The third presentation in my ACEM Fellowship Summary series. Focuses on the aetiology, diagnosis and management of acute heart failure in its many forms.

1. Acute Heart Failure
Dr Andrew Crofton

2. Introduction
 Poor prognosis with 50% mortality at 5 years
 Hospitalisation marks higher mortality than matched non-hospitalised patients
 Pathophysiology
 Definition: A complex clinical syndrome that results from any structural or
functional impairment of ventricular filling or ejection of blood
 Upregulation of neurohormonal systems to maintain perfusion ultimately increase
myocardial workload, wall tension and myocardial oxygen demand
 Natriuretic peptides (ANP, BNP and CNP) are the counter-regulatory response to the
neurohormonal system activation
 Vicious circle in APO results from rising blood pressure, reduced cardiac output and
further increased systemic vascular resistance, repeatedly

3. Classification
 Phenotypes
 Hypertensive AHF: Relatively preserved LV fx, SBP >140, APO and
<48hrs duration
 Control BP first as may be more fluid shift than overload
 Pulmonary oedema: Respiratory distress, desaturation and CXR
 Early BiPAP/CPAP to avoid intubation
 Cardiogenic shock: SBP <90 with tissue hypoperfusion
 Consider structural or ischaemic cause. Often benefit from
vasopressors and invasive haemodynamic monitoring

4. Classification
 Phenotypes
 Acute on chronic HF: Typical onset over days with peripheral
oedema and not meeting above criteria
 High-output failure: High CO, tachycardic, warm extremities and
pulmonary congestion
 E.g. anaemia or thyrotoxicosis
 Right heart failure: Raised JVP, hepatomegaly, peripheral oedema
and may have hypotension
 Pulmonary disease, valvular disease (TR) or OSA
 Treatment rests with treatment of underlying disorder, often without
volume removal as low-output state may co-exist

5. Causes
 Myocardial ischaemia: Acute or
chronic
 Systemic hypertension
 Cardiac dysrhythmias (esp. AF with
RVR)
 Valvular dysfunction
 AS, AR (consider IE or dissection)
 MS, MR (consider papillary muscle
rupture, ruptured chordae
tendinae, IE)
 Prosthetic valve dysfunction
 Cardiomyopathy
 HOCM
 Dilated
 Restrictive
 Alcohol, cocaine, thyrotoxicosis,
myxoedema
 Myocarditis: Radiation or infection
 Constrictive pericarditis
 Cardiac tamponade
 Anaemia

6. Systolic vs. diastolic failure
 Systolic = LVEF <50%
 Results in afterload sensitivity
 With circulatory stress e.g. walking, failure to improve contractility with rising
venous return results in increased cardiac pressures, pulmonary congestion and
oedema
 Diastolic dysfunction (aka HF with preserved EF)
 Impaired ventricular relaxation
 Reduced LV compliance necessitates higher atrial pressures to ensure adequate
filling, creating preload sensitivity
 Common in chronic hypertension with LV hypertrophy
 Coronary artery disease also contributes as diastolic dysfunction is seen early in
cardiac ischaemia

7. Diagnosis
 There is no singular historical or physical exam finding
that achieves sensitivity and specificity >70%
 Initial global clinical assessment has sensitivity of 61% and
specificity of 86%
 Hx of heart failure has sensitivity of 60% and specificity of
90% (+LR 5.8)
 Symptom with highest sensitivity is dyspnoea on exertion
(84%)

8. Diagnosis
 Most specific symptoms are PND, orthopnoea and oedema
(76-84%)
 Orthopnoea is a late symptom due to redistribution of
splanchnic/limb fluid into central circulation. Nocturnal cough is a
frequent manifestation and often overlooked (Harrison’s)
 PND often occurs 1-3 hours after retiring to bed and is not rapidly
relieved by sitting up (unlike orthopnoea)
 Cheyne-Stokes respiration occurs with periodic apnoea/dyspnoea
due to impaired sensitivity to reduced PaO2 and subsequent
dyspnoea as PaCO2 rises

9. Diagnosis
 Historical precipitating factors
 Non-adherence to salt/fluid restriction or medication
 Renal failure (esp. missed dialysis)
 Substance abuse e.g. meth, cocaine, ethanol
 Poorly controlled HTN
 Iatrogenic e.g. recent negative inotrope change,
NSAID/steroid initiation, inappropriate therapy
reduction, new antiarrhythmics

