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 - Frank- Starling 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

Systole: Period of isovolumic contraction.

Semilunar valves closed

AV valves opened

Diastole: Active ventricular filling.

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

Systole: Period of

Semilunar valves closed

AV valves closed

valves opened

AV valves closed

Systole: Period of isovolumic contraction. 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 – ESV70 = 125 – 55CO = SV x HR

5,250 = 70 ml/beat x 75 beats/minCO = 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 contractionIncreased 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

• 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

Effects of Autonomic Activity on Contractility

Contractility and Norepinephrine

• Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP 2nd-messenger 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 beta-receptors 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