Cardiovascular Physiology: Heart

Cardiac Cycle
 The Cardiac Cycle

Cardiac cycle = the period between the start of

one heartbeat and the beginning of the next
Consists of systole + diastole

Systole=contraction

Diastole=relaxation
 The Cardiac Cycle

 Correlate the EKG with systole + diastole

of the heart
 Electrical events occur before mechanical
contraction
 EKG animation

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 The Cardiac Cycle
Atrial Cardiac Cycle
1.Atria passively fill (end of diastole)
2.Atria isovolumetrically contract (start of systole)
3.Atria eject blood into ventricles (end of systole)
4.Atria relax (start of diastole)
Ventricular Cardiac Cycle
1.Ventricles passively fill as atria fill and contract (end of
diastole)
2.-4. Same steps as above
The Cardiac Cycle
 Blood Flow and Pressure

 During systole blood pressure increases

 During diastole blood pressure decreases

 Blood flows from high low pressure

 Contractions and valves dictate blood flow

through the heart
 The Cardiac Cycle

 Start at ventricular diastole and left side of

heart (highest pressure values)
 Blood flows from high low pressure
 Contractions and valves dictate blood flow

 Blood pressure in each chamber rises during

systole and falls during diastoles
 Isovolumetric Ventricular
contraction ejection

Atrial contraction Isovolumetric relaxation

Ventricular filling Ventricular filling

Systole
Left atrium
Right atrium Early diastole
Mid-to-late
Right ventricle diastole
Left ventricle
Phase 1 2 3 4 1
Atrioventricular valves Open Closed Open
Aortic and pulmonary Closed Open Closed
(semilunar) valves
110
Pressure (mm Hg)
Aortic pressure

70
Ventricular
Atrial pressure
40
pressure

0
130
volume (mL)

100
Ventricular
volume
60

Heart sounds

Electrocardiogram

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 The Cardiac Cycle
1. Ventricular Filling (Phase 1 on diagram)
 Blood relaxed atria atrioventricular valves ventricles
 Driven by pressure in veins (venous return)
 Atria contract more blood in ventricles atria diastole
 and ventricular systole begins

2. Isovolumetric Contraction (Phase 2)

 Ventricles start to contract (systole)
 Ventricular pressure > atrial pressure  AV valves close
 Semilunar valves are closed because ventricular pressure <
pulmonary + aortic arterial pressures
 So, no blood flowing=isovolumetric-same volume
 The Cardiac Cycle
3. Ventricular Ejection (Phase 3)
 Ventricles continue contracting
 Ventricular pressure > aortic pressure
 Blood aorta + pulmonary arteries (ventricular ejection)

4. Isovolumetric Relaxation (Phase 4)

 Eventually ventricular pressure < aortic pressure semilunar
valves close—start of diastole
 All valves are closed so some blood is still in ventricles as they
relax
 Ventricular pressure < atrial pressure so AV valves open and
ventricle passively fill with blood until they contract again
 Ventricular Pressure

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 Aortic Pressure

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 Aortic Pressure
 During ventricular contraction the aorta stored
energy by stretching (pressure reservoir)
 During ventricular diastole aorta releases pressure
to maintain blood flow to body
 This is why aortic pressure is higher than
ventricular pressure during diastole
 MAP=profusion pressure to organs
 Dicrotic notch shows semilunar valves closing
 Heart Sounds

**Heart Murmur=sounds produced by regurgitation through valves

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 Changes in Ventricular Volume

** Left ventricle
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 Cardiodynamics

Figure 20–19 A Simple Model of Stroke Volume

 Cardiodynamics
 The movement and force generated by cardiac
contractions
 End-diastolic volume (EDV)
 End-systolic volume (ESV)
 Stroke volume (SV)= volume of blood ejected per beat
 SV = EDV – ESV
 Ejection fraction
 The percentage of EDV represented by SV
 Cardiac output (CO)
 The volume pumped by left ventricle in 1 minute
 CO=SV X HR

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Catecholamines Modulate HR
KEY

Integrating center
Cardiovascular
control Efferent path
center in medulla
oblongata Effector

Tissue response

Sympathetic neurons Parasympathetic

(NE or Epi) neurons (Ach)

1-receptors of Muscarinic receptors

autorhythmic cells of autorhythmic cells

Na+ and Ca2+ influx K+ efflux; Ca2+ influx

Hyperpolarizes cell and

Rate of depolarization
rate of depolarization

Heart rate Heart rate

Catecholamines Modulate SV

Figure 13.29
Stroke Volume & Starling’s Law
Increase EDV by increasing venous return
via:
•Skeletal muscle pump
•Respiratory pump
•Sympathetic nervous system
•Arterial vasoconstriction

Increase stretch of cardiac fibers

Increase strength of contraction

Increase stroke volume

Starling’s Law

Figure 13.28
Green= w/ adrenergic stimulation
Blue= normal
Yellow and red= heart failure; increased volume does not equal increase contraction
and stroke volume
http://cardiovascres.oxfordjournals.org/content/77/4/627/F1.expansion
Stroke Volume and Heart Rate Determine Cardiac Output
CARDIAC OUTPUT

is a function of

Heart rate Stroke volume

determined by determined by

Rate of depolarization Force of contraction in

in autorhythmic cells ventricular myocardium

is influenced by

Decreases Increases increases

Contractility End-diastolic
volume
Sympathetic
Due to innervation and which varies with
parasympathetic epinephrine
innervation
increases
Venous constriction Venous return

aided by

Skeletal muscle Respiratory

pump pump

Figure 14-31
 Arterial Blood Pressure (mm Hg)

Pressure in the aorta varies with the cardiac

cycle.
Two pressure readings:
Systolic blood pressure = maximum pressure
 Due to ejection of blood into aorta
Diastolic blood pressure = minimum pressure
 Not zero due to elastic recoil of aorta
Normal BP 120/80 mm Hg
 Higher than normal= hypertension
 Lower than normal= hypotension
24
Arterial blood pressure

25
Figure 14.8
Blood pressure values: what do they mean?

Pulse pressure (PP)= SP-DP

 Force your heart generates when it contracts
 Use SP, DP, and PP as indicators of cardiovascular health
 Patient 1: 120/80; PP=?
 Patient 2: 140/100; PP=?
 Who is at greater risk?

MAP = DP + 1/3 (SP-DP)

 Pressure required to profuse brain, coronary arteries, and
kidney with blood
> 60 mm Hg

CO = MAP
TPR
CO = SV x HR 26