10. Diagnosis
 Examination
 S3 has higher LR+ for acute heart failure (LR+ 11)
 Absence does not rule out acute heart failure however
 Abdominojugular reflex +LR 6.4
 Raised JVP + LR 5.1
 Clinical judgement and a single BNP have similar accuracy
 Pulmonary crackles may be absent in chronic HF due to increased lymphatic
drainage from alveoli
 Pleural effusions tend to be bilateral and are more common in biventricular failure
(if unilateral, more often right sided)

11. Diagnosis
 CXR
 Up to 20% of patients have CXR without classic signs on first presentation to ED
(particularly in late-stage heart failure)
 Classical
 Kerley B lines
 Pleural effusions
 Upper lobe diversion
 C:T ratio >0.5
 ECG
 May reveal underlying cause or precipitant
 New AF has higher +LR for heart failure

12. Diagnosis
 Biomarkers
 BNP may add value in the undifferentiated dyspnoeic patient in
the ED
 May elevate later in flash APO
 Marked rise is associated with worse short-term outcomes
 BNP <100 makes HF unlikely (sensitivity 90%)
 BNP >500 akes HF likely (specificity 90%)

13. Diagnosis
 POCUS
 1) Is pulmonary congestion evident?
 Sonographic B lines: >2 in any one sonographic window along anterior and anterolateral
chest is highly specific
 2) Is elevated CVP evident?
 IVC >2cm and <50% collapsible
 Look for RV strain also to ensure no evidence for PE or clinically significant TR as
alternative diagnosis
 3) What is the LVEF?
 Visual estimation into normal, moderately reduced and severely reduced

14. Treatment
 Airway and breathing take precedence
 NIV reduces intubation rates and improves respiratory distress and metabolic
disturbance compared to standard therapy alone
 Unclear if reduces hospital mortality
 I&V if necessary
 Hypotensive HF
 Seen in 3% of cases
 Consider ischaemia and reperfusion therapy
 Early inotropes and invasive monitoring indicated

15. Treatment
 Hypertensive AHF
 Prompt recognition (SBP >150) and afterload reduction with vasodilators
 Nitroglycerin
 Reduces MAP by reducing preload, and afterload at high doses
 May have coronary vasodilatory effects, reducing myocardial ischaemia and improving
cardiac function
 400mcg S/L at one per minute until relief or IV infusion started
 IV 5-10mcg/min titrated up to 200mcg/min based on BP and symptoms
 Start high and titrate down rapidly as very short half-life (2 min)
 If hypotension <90 ensues and persists with cessation, consider volume depletion or RV
infarct and treat with N/S boluses
 Risk of methaemaglobinaemia if prolonged use

16. Treatment
 Hypertensive HF
 Nitroprusside
 Second-line if persistent symptoms and HTN despite GTN 200mcg/min
 More potent arterial vasodilator
 0.3mcg/kg/min titrated up every 5-10 minutes to 10mcg/kg/min
 Risk of thiocyanate toxicity if prolonged, high-dose or renal/liver failure
 End-point is control of LV filling pressures to prevent intubation
 Loop diuretics
 If continued symptoms despite BP control
 Frusemide alone without vasodilators INCREASES mortality and worsen renal function

17. Treatment
 Hypertensive HF
 Contraindications to vasodilators
 If signs of hypoperfusion/SBP< 90
 Flow-limiting, preload-dependent states such as RV infarct, aortic
stenosis, HOCM or volume depletion increase the risk
 Therapy in these situations is aimed at decreasing the outflow
gradient by slowing the heart rate and cardiac contractility with IV
beta-blockers in ICU setting
 If co-existent shock in HOCM, phenylephrine or noradrenaline are
preferred to raise systemic BP without increasing cardiac contractility

18. Treatment
 Normotensive heart failure
 Diuresis first with further treatment based on response to therapy
 Loop diuretics provide rapid symptom relief of congestive symptoms and improved effects of ACEi by
reducing intravascular volume
 IV dosing preferred (most pt’s will have bowel wall oedema limiting absorption of oral preparations)
 Effective within 10-15 minutes
 Frusemide 20-40mg IV push
 If prior use, give 1-2.5x previous total daily dose, divided in half and given q12h
 Bumetanide 1-3mg IV (1mg = 40mg frusemide)
 Torsemide 10-20mg IV (20mg = 40mg frusemide)
 DOSE trial
 Higher doses produce more rapid response with slight decrease in renal function
 Adverse effects include hypocalcaemia, hypokalaemia, hypomagnesaemia, ototoxicity (if used with
aminoglycoside)
 If symptoms worsen or fail to improve, double dose and repeat in 30-60 minutes

