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Cardiology > Pathophysiology of congestive heart failure > Flashcards

Pathophysiology of congestive heart failure Flashcards

1
Q
A
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2
Q

What is heart failure?

A

Occurs when the heart is unable to maintain an adequate circulation at normal filling pressures.

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3
Q

What are the determinants of cardiac output?

A

Preload

Afterload

Contractility

Heart rate

Distensibility

Synergy of contraction

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4
Q

What is preload?

A

the volume of blood that fills the heart during diastole

the stretching of the myocardial cells in a chamber during diastole, prior to the onset of contraction

the end-diastolic volume or end-diastolic pressure.

preload is equal to venous return plus the residual volume left in the cardiac chamber after the last contraction

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5
Q

Signs of left ventricular preload

A

pulmonary oedema as detected by crackles (if severe) or increased broncho-vesicular sounds (if mild or moderate) on pulmonary auscultation

hypoxemia/cyanosis

excessive right ventricular preload

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6
Q

Signs of right ventricular preload

A

jugular venous distention or distention of peripheral veins

positive hepato-jugular reflux test

pleural effusion as detected by increased/laboured respiration

hepatomegaly and/or splenomegaly

ascites (abdominal fluid)

subcutaneous edema

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7
Q

What is afterload?

A

Afterload refers to the arterial resistance the left ventricle encounters as it tries to eject blood.

Afterload is only conceptual and cannot be measured directly.

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8
Q

What is afterload affected by?

A

ventricular volume (size)

arterial vasomotor tone (arterial resistance)

ventricular wall thickness

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9
Q

What is afterload increased by?

A

increase in ventricular volume

increase in arterial vasomotor tone

decrease in ventricular wall thickness

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10
Q

Signs of a fall in cardiac output

A

cool extremities, fall in rectal temperature

weakness/syncope

shock

slow capillary refill time (>2 sec)

arrhythmias

reduced mentation/confusion

congestive failure signs usually coexist with a reduction in cardiac output

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11
Q

Compensatory mechanisms when the heart starts to fail

A
  1. Renin-Angiotensin-Aldosterone system (RAAS)
  2. Atrial natriuretic peptide (ANP) and BNP release
  3. Sympathetic nervous system
  4. Myocardial hypertrophy
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12
Q

Effects of RAAS activation

A

Na and water retnetion

Vasocontriction water retention

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13
Q

Atrial natriuretic peptide (ANP) and BNP release in heart failure

A

ANP is an antagonist to prevent volume overload.

ANP is released in response to atrial stretch and causes Na excretion.

It inhibits the RAAS and reduces tachycardia.

Stored and released from myocardium

Released when atria stretched

Natriuretics

Vasorelaxants

Attenuate aldosterone secretion

Inhibit sympathetic nervous system

Diagnostic markers

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14
Q

Sympathetic nervous sytem activation in heart failure

A

Noradrenaline is released in response to a fall in blood pressure or in response to exercise or excitement.

Acting via b-receptors, noradrenaline causes an increase in heart rate and contractility.

Acting via a-receptors, NA causes peripheral vasoconstriction to conserve blood flow to essential vascular beds (brain and heart) and also causes venoconstriction that increases venous return.

Respiratory sinus arrhythmia is abolished

Vagal restraint on the heart is reduced

Heart rate increases
§ Myocardial oxygen consumption increases
§ Diastole shortens and oxygen delivery to the myocardium is further decreased

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15
Q

Eccentric hypertrophy

A

Caused by volume overload

Increase in thickness and increase in radius

Leads to an overstretched ventricular myocardium so that myocytes are unable to interact and contract.

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16
Q

Concentric hypertrophy

A

Caused by pressure overload

Huge increase in thickness, and decrease in radius

Becomes so severe that MVO2 increases and the myocardium becomes hypoxic so dysrhythmias can occur. Eventually, fibrosis occurs and prevents the ventricles from relaxing, leading to diastolic failure.

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17
Q

Mechanisms of heart failure

A

Myocardial failure/pump failure

Volume overload

Pressure overload

Compliance (diastolic) failure

Abnormal heart rate/rhythm

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18
Q

Myocardial failure/pump failure

A

e.g. dilated cardiomyopathy.

This causes a failure in contractility and a decrease in forward stroke volume.

In DCM the myocardium is weak and dilated and cannot contract with sufficient force to eject the blood volume.

19
Q

Volume overload

A

Increase in ventricular volume e.g. valve regurgitation and shunts such as PDA and ASD

The force of contraction increases to expel the extra blood.

The heart dilates due to the extra blood load and chamber enlargement is seen on radiographs and echocardiography.

20
Q

Pressure overload

A

e.g. aortic stenosis, pulmonic stenosis or systemic hypertension.

Cause an increased afterload so the heart must work harder to maintain cardiac output and the heart muscle hypertrophies.

In the case of aortic stenosis, the left ventricular outflow tract is narrowed and the left ventricle must work harder to eject the blood.

The left ventricular muscle hypertrophies and prevents efficient chamber filling. The abnormally thick muscle is also prone to arrhythmias.

21
Q

Compliance (diastolic) failure

A

prevents adequate ventricular relaxation, e.g. cardiac tamponade, myocardial diseases such as HCM and AV valve stenosis

These conditions all prevent adequate relaxation of the ventricles, therefore impeding filling.

In HCM the ventricular wall becomes so thick that the ventricular lumen is obliterated and cannot fill during diastole.

