Regarding the skeletal muscle circulation, which of the following statements is INCORRECT:
The skeletal muscle circulation normally receives about 15 - 20% of the cardiac output, but this may rise to > 80% during exercise. Skeletal muscle provides a major contribution to the total peripheral resistance and sympathetic regulation of muscle blood flow is important in the baroreceptor reflex. At rest most capillaries are not perfused as their arterioles are constricted. Capillaries are recruited during exercise by metabolic hyperaemia, caused by release of K+ and CO2 from the muscle and adenosine. This overrides sympathetic vasoconstriction in working muscle; the latter reduces flow in non-working muscle conserving cardiac output.
The pulmonary circulation is not controlled by either autonomic nerves or metabolic products, and the most important mechanism regulating flow is hypoxic pulmonary vasoconstriction, in which small arteries constrict in response to hypoxia (in contrast to elsewhere in the body).
If an area of lung is poorly ventilated and the alveolar partial pressure of oxygen is low, pulmonary blood vessels are constricted and blood is diverted to areas of the lung that are better ventilated, thus maintaining optimal ventilation-perfusion matching. This effect is accentuated by high alveolar PCO2.
The response is unhelpful in the presence of global lung hypoxia, at altitude or in respiratory failure, where it may contribute to the development of pulmonary hypertension and right-sided heart failure (cor pulmonale).
The main function of the cutaneous circulation is thermoregulation. Arteriovenous anastomoses (AVAs) directly linked arterioles and venules, allowing a high blood flow into the venous plexus and thus radiation of heat. AVAs are mostly found in the hands, feet and areas of the face.
Temperature is sensed by peripheral thermoreceptors and the hypothalamus coordinates the response.
When temperature is low, sympathetic stimulation of alpha-adrenergic receptors causes vasoconstriction of cutaneous vessels minimising loss of body heat (a similar response occurs in the baroreceptor reflex). Piloerection traps insulating air.
Increased temperatures reduce sympathetic adrenergic stimulation, causing vasodilation and allowing more blood to flow to the skin and radiate its heat to the environment, whereas activation of sympathetic cholinergic fibres promotes sweating and the release of bradykinin, which also causes vasodilation.
The brain receives around 15% of the total cardiac output and has a high capillary density.
The endothelial cells of the capillaries of the blood-brain barrier have very tight junctions, and contain membrane transporters that control the movement of substances, such as ions, glucose and amino acids, and tightly regulate the composition of cerebrospinal fluid. This is continuous except where substances need to be absorbed or released e.g. pituitary gland, choroid plexus.
The precapillary cerebral vasculature typically can reflexively constrict or dilate in response to changes in mean arterial blood pressure (MAP). For clinical purposes, cerebral perfusion pressure (CPP) is defined as mean arterial blood pressure minus intracranial pressure (CPP = MAP – ICP). The autoregulation of cerebral blood flow can maintain a constant flow for blood pressures (MAP) between 50 and 170 mmHg.
CO2 and K+ are particularly important metabolic regulators in the brain, with increasing concentration causing vasodilation and a functional hyperaemia. Hyperventilation reduces blood PCO2 and can cause fainting due to cerebral vasoconstriction.
Raised ICP:
Elevation of ICP can reduce cerebral perfusion and cause or exacerbate ischaemia. The cranial cavity has a fixed volume because the cranium is a rigid, non-expansive container. When the normal intracranial volume is exceeded, intracranial pressure (ICP) rises. Venous blood and CSF can be compressed out of the container, providing a degree of pressure buffering. However, once the limit of displacement of CSF and intravascular blood has been reached, ICP rapidly increases.
The heart has a high metabolic demand and its high capillary density allow it to extract an unusually large fraction (about 70%) of oxygen from the blood.
In exercise, the reduced diastolic interval and increased oxygen consumption demand a greatly increased blood flow which is achieved by metabolic hyperaemia mediated by adenosine, K+ and hypoxia. This overrides the vasoconstriction mediated by sympathetic nerves acting at alpha-adrenergic receptors and is assisted by circulating adrenaline which causes vasodilation by acting on beta-adrenergic receptors.
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Biochemistry | Normal Value |
---|---|
Sodium | 135 – 145 mmol/l |
Potassium | 3.0 – 4.5 mmol/l |
Urea | 2.5 – 7.5 mmol/l |
Glucose | 3.5 – 5.0 mmol/l |
Creatinine | 35 – 135 μmol/l |
Alanine Aminotransferase (ALT) | 5 – 35 U/l |
Gamma-glutamyl Transferase (GGT) | < 65 U/l |
Alkaline Phosphatase (ALP) | 30 – 135 U/l |
Aspartate Aminotransferase (AST) | < 40 U/l |
Total Protein | 60 – 80 g/l |
Albumin | 35 – 50 g/l |
Globulin | 2.4 – 3.5 g/dl |
Amylase | < 70 U/l |
Total Bilirubin | 3 – 17 μmol/l |
Calcium | 2.1 – 2.5 mmol/l |
Chloride | 95 – 105 mmol/l |
Phosphate | 0.8 – 1.4 mmol/l |
Haematology | Normal Value |
---|---|
Haemoglobin | 11.5 – 16.6 g/dl |
White Blood Cells | 4.0 – 11.0 x 109/l |
Platelets | 150 – 450 x 109/l |
MCV | 80 – 96 fl |
MCHC | 32 – 36 g/dl |
Neutrophils | 2.0 – 7.5 x 109/l |
Lymphocytes | 1.5 – 4.0 x 109/l |
Monocytes | 0.3 – 1.0 x 109/l |
Eosinophils | 0.1 – 0.5 x 109/l |
Basophils | < 0.2 x 109/l |
Reticulocytes | < 2% |
Haematocrit | 0.35 – 0.49 |
Red Cell Distribution Width | 11 – 15% |
Blood Gases | Normal Value |
---|---|
pH | 7.35 – 7.45 |
pO2 | 11 – 14 kPa |
pCO2 | 4.5 – 6.0 kPa |
Base Excess | -2 – +2 mmol/l |
Bicarbonate | 24 – 30 mmol/l |
Lactate | < 2 mmol/l |