Regulation of cardiac activity

Cardiac output

Blood flow

Blood pressure
Cardiac output= stroke volume X cardiac rate

(ml/min) (ml/beat) (beats/min)

At 70 beats/min and 80 ml/beat, this comes to

about 5.5 liters per minute—

Equivalent to the total blood volume

Regulation of cardiac rate

Rhythm is set by the SA node

Sympathetic nerves
epinephrine and norepinephrine
stimulate opening of calcium and sodium
channels; increase cardiac rate

Parasympathetic (vagus) nerves

acetylcholine promotes opening of potassium
channels; reduces cardiac rate
Exercise reduces vagus inhibition and increases
sympathetic nerve activity

Cardiac control center in medulla oblongata

coordinates this activity

This in turn is regulated by higher brain activity

and pressure (baroreceptors) in aorta and
carotid arteries
Regulation of stroke volume

EDV: end-diastolic volume (blood left in ventricles

after diastole)
increase in EDV →increase in stroke volume

Total peripheral resistance to arterial blood flow

stroke volume is inversely proportional
to this (temporarily)

Strength of ventricular contraction

increased as EDV increases)
Frank-Starling law of the heart

Intrinsic variation as EDV increases, so does

force of contraction (increased stretch)

Increased peripheral resistance

↓
Increased EDV
↓
Increased stretch
↓
Next contraction is stronger

Process is highly adjustable

Contractility

Innervation from sympathetic nerves

Raises calcium levels (positive inotropic effect)
Venous return

At rest, most of the blood is in the veins

veins can “give” more and hold more
blood than arteries; venous pressure
is much lower (2 mm Hg vs. 90-100 mm Hg
mean arterial pressure)

Venous pressure determines rate of blood return

to the heart
Blood volume

Extracellular fluid distributed between

blood plasma and interstitial fluid

Affected by:
forces acting at capillaries (to draw
fluid out of or into them)

overall balance of water loss and gain

Exchange of fluid between tissues and capillaries

Glucose and various other solutes are passed

to tissues as well; balance is achieved

Movement of plasma proteins is restricted (oncotic

pressure)
osmotic pressure is higher in capillaries

Starling forces favor movement of water out of

capillaries and back into venules
exchange is continuous
some of the fluid is returned to lymph
(about 15%) and eventually to circulation
Edema- excessive fluid in tissues

Causes:
high blood pressure
venous obstruction
leakage of plasma proteins into tissue
fluid (as in inflammation)
kidney or liver disease leading to protein
loss or lack of formation
obstruction of lymphatic vessels
(filiarisis)
myxedema- increased secretion of proteins
into extracellular matrix
Regulation of blood volume by kidneys

Filtration of blood- almost all of filtrate is

reabsorbed by the kidneys

(out of daily production of ca. 180L of filtrate,

only about 1.5 L actually excreted)

Various hormones acting on, or produced by,

the kidneys
ADH (antidiuretic hormone; vasopressin)

Increase in plasma osmolality- osmoreceptors

in hypothalamus
↓
posterior pituitary releases ADH

Also triggers sensation of thirst (osmoreceptor)

Why does this happen?

dehydration
excessive salt intake

More water is reabsorbed, less is excreted

Aldosterone

reabsorption of salt (Na) by kidney

water is reabsorbed too
no dilution effect as with ADH because
both water and salt are retained

secreted by adrenal cortex

activated through renin-angiotensin-
aldosterone system

salt intake tends to inhibit renin secretion

ANF- atrial natriuretic factor

Produced by atria in response to high

blood pressure

Promotes water and salt excretion

Also antagonizes effects of angiotensin II

(therefore reduces aldosterone production
and promotes vasodilation)
Resistance to blood flow

