Heart

    Cards (40)

    • CV system:
      • heart = pump
      • arteries = outflow consuits
      • capillaries = drop off/pick up sites
      • veins = return flow conduits
    • Circulatory circuit:
      • start at right atrium and end at right atrium
    • Heart:
      four chambers:
      • left and right atria = receiving chmabers
      • left and right ventricles = pumping chambers
      right heart = pulmonary circulation:
      • pumps deoxygenated blood from body to lungs
      left heart = systemic circulation:
      • pumps oxygenated blood from lungs to body
    • Cardiac muscle:
      • contracts as single unit
      • fibres interconnected via intercalated discs
      • electrically charged
    • Coronary circulation:
      • primary blood supply to heart provided by coronary arteries from aorta
      • cardiac veins return deoxygenated blood to inferior and superior vena cava
    • Heart and exercise:
      • heart generates pressure to drive oxygenated blood through vessels to skeletal muscles
      • driven by demands of muscle for O2
      what does it do:
      • removes CO2 and wastes
      • transports hormones and molecules
      • supports temperature balance and fluid regulation
      • maintains acid-base balance
    • Matching systemic O2 supply with O2 demand:
      • VO2 = Q x a-vO2difference
      • Q = HR x SV
      • a-vO2difference = CaO2 - CvO2
      • important to increase Q with increase intensity because we would not be able to generate big enough VO2max
      • Q allows us to manage higher intensity
      • CvO2 decreases with increased intensity because more O2 is dropped off at tissue
    • Q and O2 utilization:
      • as VO2 increases, Q increases in proportion
      • increase demand = increase CO2
      • ~ 6:1 ratio
      • for every 1 L increase in VO2, we get a 6 L output of CO2
    • Cardiac output (Q):
      • total volume of blood pumped by ventricle each minute
      • influenced by HR and SV
    • HR control:
      2 mechanisms to control HR:
      intrinsic control:
      • cardiac muscle generates own signal
      • pacemaker (SA node) establishes sinus rhythm
      • without external control (~100 bpm)
      extrinsic control:
      • systems modulate intrinsic
      • causes HR to speed up or slow down
      • adjusts HR to ~35-40 bpm at rest
      • maximal effort, HR = ~220 bpm
    • Intrinsic regulation of HR:
      • SA node —> atria —> AV node —> purkinje fibres —> ventricles
      • SA node = spontaneous depolarization and repolarization to provide innate heart stimulus
      • AV node = delays impulse to provide time for atria to finish contracting and finish giving blood to ventricles
      • bundle of His
      • purkinje fibres = carry impulse rapidly through ventricles
    • Extrinsic regulation of HR:
      3 systems:
      parasympathetic:
      • releases ACh to slow down HR
      sympathetic:
      • releases NE to speed up HR and increase contractility
      • innervates heart at SA node
      endocrine:
      • release of Epi to affect SA node and increase HR
    • HR during exercise:
      • at low intensities, increase in HR due to decrease in PSNS activity
      • as intensity increases, increase in HR due to SNS activation
    • HR vs O2 uptake:
      • tight connection between HR, Q, and exercise intensity up to VO2max
    • SV:
      • amount of blood left in heart after contraction
      • EDV - ESV = SV
      ejection fraction (EF):
      • percent of EDV pumped
      • SV/EDV = EF
    • Components of SV:
      preload:
      • volume of blood in heart during diastole (before contraction)
      • end-diastolic filling
      Frank Starling Law of Heart:
      • relationship between contractile and resting length of heart muscles
      • force of contraction equals initial muscle length
      • preload stretched ventricles in diastole to produce more forceful ejection
    • Components of SV:
      contractility/inotropy:
      • enhanced contractile force to increase SV and facilitate emptying
      myocardial contractility:
      • inotropy = increasing muscle tension for given preload and rate of muscle tension development
      • increase inotropy = increase SV
      During exercise, increase inotropy:
      • increases SNS
      • decreases PSNS
      • increases endocrine (catecholamines)
    • Components of SV:
      afterload:
      • Pressure heart must generate to open aortic valve
      • increase afterload = more pressure
      • decrease afterload = less pressure
      • exercise = reduction in afterload which causes increase in SV, Q, and O2
    • SV vs O2 uptake:
      • rapid rise in SV due to decreased afterload, increased inotropy, and increased preload
      • SV plateaus as exercise continues
      • increase exercise = increase HR, which decreases the amount of time we have to fill the heart, therefore decreasing slope at which SV rises as intensity increases = plateau
