1965PubMedRequires access

TREATMENT OF SHOCK IN MAN BASED ON HEMODYNAMIC DIAGNOSIS.

MacLean Ld, Duff Jh, Scott Hm, Peretz Di

Open publisher page 104 citations

Abstract

This study assessed the hemodynamic abnormalities present in an unselected series of patients in shock. 20 patients were studied. The following types of hemodynamic abnormalities could be found: 1) cardiac deficit (cause of shock in 10 patients); 2) blood volume deficit (n=9); and 3) peripheral vascular failure (n=1). The finding that 10/20 patients had low cardiac output with a high central venous pressure or cardiac filling pressure was surprising. The hemodynamic cause of shock in these patients was only suspected clinically in 2/10 with myocardial infarction and corpulmonale respectively. In these patients further transfusions were not indicated since the central venous pressure was elevated to 10-15 cm. Response to cardiac output of isoproterenol was excellent with output of from .8-5.14 1/minute. Isoproterenol increased the cardiac output after vasoconstrictors such as metaraminol had increased blood pressure but had failed to increase cardiac output. Shock is a failure of blood flow not of blood pressure. Drugs which elevate blood pressure without increasing flow are not useful. In this study only 1 patient had a failure of resistance vessels as a cause of hypotension and since a failure of resistance vessels is the main reason for administering vasoconstrictor therapy this study does not support its use. Irreversible shock can be strongly suspected in patients who have a persistently elevated or rising arterial blood lactate level. There was no correlation between clinical diagnosis and hemodynamic abnormality. In bactermic shock for example 2 patients demonstrated a volume deficit; the other patient had a cardiac deficit. 1 probable reason for the high mortality rate of bacteremic endotoxic shock is the failure to identify the precise hemodynamic abnormality present. A useful maxim in treatment of most patients in shock is transfuse until either the blood pressure or central venous pressure rises; if the blood pressure returns to normal 1st a volume deficit probably exists. If the central venous pressure rises 1st a cardiac deficit predominates.

About this research paper

What this paper is about

This study assessed the hemodynamic abnormalities present in an unselected series of patients in shock. 20 patients were studied. The following types of hemodynamic abnormalities could be found: 1) cardiac deficit (cause of shock in 10 patients); 2) blood volume deficit (n=9); and 3) peripheral vascular failure (n=1). The finding that 10/20 patients had low cardiac output with a high central venous pressure or cardiac filling pressure was surprising. The hemodynamic cause of shock in these patients was only suspected clinically in 2/10 with myocardial infarction and corpulmonale respectively. In these patients further transfusions were not indicated since the central venous pressure was elevated to 10-15 cm. Response to cardiac output of isoproterenol was excellent with output of from .8-5.14 1/minute. Isoproterenol increased the cardiac output after vasoconstrictors such as metaraminol had increased blood pressure but had failed to increase cardiac output. Shock is a failure of blood flow not of blood pressure. Drugs which elevate blood pressure without increasing flow are not useful. In this study only 1 patient had a failure of resistance vessels as a cause of hypotension and since a failure of resistance vessels is the main reason for administering vasoconstrictor therapy this study does not support its use. Irreversible shock can be strongly suspected in patients who have a persistently elevated or rising arterial blood lactate level. There was no correlation between clinical diagnosis and hemodynamic abnormality. In bactermic shock for example 2 patients demonstrated a volume deficit; the other patient had a cardiac deficit. 1 probable reason for the high mortality rate of bacteremic endotoxic shock is the failure to identify the precise hemodynamic abnormality present. A useful maxim in treatment of most patients in shock is transfuse until either the blood pressure or central venous pressure rises; if the blood pressure returns to normal 1st a volume deficit probably exists. If the central venous pressure rises 1st a cardiac deficit predominates.

Why it matters

OpenAlex reports 104 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

This study assessed the hemodynamic abnormalities present in an unselected series of patients in shock. 20 patients were studied. The following types of hemodynamic abnormalities could be found: 1) cardiac deficit (cause of shock in 10 patients); 2) blood volume deficit (n=9); and 3) peripheral vascular failure (n=1). The finding that 10/20 patients had low cardiac output with a high central venous pressure or cardiac filling pressure was surprising. The hemodynamic cause of shock in these patients was only suspected clinically in 2/10 with myocardial infarction and corpulmonale respectively. In these patients further transfusions were not indicated since the central venous pressure was elevated to 10-15 cm. Response to cardiac output of isoproterenol was excellent with output of from .8-5.14 1/minute. Isoproterenol increased the cardiac output after vasoconstrictors such as metaraminol had increased blood pressure but had failed to increase cardiac output. Shock is a failure of blood flow not of blood pressure. Drugs which elevate blood pressure without increasing flow are not useful. In this study only 1 patient had a failure of resistance vessels as a cause of hypotension and since a failure of resistance vessels is the main reason for administering vasoconstrictor therapy this study does not support its use. Irreversible shock can be strongly suspected in patients who have a persistently elevated or rising arterial blood lactate level. There was no correlation between clinical diagnosis and hemodynamic abnormality. In bactermic shock for example 2 patients demonstrated a volume deficit; the other patient had a cardiac deficit. 1 probable reason for the high mortality rate of bacteremic endotoxic shock is the failure to identify the precise hemodynamic abnormality present. A useful maxim in treatment of most patients in shock is transfuse until either the blood pressure or central venous pressure rises; if the blood pressure returns to normal 1st a volume deficit probably exists. If the central venous pressure rises 1st a cardiac deficit predominates.

Key concepts: Medicine, Hemodynamics, Shock (circulatory), Cardiac output, Central venous pressure, Cardiogenic shock, Cardiology, Blood pressure

Related papers

Back to paper searchBrowse research topicsOriginal source
TREATMENT OF SHOCK IN MAN BASED ON HEMODYNAMIC DIAGNOSIS. — Research Paper | ScholarLens