Pathophysiology Of Heart Disease Flashcards

1
Q

Give a definition of heart failure

A

A state in which the heart fails to maintain adequate blood supply to the body despite an adequate filling pressure

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2
Q

What is the primary cause of systolic heart failure?

A

Ichaemic heart disease

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3
Q

Describe the 4 classes of heart failure

A

Class I- asymptomatic, no limitation in physicial activity

Class II- Slight limitation of physical activity, comfortable at rest

Class III- Marked limitation of physical activity, comfortable at rest

Class IV- unable to carry on any physcial activity without discomfort, symptoms at rest

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4
Q

What is the approximate normal value for cardiac output?

A

5 l/min

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5
Q

What is the approximate normal volume for stroke volume?

A

75ml/beat

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6
Q

What is an approximation of a “normal” ejection fraction?

A

50%

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7
Q

What is Starling’s Law of the Heart?

A

Stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction i.e. the end diastolic volume

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8
Q

List some causes of heart failure

A

Coronary artery disease

Hypertension

AF

Valve disease

Cardiomyopathies

Infective endocarditis

Anaemia

Endocrine disorders

Cor pulmonale

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9
Q

How can heart failure be classified based on the cause of the inadequate cardiac output?

A

Left ventricular failure

Right ventricular failure

Congestive heart failure

Low output high output heart failure (excessive afterload, excessive preload, pump failure)- LVSD, HFpEF

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10
Q

Give some of the symptoms of LVF and RVF

A

LVF: paroxysmal nocturnal dysponea, wheeze, nocturnal coughing with pink sputum (caused by pulmonary oedema)

RVF: caused by LVF usually, peripheral oedema, ascites

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11
Q

What are the three broad methods of treating heart failure?

Give some examples of each.

A

Conservative - smoking cessation, weight loss, healthy diet, exercise

Medical - ABCDDS

ACE inhibitors, Beta blockers, Candesartan(if intol. for ACEi) Digoxin, Diuretics, Spironolactone

Surgical- heart transplant, valve replacement

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12
Q

What investigations might you want to carry out to test for heart failure?

A

FBC

U & Es

LFTs

TFTs

Lipid profile

BNP (suggests measure of stretch of cardiac myocytes)

CXR: “ABCDE”

Alveolar oedema, Kerley B lines, Cardiomegaly, Dilated upper lobe vessels, pleural Effusion

ECHO

ECG

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13
Q

Name some causes of LEFT sided heart failure

A

Coronary artery disease

Hypertension

Aortic valve disease

Mitral valve disease

Myocardial disease

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14
Q

Name some causes of RIGHT sided heart failure

A

*LEFT sided heart failure*

Tricuspid valve disease

Pulmonary valve disease

Pulmonary vascular disease (Cor pulmonale)

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15
Q

Briefly explain the pathophysiology of heart failure one LVF or RVF has been established

A

Ischaemic injury leads to reduced myocardial efficiency

Increases workload, decreased cardiac output, decreased contractility

COMPENSATORY MECHANISMS: Activation of RAAS, Activation of sympathetic nervous system, increased myocyte size

These worsen HF overtime + cardiac damage

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16
Q

How do chronically activated compensatory mechanisms such a RAAS and the sympathetic nervous system lead to worsening of heart failure?

A

RAAS activated: Increased Na+ and H20 retention

Increased PRELOAD

SNS activated: Increased HR and peripheral vasoconstriction

Increased AFTERLOAD

17
Q

In HF, what is the cause of cardiac dilation?

A

Increased end-diastolic volume

18
Q

In HF, what is the cause of raised JVP?

A

Right sided-heart failure and fluid overload

19
Q

What causes hepatomegaly in right sided heart failure?

A

Congestion of the hepatic circulation

20
Q

What is heart failure with preserved ejection fraction?

A

HF that is not caused by LV systolic dysfunction, but LV diastolic dysfunction i.e. not a problem with contraction but a problem with relaxation of the LV leading to reduced filling- caused by concentric remodelling of the LV

21
Q

Explain how heart failure leads to peripheral oedema and ascites

A

Heart failure leads to increased capillary hydrostatic pressure at the venous end which pushes fluid out of the capillaries and into the interstitium

RAAS activation also leads to fluid retention

22
Q

List some of the neuro-hormonal activation that occus due to heart disease

A

Sympathetic nervous system

RAAS

Natriuretic hormones

ADH

Endothelin

Prostaglandins/ NO

Kallikrien System

TNFalpha

23
Q

Describe how the activation of the sympathetic nervous system attempts to improve cardiac output in HF and how this manifests in the long-term.

A

Increased cardiac contractility

Vasoconstruction

Tachycardia

Long- term:

Beta adrenergic receptors down-regulated

Cardiac hypertrophy, myocyte apoptosis and necrosis

Upregulation of RAAS

Reduction in HR variability

24
Q

Why is RAAS commonly activated in HF?

A

Reduced renal blood flow

Sympathetic nervous system induction of renin from the macula densa (More AngI to AngII)

25
List some of the downstream effects of elevated angiotensin II
Vasoconstriction LVH, myocyte dysfunction Aldosterone release Na+ and H20 retention Thirst Enhanced sympathetic activity
26
What is are the roles of natriuretic hormones: ANP and BNP?
Balance the effects of RAAS on vascular tone and Na/H20 balance Constrict afferent and vasodilates efferent arterioles Decrease Na+ reabsorption in the kidney Decrease renin and aldosterone secretion
27
What important role does BNP have in the diagnosis of HF?
Used as a sensitive marker for HF (released from the ventricles in response to stretch)
28
What happens to ADH levels in a patient with HF? Would you expect this? Explain.
Increased No, not expected- increased atrial pressure and blood volume should decrease the production of ADH so the body can lose some fluid RAAS and SNS seem to override this in HF and cause increased ADH
29
The hormone endothelin may be _______ in some patients with heart failure. Its role is to __________ systemic and renal blood vessels, thus _________ RAAS.
Increased Constrict Activate
30
What is the role of prostaglandin in HF?
Vasodilates Afferent renal arterioles--\> increases the effects of NA/RAAS
31
How does NO relate to heart failure?
NO synthase is blunted in HF Lose vasodilation --\> contributes to HF
32
Is TNFalpha increased or decreased in HF?
Increased
33
List some causes of increased peripheral arterial resistance in HF
Sympathetic nervous system RAAS Reduced NO Increased endothelin
34
What is cachexia and what is its relevance in HF?
Reduction in skeletal musle mass Can be caused by HF due to reduced skeletal blood flow
35
Explain the renal effects of HF and how this changes throughout its progression.
Early HF: GFR maintained by haemodynamic changes at the glomerulus Later: Increased Na+ and H20 retention, lose nephrons, kidney shrinks Late HF: renal blood flow falls--\> reduced GFR, rise in serum urea and creatinine This can be exacerbated by inhibition of AngII (HF medication)
36