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physiology allied health > Unit 5: Cardiovasular Physiology > Flashcards

Unit 5: Cardiovasular Physiology Flashcards

1
Q

preclampsia can lead to …

A

speech and language delays

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2
Q

1 cause of death

A

cardiovascular disease

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3
Q

what % of cardiovascular disease is preventable

A

80

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4
Q

why is there a delay in the av node

A

to allow time for atrial contraction to complete filling of the ventricles

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5
Q

cardiac conductance

A
  • SA node (pacemaker cells)
  • AV node
  • bundle of Hiss
  • Purkinje cells/fibers
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6
Q

generation of pacemaker action potentials

A
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7
Q

PQRS complex what does everything stand for

A
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8
Q

what does a shortened PR segment in a PQRS complex signify

A

fast heart rate (arrythmia)

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9
Q

what could disrupt the TP interval in a PQRS complex

A

potassium or electrical abnormalities

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10
Q

risk of a small or large ST segment in a PQRS complex

A
  • small = heart attack risk
  • big = myocardial disruption
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11
Q

systolic definition

A

when muscles are contracting

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12
Q

diastolic definition

A

when muscles are relaxing

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13
Q

can any of the heart functions be felt

A

yes, ventricular ejection

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14
Q

parasympathetic and sympathetic heart rate control centers

A
  • parasympathetic: vagus nerve (medulla)
  • sympathetic: cardiac nerve (T1-T4)
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15
Q

behavioral factors of ideal cardiovascular health

A
  • no smoking
  • good diet
  • being active
  • losing weight
  • managing blood pressure
  • controlling cholesterol
  • reducing blood sugar
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16
Q

what affects cardiovascular health

A
  • genetics
  • familial (trauma, finance, education)
  • preemies
  • behavior
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17
Q

acute cardiovascular response to exercise

A
  • bone marrow and EPO stimulation to make more rbcs
  • vagal tone and function increase
  • ATP, glucose, and O2 used to meet metabolic demand
    -angiogenesis (blood vessel creation)
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18
Q

hypotension

A

low blood pressure (<90/60)

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19
Q

hypertension

A
  • high blood pressure (>130/80)
  • usually silent (unless hypertensive crisis)
  • 12.8% of all deaths
  • risk factor for heart disease, heart failure, peripheral vascular disease, renal impairment, retinal hemorrhage, visual impairment and stroke
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20
Q

hypoperfusion

A

reduced amount of blood flow

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21
Q

most important hormonal system involved in Na+ and blood pressure regulation

A

renin-angiotensin-aldosterone system

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22
Q

hypovolemia

A

a state of low extracellular fluid volume, generally secondary to combined sodium and water loss

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23
Q

cardiovacular disease includes

A
  • sudden cardiac death
  • atherosclerosis
  • atrial fibrillation
  • stroke
  • heart failure
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24
Q

sudden cardiac death cause

A
  • arrythmia, errors of conduction
  • long qt 1, long qt 2, long qt 3, cpvt, brugada syndrome
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25
Q

hypertrophic cardiomyopathy

A
  • walls of the heart chamber are too thick
  • reduces the heart’s ability to do its job
  • obstructs flow of blood from the heart to the rest of the body (thickened heart muscle is too stiff to pump effectively)
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26
Q

hypertrophic cardiomyopathy symptoms

A

usually during exertion:
- shortness of breath
- chest pressure
- fainting or fatigue
- heart palpitations

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27
Q

hypertrophic cardiomyopathy cause

A

complex inherited genetic mutation

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28
Q

hypertrophic cardiomyopathy treatment

A
  • medication (2/3)
  • lifestyle changes (1/3)
  • septal myectomy (open heart surgery): a portion of the thickened heart wall is surgically removed to improve blood flow
  • septal ablation: a small portion of the thickened heart wall is intentionally scarred using a long thin tibe
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29
Q

atherosclerosis

A

narrowing or hardening of arteries due to plaque build up
- deposits of fat, cholesterol, and other substance block normal blood flow or cause a clot

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30
Q

what diseases can atherosclerosis cause

A
  • carotid artery disease (in the arteries that supply blood to the brain, can cause stroke)
  • coronary artery/heart disease (in the arteries to the heart, can cause heart attack)
  • chronic kidney disease (in the renal arteries, can cause loss of kidney function)
  • peripheral artery disease (in the arteries in the legs, can cause amputation and ulcers)
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31
Q

most common type of heart disease

A

coronary artery/heart disease

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32
Q

atrial fibrillation

A
  • abnormal electrical impulses suddenly start firing in the atria
  • most common arrythmia
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33
Q

stroke

A
  • an interruption of blood flow to the brain
  • without oxygenated blood, brain cells die
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34
Q

stroke types

A
  • ischemic
  • hemorrhagic
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35
Q

ischemic stroke

A
  • clot or mass blocks a blood vessel cutting off blood flow to a part of the brain
  • most common
  • 1/4 of cases have no known cause
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36
Q

hemorrhagic stroke

A

weakened blood vessel like an aneurysm ruptures and spills blood into the brain

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37
Q

possible hidden causes of a stroke

A
  • irregular heartbeat
  • heart structure problems
  • artery hardening
  • blood clotting disorder
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38
Q

why is it important to find the cause of a stroke

A

to implement prevention strategies

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39
Q

heart failure

A
  • a condition in which your heart does not pump blood efficiently around the body
  • makes it difficult for the body to get oxygen and blood
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40
Q

heart failure symptoms

A
  • breathlessness
  • fluid build up on the lungs
  • swollen legs, ankles, and abdomen
  • persistent cough
  • tiredness
  • palpitations
  • fainting
  • dizziness
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41
Q

heart failure causes

A
  • high blood pressure
  • coronary heart disease
  • cardiomyopathy
  • heart valve damage
  • arrhythmia
  • congenital heart disease
  • myocarditis
  • some drugs used in cancer treatment
  • excessive alcohol consumption
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42
Q

effective heart properties

A
  • regular contractions at an appropriate rate for metabolism
  • guaranteed time for ventricular filling after atrial and ventricular contractions
  • contraction duration long enough for physical movement of fluid
  • contractile strength sufficient to generate appropriate pressures
  • ventricular pressure directed towards exit valves
  • coordination of left and right atrial/ventricular contractions
  • matched volumes for emptying and filling
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43
Q

location of the heart

A
  • in the mediastinum
  • enclosed by the pericardium
  • medial
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44
Q

size of the heart

A
  • 250-350 grams
  • size of a human fist
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45
Q

adipose tissue around the heart function

A

insulate and protect

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46
Q

pericardium function

A

attaches heart to surrounding tissues
- tough double layered membraneous sac

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47
Q

pericardium components

A
  • visceral layer (attaches to heart surface)
  • parietal layer (outer pericardial layer)
  • lubricating fluid between layers reduces friction during movement of heart surface with contraction
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48
Q

myocardium

A
  • heart muscle
  • elastic, lubrication for movement
  • fibers branch and are connected with intercalated discs (connect cells, gap junctions allow for action potential conduction)
  • striated appearance
  • ordered sarcomere arrangement
  • irregular shaped cells
  • single centralized nuclei
  • sarcoplasmic reticulum and T-system present
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49
Q

what characteristic is unique to cardiac muscle

A

no requirement for external neural input

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50
Q

all cardiac cells display ?

A

pacemaker activity

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51
Q

cardiac muscle acts as a __________

A

syncytium

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52
Q

syncytium

A

network of cardiac muscle cells connected by gap junctions that allows coordinate contraction of the ventricles

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53
Q

heart activity controlled by…

A
  • ANS (sympathetic and parasympathetic)
  • control of rate and contractile strength
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54
Q

hypertrophy types

A
  • physiological
  • pathological
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55
Q

physiological hypertrophy (cause, outcome)

A
  • pregnancy
  • exercise
  • physiological stimulus
  • enhanced function
  • improved metabolism
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56
Q

hypertrophy definition

A

when heart muscles enlarge

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57
Q

pathological hypertrophy

A
  • hypertension/high afterload (fibrotic lesions)
  • infarction (fibrotic lesions, impaired electrical function)
  • diabetes (fatty and fibrotic lesions, increased ventricular mass, diastolic dysfunction)
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58
Q

heart valves function

A
  • one-way valve that prevents the backward flow of blood
  • when pressure is greater behind the valve, it opens
  • when pressure is greater in front of the valve, it closes
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59
Q

heart valves labeled

A
  • tricuspid valve: located between the right atrium and the right ventricle
  • pulmonary valve: located between the right ventricle and the pulmonary artery
  • mitral valve: located between the left atrium and the left ventricle
  • aortic valve: located between the left ventricle and the aorta
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60
Q

chordae tendinae function

A

prevent opening of valve in the wrong direction

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61
Q

bicuspid aortic valve

A
  • untreated bicuspid aortic valve can eventually lead to symptoms of heart failure (shortness of breath, fatigue, and swelling)
  • aortic aneurysm might develop downstream from the aortic valve, can lead to bleeding or rupture
  • may eventually leak (aortic regurgitation) and/or narrow (aortic stenosis)
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62
Q

aortic regurgitation

A

allows some of the blood that was pumped out of the left ventricle to leak back in

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63
Q

av stenosis

A
  • occurs when the aortic valve narrows and blood cannot flow normally
  • higher longevity is harder to repair
  • tightened fibrous valves impair function
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64
Q

myocardium progression to heart failure

A
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65
Q

coronary arteries

A
  • aortic arch
  • superior vena cava
  • inferior vena cava
  • right coronary artery
  • left coronary artery
  • right coronary artery
  • great cardiac vein
  • left pulmonary veins
  • right pulmonary veins
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66
Q

sinoatrial (SA) node

A
  • cardiac pacemaker
  • located within the right atrial wall at junction with superior vena cava
  • 80-100 action potentials per minute
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67
Q

atrioventricular (AV) node

A
  • located above cardiac septum at junction of atria and ventricles
  • 40-60 action potentials per minute
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68
Q

bundle of his

A
  • located down ventricular septum to apex
  • 20-40 action potentials per minute
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69
Q

purkinje fibers

A
  • located throughout ventricular myocardium from apex to base
  • 15-40 action potentials per minute
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70
Q

what limits the rate of production of action potentials by the SA node

A

how fast Na+ leaks in through funny channels (HCN channels)

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71
Q

electrical conduction in the heart

A
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72
Q

cardiac action potential

A
  • exhibit prolonged plateau phase (due to activation of slow L-type Ca2+ channels) accompanied by prolonged period of contraction (ensures adequate ejection time)
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73
Q

refractory period means ? is impossible

A

tetanus

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74
Q

relationship of action potentials and contractile response in cardiac muscle

A
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75
Q

action potential in cardiac contractile cells steps

A
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76
Q

phases of ventricular action potential

A
  • phase 0: rapid depolarization
  • phase 1: early repolarization
  • phase 2: action potential plateau
  • phase 3: final rapid repolarization
  • phase 4: resting membrane depolarization and diastolic depolarization
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77
Q

phase 0: rapid depolarization

A
  • excitatory stimulus or pacemaker potential depolarizes cell membrane beyond -70 mV
  • at -70 mV, Na+ channels are activated and allow inward current
  • current is brief but enormous, peaking at +47 mM membrane potential
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78
Q

phase 1: early repolarization

A
  • potential increase results in opening of outward K+ channels and inward Ca2+ channels
  • repolarization from +47 mM to +10 mV due to rapid closure of Na+ channels and activation of transient outward K+ current
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79
Q

phase 2: action potential plateau

A
  • membrane potential remains depolarized near 0 mV
  • maintained by 2 inward Ca2+ currents and 4 outward K+ currents
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80
Q

phase 3: final rapid repolarization

A

outward K+ current dominate and cause rapid repolarization

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81
Q

phase 4: resting membrane depolarization and diastolic depolarization

A
  • outward K+ channels in phase 3 deactivate, membrane is repolarized to -40 mV
  • voltage-dependent Na+ channel that causes phase 0 remains inactivated until this happens
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82
Q

sinoatrial versus ventricular myocyte action potentials

A
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83
Q

(sinoatrial action potential) the membrane is leaky to ? most of the time, but is much leakier when …

A

K+; voltage dependent potassium channels open in response to depolarization

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84
Q

(sinoatrial action potential) membrane potential determined by

A

potassium (K+)

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85
Q

(sinoatrial action potential) if depolarization occurs, what will drive membrane potential back down

A

increased K+ potential

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86
Q

(sinoatrial action potential) funny current definition and reason behind the name

A
  • current that allows Na+ to leak into SA nodal cells
  • an odd
    (funny) channel because it is voltage-dependent but opens during membrane hyperpolarisation rather than depolarisation
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87
Q

(sinoatrial action potential) key to automaticity

A

slow, depolarising baseline drift

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88
Q

(sinoatrial action potential) SA nodal cells constantly depolarise slowly, except during ?

A

hyperpolarisation – such as when K+ leaves the cell abruptly

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89
Q

(sinoatrial action potential) two sets of voltage-gated Ca2+ channels that contribute to the action potential

A
  • T-type (transient) Ca2+ channels
  • L-type (long-lasting) Ca2+ channels
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90
Q

(sinoatrial action potential) T-type Ca2+ channels

A
  • opens at a specific level of membrane depolarization
  • open transiently (T-type), providing the initial depolarising to fire the action potential
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91
Q

(sinoatrial action potential) L-type Ca2+ channels

A
  • mediate the initial depolarising to fire the action potential
  • in non-pacemaker atrial myocytes this entry of Ca2+ causes
    contraction
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92
Q

(sinoatrial action potential) resetting membrane potential

A
  • after a brief delay the L-type calcium channels close and the voltage-gated K+ channels open
  • hyperpolarisation opens the Na+ leak channels, starting the process again
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93
Q

(ventricular action potential) resting membrane potential rests at a stable level until …

A

an action potential arrives from the bundle of His

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94
Q

(ventricular action potential) bundle of His action potential arrives which leads to …

A

an increase in Ca2+ entry and contraction of the myocyte

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95
Q

(ventricular action potential) does the action potential in a ventricle look similar to an atrium?

A

no, more closely resembles the action
potential in skeletal muscle

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96
Q

(ventricular action potential) rapid cell depolarization to contractions

A
  • fast Na+ channels open
  • opens L-type Ca2+ channels (SA node cells)
  • Ca2+ entry initiates contraction
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97
Q

(ventricular action potential) contraction to resting membrane potential

A
  • voltage-gated K+ channels open as the Na+ and Ca2+ begin to close, causing hyperpolarisation
  • membrane potential back to its resting level
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98
Q

(ventricular action potential) refractory period

A
  • similar to skeletal muscle but the period is quite long so that tetanic contraction is impossible to allow ventricle filling
  • ventricular myocytes cannot sustain an action potential due to the inactivation of Na+ channels
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99
Q

what are ECGs useful for

A
  • assess heart orientation
  • localize areas that do not conduct electrical activity normally
  • assess myocardial hypertrophy or atrophy
  • accurate heart rate measurement
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100
Q

prolonged PR interval meaning

A

heart block/delay

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101
Q

short PR interval meaning

A

AP at risk of cascading on each other (can lead to ventricular tachycardia)

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102
Q

by how many seconds does atrial contraction precede ventricular contraction

A

160 msec

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103
Q

(PQRS complex) P wave

A

atrial depolarization

104
Q

(PQRS complex) PR segment

A

AV nodal delay

105
Q

(PQRS complex) QRS complex

A

ventricular depolarization (atria repolarizes simultaneous)

106
Q

(PQRS complex) ST segment

A

time during which ventricles are contracting and emptying

107
Q

(PQRS complex) T wave

A

ventricular repolarization

108
Q

(PQRS complex) TP interval

A

time during which ventricles are relaxing and filling

109
Q

different ECG abnormalities

A
  • rate abnormalities
  • rhythm abnormalities
  • cardiac myopathy
110
Q

ECG rate abnormalities

111
Q

ECG rhythm abnormalities

112
Q

ECG cardiac myopathy

113
Q

where are ion channels are related proteins responsible for de/repolarizing found

A
  • on the cell surface
  • in T-tubules
114
Q

cardiac cycle definition

A

all the events associated with the flow of blood thru the heart during a single complete heartbeat

115
Q

two phases of a heart beat

A
  • systole
  • diastole
116
Q

does myocardium contract and repolarize faster at low or high heart rates

117
Q

cardiac cycle sequence of events

A

atrial diastole -> ventricular diastole -> atrial systole -> ventricular systole

118
Q

why do valves open passively

A

pressure gradients

119
Q

mechanical phases of cardiac cycle

120
Q

end diastolic volume (EDV)

A

volume of blood in ventricle at end of diastole

121
Q

end systolic volume (ESV)

A

volume of blood in ventricle the end of systole

122
Q

stroke volume (SV)

A

volume of blood ejected from ventricle in each cycle

123
Q

ejection fraction definition and range

A
  • EDV% ejected per stroke
  • ranges 50%-75%
124
Q

what does one pressure volume loop represent

A

one cardiac cycle

125
Q

cardiac output

A

volume of blood ejected by each ventricle each minute

126
Q

venous return

A

volume of blood returning to atrium each minute

127
Q

venous return must be __________ cardiac output

128
Q

factors that influence cardiac output

A
  • metabolism (ca varies with activity level)
  • age (metabolic activity declines with age)
  • body size (co increases proportionately to body surface area)
129
Q

cardiac output controlled by

A
  • heart rate
  • stroke volume
130
Q

heart rate

A

the number of times the heart beats per minute

131
Q

what controls heart rate

A
  • SA node
  • parasympathetic (vagus) cholinergic input K+ permeability
  • sympathetic activity and epinephrine
  • exercise
132
Q

what controls stroke volume

A
  • end diastolic volume (controlled by venous return)
  • sympathetic activity and epinephrine
  • preload
  • contractility (extrinsic and intrinsic influences)
133
Q

exercises reduced heart rate to >110 bpm via…

A

symapthetic stimulation of:
- SA node (decreases K+ permeability, depolarizing effect)
- AV node (reduced delay via increase Ca2+)

134
Q

frank-starling law

A

relationship between edv, contraction strength, and sv

135
Q

frank-starling curve

A

show how changes in ventricular preload lead to changes in stroke volume

136
Q

frank-starling curve

A

show how changes in ventricular preload lead to changes in stroke volume

137
Q

frank-starling mechanism

A

Length Tension Relationship
– Varying Degree of
Stretching of Myocardium by
EDV

138
Q

preload

A
  • wall stress (force applied to unit
    cross-sectional area) in resting myocardium
  • depends on the end-diastolic pressure, chamber radius, and wall thickness
139
Q

Laplace’s Law

A
  • in a hollow sphere
  • internal pressure is proportional to the wall tension and inversely proportional to the internal radius
140
Q

tension

A

a force equal to wall stress time wall thickness

141
Q

contractility

A

the force of a contraction achieved from a given initial fiber length

142
Q

how can contractility force be increased

A
  • increased contractility
  • increasing resting fiber length through end-diastolic stretch
143
Q

positive inotropic agents

A

factors that increase contractility

144
Q

factors that increae contractility

A
  • sympathetic neurotransmitters
  • noradrenaline
  • circulating adrenaline
  • beta agonists
  • digoxin
  • reduced beat interval
145
Q

negative inotropes

A
  • ischemia
  • acidosis
  • heart failure
  • anesthetics
  • parasympathetic fiber activity
  • beta antagonists
  • calcium channel blockers
146
Q

afterload

A

force per unit cross-sectional area (stress) that opposes the shortening of an isotonically contracting muscle

147
Q

what does after load depend on

A
  • arterial pressure
  • chamber radius
  • wall thickness
148
Q

what is weakened in systolic heart failure

A

heart contractility

149
Q

cardiogenic shock

150
Q

steady state

151
Q

acute myocardial infarction

152
Q

is the circulatory system open or closed

153
Q

blood pressure

A

force exerted by blood

154
Q

blood flow pattern

A

high to low pressure

155
Q

circulatory system gradient function

A

maintain blood flow

156
Q

why does the heart have a pressure gradient

A

for bulk blood flow

157
Q

are pressures throughout vasculature constant

158
Q

pressure gradient formula (pulmonary circuit)

A

pressure in pulmonary arteries - pressure in pulmonary veins

159
Q

pulmonary arterial pressure

160
Q

pulmonary venous pressure

161
Q

total pulmonary circuit pressure gradient (#)

A

15 - 0 = 15 mmHg

162
Q

pressure gradient formula (systemic circuit)

A

pressure in aorta - pressure in vena cava (before it empties into right artium)

163
Q

mean arterial pressure (MAP) definition

A

pressure in aorta

164
Q

central venous pressure (CVP) definition

A

pressure in vena cava

165
Q

mean arterial pressure (#)

166
Q

central venous pressure (#)

167
Q

total systemic circuit pressure gradient (#)

A

15 - 0 = 15 mmHg

168
Q

is mean arterial pressure (MAP) diastolic or systolic pressure

A

both (2/3 diastolic and 1/3 systolic)

169
Q

what dictates blood flow

A
  • pressure gradients in vasculature
  • resistance in vasculature
170
Q

blood flows from ______ pressure to ______ pressure

171
Q

what does the heart create for the bulk flow of blood

A

pressure gradient

172
Q

flow formula

A

pressure gradient/resistance

173
Q

poiseuille’s law

A

resistance = (length x viscosity)/radius^4

174
Q

factors affecting resistance to flow

A
  • length of vessel
  • viscosity of fluid
  • radius of vessel (most important)
175
Q

volume flow rate formula

A

flow = volume/time

176
Q

regulation of arteriole radius

A
  • vasoconstriction
  • vasodilation
177
Q

vasoconstriction

A

decrease radius (by contracting smooth
muscle) –> increase resistance–> decrease
blood flow

178
Q

vasodilation

A

increase radiation (relax smooth muscle) –> decrease resistance –> increase blood flow

179
Q

arteriole radius depends on ?

A

contraction state of smooth muscle

180
Q

arteriole radius at rest

A

arteriolar tone (partially contracted)

181
Q

arteriole radius during vasoconstriction

A

increased contraction (decreased radius)

182
Q

arteriole radius during vasodilation

A

decreased contraction (increased radius)

183
Q

functions of arteriole radius changes

A
  • controlling blood flow to individual capillary beds
  • regulating mean arterial pressure
184
Q

types of factors that influence vasodilation and vasoconstriction

A
  • extrinsic factors
  • intrinsic factors
185
Q

extrinsic factors that influence vasodilation and vasoconstriction

A
  • autnomic nerves
  • hormones
186
Q

intrinsic factors that influence vasodilation and vasoconstriction

A
  • metabolism (active hyperemia)
  • changes in blood flow (reactive hyperemia)
  • myogenic response
  • locally secreted chemical messengers
187
Q

active hyperemia

A

increases in metabolism decrease O2 and cause vasodilation

188
Q

reactive hyperemia

A

reduction in blood flow cause vasodilation

189
Q

myogenic response

A
  • stretch of arteriolar smooth muscle
  • high perfusion pressure causes vasoconstriction
190
Q

myogenic response purpose

A

keep blood flow constant

191
Q

chemical messengers that influence vasodilation

A
  • nitric oxide
  • prostacyclin
  • adenosine
  • bradykinin
192
Q

chemical messengers that influence vasoconstriction

A

endothelin-1

193
Q

local chemical influences for intrinsic regulation of vessel radius

A
  • hypoxia
  • increased CO2
  • decreased pH
  • increase in potassium ions
  • adenosine
194
Q

local physical influences for intrinsic regulation of vessel radius

A
  • heat (increases blood flow by causing localized vasodilation)
  • cold (decreases blood flow by causing localized vasoconstriction)
  • myogenic response to stretch (autoregulation)
195
Q

how does decreased pH influence intrinsic regulation of vessel radius

A
  • carbonic acid is generated from high CO2 (metabolism waste)
  • lactic acid is produced from anaerobic metabolism of ATP production
196
Q

myogenic response to stretch (autoregulation)

A
  • arteriolar smooth muscle responds to being stretched by myogenically increasing its tone (contracting), therefore
    resisting the stretch
  • conversely, a decrease in stretch results in decreased myogenic tone
197
Q

factors affecting total peripheral resistance

A
  • arteriolar radius
  • blood viscosity
198
Q

blood viscosity

A

number of red blood cells

199
Q

central venous pressure

A

pressure in the large veins of the thoracic cavity that lead into the heart

200
Q

what does the pressure gradient between central veins and atria do

A

drive blood back the the heart

201
Q

decrease in venous pressure _________ driving force for venous return

202
Q

factors that influence central venous pressure and venous return

A
  • skeletal muscle pump
  • respiratory pump
  • blood volume
  • venomotor tone favors venous return
203
Q

respiratory pump

A
  • inspiration
  • expiration
204
Q

how does blood volume influence central venous pressure and venous return

A

decreased blood volume decreases central venous pressure (bleeding, dehydration)

205
Q

venomotor tone

A

sympathetic nerves constrict veins

206
Q

mean arterial pressure determinants

A
  • heart rate
  • stroke volume
  • total peripheral resistance
207
Q

total peripheral resistance

A

combined resistance of all blood vessels

208
Q

effects of cardiac output on mean arterial pressure

209
Q

effects of total peripheral resistance on mean arterial pressure

210
Q

mean arterial pressure

A

driving force for blood flow

211
Q

MAP < normal

A
  • hypotension
  • inadequate blood flow to tissue
212
Q

MAP > normal

A
  • hypertension
  • stress on heart and blood vessel walls
213
Q

when does systolic pressure occur

A

ventricular contraction

214
Q

systolic pressure in mmHg

215
Q

when does diastolic pressure occur

A

ventricular refilling

216
Q

diastolic pressure in nnHg

217
Q

pulse pressure

A

difference between systolic and diastolic pressure

218
Q

pulse pressure at rest

219
Q

high pulse pressure at rest is indicative of ?

A

vascular disease

220
Q

auscultation

A
  • blood pressure measurement
  • recorded at heart level via brachial artery
221
Q

korotkoff sounds

A

sounds heard during auscultation

222
Q

auscultation process

A
  • inflate cuff above expected systolic pressure
  • slowly deflate cuff (blood flows when BP > cuff pressure)
  • korotokoff sounds indicate systolic pressure
  • diastolic pressure indicated at disappearance of muffled sound
223
Q

sphygmomanometer

A

an instrument for measuring blood pressure

224
Q

sphygomanometry

225
Q

how long is short term regulation of MAP

A

seconds to minutes

226
Q

how long is long term regulation of MAP

A

minutes to days

227
Q

short term regulation of MAP

A
  • regulates cardiac output and total peripheral resistance
  • heart and blood vessels
  • primarily neural control
228
Q

long term regulation of MAP

A
  • regulates blood volume
  • involves kidneys
  • primarily hormonal control
229
Q

