This condition is caused by a failure of the left ventricle to contract forcefully enough (often as the result of damage caused by an infarct or prolonged high blood pressure). As a result, the left ventricle is unable to pump blood efficiently. This in turn leads to a build up of back-pressure into the left atria and the lungs. This pressure forces fluid out of the capillaries and into the lungs, resulting in an accumulation of fluid in the lungs, in effect the patient is drowning.
The key to the pathophysiology of acute cardiogenic pulmonary oedema is the patient history, which will typically include acute coronary syndrome and/or myocardial infarction.
With ischaemia to the anterior, lateral and in this case, also the septal region of the heart, this makes up a large area of infarct to the left ventricle. Without perfusion and the electrical activity and muscular contractility required to pump blood from the left ventricle, cardiac output is greatly reduced.
This drop in output is noticed by the aortic arch baroreceptors, which will stimulate a sympathetic tachycardia in response, as well as in the glomerulus, which, as we’ve covered in another case study, which will kick off the renin-angiotensin-aldosterone system and attempt to compensate by increasing blood volume.
With the extra fluid as well as sympathetic vasoconstriction and tachycardia attempting to correct the cardiac output, the left ventricular issue still exists, so the inability to pump effectively means that a back-flow of blood builds up into the pulmonary circuit, often rapidly.
If you imagine that cardiac output for a normal healthy male is approximately 70mls per beat, at a normal heart rate (without tachycardia) of around 60 beats per minute this is approximately 4.2 litres per minute.
The normal healthy male lungs can hold around 4-6 litres of fluid, so you can see that it wouldn’t take long for a large infarct resulting in pump restriction or pump failure to fill up the pulmonary circuit.
All of this blood filling up the lungs increases hydrostatic pressure, which naturally forces the fluid into the alveoli.
With each air pocket full of fluid, a V/Q mismatch occurs (remember our ventilation/perfusion mismatch because there’s great perfusion to the area, but no ventilation or minimal ventilation occurring) and gas exchange can’t take place.
Accumulated blood in the pulmonary circulation causes increased hydrostatic pressure that forces fluid into the alveoli of the lungs. The fluid filled alveoli are unable to effectively undertake gas exchange creating a V/Q mismatch (low V/Q ratio). This manifests in the classic symptoms of shortness of breath, crackles on auscultation, hypertension, orthopnoea and pink frothy sputum.
St John WA