Chapter 14

Cardiac output

volume of blood pumped/min by each

ventricle

Stroke volume (SV)

blood pumped/beat by each

ventricle

Heart rate (HR)

the number of beats/minute

CO = SV x HR

Total blood volume is about 5.5L

Cardiac control center

of medulla oblongata

coordinates activity of autonomic innervation

Norepinephrine and

epinephrine (“adrenaline”)

increase opening of pacemaker

HCN (hyperpolarization-activated cyclic nucleotide) channels

This depolarizes SA node faster, increasing HR

ACh promotes opening of K+

channels

Result: K+ outflow counters

Na+ influx, slowing depolarization and decreasing HR

SA node

Sympathetic nerve effect:

Increased rate of diastolic depolarization, increased cardiac rate

SA node

Parasympathetic nerve effects:

Decreased rate of diastolic depolarization, decreased cardiac rate

AV node

sympathetic nerve effects:

increased conduction rate

AV node

parasympathetic nerve effects:

decreased conduction rate

atrial muscle

sympatetic nerve effects:

icreased strength of contraction

Atrial muscle

parasympathetic nerve effects:

none

Ventricular muscle

sympathetic nerve effects:

increased strength of contraction

Ventricular muscle

p0arasympathetic nerve effect:

none

Stroke Volume

Determined by 3 variables

End diastolic volume (EDV)

volume of blood in

ventricles at the end of diastole which is also called

preload

Total peripheral resistance (TPR)

resistance to

blood flow in arteries which is also called afterload

• Afterload measures as the pressure required for

ventricular ejection

Contractility

strength of ventricular contraction

Preload/EDV

workload on the heart prior to

contraction

• Stroke volume is directly proportional to preload and

contractility (as preload and contractility increase, so

does stroke volume)

Afterload/TPR

impedes (make it harder for) ejection

from ventricle

Ejection fraction

stroke volume / preload

• Normally, EF is 50-70%, average 60%; a useful

clinical diagnostic tool.

• Less than 40% = heart failure, more than 75% =

heart hypertrophy

States that strength of

ventricular contraction

varies directly with

preload/EDV

t’s an intrinsic property of

the myocardium

• As EDV increases,

myocardium is stretched

more, causing greater

contraction and SV

(a) is state of myocardial

sarcomeres just before

filling

Actins overlap, actin-

myosin interactions are

reduced, and contraction

would be weak

In (b, c and d)

increasing interaction of

actin and myosin allowing

more force to be developed

At any given EDV, contraction

depends upon level of

sympathoadrenal activity

Norepinephrine and

epinephrine produce an

increase in HR and

contraction (positive

inotropic effect)

• Due to increased Ca2+ in

sarcomeres

Venous return = return of blood

to the heart via veins

• Controls EDV and thus SV and

CO

Dependent on:

• Blood volume and venous

pressure

• Venoconstriction caused by

sympathetic stimulation

• Skeletal muscle pumps

Blood pressure is controlled mainly by

1. HR

2. SV

3. Peripheral resistance

• An increase in any of these can result in

increased BP

Sympathoadrenal activity raises BP via arteriole

vasoconstriction and by increased CO

Kidney plays role in BP by regulating blood volume

and therefore stroke volume

Blood pressure in excess of normal range for age and

gender

> 120/80 mmHg

Elevated BP

120-129/less than 80

Hypertension stage 1

130-139/80-89

High BP hypertension stage 2

140+/90+

Hypertensive crisis

180+/120+

Hypertension

Afflicts 47% of adults in the U.S.

• Most common type is primary/essential hypertension

• Caused by complex and poorly understood

processes but to do with sodium consumption

Secondary hypertension

Possible Causes of Secondary

Hypertension

• Kidney disease – kidney disease; renal artery

disease

• Endocrine disorder – excess catecholamines;

excess aldosterone

• Nervous system disorder – including intracranial

pressure; damage to vasomotor center

• Cardiovascular disorder – complete heart block;

arteriosclerosis of aorta

Dangers of Hypertension

• Patients are often asymptomatic until substantial

vascular damage occurs

Contributes to atherosclerosis

• Increases workload of the heart leading to

ventricular hypertrophy and congestive heart

failure

• Often damages cerebral blood vessels leading

to stroke

• “Silent killer"

Treatment of hypertension

Often includes lifestyle changes such as

cessation of smoking, moderation in alcohol

intake, consistent exercise, reduced Na+ intake

(less than 5 g daily), eating fruits/vegetables etc

Treatment of hypertension

Drug treatments include diuretics to reduce fluid

volume, beta-blockers to decrease HR, calcium

blockers