3.1.1 - cardiac output - physiology

cardiac output

volume of blood ejected from each ventricle of the heart per minute

• Q (L/min) = SV (mL/beat) x HR (beats/min)

• typical adult male at rest Q: 5.25 L/min

• total blood volume: 5 L

• exercise: increases to supply working tissues with oxygen nutrients

stroke volume

volume of blood ejected by the left ventricle during each contraction

• multiplied by HR to get cardiac output

• equal to the difference between the end diastolic volume and the end systolic volume

• does not stay constant — increases and decreases to meet body demands

• can fall due to damaged ventricular myocardium or bleeding out

heart rate

SA node generated an action potential in the right atrium → the number of heart beats per minute

• multiplied by stroke volume to get cardiac output

• “normal textbook ___": 70-75 beat/min

• Ex: same size people, one being highly trained and one is couch potato — resting __ is the same in both, but highly trained athletes have lower __

  • left ventricle is thicker and the heart doesn’t need to beat as often at rest

cardiac reserve

difference between a person’s maximum cardiac output and cardiac output at rest

• avg is 4-5x the resting volume

• higher in athletes: 7-8 times resting Q and will outperform a non-athletic person

• exercise draws on this — heart pumps more blood per beat, so do not need to beat as often

• HR reaching 160 bpm then drops off

• reduced in individuals with severe heart disease and limits ability to carry out daily tasks

stroke volume factors

1) preload

2) myocardial contractility

3) afterload

preload

degree of stretch on the heart before it contracts (ventricular filling/end diastolic volume)

• a greater stretch on cardiac muscle fibers increases their force of contraction during systole (frank-starling law of the heart) — equilizes output of ventricles

• EDV: 120 mL — volume of blood filling ventricles at end of diastole (higher EDV = more forceful contraction)

• a more filled ventricle allows for more wall stretching

• higher stretch = higher stroke volume

• beat by beat equalizer

end diastolic volume (EDV)

determined by:

1) filling time: duration of ventricular diastole

2) venous return: volume of blood returning to right ventricle

• when HR increases, filling time is shorter → smaller ___ → lower preload

• venous return increases → greater volume of blood to ventricles → EDV incresades

frank-starling law of the heart (frank-starling)

manifests the length-tension relationship for cardiac muscle since EDV influences length of sarcomeres before contraction begins

• equilizes output of ventricles — same volume of blood flowing in 2 circulations, alters amt if one side is pumping more

• cardiac muscle: resting sarcomeres held at shorter length then optimum — thin filaments on both side overlap and reduce interaction b/t thick and thin filaments

• low amount of tension during contraction

• increased EDV causes stretch → sarcomeres closer to optimal lengths and greater tension → increase stroke volume

• zone of overlap is ideal and fibers can develop max tension

myocardial contractility

forcefulness of contraction of individual ventricular muscle fibers at a given preload

• positive inotropic effect: increase contractility → increase stroke volume

• negative inotropic effect: decrease contractility → decrease stroke volume

positive inotropy

agents that increase contraction and stroke volume

• increases SNS, hormones (epi, nore), increased Ca2+ levels, drugs

• enhance contractility by increasing amount of Ca2+ in sarcoplasm during cardiac APs

negative inotropy

agents that decrease contraction and stroke volume

• inhibiting SNS, excess H+ ions, increases ECF K+ levels, calcium channel blocker drugs (inhibit opening L-type voltage-gated Ca2+ channels and reduce Ca2+ influx)

afterload

pressure that must be exceeded before ejection of blood from the ventricles can occur

• ejection begins when pressure in RV exceeds pressure in pulmonary trunk (20 mmHg), and when LV exceeds pressure in aorta (80 mmHg)

• higher pressure in ventricles cause blood to push SL valves open (the pressure needed to be overcome before it opens)

• blood mores from high to low pressure — pressure gradient

• opening of aortic valve depends on compliance and total systemic vascular resistance

• increase ___ → decreases stroke volume so more blood in ventricles

• high __ → heart pumps harder to push blood

• conditions increasing include hypertension and artherosclerosis

heart rate factors

factors altering HR have chronotropic effects

1) autonomic NS

2) chemical regulation

• also age, gender, physical fitness, and body temperature

autonomic NS

sympathetic: cardiac accelerator nerve innervates SA and AV node and ventricles

• increase HR, conductivity from atria to ventricles, and force of contraction

• positive chronotropy

• thoracic spinal cord → trunk ganglia → extends to both nodes in atria AND ventricles

parasympathetic: vagus nerve innervates SA and AV node

• decrease HR and conductivity

• negative chronotropy

• brain nerve → goes to nodes only

chemical regulation

hormones: released during exercise, stress, and excitement

• norepinephrine, epinephrine, thyroid hormones

• positive chronotropy and force of contraction

ions: alterations in IC and EC concentrations of K+, Na+, Ca2+

• positive: increased EC Ca2+ → increase heart rate

• negative: increased blood K+, increased blood Na+