Pathophysiology of cardiac failure Flashcards Preview

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Flashcards in Pathophysiology of cardiac failure Deck (17)
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1
Q

Systolic ventricular dysfunction

A

– impaired cardiac contractility
 ↓ ejection fraction
– (<40%; normal ~50-65%)

2
Q

Diastolic ventricular dysfunction

A

– normal ejection fraction but impaired diastolic ventricular relaxation and decreased filling

– ↓in SV and CO

3
Q

Systolic Dysfunction commonly results from conditions that effect:

A
1. contractility
– e.g. IHD, cardiomyopathy
2. volume overload
3. pressure overload
– valvular stenosis; hypertension

this results in ↑EDV (preload), ventricular dilation, ↑ventricular wall tension

4
Q

Diastolic Dysfunction

A

Normal contraction; impaired relaxation

5
Q

causes of diastolic dysfunction

A
1. impedance of ventricular expansion
– constrictive pericarditis etc. 
2. increased wall thickness
– hypertrophy etc.
3. delayed diastolic relaxation
– aging; ischaemia 
4. ↑heart rate
6
Q

Right Ventricular Dysfunction: Causes

A

Conditions impeding flow into the lungs
– Pulmonary hypertension
– Valve damage/stenosis/incompetence

Pumping ability of right ventricle
– Cardiomyopathy
– Infarction

Left ventricular failure

Congenital heart defects

7
Q

Left Ventricular Dysfunction: Causes

A

Hypertension (↑TPR)
Acute myocardial infarction
Aortic or mitral valve stenosis or regurgitation
Increase in pulmonary pressure can lead to right ventricular failure

8
Q

Compensatory Mechanisms

A

In the early stages of heart failure, compensatory mechanisms (i.e. those involved in hypovolemia) maintain cardiac output

Longer-term, they contribute to the worsening of the condition

9
Q

Problems with the Compensatory Mechanisms: 1. Frank-Starling

A

↑ in vascular volume leads to ↑EDV

↑ in muscle stretch and O2 consumption

10
Q

Problems with Compensatory Mechanisms: 2. Sympathetic activity

A

Initially, sympathetic activity can be helpful; long-term it is not:
– Tachycardia, vasoconstriction, ↓ perfusion of tissues, cardiac arrhythmias, renin release

– ↑ the workload of the heart
• ischaemia, damage to myocytes, ↓ contractility

– Desensitisation of b but not a receptors

11
Q

Problems with Compensatory Mechanisms: 3. Renin-Angiotensin

A

↓ in renal blood flow s9mulates release of renin
↑ renin release
therefore ↑ angiotensin II formation

– Vasoconstrictor, plus stimulates aldosterone release

therefore sodium and water reabsorp9on is ↑ both directly (decreased flow rate through the kidney) and indirectly (via aldosterone)

12
Q

Angiotensin II and aldosterone are also involved inflammatory responses leading to

A

deposition of fibroblasts and collagen in the ventricles

 ↑ the stiffness and ↓ the contrac9lity of the heart, leading to myocardial remodelling and progressing dysfunction

13
Q

Strategies for treatment

A

↑ cardiac contractility

↓ preload and/or afterload to ↓ cardiac work demand

– By relaxing vascular smooth muscle
– By reducing blood volume

Inhibit the RAAS

Prevent inappropriate ↑ in heart rate

14
Q

New York Heart Association Classification of Heart Failure (NYHA) 1

A

No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath).

15
Q

New York Heart Association Classification of Heart Failure (NYHA) 2

A

Slight limitation of physical activity. Comfortable at rest. Ordinary
II physical activity results in fatigue, palpitation, dyspnea (shortness of
breath).

16
Q

New York Heart Association Classification of Heart Failure (NYHA) 3

A

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

17
Q

New York Heart Association Classification of Heart Failure (NYHA) 4

A

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