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Cardiovascular system > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Ultimately, what is inadequate in heart failure

A

Cardiac Output

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2
Q

Describe the normal circulation

A

The body has two circulations (pulmonary and systemic)

Each pump is linked to the vessels in front and behind – thus what affects one side will eventually affect the other

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3
Q

Define Cardiac output

A

The volume of blood leaving EITHER side of the heart per minute (usually in context of left ventricle)

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4
Q

What does stroke volume depend on

A

Contractility
Preload
Afterload

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5
Q

What happens to contractility in heart failure

A

Inadequate contractility can compromise SV

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6
Q

What happens to preload in HF

A

Inadequate venous return can compromise SV

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7
Q

What happens to afterload in HF

A

Excessive resistance compromises ejection volume

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8
Q

Explain the consequences of impaired contractility

A

EF reduced.
Starling curve shifts downwards
SV reduced for any end-diastolic BP (preload)

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9
Q

Describe the thresholds for EF

A 
≥55%
Normal
45-54%
Mildly reduced
30-44%
Moderately reduced

<30%
Severely reduced

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10
Q

How do we measure EF

A

Transthoracic echocardiogram (chest ultrasound).

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11
Q

Define heart failure

A

“A clinical syndrome caused by the inability of the heart to supply blood to the tissues
sufficient to meet their metabolic needs, or achieved at the expense of elevated filling pressures.”

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12
Q

Outline what is meant by heart failure

A

Inability of the heart to keep up with demand
Inadequate perfusion of organs (e.g. brain, liver, kidneys)
Congestion in lungs and legs
Collection of signs and symptoms

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13
Q

What often happens in heart failure

A

Heart rate increases to maintain Cardiac Output.

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14
Q

Describe dilated cardiomyopathy

A

Walls of ventricles are thinner- so less pressure generated- Law of Laplace.

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15
Q

Describe left heart failure

A

Dysfunction associated with the left ventricle
Ejection or filling issue
Blood backs up into the lungs causing congestion
Breathlessness, couging , wheezing
‘Respiratory symptoms’

Also dizziness and cyanosis

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16
Q

Explain the respiratory symptoms observed in left hear failure

A

Increased congestion into the pulmonary circulation, and can cause further backpressure and congestion into the systemic venous circulation.
Increases hydrostatic pressure in the lungs- leading to pulmonary hypertension and oedema- leading to SOB an other respiratory symptoms.

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17
Q

Describe right heart failure

A

Dysfunction associated with the right ventricle
Ejection or filling issue
Increased afterload of the pulmonary circulation (pulmonary hypertension)
Often secondary to left heart failure

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18
Q

What are the consequences of Right Heart Failure

A

Not enough oxygen supplied- ischaemia- cell death.

Causes congestion of the systemic veins.

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19
Q

Describe acute heart failure

A

Rapid onset

Symptoms similar to chronic HF, except the timing of onset and worsening is much more severe

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20
Q

Describe chronic heart failure

A

Slow onset

Due to Infection, pulmonary embolism, myocardial infarction or surgery

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21
Q

Describe HF with reduced EF (HFrEF)

A

Abnormal systolic function
Impaired contraction of the ventricles which despite an increase in HR results in decreased cardiac output
Typically, weakness is caused by damage or destruction of the ventricular myocytes (or valve abnormalities [decreased SV with normal/increased EDV])
Weaker ejection leads to higher diastolic pressures
Can’t expel blood

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22
Q

Describe HF with preserved EF (HFpEF)

A

Abnormal diastolic function
Normal contraction of the ventricle
Increased stiffness of ventricle, impaired relaxation or impaired filling
Because EDV is inherently reduced, the reduced stroke volume is masked when looking at ejection fraction
Can’t gain blood

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23
Q

What may cause HFpEF

A

Restrictive cardiomyopathy- ventricles are stiffer- they cannot relax- majority of cases of HF
Hypertrophic cardiomyopathy- hypertrophy of the ventricular myocardium, particularly the interventricular septum- hypertrophy inwards- smaller space for blood to fill the ventricle.

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24
Q

What are the consequences of HFpEF

A

Less space for blood to pool in diastole- reduced CO

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25
Q

Describe valve disease as a cause of heart failure

A

mitral/tricuspid problems mean ventricles cannot fill with blood, pulmonary/aortic valve means cannot expel blood (systolic issue)

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26
Q

Describe Ischaemic Heart Disease as a cause of heart failure

A

Narrowing of coronary arteries cause ischaemia in heart muscle
Most common cause of HF
Cell death
Less cells to perform role- but no oxygen supplied to be able to perform more work to compensate.

