Principles of Cardiac Output Flashcards
cardiac output (CO)
the amount of blood pumped by each ventricle per minute
stroke volume (sv)
the amount of blood pumped by each ventricle per beat
- correlates with strength of ventricular contraction
- typically about 70mL
solving for co
heart rate (HR) x stroke volume (SV)
- the entire human blood supply passes each side of the heart per minute
- co will increase if either HR or SV increases (and vice versa)
cardiac reserve
the difference in resting CO and maximal CO
- typically 4-5x resting CO (20-25L/min)
- in a highly trained athlete, maximal CO can be as much as 7x resting CO (35L/min)
solving for sv
edv - esv
EDV
typically ~120mL
- depends on how long ventricular diastole lasts and what venous pressure is
ESV
typically ~50mL
- depends on arterial pressure and the force of ventricular contraction
ejection fraction
each ventricle pumps about 60% of its blood with each contraction
factors regulating stroke volume
- preload
- frank-starling law
- contractility
- after load
- hypertension
preload
the degree to which muscle cells are stretched before contraction
- higher preload = higher SV
frank-starling law
a length tension relationship - cardiac muscle cells are stretched to their optimal length for maximal contraction
- a higher EDV will breed higher SV
- increased venous return - such as through exercise, with activity of the SNS, or increased filling time, will increase preload
- a low venous return might occur after blood loss or with tachycardia (fast heart rate)
contractility
the contractile strength achieved at a given muscle length
- will increase with rises in ca2+ - either from extracellular fluid or the sarcoplasmic reticulum
increased contractility
will increase SV and decrease ESV
increased SNS activity
increases contractility
epinephrine and norepinephrine’s effect on contractility
increase ca2+ entry and increase cross bridge cycling
positive ionotropic agents
increase contractility
- epinephrine, norepinephrine, thyroxine, glucagon, high levels of extracellular ca2+, and the drug Digitalis
negative ionotropic agents
decrease contractility
- acidosis, rising extracellular k+ levels, and the ca2+ channel blocker class of drugs (AmIodipine, cardizem)
afterload
the pressure the ventricles must overcome to eject blood
- “back pressure” on the aortic and pulmonary valves
- typically ~80 mmHg in the aorta and ~10 mmHg in the pulmonary trunk
hypertension (HTN)
(high blood pressure) increases afterload - the ventricles will have to work harder to eject blood
- ESV increases, SV decreases
regulation of heart rate
when blood volume decreases or the heart is weakened, heart rate must increase to maintain cardiac output
positive chronotropic agents
things that increase heart rate
negative chronotropic agents
things that decrease heart rate
regulation of heart rate by SNS
- Emotional and physical stressors activate the SNS – epinephrine is released, the SA Node depolarizes more rapidly
- SNS also increases heart contractility and speeds heart relaxation via enhanced Ca2+ movement
- Enhanced contractility lowers ESV so SV doesn’t decline as it typically does with an increased HR
regulation of the heart rate by PNS
- Reduces heart rate, mediated by Acetylcholine
- Acetylcholine hyperpolarizes the membranes of its effector cells by opening K+ channels
regulation of heart rate by ANS
- both the SNS and PNS are continuously sending signals to the heart - typically the PNS predominates - ‘vagal tone’
- when either the SNS or PNS is activated more strongly, the other is inhibited
vagal tone
an impairment of the vagus nerve will increase HR by ~25 bpm (75bpm-100bpm)
atrial (bainbridge) reflex
- an autonomic reflex initiated by increased venous return and increased atrial filling
- stretching of the atrial walls increases heart rate by stimulating the SA node and the atrial stretch receptors
- stretch receptor activation triggers reflexive adjustments of autonomic output to the SA node - increased HR
regulation of heart rate by chemicals
hormones and ions
regulation of heart rate by hormones
- Epinephrine: increases both heart rate and contractility
- Thyroxine: increases heart rate, enhances the effects of epinephrine and norepinephrine
regulation of heart rate by ions
normal heart function depends on normal levels of intra and extracellular ions - electrolyte imbalances can be very dangerous
- hypo/hyper calcemia (ca2+)
- hypo/hyper kalemia (k+)
hypocalcemia
too little calcium
- depresses heart function
hypercalcemia
too much calcium
- stimulates heart function and can increase risk of arrythmia
hypokalemia
too little potassium
- weakens heart contraction
hyperkalemia
too much potassium
- alters the heart’s electrical activity, can increase risk of heart block and cardiac arrest
other factors regulating heart rate
- Age: HR is 140-160 bpm in fetuses then declines
- Gender: HR is typically faster in females
- Exercise: HR increases secondary to activation of the SNS
- BP also increases
- BUT Resting HR will be lower in highly trained athletes – why?
- Temperature: heat increases HR, cold decreases HR
tachycardia
HR 100+ bpm
bradycardia
HR < 60 bpm
imbalances in cardiac output
typically, co and venous return are balanced
- congestive heart failure
congestive heart failure
- secondary to a weakened myocardium, the heart becomes an inefficient pump; circulation is not adequate to meet the tissues’ needs
causes of a weakened myocardium
- coronary atherosclerosis
- HTN
- Multiple MIs
- Dilated cardiomyopathy
coronary atherosclerosis
fat build up clogs coronary arteries, and myocardial cells are starved
HTN
an aortic diastolic BP < 90 mmHg forces the myocardium to work harder to open the aortic valve; chronically elevated afterload and ESV leads to myocardial hypertrophy
multiple MIs
dead myocytes are replaced by noncontractile scar tissue; the pumping efficiency of the heart is reduced
dilated Cardiomyopathy
the ventricles become stretched and flabby, and the myocardium becomes less effective
pulmonary congestion
- Failure of the left side of the heart
- Fluid leaks from pulmonary blood vessels into lung tissue
- Symptom: shortness of breath/dyspnea on exertion
- “Pulmonary Edema”
peripheral congestion
- Failure of the right side of the heart
- Blood stagnates in the organs and tissues
- Symptom: swelling in the distal extremities
- “Peripheral Edema”
