Acute heart failure Flashcards
acute heart failure refers to
rapid onset or worsening of the signs and symptoms of heart failure
life-threatening condition in which the heart does not pump enough blood to meet the body’s needs
may present as new onset heart failure or as acute decompensation of chronic heart failure
pathophysiology of acute heart failure
AHF involves the acute failure of the heart to pump blood to meet the body’s demand
two courses of pathology develop as a result:
1. congestion in the pulmonary or systemic circulation. pulmonary oedema develops when the left ventricle is unable to empty, which increases the hydrostatic pressure in pulmonary vasculature leading to pulmonary oedema and hypoxia. these patients are ‘wet’
2. hypoperfusion of vital organs as the cardiac output is reduced. these patients are ‘cold’
AHF patients will be classified according to:
four heamodynamic profiles:
1. WET-WARM: signs of congestion without signs of hypoperfusion (50%)
2. WET-COLD: signs of congestion with signs of hypoperfusion (45%)
3. DRY-WARM: no signs of congestion with no signs of hypo perfusion
4. DRY-COLD: no signs of congestion with signs of hypoperfusion
two pathologies in acute heart failure
- congestion: pulmonary oedema develops with the left ventricle is unable to empty, which increases hydrostatic pressure in pulmonary vasculature
- hypoperfusion: of vital organs as the cardiac output is reduced.
causes of new-onset AHF
- acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
- acute valve dysfunction
- arrhythmias
causes of acute decompensation of CHF
- infection
- acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
- uncontrolled hypertension
- arrythmias
- worsening chronic valve disease
- non-adherence with drugs/diet
- change in drug regimen
symptoms of acute heart failure
dyspnoea
reduced exercise tolerance
ankle swelling
fatigue
pink frothy sputum
orthopnoea
paroxysmal nocturnal dyspnoea
signs of pulmonary or systemic congestion
fine basal crackles (bilateral)
peripheral oedema (bilateral)
dull percussion at lung bases
raised jugular venous pressure (JVP)
hepatomegaloy
gallop rythm (S3 or S4 heart sounds)
murmur
signs of hypoperfusion
hypoxia
tachypnoea and accessory muscle use
tachycardia
cyanosis
cold, pale, and sweaty peripheries
oliguria
confusion/agitation
synocope/pre-syncope
narrow pulse pressure
DDx for AHF
asthma
chronic obstructive pulmonary disease (COPD)
pneumonia
leading cause of AHF without established CHF
myocardial infarction
a presentation of unilateral basal crackles, especially concurrent with cough and fever, is more likely to represent
a chest infection
if there is a global wheeze you should consider
asthma, although there may be a wheeze in pulmonary oedema
bedside investigations
may show hypoxia (often SpO2 < 90%)
tachycardia and taachypnoea
systolic blood pressure may be normal, elevated or reduced (hypotension is associated with cardiogenic shock and poor prognosis)
pulse pressure may be narrow (<25% of the sBP)
ECG rarely normal
what might the ECG show in acute heart failure
the ECG is rarely normal
abnormalities eg. signs of ischaemia or arrythmias are very common in AHF and an alternate diagnosis should be considered if the ECG is completely normal
lab investigations for acute heart failure
B-type natriuretic peptide (BNP)
arterial blood gas
baseline blood tests
cardiac troponin
thyroid-stimulating hormone (TSH)
D-dimer
B-type natriuretic peptide BNP
a sensitive but non-specific marker of heart failure. AHF is unlikely/can be ruled out if:
- BNP is less than 100ng/litre
- NT-proBNP is less than 300ng/litre
arterial blood gas
often shows type 1 respiratory failure, or type 2 respiratory failure in those with pre-existing chronic lung conditions
baseline blood tests
FBC, U&E, coagulation, CRP
anaemia may be a contributing factor
cardiac troponin
to detect myocardial infarction (MI) as the underlying cause, however, troponins are often elevated in AHF patients without myocardial infarction
thyroid-stimulating hormone
thyroid abnormalities may precipitate AHF
D-dimer
performed if pulmonary embolism is suspected and well’s score is low (if Well’s score is high proceed to imaging)
note that D-dimer can be positive in AHF in patients without a pulmonary embolism
imaging: chest x-ray appearance of AHF
abnormalities are present in 80% of patients in AHF
if the chest x-ray is normal, consider alternative diagnoses such as pulmonary embolism or exacerbation of asthma/COPD
it can help exclude other causes of dyspnoea such as pneumonia or pneumothorax
what does the echocardiogram assess in AHF
transthoracic ultrasound scan
should be performed early in those with suspected AHF, especially if cardiogenic shock or life-threatening cardiac abnormalities are present
- biventricular systolic and diastolic function
- valve disease
- ventricular wall rupture
- pericardial effusionon
- intracardiac shunts: the presence of a dilated inferior vena cava with reduced respiratory variation is indicative of high venous pressure
what is the relevance of a bedside lung ultrasound
may reveal extracardiac pathology such as pulmonary embolism or B-lines (consistent with interstitial oedema in pulmonary oedema)
mnemonic to remember chest x-ray findings in heart failure is ABCDE
A: alveolar oedema (perihilar/bat-wing opacification)
B: Kerley B lines (interstitial oedema)
C: cardiomegaly (cardiothoracic ratio >50%) - may be difficult to assess on an AP film
D: dilated upper lobe vessels
E: effusions (i.e. pleural effusions - blunted costophrenic angles with meniscus sign)
CHAMP conditions
these are the conditions that may have precipitated AHF, treat these urgently
acute Coronary syndrome
Hypertensive crisis
Arrythmias eg. atrial fibrillation, ventricular tachycardia, bradyarrhythmia
Mechanical problems eg. myocardial rupture as a complication of ACS, valve dysfunction
Pulmonary embolism
when should oxygen be given
if the patient is hypoxic, titrate oxygen to maintain saturations between 94-98% (or 88-92% in those with COPD), patients often require 15L/minute)
when to use loop diuretics
diuretics increase sodium excretion causing diuresis and decrease afterload
‘WET’ patients will require diuretics as the cornerstone of their management
furosemide IV initially to improve symptoms of congestion fluid overload
patients with chronic kidney disease and those already on oral diuretics will need a greater dose
Nitrates
second most used in WET patients
cause venous and/or arterial dilatation to reduce the preload and/or afterload
given to patients with concomitant myocardial ischaemia or hypertension
non-invasive ventilation
CPAP or BiPAP are used for those with cardiogenic pulmonary oedema, dyspnoea, and improves ventilation to reduce respiratory distress and drives fluid out of alveoli and into vasculature in those whose respiratory failure is not controlled with oxygen therapy given via a face mask
cardiogenic shock
some cold patients whose AHF has led to a potentially reversible cardiogenic shock may present with haemodynamic instability
specialists may consider inotropes to increase cardiac output and peripheral perfusion, and vasodepressors to increase blood pressure and vital organ perfusion
what is the aim of long-term management
pharmalogical treatment aims to increase cardiac output by optimising preload and contractility whilst decreasing afterload
what do ACEi and ARBs do
decrease activation of the renin-angiotensin aldosterone system
contraindications include a history of angiooedema, bilateral renal artery stenosis, hyperkalaemia, severe renal impairment and severe aortic stenosis
beta-blocker
decrease heart rate, myocardium oxygen demand and RAAS activation
aldosterone antagonist
antagonise aldosterone increasing sodium excretion causing diuresis and decreased after load
complications of AHF
- 40% die or are readmitted within a year
- AHF may cause arrythmias particularly atrial fibrillation
- increased risk of stroke and other thromboembolic disease following an episode of AHF
