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1. How can cardiac output, stroke volume and systemic vascular resistance be used to calculate arterial blood pressure?
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Tissue perfusion requires an adequate blood pressure, which is dependent upon the systemic vascular resistance and cardiac output; the cardiac output is a function of the heart rate and the stroke volume. These may be expressed in mathematical terms: CO = HR x SV and BP = CO x SVR, where CO is cardiac output, SV is stroke volume, HR is heart rate, BP is arterial blood pressure and SVR is systemic vascular resistance.
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2. What is Starling's law?
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The cardiac output depends on the degree of stretch of the heart muscle in diastole.
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3. Where are the receptors which monitor blood pressure?
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In the carotid sinus and the aortic arch.
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4. What determines stroke volume?
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Venous return. Increasing venous return causes an increase in stroke volume.
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5. In general, what is the cause of shock?
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Inadequate perfusion (shock) may result from factors related to the pump (the heart) and factors relating to the systemic circulation.
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6. What are the causes of cardiogenic shock?
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Massive myocardial infarction; acute ventriculoseptal defect; pulmonary embolus; mitral or aortic valve rupture; acute cardiac tamponade.
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7. What are the principal causes of reduction in systemic vascular resistance to cause a ‘hot shock’?
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Spinal shock; anaphylaxis; sepsis.
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8. What might confuse the clinical picture of shock?
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Pre-existing medical conditions and medications may confuse the clinical picture. Consider a patient with hypertension taking a β-blocker such as atenolol. For that patient a systolic blood pressure of 110 mmHg may be very low, and the atenolol prevents a compensatory tachycardia in response.
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9. What are the causes of adrenocortical shock? How is it treated?
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Loss of the hormones produced by the cortex of the suprarenal gland may follow bilateral suprarenal haemorrhage, adrenalectomy, Addison’s disease or lack of corticosteroid replacement in patients who have been on long-term glucocorticoids. Failure of aldosterone secretion results in volume depletion and glucocorticoid deficiency, which impairs autonomic responses. The ability to respond to minor stress is severely compromised and may provoke an Addisonian crisis characterized by bradycardia and postural hypotension, which is responsive to corticosteroid replacement. Adrenocortical failure should be considered in all patients with unexplained hypotension and a bolus of hydrocortisone given.
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10. How can sympathetic interruption cause shock?
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This reduces the effective blood volume by widespread vasodilatation. It follows transection of the spinal cord (spinal shock), but may also occur after a high spinal anaesthetic.
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11. What are the clinical features of vasovagal syndrome?
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The vasovagal syndrome is produced by severe pain or emotional disturbance. It is due to reflex vasodilatation together with cardiac slowing due to vagal activity. Hypotension is due to a fall in cardiac output as a result of both bradycardia and reduced venous return, the latter due to peripheral vasodilatation. Clinically, it is recognized by the presence of bradycardia and responds to the simple measure of lying the patient flat with elevation of the legs.
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12. What is septic shock? What causes it?
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Septic shock may be produced as the result of severe infection from either Gram-positive or, more commonly, Gram-negative organisms. The latter is particularly seen after colonic, biliary and urological surgery, and with infected severe burns. The principal effect of endotoxins is to cause vasodilatation of the peripheral circulation together with increased capillary permeability. The effects are partly direct, and partly due to activation of normal tissue inflammatory responses such as the complement system and cytokines such as tumour necrosis factor.
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13. What are the sequelae of shock? What will kill the patient?
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A continued low blood pressure produces a series of irreversible changes, so that the patient may die in spite of treatment. The oxygen lack affects all the vital organs. Cerebral hypoperfusion results in confusion or coma. Renal hypoperfusion results in reduced glomerular filtration, with oliguria or anuria. As renal ischaemia progresses, tubular necrosis may occur, and profound ischaemia may lead to cortical necrosis. The heart may fail owing to inadequate coronary perfusion. Pulmonary capillaries may reflect the changes in the systemic circulation with transudation of fluid resulting in pulmonary oedema, hampering oxygen transfer and causing further arterial hypoxaemia and thus tissue hypoxia. Pulmonary capillary function may also be impaired following multiple blood transfusions and contusions resulting from chest trauma, a condition known as acute lung injury (previously termed ‘shock lung’). Disseminated intravascular coagulation precipitated by sepsis may be further aggravated by hypothermia unless active re-warming is undertaken.
