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circulatory system > cardiac structure, properties, electrical activity and function > Flashcards

cardiac structure, properties, electrical activity and function Flashcards

1
Q

define incompetent valve

A

results from failure of valve to close completely, results in regurgitation/backflow of blood

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2
Q

define stenotic valve

A

results from failure of valve to open completely, obstructs forward flow of blood

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3
Q

what is the cause of heart murmurs

A

turbulent flow through diseased valves (incompetent/ stenotic) which produces abnormal heart sounds

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4
Q

characteristics of ARF/ heart disease

A

pancarditis

endocarditis on heart valves results is fibrinoid necrosis + fibrin deposition forming small vegetations along lines of closure

aschoff bodies (associates w/ zones of fibrinoid necrosis, result from inflammation in heart muscle)

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5
Q

characteristics of chronic rheumatoid heart disease

A

valvular fibrosis

fibrous lesions

permanent retraction + thickening of valve cusps

results in stenosis/ incompetence

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6
Q

effect of chronic rheumatic heart disease on mitral valve

A

shortening/ thickening/ fusion of chordae tendinae

commissural fusion + calcification (causing fishmouth/ buttonhole stenosis)

leaflet thickening

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7
Q

state which valves are most affected by rheumatic heart disease in order of most to least affected

A

mitral valve
aortic valve
tricuspid valve
pulmonary valve (almost always escapes injury)

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8
Q

characteristics of tight mitral stenosis (associated with ARF)

A

LA dilation due to pressure overload

results is atrial fibrillations (Afib) + formation of large mural thrombus

LV is generally normal

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9
Q

clinical features of ARF

A

ARF more common in children

principle manifestation is carditis

onset of symptoms in all age groups begins 2-4 weeks after initial streptococcal infection and are heralded/preceded by fever + migratory polyarthritis

cultures are negative for streptococci at time of symptom onset however serum tigers for antibodies against streptococci agents are elevated

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10
Q

how is ARF diagnosed

A

diagnosis of ARF is made based on serologic evidence of previous streptococcus infection (elevated serum tigers of antibodies against streptococci agents such as streptolysin/ DNAse)

+ 2 or more of the jones criteria

(major)
- carditis
- migratory polyarthiritis of large joints
- subcutaneous nodules (rarely noticed)
- erythema marginatum
- syndenham chorea

(minor)
-fever
- arthralgia
- EKG changes
- elevated acute phase reactants

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11
Q

what are the 2 types of infective endocarditis

A

acute IE:
occurs on previously normal valves
destructive + fatal results
rapid disease
organism is staphylococcus aureus
leads to large, friable vegetations on heart valves that can embolise around blood stream
common in IV drug abusers and affects right side valves

subacute IE:
occurs on top of already diseased valves by rheumatic heart disease/ prosthetic
slow disease
organism is less virulent streptococcus viridan
vegetations are smaller/firmer and embolization is less common than in acute IE

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12
Q

what is infective endocarditis

A

an inflammatory condition affecting the endocardium, specifically on the heart valves

leads to the development of large, friable vegetations on the heart valve

fragments of these vegetations split from the main mass and embolize around blood stream + impact distant vessels causing infarction and spreading infection

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13
Q

difference in vegetations formed by ARF and IE

A

ARF vegetations are small, 1-2mm in size

IE vegetations are large, 0.5-1cm in subacute/ 1-2cm in acute

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14
Q

morphology of IE

A

large vegetations
0.5-1cm in subacute
1-2cm in acute

vegetations may be single or confluent valve-destroying mass (forming a large mass)

in acute IE valve cusps may be perforated/ bacteria may infiltrate myocardium causing abscess formation

vegetations are on the upper/atrial surface of tricuspid and mitral valves
lower/ventricular surface of pulmonary and aortic valves

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15
Q

what are the consequences of IE

A

embolus formation - may travel along coronary arteries/ systemic circulation, can cause infection which weakens walls of vessel leading to a dilated artery (mycotic aneurysm)

valve perforation/ destruction seen in acute IE - causes infection to spread into myocardium which may lead to heart failure

immune complex tissue injury - may cause glomerulonephritis in kidney/ vascular is in skin/ arthralgia in joints (caused by deposition of immune complexes circulating in bloodstream)

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16
Q

what are the 5 phases of contractile cardiomyocyte action potential in ventricles

