CO (mL/min) = heart rate (bpm) x stroke volume (mL/beat)
Left sided heart failure is the most common type of heart failure. Causes include coronary artery disease, myocardial infarction and hypertension
Left sided HF leads to back flow into the pulmonary veins, leading to pulmonary oedema
Symptoms of left sided HF:
dysponea
reduced exercise tolerance
orthopnoea
paroxysmal nocturnal dyspnoea
nocturnal cough (with or without pink frothy sputum)
wheeze (cardiac asthma)
Right heart failure is generally as a result of left sided heart failure due to raised intrathoracic pressure
In right heart failure blood backs up into the vena cava, leading to peripheral/systemic oedema
Cor pulmonale is right ventricle dysfunction/failure due to a primary disorder of the respiratory system. The respiratory disorder leads to pulmonary hypertension and therefore increased preload
Signs of right HF:
peripheral oedema
ascites
facial engorgement
pulsation in neck + face (tricuspid regurgitation)
systolic heart failure = reduced left ventricleejection fraction. Less blood is being pumped out of the heart during systole leading to increased blood remaining in the heart. This leads to ventricular stretch, dilation and remodelling.
Diastolic heart failure = preserved left ventricle ejection fraction. Ventricular relaxation and filling is impaired.
Less than 50% function means reduced LVEF
Ejection fraction = (stroke volume / end diastolic volume) x 100
Signs of HF on examination:
pallor - pale due to poor perfusion
Oedema - peripheral / ascites
bilateral basal crackles
3rd heart sounds
murmurs
increased capillary refill time
New York heart association classification is a way of rating a patients dyspnoea from I - IV. IV means the patient is symptomatic at rest.
The RAAS is activated in HF due to reduced cardiac output and renal hypoperfusion. Angiotensin II and aldosterone lead to the retention of sodium and water. This increases the preload.
The sympathetic nervous system is activated by heart failure. It is activated by Baroreceptors and the RAAS. This increases heart rate and therefore afterload.
Natriuretic peptides are released from the heart in response to abnormal stretch and volume overload. BNP (brain natriuretic peptide) is released from the ventricles which leads to vasodilation.
Causes of heart failure include:
ischaemic heart disease
hypertension
valvular disease (commonly AS)
arrhythmias (commonly AF)
dilated cardiomyopathy
For suspected heart failure, measure NT-proBNP
> 2000 ng/L needs an urgent referral for specialist assessment and TTE within 2 weeks
400-2000 ng/L needs a specialist assessment and TTE within 6 weeks
<400 ng/L is unlikely to be heart failure
TTE is a transthoracic echocardiogram. It can assess for valve disease plus the systolic and diastolic function of the ventricles.
Gold standard imaging for heart failure is a cardiac MRI but TTE is first line
An ECG should be performed for suspected heart failure:
Raised resting heart rate
Left axis deviation
Left ventricle hypertrophy
ST and T wave abnormalities
LBBB
Atrial fibrillation as a potential cause
CXR findings suggestive of heart failure:
Cardiomegaly - increased cardiothoracic ratio
Bat wings - alveolar oedema
Prominent upper lobe vessels
Kerley B lines - interstitial oedema
Blunting of costophrenic angles - pleural effusion
Management of reduced LVEF:
ACEi + Beta blocker (can use ARB if not tolerating ACEi)
When commencing a patient on an ACEi / ARB make sure to check U&Es before and 1-2 weeks after. Also check after every dose increase.
These medications are also used in hypertension so monitor patients blood pressure.
Spironolactone is a MRA that can cause hyperkalaemia so make sure to monitor potassium levels
For all types of heart failure, diuretics are used for relief from fluid congestion. Patients with reserved LVEF tend to be on low dose furosemide.
Calcium channel blockers should be avoided in heart failure patients with reduced LVEF
All heart failure patients should receive pneumococcal and influenza vaccinations. They should also have an echocardiogram every 6-12 months.
Acute heart failure is often caused by decompensated chronic heart failure
Causes of acute heart failure:
Overload with aggressive IVI
MI
Arrhythmias
Sepsis
Hypertensive emergency
Symptoms of acute heart failure:
Chest pain - if ACS underlying cause
Acute dyspnoea
Confusion
Cough +/- frothy pink sputum
Fever - in sepsis
Palpitations - in arrhythmias
Signs of acute heart failure on examination:
Tachypnoea
Hypoxia
Tachycardia
3rd heart sound
Bilateral basal crackles- pulmonary oedema
Hypotension - cardiogenic shock
Raised JVP
Peripheral oedema
BNP should tested in suspected acute heart failure. It is sensitive but not specific. When negative it can rule out heart failure as the cause of the patients symptoms.
An ABG in acute heart failure will show type 1 respiratory failure- low oxygen without a raise in CO2
Acute heart failure treatment = SODIUM
S - Sit up
O - oxygen
D - diuretics
I - IV fluids stopped
U - underlying cause
M - monitor fluid balance
In severe cases of acute heart failure the following may be needed:
IV opiates - vasodilators (in severe hypertension or ACS)
IV nitrates - vasodilators (in severe hypertension or ACS)
Inotropes to increase cardiac output
Vasopressors such as noradrenaline to increase blood pressure
NIV or invasive ventilation
The most common cause of right heart failure is left heart failure