CH 16: Altered Perfusion Flashcards

1
Q

physical movement of air between the outside and the inside of the lungs

A

Ventilation = breathing

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2
Q

where oxygen crosses from the lungs (environment) to the circulation = where gas exchange takes place

A

Alveolar-capillary junction = gas exchange

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3
Q

process of forcing blood or other fluid to flow through a vessel
and into the vascular bed of a tissue to provide oxygen and other nutrients

A

Perfusion

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4
Q

Requirements for effective perfusion include:

A

 Adequate ventilation and diffusion
 Intact pulmonary circulation
 Adequate blood volume and components
 Adequate cardiac output
 Intact cardiac control center in the medulla of the brain
 Intact receptors
 Intact parasympathetic and sympathetic nervous systems
 Intact cardiac conduction
 Intact coronary circulation
 Intact systemic circulation
 Adequate oxygen uptake in tissues:

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5
Q

The ability to breathe in and transport oxygen across the capillaries is mandatory for effective oxygen distribution to the tissues.

A

 Adequate ventilation and diffusion

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6
Q

Pulmonary circulation is required for the
uptake of oxygen from inspired air.

A

Intact pulmonary circulation

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7
Q

An expected blood volume is required to carry oxygen (on hemoglobin) and maintain blood pressure.

A

Adequate blood volume and components

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8
Q

An optimal stroke volume, an optimal heart rate, and an efficient heart rhythm are needed to maximize perfusion to the tissues.

A

Adequate cardiac output

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9
Q

needed to regulate heart rate and force of cardiac contractions, and to detect and respond to changes in blood pressure.

A

Intact cardiac control center in the medulla of the brain

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10
Q

play a major role in sensing changes in cardiac function and blood pressure, and they provide feedback to the cardiac control center in the brain.

A

Intact receptors

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11
Q

responsible for mediating changes in the cardiovascular system based on demands.

A

Intact parasympathetic and sympathetic nervous systems: The
autonomic nervous system (ANS)

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12
Q

essential in stimulating cardiac contractility.

A

Intact cardiac conduction

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13
Q

maintains perfusion to cardiac structures, enabling the heart to distribute oxygenated blood to the remainder of the body.

A

Intact coronary circulation

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14
Q

distributes oxygenated blood to tissues and organs.

A

 Intact systemic circulation

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15
Q

Oxygen-dependent cells and tissues must be receptive to oxygen and nutrients to survive.

A

Adequate oxygen uptake in tissues

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16
Q

ventilation-perfusion ratio

A

0.8:0.9

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17
Q

how is ventilation and perfusion affected by gravity

A

lung tissues that are most dependent, or closest to the
ground, are the most ventilated and perfused.

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18
Q

job of circulation

A

delivery system of oxygen and nutrients

removes waste

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19
Q

3 circulation pathways

A

pulmonary
cardiac
systemic

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20
Q

pulmonary circulation pathway

A

lungs = where oxygen transfers from the atmosphere to the body

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21
Q

cardiac circulation pathway

A

pumps the oxygenated blood to the body

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22
Q

systemic circulation pathway

A

distributes the oxygen and nutrients to where they need to go

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23
Q

primary sites for nutrient exchange at the cellular level

A

arterioles, capillaries, and venules

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24
Q

the more capillaries that the tissue/organ possesses =

A

the more perfusion

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25
Q

the more oxygen an organ needs =

A

the more capillaries at the site

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26
Q

Pulmonary circulation location and patho

A

 Right side of heart
 Lower pressure compared to systemic circulation – this allows for more time for gas exchange
 Pulmonary arteries, capillaries and veins
o Arteries carry deoxygenated blood to the lung
o Veins carry oxygenated blood to the left side of the heart

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27
Q

systemic circulation location and patho

A

Begins at the left side of the heart – left ventricle
Composed of all arteries, capillaries, and veins except those of the
pulmonary circulation
Higher pressure than pulmonary circulation – has to work against the resistance to get to peripheral tissues

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28
Q

coronary circulation patho

A

Part of systemic system
Provides blood to the heart
Essential for life
Cardiac muscle cells require a constant supply of oxygen and nutrients; these cells have little storage capacity.
Two major vessels, the right, and left coronary artery

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29
Q

additional circulation to help out when more cardiac demand or if a vessel becomes obstructed

helps meet demands

A

Collateral circulation

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30
Q

generates an electrical signal that causes the upper heart chambers (atria) to contract.

pacemaker stimulated by calcium-sodium channels

A

SA node

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31
Q

connection between atria and ventricles

A

AV node

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32
Q

job of the AV node

A

 allows the atria to empty into the ventricles
 makes the atria and ventricles beat together

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33
Q

a group of fibers that carry electrical impulses through the center of the heart.

A

bundle of his

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34
Q

specialized conducting fibers composed of electrically excitable cells.

A

purkinjie fibers

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35
Q

cause ventricle contraction

A

bundle of his
purkinjie fibers

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36
Q

Cardiac output (CO) =

A

stroke volume x heart rate

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37
Q

amount of blood pumped in a single beat

A

stroke volume

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38
Q

CO varies based on:

A

body size
age
metabolic needs

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39
Q

average CO

A

3.5 to 8 L per minute

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40
Q

CO depends on:

A

preload
cardiac contractility
afterload
heart rate
blood volume

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41
Q

blood pressure is maintained by:

A

 Contraction of the left ventricle
 Peripheral vascular resistance
 Elasticity of the arterial walls
 Viscosity and volume of the blood

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42
Q

blood pressure is

A

CO and resistance against the arteries
pressure of blood inside systemic arteries

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43
Q

contraction of the left ventricle and ejection of blood into the aorta

A

systolic blood pressure

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44
Q

causes of systolic blood pressure increase

A

o Exercise
o Smoking
o Cardiovascular disease
o stress

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45
Q

pressure that remains in the aorta during the resting phase of the cardiac cycle

A

diastolic blood pressure

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46
Q

possible causes of diastolic elevations

A

arteries are not allowed to rest in between contractions

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47
Q

possible causes for diastolic depression

A

lack of resistance or backflow from aortic valve

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48
Q

normal MAP range

A

70-100 mm Hg

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49
Q

measure of tissue perfusion

A

mean arterial pressure

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50
Q

needed MAP for perfusion of vital organs

A

at least 60

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51
Q

neural control of blood pressure

A

Neurons of the medulla and pons – act on the ANS = Sympathetic and Parasympathetic nervous system

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52
Q

increases heart rate, cardiac contractility, and tension of blood vessels

A

SNS

53
Q

decreases heart rate

A

PNS

54
Q

how does the body know when to change

A

 Baroreceptors and chemoreceptors
 The renin–angiotensin aldosterone system
 The kidneys

55
Q

jobs of the baroreceptors

A

o Sense pressure changes in the blood vessels and heart
o Targets of HTN drugs and include beta 1 (heart), alpha 1 (vessels)
o Blocking reduces CO and vasoconstriction

56
Q

job of the chemoreceptors

A

o Located in the aorta and carotid arteries
o Detect changes in oxygen, carbon dioxide, and pH of the blood

57
Q

how the RAAS affects blood pressure

A

The kidneys sense decreased blood pressure, decreased sodium in the tubules, or SNS activation of beta cells
 Renin – enzyme released from the kidneys – converts Angiotensin I and Angiotensin II
 Angiotensin I – converted to Angiotensin II in the lungs
 Angiotensin II powerful vasoconstrictor – increases blood pressure – it also stimulates the secretion of aldosterone
 Aldosterone increases salt and water retention –increases blood volume

58
Q

factors that can alter perfusion

A

 Ventilation–perfusion mismatching
 Impaired circulation
 Inadequate cardiac output
 Excessive perfusion demands

59
Q

ventilation-perfusion mismatching

A

inadequate ventilation in well-perfused lungs
inadequate perfusion in well-ventilated lungs

60
Q

inadequate ventilation in well-perfused lungs happens with:

