Learn more about the effects of hypertensive emergencies.
Heart
Chronic hypertension activates the renin-angiotensin-aldosterone system resulting in systemic vasoconstriction and increased systemic vascular resistance. This in turn leads to left ventricular hypertrophy and reduced diastolic myocardial coronary perfusion. Further critical rises in BP, occurring in the context of a hypertensive emergency, will result in myocardial ischaemia and/or the left ventricle failing to overcome systemic vascular resistance with resultant pulmonary oedema.
Brain
Normal cerebral autoregulation results in constant cerebral blood flow in the presence of a fluctuating systemic BP. This process, however, has limits and if these are exceeded cerebral endovascular damage occurs, leading to cerebral oedema and microhaemorrhage. The clinical manifestation of autoregulatory breakdown and cerebral vascular damage is hypertensive encephalopathy which, untreated, leads to further macroscopic cerebral haemorrhage and death.
Kidneys
Chronic hypertension also results in impaired renal autoregulation as a consequence of pathological changes within renal arteries. Similar to the brain, when autoregulation fails in the kidney, it is no longer protected from critical changes in systemic BP resulting in:
Uterus
The uterine pathology associated with the hypertensive emergency eclampsia is similar to that seen in the kidney, brain and heart. Fibrinoid necrosis, platelet aggregation and thrombus formation occurs within the spiral and basal arteries which supply the placental intervillous space and the uterine decidua. This leads to reduction in placental blood flow and placental infarction and failure.