Cardiovascular/CAD/PAD/Pulmonnary Flashcards

Flash cards for exam 3

1
Q

Blood flows from the RA thru the __ valve

A

Tricuspid

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2
Q

Blood flows from the LA thru the __ valve

A

Mitral

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3
Q

Blood flows from the RV thru the __ valve

A

Pulmonary

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4
Q

Blood flows from the LV thru the __ valve

A

Aortic

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5
Q

Heart valves in order of flow:

A

Tricuspid
Pulmonary
Mitral
Aortic

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6
Q

Average stroke volume:

A

70mL/Beat

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7
Q

Cardiac output is determined by:

A

SV X BPM

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8
Q

Ability of the heart muscle to pump effectively!

A

Cantractility

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9
Q

Volume of blood in ventricles before contraction

A

Preload

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10
Q

Pulmonary vascular Resistance

A

RV afterload

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11
Q

Systemic vascular resistance

A

LV afterload

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12
Q

RV afterload can cause

A

right sided heart failure

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13
Q

LV after load can be too high due to:

A

HTN or atherosclerosis/arteriosclerosis

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14
Q

RV afterload can be caused by

A

atherosclerosis/arteriosclerosis of pulmonary vessels; stiff, noncompliant lung tissue

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15
Q

Normal preload value:

A

~4-6 L/min

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16
Q

Blood flow back to the heart

A

venous return

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17
Q

Most venous disorders occur in:

A

the legs

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18
Q

CVI

A

chronic venous insufficiency

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19
Q

DVT

A

deep vein thrombosis

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20
Q

CVI & DVT are usually related to problems pertaining to:

A

maintaining forward flow

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21
Q

AKA “valve incompetence”

A

Venous insufficiency

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22
Q

Pooling of blood due to venous insufficiency

A

venous congestion

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23
Q

Factors contributing to venous congestion

A

Gravity (standing for long periods)

Valve incompetence

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24
Q

Worn out, “floppy” valves in leg veins

A

Venous insufficiency

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25
Q

Blood pooling due to worn out, floppy leg vein valves

A

Venous stasis

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26
Q

Venous stasis causes an increase in:

A

hydrostatic pressure

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27
Q

Increased hydrostatic pressure can result in:

A

fluid shifting into the legs > edema

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28
Q

Mini concept map for Venous stasis ulcers

A

Venous stasis > increased hydro. pressure > fluid shift into tissue > edema > improperly functioning skin cells due to pressure > skin breaks easily > venous stasis ulcers

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29
Q

Another possible sequela to Venous insufficiency caused by increased hydrostatic pressure

A

Varicose veins

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30
Q

Contributing factors to CVI

A
Aging
Genetics
Obesity
Pregnancy
Job functions (standing)
Immobility
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31
Q

Pathologic clot that forms in walls of veins, especially in veins of thighs & calves

A

deep vein thrombosis

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32
Q

Inflamed tissue around a DVT

A

thrombophlebitis

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33
Q

S/S of DVT

A

SHEP
Usually occurs unilaterally
May be extreme or discrete
May have no S/S

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34
Q

Risk factors of DVT are called:

A

Virchow’s Triad

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35
Q

Virchow’s triad consists of:

A

Injury to venous endothelium
Stasis of blood flow (due to immobility or venous insufficiency)
States of hyper-coagulability (dehydration, individual tendencies to clot easily)

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36
Q

Individual tendency to clot easily is called

A

coagulopathy

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37
Q

Potentially deadly sequela of DVT

A

Pulmonary embolism

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38
Q

Mini concept map of PE

A

DVT > thrombus or part breaks loose & travels > embolus > embolus travels to/thru the heart > embolism lodges into pulmonary arterioles

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39
Q

Oxygenated blood blocked from entering the pulmonary capillaries due to an embolism can cause:

A

SOB, chest pain

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40
Q

Hemoptysis as a S/S of PE is caused by:

A

inflammation of alveolar tissue causing leakage of blood/fluids into the alveolar space

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41
Q

S/S of PE include:

A

SOB, chest pain, shock, hemoptysis, death

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42
Q

Treatment/prevention of PE includes:

A

Encouraging mobility & hydration
Elevating feet & legs
Monitor skin for breakdown & stasis ulcers
Anticoagulants

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43
Q

Ability of arteries to work efficiently is determined by

A

vasomotor tone

State of the lumen

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44
Q

__ can be determined by vasomotor tone

A

BP

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45
Q

Normal, healthy arterial lumens should be

A

smooth and patent (free of any sort of blockage)

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46
Q

Delivery of O2 & nutrients to tissue beds via the arterial system

A

perfusion

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47
Q

Good perfusion results in:

A

adequate delivery of O2 & nutrients
Normal pulses & BP
Normal cap refill
Normal organ function

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48
Q

Strength & quality of pulses are indicative of:

A

state of the lumen & vasomotor tone

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49
Q

AKA “arterial disease”

A

arterial insufficiency

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50
Q

Common to all arterial disorders is:

A

ischemia

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51
Q

Arterial dz is almost always due to

A

athero/arteriosclerosis

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52
Q

Atherosclerosis=

A

stiffening of arteries & buildup of fat & other substances in arterial walls

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53
Q

Chronic dz of arterial system usually related to aging, where arterial walls become thick & hard

A

arteriosclerosis

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54
Q

Etiology of arteriosclerosis is caused by vessel damage from:

A
HTN
smoking
diabetes
infection
high cholesterol
aging
genetics
free radicals
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55
Q

Mini concept map of arteriosclerosis

A

tunica intima microscopically damage > collagen fibers enter vessel wall > stiffening of vessel wall > decreased elasticity & arterial compliance

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56
Q

Atherosclerosis develops from:

A

atherous involvement of arteriosclerosis

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57
Q

“fatty deposits”

A

Athero

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58
Q

Atherosclerotic walls have deposits of:

A

collagen as well as LDLs

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59
Q

Fatty deposits in arterial walls cause:

A

irritation

inflammatory & coagulation responses

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60
Q

Formation of a fibrous capsule with a fatty middle section

A

Plaque

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61
Q

Formation of plaque is caused by:

A

stiff arteries, fat deposits, and inflammatory & clotting responses

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62
Q

Sequela of plaque growing & protruding into the lumen

A

Ischemia

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63
Q

Buildup of blockage in/along arterial walls results in:

A

loss of vasomotor tone and non-patent lumen

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64
Q

If arterial pathology exists in one area…

A

it is usually occurring system-wide

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65
Q

Narrowed, stiff, atheromatous arteries often result in:

A

compromised perfusion > ischemia

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66
Q

Characteristics of ischemic pain:

A

increased with exacerbation
decreases with rest
present in tissue distal to the plaque or narrowed arteries

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67
Q

S/S of ischemia seen in the periphery

A

diminished/absent pulses
delayed cap refill
pale, cool skin/mucous membranes
delayed healing

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68
Q

Specific S/S of ischemia in the heart

A

Altered function

decreased cardiac output

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69
Q

Specific S/S of ischemia in the brain

A

Altered LOC

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70
Q

Specific S/S of ischemia in the kidneys

A

Decreased urine output

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71
Q

Non-modifiable risk factors of arterial dz

A
Family HX (tendency to atherosclerosis &hypercholesterolemia)
Advanced age > stiffer arteries
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72
Q

Modifiable risk factors for arterial dz

A

Diet, obesity, sedentary lifestyle
Alcohol consumption
DM2
Cigarettes/nicotine

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73
Q

Characteristic of DM2, increased circulating LDLs

A

lipodystrophy

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74
Q

Nicotine is a powerful ___

A

vasoconstrictor

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75
Q

Cardiovascular dz can be described as ___

A

atherosclerosis of coronary arteries

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76
Q

Venous insufficiency is often due to ___ and results in ___

A

bad valves in leg veins; venous congestion & peripheral edema

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77
Q

Arterial insufficiency is almost always due to ___ and results in ___

A

atherosclerosis; ischemia

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78
Q

PAD =

A

Peripheral artery disease

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79
Q

PAD is a dz of ___

A

any arterial vessels outside the heart, but most commonly refers to arterial problems of the legs

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80
Q

PAD usually manifests as __ due to __

A

problems of ischemia; narrowed peripheral arteries

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81
Q

S/S of PAD

A
Intermittent claudication
Cool, pale feet
Diminished pulses & delayed cap refill
No hair growth on legs (shiny skin)
Ischemic skin ulcers
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82
Q

5 Ps of PAD

A
Pain
Pallor
Paresthesias 
Pulselessness
Poikilothermia
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83
Q

Poikilothermia =

A

cold, pale feet

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84
Q

Arterial thrombi form where __

A

flow is sluggish, and/or where there is narrowing/injury to vessel walls

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85
Q

Veinous thrombi block blood flow ___, causing ___

A

to the heart; congestion distal to the blockage

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86
Q

Arterial blockage results in ___

A

ischemia to distal tissue

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87
Q

If narrowing/injury/atherosclerosis occurs at an arterial bifurcation:

A

a thrombus might form

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88
Q

Emoboli of a bifurcation thrombus would travel to:

A

distal arteries &arterioles

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89
Q

Hypertension is ___

A

consistent elevation of systemic arterial BP over 140/90

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90
Q

2 categories of HTN

A

primary & secondary

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91
Q

Secondary HTN is caused by ___

A

altered hemodynamics associated with a dz process

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92
Q

Primary HTN, AKA ___, is caused by ___

A

Essential HTN; a complex set of factors

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93
Q

__% of hypertensives have primary HTN

A

92-95

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94
Q

Non-modifiable Risk factors of HTN

A
Family HX (inherited tendency)
advanced agin
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95
Q

Modifiable risk factors of HTN

A

Diet, obesity, sedentary lifestyle
Heavy alcohol consumption
DM2
Cigarette smoking/nicotine intake

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96
Q

Certain conditions usually present in HTN to come degree:

A

Atherosclerosis

Overactivity of SNS & RAAS

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97
Q

Atherosclerosis contributes to HTN due to __

A

decreased elasticity of vessels

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98
Q

__ is consistently released by intracardiac nerve fibers, causing over stimulation of ___ to increase __ & __

A

Epinephrine
beta receptors
HR & contractility

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99
Q

Mini concept map of increased HR & contractility due to SNS overactivity

A

greater cardiac output & ejection pressure > pathologically larger volume of blood & pressure > sustained increase in BP

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100
Q

RAAS is usually a ___ triggered by ___

A

compensatory mechanism; drop in BP

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101
Q

For unknown reasons the RAAS sometimes becomes ___ causing ___

A

chronically activated; chronically high BP & blood volume

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102
Q

Vicious cycle of chronic HTN

A

arterial walls stimulated to strengthen via hypertrophy & hyperplasia > decreased lumen size > HTNn increases even more

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103
Q

Chronic HTN damages the __

A

tunica intima

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104
Q

S/S of HTN are often __

A

secondary to years of vascular damage

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105
Q

3 systems most often affected by HTN

A

Neuro
Renal
Cardiovascular

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106
Q

Neurological effects of HTN on the brain

A

Strokes due to ischemia from narrowed vessels

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107
Q

Effects of HTN on the eyes

A

ischemia & infarcts of parts of retina, vision changes

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108
Q

Effects of HTN on the renal system

A

High pressures & vessel damage can cause spilling of blood & protein into urine > eventually kidney failure

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109
Q

Effects of HTN on the cardiovascular system

A

increased workload ejecting blood against narrowed, stiff arteries;
Multiple problems including MI

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110
Q

Local dilation or out pouching of arterial vessel walls

A

Aneurysms

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111
Q

Pathology of aneurysms

A

Atherosclerosis & HTN cause weakness in arterial walls which can cause bulges in certain areas;
Minute injuries to intimal lining accumulate & allow blood to seep into muscle & tissue layers of arteries, which increase the size & chances of rupture

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112
Q

Areas of typical aneurysms

A

brain & aorta

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113
Q

The aorta is susceptible to aneurysms due to:

A

constant stress, especially from higher pressure of HTN

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114
Q

S/S of AAA

A

pulsatile, palpable mass inn abdomen; abdominal pain

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115
Q

S/S of thoracic aortic aneurysm

A

S/S usually resemble that of MI (chest pain, diminished pulses unilaterally)