22
Q

Abnormal heart rate/rhythm

A

tachycardia can provoke a cardiomyopathy if sustained over a long enough period

A sustained tachycardia can result in a cardiomyopathy where the affected heart becomes dilated and hypocontractile.

Similarly, a profound bradycardia can cause low output failure.

23
Q

Forward (low output) heart failure

A

Leads to a fall in systemic blood pressure.

Right-sided forward failure leads to a reduction in blood supply to the lungs.

Left sided failure leads to low output to the body.

24
Q

Clinical signs of forward heart failure:

A

Exercise intolerance- Poor muscle perfusion

Pallor- Peripheral vasoconstriction

Tachycardia- Catecholamine release (sympathetic tone increase)

Weak femoral pulses- Poor contractility

Azotaemia- Poor renal perfusion

Increased thirst- Angiotensin II

25
Q

Backward failure (congestive heart failure)

A

In contrast to forward failure, the clinical signs are different for left and right-sided failure.

Congestion occurs due to damming of the blood behind a failing heart.

The same basic processes occur that lead to pulmonary oedema (left-sided) or body cavity effusions (right-sided).

26
Q

Clinical signs of left-sided backward failure:

A

Dyspnoea/tachypnoea
- Pulmonary oedema, pleural effusion in cats

Cough (especially in dogs)
- Left-sided cardiomegaly compressing left main-stem bronchus (harsh), pulmonary oedema (soft)

Respiratory crackles and wheezes
Absence of lung noise
- Pulmonary oedema, pulmonary effusion

27
Q

Clinical signs of right-sided backward failure:

A

Jugular distension
- Increased RA pressure

Hepatomegaly
- Increased vena cava pressure

Ascites
- Venous congestion of liver

Positive hepatojugular reflex
- Blood displaced from liver to jugular

Pleural effusion (dogs)
- Increased pressure in azygous and bronchial veins

Peripheral oedema
- Increased systemic venous pressure and venoconstriction

28
Q

New York Heart Association classification scheme for congestive heart failure

A

Class 1 No clinical signs but evidence of heart disease

Class 2 Exercise intolerance or dyspnoea after marked exercise

Class 3 Marked exercise intolerance, dyspnoea after mild exercise

Class 4 Cannot exercise, dyspnoea at rest

29
Q

4 basic stages of myxomatous mitral valve degeneration

A

Stage A: patients at high risk

Stage B: patients with structural heart disease
B1: asymptomatic with no imaging evidence of structural change
B2: asymptomatic patients with haemodynamically significant valve regurgitation

Stage C: patients with past or current clinical signs

Stage D: patients with end-stage disease with clinical signs of heart failure caused by CVHD that are refractory to ‘‘standard therapy’’

30
Q

Stage A of myxomatous mitral valve degeneration and failure

A

patients at high risk for developing chronic valvular heart disease (CVHD) but that currently have no identifiable structural disorder of the heart (eg, every Cavalier King Charles Spaniel without a heart murmur).

31
Q

Stage B of myxomatous mitral valve degeneration and failure:

A

identifies patients with structural heart disease (eg, the typical murmur of mitral valve regurgitation is present), but that have never developed clinical signs caused by heart failure.

Because of important clinical implications for prognosis and treatment, the panel further subdivided Stage B into Stage B1 and B2.

32
Q

Stage B1 of myxomatous mitral valve degeneration and failure:

A

asymptomatic patients that have no radiographic or echocardiographic evidence of cardiac remodelling in response to CVHD.

33
Q

Stage B2 of myxomatous mitral valve degeneration and failure:

A

asymptomatic patients that have hemodynamically significant valve regurgitation, as evidenced by radiographic or echocardiographic findings of left-sided heart enlargement.

34
Q

Stage C of myxomatous mitral valve degeneration and failure:

A

patients with past or current clinical signs of heart failure associated with structural heart disease.

Because of important treatment differences between dogs with acute heart failure requiring hospital care and those with heart failure that can be treated on an outpatient basis, these issues have been addressed separately by the panel.

35
Q

Stage D of myxomatous mitral valve degeneration and failure:

A

patients with end-stage disease with clinical signs of heart failure caused by CVHD that are refractory to ‘‘standard therapy’’.

Such patients require advanced or specialized treatment strategies in order to remain clinically comfortable with their disease.

36
Q

4 phases of diastole

A

Isovolumic relaxation

Rapid early mitral filling

Diastasis

Atrial contraction

37
Q

Isovolumic relaxation

A

from closure of aortic valve to opening of the mitral valve

38
Q

Rapid early mitral filling

A

Passive

39
Q

Diastasis

A

a pause during which there is little change in ventricular volume or pressure

40
Q

Atrial contraction

A

atrial systole and its contribution to ventricular filling

41
Q

What is failure of relaxtion caused by?

A

Increased afterload

Ventricular hypertrophy

Abnormal calcium movement

Obstruction to ventricular filling

Increased chamber stiffness

42
Q

Ventricular hypertophy causes

A

Hypertrophic cardiomyopathy

Aortic stenosis

Pulmonic stenosis

Heartworm disease

Systemic hypertension

43
Q

Obstruction to ventricular filling causes

A

AV valve stenosis

Intracardiac neoplasia

Pericardial disease - causes tamponade

44
Q

Increased chamber stiffness causes

A

Fibrosis

Ischaemia

Hypertrophy
§ HCM
§ Aortic/pulmonic stenosis
§ Heartworm
§ Hypertension

Tamponade

Cardiology (10 decks)

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