8/22/2019 Cardiac Physiology1

1/30

Cardiac Physiology(I)

A. Rhan Akar

Ankara University

School of Medicine

December- 2003

8/22/2019 Cardiac Physiology1

2/30

Cardiovascular System

Primary function: convection

mass movement of fluid caused by

pressure difference

Heart- driving force

Arteries- distribution

Microcirculation- exchange

Veins- reservoir

8/22/2019 Cardiac Physiology1

3/30

The Heart

central part of the circulatory system

driving blood through

systemic

(high pressure system)

pulmonary circulations

(low pressure system)

8/22/2019 Cardiac Physiology1

4/30

Left ventricular wall is three timesthicker than right

ventricle

Right ventricle crescent-shaped

Left ventricle- cylindrical

Conducting tissue ( Purkinje fibers) in the septum

Interventricular

septum

RV wall LV wall

8/22/2019 Cardiac Physiology1

5/30

ejects blood primarily by reducing the

cross-sectional area of the cylinder

changes in volume are a function of

changes in the radius squared

area= . r2

Left Ventricle

8/22/2019 Cardiac Physiology1

6/30

volume of blood ejected by

one ventricle per minute

CO = stroke volume x heart rate

~ 5 L = (70-80 ml) x (65-75 beats/min)

Cardiac Output

8/22/2019 Cardiac Physiology1

7/30

Stroke volume Heart rateCO

Sympathetic activity

Parasympathetic (vagal) activity

Catecolamines

Preload

Afterload

Contractility

.=

8/22/2019 Cardiac Physiology1

8/30

Haemodynamics

study of factors that determine blood

flow and blood pressure in the body

8/22/2019 Cardiac Physiology1

9/30

Pressure = force per unit area (dynes/cm2)

1 mmHg = 1.36 cmH2O = 1330 dynes/cm2

8/22/2019 Cardiac Physiology1

10/30

Total energy = Kinetic energy+ Potential energy

Momentum that blood gains

because of its mass (m) and

velocitym . v2

2

Hydrostatic pressure

Lateral pressure

8/22/2019 Cardiac Physiology1

11/30

Flow (Q)

Mass movement of avolume of fluid per unit time

ml/sec

L/min

Continuity principle:flow through each vascular

component must be equal to each other

To keep the flow rate equal, the veloci tyof flow

must vary inversely with the cros s-sect ional area

Narrow segmentrepresents an area of in creased

veloci tywhich results in a Bernoulli effect

(conversion of potential energy into kinetic

energy)

8/22/2019 Cardiac Physiology1

12/30

Poiseuilles Law(for laminar flow)

Q =P . . r4

8 . . L

P= pressure gradient

r= radius of the tube

= viscosity of the fluidL= length of the tube 8 . . L

. r4

Resistan

ce

8/22/2019 Cardiac Physiology1

13/30

Ohms Law

Current (flow) =

Voltage (pressure gradient)

Resistance

8/22/2019 Cardiac Physiology1

14/30

P

R

Law of Flow (Darcy)

flow is proportional to driving pressure

inversely proportional to resistance

Q =

8/22/2019 Cardiac Physiology1

15/30

SVR = P/Q (mmHg/L/min)

1 peripheral resistance unit (PRU) = 1 mmHg/ml/sec

Systemic circulation resistance= 1 PRU

Pulmonary circulation resistance= 0.1-0.2 PRU

8/22/2019 Cardiac Physiology1

16/30

Frank Starling effect

Energy produced by the heartwhen it contracts is a function of the

end-diastol ic leng thof the muscle

fibers

8/22/2019 Cardiac Physiology1

17/30

Direct linear relationship

Tension in an individual fiber

Pressure development in the ventricle

8/22/2019 Cardiac Physiology1

18/30

Frank curve for isolated muscle

8/22/2019 Cardiac Physiology1

19/30

depends volume of blood before contraction(LVEDV)

physiologically determined by the venous

returnwall stress at the end of diastole

LVEDP determines the LVEDV and hencethe resting length of the ventricular musclefibers

Preload

8/22/2019 Cardiac Physiology1

20/30

Frank Starling Increased ventricularend-diastolic volume

and pressure

increases the force of

contraction

The time required to

generate peak

pressure is

unchanged

8/22/2019 Cardiac Physiology1

21/30

Contractility (Inotropism)

increased contractile force at a constant preloador ventricular volume

Activation of1 receptors

Sympathetic nerve stimulation

Epinephrine, norepinephrine

Digitalis

8/22/2019 Cardiac Physiology1

22/30

Contractility alter the

peak force developed

and the duration of thecontractile process

Contractility

8/22/2019 Cardiac Physiology1

23/30

Frank Starling

Ventricular function curve

(venous pressure)

8/22/2019 Cardiac Physiology1

24/30

Contractility @ Maximal velocity of shortening

Positive inotropism can be defined as anincrease in the maximal velocity of shortening

(Vmax)

8/22/2019 Cardiac Physiology1

25/30

Force velocity curve for isolated muscle

(afterload)

8/22/2019 Cardiac Physiology1

26/30

Negative Inotropic Mechanisms

Hypoxia

Acidosis

Myocardial ischaemia or infarct

8/22/2019 Cardiac Physiology1

27/30

The increase in the radius-to-thicknessratio increases wall stress (or afterload)

(maladaptive)

at any given radius (LV size), the greaterthe pressure developed by the LV, the

greater the wall stress

pressure x radius (r)Wall stress (T)=

2 thickness (h)

Law of Laplace

8/22/2019 Cardiac Physiology1

28/30

A practical application of Law of Laplace.

8/22/2019 Cardiac Physiology1

29/30

8/22/2019 Cardiac Physiology1

30/30

V = 4/3r3In a sphere;

Left ventricle has three axes;

Antero-posterior (DA)

Lateral diameter (DL)

Maximal length (LM)

V = 4/3 (DA/2) x (DL/2) x (LM/2)

V= volume

r= radius