A

phase 0 - initial rapid depolarization (Na influx)

phase 1- rapid, partial, early repolarization (K outflux, opening of L-type voltage gated Ca channels)

phase 2- prolonged period of slow repolarization/ plateau phase (simultaneous K outflux + Ca influx)
phase 3- rapid repolarization (inactivation of L type
Ca channels + continued K outflux)

phase 4- complete repolarization/ RMP

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17
Q

which phase corresponds to absolute and relative refractory periods respectively

A

ARP = phase 2
RRP = phase 3

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18
Q

what are the 3 phases that make up pacemaker potential

A

phase 4- diastolic depolarization (influx of Na through h/funny channels + Ca influx through T channels at -55mV for more rapid depolarization)

phase 0- depolarization (Ca influx through L type channels up to +10mV)

phase 3- repolarization (Ca channel inactivation + opening of K channels)

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19
Q

what are the factors affecting myocardial rhythmicity

A

sympathetic nerve stimulation at SAN, increases rate of phase 4/ depolarization therefore threshold potential is reached faster and heart rate increases

parasympathetic nerve stimulation via the vagus nerve slows heart rate by hyperpolarisation of SAN cells so rate of depolarization at phase 4 is therefore also reduced therefore it takes longer for threshold potential to be reached

hyperkalaemia, a rise in plasma K, consequence of acidosis/ inadequate excretion of K from body, life threatening because it can lead to depolarization of cardiomyocytes (resting potential rises to 0) meaning Na channels stay inactivated (membrane cannot return to -ve potential) which may lead to cardiac arrest

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20
Q

define myocardial excitability

A

ability of cardiac muscle to respond to a stimulus by generating an action potential followed by contraction

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21
Q

what are the 4 properties of cardiac muscles

A

automaticity (spontaneous depolarization)

excitability

conductivity

contractility

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22
Q

characteristics of absolute refractory period in cardiomyocytes

A

no sensitivity to additional stimulation as all Na channels are active

cardiomyocytes cannot respond to restimulation whatever the strength of stimulus may be as Na voltage gated channels are inactive therefore further stimulation cannot produce action potential

corresponds to depolarization + 2/3 of repolarization (phases 0, 1, 2, beginning of phase 3)

mechanically corresponds to whole period of systole and early diastole

duration in ventricles = 0.25-0.3s
duration in atria = 0.15s

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23
Q

characteristics of relative refractory period in cardiomyocytes

A

reduced sensitivity to additional stimulation as only some Na channels are active

cardiomyocytes can respond to restimulation by a greater than normal stimulus as some Na channels are active, causes premature contraction

corresponds to last 1/3 of repolarization (rest of phase 3)

mechanically corresponds to middle of diastole

duration in ventricles = 0.05s
duration in atria = 0.03s

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24
Q

what is the significance of long refractory period in cardiomyocytes

A

lasts almost as long as entire systole

prevents sustained tetanic contractions (sustained muscle contraction)

mechanism allowing sufficient time for ventricles to empty + refill prior to next contraction essential for pumping function of heart

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25
Q

factors affecting myocardial excitability

A

1- innervation
- sympathetic stimulation leads to increased excitability
- parasympathetic stimulation (vagal nerve) decreases excitability

2- ECF ion conc.
- hyperkalemia, increases excitability initially however, if sustained it results in inactivation of Ca and K channels causing loss of excitability leading to cardiac arrest and heart stops in diastole
- hypokalemia decreases excitability

  • hypercalcemia decreases excitability
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26
Q

define myocardial conductivity

A

ability of myocardiocytes to transmit impulse generated in SAN to the rest of the heart

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27
Q

why is the SAN the primary pacemaker/ why do cardiac impulses originate from the SAN

A

because its the region of the heart w/ the fastest intrinsic spontaneous discharge rate (110-120bpm)

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28
Q

where in the heart are the SAN and AVN found

A

SAN - right atrium near SVC

AVN - right atrium at posterior part of inter atrial septum close to opening of coronary sinus

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29
Q

which cardiac cells have the longest refractory period

A

AVN + purkinje fibers

this allows only forward conduction from atria to ventricles preventing re-entry of cardiac impulses from ventricles to atria

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30
Q

conduction speed in AVN

A

AVN has the slowest conduction velocity (0.05m/s)
long absolute refractory period
leads to 0.1s of AVN delay

this is caused by the small diameter of AVN cells and slow conductive fibers

AVN delay is shortened by sympathetic stimulation/ prolonged by vagal stimulation