27
Q

Describe MI as a cause of heart failure

A

Significant occlusion leads to death of heart muscle

28
Q

Describe hypertension as a cause of heart failure

A

Hypertension increases afterload which means ventricle must work harder
Compensatory left ventricle hypertrophy occurs- this impairs diastolic filling- increasing myocardial oxygen demand
(need more oxygen which not supplied so die), so muscle grows inward (reducing space for filling)

29
Q

Describe dilated cardiomyopathy as a cause of heart failure

A

Dilated LV reduces generatable pressures which reduces ejection

30
Q

Describe hypertrophic cardiomyopathy as a cause of heart failure

A

Increased LV thickness reduces internal ventricular volume & impedes filling

31
Q

List the most common causes of HF in order

A
  1. CAD
  2. Hypertension and cardiomyopathy
  3. Valve disease
  4. Myocarditis and neoplasia
  5. other
32
Q

What is the most common cause of RHF

A

LHF

33
Q

Describe the causes of RHF

A

Right ventricular MI
Cor pulmonale: RHF due to disease of the pulmonary vasculature. It can be caused by recurrent pulmonary emboli, primary pulmonary hypertension or any widespread hypoxic pulmonary vasoconstriction such as COPD. All of these increase pulmonary vascular resistance causing pressure and volume overload of the right ventricle.
Decreased right ventricular CO limits LV preload and thus LV SV

34
Q

Describe the features of HF seen in the patient

A

orthopnoea- shortness of breath in supine position. When supine, blood redistributes to the intrathoracic compartment increasing pressures and alveolar oedema. It can be relieved by sitting upright, and patients will report that they have to sleep with multiple pillows.
Exertional breathlessness
Weight loss
Anorexia
Paroxysmal nocturnal dyspnoea- patients wake up in the night gasping for breath- alveolar oedema caused by pulmonary venous congestion
Fatigue
Nocturia- peripheral oedema is reabsorbed in the circulation when supine- circulating volume increases and is compensated by an increase in urinary output.

35
Q

Describe the clinical features of HF

A

ascites, hepatomegaly ( due to hepatic venous congestion), increased JVP, reduced pulse volume, tachycardia
Pitting oedema- due to oedema from increased fluid filtration caused by increased venous pressure.

36
Q

Describe some of the investigations that we may use for HF.

A

Chest X-Ray- May show an enlarged heart shadow due to dilatation and alveolar shadowing due to oedema. There may be small bilateral pleural effusions. Width of heart shadow greater than half the transthoracic diameter.
Echocardiogram- Key investigation- allows quantification of EF- indicating the degree of systolic dysfunction. Allows assessment of ventricular dilatation and valvular disease
BNP- B natriuretic peptide- released in response to vascular stretch and is a very sensitive marker for heart failure
Exercise Test
Ambulatory ECG- atrial fibrillation, ventricular hypertrophy or left bundle branch block- if ischaemic- ST elevation indicates previous MI.
Angiogram

37
Q

Describe raised jugular venous pressure

A

Direct measure of pressure in right atria (increases with increase in RJVP)- shows degree of HF
Increased pressure in right side of heart leads to pressures backing up into systemic veins, especially visible in jugular vein.

38
Q

Describe pitting oedema

A

Fluid accumulation in tissue (especially of lower extremities) leads to a pitting effect when physically depressed. The indentation is visible for a short period

39
Q

Describe Ascites

A

Fluid accumulation in peritoneal cavity

40
Q

What is meant by natriuresis

A

Sodium excretion

41
Q

What are the effects of BNP and when is it released

A

Released from ventricular myocytes in response to stretch

Vasodilation of microvessels- reducing BP, afterload- less strain on ventricles
Reduced aldosterone secretion- LESS NA+ absorption
Reduced sodium reabsorption
Inhibits renin secretion

Reduced ECF- reducing circulatory volume and thus pressure
Reduced pressures

42
Q

Describe the use of BNP in HF

A

Good marker of HF

BNP > 100 pg/mL (<70y) or >300 (>70y) suggestive of heart failure

43
Q

Describe the conservative treatment of HF

A

Weight loss
Smoking cessation
Less alcohol
Regular exercise

44
Q

What are the aims of treatment for HF

A

Decrease preload
Decrease afterload by reducing both ventricular volume and pressure
Limit heart rate
Reverse or limit ventricular remodelling.

45
Q

Which treatments should we start with

A

ACE inhibitors and beta blockers.

Also diuretics- to get rid off excess fluid.

46
Q

Describe ACE inhibitors

A

Limits ventricular remodelling
Reduces afterload of the heart (by removing its vasoconstrictor effect)
Limits salt and water retention.

47
Q

Describe beta blockers

A

Beta blocker
bisoprolol or carvedilol;
NOT atenolol or metoprolol

Reduce heart rate, increase coronary blood flow
The decreased contractility and heart rate, however, may worsen symptoms and thus they should only be given in low doses

48
Q

What should be given next if EF is still low

A

As EF<35% if still symptomatic spironolactone or eplerenone

49
Q

Which treatments should then be considered if the patient is still symptomatic

A

ivabradine (if HR>70) to cause vasodilation and sacubitril (inhibits enzyme to break down BNP)/valsartan (stops aldosterone being produced)- if ACE I tolerated.

50
Q

When should you consider Cardiac Resynchronisation therapy

A

if LBBB/RBBB, then this can allow more efficient contraction
Consider CRT if
QRS >130ms and LBBB or QRS >150 and RBBB

51
Q

What are the NICE guidelines for the treatment of HF

A

New HF diagnosis
Start ACE inhibitor and titrate upwards
(Angiotensin receptor blocker if ACE-intolerant)
Add beta blocker and titrate upwards
(Assuming no contraindications and patient is stable)
Add spironolactone (diuretic)
(if patient remains moderately to severely symptomatic)

52
Q

What must also be given alongside these treatments

A

Add diuretic
In most cases

Add digoxin
If normal rhythm and symptomatic despite ACE inhibitor and beta blocker

If AF present

53
Q

Describe the non-pharmacological treatment for fluid control

A

Haemoflitration
Peritoneal dialysis
Haemodialysis

54
Q

Describe the devices available for patients with HF

A

Intra-aortic ballooning
CRT
Ventricular Assist Device (VAD)/Total artificial heart.

55
Q

Describe the surgical treatments of HF

A

Coronary artery bypass graft

Valve surgery

Transplant- severe, intractable HF- life-long immunosuppression.

56
Q

Describe the VAD

A

Implantation of mechanical ventricular assist devices which take over the work of the failing ventricles- used as a temporary solution until transplantation.

57
Q

Describe the Law of LaPlace

A

Wall stress= PR/2 x wall thickness
=PV/LV mass
Increased wall thickness reduced wall stress but less space for the blood to pool.

58
Q

Describe compensatory hypertrophy

A

reduces wall stress in response to acute load, but then leads to dilated cardiomyopathy as ventricle volume has reduced - increasing wall stress; thin wall can no longer contract with enough force to eject blood

59
Q

Describe the beneficial physiological response to heart failure

A

BNP released when ventricular myocytes stretched; vasodilation, reduced aldosterone and reduced BP

60
Q

Describe the pathological response to heart failure

A

Reduced renal perfusion leads to activation of RAAS, leading to aldosterone production and hence vasoconstriction, sodium/water retention, and blood pressure increases
This is initially in place to increase filling pressures and to maximise stroke volume, but soon filling pressures become excessive and stroke volume decreases due to over-stretching of the myocytes- moves them onto the downward part of the starling curve.

61
Q

What are the consequences of compensatory tachycardia

A

Reduces the duration of diastole, and thus the duration of coronary flow.
With the increase in contractility, myocardial oxygen demand is increased while oxygen delivery is reduced. These two factors combined may cause myocardial ischaemia, which will further impair function.

62
Q

What is it like to live with HF

A

Patient is breathless and tired, sometimes at rest
Heart is damaged and a less effective pump
Marked neurohormonal activation
Poor QoL
Life expectancy is reduced

63
Q

What is the functional NHYA classification

A

Based on a patients
physical limitations

Class 1- No limit of physical activity. Ordinary physical activity does not cause fatigue, palpitations or dyspnoea
Class 2- Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitations and dyspnoea
Class 3- Marked limitation of physical activity. Comfortable at rest but less than ordinary physical activity results in fatigue, palpitations and dyspnoea
Class 4- Unable to carry out any physical activity without discomfort.

64
Q

Describe the progression of heart failure

A

becomes more severe till death, and coronary events (e.g. MI) speeds up process of dying
sudden death always a risk.

Cardiovascular system (19 decks)

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