most important hormonal system involved in regulating Na+

A

renin-angiotensin-aldosterone system

230
Q

neural control of MAP

A

negative feedback loops

231
Q

negative feedback loop of MAP neural control

A
  • detector = baroreceptors
  • integration center = cardiovascular centers in the brainstem
  • controllers = autonomic nervous system
  • effectors = heart and blood vessels
232
Q

baroreceptor definition

A
  • stretch receptors
  • specialized nerve endings that respond to a vessel wall stretch
233
Q

arterial baroreceptors

A
  • high pressure baroreceptors
  • sinoaortic baroreceptors
234
Q

location of arterial baroreceptors

A
  • carotid sinus
  • aortic arch
235
Q

cardiovascular control center

A
  • medulla oblongata
  • sympathetic nervous system
  • parasympathetic nervous system
236
Q

location of cardiac and venous baroreceptors

A
  • walls of large systemic veins
  • walls of atria
237
Q

low pressure baroreceptors

A

volume receptors

238
Q

autonomic output to cardiovascular effectors, parasympathetic input to ?

A
  • SA node (decrease heart rate)
  • AV node
239
Q

autonomic output to cardiovascular effectors, sympathetic input to ?

A
  • SA node (increase heart rate)
  • AV node
  • ventricular myocardium (increase contractility)
  • arterioles (increase resistance)
  • veins (increase venomotor tone)
240
Q

baroreceptor reflex

A

negative feedback loop to maintain blood pressure at normal level

241
Q

components of baroreceptor reflex

A
  • detector = baroreceptors
  • afferents = nerves
  • integration center = cardiovascular control center
  • efferents = autonomic nervous system
  • effectors = heart, arterioles, veins
242
Q

types of baroreceptors

A
  • A fibers (myelinated)
  • C fibers (unmyelinated)
243
Q

A fiber baroreceptors

A
  • low pressure (30-90 mmHg)
  • important at rest
244
Q

C fiber baroreceptors

A
  • high pressure (70-140 mmHg)
  • increasingly active at higher pressures
245
Q

baroreceptor reflex - a person who had been lying down stands up too quickly

A
  • gravity causes venous pooling in the legs
  • decreases in venous resistance = decrease in cardiac output
  • decrease in blood pressure
  • baroreceptors sense the decrease and reflex occurs
  • reflex causes increased sympathetic and decreased parasympathetic activity
  • cardiac output and total peripheral resistance increase
  • blood pressure is increased to normal
246
Q

extra inputs to cardiovascular system control

A
  • bainbridge reflex
  • atrial stretch receptors
247
Q

bainbridge reflex

A
  • vena cava stretch receptors –> neural mediated increase heart rate
  • avoids venous congestion
248
Q

atrial stretch receptors

A
  • myelinated vagal afferents sensitive to blood volume
  • located at junction of great veins and atria
  • influence endocrine regulation regulation of blood volume
249
Q

hemorrhage causes

A
  • baroreceptor reflex
  • increase in sympathetic activity
  • decreases in parasympathetic activity
250
Q

response to hemorrhage

A
  • reflex compensation
  • MAP compensated only to near-normal level
251
Q

baroreceptor reflex in the GI tract

A
  • increased resistance
  • decreased blood flow
252
Q

baroreceptor reflex in the brain

A
  • vasculature not subject of extrinsic control
  • no change in resistance
  • blood diverted from GI tract to brain
253
Q

hormones that control mean arterial pressure

A
  • epinephrine
  • vasopressin
  • angiotensin II
254
Q

epinephrine control of mean arterial pressure

A
  • released by adrenal medulla in response to sympathetic activity
  • increases mean arterial pressure
  • increases heart rate and stroke volume
  • increases total periphery resistance on arterial smooth muscle
  • increases venomotor tone on smooth muscle of veins
255
Q

vasopressin and angiotension II control of mean arterial pressure

A
  • vasoconstrictors
  • increases total periphery resistance
  • increase mean arterial pressure

physiology allied health (6 decks)

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