AHF Triggers
there are many triggers for AHF, which if recognized and treated with help improve outcomes
- Cardiac: ACS, Arrhythmia, Aortic Dissection, Acute Valve Incompetence, VSD, Malignant Hypertension
- Respiratory: PE, COPD
- Infection: Pneumonia, Sepsis, Infective endocarditis
- Toxins/Drugs: Alcohol, Recreational drugs, NSAIDs, Steroids, Cardiotoxic meds
- Increased Sympathetic Drive: Stress
- Metabolic: DKA, Thyroid dysfunction, Pregnancy, Adrenal Dysfunction
- Cerebrovascular Insult
Presentation & Clinical Classification
The presentation of AHF can vary but tends to fall in to the following 4 categories, which can be determined clinically and can help guide your approach to treatment; warm-dry, warm-wet, cold-dry, cold-wet.
It is worth noting that the vast majority of patients will be norm-hypertensive. However, 5-8% are Hypertensive this confers a very poor prognosis.
Investigations
- ECG: Rarely normal (High NPV), and may identify underlying cause
- CXR: Pulmonary congestion, Effusion, Cardiomegaly (20% will have an almost “Normal” CXR)
- BNP: Can be helpful (we have it)
- >845 show increased mortality
- <100 AHF is unlikely
- BNP is not a specific test and will elevate for many reasons
- POCUS: This can be very useful in identifying cases but training is required [Bilat B lines in 2 zones each side]
- Condition specific tests: Try to identify the underlying trigger dependent on history and exam (e.g. ABG, Trop, U&E, TFT, LFT, CTPA)
- ECHO: this is important but not necessary in the ED phase (unless the patient has haemodynamic instability i.e. cardiogenic shock)
Treatment – Time Matters!!!
- Mortality increased by 1%/hour IV treatment not started
- Treatment after 12hrs from onset makes little difference
Treat The Cause!: If you can identify the trigger treat it it will in turn improve the AHF. (e.g. AMI, Arrythmia(Tachy/Brady), Massive PE)
- Vasodilator: has 2 effects reducing vascular resistance and thus increasing stroke volume [NOT to be used if sBP<90mmHg]
- Diuretic: commonly we use frurosemide 20-40mg IV, however, depending on the patient higher doses can be used. [Doses over 160mg has been shown to increase mortality!]
- Oxygen: maintain SaO2 of 95% OR 88-92% if at risk of hypercapnic coma [Avoid hyperoxia]
- NIV: recommended in respiratory distress (RR >25bpm, SpO2 <90%) & start ASAP, this can reduce intubations and make the patient feel more comfortable. However, doesn’t increase survival NIV Guide-HERE
- SHOCK!!!: there is no agreement on the best treatment, ICU & Medical/Cardiology input is vital, as inotropes & vasporessors (Noradrenaline recommended) will need to be considered.
ESC Guide – 2016 Heart Failure
