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Flashcards in CVS S11 - Heart Failure Deck (37):
1

Define Heart Failure

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

2

What are some of the causes of heart failure?

Most commonly ischaemic heart disease

Can also be:
- Hypertension
- Dilated cardiomyopathy (Bugs, alcohol, drugs, poison, pregnancy)
- Valvular disease (acquired or congenital)
- Hypertrophic cardiomyopathy
- Pericardial disease
- High output heart failure
- Arrhythmia

3

How does the relationship between end diastolic pressure and cardiac output change in heart failure?

As heart failure progresses the heart can no longer generate the same force of contraction (and hence cardiac output) at a given level of filling (end diastolic volume).

Make sure you recognise the graph of this relationship showing the difference between a healthy heart, mild failure and gross failure

4

How is heart failure classified?

Class I to IV depending on symptom severity

5

Describe class I heart failure

No symptomatic limitation of physical activity

6

Describe class II heart failure

Slight limitation of physical activity

Ordinary physical activity results in symptoms

No symptoms at rest

7

Describe class 3 heart failure

Marked limitation of physical activity

Less than ordinary physical activity results in symptoms

No symptoms at rest

8

Describe class IV heart failure

Inability to carry out any physical activity without symptoms

May have symptoms at rest

Discomfort increases with any degree of physical activity

9

What proportion of hospital admissions is for heart failure annually?

What proportion of general medical care and care of the elderly hospital admissions are due to chronic heart failure?

In what subset of the population is heart failure the commonest cause of hospitalisation?

How common are heart failure consultations in primary care?

0.2%

5+%

>65yrs

2nd most common after hypertension

10

What are the 4 main factors affecting cardiac output?

Preload (Venous capacity)
Afterload (peripheral impedance/TPR)
Myocardial contractility
Heart rate

11

On which side of the heart can heart failure occur?

Left, right or both

12

How can types of heart failure be classified?

Left sided HF
Right sided HF
Congestive HF (both)

Systolic HF
Diastolic HF

13

What are some of the features of systolic heart dysfunction?

Increased LV capacity (dilation)
Reduced LV output
Thinning of the myocardial wall (Fibrosis, necrosis, matrix proteinases)
Mitral valve incompetence
Neurohormonal activation
Cardiac arrhythmias

14

What are some of the structural changes that occur during heart failure?

Loss of muscle
Uncoordinated or abnormal contraction (ECG changes)

Changes in ECM:
- Increased Collagen (mostly type 3) from 5% to 25%
- Slippage of myocardial fibre orientation

Changes in cellular structure and function:
- Myocytolysis and vacuolation of cells
- SR dysfunction
- Changes in Ca2+ availability and Ca2+ receptor regulation
- Diastolic failure = concentric hypertrophy
- Systolic failure = Eccentric hypertrophy

15

What factors are involved in neurohormonal activation in heart failure?

SNS
RAAS
Natriuretic hormones
Anti-diuretic hormones
Endothelin
Prostaglandins/NO
TNF-alpha

16

Describe how the SNS responds to HF

Early compensation:
- Increase in SNS output
- Improved CO, contractility, HR
- Vasoconstriction (arteries and veins)

Long term deleterious effects:
- Downregulation/uncoupling of b-adrenoceptors
- NA induces cardiac hypertrophy, myocyte apoptosis and necrosis via alpha receptors
- Upregulates RAAS

Also reduces heart rate variability (reduced PSNS and increased SNS)

17

Describe the RAAS and its effects on the CVS

Renin-angiotensin-aldosterone system

Reduced renal blood flow induces SNS output via macula densa (deleterious effects in HF)

Kidney releases renin in response to SNS

Renin is an enzyme that cleaves angiotensinogen to form angiotensin I

Angiotensin I is converted to angiotensin II by angiotensin cleaving enzymes (ACE)

Angiotensin II causes:
- Vasoconstriction
- Promote LV hypertrophy and myocyte dysfunction/apoptosis

Also promotes release of aldosterone causing:
- Na+/H2O retention
- Increased BP

18

Describe action of the natriuretic hormones

Atrial natriuretic peptide:
- Released in response to atrial stretch
- Predominant renal effect is to constrict afferent and dilated efferent arterioles
- Decreases Na+ absorption in collecting duct
- Inhibits secretion of renin and aldosterone
- Systemic arterial and venous dilation

Brain natriuretic peptide:
- Released in response to ventricular stretch
- Similar effects to Atrial version

These peptide balance the effects of the RAAS on vascular tone and Na+/H2O balance

19

Describe the action of anti-diuretic hormone (vasopressin) in HF

Increases H2O retention by the kidneys

Hypo-natraemia can result

Normally hypo-natraemia inhibits ADH release

But in HF it is increased:
- Increased H2O retention
- Tachycardia and vasoconstriction

20

Describe the actions of Endothelin and its role in HF

Secreted by vascular endothelial cells

Potent systemic and renal vasoconstrictor

Acts via autocrine activity

Activates RAAS in the kidney (reduced renal blood flow)

Evidence of increased levels in HF

Correlated with severity of HF

21

What are the actions of prostaglandins on the CVS?

