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Patho Exam 4 > CH 16: Altered Perfusion > Flashcards

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
the more oxygen an organ needs =
the more capillaries at the site
26
Pulmonary circulation location and patho
 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
27
systemic circulation location and patho
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
28
coronary circulation patho
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
29
additional circulation to help out when more cardiac demand or if a vessel becomes obstructed helps meet demands
Collateral circulation
30
generates an electrical signal that causes the upper heart chambers (atria) to contract. pacemaker stimulated by calcium-sodium channels
SA node
31
connection between atria and ventricles
AV node
32
job of the AV node
 allows the atria to empty into the ventricles  makes the atria and ventricles beat together
33
a group of fibers that carry electrical impulses through the center of the heart.
bundle of his
34
specialized conducting fibers composed of electrically excitable cells.
purkinjie fibers
35
cause ventricle contraction
bundle of his purkinjie fibers
36
Cardiac output (CO) =
stroke volume x heart rate
37
amount of blood pumped in a single beat
stroke volume
38
CO varies based on:
body size age metabolic needs
39
average CO
3.5 to 8 L per minute
40
CO depends on:
preload cardiac contractility afterload heart rate blood volume
41
blood pressure is maintained by:
 Contraction of the left ventricle  Peripheral vascular resistance  Elasticity of the arterial walls  Viscosity and volume of the blood
42
blood pressure is
CO and resistance against the arteries pressure of blood inside systemic arteries
43
contraction of the left ventricle and ejection of blood into the aorta
systolic blood pressure
44
causes of systolic blood pressure increase
o Exercise o Smoking o Cardiovascular disease o stress
45
pressure that remains in the aorta during the resting phase of the cardiac cycle
diastolic blood pressure
46
possible causes of diastolic elevations
arteries are not allowed to rest in between contractions
47
possible causes for diastolic depression
lack of resistance or backflow from aortic valve
48
normal MAP range
70-100 mm Hg
49
measure of tissue perfusion
mean arterial pressure
50
needed MAP for perfusion of vital organs
at least 60
51
neural control of blood pressure
Neurons of the medulla and pons – act on the ANS = Sympathetic and Parasympathetic nervous system
52
increases heart rate, cardiac contractility, and tension of blood vessels
SNS
53
decreases heart rate
PNS
54
how does the body know when to change
 Baroreceptors and chemoreceptors  The renin–angiotensin aldosterone system  The kidneys
55
jobs of the baroreceptors
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
job of the chemoreceptors
o Located in the aorta and carotid arteries o Detect changes in oxygen, carbon dioxide, and pH of the blood
57
how the RAAS affects blood pressure
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
factors that can alter perfusion
 Ventilation–perfusion mismatching  Impaired circulation  Inadequate cardiac output  Excessive perfusion demands
59
ventilation-perfusion mismatching
inadequate ventilation in well-perfused lungs inadequate perfusion in well-ventilated lungs
60
inadequate ventilation in well-perfused lungs happens with:
asthma pneumonia pulmonary embolism
61
inadequate perfusion in well-ventilated lungs happens with:
vascular obstruction (pulmonary embolus)
62
not enough or too much blood flow to tissues or organs
impaired circulation
63
impaired circulation can be from:
 Injury to vessels  Obstruction  Inadequate movement of blood  Not enough blood
64
loss of blood due to injury
hemorrhage
65
lipid deposits on the lining of arteries - plaques
atherosclerosis
66
clot due to vessel damage of turbulent of stagnant flow
thrombosis
67
bulges caused by weakness in a vessel
aneurysms
68
prolonged bed rest and varicose veins
venous stasis
69
causes of vessel wall damage
excessive clotting alterations in blood flow, turbulence or sluggish movement
70
causes of turbulent of stagnant flow
o Venous stasis o Turbulence such as around areas of atherosclerosis o Aneurysms
71
excessive clotting
hypercoagulability
72
possible causes of hypercoagulability
 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
possible outcome of hypercoagulability
 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
process of obstructing a vessel
infarction can cause sudden death
75
often originate in the deep veins of the legs (DVT) – often at a bifurcation break off and lodge into the pulmonary arteries (PE)
