cardiac structure, properties, electrical activity and function

Question 1

define incompetent valve

Answer 1

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

Question 2

define stenotic valve

Answer 2

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

Question 3

what is the cause of heart murmurs

Answer 3

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

Question 4

characteristics of ARF/ heart disease

Answer 4

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)

Question 5

characteristics of chronic rheumatoid heart disease

Answer 5

valvular fibrosis

fibrous lesions

permanent retraction + thickening of valve cusps

results in stenosis/ incompetence

Question 6

effect of chronic rheumatic heart disease on mitral valve

Answer 6

shortening/ thickening/ fusion of chordae tendinae

commissural fusion + calcification (causing fishmouth/ buttonhole stenosis)

leaflet thickening

Question 7

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

Answer 7

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

Question 8

characteristics of tight mitral stenosis (associated with ARF)

Answer 8

LA dilation due to pressure overload

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

LV is generally normal

Question 9

clinical features of ARF

Answer 9

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

Question 10

how is ARF diagnosed

Answer 10

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

Question 11

what are the 2 types of infective endocarditis

Answer 11

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

Question 12

what is infective endocarditis

Answer 12

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

Question 13

difference in vegetations formed by ARF and IE

Answer 13

ARF vegetations are small, 1-2mm in size

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

Question 14

morphology of IE

Answer 14

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

Question 15

what are the consequences of IE

Answer 15

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)

Question 16

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

Answer 16

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

Question 17

which phase corresponds to absolute and relative refractory periods respectively

Answer 17

ARP = phase 2
RRP = phase 3

Question 18

what are the 3 phases that make up pacemaker potential

Answer 18

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)

Question 19

what are the factors affecting myocardial rhythmicity

Answer 19

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

Question 20

define myocardial excitability

Answer 20

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

Question 21

what are the 4 properties of cardiac muscles

Answer 21

automaticity (spontaneous depolarization)

excitability

conductivity

contractility

Question 22

characteristics of absolute refractory period in cardiomyocytes

Answer 22

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

Question 23

characteristics of relative refractory period in cardiomyocytes

Answer 23

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

Question 24

what is the significance of long refractory period in cardiomyocytes

Answer 24

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

Question 25

factors affecting myocardial excitability

Answer 25

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

Question 26

define myocardial conductivity

Answer 26

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

Question 27

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

Answer 27

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

Question 28

where in the heart are the SAN and AVN found

Answer 28

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

Question 29

which cardiac cells have the longest refractory period

Answer 29

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

Question 30

conduction speed in AVN

Answer 30

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

Question 31

what is the significance of slow conduction in AVN

Answer 31

allows atria to empty completely before beginning of ventricular contraction protects ventricles from abnormal atrial rhythms (Afib)

Question 32

what are the functions of the AVN

Answer 32

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

Question 33

functional differences between AVN and SAN

Answer 33

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

Question 34

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

Answer 34

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

Question 35

define WPW/ pre-excitation syndrome

Answer 35

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

Question 36

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

Answer 36

-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

Question 37

what is the force of muscle contraction dependent on

Answer 37

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

Question 38

factors affecting force of contraction

Answer 38

sympathetic NS activation drugs increasing intracellular Ca

Question 39

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

Answer 39

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

Question 40

what are positive inotropes + examples

Answer 40

agents which increase the force of contraction examples include - sympathetic stimulation - sympathomimetic agents

Question 41

what are negative inotropes + examples

Answer 41

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

Question 42

what are the 2 types of contraction

Answer 42

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

Question 43

phases of the cardiac cycle

Answer 43

atrial systole - 0.1s ventricular systole - 0.3s isovolumetric contraction rapid ejection reduced ejection diastole - 0.4s isovolumetric relaxation maximum filling reduced filling

Question 44

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

Answer 44

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

Question 45

location + organization of CVC/ vasomotor center

Answer 45

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

Question 46

describe vasoconstrictor area in CVC

Answer 46

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)

Question 47

describe vasodilator area in CVC

Answer 47

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)

Question 48

describe sensory area in CVC

Answer 48

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

Question 49

what is the function of vagal/parasympathetic fibers to heart

Answer 49

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

Question 50

what is the vagal/ventricular escape phenomenon

Answer 50

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)

Question 51

what is the function of sympathetic fibers to heart

Answer 51

positive chronotropic effect (rate of contraction) positive inotropic effect (force of contraction) positive dormotropic effect (conductivity) increased excitability decreased effects of vagal stimulation

Question 52

describe vagal tone of the heart

Answer 52

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

Question 53

factors affecting HR

Answer 53

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

Question 54

nervous regulation of the heart

Answer 54

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)

Question 55

what are the vasosensory areas and their buffer nerves

Answer 55

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

Question 56

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

Answer 56

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

Question 57

what are the baroreceptors reflexes

Answer 57

decreased HR and force of contraction generalized peripheral vasodilation decreased ADH secretion (increased urine volume)

Question 58

where are peripheral chemoreceptors found + their function

Answer 58

carotid and aortic bodies where rate of blood flow is very high increase respiration/ vasoconstriction in response to decreased oxygen/ increased CO2/ H+

Question 59

describe the CNS ischemic response

Answer 59

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

Question 60

describe cushings reflex

Answer 60

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

Question 61

causes of increased HR

Answer 61

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

Question 62

causes of decreased HR

Answer 62

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

Question 63

define cardiac output

Answer 63

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

Question 64

factors affecting cardiac output

Answer 64

metabolism exercise age size of body

Question 65

define cardiac index

Answer 65

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

Question 66

define stroke volume

Answer 66

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)

Question 67

how to calculate cardiac output (CO)

Answer 67

CO = HR x stroke volume stroke volume = EDV - ESV

Question 68

define ejection fraction

Answer 68

% 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%

Question 69

conditions affecting CO

Answer 69

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

Question 70

factors affecting CO

Answer 70

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)

Question 71

explain how VR affects CO

Answer 71

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)

Question 72

what are the intrinsic auto-regulatory mechanisms controlling CO

Answer 72

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

Question 73

what are the mechanisms that increase CO when VR is increased

Answer 73

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

Question 74

what are the factors that affect VR

Answer 74

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

Question 75

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

Answer 75

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

Question 76

what is the effect of standing on VR

Answer 76

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)

Question 77

explain how myocardial contractility affects CO

Answer 77

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)

Question 78

what affects level of contractility

Answer 78

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

Question 79

explain how afterload/ ABP affects CO

Answer 79

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

Question 80

explain how changes in HR affects CO

Answer 80

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

Question 81

explain how changes in blood volume/ viscosity affects CO

Answer 81

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

Question 82

L 22