Lecture 20 Flashcards
(21 cards)
Cardiac output
Volume of blood pumped (per ventricle) per given time (mLs/min). Indicator of total blood pumped around the body.
CO = HR * SV
Modulation of heart rate
HR is initiated by autorhythmic cells but can be altered by neural and hormonal input via ANS.
Parasympathetic NS
Ach released and binds to muscarinic receptors on pacemaker cells causing increase in K+ efflux and decrease Ca2+ influx causes hyperpolarisation and decrease depolarisation cells causing decreases HR. Basically decreases slope of pacemaker potential.
Sympathetic NS
Noradrenaline released which binds to B1 receptors on pacemaker cells which causes an increase influx of Na+ and Ca2+ leads to increase depolarisation rate leads to increase in HR. Increase slope of pacemaker potential.
Modulation of SV
- Modulating length of muscle fibres (increases ventricular stretch)
- Increase contraction strength
Length-tension relationship
Length of the sarcomere and so, length of myosin/actin directly relates to the force generated by muscle fibres. Stretching fibres increases overlap between actin and myosin increase force generated.
Frank-Starling Law of the heart
If more blood goes to heart, muscle fibres can stretch and therefore contract more forcefully.
Altering end diastolic volume
EDV is determined by venous return. Altered by contraction/compression of veins, pressure changes in abdomen and thorax and sympathetic innovation of veins.
skeletal muscle pump
A lot of veins innovate large muscle groups. There are points of constriction on the veins caused by innervation into different muscle groups. When muscle contract, it pushes blood away from constriction point. Blood flows increases but decreases, but, venous valves ensures that blood ALWAYS flows to heart.
Respiratory pump
When right ventricle closes, it causes suction effect which draws blood back into heart. Breathing causes same effect. When breathing in, diaphragm and volume increases which decreases pressure which draws blood from areas with high atmospheric pressure to the chest and eventually back to the heart.
Altering contractility of heart
For same amount of blood to heart, even more exits under control of noradrenaline.
Altering contractility of heart steps
- SNS releases adrenaline and noradrenaline
- They bind to B1 receptors on contractile cells
- Voltage-gated Ca2+ channels phosphorylate causing an influx of Ca2+ and phospholambin which increases ATP-ase and Ca2+ binding to SR.
- Increase Ca2+ stores in SR or Ca2+ is removed from troponin complex.
- Contractions more forceful or, shorter.
Distribution of blood
Arteries are low volume vessels while veins are high volume vessels (contains 60% circulating blood at a time). Hence, veins acts as volume reservoirs of blood as a way to bring blood back to heart and influence SV. Increase venous return = Increase SV = increase CO
Blood flow from high to low pressure
Change pressure= high - low pressure.
There must be a pressure gradient for blood flow. Flow is directly proportional to pressure change. Magnitude of P is not important, just pressure change.
Resistance
Opposition to the flow of blood. Blood takes path of least resistance therefore, increase R = decrease blood flow.
What is resistance impacted by
Radius of vessel, length of tube, viscocity of fluid
Resistance/flow formulas
R = 1/r^4
flow directly proportional to pressure change
Flow is inversely proportional to resistance
Flow is proportional to pressure change/resistance.
Driving pressure in arterial system
After breathing, the force is not immediately lost due to the presence of elastin which absorbs the force. This causes the wall to expand. When pressure decreases in LV, the valve closes and the elastin recoils. The absorbed force is imparted into the flow of the blood. Elastic recoils maintains pressure needed for systemic circulation. Driving force of pressure on blood when it leaves heart is pulse pressure.
Pulse pressure formula
systolic pressure - diastolic pressure
Mean arterial pressure
average pressure diving blood to tissue. Rough average of diastolic and systolic as heart spends more time is diastole than systole. MAP influenced by R and CO. If flow in>flow out, MAP increases. Vice versa.
MAP formula
Diastolic pressure + 1/3 Pulse Pressure
CO * arteriole resistance.