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Heart as a Pump
Outline
‡Overview of heart anatomy and function
‡Cardiac cycle
‡Volume-‐Pressure Diagram
‡Cardiac Output and Venous Return
‡Regulation of Cardiac Output
Learning Objectives
•Describe the cardiac cycle by explaining Fig. 9-6
in Guyton and Hall
•Analyze ventricular pumping with a volume ‐
pressure diagram
•Understand cardiac output and venous return
- quantitatively know cardiac output
•Know how cardiac output is regulated - FrankStarling mechanism and autonomic regulation
Cardiovascular System
Note, right side is the right side of the person or
animal.
Two pumps in the heart:
Right side pumps blood through the lungs
Left side through the peripheral organs
Each side has an atrium and a ventricle
Atrium is a primer pump for the ventricle
Ventricle supplies the main pumping force
Heart Anatomy
Atrioventricular valves: tricuspid (right) and mitral (left)
Semilunar valves: pulmonary (right) and aortic (left)
Cardiac Cycle
•The cardiac cycle includes the events that
occur from the beginning of one heartbeat to
the beginning of the next
•The cardiac cycle consists of two periods:
- Diastole - period of relaxation when the heart fills
with blood
- Systole - period of contraction
Beginning just after a
ventricular contraction
Semilunar
valves closed
AV valves
opened
Diastole: Passive ventricular filling. The AV valves open and
blood flows into the relaxed ventricles, accounting for most of the
ventricular filling.
Semilunar
valves closed
AV valves
opened
Diastole: Active ventricular filling.
Semilunar
valves closed
AV valves
opened
Diastole: Passive ventricular
filling.
Semilunar
valves closed
AV valves
opened
Diastole: Active ventricular filling. The atria contract and
complete ventricular filling.
Semilunar
valves closed
AV valves
closed
Semilunar
valves closed
AV valves
opened
Diastole: Active ventricular filling.
Systole: Period of isovolumic
contraction.
Semilunar
valves closed
AV valves
closed
Systole: Period of isovolumic contraction. Ventricular contraction
causes the AV valves to close, which is the beginning of
ventricular systole. The semilunar valves were closed in the
previous diastole and remain closed during this period.
Semilunar
valves closed
Semilunar
valves
opened
AV valves
closed
AV valves
closed
Systole: Period of
isovolumic contraction.
Systole: Period of
ejection.
Semilunar
valves opened
AV valves
closed
Systole: Period of ejection. Continued ventricular contraction pushes
blood out of the ventricles, causing the semilunar valves to open.
Semilunar
valves opened
AV valves
closed
Systole: Period of
ejection.
Semilunar
valves closed
AV valves
closed
Diastole: Period of isovolumic relaxation.
Semilunar
valves closed
AV valves
closed
Diastole: Period of isovolumic relaxation. Blood flowing back
toward the relaxed ventricles causes the semilunar valves to close,
which is the beginning of ventricular diastole. Note that the AV valves
closed, also.
Semilunar
valves closed
AV valves
closed
Semilunar
valves closed
AV valves
opened
Diastole: Passive ventricular
filling.
Diastole: Period of
isovolumic relaxation.
