Neobook — clinical reference

Introduction
Identification
Management
Relevant history, Examination
Investigations
Referral criteria
Discharge criteria/checklist
Follow-up
Treatment Algorithm

Introduction/ Description

Heart failure is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood.

Identification/recognition/diagnosis of problem

The acute decompensated heart failure patient appears extremely ill, restless, poorly perfused and sweaty (peripheries often cold and clammy), tachypnoeic, tachycardic, hypoxic with increased work of breathing (using respiratory accessory muscles) and frothy sputum (may be pink/ blood tinged).

Causes of heart failure:the FAILURE mnemonic

Forgot medication
Arrhythmia/ Anaemia
Ischaemia/ Infarction/ Infection
Lifestyle: taken too much salt
Upregulating of cardiac output: pregnancy, hyperthyroidism
Renal failure/ Retention of fluid: Steroids, NSAIDs
Endocardium: valve abnormalities

Differential Diagnosis

Acute Renal Failure
Acute Respiratory Distress Syndrome
COPD, emphysema
Myocardial Infarction
Pneumonia
Pneumothorax
Neurogenic pulmonary oedema
Pulmonary Embolism
Pulmonary Fibrosis

Management

Immediate action

Stabilise using ABCs, perform blood glucose, apply oxygen if hypoxic and establish IV access.
Main goal is to redistribute fluid out of the lungs
Decrease preload (right-sided over filling) using nitrates (± furosemide)
Decrease afterload (“unload” the left side of the heart) using ACE inhibitors
Consider non-invasive Positive Pressure Ventilation (CPAP) in respiratory failure
Increase contractility (left ventricular systolic function) using inotropes
Treat the cause aggressively

Dose charts

Preload reduction: Give nitrates
GTN spray (one dose) or Isordil 5mg sublingually can be used, and repeated in 5-10 minutes Nitrate infusion: Mix 50 mg GTN in 200 mL Saline 0.9% Rate: 0 – 48 mL/h (0 – 200 μg/min). Start at 20 mL/h and titrate up or down in 2 – 4 mL/h increments Avoid lowering the systolic blood pressure below 90 – 100 mmHg	More effective and safer than morphine or furosemide for preload reduction Can be used in pre-hospital setting Sublingual GTN provides rapid and effective initiation of treatment This can be followed by IV nitrates if symptoms are severe
Consider furosemide
Mainly indicated if pulmonary oedema due to fluid retention and required to offload excess fluid. No added benefit in normovolaemic patients Diuretic naive: IV Furosemide 1mg/kg Patient already on diuretics: use same dose that the patient takes but give it IV Large doses can be placed in a normal saline bag and run as continuous infusion	May reduce blood pressure No consistent data regarding any immediate direct venodilating effect Decreases preload through diuresis, but this is a delayed effect Overall produces adverse hemodynamic effects early-on
Consider morphine
If used, IV Morphine should be titrated in small doses (e.g. 2.5 mg IV as needed; not exceeding 0.1mg/kg)	May reduce blood pressure and respiratory drive No good evidence to support any immediate reduction in preload centrally Nitrates are more effective and safer May provide some anxiolysis
Afterload Reduction: Give ACE inhibitors
SBP > 110: Captopril 25mg sublingual (crushed) SBP 90- 110 mmHg: Captopril 12.5 mg sublingual (crushed)	Combination with nitrates exceeds benefit of either drug on its own Acceptable alternative to IV nitrates (single agent) Rapid reduction in afterload and preload Rapid reduction in subjective level of distress (decreased anxiety) Decreases need for intubation, ICU use Useful in patients with known severe MR, AS
Inotropic support
Inotropes should ideally be started in the Emergency Centre (involve a senior early) Dopamine and / or Dobutamine may require large dosages in severe CHF Tachycardia, arrhythmias and increased myocardial oxygen consumption are side effects Milrinone (where available) provides preload and afterload reduction in addition to inotropic support - superior to dobutamine for the patient with borderline hypotension
Non-invasive Positive Pressure Ventilation (NPPV)
Consider CPAP via a tight fitting facemask if there is respiratory failure and acidosis Start with low PEEP of 5 and then slowly increase as needed. Explain to the patient and hold the mask onto his/ her face, only strapping it on if the patient has settled If combative, confused consider intubation CPAP can be started almost immediately in severe cases along with other treatments Decreases work of breathing, improves oxygenation, CO₂ exchange, preload, afterload, cardiac output and reduces need for endotracheal intubation

Relevant history, Examination

History

Assess clinical severity by history and physical examination
Assess cardiac structure and function
Determine the aetiology, with particular attention to reversible causes
Evaluate for coronary disease and myocardial ischemia
Evaluate the risk of life-threatening arrhythmia
Identify any exacerbating factors
Identify comorbidities which influence therapy
Identify barriers to treatment adherence
Presence of paroxysmal nocturnal dyspnoea or orthopnoea
Presence of dyspnoea on exertion

New York Heart Association Functional Classification should be noted

Class I No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnoea.
Class II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitations, or dyspnoea.
Class III
- IIIA: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnoea.
- IIIB: Marked limitation of physical activity. Comfortable at rest, but minimal exertion causes fatigue, palpitation, or dyspnoea.
Class IV Unable to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency present at rest. If any physical activity is undertaken, discomfort is increased.

Examination

weight and vital signs with assessment for orthostatic changes
Presence and degree of crackles, S₃ gallop, jugular venous pressure elevation, hepatic enlargement and tenderness, positive hepatojugular reflux, oedema and ascites

Investigations

Arterial blood gas: early indication of respiratory status (e.g. acidosis, failure)
Renal function, FBC
Glucose and urine analysis (point of care)
Cardiac Markers (troponin) only if clinically indicated
ECG: look for
Evidence of myocardial infarction or ischaemia
Arrhythmia
Left ventricular hypertrophy or other chamber enlargement (etiology)
Chest X-Ray
Echo: if trained in use, focussed emergency cardiac ultrasound can give valuable information about left ventricular function

Referral criteria

Although nitrates and ACE inhibitor (and furosemide if used) can be initiated within primary care, referral to secondary or tertiary care will be required to continue treatment. Observation is often required for an extended period of time within a high care setting. Transfer/ referral may be required to accommodate this if not locally available. Escalation of care to intubation will require intensive care referral.

Discharge criteria/checklist

No longer hypoxic on room air
Vital signs have returned to within normal parameters
Return to baseline effort tolerance
Cause of failure identified and appropriately addressed
Patient understanding of dietary sodium restriction checked
Patient understanding of medical regimen checked
Medication adjusted as required
Follow up arrangements made as required

Follow-up: elements to focus on in follow-up

Functional capacity and activity level
Changes in body weight
Patient understanding of and compliance with dietary sodium restriction
Patient understanding of and compliance with medical regimen
History of arrhythmia, syncope, presyncope, palpitation
Adherence and response to therapeutic interventions
The presence or absence of exacerbating factors for HF, including worsening ischemic heart disease, hypertension, and new or worsening valvular disease.

Treatment algorithm for acute decompensated heart failure

References

Rossiter D, Blockman M (eds.). South African Medicines Formulary. 11^th Ed. Cape Town: Health and Medical Publishing Group; 2014

Cameron P, Jelinek G, Kelly A, et al. Textbook of Adult Emergency Medicine. 4^th Ed. Elsevier; 2015

Acute Decompensated Heart Failure

Drugs mentioned