19. Treatment
 Normotensive HF
 Ultrafiltration
 No benefit seen over bolus diuretic therapy
 Consider if all medical strategies not effective in obvious volume overload
 Morphine
 Relieves congestion and anxiety BUT is associated with need for mechanical ventilation, prolonged
hospitalisation, ICU admission and mortality
 If desired for venodilation or pain control, 2-4mg IV boluses with close monitoring is an option
 This trial only used morphine in severe cases so probably biased but definitely has a secondary role to
loop diuretics and nitrates
 Nesiritide
 Vasodilator (recombinant BNP) with no significant effect on hospitalisation or mortality (ASCEND-HF trial)
 Increased risk of hypotension
 Optional if nitrates ineffective or contraindicated

20. Treatment
 Normotensive HF
 ACEi and ARB’s
 Not utilised in the ED for acute management but indicated for chronic heart failure with reduced EF
 Beta-blockers
 Reduce mortality in chronic heart failure but generally witheld in acute heart failure due to risk of
deterioration
 May have a place in management of rate-related failure but very dangerous
 Drugs to avoid
 CCB
 Myocardial depressant activity (like beta-blockers)
 Trials show no benefit and worse outcomes
 NSAID’s
 Risk of sodium and water retention, blunt the effect of diuretics +- renal impairment and may increase
morbidity and mortality

21. Treatment
 Anticoagulation
 1.3-2.4% annual risk of stroke in HF
 Warfarin indicated if HF and AF or HF with history of systemic or pulmonary emboli
 If documented LV thrombus, need 3 months of therapy
 Aspirin is recommended for HF patients with IHD to prevent MI and death
 ICD
 Prophylactic use in NYHA II-III reduces sudden cardiac death
 Should be considered for these patients with EF <30-35% who are already on
optimal background therapy
 May be combined with biventricular pacemaker (CRT)

22. Treatment
 Cardiac resynchronisation therapy
 1/3 of patients with depressed EF and symptomatic HF have QRS >120ms
 Mechanical consequences of inter- or intraventricular conduction disturbance
include suboptimal ventricular filling, reduced LV contractility, prolonged duration
of MR and paradoxical septal wall motion
 CRT reduces severity of MR, mortality, hospitalisation, reversal of LV remodelling
and improved QoL and exercise capacity
 Indicated for patients in sinus rhythm with EF <35% and QRS >120ms and those who
remain symptomatic (NYHA III-IV) despite optimal medical therapy

23. Disposition
 Need to consider clinical gestalt, physiological risk profile and barriers to self-
care/support
 Caregiver support, hospitalisation history, symptom monitoring, education, access
to medical care, disease knowledge, medication adherence all come into
consideration
 Is ED SSU an option?
 Studies have shown this can be safely done if no high-risk markers
 Can monitor for complete symptom resolution within 12-24 hours (typical), can
have BP/UO/weight/HR monitoring, any further diagnostic testing organised (labs,
echo) and can perform heart failure education, confirm outpatient appointments
and arrange follow-up

24. Disposition
 Exclusion criteria for SSW/Discharge
 Positive troponin
 BUN >40mg/dL
 Creatinine >3mg/dL
 Sodium <135
 New ischaemic changes
 New onset acute HF
 IV vasoactive infusions being titrated
 Significant cormorbidities requiring acute interventions
 RR >32 or NIV
 Signs of poor perfusion
 Poor social support and/or follow-up

25. Disposition
 High-risk markers (seen in 50%)
 Renal dysfunction
 Low BP
 Low serum sodium
 Elevated BNP
 Elevated troponin
 Studies have shown 75% of patients will respond to therapy, will have no
identifiable high-risk features and can be discharged home
 Rates of re-admission are similar to or better than those that are admitted
 Outpatient follow-up within 5 days reduces re-admission rates
 If inadequate response to initial therapy, high-risk fratures need admission

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