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.

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:
Erythromycin
Amiodarone
Quinidine
Methadone
Procainamide
Sotalol
Terfenadine
Tricyclic antidepressants
Jervell-Lange-Nielsen syndrome (autosomal dominant)
Romano Ward syndrome (autosomal recessive)
Hypothyroidism
Hypocalcaemia
Hypokalaemia
Hypomagnesaemia
Hypothermia
Rheumatic carditis
Mitral valve prolapse
Ischaemic heart disease

The causes of a prolonged QT interval include:

Hypomagnesaemia
Hypothermia
Hypokalaemia
Hypocalcaemia
Hypothyroidism
Jervell-Lange-Nielsen syndrome (autosomal dominant)
Romano Ward syndrome (autosomal recessive)
Ischaemic heart disease
Mitral valve prolapse
Rheumatic carditis
Erythromycin
Amiodarone
Quinidine
Tricyclic antidepressants
Terfenadine
Methadone
Procainamide
Sotalol

Cardiac output (CO) is calculated by multiplying stroke volume (SV) by heart rate (HR):
CO = HR x SV

As 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.

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 hypertension
Pulmonary embolism
Heart failure
Pleural effusion
Decreased cardiac output
Cardiac tamponade
CVP is reduced by the following factors:
Distributive shock
Negative pressure ventilation
Hypovolaemia
Deep inhalation

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 pressure
Pi= interstitial hydrostatic pressure
πp= plasma oncotic pressure
πi= 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.

There are 4 classes of haemorrhage. Classification is based on clinical signs and physiological parameters.

In CLASS I:Blood loss (ml) is < or = 750
Blood loss(% blood volume) < or = 15%
Pulse rate (bpm) is <100
Respiratory rate is 14-20
Urine output (ml/hr) is >30
Pulse pressure is normal or increased
Systolic BP is normal
CNS/mental status patient is slightly anxious

In CLASS II:
Blood loss (ml) is 750 – 1500
Blood loss(% blood volume) is 15 – 30%
Pulse rate (bpm) is 100 – 120
Respiratory rate is 20-30
Urine output (ml/hr) is 20-30
Pulse pressure is decreased
Systolic BP is normal
CNS/mental status patient is mildly anxious

In CLASS III:
Blood loss (ml) is 1500 – 2000
Blood loss(% blood volume) is 30- 40%
Pulse rate (bpm) is 120 – 140
Respiratory rate is 30-40
Urine output (ml/hr) is 5-15
Pulse pressure is decreased
Systolic BP is decreased
CNS/mental status patient is anxious, confused

In CLASS IV:
Blood loss (ml) is >2000
Blood loss(% blood volume) is >40%
Pulse rate (bpm) is >140
Respiratory rate is >40
Urine output (ml/hr) is negligible
Pulse pressure is decreased
Systolic BP is decreased
CNS/mental status patient is confused, lethargic

Plasma oncotic pressure (πp) is typically 25-30 mmHg.

70% of π p is generated by albumin so Hypoalbuminemia will decrease π p

The osmotic power of albumin is enhanced by the Gibbs-Donnan effect.

The influence of π p on fluid movement is negligible if the capillary reflection coefficient is 0.1. Another way of saying a vessel is highly permeable is saying the reflection coefficient is close to 0.

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 SV

As 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.