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31
Q

what is the significance of slow conduction in AVN

A

allows atria to empty completely before beginning of ventricular contraction

protects ventricles from abnormal atrial rhythms (Afib)

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32
Q

what are the functions of the AVN

A

receives impulse originating from SAN and transmits it to ventricles through bundle of his

AV nodal delay (which allows for complete atrial emptying before ventricular contraction + protects ventricles from abnormal atrial rhythms)

can initiate cardiac impulses but at a slower rate (40-60bpm) if SAN gets damaged

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33
Q

functional differences between AVN and SAN

A

initial resting potential of AVN is -80mV compared to -60mV of SAN

depolarization of AVN doesn’t exceed +5-+10mV

depolarization in phase 4 is slower because of absence of a population of Na channels causing the slower intrinsic rate of firing

34
Q

what is the significance of purkinje fibers having the fastest conduction rate of all cardiac muscle

A

ensures simultaneous contraction of all parts of ventricles, essential from pumping function of heart

35
Q

define WPW/ pre-excitation syndrome

A

the presence of an electrical leak in the fibrous ring separating atria from ventricles (anulus fibrosis) leading to an alternative direct route for spread of action potential from atria to ventricles resulting in arrhythmia

36
Q

what are the steps of transmission of a cardiac impulse through the heart

A

-cardiac impulse originates in the SAN
-impulse spreads across left/right atria
- impulse proceeds across internodal pathway
- impulse reaches AVN and passes to bundle of his
- wave of depolarization spreads on top of ventricular septum to purkinje fibers down each side of the septum before spreading to all parts of the ventricles

37
Q

what is the force of muscle contraction dependent on

A

the no. of actomyosin cross bridges formed which in turn is dependent on the conc. of Ca inside the cell

38
Q

factors affecting force of contraction

A

sympathetic NS activation

drugs increasing intracellular Ca

39
Q

how does physiologic stimulation of sympathetic nerves to the heart result in an increased force of contraction

A

B1-ADR activation leads to rise in intracellular cAMP, a secondary messenger which activates several protein kinases causing phosphorylation of protein phospholamban

protein phospholamban accelerates the transport of Ca into the SR, favoring the retention of Ca in SR at the expense of efflux back across plasma membrane (more Ca gets reabsorbed into SR instead of effluxed back through membrane)

contractility of the heart is therefore increased by raising the amount of Ca stored in the SR (more Ca gets released into myocyte which increases the force of contraction)

rate of relaxation of cardiac muscle is also increased as Ca re-enters the SR more quickly

effects of cAMP can be manipulated by caffeine/ milrinone which as as phosphodiesterase inhibitors therefore prolonging the half life of cAMP

sympathetic stimulation also causes phosphorylation of L-type Ca channels which increases their permeability to Ca allowing more entry of Ca from ECF into the myocyte

40
Q

what are positive inotropes + examples

A

agents which increase the force of contraction

examples include
- sympathetic stimulation
- sympathomimetic agents

41
Q

what are negative inotropes + examples

A

agents which decrease the force of contraction

examples include
- intracellular acidosis (high H+)
- reduced binding of Ca to troponin which decreases the no. of cross bridges formed
- Ca channel blocking drugs

42
Q

what are the 2 types of contraction

A

isometric - fibers contract w/o shortening, tension developed rises very high, most energy is liberated as heat, no work is done, pressure inside heart raises to a high level essential to opening aortic/ pulmonary valves, volume of heart remains constant

isotonic - fibers shorten to contract, tension doesn’t increase/ remains same throughout work, pressure inside heart raises only slightly, volume of heart decreases as it pumps blood into lungs/body by decreasing in size

43
Q

phases of the cardiac cycle

A

atrial systole - 0.1s

ventricular systole - 0.3s
isovolumetric contraction
rapid ejection
reduced ejection

diastole - 0.4s
isovolumetric relaxation
maximum filling
reduced filling

44
Q

what is the effect of heart rate on the duration of the cardiac cycle

A

when HR increases the duration of each cardiac cycle decreases + duration of action potential decreases

duration of diastole decreases by a greater % than the the duration of systole

meaning that the heart doesn’t remain relaxed long enough to allow complete filling of the cardiac chambers before the next contraction

45
Q

location + organization of CVC/ vasomotor center

A

located bilaterally, mainly in medulla oblongata + lower 1/3 of pons
contains vasoconstrictor/ vasodilator/ sensory areas

