Lec 20 Flashcards
Systole
Contraction
Diastole
Relaxing
During diastole
Chambers are filing with blood
Late diastole
Both chambers are relaxed
Ventricle fill passivley
Atrial systole
Atrial contraction 15% of blood
Isovolumic Ventricular Contraction
Pushes AV valves close
Not enough pressure to semilunar valve
Ventricular ejection
Ventricular pressure rises
Semilunar valve open
Isovolumic ventricular relaxation
Semilunar valve close
AV close (not enough pressure to open)
S1
AV valve shut
S2
Semilunar valve shut
End-diastolic volume
Volume of blood in ventricle at the end of ventricular diastole
End systolic volume
Volume blood in ventricle at end of ventricular ejection
Stroke volume
EDV-ESV
What can pumped out of heart
Average resting SV= 70ml/beat
Pressure/volume diagram of left ventricle
Volume =x-axis
Pressure = y-axis
Pressure/volume diagram of left ventricle
1- passively feeling the ventricle (no pressure change)
2- Atria contracted (max vol reach 135)—pressure increase slightly
3- Isovolumic ventrical systole (high increase in pressure)—no vol change
4- Ventricular ejection (min vol reach65)
5- ventricular diastole/Isovolumic ventricular relaxation (high pressure decrease)— no vol change
Cardiac output
Vol of blood pumped by one ventricle in a given period of time
HR * SV
Average restingn CO
5L/min
Autonomic innervation of heart
sympathetic
From: Thoracic and Lumbar
To: SA node/AV node/Ventricular myocardium
parasympatethic
From: medulla
To: SA node/AV node
Autonomic effect on SA node
Modulation of heart rate (chronotropic effect)
—parasympathetic or sympathetic
same effect on AV node but SA node will overwrite it
Autonomic effect on Ventricular myocyte
Modulation of contractility (Inotropic effect)
—only sympathetic
*by removing sympathetic, contractility reduces
Chronotropic and inotropic
Are usually together
Chronotropic effect
Sympathetic: NE on Betta1 receptor
Parasympathetic: ACh on M2 receptor
Contraction force formula
HR * Stroke Volume
Contraction force determined by
1- sarcomere length EDV
only true in cardiac not smooth
2- contractibility of muscle
Frank-starling curve
Length-tension relationship
Greater stretch= greater force to contract
Increase EDV factors
1- increase venous retuurn
2- decrease HR — more filling time
Sympathetic effect on ventricular contractility
Sympathetic increase
Less time
Higher HR
Higher contractility
Increase stroke volume
SNS on myocyte contractibility
-Epinephrine and Norepinephrine
-Bind to Betta1 receptors
-Activate cAMP (GS) secondary messenger
-Result in
phosphorylation of voltage gated Ca channels
phospholamban
Phosphrylation of voltage gated ca channels
cAMP activate PKA
Voltage Ca channels opening time increase
Higher Ca entry from ECF
More CA released/Ca store in SR
More forceful contraction
Phosphorylation of phospholamban
Higher Ca-ATPase on SR:
1.1- Ca store in Sr
1.2- Ca more release
more forceful contraction
2.1- Ca removed from cytosol faster
2.2- Shorter Ca-troponin binding time
shorter duration of contraction