Cardiac Cycle in Left Side
Mechanical Events:
The Cardiac Cycle
The Cardiac Cycle
• Cardiac cycle refers to all events associated with
blood flow through the heart from the start of one
heartbeat to the beginning of the next
• During a cardiac cycle
– Each heart chamber goes through systole and diastole
– Correct pressure relationships are dependent on careful
timing of contractions
Phases of the Cardiac Cycle
• Atrial diastole and systole – Blood flows into and passively out of atria (80% of total)
• AV valves open
– Atrial systole pumps only about 20% of blood into ventricles
• Ventricular filling: mid-to-late diastole
– Heart blood pressure is low as blood enters atria and flows
into ventricles
– 80% of blood enters ventricles passively
– AV valves are open, then atrial systole occurs
– Atrial systole pumps remaining 20% of blood into ventricles
Phases of the Cardiac Cycle
• Ventricular systole
– Atria relax
– Rising ventricular pressure results in closing of AV
valves (1st heart sound – “lubb”)
– Isovolumetric contraction phase
• Ventricles are contracting but no blood is leaving
• Ventricular pressure not great enough to open semilunar
valves
– Ventricular ejection phase opens semilunar valves
• Ventricular pressure now greater than pressure in arteries
(aorta and pulmonary trunk)
Phases of the Cardiac Cycle
• Ventricular diastole
– Ventricles relax
– Backflow of blood in aorta and pulmonary trunk
closes semilunar valves (2nd hear sound - “dubb”)
• Dicrotic notch – brief rise in aortic pressure caused by
backflow of blood rebounding off semilunar valves
– Blood once again flowing into relaxed atria and
passively into ventricles
Normal Volume of Blood in Ventricles
•After atrial contraction, 110-120 ml in each
ventricle (end-diastolic volume)
•Contraction ejects ~70 ml (stroke volume
output)
•Thus, 40-50 ml remain in each ventricle (End‐
systolic volume)
•The fraction ejected is then ~60% (ejection
fraction)
Left Ventricle Volume-‐Pressure
Curve
Be able to use these pressure
and volume values
Aortic valve closes
Aortic valve opens
Mitral valve opens
Mitral valve closes
End-systolic volume
End-diastolic volume
Preload and Afterload
•Preload - tension on muscle when it begins to
contract (end-diastolic pressure)
•Afterload - load against which the muscle
exerts its contractile force, which is the
pressure in the artery leading from the
ventricle. Phase III on volume-pressure
diagram
Cardiac Output and Venous Return
•Cardiac output is the quantity of blood
pumped into the aorta each minute.
Cardiac output = stroke volume x heart rate
•Venous return is the quantity of blood flowing
from the veins to the right atrium.
•Except for temporary moments, the cardiac
output should equal the venous return
Normal Cardiac Output
•Normal resting cardiac output:
- Stroke volume of 70 ml
- Heart rate of 72 beats/minute
- Cardiac output ~ 5 litres/minute
•During exercise, cardiac output may increase
to > 20 liters/minutes
•You should be able to get stroke volume and
heart rate from volume-‐pressure curves and
ECG recordings, respectively
Cardiac Output
• Stroke Volume = the vol of blood pumped by
either the right or left ventricle during 1
ventricular contraction.
SV = EDV – ESV
70 = 125 – 55
CO = SV x HR
5,250 = 70 ml/beat x 75 beats/min
CO = 5.25 L/min
Cardiac Output
• Regulation of Stroke volume
• Preload: Degree of stretch of heart muscle (Frank-Starling) –
greatest factor influencing stretch is venous return (see Below)
• Contractility – Strength of contraction
Increased Ca2+ is the result of sympathetic nervous system
A Simple Model of Stroke Volume
Cardiac Output
• Other chemicals can affect contractility:
- Positive inotropic agents: glucagon, epinephrine,
thyroxine, digitalis.
- Negative inotropic agents: acidoses, rising K+, Ca2+
channel blockers.
Afterload: Back pressure exerted by arterial blood.
Regulation of Heart Rate
• Autonomic nervous system
• Chemical Regulation: Hormones (e.g., epinephrine, thyroxine)
and ions.
Regulation of Cardiac Output
• Frank-Starling Mechanism -‐ Cardiac output
changes in response to changes in venous
return.
• Autonomic control -‐ Control of heart rate and
strength of heart pumping by the autonomic
nervous system.
Chemical Regulation of the Heart
• The hormones epinephrine and thyroxine
increase heart rate
• Intra- and extracellular ion concentrations
must be maintained for normal heart
function
Regulation of Stroke Volume
• SV: volume of blood pumped by a ventricle per beat
SV= end diastolic volume (EDV) minus end systolic volume
(ESV); SV = EDV - ESV
• EDV = end diastolic volume
– amount of blood in a ventricle at end of diastole
• ESV = end systolic volume
– amount of blood remaining in a ventricle after contraction
• Ejection Fraction - % of EDV that is pumped by the
ventricle; important clinical parameter
– Ejection fraction should be about 55-60% or higher
Factors Affecting Stroke Volume
• EDV - affected by
– Venous return - vol. of blood returning to heart
– Preload – amount ventricles are stretched by
blood (=EDV)
• ESV - affected by
– Contractility – myocardial contractile force due
to factors other than EDV
– Afterload – back pressure exerted by blood in
the large arteries leaving the heart
Frank-Starling Law of the Heart
• Preload, or degree of stretch, of cardiac muscle cells
before they contract is the critical factor controlling
stroke volume; EDV leads to stretch of myocardium.