46
Q

describe vasoconstrictor area in CVC

A

located in rostral ventro-lateral medulla (RVLM)
sends fibers to thoraco-lumbar segments of spinal cord
activity is sympathetic postganglionic fibers leads to generalized vasoconstriction elevating ABP (depressor effect)

47
Q

describe vasodilator area in CVC

A

located in caudal ventro-lateral medulla (CVLM)
receives impulses from sensory neurons
not connected to any vasodilator fibers
when stimulated it inhibits vasoconstrictor area causing generalized vasodilation lowering BP (depressor effect)

48
Q

describe sensory area in CVC

A

located in posterolateral part of medulla oblongata + lower pons (in nucleus tractus solitarius/ NTS)
lateral portion - sends excitatory signals through sympathetic nerves to heart
medial portion - sends signals to adjacent nucleus ambiguous in MO from which preganglionic parasympathetic vagal fibers arise that relay in terminal ganglia in nodal tissue of RA, postganglionic fibers supply atria/ bundle of his/ coronary vessels (right vagus supples SAN/ left vagus supplies AVN) causing inhibition

49
Q

what is the function of vagal/parasympathetic fibers to heart

A

negative chronotropic (rate of contraction) effect

negative inotropic (force of contraction) effect

negative dormotropic effect (decreased conduction at AVN)

decreased excitability

decreases release of NA (vasopressor) from nearby sympathetic nerve fibers

50
Q

what is the vagal/ventricular escape phenomenon

A

vagal fibers to heart produce a negative dormotropic effect which leads to decreased conduction at AVN, strong vagal activity may lead to complete AV block where ventricles stop beating, they may then regain their function by idioventricular rhythm (a slow regular ventricular rhythm, typically with a rate of less than 50, absence of P waves, and a prolonged QRS interval)

51
Q

what is the function of sympathetic fibers to heart

A

positive chronotropic effect (rate of contraction)

positive inotropic effect (force of contraction)

positive dormotropic effect (conductivity)

increased excitability

decreased effects of vagal stimulation

52
Q

describe vagal tone of the heart

A

continuous inhibitory impulses transmitted by vagi to check inherently high rhythm of SAN (110-120 bpm) at the basal level of ABP

its reflexly produced through baroreceptors

high ABP, more impulses sent through baroreceptors to CVC (sensory area/ medial portion), more inhibitory impulses sent by vagus to heart, lower HR

53
Q

factors affecting HR

A

gender (females > males due to lower ABP w/ a weaker vagal tone)

age (higher in young due to increased BMR and in elderly)

circadian rhythm (lowest in early morning/ highest in evening)

rest

muscular exercise

posture (HR increases by up to 25% when standing)

emotions

metabolic rate

respiration

54
Q

nervous regulation of the heart

A

afferent impulses from CVS (baroreceptors/ low pressure baroreceptors/ peripheral chemoreceptors)

afferent impulses from other regions of the body (contracting voluntary muscles/ painful stimuli)

afferent impulses from higher centers (cerebral cortex, lambic system, hypothalamus respond to emotions/ respiratory center/ CNS ischemic response/ cushing’s reflex)

55
Q

what are the vasosensory areas and their buffer nerves

A

carotid sinus, supplies by coronary sinus nerve, a branch of glossopharyngeal IX cranial nerve

aortic arch, supplies by aortic depressor nerve, a branch of vagus X cranial nerve

56
Q

where are the low pressure baroreceptors/ serial stretch receptors found + their function

A

4 chambers of the heart/ SVC/ IVC pulmonary artery

increase HR by distention caused by increased blood volume/ venous return

mechanisms of increasing HR include direct stretching of SAN/ brain bridge reflex where increased venous return stimulates type B receptors that discharge during atrial diastole to medullary/vasomotor centers via the vagus nerve leading to decreased vagal tone + increased sympathetic tone of heart

57
Q

what are the baroreceptors reflexes

A

decreased HR and force of contraction

generalized peripheral vasodilation

decreased ADH secretion (increased urine volume)

58
Q

where are peripheral chemoreceptors found + their function

A

carotid and aortic bodies where rate of blood flow is very high

increase respiration/ vasoconstriction in response to decreased oxygen/ increased CO2/ H+

