case review: GTN in acute heart failure and pulmonary oedema

what?

90yof, sudden onset acute dyspnoea at 0200, worsening through the night; on a background of 2 days mild dyspnoea, coughing up 'yellow' sputum. Only medical history is hypertension.

on arrival:
found in bed, pale and diaphoretic, panting. Venous distention observed on upper chest/neck.

on examination:
A: clear self maintained
B: Tachypnoeic, oxygen saturations initially unreadable due to low PI%, eventually captured 86% on room air. On auscultation, bilateral crackles -- like crunching snow
C: tachycardic at 116, deteriorating to 135 on route to A&E. Hypertensive aound 176 systolic, dubious(due to road chatter) auto sphygmomanometer readings of ~140 systolic. 12 lead ECG shows atrial fibrillation with rapid ventricular response + left bundle branch block.
D: GCS 15. Normoglycaemic.
E: Apyrexic. Denies any pain. Bilateral peripheral pitting oedema.\

treatment
Oxygen delivered via nonrebreather mask at 15 litres per minute. Attempted to titrate down to 4LPM via nasal cannula but only held saturations of 89%.

Impression: Acute heart failure. Unable to conclusively rule out sepsis or PE. Pre alerted and transported emergently to ED.

GTN was considered by crew, but had confusion around the definition of 'uncontrolled hypertension' as opposed to hypertension, and it was withheld.

On arrival, patient was catheterised, given GTN, and started on digoxin and IV furosemide.

so what?

Glyceryl Trinitrate(GTN) is a nitrate medication, most commonly found in sublingual spray presentation. Its primary indication is the treatment of suspected or confirmed cardiac chest pain¹. UK guidelines also provide an indication for acute heart failure with 'ischemia' or 'uncontrolled hypertension'.

Its primary action is vasodilation. In angina, this counteracts coronary vasospasm, relieving chest pain. It also reduces left ventricular volume, resulting in lower myocardial demand². This is theorised to improve mortality in the event of myocardial ischaemia e.g. infarction.

This leads into its usage in acute heart failure. The theory goes that by inducing hypotension and vasodilation, GTN can reduce preload, ameliorating pulmonary oedema. However, this appears to be a point of contention, with sources like the JRCALC guidelines NICE³ disagreeing. NICE states very simply that nitrates should not be offered 'routinely' to patients with acute heart failure. JRCALC says that while there is theoretical benefit and evident symptomatic relief, there is no 'robust' evidence confirming these effects. One could argue that inducing hypotension in a decompensating patient is the opposite of beneficial, and as such it is heavily cautioned.

now what?

After closer inspection of the JRCALC guidelines, GTN administration in acute heart failure is largely supported in a patient with a systolic blood pressure over 140mmHg. However, the current body of evidence does not conclusively offer benefits nor risks. The question then arises -- should it be given in heart failure at all?

The bigger picture is that patients in acute heart failure need CPAP, diuretics, and possibly beta blockade or even PCI. GTN is unlikely to make a big difference. The most important thing a prehospital clinician without access to IV furosemide or CPAP can do is recognise pulmonary oedema early and undertake time-critical conveyance to the nearest appropriate hospital.