Describe the circulatory response to exercise
During exercise, there is an increased blood flow to skeletal muscle. In order to increase cardiac output, the heart rate increases to match the demands of the muscle (there is little increase in stroke volume).Compression of the veins by contracting skeletal muscle increases venous return to the heart
Cerebral cortex initiating the exercise activates vasomotor responses (controlled by the medulla oblongata). Sympathetic activity increases heart rate and contractility and vagal tone is inhibited which also increases heart rate.
As cardiac output increases, there is a slight increase in arterial pressure, and a fall in TPR. Venous pressure remains the same. Blood flow is redistributed away from the GI tract and kidneys to the skeletal muscle.
Describe the circulatory response to standing from a lying position
When lying down, the venous system of the lower limbs is at the level of the heart and blood is returned in a steady, stable situation.
Gravity acts on the vascular volume so blood accumulates in the lower extremities. Therefore, venous volume and pressure becomes very high in the feet and lower limbs when standing. This shift in blood volume decreases central venous pressure.
This venous return to the heart and left ventricular stroke volume also falls because of reduced pulmonary venous return (decreased left ventricular preload). This causes cardiac output and arterial blood pressure to fall. This fall in arterial pressure can reduce cerebral blood flow to the point where a person might experience syncope
Describe the reflex responses to the drop in arterial pressure caused by standing up
When a person stands up, baroreceptor reflexes in the carotid sinus and aorta sense the fall in arterial pressure and activate vasomotor centres of the brain.
This activates the sympathetic nervous system to increase SVR,decrease venous compliance (due to sympathetic activation of veins), decreased stroke volume, and increase heart rate.
Describe the immediate circulatory response to haemorrhage
Haemorrhage causes a large decrease in blood volume which leads to reduced cardiac output and organ perfusion
Acute blood loss causes a fall in central venous pressure and therefore venous return. This reduces cardiac output and arterial pressure.
Baroreceptors activate sympathetic fibres to increase heart rate and contractility, and constrict blood vessels (raise SVR). The heart rate can become very high (pulse is weak and thready)
Blood flow is redistributed to from the GI tract, skeletal muscle and kidneys to the brain and heart.
Kidneys secrete more renin following haemorrhage which leads to increased levels of angiotensin II which is a potent vasoconstrictor.
Describe the intermediate term circulatory responses to haemorrhage
Hypotension and contrction of small arteries/arterioles causes a fall in hydrostatic pressure. The pressure gradient is reduced and less fluid leaves the capillaries and there is a net reabsorption of fluid from the tissues back into the capillaries. This increases plasma volume.
Note: increase is plasma volume dilutes hematocrit and plasma proteins.
What are the longer term physiological responses to haemorrhage?
Restoration of extracellular blood volume: Angiotensin II stimulates release of aldosterone which increases renal absorption of Na+ and water, and secretion of vasopressin which reduces water loss and stimulates thirst.
Restore hematocrit by increased RBC production, stimulated by EPO release from the kidneys
Restore pasma proteins through synthesis in the liver
How do long term increases in blood volume affect circulatory responses?
High Na+ diets/changes in renal function may lead to increases in extracellulaar fluid volume.
Increase in blood volume will raise venous pressure, so end-diastolic volume and cardiac output increases. There is an increase in arterial pressure which increases flow. This causes a washout of vasodilator metabolites and may lead to an autoregulatory increase in SVR. Leads to hypertension
These changes are reversible in the short term however long term exposure causes remodelling of the blood vessel walls and the baroreceptor reflex adapts to high pressure.
Describe the circulatory consequences of hypovolemic shock
Reduction in blood volume, causes hypotensionFall in blood pressure activates the baroreceptor reflex, which produces an increase in heart rate (tachycardia) and an increase in TPR by vasoconstriction and venoconstriction.
Because of the combination of raised HR and TRP, the pulse is weak (thready). These adaptations maintain MAP and perfusion of the heart and brain.
Activation of sympathetic nervous system increases sweating, hands are cold and clammy. Vasocontriction causes pallor. Low blood pH increases resp rate (tachypnoea)
Describe the circulatory consequences of heart failure
Heart failure occurs when the heart is unable to maintain cardiac output despite normal venous pressure.
Blood pressure falls due to reduced CO, so blood accumulates is the venous circulation, causing a rise in central venous pressure.
[Patient may have raised JVP due to accumulation of blood in the right atrium and vena cava backing up in the internal jugular vein]
Compensation can include increased resistance of the vessels and and increase in heart rate.
Describe the circulatory consequences of vasodilatation
Vasodilation causes a fall in TPR, blood pressure falls as a result.
Decerase in blood pressure causes an increase in cardiac output by increasing the heart rate (tachycardia)
Patients have warm, dry peripheries, a short capillary refill time and a bounding pulse.
What are the three factors that can lead to shock?
Inadequate circulating volume
Failure of the heart
Damage to the control of resistance
How does shock occur?
When the cardiac output is insufficient to maintain adequate tissue perfusion