59
Q

describe the CNS ischemic response

A

afferent impulse from a higher brain center for nervous regulation of HR

ABP <60 mmHg results in ischemia of vasomotor centers w/ increased CO2 + lactic acid which stimulates them causing activation of sympathetic NS leading to peripheral vasoconstriction especially in skin/kidneys

60
Q

describe cushings reflex

A

afferent impulse from a higher brain center for nervous regulation of HR

caused by increased intracranial pressure which leads to compression of cerebral vessels causing a hypoxia state which activates RVLM neurons leading to systemic vasoconstriction increasing ABP which reflexively decreases HR

61
Q

causes of increased HR

A

decreased stimulation of baroreceptors (decreased ABP —> increased HR)

stimulation of arterial stretch receptors

during inspiration

muscular exercise

mild/moderate painful stimuli

mild/moderate emotions (stress/anger)

moderate hypoxia (directly stimulates SAN/ RVLM)

catecholamines

thyroxin

increased body temp

62
Q

causes of decreased HR

A

increased stimulation of baroreceptors (increased ABP —> decreased HR)

severe emotions (fear/grief)

severe pain/ pain in trigger areas

during expiration

increased intracranial pressure (cushings reflex)

severe pre-mortal hypoxia/ acidosis

hyperkalemia

63
Q

define cardiac output

A

vol. of blood pumped out be each ventricle per minute

at rest = 5-6 L/min
in severe exercise = 25L/min in non-athletes / 35L/min in athletes

64
Q

factors affecting cardiac output

A

metabolism

exercise

age

size of body

65
Q

define cardiac index

A

cardiac output (volume of blood pumped out by each V/min) per m^2 of body surface area

normal value = 3.2L/m^2/min at rest

66
Q

define stroke volume

A

vol. of blood pumped by each V per beat

70-90ml in average size, resting, supine position

ventricular end diastolic volume - end systolic volume = stroke volume

EDV = 130ml
ESV = 50ml (increased ABP or decreased cardiac contractility increase ESV which decreases SV)

67
Q

how to calculate cardiac output (CO)

A

CO = HR x stroke volume

stroke volume = EDV - ESV

68
Q

define ejection fraction

A

% of end diastolic blood volume that’s ejected per beat

index of ventricular function

EF = (SV/EDV) x 100

at rest it ranges from 60-70%

69
Q

conditions affecting CO

A

increases during:
- exercise
- excitement
- anxiety
- eating
- in pregnant women
- exposure to high environmental temp

decreases during:
- on standing from lying down in heart disease (postural hypotension)

no change during:
- sleep
- exposure to moderate change in temp

70
Q

factors affecting CO

A

CO = HR x SV
changes in HR/ SV/ both produce changes in CO

  • venous return (preload)
  • cardiac contractility/ systolic performance of ventricle
  • ABP (after load)
  • HR
  • blood volume +viscosity

preload = EDV
after load = resistance against which blood in expelled (ABP/ pressure in aorta)

71
Q

explain how VR affects CO

A

factors affecting VR/ peripheral circulation are the primary controllers of CO

VR = vol. of blood flowing from veins into RA/ min

VR determines stroke volume + cardiac output by affecting EDV

during rest, VR is 5-6L/min which is equal to CO (controlled via intrinsic auto-regulatory mechanisms)

72
Q

what are the intrinsic auto-regulatory mechanisms controlling CO

A

sympathetic tone of heart can increase CO by up to 15-25L/min (during muscular exercise), known as cardiac permissive level

outputs greater than the cardiac permissive level can still by ejected by:
1. neuro-hormonal mechanisms such as
- increasing sympathetic activity
- secretion of catecholamines from adrenal medulla
2. cardiac hypertrophy which can increase CO by 35L/min in athletes

73
Q

what are the mechanisms that increase CO when VR is increased

A

Frank-Starling law - extra blood in ventricles stretches cardiac muscle to grater extent causing muscle to contract w/ increased force causing an increase in SV therefore increasing CO

brain bridge reflex/ atrial stretch receptor reflex - increased VR stretches wall of RA sending more impulses via atrial stretch receptor which increases sympathetic tone causing an increase in HR therefore increasing CO

