Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio Exam 1 > 6 - Pathophysiology of Congestive Heart Failure > Flashcards

6 - Pathophysiology of Congestive Heart Failure Flashcards

1
Q

What is heart failure?

A

Heart failure is the inability of the heart to meet the metabolic demands of the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is congestive heart failure?

A

Clinical syndrome of CHF

  • Dyspnea
  • Increased fatigue
  • Fluid accumulation
  • Exercise intolerance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the difference between CHF and cardiomyopathy

A

Cardiomyopathy is a structural abnormality of the cardiac tissue

While cardiomyopathies can result in heart failure, they are not equivalent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe acute heart failure

A

Symptoms which manifest over a very short period of time (hours, days or weeks)

  • Acute myocardia ischemia
  • Arrhythmias
  • Rupture of a papillary muscle or chordae tendinea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What systems attempt to compensate for the decreased heart function seen in CHF?

A
  • Peripheral vasculature
  • Kidneys
  • Skeletal muscles
  • Neurohumoral activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the effect of these compensatory mechanisms in the long term and in the short term?

A

Short term
- Alleviate some of the symptoms of CHF

Long term
- Further impair function

Note that there is a PROGRESSIVE nature of the disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the New York Heart Association classifications for heart failure

A

Class I - Asymptomatic
Class II - Symptoms with significant exertion
Class III - Symptoms on minor exertion
Class IV - Symptoms at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How many people in the US are affected by heart failure? How many new cases per year?

A

6 million people

500,000 diagnoses per year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the top two risk factors for heart failure?

A

The risk of HF increases with prior coronary artery disease and hypertension

75% of diagnosed patients have a hx of this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What other risk factors exist for heart failure?

A
  • Diabetes
  • Vascular disease
  • Cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is ejection fraction?

A

The percentage of the end diastolic volume (after filling) that is effectively pumped out of the heart

EF = (SV/EDV)*100

EF = ejection fraction
SV = stroke volume
EDV = end diastolic volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does heart failure with a preserved ejection fraction suggest?

A

HF with a preserved EF suggests the compensatory mechanisms are able to sustain the circulatory demands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does heart failure with a low ejection fraction suggest?

A

A low EF denotes cardiac congestion (more volume is staying in the ventricular chamber with each heart beat).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What level (percentage) of ejection fraction is used to indicate a significantly compromised cardiac function?

A

40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Heart failure can be summarized as…

A

The net result is the mismatch between metabolic demand and appropriate cardiac function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes right heart failure?

A

AKA cor pulmonale

  • Vascular dysfunction
  • Hypoxia
  • Parenchymal disease in the lungs
  • Severe left-sided congestion leads to right-sided dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does left-heart dysfunction lead to right heart failure?

A

Severe left-sided congestion can result in right-sided dysfunction, as pulmonary edema and pulmonary venous pressure alter the afterload of the right heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the goal of compensatory mechanisms in CHF?

A
  • Increasing cardiac output

- Increasing the circulating volume to offset the circulatory demands of the periphery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the three categories of changes seen in HF?

A

1 - Protein changes
2 - Neurohumoral changes
3 - Hemodynamic changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do proteins change in HF?

A

Both the expression and function of many proteins are altered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What specific alterations do we see?

A

Changes in proteins related to muscle excitation-contraction coupling, such as…

  • Proteins in the contractile apparatus (sarcomeric proteins)
  • Proteins for calcium cycling (membrane channels, SR channels)
  • Proteins for mitochondrial function (to provide ATP source for contraction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do changes in calcium cycling affect HF patients?

A

Changes in calcium cycling impairs the contraction and relaxation of the myocytes and can contribute to the exercise intolerance suffered by patients with HF, as upon exertion, the heart is functionally unable to match the increased demand

23
Q

How is the autonomic nervous system altered in HF?

A

Sympathetics are activated, parasympathetics are defective

24
Q

What does the activated sympathetic nervous system do in HF?

A

Induces peripheral vascular resistance

25
Q

What event occurs alongside the increased peripheral vascular resistance in HF patients?

A

The release of vasoactive agents

  • Endothelin
  • Vasopressin
  • Angiotensin II

Also, the volume in the vascular circuit increases stress which reduces endothelial-dependent vasodilation

26
Q

What two reflexes are altered in this case?

A
  • Baroreflex (inhibitory reflex) is lowered

- Chemoreflex (excitatory reflex) is increased

27
Q

How is the sensitivity of the sympathetic nervous system altered in HF?

A

Beta adrenergic receptors are desensitized

  • Upon stimulation, the intracellular effect is greatly diminished
  • Much lower inotropic and chronotropic responses are elicited
28
Q

What medications are used to address the concernt of desensitized beta adrenergic receptors?

