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WEEK 20:

Cardiac Function:

QuestionAnswer
formula for cardiac output cardiac output (L/min) = stroke volume (L/beat) x heart rate (bpm)
cardiac output at rest 5L/min = 70mL/beat x 70bpm
cardiac output during exercise 22L/min = 110ml/beat x 200bpm
cardiac output depends on (2) factors affecting heart rate and factors affecting stroke volume
how to measure heart rate (3) pulse oximeter, counting pulses in major arteries (radial, brachial, femoral), and analysis of ECG
pulse oximeter measures automatically beat by beat but can be affected by physical factors eg cold peripheries and does not show character of pulse or regularity/ irregularity
peripheral pulses count number of pulses in 60 secs which allows you to estimate character of pulse and regularity/ irregularity
normal heart rate range 60-100bpm
ECG as a mean of measuring heart rate often detect most common arrhythmias, count number of QRS complexes/R waves in 10secs (so x6 to get HR)
heart rate influenced by (4) SNS, PNS, hormones and extra/intracellular ions (alter membrane potential)
factors affecting heart rate intrinsic rate (SAN and AVN conduction)
stroke volume determined by interaction of (3) preload (volume of blood in ventricles before systole), cardiac contractility (how efficient myocardium is at contracting), and after load (pressure needed for ventricles to contract and open valves)
stroke volume difference between end diastole volume (EDV) and end systolic volume (ESV)
slide 8** factors affecting stroke volume** posture, intrathoracic pressure (breathing in/out), filling time, atrial contractility
Frank Starling Curve force of contraction of cardiac muscle fibres is proportional to degree of stretch (increased stretch EDV means increased force of contraction therefore increased contractility)
cardiac contractility and stroke volume increases and depends on amount of force generated by cardiac muscles which depends on degree of stretch (eg increases if SNS activity increases)
cardiac contractility and stroke volume decreases and depends on hypoxia, acidosis, heart failure, and reduced SNS
increased aortic pressure means increased afterload (pressure needed to contract ventricle) increases which will reduce stroke volume at constant preload
velocity of ventricular contraction at fixed length is greatest when afterload is low (as needs less pressure and therefore effort to contract)
slide 13-16 relationship between stroke volume, pressure and volume graph** LV pressure mmHg on Y axis and LV volume ml on X axis
explain the stroke volume graph**
increased EDV (preload)/ increased cardiac contractility leads to increased stroke volume
increased aortic pressure (afterload) leads to decrease in stroke volume
Created by: kablooey
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