Cardiovascular System

1. Transport oxygen and nutrients to cells
2. transport carbon dioxide and other metabolites away from cells
3. distribute hormones
4. defence (immune cells)
5. thermoregulation

1. ventricles
2. atria
3. inside lined with endocardium, outside epicardium
4. valves
   1. semilunar, both 3 cusps
   2. AV, LHS mitral= BICUSPID RHS TRICUSPID
5. chordae tendinae + papillary muscle

1. non conducting connective tissue
2. structural integrity
3. break up continuity between A and V allow separate contraction

1. VEINS
   1. bigger
   2. may have valves
   3. less muscle
   4. most blood is sitting in the venous system
2. ARTERIES
   1. Thicker muscle
   2. elastic to allow for stroke volume
   3. arterioles- resistance vessels decrease in diamater decrease blood pressure, increase resistance to blood flow

1. arterioles and venules rally thin muscle layer
2. microcirculation, exchange happens
   1. Arteriole end- high hydrostatic pressure forces fluid out into tissues
   2. Venous end- osmotic pull from proteins in capillary returns fluid to blood
   3. starling forces
   4. lymphatic system returns the rest to CVS via lymphatic duct

1. parasympathetic, vagus nerve innervates SAN and AVN

   Annotations:

   • dominant at rest
2. Adrenergic nerve innervate SAN and AVN

1. cardiac muscle can beat spontaniously generating own action potential
2. functional syncytium- cells electrically coupled by intercalated discs
3. v central nuclei
4. calcium-induced calcium release excitation coupling

   Annotations:

   • calcium ions enter the cell deplarising it, this triggers calcium ions to be released from the sarcoplasmic reticulum so the muscle contracts

1. 1- Slow region of gradual depolarisation thanks to sodium ion leak channels letting sodium ions into the cell
2. 2-depolarisation reaches a threshold value and voltage gated calcium ion channels open
3. 3- calcium ions rush into the cell causing rapid depolarisation

1. 1- Fast sodium ion channels open causing rapid depolarisation
2. 2- at a threshold the fast sodium ion channels close
3. 3-plateu as calcium ions enter via voltage gated channels
4. 4- repolarisation

Annotations:

• so to alter cardiac oputput we must either alter stroke volume or heart rate

1. SAN- innervated by SNS and PNS
   1. PNS releases acetylcholine which closes the sodium ion leak channels so it takes longer to reach threshold value
   2. SNS- releases noradrenaline binds to beta-adrenoreceptors to open more sodium ion leak channels
2. AVN innervated by both
   1. PNS increases refractory period, SNS decreases refreactory period

Annotations:

• increase the force generated by the contractile cells in the heart

1. ATRIAL MYOCYTES respond to both SNS and PNS
2. VENTRICULAR MYOCYTES- does not directly respond to PNS, instead PNS affects SNS decreasing noradrenaline release

1. filling pressure of the heart
2. affected by central venous pressure
3. INCREASED PRELOAD= INCREASED VENTRICULAR PRESSURE
4. MORE BLOOD ENTERS THE VENTRICLES SO VENTRICLE MUSCLE IS STREACHED
   1. increased strength of contraction, increases stroke volume= increase cardiac output
5. 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

1. pressure against which the heart ejects
2. determined by arterial pressure (resistance vessels?)
3. direct oposition to ejection, increase in afterload decrease stroke volume
   1. decrease cardiac output

1. MAP= CARDIAC OUTPUT X TOTAL PERIPHERAL RESISTANCE
2. to alter we must either alter heart rate, stroke volume or resistance

1. 1- changes in pressure sensed by baroreceptors in adventitia of corotid arteries and aortic arch e.g. sense BP increase
2. 2- impulses send from baroreceptors to medulla oblongata
3. 3- increase PNS (vagal) output to decrease heart rate therefore cardiac outptu
4. 4- decrease sympathetic, decrease arteriolar tone (decrease resistance, decrease cardiac contractility and heart rate

1. if we increase circulating blood volume, increase preload, increase cardiac output so increase MAP
2. 1- Renin release stimulates angiotensin II production
3. 2- angiotensin II is a vasoconstrictor incresaes TPR and therefore MAP
4. 3-stimulate ADH, retain water increase circulating volume
5. 4- aldesterone releaed so kidney retains more sodium so even more water is absorbed

1. BLOOD LOSS- BIG DECREASE IN VOLUME
   1. decrease arterial pressure
      1. barroreceptor reflex
   2. decrease in venous return
      1. decrease discharge of atrial volume receptors
         1. ADH RELEASE
         2. EXCITE SYMPATHETIC PATHWAY TO KIDNEY
            1. renal vasoconstriction
               1. incrase MAP
            2. Renin release
               1. angiotensin II produced
                  1. vasoconstriction and aldesterone production
                     1. water retention= increase in mean arterial pressure