A

Beta (adrenergic) blockers

Exact mechanism of action is not clear

29
Q

The activation of the following humoral substances is beneficial in the short term but harmful in the long term

A
  • Vasoconstrictors
  • Vasodilators
  • Anti-naturetic substances
  • Anti-diuretic substaces
30
Q

What is RAAS?

A

Renin-Angiotensin-Aldosterone System

31
Q

When in the progression of HF is RAAS activated?

A

Early on in order to counteract the reduction in cardiac output by increasing sodium and water retention, vasoconstriction and thirst

32
Q

How does the RAAS implicate HF in the long term?

A
  • Initiates remodeling processes within the heart and vasculature
  • Promotes CNS dysfunction (sustained SNA)
  • Can lead to electrolyte disturbances (potassium secretion is enhanced by aldosterone)
33
Q

Why would therapeutic strategies to preventing RAAS activation be advantageous in the long run?

A

They prolong the progression to decompensated HF

34
Q

Describe systolic dysfunction in HF

A

Impaired contractility of the heart muscle

  • Reduces stroke volume
  • Reduces cardiac output
35
Q

What are the compensatory mechanisms used to compensate for systolic dysfunction?

A

Try to increase in preload by…

  • Sympathetic stimulation to increase venous return promote fluid retention to increase end diastolic volume
  • Sympathetic stimulation to increase contractility of the heart and therefore stroke volume
36
Q

What do these mechanisms result in in the long run?

A
  • Ventricular remodeling (hypertrophy) which increases the filling of the heart to increase stroke volume
  • As contractility continues to be reduced, hypertrophy increases further and therefore stroke volume is again lowered and cardiac output decreases
37
Q

How will a vasodilater be useful in treating this condition?

A

A vasodilator reduces afterload, so the heart has can eject a larger stroke volume, improving hemodynamics

38
Q

How is diastolic dysfunction compromised in HF?

A

Although diastolic dysfunction is not usually the initial insult, it can occur with time

Hypertrophy and other remodelling activities (fibrosis) compromise ventricular relaxation

39
Q

What happens when ventricular relaxation is impaired?

A

Pure diastolic dysfunction does not (at first) reduce stroke volume but generates higher diastolic pressures within the ventricles, which can lead to impaired filling

40
Q

What causes diastolic dysfunction in HF?

A

Diastolic function is impaired as a result of impaired calcium cycling, decreased tissue compliance, increased ventricular stiffness and depressed ATP levels

41
Q

Why is central venous pressure elevated in HF? Why is this relevant?

A

Central venous pressure is an independent prognostic indicator of HF disease progression and outcomes

42
Q

Describe the trend of central venous pressure elevation in HF

A
  • The initial reduction in cardiac output reduces venous return and increases venous pressure
  • Sympathetic activation acutely increases venous tone and increases cardiac output through increased fluid returning to the heart
  • With further neurohumoral activation, more fluid is retained and venous pressure increases
  • s more and more fluid is retained, the failing heart cannot match the volume demand, causing greater increases in venous pressure

This leads to a downward spiral of fluid retention and cardiac congestion

43
Q

What symptoms are attributed to fluid accumulation?

A

Pulmonary and peripheral edema

44
Q

What symptoms are attributed to reduction in ejection fraction (decreased cardiac output)?

A

Overall fatigue, exercise intolerance and inadequate perfusion of skeletal muscle

45
Q

What symptoms are attributed to inadequate perfusion of the brain?

A

Confusion

46
Q

What symptoms are attributed to pulmonary edema resulting in excessive ventilation?

A

Shortness of breath

47
Q

What is cachexia?

A

weakness and wasting of the body due to severe chronic illness

48
Q

What accounts for HF patients developing cachexia?

A

Cachexia can also be seen in HF patient, possibly through reduction in anabolism/ increase in catabolism throughout the body

49
Q

What are the four main treatments for HF patients?

A
  • Diuretics
  • ACEi, ARB
  • Beta blockers
  • Statins
50
Q

What is the goal of using diuretics?

A

Reduce volume

51
Q

What is the goal of using ACEi or ARBs?

A 
ACEi = angiotensin converting enzyme inhibitors
ARB = angiotensin receptor blockers

Reduce remodeling, afterload, myocardial metabolic demand

52
Q

What is the goal of using beta blockers?

A

Counter sympathetic effects (need to be monitored carefully)

53
Q

What is the goal of using statins?

A

Dyslipidemia and pleiotrophic effects

Statins have been shown to be particularly efficacious in HF patients with underlying CAD; this class of drugs has been shown to have pleiotropic properties that ameliorate some of the systemic dysfunctions seen in HF

54
Q

What is important to keep in mind when treating HF patients?

A

Also, maintaining the treatment of the underlying etiology is important; for example, patients with CAD caused by hyperlipidemia are urged to continue their anti-hyperlipidemics

Cardio Exam 1 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions