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3A Geriatrics > HF part 2 > Flashcards

HF part 2 Flashcards

1
Q

Defintion of HF

A

Cardiac output is not able to meet metabolic demands. This can be new-onset or as an acute decompensation of chronic heart failure.

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2
Q

Epidemiology

A
  • In the UK, heart failure is responsible for over 67,000 hospital admissions per year
  • > 65 years of age
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3
Q

RFs for HF

A
  • Increasing age
  • Coronary artery disease
  • Hypertension
  • Valvular disease: commonly senile calcification of the aortic valve
  • Diabetes
  • Atrial fibrillation
  • Renal insufficiency
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4
Q

What is acute decompensated HF?

A
  • either new-onset heart failure without any previous cardiac dysfunction
  • or as an acute decompensation of chronic heart failure.
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5
Q

What are the causes of acute decompensation of heart failure?

A
  • HT
  • Obesity
  • AF & Arrhythmias
  • Excess alcohol
  • NSAIDs
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6
Q

What happens when HF starts and as it progresses

A
  • Many systems initiate physiological compensatory changes to maintain CO and peripheral perfusion to negate HF effects
  • Overtime compensatory changes become overwhelmed and become pathophysiological
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7
Q

General pathophysiology of Acute decompensated HF

A
  • Reduced CO > Sympathetic NS activated
  • Causes tachycardia + increased myocardial contractility + peripheral vasoconstriction + RAAS > Leads to increased salt + water retention
  • BNP released by ventricular myocytes in response to increased stretching
  • Leads to pulmonary + venous congestion
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8
Q

Pulmonary oedema and venous congestion presentations

A
  • Pulmonary oedema: shortness of breath
  • venous congestion causes peripheral oedema
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9
Q

Signs of acute decompensated HF

A
  • Cool peripheries
  • Signs of congestive heart failure: peripheral, pitting oedema and raised JVP
  • Displaced apex beat
  • Hypotension
  • Crackles on auscultation: left-sided failure; usually coarse bi-basal crackles
  • Third heart sound (S3)
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10
Q

Symptoms of acute decompensated HF

A
  • Dyspnoea: due to pulmonary oedema
    • Often a history of orthopnea and paroxysmal nocturnal dyspnoea
  • Fatigue and weakness
  • Cardiogenic wheeze
  • Symptoms of congestive heart failure: swelling of the peripheries and ascites
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11
Q

Investigations

A
  • FBC
  • U&Es
  • ABG
  • BNP or NT-proBNP
  • ECG
  • CXR
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12
Q

Whats seen on CXR?

A
  • A-Alveolar oedema (batwing opacities)
  • B- Kerley Blines
  • C-Cardiomegaly
  • D-Dilated upper lobe vessels
  • E- PleuralEffusion
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13
Q

Acute managment for Acute Decompensated HF

A
  • Stabilise the patient: administer oxygen to maintain a SpO2≥94%
  • Fluid restriction: fluid intake is usually limited to <1.5L/day
  • IV diuretic: usually a loop diuretic e.g. furosemide to relieve fluid overload
  • Inotropes or vasopressors e.g. dobutamine: only offer to patients with heart failure and cardiogenic shock (i.e. haemodynamically unstable)
  • Non-invasive ventilation (NIV): consider NIV if the patient does not stabilise with initial medical management
    • Continuous positive airway pressure (CPAP)
  • Intubation and ventilation: if CPAP is unsuccessful
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14
Q

Surgical management

A
  • If acute heart failure is due to aortic stenosis: offersurgical aortic valve replacement
  • Mechanical assist device: pump that can temporarily help the pumping action of the heart
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15
Q

Long term management

A
  • ACE-inhibitor e.g. ramiprilanda cardioselective β-blocker e.g. bisoprolol
    • Improved prognosisby slowing, or even reversing, ventricular remodelling
  • Fluid restriction: fluid intake is usually limited to <1.5L/day
  • Loop diuretic (e.g. furosemide) forsymptomaticrelief of oedema
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16
Q

HF complications

A

Arrhythmias: can both precipitate acute heart failure and occur as a result of it. Atrial fibrillation is one of the most common arrhythmias associated with heart failure.

