PubMed · 6671621
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R R Zimlichman, C Chaimovitz. 1983-11-01. [Hemodynamic changes in essential hypertension].. https://pubmed.ncbi.nlm.nih.gov/6671621/
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Cardiogenic shock (CS), defined as forward failure combined with systolic blood pressure < 90 mm Hg and reduced organ perfusion despite adequate volume loading, still has a grim prognosis with mortality rates of 80-100% if the causes are left untreated. The most frequent conditions underlying CS are acute myocardial infarction, acute and severe aortic or mitral incompetence, rapidly progressive dilatative cardiomyopathy and hypertrophic obstructive cardiomyopathy. Whereas correct conservative management by drugs and pacing may be life saving in the latter, the other conditions require early invasive management. Indications for cardiac surgery and circulatory assistance are given for mechanical complications leading to CS. In CS complicating myocardial infarction, comprehensive management with early invasive revascularization and intraaortic balloon pumping may result in improved survival compared with the disappointing outcome of medical treatment, including fibrinolysis. This strategy can be offered to the majority of infarct patients in CS, who are primarily admitted to hospitals not equipped for interventional cardiology or cardiac surgery. Between-hospital transfer of these patients for PTCA (or surgery) and advanced intensive care has been shown to be feasible and safe.
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The wide spectrum of pulmonary vascular disorders in liver disease and portal hypertension ranges from the hepatopulmonary syndrome characterized by intrapulmonary vascular dilatations, to pulmonary hypertension (portopulmonary hypertension), in which pulmonary vascular resistance is elevated. Since hepatopulmonary syndrome and portopulmonary hypertension have been reported in patients with nonhepatic portal hypertension, the common factor that determines their development must be portal hypertension. The clinical presentations are very different, with gas exchange impairment in the hepatopulmonary syndrome and haemodynamic failure in portopulmonary hypertension. The severity of hepatopulmonary syndrome seems to parallel the severity of liver failure, whereas no simple relationship has been identified between hepatic impairment and the severity of portopulmonary hypertension. Resolution of hepatopulmonary syndrome is common after liver transplantation, which has an uncertain effect in portopulmonary hypertension. The pathophysiology of both syndromes may involve vasoactive mediators and angiogenic factors.