PHYSICAL EXAMINATION

LABORATORY STUDIES

DIAGNOSIS

Hemorrhagic shock

COURSE

The patient was infused with 2 L of typed and crossmatched blood. This restored the blood pressure toward normal, and pulse and respiratory rates declined. Mixed venous blood gas values returned toward normal. The patient was transferred to surgery for repair of the damaged artery.

PATHOPHYSIOLOGY OF KEY SYMPTOMS

Arterial blood pressure is the regulated variable in the cardiovascular system. Arterial pressure results from the accumulation of blood in the aorta and large arteries. Consequently, arterial blood pressure represents a balance between the volume entering the aorta (cardiac output of the left ventricle) and the volume leaving the artery and flowing into the capillaries (determined by total peripheral resistance).

Cardiac output is determined by the pumping ability of the heart and is limited by the venous return. Pumping ability of the heart is a function of heart rate and stroke volume, and stroke volume is a function of the ventricular preload and the cardiac contractility. Venous return ultimately limits cardiac output because as cardiac output exceeds venous return the preload on the ventricle falls, resulting in a reduced cardiac output. The heart cannot pump more blood than the volume that flows into it from the vena cava.

Arterial blood pressure is sensed by the stretch receptors of the aortic arch and the carotid sinus, collectively called arterial baroreceptors. A drop in arterial blood pressure unloads the baroreceptors and causes a sympathetic activation and a parasympathetic inhibition (Fig. 7-1). Sympathetic activation causes increases in heart rate, ventricular contractility, and total peripheral resistance and a decrease in venous capacitance (Table 7-1). These changes cause an increase in cardiac output and a reduction in the volume of blood exiting the arteries. Consequently, arterial pressure recovers toward normal.

FIGURE 7–1 Activation of the baroreceptors at different levels of arterial pressure. I, change in carotid sinus nerve impulses per second; P, change in arterial blood pressure in millimeters of mercury.

TABLE 7–1 Autonomic Effects on Various Organs of the Body

The initial event in this patient was the loss of circulating blood volume. Estimated blood volume for this individual is 5 L, which accounts for 8% of body weight. Blood loss caused a drop in venous volume and venous pressure and, consequently, a fall in cardiac preload (see Fig. II-2, p. 21). The fall in preload causes a drop in cardiac output and, therefore, a drop in arterial blood pressure (Fig. 7-2).

FIGURE 7–2 Basic renal body fluid feedback mechanism for control of blood volume, extracellular fluid volume, and arterial pressure. Solid lines indicate positive effects, and dashed lines indicate negative effects.