PHG 216 / 231

Introductory Cardiovascular and Respiratory

Systems
CARDIOVASCULAR PART
By
Dr. A. A. ADEJARE
Department of Physiology
Faculty of Basic Medical Sciences
College of Medicine of the University of Lagos
Email: aadejare@unilag.edu.ng
 Cardiac output
• CO is defined as the volume of blood pumped by each ventricle into the aorta per
minute.
• It is also the volume of blood flowing through either the systemic or the pulmonary
circuit per minute.
• determined by multiplying the heart rate (HR)—the number of beats per minute— and
the stroke volume (SV)—the blood volume ejected by each ventricle with each beat:
• CO = HR x SV
• Thus, if each ventricle has a rate of 72 beats/min and ejects 70 ml of blood with each
beat, the cardiac output is:
• CO = 72 beats/min x 0.07 L/beat = 5.0 L/min (men 5.6, women 4.9)
 Variations in CO

• A. Physiological variations
• 1. Age: less in children
• 2. sex: less in females
• 3. body size: greater in huge individuals
• 4. Diurnal variations: low in the morning
• 5. environmental temperature: increase >30⁰C affects CO
• 6. emotional conditions: anxiety increases CO
• 7. level of body metabolism: increases after meals
• 8. increases during exercise
• 9. high altitude: increased by hypoxia
• 10. decreases when body is shifted from recumbent to upright positions
• 11. pregnancy: increases 7-9months
• 12. sleep; decreases during sleep
• B. Pathological variations
• 1. Fever: increases CO
• 2. Anemia: decreases CO
• 3. Hyperthyroidism: increases CO, hypothyroidism reduces it
• 4. atrial fibrillation: decreases CO
• 5. Heart failure decreases CO
• 6. Shock decreases CO
• 7. Hemorrhage decreases CO
• Conditions in which CO is pathologically low
• A. cardiac factors
• (1) severe coronary blood vessel blockage and consequent myocardial infarction,
• (2) severe valvular heart disease,
• (3) myocarditis,
• (4) cardiac tamponade,
• (5) cardiac metabolic derangements.
• B. peripheral factors
• (6) decreased blood volume
• (7) acute venous dilation
• (8) obstruction of the large veins
• (9) Decreased tissue mass, especially decreased skeletal muscle mass
 Regulation of CO
• A. Cardiac factors
• 1. Force of contraction of the heart
• 2. Heart rate
• B. Peripheral factors
• 3. Venous return
• 4. Peripheral resistance
 1. Force of contraction of the heart (Frank-Sterling law of the heart)

• States that the force of contraction of the heart is directly proportional to the
initial length of muscle fibers before the onset of contraction.
• This force depends on:
• 1. Preload: which is the stretching of the cardiac muscle fibers at the end of
diastole just before contraction
• 2. changes in the magnitude of sympathetic nervous system input to the
ventricles; and
• 3. Afterload: is the force against which the ventricles must contract and eject the
blood.
• The afterload for left ventricle is determined by the aortic pressure.
• Afterload is inversely proportional to the force and CO
 EDV (preload): Control of stroke volume
• a more forceful contraction can produce an increase in stroke volume by causing
greater emptying. Changes in the force of contraction can be produced by the
three factors,
• Mechanism: the greater the end-diastolic volume, the greater the stretch, and the
more forceful the contraction.
 1. EDV (preload)
• Reason: The normal point for cardiac muscle in a resting individual is not at its
optimal length for contraction, as it is for most resting skeletal muscles, but is on
the rising phase of the curve. For this reason, additional stretching of the cardiac
muscle fibers by greater filling causes increased force of contraction.
• Thus, an increase in the venous return—the flow of blood from the veins into the
heart—automatically forces an increase in cardiac output by increasing end-diastolic
volume and thus stroke volume.
• Importance: to balance blood volume in the two circulations
 2. Sympathetic nerve stimulation
• Increased ionotropy and dromotropy
• Effect is independent of a change in end-diastolic ventricular volume
• increased contractility leads to a more complete ejection of the end-diastolic ventricular
volume.
• Increased contractility causes an increased ejection fraction (defined as the ratio of
stroke volume (SV) to end-diastolic volume (EDV))
• EF = SV / EDV (50-75%)
 Sympathetic effects
• Increased sympathetic stimulation also
causes both the contraction and relaxation of
the ventricles to occur more quickly
• Mechanism:
• (1) opening more plasma-membrane calcium
channels during excitation;
• (2) stimulating active calcium pumping into
the sarcoplasmic reticulum; and
• (3) altering the binding of calcium by
troponin.
 3. Afterload (aortic pressure to pump against)
• An increased arterial pressure tends to reduce stroke volume
• the arterial pressure constitutes the “load” for contracting ventricular muscle.
• The greater this load, the less the contracting muscle fibers can shorten
• Factors that can cause hyper-
effectivity of the heart
• 1. nervous stimulation
• 2. hypertrophy of the heart muscle
• Factors that can cause hypo-
effectivity of the heart
• 1. inhibition of nervous excitation
of the heart
• 2. pathological factors: arrhythmia,
valvular heart diseases,
hypertension
• 2. Heart rate:
• SNS increases
• PNS decreases
• The HR maintains the ABP when the VR and CO increase
 Control of heart rate
• Parasympathetic reduces HR (pronounced at rest): decreases the slope of the
pacemaker potential by decreasing the If(sodium) and T-type calcium currents. This
causes the SAnode cells to reach threshold less rapidly and the heart rate to
decrease, decrease conduction velocity
• hyperpolarizes the plasma membrane of SA node cells by increasing the
permeability to potassium. The pacemaker potential thus starts from a more
negative value (closer to the potassium equilibrium potential).
• Sympathetic increases HR: increases the slope of the pacemaker potential by
increasing the If(sodium) and T-type calcium currents. This causes the SAnode
cells to reach threshold more rapidly and the heart rate to increase. Increase
conduction velocity
• Epinephrine increases heart rate
• Body temperature, plasma electrolyte concentration, hormones
 3. Venous return
• VR depends on
• 1. Respiratory pump: is the respiratory activity that helps return of the blood back to
the heart during inspiration. There is increased VR during inspiration and reduced
VR during expiration.
• 2. Muscle pump: is the muscular activity that helps return of the blood back to
heart. During skeletal muscle contraction, proximal valves open while distal valves
close.
• 3. Gravity: causes venous pulling and reduction in VR
• 4. Venous pressure: venous gradient from the veins (12-18mmHg) to the RA
(<4mmHg) affects VR
• 5. Vis-a-Tergo: residual force of propulsion from the LV
• 6. Vis-a-fronte: force of thoracic aspiration during inspiration
• 7. Sympathetic tone: VR is aided by the vasomotor tone ie venoconstriction
 4. Peripheral resistance
• PR is the load against which the heart has to pump the blood. The resistance is
offered at the arterioles.

• Increases in PR only alters the CO to maintain the ABP ie under most normal
conditions, the long term CO level varies reciprocally with changes in PR
• Conditions in
Applied physiology
which CO is
pathologically
high via low TPR
• Beriberi
• Arteriovenous
fistula (shunt).
• Hyperthyroidism
• Anemia
Summary of factors determining CO
 MEASUREMENT OF CO
• 1. By direct methods: using
• A. cardiometer
• B, flowmeter
• 2. By indirect methods
• A. Using Ficks principle
• B. indicator dilution method
• 3. thermodilution technique
• 4. Esophageal Doppler transducer technique
• 5. Doppler echocardiography
• 6. ballistocardiographic method
• 7. Radionuclide ventriculography