Prostaglandin E2 and I2:
- Stimulated by NA and RAAS
- Act as vasodilators on afferent renal arterioles to attenuate effects of NA/RAAS
- NSAID Rx blocks de novo PG synthesis

22

What is the effect of nitric oxide on the CVS?

What is its role in HF?

Usually a potent vasodilator produced by endothelial cells via NO synthase

NO synthase may be blunted by HF

Loss of vasodilator balance

23

What is the effect of bradykinin on the CVS?

Promotes natriuresis and vasodilation

Stimulates Prostaglandin production

24

What is the role of TNF-alpha on the CVS?

Depresses myocardial function
May stimulate NO synthase
May have role in cachexia
Increased in HF

25

How is the skeletal muscle affected by HF?

Reduced blood flow leads to reduction in mass:
- Affects all limbs
- Respiratory muscle (E.g. Diaphragm)

Causes abnormalities in structure and function

Contributes to fatigue and exercise intolerance

26

What are the renal effects of HF?

GFR is maintained by haemodynamic changes in the glomerulus in early HF

Increased Na+/H2O retention due to neurohormonal activation (raises BP)

In severe HF, renal blood flow falls and GFR is reduced (causing rise in serum urea and creatinine

This can be exacerbated by treatment inhibiting production or action of angiotensin II

27

What is the involvement of anaemia in HF?

Contributes to symptoms (tiredness, fatigue)
Common, easily treated

Can be caused by:
- Chronic renal failure
- ACEI, Aspirin
- Iron malabsorption
- Expanded plasma volume

28

What are the major predisposing factors of Diastolic heart failure?

What percentage of HF patients overall are DHF?

How does mortality compare to SHF?

Frequently elderly and female
Often history of hypertension/diabetes/obesity

20 - 50% of all HF patients

Hostiptalisation and mortality similar to SHF

29

What are the key features of Diastolic HF?

Concentric LV hypertrophy
reduced LV compliance
Impaired LV relaxation and filling
Increased LA and PA pressures
Unable to compensate by increasing LV end diastolic pressure
Low CO results
Triggers neurohormonal activation same as SHF

30

What are the symptoms/signs of Left HF?

Fatigue
Exertional dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea

In more severe left HF:
- Tachycardia
- Cardiomegaly (displaced apex beat)
- 3rd or 4th heart sound (gallop rhythm)
- Functional murmur of mitral regurg.
- Basal pulmonary crackles
- Peripheral oedema

31

What are the causes of right heart failure?

Chronic lung disease
Pulmonary embolism/hypertension
Pulmonary/tricuspid disease
Left to right shunts (ASD/VSD)
Isolated RV cardiomyopathy
Secondary to LHF (most common cause!)

32

What are the symptoms of right heart failure?

Distension and fluid accumulation in areas drained by systemic veins (Increased vBP)

Fatigue, dyspnoea, anorexia, nausea
Increased JVP
Tender, smooth hepatic enlargement
Dependent pitting oedema
Ascites
Pleural effusion

33

What are the principles of HF management?

Correct underlying cause
Non-pharmacological measures

Pharmacological measures:
- Symptomatic improvement
- Delay progression
- Reduce mortality

Treat complications/associated conditions/risk factors
- E.g. Arrhythmias

34

What are the major factors involved in lifestyle modification for treatment of HF?

Reduce Salt intake
Reduce alcohol
Increase aerobic exercise
reduce BP

35

What are the major factors involved in pharmocalogical intervention for treatment of HF?

Diuretics
ACEI/ Angiotensin receptor antagonists
Nitrates
B-blockers
Spironalactone (aldosterone antagonist diuretic)
Digoxin
Antiarrythmics
Ionotropes - acute setting
Phosphodiesterase inhibitors - acute setting (increase cAMP levels in cardiomyocytes)

36

What are the major surgical interventions for treatment of HF?

Heart transplant
Mechanical assist devices
Valve surgery
Revascularisation (CABG/PCI)
Implantable pacemakers/defibrillators

37

Describe how treatment of HF is staged and the treatments used at each stage

Stage A (High risk, no symptoms):
- Risk factor reduction, education
- Treat hypertension, diabetes, dyslipidaemia
- ACEI or ARAs in some patients

Stage B (Structural HF, no symptoms):
- ACE inhibitors or ARAs in all patients
- B-blockers in some

Stage C (Structural HF, previous or current symptoms):
- ACEI and B-blockers in all
- Dietary Na+ restriction
- Diuretics, digoxin
- Cardiac resynch is bundle branch block present
- Revascularisation/mitral valve surgery
- Aldosterone antagonists (spironolactone)

Stage D (Refractory symptoms requiring special intervention):
- Ionotropes
- Ventricular assist device
- Transplantation
- Hospice care