Heart Failure
So heart failure is a term used to describe the chronic condition of pump failure. This maybe related to a myocardial damage (in either a systolic or diastolic dysfunction), valvular pathology, arrhythmia or through toxic effects (ie Acidosis) limiting myocyte function.
Patients presenting to A+E with acute heart failure are often a decompensation of their known heart failure with a precipitant (ie MI, arrhythmia) or maybe a new presentation of Heart Failure.
How do these patient present?
So the easiest way to think about these patients is are they perfusing or are they shocked and are they congested or are they dry?
This gives you 4 types of heart failure patients – cold and wet, cold and dry. Warm and wet, warm and dry.
The easiest to recognize is the wet patients as they present more classically, fortunately they are the more common and the easier to treat.
Pulmonary oedema is the reason these patients are wet and it’s the source of their signs and symptoms – orthopnoea, PND, pink frothy sputum.
Lets talk about the Physiology behind it.
Like we said, fundamentally Heart Failure is the pump not working properly. So lets start there.
- If the LV doesn’t empty properly there is a gradual rise in end diastolic volume and as such pressure.
- Given the pulmonary system, particular the pulmonary veins, are a low pressure system this can lead to increased hydrostatic pressure and so you have transudate into the interstitium and then the alveoli. This is usually balanced with the lymphatic drainage but once this balance is tipped you end up with accumulating fluid, increasing diffusion distances and reducing the surface area for gas exchange – causing hypoxia
- Hypoxia in the lung causes vasoconstriction and a hypoxic state causes catecholamine release causing systemic vasoconstriction.
o The increased systemic vascular resistance puts increasing strain on the LV and the pulmonary vasoconstriction puts more strain on the RV.
- In addition to the vasoconstriction the catecholeamine release also causes activation of the renin-angiotensin-aldosterone system increases water and sodium retention.
o This leads to further demand on the LV and RV as well as increasing O2 demand and creates a cycle that leads to respiratory and circulatory collapse.
Clinical Assessment
There is a spectrum of patients that attend A+E with heart failure and there is no single test that will give us a diagnosis. The clinical picture is our best bet and so we need a good history and a thorough examination.
On one end is the heart failure patient who has a gradual deterioration and now is left a little too breathless and possibly a little hypoxic and so cant manage at home. At the other end of the spectrum is the acute decompensation presenting with cardiogenic pulmonary oedema. This patients typically come in early in the morning – it’s the 4-6 am resus call usually.
In our clinical assessment we want to look for the onset of symptoms, the clinical picture (ie wet or dry and hot or cold) and we want to establish any precipitants (MI). Often these patients are co-morbid and pulmonary oedema can be challenging to distinguish with COPD or asthma.
In typical situations – the pulmonary oedema signs are typically bilateral and more pronounced at the bases.
However, depending on the type of heart failure they are presenting with the other features maybe varied – cold (poorly perfused) patients are likely to be hypotensive or normotensive with poor flow, warm patients (well perfused) are likely to be hypertensive.
Investigations
When it comes to investigating these patients there is no one test that will help that we can easily get in A+E.
The best test to confirm heart failure is an echo, however this will not help you differentiate whether that wheeze and SOB is pulmonary oedema or COPD, it will only tell you that the heart doesn’t work well.
BNPs are sensitive but not specific – they make a useful rule out tool if you have the hours to wait for it come back but only if it comes back conclusively (<100 in BNP and <300 in proN BNP)
Likewise a CXR, the signs of pulmonary oedema with effusions, bat wings, upper lobe diversion and cardiomegaly maybe present but there absence doesn’t mean that its not heart failure. It is helpful to look for other parts of the differential ie Pneumothorax or Pneumonia.
The most useful features are an ECG – most patients will with heart failure will have a non specifically abnormal ECG and it will also potentially show any precipitant arrhythmia or MI – and lung US to demonstrate signs of oedema. As with all US it is more user and patient dependent then most of the testing we have available in A+E. LITFL, as always has a helper on B-lines
Management
So our guiding principles of all management and resus doesn’t change with heart failure – we want to restore normal physiology as well we can to facilitate oxygen delivery to the tissues.
Initial simple management can go a long way – sit the patient up, put on O2.
Just the application of O2 can reverse some of the catecholeamine release and vasoconstriction and can go a long way to improve the patient.
The application of PEEP in hypoxic patients who aren’t too hypotensive will also help – the increase in intrathoracic pressure provided by PEEP will reduce both the preload and afterload, taking some of the work off the heart. It will also help in recruiting lung, easing the work of breathing and reversing any shunt in the lung.
Loop diuretics are commonly used – the initial effect of furosemide is venodilation reducing preload and then the inhibition of Na reabsorption in the Loop of Henle creates a diuretic effect, reversing the consequences of RAAS activation. The suggested dosing of furosemide is 20-40mg IV initially, however, given the vasoconstricted state of most patients with heart failure and pulmonary oedema, it may take over an hour to have a diuretic effect due to poor renal perfusion. The initial benefit seen is usually from vasodilation.
Vasodilation can also be achieved by using nitrates and historically nitroprusside. At low doses GTN causes venous dilation and at higher doses it causes arterial vasodilation. In the hyper/normotensive heart failure patient they can have significant role in improving cardiac function by reducing afterload and preload. In extremis a GTN spray can be administered whilst other treatments are being established but the usual practice is to use an infusion (10-20micrograms/min, increasing every 3-5mins to a max of 200mcg/min). Remembering that there can be a lag in its effect when at low infusion rates due to the dead space of the cannula (ie 1-2mm maybe in the cannula before it enters the body to have a physiological effect)
Inotropes. In the hypotensive and dry patients a small fluid bolus can be helpful as they likely have a very low preload, however in the wet patients the only real option when they are hypotensive is inotropes. Dobutamine is the first choice inotrope, however they are very much a last resort as they are associated with higher mortality and logically are limited in heart failure patients as they ask a failing heart to beat harder and fast with increased O2 demand. The place where they have a role maybe around MI and PCI or post ROSC where myocardial stunning and resolution of the initial insult has occurred.
Opiates have been shown to cause harm in acute heart failure and should only be used when also treating a precipitant primary myocardial infarction.