Download CRRM1.29 - Haemorrhage and Hypertension

CRRM1.29: HAEMORRHAGE AND HYPERTENSION
06/02/08
LEARNING OUTCOMES
Explain the basic mechanisms active in hypertension, haemorrhage and shock
SHOCK
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A fit, young and healthy individual can lose approximately 30% of blood volume before blood pressure
control mechanisms fail
When blood pressure can no longer be maintained for adequate perfusion of the brain and heart,
shock occurs
Shock is defined as an acute failure of the CVS to supply nutritional blood flow to all tissues
o Hypovolaemic shock is due to an acute loss in blood volume (e.g. haemorrhage)
o Septicaemic shock is due to bacterial toxins
o Cardiogenic shock is due to mechanical or electrical ventricular failure
During shock:
o Systolic, diastolic and pulse pressures are all reduced
o Pulse is rapid and weak
o Veins within the skin collapse making it pale, cold and moist
HAEMORRHAGE
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In haemorrhage decreasing blood volume reduces venous return which in turn reduces cardiac output
o Arterial BP drops which is sensed by baroreceptors
o Local blood flow drops resulting in stagnant hypoxia which is sensed by chemoreceptors
Overall triggers an increase in sympathetic activity:
o HR and contractility increases
o Peripheral vasoconstriction
o Increased sympathetic output to juxtaglomerular apparatus (JGA) in the kidneys
Low blood volume triggers the release of vasopressin (ADH) – further vasoconstriction and antidiuretic effects
Reduced renal perfusion stimulates the renin-angiotensin system (RAS):
o JGA stimulation increases renal renin secretion
o Angiotensinogen in the plasma is converted by renin into angiotensin I
o Angiotensin converting enzyme (ACE) then converts angiotensin I to angiotensin II
Angiotenin II acts to:
o Induce vasoconstriction
o Promote aldosterone release
o Stimulate thirst
Aldosterone promotes sodium and water re-absorption in the kidneys to increase blood volume
Longer-term response to haemorrhage is to activate the internal perfusion mechanism:
o Capillary pressure falls increasing water absorption from the interstitium
o Glucose is released from the liver to increase plasma osmolarity
HYPERTENSION
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Hypertension is defined as a chronic, usually progressive raised arterial blood pressure
Approximately 30% of the adult population suffer from some degree of hypertension
Normal BP averages at 120/80; over 140/90 qualifies as hypertension (adjust for age)
o < 160/100 is mild
o < 180/110 is moderate
o < 210/120 is severe
There are two main forms of hypertension:
o Essential – no known cause; accounts for 95% of cases
o Secondary – the result of a particular condition, usually renal disease (e.g.
hyperaldosteronism, renal artery stenosis, phaeochromocytoma)
o Also white coat hypertension (rare) – elevated in presence of clinician
Essential hypertension usually results from an increased peripheral resistance with a normal cardiac
output due to:
o Decreased response to endogenous vasodilators e.g. NO
o Impaired baroreceptor reflex
Increased local RAS activity is thought to be involved in the aetiology of essential hypertension
o Bradykinin is a potent vasodilator that is inactivated by ACE
Hypertension increases the risk of MI, CHD, strokes, renal failure and atherosclerosis
Examination of a hypertensive patient usually includes fundoscopy (observation of retina and blood
vessels) – abnormalities can indicate malignant hypertension (often fatal)
Investigations typically include:
o ECG monitoring
o Urine test for protein and blood
o Serum urea, creatinine and electrolytes
Low serum potassium may indicate an endocrine disorder
Treatments include:
o Weight reduction / diet alteration (low sodium and fat)
o Limited alcohol consumption
o Diuretics to reduce extracellular fluid (not often used in younger patients)
o β-blockers
o ACE inhibitors
o Peripheral vasodilators (α-antagonists) – in resistant cases