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