HF part 2 Flashcards
Defintion of HF
Cardiac output is not able to meet metabolic demands. This can be new-onset or as an acute decompensation of chronic heart failure.
Epidemiology
- In the UK, heart failure is responsible for over 67,000 hospital admissions per year
- > 65 years of age
RFs for HF
- Increasing age
- Coronary artery disease
- Hypertension
- Valvular disease: commonly senile calcification of the aortic valve
- Diabetes
- Atrial fibrillation
- Renal insufficiency
What is acute decompensated HF?
- either new-onset heart failure without any previous cardiac dysfunction
- or as an acute decompensation of chronic heart failure.
What are the causes of acute decompensation of heart failure?
- HT
- Obesity
- AF & Arrhythmias
- Excess alcohol
- NSAIDs
What happens when HF starts and as it progresses
- Many systems initiate physiological compensatory changes to maintain CO and peripheral perfusion to negate HF effects
- Overtime compensatory changes become overwhelmed and become pathophysiological
General pathophysiology of Acute decompensated HF
- 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
Pulmonary oedema and venous congestion presentations
- Pulmonary oedema: shortness of breath
- venous congestion causes peripheral oedema
Signs of acute decompensated HF
- 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)
Symptoms of acute decompensated HF
-
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
Investigations
- FBC
- U&Es
- ABG
- BNP or NT-proBNP
- ECG
- CXR
Whats seen on CXR?
- A-Alveolar oedema (batwing opacities)
- B- Kerley Blines
- C-Cardiomegaly
- D-Dilated upper lobe vessels
- E- PleuralEffusion
Acute managment for Acute Decompensated HF
- 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
Surgical management
- 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
Long term management
-
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
HF complications
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.
What is Cor Pulmonale?
Right sided heart failure caused by respiratory disease
Pathophysiology of Cor Pulmonale
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.
Presentation of Cor Pulmonale
- Early - asymptomatic -
- SOB
- Peripheral oedema
- Syncope
- Chest pain
Resp causes of Cor pulmonale
COPD is the most common cause
Pulmonary Embolism
Interstitial Lung Disease
Cystic Fibrosis
Primary Pulmonary Hypertension
Signs of Cor pulmonale
- 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
What does HF do to venous return?
- 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
What happens in progressive HF to venous return?
- failing myocardium actually doesn’t contract as much in response to increased preload meaning cardiac output cannot be maintained and may decrease
What is afterload?
the load or resistance against which the ventricle contracts
What happens when there’s an increase in afterload?
- 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
Sympathetic system activation of heart
- 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
What happens in sympathetic system in HF
- 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
What does angio tensin 2 do
stimulates the release of aldosterone from the adrenal cortex
above the kidneys
What does aldosterone do
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
Why does ventricular hypertrophy happen?
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
3 cardinal symptoms of HF
shortness of breath, fatigue & ankle swelling
Overrall symptoms of HF
- Dyspnoea especially when lying flat (orthopnoea)
- Cold peripheries
- Raised jugular venous pressure (JVP)
- Murmurs and displaced apex beat
- Cyanosis
- Hypotension
- Peripheral or pulmonary oedema
Blood tests for HF
BNP
CXR for HF
Alveolar oedema
Cardiomegaly
Dilated upper lobe vessels of lungs
Effusions (pleural)
What loop diuretics and thiazide diueritcs could you use?
Loop: furosemide
Thiazide: bendroflumethiazide
What can aldosterone antagonist do?
inhibiting ADH release resulting in water loss
spirolactone & epelerone
ACEi
Ramipril, enalipril, captopri
SE: cough , hypotension, hyperkalaemia and renal dysfunction
BBs to use
Bisoprolol, nebvilol, carvedilol Digoxin
