lecture 15 Flashcards
(26 cards)
the cardiovascular system
four major parts:
1. heart “pump”
2. arteries “outflow conduits”
3. capillaries “drop/pick-up site”
4. veins “return flow conduits”
the heart
four chambers
- right and left atria (RA, LA): top, receiving chambers
- right and left ventricles (RV, LV): bottom, pumping chambers
right heart: pulmonary circulation
- pumps deoxygenated blood from body to lungs
- superior/inferior vena cana —> RA —> tricuspid valve —> RV —> pulmonary valve —> pulmonary arteries —> lungs
left heart: systemic circulation
- pumps oxygenated blood from lungs to body
- lungs —> pulmonary veins —> LA —> mitral valve —> LV —> aortic valve —> aorta
cardiac muscle
- contracts as one single unit, individual cardiac muscle fibers are interconnected end-to-end by intercalated discs
- skeletal muscle (voluntary)
- cardiac muscle (involuntary)
coronary circulation
- primary blood supply to heart is provided by coronary arteries which arise from arota
- cardiac veins return deoxygenate blood to the inferior and superior vena cavae
how do we match 2 supply with O2 demand (VO2)?
the heart and exercise
the heart and exercise
- heart generates pressure to drive oxygenated blood through vessels to skeletal muscle
- like a garden hose - driven by the demands of active skeletal muscle for O2 but also:
- removes CO2 and other wastes
- transports hormones and other molecules
- supports temperature balance and cntrols fluid regultion
- maintains cid-base balance
matching systemic O2 supply with O2 demand (VO2)
cardiac output —> extremely important to maintain high VO2max
fick’s principle
VO2 = Q x a-VO2diff
Q = HR x SV
a-VO2diff = CaO2 (arterial) - CvO2 (venous)
CaO2 = hemoglobin, saturation fo hemoglobin, and partial pressure of oxygen
to change VO2, cardiac output is what changes VO2 not a-VO2diff
cardiac output and oxygen utilization
cardiac output relates closely to VO2 by a ratio of ~6:1
per 1L/min of increase in VO2, cardiac output increases by 6
Cardiac output (Q)
total volume of blood pumped by the ventricle each minute (L of blood per minute)
VO2 = Q x a-VO2diff
Q = HR x SV
HR - heart rate —> # of times the heart contracts in 1 minute (beats/min)
left and right sides of the heart pump the same amount of blood or the heart will fail
- same Cardiac output
heart rate (HR) control
- cardiac muscle possesses two mechanisms by which rhythm is controlled:
- intrinsic control
- cardiac musce has ability to generate its own electrical signal (“spontaneous rhythmicity”)
- pacemaker (SA node) - establishes sinus rhythm
- without external control - averages ~ 100 beats/min (transplant) - extrinsic control
- systems that modulate intrinsic electrical impulses
- causes heart to speed up (e.g. “anticipation”) or slow down
- adjusts HR to 35 to 40 beats/min at rest in endurance athletes
- during maximal effort (exercise), HR can hit 220 beats/min
ventricular depolarization
P —> QRS —> ST —> T
intrinsic regulation of HR
- normal route of myocardial impulse transmission
SA node —> atria —> AV node —> AV bundle (Purkinje fibers) —> ventricles
- sinoatrial (S-A) node
- spontaneously depolarizes and repolarizes to provide “innate” heart stimulus - atrioventricular (A-V) node
- delays impulse about 0.10 sec to provide sufficient time for atria to contract and force blood into ventricles - A-V bundle or bundle of His
- Purkinje Fibers
- speed impulse rapidly through ventricles
A. normal route from excitation and conduction of cardiac impulse
B. time sequence for electrical impulse transmission from SA node throughout myocardium
extrinsic regulation of HR
- modulation of intrinsic rate at SA and AV node
3 extrinsic systems modulate HR:
- parasympathetic nervous system (like car break)
- sympathetic nervous system (like car accelerator)
- endocrine system
- beta blockers are prescribed to help the heart take a break/calm down (ACh, Epi, NE)
the rise in HR during exercise
- decrease PNS input to SA node (-vagus)
- increase SNS input to SA node (+sympathetic)
heart rate vs Oxygen Uptake
there is a tight coupling between heart rate, cardiac output and exercise intensity (i.e. VO2) up to VO2max
cardiac output (Q)
total volume of blood pumped by the ventricle each minute (L of blood per minute)
VO2 = Q x a-VO2diff
Q = HR x SV
SV —> stroke volume: volume of blood pumped in one heartbeat (mL)
cardiac cycle
bood pressure machine 120/80 (aortic pressure)
- when aortic valve opens its 80 and before it closes it goes up to 120
end-diastolic volume (EDV) to end-systolic voume (ESV)
- the stroke volume is the difference between the two of them
stroke volume
- calculating stroke volume
- during systole, most (not all) blood ejected
- EDV - ESV = SV
- 100mL - 40mL = 60mL - calculating ejection fraction (EF)
- % of EDV pumped
- SV/EDV = EF
- 60mL/10mL = 0.6 = 60%
- clinical index of heart contractile function
a) calculation of stroke volume (SV), the difference betwen end-diastolic volume (EDV) and end-systolic volume (ESV)
b) calculation of ejection fraction (EF)
c) calculation of cardiac output (Q)
cardiac output (Q)
total volume of blood pumped by the ventricle each minute (L of blood per minute)
VO2 = Q x a-VO2diff
Q = HR x SV
SV = preload, contractility (inotropy), afterload
preload —> volume of blood received by the heart during diastole (EDV)
contractility —> inotropy = enhancd contractile force to augment stroke power and facilitate emptying
afterload —> pressure heart must generate to open aortic valve
end-diastolic filling
- frank-starling law of the heart
- describes the relationship between contractile force and resting length of the heart’s muscle fibers
- the force of contraction of cardiac muscle is proportional to its initial length (i.e. during end diastole)
- the preload stretches the ventricle in diastole to produce a more forceful ejection of blood
- increase EDV = increase SV - during exercise,increase EDV (increase preload)
- increase venous return (more blood coming back to the heart)
- effect is attenuated at faster HR
myocardial contractility
- inotropy (length-independent)
- cardiac muscle cannot modulate force through changes in motor nerve activity
- increase inotropy = increase muscle tension for a given preload (or EDV) and rate of muscle tension development
- increase inotropy = increase stroke volume - during exercise, increase inotropy
- increase firing of sympathetic nerves innervating ventricle
- decrease firing activity of parasympathetic nerves
- increase circulating catecholamines (Epi and NE)
overcoming afterload
pressure heart must generate to open aortic valve
for a normal curve —> decrease afterload, is above the normal curve - increase afterload, is below the normal curve
stroke volume vs oxygen uptake
SV increases, then plateaus
from 60mL/b, then plateaus around 140mL/b
determinants of cardiac output
heart rate, preload, contractility, afterload, and stroke volume all contribute to cardiac output
HR, SV, Q vs VO2
increase VO2 = Q x a-VO2diff
Q = (increase HR x increase SV)