74
Q

what are the factors that affect VR

A

venous pressure gradient - difference between mean pressure in systemic circulation (7-10mmHg) and RA pressure (2mmHg / 0mmHg in standing position), the greater the VPG the greater the VR and vice versa

skeletal muscle pump - contraction compresses capillaries/ venues in skeletal muscles propelling blood towards heart, occurs by muscle tone/ during exercise

valves in veins - prevent back flow of blood in veins

arteriolar diameter - dilation in skin during hot weather/ splanchnic area during digestion decreases resistance to blood flow + increases VR

capillary tone - 90% are partially/totally closed under normal conditions, severe dilation w/ histamine release/ on tissue injury leads to pooling of blood in capillaries which decreases mean circulatory pressure (decreased venous pressure gradient) therefore decreasing VR + CO causing circulatory shock

respiratory pump - during inspiration, thoracic pressure becomes more -ve so thoracic veins dilate + resistance to blood flow is decreased, at the same time intra-abdominal pressure increases as diaphragm descends which compresses/constricts and increases pressure in abdominal veins, the increase in pressure gradient between thoracic and abdominal veins helps VR towards heart (high pressure in abdomen to low pressure in thorax)

sympathetic stimulation - increases venous tone (partial constriction during rest caused by continuous sympathetic discharge creating an upstream pressure which maintains VR against gravity) + cardiac suction forces ( during ventricular diastole V expands increasing inflow from A decreasing atrial pressure resulting in sanction of blood from veins)

blood volume - decrease in blood volume decreases mean circulatory pressure which decreases venous pressure gradient resulting in a reduction in VR + vice versa

gravity - opposes VR from lower limbs, this effect is normally antagonized by thoracic + muscular pumps/ venomotor tone/ cardiac suction forces

75
Q

what does mean systemic filling pressure/ mean pressure in systemic circulation depend on

A

blood volume (proportional)

venous compliance (indirectly proportional) (more blood stays in veins instead of returning to heart)

76
Q

what is the effect of standing on VR

A

when standing, effect of gravity is greater than venous pressure gradient
this causes blood to pool down in veins of lower limbs
which increases capillary blood pressure
so fluid escapes into interstitial spaces
resulting in a 15% decrease in blood volume in 15mins
VR is decreased
therefore CO is decreases
syncope (fainting)

this is prevented by
contraction of muscles in lower limbs (muscular pump)
venomotor tone (partial constriction during rest caused by continuous sympathetic discharge creating an upstream pressure which maintains VR against gravity)
cardiac suction forces (V diastole)

77
Q

explain how myocardial contractility affects CO

A

defined as the force generated by V muscle during systole

determined by the no. of actomyosin cross bridges formed which depends on:

  • preload/ frank-sterling law (pre stretch of V muscle at end of diastole/ EDV)
  • level of contractility (change in force of contraction)
78
Q

what affects level of contractility

A

neural input - sympathetic stimulation of heart increases force of contraction by increasing Ca entry from ECF causing an increase in ejection fraction/ catecholamines increase +ve inotropic effect of NA released from nerve endings

changes in HR - high HR produces small increase in contractility because Ca enters cell more rapidly than it’s reabsorbed by SR resulting in an increase in intracellular Ca, increased contractility compensates for reduced filling time

Ca availability - increase contractility

digitalis/ other inotropic drugs - increase contractility

heart failure/ hypoxia/acidosis - decrease contractility

79
Q

explain how afterload/ ABP affects CO

A

increased ABP/ peripheral vascular resistance causes initial decrease in SV + CO for several beats

EDV of next beat increases leading to increase in force of contraction (frank-starling law) therefore CO returns to normal

changes in ABP don’t affect CO as long as VR remains constant

80
Q

explain how changes in HR affects CO

A

proportional relationship (if HR increases/decreases within limits)

excessive acceleration/slowing of HR is associated with a decrease in CO (inversely proportional relationship)

if HR increases above limits where it shortens diastolic time during which filling takes place the CO will decrease rather than increase

HR <70bpm, SV increases (enough time for max filling) so CO remains constant

HR <50bpm, increase in SV doesn’t compensate for slowing of heart so CO is decreased

HR from 180-200bpm, SV is decreased because of shortening of diastolic time but CO remains constant/ increases slightly due to heart acceleration

HR >180-200bpm, diastolic times becomes shorter and decreased EDV/ force of contraction/ SV/ CO, decrease in SV is not compensated for by heart acceleration

81
Q

explain how changes in blood volume/ viscosity affects CO

A

increased blood vol increases VR
hemorrhage decreased VR + CO

increased blood viscosity increases resistance against blood returning to heart/ decreases VR
decreased blood viscosity (e.g- anemia) increases VR + CO

82
Q

L 22

A

circulatory system (4 decks)

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