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Factors that Contribute to Cardiac Output (Stroke Volume (represesnts the…
Factors that Contribute to Cardiac Output
Cardiac Output - the volume of blood per minute pumped out by one ventricle
Cardiac output increases when Heart Rate and/or Stroke Volume increases
CO = HR x SV
Units of mL/min or L/min
Heart Rate
Regulation of Heart Rate
Autonomic Nervous System Regulation of HR: during rest both divisions of the ANS continuously send impulses to the SA node
PNS dominates the autonomic stimulation
PNS Alters the membrane potential to slow the SA Node: acetylcholine hyperpolarizes pace maker cells by opening K+ channel which slowed heart rate.
Heart exhibits a vagal tone: the inherent rate of SA node is 100 beats/minute but is reduced to the sinus rhythm of 75 beats/minute
SNS alters the membrane potential to speed up the SA node: Norepinephrine is released and binds to β1-adrenergic receptors on heart, reducing repolarization and making it easier to depolarize
stimulated by stress, anxiety, excitement, or exercise.
Chemical Regulation of HR
Hormones
Epinephrine - enhances HR and Contractility
Thyroxine produced and released by the thyroid, can cause increased heart rate and enhances norepinephrine and epinephrine.
Ions: proper heart function requires having normal levels of intracellular and extracellular ions, and without them it can pose a real danger to the heart.
Other Factors that regulate HR
Age- HR declines with age
Gender- Women have a faster HR than men
Exercise- Increases HR
Body Temperature- Increased body temp increases HR
Number of times the heart beats per minute (bpm)
Average heart rate of an individual is 75 bpm
Stroke Volume
the volume of blood pumped out by one ventricle with each beat
correlates with the force of ventricular contraction
normal resting value for stroke volume is (70ml/beat)
SV = CO/HR
represesnts the diference between end diastolic volume (EDV), the amount of blood that collects in a ventricle during distole and end systolic volume (ESV), the volume of blood remaining in a ventricle after it has contracted
EDV is determined by how long ventricualt diastole lastsa nd by venous pressure, normall 120 ml
ESV is determined by arterial blood pressure and the force of ventricular contraction , approx. 50 ml
SV = EDV - ESV
Factors affecting Stroke Volume
Preload: "degree of stretch" of cardiac muscle cells before they contract
Venous Return: amount of blood returning to the heart; most important part of preload;
Slow heart rate and exercise increase venous return
blood loss and extremely rapid heartbeat decrease venous return
increased Venous return -> increased EDV -> increased SV -> increased CO
Contractility: the contractile strength achieved at a given muscle length. enhanced contractility means more blood is ejected from the heart = greater SV and ESV is lower
positive inotropic agents Increase contractility
Increased sympathetic Stimuli
Hormones: epinephrine, thyroxine and glucagon
Ca+ which is required for binding to troponin
Norepinephrine increases heart contractility via calcium ion release through a cyclic AMP second messenger system
Negative Inotropic agents decreased contractility
Acidosis
increased extracellular K+
calcium channel blockers
Afterload:the pressure that the ventricles must overcome t o eject blood; the pressure that atrial blood exerts on aortic and pulmonary valves
Healthy People: afterload is not a major determinant of SV because it is relatively constant.
People with Hypertension: afterload reduces the ability of the ventricles to eject blood , which means more blood remains in the heart after systole increasing the EVS and Reducing stroke volume
Created by Emma Armington, Sarah Hershey, Vivian Bui, and Hannah Slaga