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Medical Studies 1 > 3.4 Pathophysiology of Heart Failure > Flashcards

3.4 Pathophysiology of Heart Failure Flashcards

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USMLE® Step 1 flashcards
1
Q

List some common causes of systolic and diastolic dysfunction

A
  • Myocardial infarction
  • Arrhythmia
  • Coronary Artery Disease
  • Cardiomyopathy
  • Hypertension
  • Valvular pathology
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2
Q

Why can diastolic heart failure lead to an increased ejection fraction?

A

Because it decreases end diastolic volume, which is inversely proportional to stroke volume

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3
Q

What is heart failure called on both sides?

A

Biventricular heart failure

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4
Q

Mechanism: how can hypertension lead to left sided systolic heart failure?

A
  • Increased peripheral resistance
  • Left ventricular hypertrophy
  • Increased myocardial oxygen demand
  • Coronary arteries are compressed
  • Not enough oxygen, myocardium cannot function optimally
  • Left sided heart failure
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5
Q

Is systolic or diastolic heart failure more common in left-sided heart failure?

A

Systolic

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6
Q

Explain how left ventricular hypertrophy can lead to left sided diastolic heart failure

A
  • Increased muscle size
  • Decreased room for filling of ventricle
  • Diastolic heart failure
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7
Q

What is a major, major sign of heart failure, and how can it manifest itself clinically?

A

Major, major sign: pulmonary oedema
Manifests:
- Dyspnoea
- Orthopnea
- Paroxysmal nocturnal dyspnoea

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8
Q

How can left sided heart failure lead to right sided heart failure?

A
  • Left sided heart failure
  • Blood is not circulating as efficiently
  • Blood is backed up in the lungs
  • Increased pressure in pulmonary artery
  • Right ventricle fails to pump hard enough
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9
Q

How can a left-to-right shunt lead to systolic and diastolic right sided heart failure?

A
  • Blood shunted to right side (high to low pressure)
  • Increased fluid volume in right side of heart
  • Right sided hypertrophy
  • Decreased filling space (diastolic)
  • Ischaemia due to increased demand (systolic)
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10
Q

Define heart failure

A

Structural and/or functional abnormality of the heart that results in elevated intracardiac pressures and/or inadequate cardiac output at rest and/or during exercise

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11
Q

LVEF for HFrEF

A

<= 40%

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12
Q

LVEF for HFpEF

A

> = 50%

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13
Q

Criteria for HFpEF other than (EF)

A
  • LV diastolic dysfunction
    and/or
  • Evidence of raised LV filling pressures
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14
Q

Describe the neurohumoral mechanism that is activated in response to reduced stroke volume from the heart

A
  • Sympathetic activation (chronotopic; increased heart rate + inotropic; increased contractility)
  • Renal hypoperfusion + sympathetic activation activates the RAS
  • Increased blood volume increases CO (via RAS system), and increased arterial pressure due to vasoconstriction
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15
Q

What is a potential negative side effect of prolonged RAAS activation?

A

Cardiac fibrosis

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16
Q

List the two kinds of natriuretic peptides released from the heart, and state which chambers they are released from

A

Atrial Natriuretic Peptide (Atria)
Brain Natriuretic Peptide (BNP)

17
Q

What are the effects of natriuretic peptides, and when are they released?

A
  • Cause loss of sodium through urine, leading to decreased blood pressure
  • Released in response to volume overload in heart
18
Q

Describe early pathological remodelling of the heart following an ischaemic event (<72hr). Specify the histological changes.

A
  • Wall thinning
  • Chamber dilation
  • Increased wall stress

Histological changes:
- Formation of a fibrous scar in myocardium

19
Q

Describe late pathological remodelling of the heart following an ischaemic event (>72hr). Specify the histological changes.

A
  • Increased SNS and RAAS due to decreased cardiac output
  • Leads to myocardial hypertrophy and fibrosis

Histological changes:
- Myocyte hypertrophy
- Increased interstitial collagen

20
Q

Briefly explain how heart failure can be progressive

A
  • Left ventricular remodelling in response to damage
  • Maladaptive alterations lead to increased energy demand and ECM degradation, further increasing remodelling and perpetuating a decline in cardiac function
21
Q
A
21
Q

Normal LVEF

A

60%+

22
Q
A
22
Q

Normal LVEF

A

60%+

23
Q

Normal LVEF

A

60%+

24
Q

Approximately what percentage of heart failure patients have HFpEF?

A

50%

25
Q

List three signs that can be used to diagnose HFpEF

A
  • Increase in BNP
  • CV imaging showing impaired diastolic function
  • Raises LV filling pressures during catheterisation
26
Q

How can increased pre-diastolic pressure within the ventricles lead to decreased stroke volume?

A
  • Ventricular filling stops when the pressure in the ventricles exceeds the pressure in the atria
  • If the pressure in the ventricles is higher, this occurs sooner, meaning there is less time for blood to enter ventricles
  • Therefore, less blood is pumped out with each beat, even if ejection fraction is maintained (like in HFpEF)
27
Q

What are some primary risk factors for HfpEF?

A
  • Age
  • Hypertension
  • Obesity
  • Atrial fibrilation
  • Type 2 diabetes
28
Q

Basic mechanism of HFpEF

A
  • Stiffening of LV due to risk factors, but systolic function preserved
  • Increased pressure in LV
  • Increase LA pressure, as more blood remains in LA
  • Remodelling of LA
  • Diastolic dysfunction
29
Q

How can LV heart failure cause peripheral oedema?

A
  • LV function decreases
  • Pressure backs up in pulmonary circulation (orthopnea/dyspnoea), and eventually backs up into right side of heart, inhibiting venous return
  • Fluid remains in the peripheral circulation, where it extravasates and causes oedema
30
Q

How can congestive cardiac failure cause nocturia?

A
  • In heart failure, renal perfusion decreases
  • In the supine position, renal perfusion improves, leading to increased urine production and thus nocturia
31
Q

How does an echocardiogram assist in the diagnosis of heart failure?

A

It provides a representation of chamber size and structure, and the relative movement of valves, enabling heart function to be assessed.

Medical Studies 1 (90 decks)

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