CV Anatomy Review Flashcards
Heart function
creates pressure to pump blood
Purposes of the cardiorespiratory system
Transport O2 and nutrients to tissues
Removal of CO2 wastes from tissues
Regulation of body temperature
Capillaries function
responsible for all exchange of O2, CO2, and nutrients with tissues
Myocardium receives blood via
coronary arteries
Coronary arteries are responsible for
meeting high demand for oxygen and nutrients
Myocardial infarction
blockage in coronary blood flow results in cell damage
Plasma
liquid portion of blood
contains ions, proteins, hormones
Red blood cells
contain hemoglobin to carry oxygen
largest fraction of cells in the blood
White blood cells
Important in preventing infection
Platelets
important in blood clotting
hematocrit
percentage of blood composed of RBC
What percentage of hematocrit is blood?
42%
Systole
Contraction phase
Ejection of blood
How much blood is ejected from ventricles per beat?
2/3
Why does 1/3 blood remain in the ventricle after contraction?
to prevent collapse
keeps structural integrity
Diastole
Relaxation phase
Filling with blood
At rest, which part of the heart cycle is longer?
diastole is longer than systole
During exercise, what happens to diastole and systole?
both are shortened
diastole shortens more
What is normal arterial blood pressure?
<120/<80 mmHg
Systolic pressure
pressure generated during ventricular contraction
Diastolic pressure
pressure in the arteries during cardiac relaxation
Pulse pressure
difference between systolic and diastolic
Mean arterial pressure
Average pressure in the arteries during cardiac cycle at rest
Contraction of the heart depends on
electrical stimulation of the myocardium
Sinoatrial node
SA node
Part of conduction system
pacemaker, initiates depolarization
Atrioventricular node
AV node
Part of conduction system
Passes depolarization to ventricles
Why is there a brief delay between the SA and AV node?
to allow for ventricular filling (blood transfer from atria to ventricle)
Bundle branches
extend from AV node
connect atria to left and right ventricular
Purkinje fibers
spread wave of depolarization throughout ventricles
Parasympathetic nervous system releases Ach on SA node via the
vagus nerve
How does the PNS slow HR?
by inhibiting SA and AV node
Decrease in parasympathetic tone =
increase in HR (this typically causes rise in HR up to ~ 100 bpm)
Sympathetic nervous system releases norepinephrine via
cardiac accelerator nerves
Sympathetic nervous system increases HR by
stimulating SA and AV node (this typically causes rise in HR beyond 100 bpm)
How does HR respond at onset of exercise?
- initial increase due to parasympathetic withdrawal
- later increase due to SNS stimulation
Heart rate variability
how well sympathetic and parasympathetic nervous system are coordinating
standard deviation of the R-R interval on an EKG
Wide variation in HRV…
is considered healthy (reflects “autonomic balance”)
collaboration most of the time
Low HRV is a predictor of
cardiovascular morbidity and mortality in patients with existing cardiovascular disease
Low HRV
SNS or PNS takes precedent most of the time
Cardiac output
the amount of blood pumped by the heart each minute
Cardiac output equation
Q = HR x SV
product of heart rate and stroke volume
Stroke volume
amount of blood ejected in each beat
CO depends on
training state and gender
End-Diastolic Volume
Volume of blood in the ventricles at the end of diastole (aka “preload”), at the end of filling
Frank-Starling mechanism
greater EDV results in a more forceful contraction
- due to stretch of ventricles
EDV is dependent on
venous return
Venous return is increased by
- Venoconstriction
- Skeletal muscle pump
- Respiratory pump
Venoconstriction
increased pressure in veins
Skeletal muscle pump
rhythmic skeletal muscle contractions force blood in the veins toward the heart
What is the function of one-way valves in veins?
prevent backflow of blood
Respiratory pump
breathing puts pressure on veins in thoracic cavity, increases pressure… pushes blood towards the heart
What do changes in thoracic pressure do?
pull blood toward heart
Stroke Volume is dependent on 3 factors
- EDV
- Average aortic blood pressure
- Strength of ventricular contraction (contractility)
Average aortic blood pressure
pressure the heart must pump against to eject blood (“afterload”)
Strength of the ventricular contraction “contractility” is enhanced by:
circulating epinephrine and norepinephrine
direct sympathetic stimulation of the heart
Oxygen demand by muscles during exercise
is 15-25x greater than at rest
Increased O2 delivery during exercise is accomplished by:
- Increased cardiac output
- Redistribution of blood flow
- from inactive organs to working skeletal muscle
CO during exercises increases due to
increased HR (linear increase to max)
increased SV
Max heart rate adult equation
220-age (years)
Increase in SV during exercise
increase, then plateau at 40-60% VO2 max
no plateau in highly trained subjects
Transition from rest to exercise
Rapid increase in HR, SV, CO
Plateau in submaximal (below lactate threshold) exercise
Transition from exercise to recovery
Decrease in HR, SV, and CO toward resting levels
Depends on:
- Duration and intensity of exercise
- Training state of subject (more trained = back to recovery faster)
Regular exercise is cardioprotective, which means
reduces incidence of heart attacks
improves survival from heart attack
Exercise reduces the amount of myocardial damage from heart attack by
improvements in heart’s antioxidant capacity (ability to remove free radicals)
improved function of ATP- sensitive potassium channels
