Download Anatomy and physiology of the cardiovascular system

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts

Quantium Medical Cardiac Output wikipedia, lookup

Dextro-Transposition of the great arteries wikipedia, lookup

Antihypertensive drug wikipedia, lookup

Jatene procedure wikipedia, lookup

Cardiac surgery wikipedia, lookup

Lutembacher's syndrome wikipedia, lookup

Coronary artery disease wikipedia, lookup

Management of acute coronary syndrome wikipedia, lookup

Arrhythmogenic right ventricular dysplasia wikipedia, lookup

Electrocardiography wikipedia, lookup

Heart failure wikipedia, lookup

Mitral insufficiency wikipedia, lookup

Cardiac contractility modulation wikipedia, lookup

Transcript
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)