Venous thromboemboli
76
most often originate in the heart as atherosclerotic plaques, and they can travel to the brain, intestines, lower extremities, or kidneys.
Arterial thromboemboli
77
Cardiac output is inadequate when
the heart is unable to successfully eject the necessary amount of blood to the pulmonary and systemic circulation.
78
causes of inadequate cardiac output
 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
impaired cardiac output clinical manifestations
Changes in blood volume Changes in peripheral vascular resistance Thrombosis – DVT or PE
80
excessive perfusion demands from: ex:
altered or excessive tissue metabolism ex: hyperthyroidism
81
diagnostic tests to determine altered perfusion
Echo Cardiac catheter chest x-ray ECG pressure measurements
82
circulatory failure and impaired perfusion of vital organs
shock
83
3 classifications of shock
cadiogenic hypovolemic massive systemic vasodilation
84
cardiogenic shock is inadequate cardiac pumping that leads to:
o reduced cardiac output o low blood pressure o restricted movement of oxygenated blood through the circulation
85
cardiogenic shock leads to
hypotension and pulmonary edema
86
leading cause of cardiogenic shock
MI
87
inadequate blood/plasma volume
hypovolemic shock
88
causes of hypovolemic shock
o Hemorrhage o Burns o Diarrhea o Polyuria – like in DI
89
hypovolemic shock results in
low venous return and reduced circulation reduced oxygen transport organ failure
90
types of massive systemic vasodilation shock
septic neurogenic anaphylactic
91
overwhelming infection
septic shock
92
brain of spinal cord injury
neurogenic shock
93
hypersensitivity response
anaphylactic shock
94
clinical manifestations of shock
 Chest pain  Shortness of breath  Labored breathing  Diaphoresis  Nausea  Vomiting  And condition-specific manifestations
95
Total occlusion of one or coronary arteries
Myocardial Infarction (MI)
96
most common cause of MI
atherosclerosis
97
risk factors for MI
o Family history o Hypertension o Smoking o Cholesterol levels o Comorbid diabetes mellitus
98
labs and tests for MI
troponin CK-MB ECG
99
the heart is unable to maintain blood circulation or meet the demand of the tissues and organs
heart failure
100
causes of HF
secondary to other conditions
101
HF can be secondary to these conditions:
 MI  Heart defects  Infection  Inflammation of heart tissue  Hypertension  Fluid volume overload  Anemia
102
Left sided HF patho
Left ventricle – can become larger hypertrophy – becomes ineffective
103
left sided HF clinical manifestations
o Fluid in the lungs – pulmonary edema o Bilateral rhonchi or crackles in the bases
104
right sided HF
 Right side of heart  Loses Ability to move deoxygenated blood to the lungs
105
clinical manifestations of right sided HF
Peripheral edema extremities, hepatomegaly, spleenomegaly, GI tract, peritoneum
106
causes of right sided HF
Cor pulmonale – right heart structure is altered o Lung injury o Infections o Inflammation o Pulmonary edema o Left heart failure (most common!!)
107
overtime, right sided HF can trigger
dysrhythmias deprive vital organs of oxygen
108
myocardial hypertrophy can contribute to:
contractility but eventually impairs diastole and promotes oxygen deprivation to the myocardium.
109
congestion of peripheral tissues
right HF
110
decreased cardiac output pulmonary congestion
left HF
111
side effects of decreased cardiac output
activity intolerance signs of decreased tissue perfusion
112
side effects of pulmonary congestion
impaired gas exchange cyanosis signs of hypoxia pulmonary edema cough with frothy sputum orthopnea paroxysmal nocturnal dyspnea
113
vasodilation =
increased blood flow
114
more capillaries =
more perfusion
115
arteries carry what where
deoxygenated blood to lungs
116
veins carry what where
oxygenated blood to left side of heart
117
high peripheral resistance means heart works
much harder
118
depolarization of the atria
P wave
119
ventricles contract
QRS
120
repolarization of ventricles - finds MI
ST
121
ST depression means
ischemia
122
ST elevation means
cells died = MI
123
stretch of myocardium
preload
124
force of contraction
cardiac contractility
125
tension on the ventricles
afterload
126
how to make adjusts to BP
CO peripheral vascular resistance SNS
127
causes of injury to lining in atherscherosis
HTN smoking environmental exposure
128
eventual conclusion of atherschelrosis
occlude the artery and break off and become a thrombus
129
excessive perfusion demands from: ex:
altered or excessive tissue metabolism ex: hyperthyroidism

Patho Exam 4 (2 decks)

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