In skeletal muscle, blood flow is closely related to metabolic rate. Due to the contraction of precapillary sphincters, most capillaries are blocked off from the rest of the circulation at rest and are not perfused. This causes an increase in vascular tone and vessel constriction. As metabolic activity rises, this develops redundancy in the system, allowing it to cope with greater demand. During exercise, metabolic hyperaemia, which is induced by the release of K+, CO2, and adenosine, recruits capillaries. Sympathetic vasoconstriction in the active muscles is overridden by this. Simultaneously, blood flow in non-working muscles is restricted, preserving cardiac output. During exercise, muscle contractions pump blood through the venous system, raising the pressure differential between arterioles and venules and boosting blood flow via capillaries.Capillary angiogenesis is evident when muscles are used repeatedly (e.g. endurance training). It is a long-term effect, not a quick fix for increased blood flow.The local partial pressure of alveolar oxygen is the primary intrinsic control of pulmonary blood flow (pAO2). Low pAO2 promotes arteriole vasoconstriction and vice versa. The hypoxic pulmonary vasoconstriction (HPV) reflex allows blood flow to be diverted away from poorly ventilated alveoli and towards well-ventilated alveoli in order to maximize gaseous exchange.

Cardiac output (CO) is calculated by multiplying stroke volume (SV) by heart rate (HR):CO = HR x SVAs a result, both stroke volume and heart rate are exactly proportional to cardiac output. There will be an increase in cardiac output if the stroke volume or heart rate increases, and a reduction in cardiac output if the stroke volume or heart rate lowers.

There are 4 classes of haemorrhage. Classification is based on clinical signs and physiological parameters.In CLASS I:Blood loss (ml) is < or = 750Blood loss(% blood volume) < or = 15%Pulse rate (bpm) is 30Pulse pressure is normal or increasedSystolic BP is normalCNS/mental status patient is slightly anxious In CLASS II:Blood loss (ml) is 750 – 1500Blood loss(% blood volume) is 15 – 30%Pulse rate (bpm) is 100 – 120Respiratory rate is 20-30Urine output (ml/hr) is 20-30Pulse pressure is decreasedSystolic BP is normalCNS/mental status patient is mildly anxiousIn CLASS III:Blood loss (ml) is 1500 – 2000Blood loss(% blood volume) is 30- 40%Pulse rate (bpm) is 120 – 140Respiratory rate is 30-40Urine output (ml/hr) is 5-15Pulse pressure is decreasedSystolic BP is decreasedCNS/mental status patient is anxious, confusedIn CLASS IV:Blood loss (ml) is >2000Blood loss(% blood volume) is >40%Pulse rate (bpm) is >140Respiratory rate is >40Urine output (ml/hr) is negligiblePulse pressure is decreasedSystolic BP is decreasedCNS/mental status patient is confused, lethargic

Short vessels called arteriovenous anastomoses (AVAs) link tiny arteries and veins. They have a large lumen diameter. The strong and muscular walls allow AVAs to completely clog the vascular lumen, preventing blood flow from artery to vein (acting like a sphincter). When the AVAs open, they create a low-resistance connection between arteries and veins, allowing blood to flow into the limbs’ superficial venous plexuses. There is no diffusion of solutes or fluid into the interstitium due to their strong muscle walls.AVAs are densely innervated by adrenergic fibres from the hypothalamic temperature-regulation centre. High sympathetic output occurs at normal core temperatures, inducing vasoconstriction of the AVAs and blood flow through the capillary networks and deep plexuses. When the temperature rises, sympathetic output decreases, producing AVA vasodilation and blood shunting from the artery to the superficial venous plexus. Heat is lost to the environment as hot blood rushes near to the skin’s surface.AVAs are a specialized anatomical adaptation that can only be found in large quantities in the fingers, palms, soles, lips, and pinna of the ear.

