Download Anatomy and physiology of the cardiovascular system

Anatomy and physiology of the
cardiovascular system
Dr Cath Spoors
Consultant, Anaesthesia and Burns Intensive Care
Broomfield Hospital, Chelmsford
Cardiovascular system
• Giant circular shuttle system
• Transport
– Oxygen, nutrients, cells
– CO2, waste products
• Distribution
– The right stuff to the right place at the right time
What price failure?
What price failure?
What price failure?
What price failure?
What price failure?
30% arteries 5% capillaries 65% veins
Large arteries
• Elastic arteries – large and proximal. Vessel
wall distension in the presence of a competent
aortic valve acts as a secondary pump
• Muscular arteries – high-pressure conduits.
Pressure waves within them are palpable as
peripheral pulses.
Arterioles
• Control of local blood flow
• Major determinant of systemic vascular
resistance (SVR) and therefore blood pressure
• Independent in any given organ bed (control
distribution of cardiac output around the
body)
• Influence capillary hydrostatic pressure
Control of blood flow
• Myogenic – stretch causes vasoconstriction, slackening causes
vasodilation. Important in brain and kidney
Control of blood flow
• Metabolic – substances produced by active
tissues cause vasodilatation to “attract” more
blood to the area (bradykinin, CO2). Hypoxia also
causes vasodilatation
• Sympathetic – basal arteriolar tone. α1 receptors
– vasoconstriction (most beds esp skin, gut,
kidneys). Β2 receptors – vasodilatation (skeletal
muscle). Brain and heart less affected by
neurogenic control
• Hormonal – adrenaline on adrenoceptors
Capillaries
• Continuous – muscle, brain, connective tissue.
Cells joined by tight junctions. Water, oxygen,
carbon dioxide and small water-soluble
molecules can pass relatively easily. Larger
molecules must be transported across
• Fenestrated – intestine, kidneys. Contain pores
which allow rapid exchange of water and small
molecules
• Sinusoidal – liver, bone marrow – whole blood
can pass out into the interstitium
Capillaries
• Gradients
Capillaries
• Gradients
Capillaries
• Gradients
Veins and the venous reservoir
• Low-pressure system for conducting blood back to
heart
• Valves to prevent stasis
• Distend – can accommodate large volumes with little
pressure change. “Buffer” for blood volume
• Venous reservoirs in lungs, liver, gut and skin – under
sympathetic control
• Skeletal muscle augments return of venous blood to
heart
• Respiratory pump increases intrathoracic and right
ventricular volume by sucking in blood from veins
Cardiac output
• The volume of blood pumped out of the left
ventricle per unit time
• Approx 3.5-7.5L/min in adults
Cardiac output
• The volume of blood pumped out of the left
ventricle per unit time
• Approx 3.5-7.5L/min in adults
Cardiac output
• The volume of blood pumped out of the left
ventricle per unit time
• Approx 3.5-7.5L/min in adults
Venous return
• The volume of blood returned to the right
atrium per unit time
Cardiac output
• The volume of blood pumped out of the left
ventricle per unit time
• Approx 3.5-7.5L/min in adults
Venous return
• The volume of blood returned to the right
atrium per unit time
Determinants of stroke volume
• Preload
• Afterload
• Contractility
Determinants of heart rate
• Autonomic function
• Dysrhythmias
• Pacemakers
Preload
• Myocardial muscle cells obey Starling’s law
(force-length relationship)
Preload
• Myocardial muscle cells obey Starling’s law
(force-length relationship)
Preload
• Myocardial muscle cells obey Starling’s law
(force-length relationship)
Determinants of preload
• Volume status
– Hypovolaemia reduces pre-load and cardiac efficiency
– Hypervolaemia over-distends the right heart and reduces
efficiency
• PEEP
– High PEEP (recruitment manoeuvres) can reduce venous
return by increasing thoracic pressure which impedes flow
into the heart
• Arrhythmias
– The chambers need time to fill; if the duration of diastole
is reduced this will impede ventricular filling
• Regurgitant cardiac valves
• Cardiac tamponade
Afterload
• The force opposing shortening of muscle
fibres during contraction
• Increases in afterload will reduce the stroke
volume
• Increases with increased pressure in the
chamber cavity
• Increases with diameter of the chamber cavity
• Decreases with wall thickness
Afterload
• Most afterload is provided by systemic
vascular resistance
• Arterial dilatation will reduce afterload but
this may compromise coronary perfusion
Afterload
• Most afterload is provided by systemic
vascular resistance
• Arterial dilatation will reduce afterload but
this may compromise coronary perfusion
Contractility
• This is the contractile energy of the heart not related to
preload or afterload
• Increased contractility will give an increased stroke volume
• Increased by
– Sympathetic stimulation (catecholamines)
– Extracellular calcium levels
– Increased heart rate (Bowditch effect)
• Decreased by
–
–
–
–
Ischaemia
Drugs
Sepsis
Toxins
Contractility
• This is the contractile energy of the heart not related to
preload or afterload
• Increased contractility will give an increased stroke volume
• Increased by
– Sympathetic stimulation (catecholamines)
– Extracellular calcium levels
– Increased heart rate (Bowditch effect)
• Decreased by
–
–
–
–
Ischaemia
Drugs
Sepsis
Toxins
Determinants of heart rate
• In sinus rhythm, the SA node determines the
heart rate
• Control is by reciprocal action of sympathetic and
parasympathetic nerves
• Circulating catecholamines also increase heart
rate
• β1 adrenoceptors in the SA node speed up;
muscarinic (parasympathetic) slow down
• Optimisation is the key to heart rate
manipulations – trade off between cardiac work
(oxygen demand), output, and venous return
(filling)