    • Qmax and VO2max:
      • increase Q = increase VO2max
      • endurance athletes that have high VO2max also have high Q
      • HR = limiting factor for ability to sustain higher intensities
    • Fick principle:
      • increase in VO2 is determined by Q
      • VO2max related to maximum ability of heart to pump blood
    • Central delivery of O2 blood:
      • SV fills chambers during diastole —> increases with increased intensity
    • CV system:
      • arteries = carry blood away from heart
      • arterioles = control blood flow
      • capillaries = area of exchange
      • venules = collect blood from capillaries
      • veins = carry blood to heart
    • Arteries and arterioles:
      • high-pressure tubing
      • pressure = high on arterial side, low on venous side
      • connect left ventricle to tissue
      • walls contain circular layers of smooth muscle that constrict and relax to control blood flow
      • innervated by SNS (NE released = constriction)
      • no gas exchange
    • Capillaries:
      • exchange
      • gas, nutrients, and waste products
      • velocity decreases as blood moves to and through capillaries because blood is moving away from area of high pressure (heart) to low pressure (veins)
    • Blood flow and VO2:
      • they follow each other
      • as one rises/lowers, the other rises/lowers
      • blood flow and VO2 rise to match O2 demands
      • relationship with metabolic rate of muscles
    • Hemodynamics:
      pressure:
      • force that drives flow
      • provided by heart contraction
      • from region of high pressure to low pressure (no gradient = no flow)
      resistance:
      • force that opposes flow
      • provided by physiological properties of vessels —> pressure differential
      • modification of vessel radius
    • Blood flow (Q):
      • total volume of blood pumped through vessel per minute
      • Q = MAP / TPR
      • increase pressure and decrease resistance = increase Q
      • decrease pressure and increase resistance = decrease Q
    • MAP:
      P = arterial pressure - venous pressure
      arterial pressure = 2/3 DBP + 1/3 SBP
    • Arterial blood pressure:
      • systolic = highest pressure in artery during contraction
      • diastolic = lowest pressure in artery during relaxation
      • mean arterial pressure (MAP) = average pressure on arterial vessel walls over entire cardiac cycle
    • Facts about pressure:
      • diastolic pressure stays the same with varying intensities
      • but systolic pressure changes (ex. increases with greater intensity)
    • MAP:
      • venous pressure = CVP (central venous pressure)
      • represents blood coming back to heart
    • Venous blood pressure:
      CVP:
      • blood pressure taken in vena cava or right atrium pressure
      • reflects amount of blood returning to heart and ability of right heart to pump blood into pulmonary circulatory
      • range = 0-8 mmHg.
      • right atrial pressure doesn't change much during exercise
    • TPR:
      resistance = n x L x r^4
      • we only really manipulate radius (r^4) because viscosity (n) and length of vessel (L) don’t change as often
      • r^4 has a powerful impact on resistance
      • increase r^4 = decrease resistance
      • decrease r^4 = increase resistance
    • TPR:
      • resistance to Q offered by all systemic vasculature, excluding pulmonary vasculature
      3 factors affect resistance of Q:
      • Poiseuille’s Law —> n, L, r^4
      • we can only acutely change r^4 (vasoconstriction and vasodilation)
      • arterioles = resistance vessels (they control TPR; responsible for 70-80% of pressure drop from left ventricle to right atrium)
      • TPR = MAP / Q
    • Blood flow and exercise:
      • at rest, muscles receive ~ 1L/min of Q
      • with increased intensity, blood to muscle rises (80-85% of total Q)
      • brain always receives steady flow of blood
      • vessels constrict to redirect blood from areas that do not need it to areas that do (kidneys and splanchic)
    • Distribution of blood flow:
      • blood to sites that most need it
      at rest:
      • liver and kidneys receive 50% of Q
      • muscles receive 20% of Q
      exercise:
      • muscles receive 80% of Q
    • Q and muscle blood flow:
      • active muscle = decrease resistance
      • non-active muscle = increase resistance
    • Muscle blood flow:
      • resistance = most powerful tool to modify blood flow
    • Arterioles and smooth muscle:
      • arterioles have strong muscular walls of smooth muscle
      • smooth muscle uses cross-bridge cycling, actin and myosin, and Ca2+
      • increase Ca2+ = contraction
      • decrease Ca2+ = relaxation
      • innervated by SNS and controlled by hormones
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