A

asthma
pneumonia
pulmonary embolism

61
Q

inadequate perfusion in well-ventilated lungs happens with:

A

vascular obstruction (pulmonary embolus)

62
Q

not enough or too much blood flow to tissues or organs

A

impaired circulation

63
Q

impaired circulation can be from:

A

 Injury to vessels
 Obstruction
 Inadequate movement of blood
 Not enough blood

64
Q

loss of blood due to injury

A

hemorrhage

65
Q

lipid deposits on the lining of arteries - plaques

A

atherosclerosis

66
Q

clot due to vessel damage of turbulent of stagnant flow

A

thrombosis

67
Q

bulges caused by weakness in a vessel

A

aneurysms

68
Q

prolonged bed rest and varicose veins

A

venous stasis

69
Q

causes of vessel wall damage

A

excessive clotting
alterations in blood flow, turbulence or sluggish movement

70
Q

causes of turbulent of stagnant flow

A

o Venous stasis
o Turbulence such as around areas of atherosclerosis
o Aneurysms

71
Q

excessive clotting

A

hypercoagulability

72
Q

possible causes of hypercoagulability

A

 Autoimmune mechanisms that activate platelets and alter coagulation factors
 Certain types of cancer, or myeloproliferative disorders, such as thrombocythemia (excess platelets)
 Sickle cell disease
 Polycythemia vera
 Use of oral contraceptives
 Vascular changes in the late stage of pregnancy

73
Q

possible outcome of hypercoagulability

A

 The thrombus continues to grow and occlude the vessel completely.
 The thrombus is degraded by enzymes and decreases in size.
 All or part of the thrombus breaks off and travels through the circulation.

74
Q

process of obstructing a vessel

A

infarction
can cause sudden death

75
Q

often originate in the deep veins of the legs (DVT) –
often at a bifurcation break off and lodge into the pulmonary arteries (PE)

A

Venous thromboemboli

76
Q

most often originate in the heart as atherosclerotic plaques, and they can travel to the brain, intestines, lower extremities, or kidneys.

A

Arterial thromboemboli

77
Q

Cardiac output is inadequate when

A

the heart is unable to successfully eject
the necessary amount of blood to the pulmonary and systemic circulation.

78
Q

causes of inadequate cardiac output

A

 Changes in, or
o blood volume: dehydration or hemorrhage
o composition: anemia not enough RBCs to carry O2
o viscosity: thicker viscosity increases peripheral resistance reduces blood flow
 Impaired ventricular pumping
o Loss of muscle function – for example heart failure
 Structural heart defects, such as
o valve defects, allow the leaking or regurgitation of blood
o openings between chambers
o narrowing of the aorta
 Conduction defects that lead to an unresponsive heart rate and rhythm –
o Example cardiac dysrhythmias – inability to maintain an efficient heart rhythm.
o Can stem from the SA node, AV node, or cardiac cells, or the atria and ventricles –
o Ventricular dysrhythmias are very troublesome, example v fib a fib
 Excessive or significantly reduced peripheral vascular resistance
o Hypotension or hypertension

79
Q

impaired cardiac output clinical manifestations

A

Changes in blood volume
Changes in peripheral vascular resistance
Thrombosis – DVT or PE

80
Q

excessive perfusion demands from:
ex:

A

altered or excessive tissue metabolism
ex: hyperthyroidism

81
Q

diagnostic tests to determine altered perfusion

A

Echo
Cardiac catheter
chest x-ray
ECG
pressure measurements

82
Q

circulatory failure and impaired perfusion of vital organs

A

shock

83
Q

3 classifications of shock

A

cadiogenic
hypovolemic
massive systemic vasodilation

84
Q

cardiogenic shock is inadequate cardiac pumping that leads to:

A

o reduced cardiac output
o low blood pressure
o restricted movement of oxygenated blood through the circulation