Related to pressure difference between the ends

of the vessel

Inversely related to resistance of blood flow

through vessel

In body, vasodilation in one organ system might

be offset by vasoconstriction in another
Regulation of blood flow

Sympathetic nervous system

overall, increase in cardiac output and in
peripheral resistance

vasoconstriction in arterioles of viscera

and skin

vasodilation in skeletal muscles

(depends on receptors)

Parasympathetic- vasodilation effect confined

to GI, genitalia, salivary glands
Paracrine regulation, e.g., inflammation

Intrinsic (autoregulation)
myogenic- response to changes in blood
pressure

metabolic-oxygen, carbon dioxide levels

local vasodilation
Regulation of blood flow to the heart

Alpha and beta adrenergic receptors

(constriction and dilation; norepinephrine
and epinephrine)

Also intrinsic regulation

increased metabolic rate- oxygen need,
accumulation of carbon dioxide, etc.
smooth muscle stimulated to cause
relaxation and dilation
How are aerobic requirements of heart met?

Lots of capillaries
Myoglobin releases oxygen during systole
(blood flow is reduced at that time)
capacity for aerobic respiration:
extra mitochondria, enzymes

Blockages in blood supply are corrected by

angioplasty, bypass, etc.
Blood flow through skeletal muscles

High vascular resistance at rest

Blood flow decreases when muscle contracts

Intrinsic metabolic control promotes blood

flow through muscles during exercise

20-25% of total blood flow through muscles

at rest

Up to 85% during exercise

Blood flow to brain

Intrinsic mechanisms maintain constant flow

myogenic responses to changes in blood
pressure
sensitive to CO2 levels in arterial blood

metabolic responses- local vasodilation

Blood flow to skin is highly sensitive to action

of sympathetic nervous system
Blood pressure

Blood flow resistance highest in arterioles

Flow rate lowest in capillaries

Blood pressure can be raised by:

vasoconstriction of arterioles
increase in cardiac output
(higher cardiac rate or stroke volume)

Various factors can affect these: kidneys,

sympathetic nervous system, etc.
Pressure receptors (baroreceptors)

Action potentials will increase or decrease

as pressure rises or falls

Baroreceptor reflex activated when blood

pressure rises or falls. Activated when a
person changes position

Vasomotor control centers- constriction/dilation

Cardiac control centers- cardiac rate

Blood pressure also regulated by:

Atrial stretch receptors

ADH release
Renin-angiotensin-aldosterone
ANF
Measurement of blood pressure
sphygmomanometer

Systolic/diastolic pressure, e.g., 120/80

exercise tends to raise systolic more
changing position tends to affect diastolic

Pulse pressure: systolic- diastolic

reflects stroke volume
drops in dehydration or blood loss

Pulse rate reflects cardiac rate

Mean arterial pressure= diastolic + 1/3 pulse

pressure
Pathophysiology of cardiovascular system

Hypertension
Secondary- results from known diseases
(table 14.10)
processes that affect blood flow; damage
to tissue that results in release of
vasoactive chemicals; damage to sympa-
thetic nervous system, etc.

Essential- accounts for most cases of hypertension

Increased total peripheral resistance

Low renin secretion?

High salt intake?
Stress?

Inability of kidneys to regulation salt and water

excretion?
Consequences of high blood pressure

Can damage cerebral blood vessels and lead

to stroke

Causes heart to work harder (harder to eject

blood if peripheral resistance is high)

Contributes to atherosclerosis

Treatments are many and varied

diet, diuretics, various receptor blockers
Shock due to loss of blood flow
hypovolemic- blood LOSS

septic- blood-borne infection; nitric oxide

formation might be the culprit

anaphylactic- severe allergic reaction

(histamine)

cardiogenic- infarction causes extensive

damage to heart muscle
Congestive heart failure- cardiac output is
inadequate
causes: heart disease, hypertension,
electrolyte imbalance

Digitalis increases contractility of heart muscle

Diuretics lower blood volume

Nitroglycerin is a vasodilator

Make heart work more efficiently; reduce stress

on heart