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10 AClJTE CARE HANDBOOK FOR PHYSICAL THERAPISTS

duction can decrease CO (refer to the discussion of rhythm and conduction disturbances in the Pathophysiology section)?

Netlral lnptlt

The SA node has its own inherent rate. Neural input can, however,

influence HR, HRV, and contractility through the autonomic nervous

system.J•s

Parasympathetic system (vagal) neural input generally decelerates

cardiac function, thus decreasing HR and contractility. Parasympathetic input travels through the vagus nerves. The right vagus nerve primarily stimulates the SA node and affects rate, whereas the left vagus nerve primarily stimulates the AV node and affects AV conduction.J,8

Sympathetic system neural input is through the thoracolumbar

sympathetic system and serves to increase HR and augment ventricular contractility, thus accelerating cardiac function.3

Endocrine Input

In response to physical activity or stress, a release in catecholamines

increases HR, contractility, and peripheral vascular resistance for a

net effect of increased cardiac function.' Refer to Table 1-3 for the

cardiac effects of hormones.

Local Input

Tissue pH, concentration of carbon dioxide (C02), concentration of oxygen (02)' and metabolic products (e.g., lactic acid) can affect vascular tone.' During exercise, increased levels of CO2, decreased levels of 02'

decreased pH, and increased levels of lacric acid ar the tissue level dilate

local blood vessels and therefore increase CO distribution to thar area.

Cardiac Reflexes

Cardiac reflexes influence HR and contractility and can be divided

into three general categories: baroreflex (or pressure), Bainbridge

reflex (or stretch), and chemoreflex (or chemical reflexes).

CARDIAC SYSTEM

1 t

Table 1-3. Cardiac Effects of Hormones

Hormone

Primary Site

Stimulus

Cardiac Effect

Norepinephrine Adrenal

Stress/exercise

Vasoconstriction

medulla

Epinephrine

Adrenal

Stress/exercise

Coronary artery

medulla

vasodilation

Angiotensin

Kidney

Decreased arte-

Vasoconstriction,

rial pressure

increases blood

volume

Vasopressin

Posterior

Decreased arte-

Potem vasoconstriaor

pituitary

rial pressure

Bradykinin

Formed by

Tissue damage!

Vasodilation,

polypep-

inflammation

increased capil-

tides in

lary permeabiliry

blood when

activated

Histamine

Throughout

Tissue damage

Vasodilation,

tissues of

increased capil-

body

lary permeability

Atrial natri-

Atria of heart

Increased atrial

Decreased blood

uretic pep-

stretch

volume

tides

Aldosterone

Adrenal

Angiotensin II

Increases blood

cortex

(stimulated) by

volume, kidneys

hypovolemia

excrete more

or decreased

potassium

renal perfusion

Source: Data from AC Guyton.JE Hall. Textbook of Medical Physiology (9th cd). Phil-

adelphia: Saunders, 1996.

Baroreflexes are activated through a group of mechanoreceptors

located in the heart, great vessels, and intrathoracic and cervical

blood vessels. These mechanoreceptors are most plentiful in the walls

of the internal carotid arteries.] Mechanoreceptors are sensory receptors that are sensitive co mechanical changes, such as pressure and Stretch. Activation of the mechanoreceptors by high pressures results

in an inhibition of the vasomotor center of the medulla that increases

vagal stimulation. This chain of events is known as the baroref/ex and

results in vasodilation, decreased HR, and decreased contractility.

12

ACUTE CARE HANDBOOK ';OR PHYSICAL THERAPISTS

Mechanoreceptors located in the right atrial myocardium

respond to stretch. With an increased volume in the right atrium,

there is an increase in pressure on the atrial wall. This reflex,

known as the Bail1bridge reflex, stimulates the vasomOtor center of

the medulla, which in turn increases sympathetic input and

increases HR and contractility.) Respiratory sinus arrhythmia, an

increased HR during inspiration and decreased HR during expiration, may be facilitated by changes in venous return and SV caused by changes in thoracic pressure induced by the respiratory cycle.

At the beginning of inspiration, when thoracic pressure is

decreased, venous return is greater, and therefore there is a greater

stretch on the atrial wall .'

Chemoreceptors located on the carotid and aortic bodies have a

primary effect on increasing rate and depth of ventilation in response

to CO, levels, but they also have a cardiac effect. Changes in CO,

during the respiratory cycle may also result in sinus arrhythmia.3

Coroltary Perfusiolt

For a review of the major coronary arteries, refer to F igure I - I . Blood

is pumped to the large superficial coronary arteries during ventricular

systole. At this time, myocardial contraction limits the flow of blood

to the myocardium; therefore, myocardial tissue is actually perfused

during diastole.

Systemic Circulatiolt

For review of the primary anatomic structures and distribution of

the systemic circulation, refer to F igure ] -4. Systemic circulation is

affected by roral peripheral resistance (TPR), which is the resistance to blood flow by the force created by the aorta and arterial system. Two factors that contribute to resistance are ( 1 ) vasomotor

tone, in which vessels dilate and constrict, and (2) blood viscosity,

in which greater pressure is required to propel thicker blood. Also

called systemic vasClilar resistaltce, TPR and CO influence blood

pressure (BP).3 This relationship is illustrated in the following

equation:

BP = CO xTPR