Cardiac Output

Cardiac Output

Chronotropic Effects of Nervous System

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Cardiac Output
Amount ejected by each ventricle in one min
Cardiac Output (CO) = Heart Rate (HR) x
Stroke Volume (SV)
About 5 L/min at rest
vigorous exercise increases CO to 21 L/min for fit
person and up to 35 L/min for world class athlete
(4-7x increase)

Cardiac reserve: difference between a

persons maximum and resting CO
Increase with fitness, decrease with disease
19-2

Heart Rate
Pulse: surge of pressure in artery
HR measured by recording pulse of artery close
to surface

Tachycardia: resting adult HR > 100 bpm

stress, anxiety, drugs, heart disease or elevated
body temperature

Bradycardia: resting adult HR < 60 bpm

in sleep and response to hypothermia

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Chronotropic Effects
Chronotropic factors change heart rate

Positive chronotropic agents: increase HR

Negative chronotropic agents: decrease HR
Cardiac centers of medulla oblongata
an autonomic control center with two neuronal
pools:
o a cardioacceleratory center: stimulatory via
sympathetic nerves (SA node, AV node,
ventricles, and atrial leading to Incrased HR)
o a cardioinhibitory center: inhibitory via
parasympathetic vagus nerve (does not reach

19-4

Sympathetic Nervous System

Sympathetic nerves secrete norepinephrine, which
binds to -adrenergic receptors in the heart
Binding activates the cAMP 2nd messenger system
in nodal cells and cardiocytes
cAMP activates a kinase which activate enzymes
which do the following:

1) open special Na+ channels in plasma

membrane of nodal cells
2) open slow, long-lasting calcium channels in
the plasma membrane of cardiocytes
3) open calcium channels on the SR of
cardiocytes

19-5

Sympathetic Nervous System

In cardiocytes, opening more calcium channels
on cell surface and on SR means more calcium
enters from outside cell and more calcium from
inside SR per unit time

Sympathetic can increase HR up to 230 bpm

Limited by refractory period of SA node
Cardiac output peaks at a HR of 160-180 bpm
At HR greater than 160-180 bpm, the ventricles
do not have sufficient time to fill between
contractions
At higher HR, SV and CO decrease

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Parasympathetic Nervous System

Cardioinhibitory center via vagus nerves
affect SA and AV nodes
Cholinergic, inhibitory effects

Secretes acetylcholine (ACh) which binds to

muscarinic receptors on nodal cells: opens K+
channels
nodal cells hyperpolarized as K+ exit

depolarize less frequently: HR slows

Vagus nerves act faster on heart than sympathetic

nerves
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Inputs to Cardiac Centers

Cardiac centers in medulla integrate stimuli
from cerebral cortex, limbic system, hypothalamus
sensory or emotional stimuli (e.g., love, stress and anger)
can increase HR

The medulla cardiac centers also receive input and

integrate it from receptors in the muscles, joints,
arteries, and brainstem.
Proprioceptors
inform cardiac centers about changes in activity, increase
in HR before metabolic rate increases

19-9

Inputs to Cardiac Centers

Baroreceptors (pressure sensors)
send a constant flow of information to the cardiac centers on
heart rate and blood pressure
aortic arch, internal carotid arteries, large veins, pulmonary
vessels and heart wall

A negative feedback loop exists called a baroreflex which

helps keep BP approximately constant.
BP , signal firing rate to medulla increases, decrease
sympathetic output, increase parasympathetic output, HR
BP , signal firing rate to medulla decreases, increase
sympathetic output, decrease parasympathetic output, HR
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Inputs to Cardiac Center

Chemoreceptors
aortic arch, carotid arteries (peripheral) and medulla
oblongata (central)
sensitive to blood levels of pH, CO2 and oxygen
main role is to adjust respiration rate but affect heart rate
CO2 (hypercapnia) causes H+ levels, may create
acidosis (pH < 7.35)
hypercapnia and acidosis signal medulla to increase HR

hypocapnia and above normal pH signal medulla to

decrease HR

19-11

Inputs to Cardiac Center

Chemoreceptors
chemoreflex which is a negative feedback loop which
keeps blood chemical levels constant by varying cardiac
output and blood flow
For normal systemic BP, increasing CO2 and acid levels in
tissues or in brain requires increased perfusion rate and
respiration rate for removal of CO2 and acid from tissues
and blood.
Thus, ventilation rate in lungs increases and, for constant
TPR, HR increases, which increases CO.
hypoexmia leads to reduced heart rate
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