Heart Failure Flashcards

1
Q

What does heart failure represent?

A

Clinically represents end point of number of diseases that can affect the heart.
Cardiac output insufficient to meet the body’s demand

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2
Q

What are the most common causes?

A

Hypertension
Diabetes
Ischaemia
Acute MI
Valvular disease
Cardiomyopathy
Pericardial disease
Infection

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3
Q

What is the Frank-Starling mechanism?

A

When ventricular end-diastolic volume increases, stroke volume increases

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4
Q

What is cardiac pre-load?

A

So stretch (on normal myocyte) augments contraction (within limits) in response ti stretch

This is cardiac preload – so within limits, stretch on a normal myocyte with augment contraction and refer this to preload

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5
Q

What increases cardiac output?

A

When cardiac muscle is stretched (more blood entering the ventricle) -
Stretched muscle contracts with greater force -
So automatically pumping extra blood out -
Increase venous return when you increase cardiac output

So stretch (on normal myocyte) augments contraction (within limits) in response to stretch

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6
Q

What is after-load?

A

Afterload is the load against which the heart must contract to eject blood from the ventricle

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7
Q

What can cause ventricular remodelling?

A

An increase in afterload (pressure overload)

An increase in preload (volume overload)

Myocardial injury (usually due to MI)

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7
Q

What is ventricular remodelling?

A

Can be defined as any structual change of the ventnricle in reponse to change in loading conditions – includes changes in ventricular mass, chamber size and shape – can help to maintain cardiac output and then worsening heart failure

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7
Q

Can ventricular remodelling be reversed?

A

Yes

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8
Q

What is concentric hypertrophy?

A

Increased amount of work that is demanded of the heart eg. chronic hypertension

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9
Q

What is eccentric hypertrophy?

A

Increased filling pressure or a diastolic overload

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10
Q

What is the ejection fraction?

A

Proportion of the volume of blood present at the end of diastole that is ejected from the ventricle on contraction

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10
Q

How can the systolic function of the LV be approximated by?

A

Ejection fraction

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11
Q

How do you work out ejection fraction?

A

EDV - ESV / EDV

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12
Q

What is the normal ejection fraction percentage?

A

50-60%

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13
Q

What does the LVEF correlate and not correlate to?

A

Not correlate = functional capacity
Does describe the pattern of ventricular remodelling

14
Q

What is the value for heart failure reduced ejection fraction?

A

EF < 45%

14
Q

What is the value for heart failure normal ejection fraction?

A

EF > 45%

15
Q

What is the progression of HF?

A

Damage to the myocardium
(essentially adaptive mechanism / neurohumoral activation)
Systemic body response
(long term systemic response is harmful to the patient)
Progression of damage to myocardium
(downward clinical spiral)
Death

16
Q

What is neurohumoral activation?

A

Activation of nervous system, different endocrine signals and essentially adaptive mechanism to help heart maintain cardiac output

17
Q

What is long-term systemic response?

A

Changed in circulating blood volume, changes in other systems – can be harmful to patient

18
Q

Why can HF lead To death?

A

If unable to intervene somewhere in the spiral and try and restire normal function of the myocardium

19
Q

What are the changes observed in HF?

A

Ventricular remodelling (dilatation and hypertrophy)
Changed in:
Cardiac function
Neurohumoral status (activation of sympathetic nervous and renin-angiotensin-aldosterone system)
Systemic vascular function
Blood volume

20
Q

What are the signs and symptoms of HF?

A

Breathlessness on exertion and at rest
Orthopnoea (SOB when supine) - most commonly you see an increase in venous return when lay down in normal healthy person, no matter heart can effectively pump excess. In pt with HF the left ventricle is often weakened and isn’t able to do that
Paroxysmal nocturnal dysponea
Defined by New York Heart Association

Fatigue and ‘lack of energy’
SOB/dyspnea
Ptting oedema – particularly around ankles
Coughing
Elevated JVP
Pulmonary oedema/pleural effusion – fluid in pleural space, lining of the lungs
Ascites – fluid in the abdomen
Tachycardia
S3 gallops (3rd heart sound – deceleration of blood entering the LV from LA)

21
Q

What are the stages of HF?

A

Stage 1: no symptoms / no limitations of ‘ordinary’ physical activity
Stage 2: mild symptoms slight limitations of ordinary activity
Stage 3: marked limitations during less-than-ordinary activity
Stage 4: severe limitations, experiences symptoms at rest

22
Q

What investigations are undertaken to diagnose HF?

A

Diagnosis based on overall picture (signs, symptoms and evidience of funtional or structural change)
FBC – full blood count
Haematinicins
U+E
TFT
CXR – chest xray
BNP – brain derived natriuretic peptide – polypeptide produced by ventricles in response to stretching. If normal unlikely patient has HF but higher levels coreelate with functionally worse clinical outcomes
ECG – AF and other arrhythmias, evidence of an old MI, LBBB, left ventricular hypertrophy
Echo – ejection fraction, assessment of valves, assessment of previous MI, infarction of chamber dimensions

23
Q

What is the management for someone with HFNEF >45%?

A

Diuretics, managing hypertension and underlying causes eg. Diabetes

24
Q

What is the management for someone with HFRNEF <45%?

A

ACE inhibitors, beta blockers, aldosterone receptor antagonists, devises