– preload  stretch of muscle  force of contraction  SV
– Unlike skeletal fibers, cardiac fibers contract MORE FORCEFULLY when
stretched thus ejecting MORE BLOOD (SV)
– If SV is increased, then ESV is decreased!!
• Slow heartbeat and exercise increase venous return (VR)
to the heart, increasing SV.
– VR changes in response to blood volume, skeletal muscle
activity, alterations in cardiac output
– VR  EDV and in VR   in EDV
– Any  in EDV   in SV
• Blood loss and extremely rapid heartbeat decrease SV.
Frank-Starling Law of the Heart
•
•
Relationship between EDV,
contraction strength, and SV.
Intrinsic mechanism:
– As EDV increases:
• Myocardium is
increasingly stretched.
• Contracts more forcefully.
•
As ventricles fill, the
myocardium stretches:
–
•
•
Increases the number of
interactions between actin and
myosin.
Allows more force to develop.
Explains how the heart can
adjust to rise in TPR.
Figure 14.3
Extrinsic Control of Contractility
• Contractility:
– Strength of contraction at
any given fiber length.
• Sympathoadrenal
system:
– NE and Epi produce an
increase in contractile
strength.
• + inotropic effect:
– More Ca2+ available
to sarcomeres.
• Parasympathetic
stimulation:
– Does not directly
influence contraction
strength.
Figure 14.2
Frank-Starling Mechanism
The force of cardiac muscle contraction
increases as the muscle stretches,
within limits.
Due to more optimal overlap of actin
and myosin filaments during stretch same in skeletal muscle
So, with increase venous return and
increased stretching, the force of
contraction increases and the stroke
volume increases.
Moreover, stretching of the SA node
increasing the firing rate of the pacemaker
(increasing heart rate).
Frank-‐Starling
Summary: within physiological limits, the heart
pumps all the blood that returns to it from the
veins.
Venous return increases when there is an
increase in the blood flow through peripheral
organs. So, peripheral blood flow is a major
determinant of cardiac output
Factors Affecting Stroke Volume
Extrinsic Factors Influencing Stroke
Volume
• Contractility is the increase in contractile strength, independent of stretch
and EDV
• Referred to as extrinsic since the influencing factor is from some external
source
• Increase in contractility comes from:
– Increased sympathetic stimuli
– Certain hormones
– Ca2+ and some drugs
• Agents/factors that decrease contractility include:
– Acidosis
– Increased extracellular K+
– Calcium channel blockers
Effects of Autonomic Activity on
Contractility
• Sympathetic stimulation
–
–
–
–
Release norepinephrine from symp. postganglionic fiber
Also, EP and NE from adrenal medulla
Have positive ionotropic effect
Ventricles contract more forcefully, increasing SV, increasing
ejection fraction and decreasing ESV
• Parasympathetic stimulation via Vagus Nerve -CNX
– Releases ACh
– Has a negative inotropic effect
• Hyperpolarization and inhibition
– Force of contractions is reduced, ejection fraction decreased
Contractility and Norepinephrine
• Sympathetic
stimulation
releases
norepinephrine
and initiates a
cyclic AMP 2ndmessenger
system
Figure 18.22
Preload and Afterload
Figure 18.21
Effects of Hormones on
Contractility
• Epi, NE, and Thyroxine all have positive
ionotropic effects and thus contractility
• Digitalis elevates intracellular Ca++
concentrations by interfering with its removal
from sarcoplasm of cardiac cells
• Beta-blockers (propanolol, timolol) block betareceptors and prevent sympathetic stimulation
of heart (neg. chronotropic effect)
Autonomic Control of Cardiac Output
Sympathetic increases cardiac output
Can increase heart rate 70 to 180-200 BPM
‡
Can double force of contraction
‡
Sympathetic nerves release norepinephrine
Believed to increase permeability of Ca2+ and
‡
Na+.
Parasympathetic (vagal) decreases cardiac
output
Can decrease heart rate to 20-40 BPM
‡
Can decrease force of contraction by 20-30%
‡
Parasympathetic nerves release acetylcholine
Increases permeability to K+
‡
Cardiac Output and Peripheral
Resistance
Increasing the peripheral resistance
decreases cardiac output.
cardiac output =
arterial pressure
total peripheral resistance
Other Factors Affecting Cardiac Output
• Age
• Gender
• Exercise/body temperature