Pathophysiology of Heart Failure Flashcards

1
Q

What is afterload?

A

The force the contracting heart must generate to eject blood from the heart

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2
Q

What are the patients symptoms in Class I HF as defined by th New York Heart Association?

A

No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea

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3
Q

What is ascites?

A

An abnormal buildup of fluid in the abdomen

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4
Q

What can right sided heart failure cause?

A
  • Conjestion of peripheral tissues
  • Oedema and ascites
  • GI tract conjestion
    anorexia, GI distress, weight loss
  • Liver conjestion
    Impaired liver function
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5
Q

What can left sided heart failure cause?

A
  • Decreased CO
  • Activity intolerence, signs of decreased tissue perfusion
  • Cyanosis and signs of hypoxia
  • Pulmonary conjestion
  • Cough with frothy sputum
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Right heart failure
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6
Q

What is class II HF as defined by the NYHA?

A

Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnoea

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7
Q

What is class III HF as defined by the NYHA?

A

Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitations, or dyspnea

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8
Q

What is class IV HF as defined by the NYHA?

A

Unable to carry on any physical activity without discomfort. Symptoms of HF at rest. If any physical activity is undertaken, discomfort increases.

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9
Q

What is preload?

A

Determined by venous return; EDV.

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10
Q

What are the main components of afterload?

A

Vascular resistance; ventricular wall tension

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11
Q

What is the normal ventricular ejection fraction?

A

~50-60%

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12
Q

What is systolic ventricular dysfunction?

A

Impaired cardiac contractility therefore decreased ejection fraction (<40%)

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13
Q

What is diastolic ventricular dysfunction?

A
  • Normal ejection fraction but impaired diastolic ventricular relaxation and decreased filling
  • Therefore decrease in SV and CO
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14
Q

Systolic dysfunction commonly results from conditions that affect what?

A
  • Contractility
  • Volume overload
  • Pressure overload
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15
Q

Diastolic dysfunction commonly results from what?

A
  • Impedance of ventricular expansion
  • Increased wall thickness
  • Delayed diastolic relaxation
  • Increased HR
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16
Q

What does systolic dysfunction result in?

A
  • Increased EDV (preload)
  • Ventricular dilation
  • Increased ventricular wall tension
17
Q

What is more common diastolic or systolic dysfunction?

A

Systolic dysfunction

18
Q

What are the causes of right ventricular dysfunction?

A
  • Conditions impeding flow into the lungs
  • Pumping ability of right ventricle
  • Left ventricular failure
  • Congenital heart defects
19
Q

What are the causes of left ventricular dysfunction?

A
  • Hypertension (increased TPR)
  • Acute MI
  • Aortic or mitral valve stenosis or regurgitation
  • Increase in pulmonary pressure can lead to right ventricular failure
20
Q

Are the body’s intrinsic mechansisms good for dealing with HF?

A
  • In they early stages they are good as the compensatory mechanisms maintain cardiac output.
  • Longer-term, they contribute to the worsening of the condition
21
Q

What receptors are desensitised by sympathetic activity?

A

Beta but not alpha receptors

22
Q

How does increased sympathetic activity affect the heart long term?

A
  • Tachycardia, vasoconstriction, decreased perfusion of tissues, cardiac arrhythmias, renin release
  • Increased workload of the heart which leads to ischaemia and damage to myocytes which decreases contractility
  • Dessensitisation of B1 receptors
23
Q

What are the strategies for treating HF?

A
  • Increasing cardiac contractility
  • Decreasing preload and/or afterload to decrease cardiac work demand
    By relaxing smooth muscle
    By reducing blood volume
  • Inhibit the RAAS
  • Prevent inappropriate increase in HR
24
Q

What are the problems with the RAAS in treating HF?

A
  • Decreased renal blood flow stimulates release of renin
  • Renin release therefore increases angiotensin II formation (vasoconstrictor, plus stimulates aldosterone release)
  • Sodium and water reabsorption is increased both directly (decreased flow rate through the kidney) and indirectly (via aldosterone)