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Physiology of Heart (Cardiac muscle contraction (Ventricular Pressure…
Physiology of Heart
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Special Circulation
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Cerebral circulation
Almost entirely by local metabolites, exhibit autoregulation and active and reactive hyperemia
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Cardiac Function Cruve
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Vascular function curve, decrease in venous return as right atrial pressure increase (Venous return depends on pressure differences)
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mean systematic pressure when venous return = 0, as there is no more blood flow.
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decrease in TPR (dilation of arterioles) result in clockwise rotation of vascular function curve: for a given right atrial pressure, venous return is increased and this is due to lower resistance
Also cause a decrease in arterial pressure and decrease in afterload (can pump more), causing cardiac function curve to shift up
- overall effect on right atrial pressure depends on extend of both changes, and it will decrease or increase slightly, or stays the same, but will generally increase cardiac output
+ve inotropic effect shits cardiac function curve up as increase in stroke vol and increase in cardiac output for any give right atrial P
- increase cardiac output and decreased right atrial pressure
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ECG
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PR interval: time from initial depolarization of atria to that of ventricles
Includes isoelectric portion --> AV node conduction
Usually 160ms
QRS Complex: depolarization of ventricles, about same duration as P wave
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QT interval: first ventricular depolarization to last ventricular repolarization, ST correlates to plateau of ventricular AP
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Microcirculation
Starling equation:
Jv = Kf [(Pc - Pi)-(pi.c - pi.i)]
Jv = fluid movement
Kf = hydraulic conductance
P = pressure
pi = oncotic pressure
c = capillary
i = interstital
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KfL not influenced by factors such as change in arteriolelar resistance, hypoxia, but is increased in capillary injury
Hydrostatic pressure favours filtration, determined by arterial and venous pressure (Pc)
Pi usually zero
Closer to Arterial pressure but more affected by changes in venous changes, and is normally highest at arteriolar end and lowest at venous end due to decline
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Thus, increase in filtration could be due to increase in Pc or decrease in pi.c
Heart Pumping
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In steady state, cardiac output from the heart should equal venous return to the heart
Circuitry
- O2-ted blood fills left ventricle from the left atrium through the mitral valve
- Blood is ejected from left ventricle to the aorta through aortic valve
- Cardiac output distributed among various organs
- Blood flow from organs collected in veins
Three mechanisms to change blood flow:
- Cardiac output constant, blood flow redistributed through selective alteration of TRP
- Change in cardiac output but keep distribution constant
- Change both
- venous return to right atrium
- Fills right ventricle through tricuspid valve
- Blood ejected from the right ventricle through pulmonary valves to the pulmonary artery
- Blood flow from lungs returned to the heart via pulmonary vein
Temperature regulation
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Generating heat
Thyroid hormones stimulate Na+-K+ ATPase, increase O2 consumption, increase metabolic rate and increase heat production -> thermogenic hormones
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Hemodynamics
Types of blood vessels
Arteries:
- aorta largest artery of systemic circulation
- medium and small sized arteries branch off aorta
- Thick-walled, with extensive elastic tissue, smooth muscle and connective tissue
- Thickness due to high pressure
- Vol of blood in arteries called stressed vol (blood vol under high pressure)
Arterioles:
- Smallest branches of arteries
- Have extensive smooth muscle
- site or highest resistance to blood flow
- Tonically active (always contracted)
- a1-adrenergic receptors found on arterioles of several vascular beds (e.g. skin and splanchnic vasculature)
- B2-adrenergic receptors found in arterioles of skeletal muscles(less common)
- site where resistance can be changed by alterations
Capillaries:
- single layer endothelial cells to facilitate exchange
- lipid soluble substances (such as gas) pass through endothelial cells (can go through cell membrane)
- water soluble substances cross through water-filled spaces between endothelial cells or through large pores in walls of some capillaries
- selective perfusion through arteriole constriction/dilation and precapillary sphincters
Venules and Veins:
- Thin walled, with a modest amount of elastic tissue, smooth muscle and CT.
- due to less elastic tissue, have a large capacitance (to hold blood) -> larger accomodation of blood with less change in pressure
- Contains the largest percentage of blood in CVS
- Vol of blood called unstressed Vol
- Smooth muscle innervated by a1 adrenergic receptors to change capacitance (and unstressed vol)
Equations
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Q= P/R
Q=Flow (mL/min)
P = Pressure difference (mm Hg)
R = Resistance (mm Hg/mL/min)
TPR = total peripheral resistance
Cardiac output = Q
Difference in pressure between aorta and vena cava = P
Resistance in single organ
Renal blood flow = Q
Difference in P between renal artery and renal vein = P
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Pressure in CVS
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remains relatively constant from aorta to the large arteries due to large vol of blood pumped in and the low compliance of the arterial wall. Remains high due to high elastic recoil of arterial walls -> little energy is lost as blood flows
Drops when we reach small arteries, and most significant at arterioles due to high resistance
Decreases further in capillaries due to frictional resistance and filtration of fluid out of capillaries
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Cardiac Cycle
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Atrial systole happens at end of ventricular filling as a kick, faster ventricular filling happens upon opening of mitral valve due to pressure difference
1sr sound when mitral valve close, 2nd when aortic valve close
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