The pressure measured in the right atrium or superior vena cava is known as central venous pressure (CVP). In a spontaneously breathing subject, the usual CVP value is 0-8 cmH2O (0-6 mmHg).The structure of the CVP waveform is as follows:The CVP’s components are listed in the table below:Component of the waveformThe cardiac cycle phase.mechanical eventmechanical event Diastole Atrial contractiona wave C  wave v waveEarly systoleThe tricuspid valve closes and bulges Late Systole Filling of the atrium with systolic blood x descenty descentMid systoleRelaxation of the atrium Early diastoleFilling of the ventricles at an early stage

Syncope and sudden death due to ventricular tachycardia, particularly Torsades-des-pointes is seen in prolongation of the QT interval.The causes of a prolonged QT interval include:ErythromycinAmiodaroneQuinidineMethadoneProcainamideSotalolTerfenadineTricyclic antidepressantsJervell-Lange-Nielsen syndrome (autosomal dominant)Romano Ward syndrome (autosomal recessive)HypothyroidismHypocalcaemiaHypokalaemiaHypomagnesaemiaHypothermiaRheumatic carditisMitral valve prolapseIschaemic heart disease

The pressure measured in the right atrium or superior vena cava is known as central venous pressure (CVP). In a spontaneously breathing subject, the usual CVP value is 0-8 cmH2O (0-6 mmHg).At the conclusion of expiration, the CVP should be measured with the patient resting flat. The catheter’s tip should be at the intersection of the superior vena cava and the right atrium. An electronic transducer is installed and zeroed at the level of the right atrium to measure it (usually in the 4th intercostal space in the mid-axillary line).CVP is a good predictor of preload in the right ventricle. Hypovolaemia is indicated by a volume challenge of 250-500 mL crystalloid eliciting an increase in CVP that is not sustained for more than 10 minutes.CVP is influenced by a number of factors, including:Mechanical ventilation (and PEEP)Pulmonary hypertensionPulmonary embolismHeart failurePleural effusionDecreased cardiac outputCardiac tamponadeCVP is reduced by the following factors:Distributive shockNegative pressure ventilationHypovolaemiaDeep inhalation

The terminology cardiac output refers to the amount of blood pumped by the heart in one minute. Women’s rates are around 5 L/min, whereas men’s rates are somewhat higher, around 5.5 L/min.Cardiac output (CO) is calculated by multiplying stroke volume (SV) by heart rate (HR):CO = HR x SVAs a result, both stroke volume and heart rate are exactly proportional to cardiac output. There will be an increase in cardiac output if the stroke volume or heart rate increases, and a reduction in cardiac output if the stroke volume or heart rate lowers.

Starling’s equation for fluid filtration describes fluid flow at the capillary bed.Filtration forces (capillary hydrostatic pressure and interstitial oncotic pressure) stimulate fluid movement out of the capillary, while resorption forces promote fluid movement into the capillary (interstitial hydrostatic pressure and plasma oncotic pressure). Although the forces fluctuate along the length of the capillary bed, overall filtration is achieved.At the capillary bed, there is fluid movement.The reflection coefficient (σ), the surface area accessible (S), and the hydraulic conductance of the wall (Lp) are frequently used to account for the endothelium’s semi-permeability, yielding:Volume / min = LpS [(Pc- Pi) –  σ(πp– πi)]Volume /min = (Pc-Pi) – (πp–πi) describes the fluid circulation at the capillaries.Where:Pc= capillary hydrostatic pressurePi= interstitial hydrostatic pressureπp= plasma oncotic pressureπi= interstitial oncotic pressure

Short vessels called arteriovenous anastomoses (AVAs) link tiny arteries and veins. They have a large lumen diameter. The strong and muscular walls allow AVAs to completely clog the vascular lumen, preventing blood flow from artery to vein (acting like a sphincter). When the AVAs open, they create a low-resistance connection between arteries and veins, allowing blood to flow into the limbs’ superficial venous plexuses. There is no diffusion of solutes or fluid into the interstitium due to their strong muscle walls.AVAs are densely innervated by adrenergic fibres from the hypothalamic temperature-regulation centre. High sympathetic output occurs at normal core temperatures, inducing vasoconstriction of the AVAs and blood flow through the capillary networks and deep plexuses. When the temperature rises, sympathetic output decreases, producing AVA vasodilation and blood shunting from the artery to the superficial venous plexus. Heat is lost to the environment as hot blood rushes near to the skin’s surface.AVAs are a specialized anatomical adaptation that can only be found in large quantities in the fingers, palms, soles, lips, and pinna of the ear.