17
Q

What is Cor Pulmonale?

A

Right sided heart failure caused by respiratory disease

18
Q

Pathophysiology of Cor Pulmonale

A

Increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries.

Leads to back pressure of blood in:
right atrium
vena cava
systemic venous system.

19
Q

Presentation of Cor Pulmonale

A
  • Early - asymptomatic -
  • SOB
  • Peripheral oedema
  • Syncope
  • Chest pain
20
Q

Resp causes of Cor pulmonale

A

COPD is the most common cause
Pulmonary Embolism
Interstitial Lung Disease
Cystic Fibrosis
Primary Pulmonary Hypertension

21
Q

Signs of Cor pulmonale

A
  • Hypoxia
  • Cyanosis
  • Raised JVP (due to a back-log of blood in the jugular veins)
  • Peripheral oedema
  • Third heart sound
  • Murmurs (e.g. pan-systolic in tricuspid regurgitation)
  • Hepatomegaly due to back pressure in the hepatic vein
22
Q

What does HF do to venous return?

A
  • Reduc in vol of blood ejected with each heart beat - increase in vol of blood remaining in systole
  • Preload volume stretches myocardial fibres + myocardial contraction is restored since stretching of fibres will increase force of contraction
23
Q

What happens in progressive HF to venous return?

A
  • failing myocardium actually doesn’t contract as much in response to increased preload meaning cardiac output cannot be maintained and may decrease
24
Q

What is afterload?

A

the load or resistance against which the ventricle contracts

25
Q

What happens when there’s an increase in afterload?

A
  • Increase in EDV + Dec in SV Leads to Dec in CO
  • Causes increased EDV + dilation of ventricles which increases problem of afterload
  • If ventricles dilated its gotta work harder
26
Q

Sympathetic system activation of heart

A
  • When baroreceptors detect a drop in
    arterial pressure or an increase in venous pressure (due to back flow of blood) they stimulate sympathetic activation
  • increases the force of contraction (positively inotropic) of the heart (which increases stroke volume) as well as heart rate - both resulting in an increase in cardiac output
27
Q

What happens in sympathetic system in HF

A
  • Chronic sympathetic activation - down regulation of receptors by SNS resulting in less receptors to act on
  • so sympathetic activation is diminsed and CO stops inceasing in response to sympathetic activation
28
Q

What does angio tensin 2 do

A

stimulates the release of aldosterone from the adrenal cortex
above the kidneys

29
Q

What does aldosterone do

A

increased Na+ reabsorption and thus water reabsorption as well as the release of ADH which stimulates water retention

increased volume of the blood which in turn increases blood pressure and thus venous pressure which in turn increases pre-load thereby increasing the stretching of the heart and thus force of contraction and thus stroke volume and thus cardiac output

30
Q

Why does ventricular hypertrophy happen?

A

chronic hypertension which results in increased blood pressure thereby increasing afterload so heart pumps against more resistance and thus cardiac myocytes grow bigger to compensate for this

31
Q

3 cardinal symptoms of HF

A

shortness of breath, fatigue & ankle swelling

32
Q

Overrall symptoms of HF

A
  • Dyspnoea especially when lying flat (orthopnoea)
  • Cold peripheries
  • Raised jugular venous pressure (JVP)
  • Murmurs and displaced apex beat
  • Cyanosis
  • Hypotension
  • Peripheral or pulmonary oedema
33
Q

Blood tests for HF

A

BNP

34
Q

CXR for HF

A

Alveolar oedema
Cardiomegaly
Dilated upper lobe vessels of lungs
Effusions (pleural)

35
Q

What loop diuretics and thiazide diueritcs could you use?

A

Loop: furosemide
Thiazide: bendroflumethiazide

36
Q

What can aldosterone antagonist do?

A

inhibiting ADH release resulting in water loss
spirolactone & epelerone

37
Q

ACEi

A

Ramipril, enalipril, captopri
SE: cough , hypotension, hyperkalaemia and renal dysfunction

38
Q

BBs to use

A

Bisoprolol, nebvilol, carvedilol Digoxin

3A Geriatrics (12 decks)

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