Principles of Cardiac Output Study Guide Flashcards
Cardiac Output (CO)
the amount of blood pumped by each ventricle per minute 5-6L/min
Stroke Volume (SV)
the amount of blood pumped by each ventricle per beat
- Correlates with strength of ventricular contraction
- Typically, about ~70mL
equation for CO.
CO = Heart Rate (HR) x Stroke Volume (SV)
- ex: CO = 75 bpm x 70mL/min = 5250mL/min = 5.25L/min
cardiac reserve
the difference in resting CO and maximal CO (typically 4-5x resting CO, but in athletes can be as much as 7x CO)
How do EDV and ESV relate to SV and therefore CO?
EDV - ESV = SV
Bigger SV = bigger CO
typical ejection fraction for a healthy heart
Each ventricle pumps abt 60% of its blood w each contraction 70mL/120mL x 100 = 60%
3 factors that regulate stroke volume
preload, afterload, contractility
Preload
the degree to which muscle cells are stretched before contracting
- Higher Preload = Higher SV
- Preload increases with increased venous return – through exercise w increased SNS activity, and increased filling time
Afterload
the pressure the ventricles must overcome to eject blood, ‘back pressure’ on the aortic and pulmonary valves 80 mmHg in aorta and 10 mmHg in pulmonary trunk
- Hypertension increases afterload - ventricles have to work harder to eject blood
Contractility
the contractile strength achieved at a given muscle length, increases with rises in ca2+ and increased SNS activity
Frank-Starling Law
A length tension relationship – cardiac muscle cells are stretched to their optimal length for maximal contraction
Ionotropic agents
increase contractility
Positive ionotropic agents
Epinephrine, norepinephrine, thyroxine, glucagon, high levels of extracellular ca2+, and the drug digitalis
negative ionotropic agents.
acidosis, rising extracellular K+ levels, and Ca2+ channel blocker class of drugs (amlodipine, cardizem)
Chronotropic agents
increase/decrease heart rate
positive chronotropic agents
epinephrine, thyroxine, hypercalcemia
negative chronotropic agents
hypocalcemia
How to calculate your maximal heart rate
Age - 220
How does maximal heart rate guide your exercise routines?
You want to be in the 50-85% range for exercise, so for example, a 20 year old would subtract 220 from their age (=200) and then aim to have the heart rate be 100-170 bpm
how SNS regulates heart rate
- 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
how PNS regulates heart rate
- Reduces heart rate, mediated by Acetylcholine
- Acetylcholine hyperpolarizes the membranes of its effector cells by opening K+ channels
vagal tone
Both the SNS and PNS are continuously sending signals to the heart – typically, the PNS predominates (lowers heart rate)
- An impairment of the vagus nerve will increase resting HR by ~25 bpm (75 bpm to 100 bpm)
* When either the SNS or PNS is activated more strongly, the other is inhibited
Define the atrial or 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 atrial stretch receptors
- Stretch receptor activation triggers reflexive adjustments of autonomic output to the SA node – increased HR
Epinephrine
increases both heart rate and contractility
Thyroxine
increases heart rate, enhances the effects of epinephrine and norepinephrine
Hypocalcemia
depresses heart function
Hypercalcemia
stimulates heart function and can increase risk of arrythmia
Hypokalemia
weakens heart contraction
Hyperkalemia
alters the heart’s electrical activity, can increase risk of heart block and cardiac arrest
age & heart rate
HR is 140-160 bpm in fetuses then declines
gender & heart rate
HR is typically faster in females
exercise & heart rate
HR increases secondary to activation of the SNS
- BP also increases
- BUT Resting HR will be lower in highly trained athletes
temperature & heart rate
heat increases HR, cold decreases HR
Congestive Heart Failure
weakened myocardium causes the heart tp become an inefficient pump; circulation is not adequate to meet the tissues’ needs
4 ways myocardium can weaken
- Coronary Atherosclerosis: fat clogs coronary arteries
- HTN: an aortic diastolic BP < 90mmHg 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
side of the heart that is failing when peripheral congestion is seen
failure of right side of heart
side of the heart that is failing when pulmonary congestion is seen
failure of left side of heart
Diuretics
increase excretion of Na+,H2O by the kidneys (used to manage heart failure)
Digitalis
increases heart contractility (used to manage heart failure)
4 primitive chambers of the heart and what they become as the heart matures
- Sinus Venosus: receives all venous blood from the embryo – becomes the smooth-walled portions of the atria, the coronary sinus, and the SA node
- Atrium: becomes the pectinate muscle-ridged parts of the atria
- Ventricle: the strongest part of the embryonic heart – becomes the left ventricle
- Bulbus Cordis: has a cranial extension – the truncus arteriosus – becomes the pulmonary trunk, part of the aorta, and most of the right ventricle
gestational age that the fetal heart contracts
22 days
two ways nonfunctional fetal lungs are bypassedand what they become after birth
- Foramen Ovale: a hole in the interatrial septum, a bypass for the lungs – becomes the Fossa Ovalis in adults
- Ductus Arteriosus: a shunt between the pulmonary trunk and the aorta, another bypass for the lungs – becomes the Ligamentum Arteriosum in adults
two classes of congenital heart defects
- Mixing of O2 rich and O2 poor blood – inadequately oxygenated blood reaches the body’s tissues
*Ex: septal defects, patent ductus arteriosus - Narrowed valves/vessels increase the heart’s workload
*Ex: Coarctation of the Aorta - really narrow aorta (heart has to work harder to push blood through)
Tetralogy of Fallot (4)
a serious condition in which cyanosis appears within minutes of birth - encompasses both types of defects
4 features of Tetralogy of Fallot
- narrowed pulmonary trunk/pulmonary valve stenosed
- hypertrophied right ventricle
- ventricular septal defect
- aorta receiving blood from both chambers
Explain how a highly trained aerobic athlete could have a resting HR as low as 30-40 bpm.
The heart becomes more powerful, efficient, and enlarged with vigorous exercise, which means it can pump more blood, and when CO increases, HR increases
