

2) Sympathetic stimulation

3) Ischemia

4) Increased wall tension/stretch

5) Iatrogenic factors: hypokalemia, hypomagnesemia

Front 63

What is treatment/prevention for life-threatening arrhythmias in CHF?

Back 63

Automatic implantable cardiac defibrillator (AICD)
Drug therapy usually not effective, limited by proarrhythmia
Amiodarone of some use, inferior to AICD

Front 64

How can the neurohumoral storm be blocked?

Back 64

Pharmacologically.

Give vasodilators to patients with borderline hypotension. This reduces afterload.

Negative inotropes (beta blockers) work to decrease arrhythmias, ischemia, persistent cell death.

Front 65

How do negative inotropes (eg, beta blockers) work in CHF?

Back 65

They reduce one component of the neurohormonal storm (sympathetic NE stimulation).

Thus, they decrease arrhythmias, ischemia, persistent cell death.

Over time they improve mortality.

Front 66

Elevated left atrial/pulmonary capillary wedge pressure cause what symptoms?

Back 66

Pulmonary edema symptoms - orthopnea, dyspnea, paroxysmal nocturnal dyspnea

Front 67

Elevated left atrial/pulmonary capillary wedge pressure cause what signs?

Back 67

Rales

Front 68

Elevated right atrial pressure causes what symptoms?

Back 68

Symptoms:
Hepatic congestion: nausea, vomiting
GI congestion: nausea, bloating
Swelling
Dyspnea due to pleural effusions

Front 69

Elevated right atrial pressure causes what signs?

Back 69

Elevated jugular venous pressure, peripheral edema, “pulsatile” liver edge, hepatojugular reflux

Front 70

Low forward CO causes what symptoms?

Back 70

Fatigue, lightheadedness, orthostatic symptoms