CVS - Pathophysiology Of Heart Failure Flashcards Preview

CJ: UoL Medicine Semester Two (ESA2) > CVS - Pathophysiology Of Heart Failure > Flashcards

Flashcards in CVS - Pathophysiology Of Heart Failure Deck (26):
1

What is heart failure?

A pathophysiological state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure

2

What is the main cause of systolic heart failure?

Ischaemic heart disease

3

What are the four classes of heart failure?

- CLASS I: no limitation of physical activity
- CLASS II: slight limitation of physical activity, no symptoms at rest
- CLASS III: marked limitation of (even 'less than normal' levels of) physical activity, no symptoms at rest
- CLASS IV: inability to carry out any physical activity without symptoms, may have symptoms at rest, discomfort increases with any degree of physical activity

4

What is the stroke volume of the average heart?

75 ml/beat

5

What are the four factors which contribute to cardiac output?

Heart rate, venous capacity (LV preload), myocardial contractility, aortic and peripheral impedance (after load)

6

What is left ventricular systolic dysfunction?

Increased left ventricle capacity and reduced left ventricle cardiac output due to thinning of the myocardial wall. Fibrosis and necrosis of myocardium and activity of matrix proteinase leads to the ventricle wall becoming thinner. A gap develops between the cusps of the mitral valve, leading to mitral valve incompetence

7

What are the changes of cellular structure and function which occur due to heart failure?

- myocytolysis and vacuolation of cells
- myocyte hypertrophy
- sarcoplasmic reticulum dysfunction
- changes to calcium availability and/or receptor regulation

8

What are the broad changes which occur in the heart as a result of heart failure?

- loss of muscle
- uncoordinated or abnormal myocardial contraction
- changes to the extra-cellular matrix (increase in collagen, slippage of myocardial fibre orientation)
- changes of cellular structure and function

9

How is the sympathetic nervous system's response to poor contractility mediated?

By baroreceptors

10

How does the sympathetic nervous system help improve cardiac output?

It improves cardiac contractility, causes arterial and venous vasoconstriction and causes tachycardia

11

What are the negative effects of sympathetic nervous system regulation of the heart?

Nodadrenaline induces cardiac hypertrophy and myocyte apoptosis/necrosis via alpha-receptors. It also induces up-regulation of the RAAS

12

What are the roles of angiotensin II?

- potent vasoconstrictor
- promotes LVH and myocyte dysfunction
- promotes aldosterone release
- promotes Na+/H2O retention
- may stimulate thirst

13

How does renin leads to aldosterone release?

- liver, vessels and brain release renin substrate (angiotensinogen)
- this is converted to angiotensin I by renin from the kidney
- angiotensin I is converted to angiotensin II by angiotensin converting enzyme (from lungs and vasculature)
- angiotensin II stimulates aldosterone release

14

What are the functions of ANP?

- constricts afferent and vasodilator efferent arterioles to kidney
- decreases Na+ reabsorption in the collecting duct
- inhibits secretion of renin and aldosterone

BNP has similar effects, and CNP has limited effects in CNS and endothelium

15

What is different about ADH levels in hyponatraemia?

They are increased, meaning that there is increased H2O retention and increased systemic resistance, resulting in increased cardiac output

16

What is endothelin?

Secreted by vascular endothelial cells, potent system and renal vasoconstrictor which acts via autocrine activity. It also activates RAAS. There are increased levels in heart failure patients

17

What is the role of prostaglandins in heart failure?

Act as vasodilators on afferent renal arterioles to attenuate the effects of noradrenaline/RAAS

18

What is the role of bradykinin in heart failure?

Promotes natriuresis and vasodilation, stimulates production of prostaglandins

19

How does heart failure lead to oedema?

Heart failure leads to increased capillary hydrostatic pressure, which overcomes the osmotic pressure and results in fluid moving from capillaries into interstitial fluid.

20

What skeletal muscle changes occur as a result of heart failure?

- reduced skeletal muscle blood flow
- reduction in skeletal muscle mass (cachexia), which affects all muscle including limbs and respiratory
- abnormalities of structure and function contribute to fatigue and exercise intolerance

21

What are the renal effects of heart failure?

- increased sodium and water retention
- in early heart failure, the glomerular filtration rate is maintained by haemodynamic changes at glomerulus
- in severe heart failure, renal blood flow falls leading to reduced GFR and a rise in serum urea/creatinine

22

What are the key factors that lead to heart failure with preserved ejection fraction?

- elderly
- female
- history of hypertension, diabetes and/or obesity

23

What are the characteristics of HFpEF?

- reduced LV compliance and impaired myocardial relaxation
- thicker and shorter cardiomyocytes
- increased deposition of collagen
- impaired diastolic LV filling, dependent on high LA pressure which can also cause RV dysfunction
- triggers neurohormonal activation

24

What are the signs/symptoms of left sided heart failure?

- fatigue
- exertional dyspnoea
- orthopnoea
- paroxysmal nocturnal dyspnoea
- tachycardia
- cardiomegaly
- 3rd/4th heart sound
- functional murmur of mitral regurgitation
- basal pulmonary crackles
- peripheral oedema

25

What can cause right heart failure?

- chronic lung disease
- pulmonary embolism/hypertension
- pulmonary/tricuspid valvular disease
- left-to-right shunts
- isolated right ventricular cardiomyopathy

26

What are the signs/symptoms of right heart failure?

They all relate to distension and fluid accumulation in areas drained by systemic veins:
- fatigue, dyspnoea, anorexia, nausea
- increased JVP
- tender, smooth hepatic enlargement
- dependent pitting oedema
- ascites
- pleural effusion

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