Acute Heart Failure

Notes

Cardiology | Cardiovascular Emergencies | Critical Care Medicine | Heart Failure

Overview

Heart failure is a condition in which the heart does not pump enough blood to meet all the needs of the body. It is caused by heart muscle damage or dysfunction, valve problems, heart rhythm disturbances and other rarer causes. Acute heart failure can present as new-onset heart failure in people without known cardiac dysfunction, or as acute decompensation of chronic heart failure. Acute heart failure is a common cause of admission to hospital.

Definition

Heart failure: Reduced CO and/or elevated intracardiac pressures at rest or during stress. Caused by a structural and/or functional cardiac abnormality
Acute heart failure: Describes a patient with acute-onset dyspnoea and pulmonary oedema, but can also apply to cardiogenic shock where the patient is hypotensive and oliguric.
Acute decompensated heart failure: Defined as the sudden or gradual onset of the signs or symptoms of heart failure (usually person with chronic heart failure) requiring unplanned office visits, emergency room visits, or hospitalization.

Cardiac Physiology

Cardiac Output

The amount of blood pumped by the heart per minute

Factors influencing Cardiac Output

Pre-load:
- The end-diastolic ventricular volume which is used to determine the venous return.
- Venous return: depends on the intravascular volume and venous tone
After-load:
- The ventricular pressure at the end of systole
- Calculated = pressure gradient across the vascular bed/CO
Heart rate:
- Number of heart beats in 60 seconds
- 60-100bpm normal
Contractility:
- Ability of the heart muscle to contract (myocardial fibres shorten)

Remember

The four determinants of Cardiac Output are preload, afterload, heart rate and contractility.

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Cardiac Output

Aetiology and Risk Factors

Aetiology

Remember

Most commone cause of acute heart failure (Severe pulmonary oedema is usually left ventricular failure (post MI), valvular heart disease, arrhythmia and ARDS.

Causes	Examples
Coronary artery disease (Most common cause)	Post MI
Infection	Systemic sepsisMyocarditis
Mechanical	EndocarditisPulmonary emboliValve problemsSeptal defectsTamponade
Drugs	B-BlockersCalcium antagonistsCytotoxic therapy
Hypoxaemia
Metabolic	AcidaemiaThiamine deficiencyHypocalcaemiaHypophosphataemia
Myocardial contusion	Blunt thoracic trauma
Myocardial infiltration	TumourSarcoidosisAmyloidosis

Pathophysiology

Acute heart failure is most often caused by a cardiac problem such as following a MI. The diagram below illustrates what happens following an MI and the bodies response to these changes.

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Cardiogenic shock

Clinical Manifestation

Symptoms

Palpitations
Shortness of breath on exertion
Shortness of breath at rest
Fatigue
Orthopnoea
Paroxysmal nocturnal dyspnoea

Think

Has there been any drugs recently given of other illnesses that could cause these symptoms.

Signs

Distress
Tachycardia
Tachypnoea
Hypotension
Displaced apex beat
Gallop rhythm 3rd heart sound
↑JVP
Peripheral oedema
Pulmonary congestion – basal crepitations

The third heart sound (S3), also known as the “ventricular gallop”, occurs just after S2 when the mitral valve opens allowing passive filling of the left ventricle. The S3 sound is actually produced by the large amount of blood striking a very compliant left ventricle (systolic heart failure meaning dilated ventricles). Remember S3 can be a normal finding in children, pregnant females, and well trained athletes, however a S4 heart sound is almost always abnormal.

Diagnosis

Remember

Acute heart failure has an underlying cause. Other then finding what the cause is, it is important to keep differentials below in mind.

Obesity
Chest disease—including lung, diaphragm, or chest wall
Venous insufficiency in lower limbs.
Drug-induced ankle swelling (e.g.dihydropyridine calcium blockers)
Drug-induced fluid retention (e.g. NSAIDs)
Hypoalbuminaemia
Intrinsic renal disease
Intrinsic hepatic disease
Pulmonary embolism
Depression and/or anxiety disorders
Severe anaemia
Thyroid disease
Bilateral renal artery stenosis

Investigations

Serology

ECG – Sign of MI, dysryhtmias?
EUC
Cardiac enzymes
ABG
BNP

Imaging

Chest X-ray
- Alveolar oedema (Bat wings)
- Kerly B lines (Interstitial oedema)
- Cardiomegaly
- Dilated veins
- Pulmonary Effusion
ECG
Echocardiogram – check for cardiac abnormalities

Treatment

Resuscitation – Begin treatment before investigations

Airway
Breathing
- Respiratory rate
- O2 sats
- Provide O2
Circulation
- Heart rate, Blood pressure, JVP, ECG
- IV access
- Take bloods – ABG
- Pain relief: morphine? GTN?
- Fluid??
Disability and Exposure
- BGL, temp
- Head to toe of patient

Acute Management

Sit patient upright – Oxygen
Pharmacological intervention – Start with low doses and titrate slowly
- Morphine
- Loop diuretics added – help control fluid overload
- +/- GTN spray/infusion for high BP – DO NOT USE IF LOW BP
+/- Ionotropic drugs – affect the strength and contraction of the heart (for reversible cardiogenic shock)
+/- CPAP – if patient worsening
Cardiologist consult

Once stable and improving

Monitor
- Fluid status
- Kidney function – electrolyte concentrations
Repeat Chest X-ray
Oral Frusemide
ACEI – improves prognosis (ARB alternative therapy for intolerance)
B-blockers OR spironolactone– started when the patient is stable and euvolaemic
Mechanical support of the circulation – if patient deteriorates
- Intra-aortic balloon pump
- Extracorporeal membrane oxygenation
- Ventricular assist devices
Cardiac transplantion?

ANTIHYPERTENSIVE DRUGS
Drug Class	MOA	Adverse effects (Contraindications)
ACE Inhibitors	Angiotensin converting enzyme inhibitor inhibits Angiotensin II a potent vasoconstrictor. Also prevents aldosterone release (Na+ and fluid lost and K+ retained)	Hypotension, Rash, Cough, taste disturbance, angioedema (Pregnancy, renal stenosis)
Beta Blockers		Worsening of the failure, severe hypotension, bradyarrhythmias (Chronic obstructive lung disease, Peripheral vascular disease)
Diuretics	Inhibit the reabsorption of sodium from the nephron and so inhibits water reabsorption
Nitrates	Dilates venous vessels, decreasing preload.

Watch Pharmacology – Antihypertensives

IONOTROPIC DRUGS
Drug Class	MOA	Adverse effects (Contraindications)
Catecholamines (Adrenaline)	Predominately acts on alpha and beta receptors in the heartperipheral vasoconstriction (alpha adrenergic action)Positive inotropic effect on the heart and dilation of coronary arteries (beta adrenergic action)
Phosphodiesterase inhibitors (Milrinone)	Competitively inhibit the phosphodiesterase III isoenzyme responsible to the breakdown of cAMP, increasing inracellular cAMP levels and improving myocardial contractility independent of beta-receptor stimulation
Cardiac glycosides (Digoxin)	Slows HR and reduces AV nodal conduction by an increase in vagal tone and a reduction in sympathetic activity. Increases the force of myocardial contraction by increasing the release and availability of stored intracellular calcium
Calcium and calcium sensitisers (Levosimendan)	Binds to and sensitises cTnC to calcium without raising intracellular calcium – Improves cardiac performance and contractility during systole without impairing ventricular relaxation during diastole