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MD3001 - Cardiology Disease and Pathology > Pathophysiology of cardiac failure > Flashcards

Pathophysiology of cardiac failure Flashcards

1
Q

Cardiac Output =

A

SV x HR

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2
Q

What determines preload?

A

venous return

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3
Q

What is afterload?

A

Force the contracting heart muscle must generate to eject blood from the heart

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4
Q

What are the main components of afterload?

A
  • Vascular resistance
  • Ventricular wall tension
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5
Q

What determines myocardial contractility?

A

Sympathetic nervous system

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6
Q

What does an increase in contractility generate?

A

increases CO independent of preload and afterload

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7
Q

Classify stage 1 heart failure

A

No limitation on physical activity

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8
Q

Classify stage 2 heart failure

A

Slight limitation on physical activity

Physical activity results in fatigue, palpitation, dyspnoea

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9
Q

Classify stage 3 heart failure

A

Marked limitation of physical activity

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10
Q

Classify stage 4 heart failure

A

Unable to carry on any physical activity without discomfort. Will experience symptoms of heart failure at rest

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11
Q

What is systolic ventricular dysfunction?

A

Impaired cardiac contractility therefore a decreased ejection fraction

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12
Q

What is diastolic ventricular dysfunction?

A

Normal ejection fraction but impaired diastolic ventricular relaxation and decreased filling. Heart is pumping less volume than normal

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13
Q

What are the 3 factors that cause systolic dysfunction when affected?

A
  • Contractility
  • Volume overload
  • Pressure overload - valvular stenosis
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14
Q

What are the results of systolic dysfunction?

A
  • Increased EDV
  • ventricular dilation
  • Increased ventricular wall tension (leads to long term remodelling)
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15
Q

What is more common; systolic or diastolic dysfunction?

A

systolic dysfunction

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16
Q

What are the causes of diastolic dysfunction?

A
  • Impedance of ventricular expansion - constrictive pericarditis
  • Increased wall thickness; hypertrophy
  • Delayed diastolic relaxation; aging, ischaemia
  • Increase HR; less opportunity for the heart to relax
17
Q

What does cardiac tamponade cause in the pericardium?

A

reduces the space that the heart occupies

18
Q

What conditions cause impaired diastolic filling?

A
  • Left ventricular hypertrophy
  • Restrictive cardiomyopathy
  • Myocardial fibrosis
  • Transient myocardial ischaemia
  • Pericardial constriction or tamponade
19
Q

What causes impaired contractility in systolic dysfunction?

A
  • Coronary artery disease
    • Myocardial Infarction
    • Transient myocardial ischaemia
  • Chronic volume overload
    • Mitral regurgitation
    • Aortia regurgitation
  • Dilated cardiomyopathies
20
Q

What causes increase afterload (chronic pressure overload) in systolic dysfunction?

A
  • Advanced aortic stenosis
  • Uncontrolled severe hypertension
21
Q

What is LHS HF most likely to cause?

A

RHS heart failure

22
Q

What occurs in RHS heart failure?

A

Congestion of peripheral tissues:

  • Oedema and ascites
  • Liver congestion; impaired liver function
  • GI tract congestion; anorexia, GI distress, weight loss
23
Q

What is an ascites?

A

swelling of abdominal region due to back up of fluid in the portal system

24
Q

What occurs in LHS heart failure?

A
  • Decreased cardiac output
    • Activity intolerence and signs of decreased tissue perfusion; cyanosis and hypoxia
  • Pulmonary congestion
    • Othopnea
    • Parxysmal nocturnal dyspnoea
    • Cough with frothy sputum
25
Q

What conditions mpede flow into the lungs in RV dysfunction?

A
  • Pulmonary hypertension
  • Valve damage/stenosis/incompetence
26
Q

What conditions affect the pumping ability of the RV?

A
  • Cardiomyopathy
  • Infarction
27
Q

What are the causes of Left ventricular dysfunction?

A
  • Hypertension (increase TPR)
  • Acute MI
  • Aortic or mitral valve stenosis or regurgitation
  • Increase in pulmonary pressure can lead to RV failure if you have LV failure
28
Q

What are the main compensatory mechanisms that ultimately contribute to heart failure?

A
  • Sympathetic nerve activity
  • Renin-angiotensin-aldosterone
  • Frank-Starling (length-tension) mechanism
  • Fluid movements
29
Q

What is the problem with the frank-starling mechanisms in systolic dysfunction

A
  • Increased vascular volume –> increased EDV
  • Increase in muscle stretch and O2 consumption
  • Walls of the ventricles are stretch beyond the optimal length resulting in an decreased force of contraction
  • Increasing HR has very little impact on SV
30
Q

What are the problems with sympathetic activity in systolic dysfunction?

A
  • Tachycardia, vasoconstriction, decreased perufsion, cardiac arrhythmias, renin release
  • Increase the workload of the heart - causes ischaemia, damage to myoctes and decreased contractility
  • Desensitisation of beta but not alpha receptors

**Numb to the effect of adrenaline

31
Q

What are the problems with Renin-Angiotensin system in systolic dysfunction?

A
  • Decrease in renal blood flow stimulate renin
  • Renin –> Angiotensin II (constriction and remodelling)
  • Angiotensin II = vasocontrictor and stimulates aldosterone release
  • Sodium and water retention increase
32
Q

What are the other functions of angiotensin and aldosterone and what are the results of this on the heart?

A
  • Angiotensin II and aldosterone are involved in inflammatory responses leading to the deposition of fibroblasts and collagen in the ventricles
  • Increase in stiffness and decrease contractility of the heart leading to remodelling and progressing dysfunction
33
Q

Strategies for the treatment of heart failure

A
  • Increase cardiac contractility
  • Decrease proload or afterload
    • By relaxing vascular smooth muscle
    • Reducing blood volume
  • Inhibit RAAS
  • Prevent inappropriate increase in HR

MD3001 - Cardiology Disease and Pathology (10 decks)

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