85
Q

cardiogenic shock leads to

A

hypotension and pulmonary edema

86
Q

leading cause of cardiogenic shock

A

MI

87
Q

inadequate blood/plasma volume

A

hypovolemic shock

88
Q

causes of hypovolemic shock

A

o Hemorrhage
o Burns
o Diarrhea
o Polyuria – like in DI

89
Q

hypovolemic shock results in

A

low venous return and reduced circulation
reduced oxygen transport
organ failure

90
Q

types of massive systemic vasodilation shock

A

septic
neurogenic
anaphylactic

91
Q

overwhelming infection

A

septic shock

92
Q

brain of spinal cord injury

A

neurogenic shock

93
Q

hypersensitivity response

A

anaphylactic shock

94
Q

clinical manifestations of shock

A

 Chest pain
 Shortness of breath
 Labored breathing
 Diaphoresis
 Nausea
 Vomiting
 And condition-specific manifestations

95
Q

Total occlusion of one or coronary arteries

A

Myocardial Infarction (MI)

96
Q

most common cause of MI

A

atherosclerosis

97
Q

risk factors for MI

A

o Family history
o Hypertension
o Smoking
o Cholesterol levels
o Comorbid diabetes mellitus

98
Q

labs and tests for MI

A

troponin
CK-MB
ECG

99
Q

the heart is unable to maintain blood circulation or meet the demand of the tissues and organs

A

heart failure

100
Q

causes of HF

A

secondary to other conditions

101
Q

HF can be secondary to these conditions:

A

 MI
 Heart defects
 Infection
 Inflammation of heart tissue
 Hypertension
 Fluid volume overload
 Anemia

102
Q

Left sided HF patho

A

Left ventricle – can become larger hypertrophy – becomes ineffective

103
Q

left sided HF clinical manifestations

A

o Fluid in the lungs – pulmonary edema
o Bilateral rhonchi or crackles in the bases

104
Q

right sided HF

A

 Right side of heart
 Loses Ability to move deoxygenated blood to the lungs

105
Q

clinical manifestations of right sided HF

A

Peripheral edema extremities, hepatomegaly, spleenomegaly, GI tract, peritoneum

106
Q

causes of right sided HF

A

Cor pulmonale – right heart structure is altered
o Lung injury
o Infections
o Inflammation
o Pulmonary edema
o Left heart failure (most common!!)

107
Q

overtime, right sided HF can trigger

A

dysrhythmias
deprive vital organs of oxygen

108
Q

myocardial hypertrophy can contribute to:

A

contractility but eventually impairs diastole and promotes oxygen deprivation to the myocardium.

109
Q

congestion of peripheral tissues

A

right HF

110
Q

decreased cardiac output
pulmonary congestion

A

left HF

111
Q

side effects of decreased cardiac output

A

activity intolerance
signs of decreased tissue perfusion

112
Q

side effects of pulmonary congestion

A

impaired gas exchange
cyanosis
signs of hypoxia
pulmonary edema
cough with frothy sputum
orthopnea
paroxysmal nocturnal dyspnea

113
Q

vasodilation =

A

increased blood flow

114
Q

more capillaries =

A

more perfusion

115
Q

arteries carry what where

A

deoxygenated blood to lungs

116
Q

veins carry what where

A

oxygenated blood to left side of heart

117
Q

high peripheral resistance means heart works

A

much harder

118
Q

depolarization of the atria

A

P wave

119
Q

ventricles contract

A

QRS

120
Q

repolarization of ventricles - finds MI

A

ST

121
Q

ST depression means

A

ischemia

122
Q

ST elevation means

A

cells died = MI

123
Q

stretch of myocardium

A

preload

124
Q

force of contraction

A

cardiac contractility

125
Q

tension on the ventricles

A

afterload

126
Q

how to make adjusts to BP

A

CO
peripheral vascular resistance
SNS

127
Q

causes of injury to lining in atherscherosis

A

HTN
smoking
environmental exposure

128
Q

eventual conclusion of atherschelrosis

A

occlude the artery and break off and become a thrombus

129
Q

excessive perfusion demands from:
ex:

A

altered or excessive tissue metabolism
ex: hyperthyroidism