Acute heart failure is a common emergency presentation with high mortality and morbidity. While clinical examination findings are not always sensitive or specific, prompt recognition and stabilization of the patient is a priority. Presentations can include shortness of breath, frothy sputum, collapse, or cardiac arrest. Investigations including ECG, cardiac enzymes, BNP, CXR, and echocardiogram help determine the cause and assess cardiac function. Initial stabilization involves propping the patient up, administering oxygen, diuretics, and monitoring vital signs to optimize hemodynamic status before further treatment.

1. Acute heart failure AIMS

2. Common emergency presentation High mortality & morbidity in survivors Diagnosis not always straightforward Classic examination findings not sensitive or specific Prompt recognition & stabilization of patient- priority

3. At 40 yrs age- lifetime risk: 21% Increasing prevalence In extremis + rapid deterioration Often respond very rapidly to treatment Very satisfying condition to treat Outlook poor despite initial clinical improvement

4. Presentations Acute SOB, frothy sputum Collapse Shock Cardiac arrest

5. Acute pulmonary oedema SPOTTER Extreme SOB, puffing, unable to speak Profuse sweating, cold clammy extremities Tachycardia irregularity BP fall ± Basal creps Rarely wheeze predominant !!! ( asthma)

6. Collapse/ cardiac arrest Severe HF of any cause:- prone for malignant arrythmias, PE  Present as collapse Very poor outcomes Survival to discharge ???

7. Aetiology CAD Hypertensive heart disease Fluid overload Acute valvular regurgitations Arrythmias Pulmonary embolism Acute hepatic venous thrombosis IWMI+RVMI Tamponade

8. CAD Most common cause Can be the 1 st manifestation SOB >>> chest pain RVMI common in the setting of IWMI LV > 40% infarct size

9. HHD 1 st presentation Accelerated hypertension Onset of HF lowers previously high BP Diastolic dysfunction is the basis Age

10. Pulmonary oedema Mechanisms pulm capillary pressure Capillary permeability Oncotic pressure

11. pulm capillary pressure LA pressure MV disease Arrythmias Aortic valve disease Ischemia cardiomyopathy LVEDP Accelerated HBP Pericardial constriction Fluid overload Reno-vascular disease High-output states Neurogenic IC bleed Cerebral oedema Post-ictal high altitude

12. Capillary permeability ARDS Oncotic pressure fall Loss:- NS, Cirrhosis Production:- cirrhosis, sepsis Dilution:- crystalloids

14. Investigations ECG Entirely normal # systolic HF ACS Arrythmias Serial ECG always essential

15. Cardiac enzymes Essential to r/o AMI even in the absence of chest pain !! Ideally tropT / trop-I : at presentation & 12 hrs later BNP :- very useful in r/o AMI in a breathless patient

16. CXR NEVER delay treatment pending CXR Portable CXR: cardiomegaly ?? Peri-hilar bat’s wing shadowing diagnostic Look for pericardial effusion, pneumothorax, consolidation

17. ECHO:- preferably as early as possible To identify cause Assess LV function, Diastolic dysfunction Cardiac tamponade

18. STABILIZATION

19. Actions in order Propped up position IV Morphine 100% Oxygen IV Lasix Monitor ECG Venous access Ensure optimal BP Emergency blood samples ABG SpO2

20. Assess respiratory function Wheeze: interstitial oedema Aminophylline helpful- bolus Indications for further support Exhaustion Persistent low paO2 < 8kPa Rising pCO2 Worsening acidosis

21. Hemodynamic status PCWP > 18 mmHg diagnostic BP < 100 > 100

22. Patient in shock Insert central line Renal dose Dopamine ( 2.5-5 µg/kg/mt) Urgent ECHO for any mechanical causes Increase Dopamine (but not > 10-20 )  raises pulm filling prssures Nor adrenaline preferred to high dose dopamine Once Bp restored add vasodilators

23. SBP >100 Further doses of IV lasix 60-80 mg q8h or even 20-80 mg/hr infusion NTG infusion at 2-10 mg/hr titrate to keep BP> 100 Vasodilators : ACEI

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