Hypovomemic Shock




A patient is brought into the emergency room following a leg laceration. Blood loss is estimated at 1000ml.
Discuss the (cardiovascular) physiological response to this injury.

The body acts to defend itself from hypovolemia by way of a series of reflex mechanisms involving the cardiovascular and neurohormonal systems. The reflex compensatory responses occur in the macrocirculation, in the kidney and in the microcirculation.

Macrovascular compensation:

The initial loss of volume leads to a reduction in venous return and consequent reduction in end diastolic volume. Cardiac output is determined by heart rate times stroke volume. Stroke volume relates to end diastolic volume on the Starling curve ( the patent moves from point a to point b:

The result is a decrease in cardiac output.

Reduced cardiac output leads to reduced stretching of the baroreceptors in the aortic arch and the carotid sinus. This leads to increased inhibition of the cardioinhibitory centre, reducing parasympathetic output, and increased sympathetic activity from the vasomotor centre. The result is increased vasoconstriction and venoconstriction, increased heart rate and contractility and consequently increased cardiac output. Blood is shunted from capacitance vessels to arteries, and fluid is sequestered from the extravascular space to the intravascular space. This process is known as autotransfusion. Blood is preferably shunted to essential organs such as the brain, the heart and the kidneys, which are further protected by autoregulatory reflexes.

Reduced renal blood flow is sensed by the mesangial cells of the juxtaglomerular apparatus, leading to increased production of renin. Renin accelerates the production of angiotensin II which causes vasoconstriction (by increasing intracellular Ca2+ ions), enhances SNS activity, and facilitates the  release of aldosterone from the adrenal cortex, which increases the reabsorption of salt and water. This effect is enhanced by the production of Antidiuretic Hormone (vasopressin), which is stimulated by the osmoreceptors in the hypothalmus, and by trauma and angiotensin II. ADH is a potent vasoconstrictor and also facilitates the reabsorption of water from the collecting ducts of nephrons.

This state is known as compensated shock.

In a 70kg patient, approximately 20% of blood volume will have been lost. The clinical signs of shock are often subtle: blood pressure may be normal, the is a tachycardia, cold and clammy peripheries, decreased capillary refill and a widened core to peripheral temperature gradient.

When 20 40 % of circulating volume has been lost (1000 2000ml), the blood pressure begins to fall, there is profound peripheral vasoconstriction and tachycardia. When greater than 40% of circulating volume has been lost (>2000ml), blood pressure may become unrecordable and there are signs of end organ failure: oliguria and confusion. The urinary output is probably the most reliable way of estimating circulating volume.

Microvascular compensation:

In hypovolemia, extracellular and interstitial fluid is mobilized into the bloodstream as a form of auto-transfusion. The microcirculation shuts down (vasoconstriction mediated by epinephrine, vasopressin an angiotensin II), and the patient feels cold and clammy. The reduced girth of smaller blood vessels increases velocity of flow and this has the effect of sucking fluid from the extracellular space into the bloodstream.




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