Cardiovascular System

Cardiovascular System

1. Anatomy Cardiovascular system

   • Functions
     • Transport oxygen and nutrients to cells
     • transport carbon dioxide and other metabolites away from cells
     • distribute hormones
     • defence (immune cells)
     • thermoregulation
   • Heart
     • ventricles
     • atria
     • inside lined with endocardium, outside epicardium
     • valves
       • semilunar, both 3 cusps
       • AV, LHS mitral= BICUSPID RHS TRICUSPID
     • chordae tendinae + papillary muscle
   • Cardiac Skeleton
     • non conducting connective tissue
     • structural integrity
     • break up continuity between A and V allow separate contraction
   • Large Vessels
     • VEINS
       • bigger
       • may have valves
       • less muscle
       • most blood is sitting in the venous system
     • ARTERIES
       • Thicker muscle
       • elastic to allow for stroke volume
       • arterioles- resistance vessels decrease in diamater decrease blood pressure, increase resistance to blood flow
   • Small Vessels
     • arterioles and venules rally thin muscle layer
     • microcirculation, exchange happens
       • Arteriole end- high hydrostatic pressure forces fluid out into tissues
       • Venous end- osmotic pull from proteins in capillary returns fluid to blood
       • starling forces
       • lymphatic system returns the rest to CVS via lymphatic duct

2. Regulation heartbeat/ cardiac cycle

   • Atrial Systole>Ventricle Systole>ejection of blood, diastole, ventricle and arteries fill
   • electrically- Sinoatrial node (atria contract), atrioventricular node, bundle of His, purkinje fibres- ventricles contract
   • Influence heart rate?
     • parasympathetic, vagus nerve innervates SAN and AVN
       • dominant at rest
     • Adrenergic nerve innervate SAN and AVN
   • cardiac muscle
     • cardiac muscle can beat spontaniously generating own action potential
     • functional syncytium- cells electrically coupled by intercalated discs
     • v central nuclei
     • calcium-induced calcium release excitation coupling
       • calcium ions enter the cell deplarising it, this triggers calcium ions to be released from the sarcoplasmic reticulum so the muscle contracts
   • CARDIAC ACTION POTENTIALS IN SAN
     • 1- Slow region of gradual depolarisation thanks to sodium ion leak channels letting sodium ions into the cell
     • 2-depolarisation reaches a threshold value and voltage gated calcium ion channels open
     • 3- calcium ions rush into the cell causing rapid depolarisation
   • CARDIAC ACTION POTENTIALS IN THE VENTRICLES
     • 1- Fast sodium ion channels open causing rapid depolarisation
     • 2- at a threshold the fast sodium ion channels close
     • 3-plateu as calcium ions enter via voltage gated channels
     • 4- repolarisation

3. Regulation of Cardiac Output

   • Cardiac output= stroke volume x heart rate
     • so to alter cardiac oputput we must either alter stroke volume or heart rate
   • Altering heart rate
     • SAN- innervated by SNS and PNS
       • PNS releases acetylcholine which closes the sodium ion leak channels so it takes longer to reach threshold value
       • SNS- releases noradrenaline binds to beta-adrenoreceptors to open more sodium ion leak channels
     • AVN innervated by both
       • PNS increases refractory period, SNS decreases refreactory period
   • increasing stroke volume- myocardial contractility
     • increase the force generated by the contractile cells in the heart
     • ATRIAL MYOCYTES respond to both SNS and PNS
     • VENTRICULAR MYOCYTES- does not directly respond to PNS, instead PNS affects SNS decreasing noradrenaline release
   • PRELOAD
     • filling pressure of the heart
     • affected by central venous pressure
     • INCREASED PRELOAD= INCREASED VENTRICULAR PRESSURE
     • MORE BLOOD ENTERS THE VENTRICLES SO VENTRICLE MUSCLE IS STREACHED
       • increased strength of contraction, increases stroke volume= increase cardiac output
     • STARLINGS LAW OF THE HEART- force of muscle fibre contraction is proportional to length of fibre, so if we stretch the fibre we get a stronger contraction
   • AFTERLOAD
     • pressure against which the heart ejects
     • determined by arterial pressure (resistance vessels?)
     • direct oposition to ejection, increase in afterload decrease stroke volume
       • decrease cardiac output

4. Regulation blood pressure

   • Mean arterial pressure (MAP)
     • MAP= CARDIAC OUTPUT X TOTAL PERIPHERAL RESISTANCE
     • to alter we must either alter heart rate, stroke volume or resistance
   • Short term regulation
     • 1- changes in pressure sensed by baroreceptors in adventitia of corotid arteries and aortic arch e.g. sense BP increase
     • 2- impulses send from baroreceptors to medulla oblongata
     • 3- increase PNS (vagal) output to decrease heart rate therefore cardiac outptu
     • 4- decrease sympathetic, decrease arteriolar tone (decrease resistance, decrease cardiac contractility and heart rate
   • Long term regulation
     • if we increase circulating blood volume, increase preload, increase cardiac output so increase MAP
     • 1- Renin release stimulates angiotensin II production
     • 2- angiotensin II is a vasoconstrictor incresaes TPR and therefore MAP
     • 3-stimulate ADH, retain water increase circulating volume
     • 4- aldesterone releaed so kidney retains more sodium so even more water is absorbed
   • KEY EXAMPLE- HAEMORRHAGE
     • BLOOD LOSS- BIG DECREASE IN VOLUME
       • decrease arterial pressure
         • barroreceptor reflex
       • decrease in venous return
         • decrease discharge of atrial volume receptors
           • ADH RELEASE
           • EXCITE SYMPATHETIC PATHWAY TO KIDNEY
             • renal vasoconstriction
               • incrase MAP
             • Renin release
               • angiotensin II produced
                 • vasoconstriction and aldesterone production
                   • water retention= increase in mean arterial pressure

Imagens e arquivos do mapa