Download Phases of the Cardiac Cycle Atrial systole begins: Atrial

Phases of the Cardiac Cycle
a) Atrial systole begins: Atrial contraction forces a small amount of additional blood into
relaxed ventricles
b) Atrial systole ends and atrial diastole begins
c) Ventricular systole- first phase: Ventricular contraction pushes AV valves closed but
does not create enough pressure to open semilunar valves
d) Ventricular systole- second phase: As ventricular pressure rises and exceeds pressure in
the arteries, the semilunar valves open and blood is ejected
e) Ventricular diastole- early: As ventricles relax, pressure in ventricles drops; blood
flows back against cusps of semilunar valves and forces them closed.
f) Ventricular diastole- late: All chambers are relaxed. Ventricles fill passively.
Blood Flow through the heart
 IVC/SVCRight AtriumTricuspid Valve Right Ventricles Semi-Lunar Valve of
Pulmonary ArteryPulmonary Arteries Lungs Pulmonary Veins Left Atrium
Bicuspid Valve Left VentricleSemi-Lunar ValveAortaBodyIVC/SVC
(Repeat)
*Sings*Just Keep Swimming! Just Keep Swimming!*Sings*
Normal Heart Sounds:
 S1
o “Low rumbling” sound caused by closure of the mitral and tricuspid valves
o Occurs at beginning of ventricular systole
 S2
o Caused by closure of the aortic and pulmonic valves
o Occurs at the end of ventricular systole
Effect of Inspiration on Heart Sounds:
 Inspiration causes more space in the thoracic cavity, this means less pressure on the IVC
and SVC.
Possible Pathology:
 S3
o Low intensity rumble in early diastole, just after the opening of the AV valves
during the rapid filling of the ventricle.
o Is produced by rapid filling of a dilated ventricle (i.e. systolic heart failure,
valvular regurgitation, etc)
o Common in children, but usually pathologic in adults
 S4
o Low frequency sound in late diastole and is coincident with atrial contraction
during the last part of the filling phase
o Produced when atrium contracts against and tries to fill a non-compliant ventricle
(i.e., stiff ventricle) as occurs with ventricular hypertrophy
o S4 is NOT audible is healthy adults
o Fairly common in older people as ventricular compliance  with age
Preload:
 The amount the sarcomere is stretched prior to contraction
 Clinical assessment of preload?
o End-diastolic volume
o End-diastolic pressure
o Right atrial pressure
o Central venous pressure
Starlings Law of the heart Increasing venous return and ventricular preload leads to an increased stroke volume
Factors Effecting Preload:
 Atrial Contraction
 Venous Pressure
 Ventricular Compliance
 Heart Rate
Side Note: Decreased Compliance leads to decreased stretch of the heart. As per Frank Starlings
Law this means less force of contraction. With less force of contraction there will be a greater
end systolic volume which will cause a decrease stroke volume. Since CO = Stroke Volume X
HR a decreased Stroke Volume means decrease in overall cardiac output. I think that’s what he
was getting to with slide 18? Confusing?
Afterload:
 The force against which the ventricle must work to eject blood into the arteries
 Clinical assessment of afterload?
o Systolic arterial pressure
 One way to estimate this is to estimate wall stress. Wall stress in proportional to
intraventricular pressure and its radius (assume sphere) and inversely proportional to wall
thickness x 2
 Thus, and increase in radius of ventricle or intraventricular pressure increases wall stress
or afterload while an increase in wall thickness decreases wall stress or afterload.
Contractility (Inotropy):
 the ability of cardiac muscle to develop force, independent of preload or afterload
 Clinical assessment of contractility?
o Rate of rise of LVP during isovolumic contraction
o Doppler estimates myocardial shortening velocity
o Doppler estimates blood ejection velocity through aortic valve
 Caused by cellular mechanisms that regulate actin/myosin interaction, sympathetic
regulation:
o L-type Ca2+ channel phosphorylation
o  Ca2+ release
o Phosphorylation of SERCA
  Ca2+ sequestration in SR
  Ca2+ clearance from sarcoplasm
Factors that Increase Inotropy
 Catecholamines
o Cardiac Sympathetic Nerves
o Adrenal Catecholamines
 Bowditch/Treppe Effect
 Positive Inotropic Agents (Digoxin)
Factors that Decrease Inotropy
 Beta Adgrenergic Antagonist
 Calcium Channel Blockers
Drugs in the setting of an Myocardial Infarct

Remember the saying MONA-B (Morphine, Oxygen, Nitroglycerin, Asparin, Beta
Blocker)
 Oxygen- helps out with an increased myocardial oxygen demand
 Morphine- reduces pain (and preload/afterload)
 Nitroglycerin- Reduces Preload/Afterload
 Beta Blockers- Reduces Heart Rate
Conclusion:




 wall stress =  O2 consumption
Remember that wall stress is an index of afterload
Changes in stroke volume have a smaller effect on MVO2 than changes in heart rate, inotropy or
afterload
Know what causes change in CO through SV, and HR.
Equation Page
Stroke volume = End Diastolic volume – End Systolic volume


Normal SV : 70 ml
On average, RVSV = LVSV
Ejection fraction = Stroke volume / End diastolic volume
Or
Ejection Fraction =( (End Diastolic Volume-End Systolic Volume)/End Diastolic Volume) X 100


Normal Resting EF: 55 to 65 %
Ejection fraction is an indicator of ventricular contractility
Compliance= ∆ Volume/ ∆Pressure
Wall Stress (𝝈) = Pressure X Radius/ 2 X Wall Thickness
Myocardial Oxygen Consumption (MVO2) = Coronary Blood Flow X (Coronary Arterial O2 Content
(CaO2)-Coronary Venous Flow (CvO2))
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