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116
Q

Educational aspects of nursing implications for managing HTN

A

managing stress, smoking cessation, moderation of alcohol intake

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117
Q

Dietary aspects of managing HTN

A

low LDL intake; high intake of HDL & omega-3 fats

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118
Q

Desired daily intake of HDL:

A

40 mg/dL

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119
Q

Medicinal approaches for overactivity of SNS

A

beta & Ca channel blockers

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120
Q

Medicinal approaches for overactivity or RAAS

A

ACE inhibitors or angiotensin receptor blockers

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121
Q

Symbolizes ventricular repolarization on an EKG

A

T wave

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122
Q

Symbolizes ventricular depolarization on an EKG

A

QRS complex

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123
Q

Consistent, regular pattern or PQRST

A

sinus rhythm

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124
Q

Good CO is linked with ___

A

S/S of good perfusion

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125
Q

S/S of good perfusion

A

normal BP, pulses, cap refill, mentation, and skin color/ and warmth

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126
Q

SV is affected by:

A

contractility
preload
afterload

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127
Q

CO can improve or deteriorate based on:

A

changes in HR/rhythm; changes in SV

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128
Q

Definition: how well cardiomyocytes responds to electrical impulses

A

contractility

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129
Q

The effect of different factors on contractility

A

Inotropic

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130
Q

Some thing that enhances contractility

A

Positive inotropic effect

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131
Q

Something that decreases contractility

A

Negative inotropic effect

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132
Q

Amount or volume of blood in the ventricles before contraction

A

Preload

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133
Q

Any form of resistance to ejection of blood from any heart chamber

A

afterload

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134
Q

Normal after load exists when the receiving arteries have:

A

good vasomotor tone; smooth, patent lumens

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135
Q

Normal RV after load is called:

A

pulmonary vascular resistance

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136
Q

Normal LV after load is called:

A

systemic vascular resistance

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137
Q

HR >100BPM

A

tachycardia

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138
Q

Describe the neurohormonal effect on the SNS during physical exertion or stress:

A

Epinephrine binds to beta receptors, causing HR to increase

139
Q

Hypopolarization causes cardiomyocytes to ___

A

contract more quickly

140
Q

The PNS effect on HR involves the release of ___ by the ___

A

acetylcholine; vagus nerve

141
Q

Interference in impulse conduction due to ischemic or infarcted cardiac tissue causes:

A

dysrhythmias

142
Q

Chaotic electrical impulses in the atria that cause atrial “quivering”

A

Afib

143
Q

Percentage of elderly that have Afib

A

~3%

144
Q

Afib can cause a small, but sometimes significant ___

A

decrease in CO

145
Q

Arterial thrombi in the LA that break loose can cause:

A

stroke

146
Q

Arterial thrombi in the RA that break loose can cause:

A

PE

147
Q

Increased preload, pathologically, relates to:

A

increased blood volume/fluid volume overload

148
Q

Decreased preload, pathologically, relates to:

A

decreased blood volume/fluid volume deficit

149
Q

Fluid volume deficit eventually leads to:

A

decreased BP & CO

150
Q

Pathologically increased after load in the RV can be caused by:

A

atherosclerosis of pulmonary arteries, or chronic disorders such as bronchitis

151
Q

Pathologically increased after load in the LV can be caused by:

A

Atherosclerosis of the aorta & systemic arteries; peripheral vasoconstriction; HTN; pathologically high blood volume

152
Q

Pathologically decreased afterload in the LV is usually due to:

A

massive peripheral vasodilation/shock

153
Q

A disorder in which the coronary arteries are narrowed or occluded

A

Coronary artery disease

154
Q

Risk for CAD increases with high serum levels of:

A

hemocysteine

155
Q

Risk of CAD is linked with ___ due to inflammatory process of plaque formation

A

elevated CRP

156
Q

Cardiac cell ischemia has a ___ effect, leading to ___

A

negative inotropic; decreased CO

157
Q

If not reversed, CAD can lead to:

A

cell death/necrosis

158
Q

Most common symptom of CAD

A

angina

159
Q

Ischemic pain in the heart muscle tissue

A

Angina

160
Q

Classification of CAD is based on:

A

degree of coronary artery occlusion & ischemia

161
Q

2 categories of CAD, based on symptoms

A

Stable Angina; Acute coronary syndrome

162
Q

___ is established thru arteriogenesis to compensate for slow development of plaque

A

Collateral circulation

163
Q

Acute coronary syndrome manifests as __ or __

A

Unstable angina or MI

164
Q

Necrosis of myocardial cells

A

MI

165
Q

2 enzymes that indicate MI upon lab testing

A

Creatine kinase; troponin

166
Q

2 internal compensatory mechanisms of CAD patients

A

Collateral circulation; hypertrophy of cardiac muscle cells

167
Q

A heart murmur is caused by ___ or ___

A

cardiac valve stenosis (valvular prolapse/ insufficiency)
or
regurgitation (back flow)

168
Q

Right sided heart valves

A

Tricuspid, Pulmonary

169
Q

Left sided heart valves

A

mitral, aortic

170
Q

Valve malfunction may be caused by autoimmune disorders, such as:

A

rheumatic fever

171
Q

Stenosis impedes blood flow because of:

A

narrowed or constricted valve orifices

172
Q

A state of incompetent, floppy valves is called:

A

valvular prolapse
valve insufficiency
regurgitation

173
Q

General term used to describe types of cardiac dysfunction secondary to failure of the heart to effectively propel blood forward

A

Heart failure

174
Q

3 aspects of the pathology of HF

A
weakened contractility (pump problem)
increased afterload (resistance)
Increased preload (fluid volume overload)
175
Q

One sequela of HF pertaining to the kidneys is:

A

Diminished CO stimulates the kidneys to secrete Renin as part of the RAAS, causing retention of fluids, making the problem worse instead of better

176
Q

4 sequela of venous insufficiency

A

localized edema
local skin breakdown
Local skin discoloration
Varicose veins

177
Q

Renin stimulates:

A

secretion of angiotensin I

178
Q

Angiotensin 2 stimulates:

A

peripheral vasoconstriction, secretion of Aldosterone from Adrenal glands

179
Q

Effects of Aldosterone:

A

causes distal convoluted tubules to reabsorb Na > increases tonicity > water is shifted from tissues into blood > increased UO

180
Q

Increased systemic tonicity triggers release of __ which aids in fluid retention

A

ADH

181
Q

Most common type of hypertension

A

Primary/Essential

182
Q

Factors contributing to left heart failure

A

Weekend LV w/ decreased contractility
and/or
High afterload

183
Q

High afterload can be due to:

A

HTN and/or
pathologically increased arterial vasoconstriction and/or
narrowed/blocked systemic arteries

184
Q

Common sequela of LHF

A

Fluid overload overwhelms the LV, causing fluid to backup in the lungs > pulmonary edema

185
Q

Weakened LV contractility can be caused by:

A
Ischemia/MI and/or
Electrolyte imbalance and/or
HR/rhythm problems
And/Or
High afterload
186
Q

Sequela of RHF

A

RV overwhelmed by fluid overload (high preload) > fluid buildup in systemic veins > peripheral edema

187
Q

RAAS complication of RHF

A

Aldosterone secreted by adrenal glands causes retention of Na+ > H2O retention > further increased preload

188
Q

General S/S of decreased CO

A
Fatigue, weakness
mentation changes
hypotension
dyspnea
delayed cap refill
Oliguria
189
Q

S/S of pulmonary Edema (fluid backup)

A
Fluid congestion in lungs
Crackles on auscultation 
Pink, frothy sputum
Orthopnea
Increased RR
Decreased SpO2
190
Q

S/S of peripheral Edema

A

JVD
Pedal edema
Liver congestion/enlargement
Ascites (abdominal edema)

191
Q

Definition: when RHF is caused by pathologically increased pulmonary vascular resistance

A

Cor pulmonale

192
Q

Lung congestion is caused by ___
But
Lung congestion causes __

A

LHF; RHF

193
Q

Fluid volume overload triggers the __

A

NPS

194
Q

NPS causes the kidneys to ___, > ___

A

excrete more Na+ > water follows

195
Q

In volume overload, the ventricles secrete ___ and the atria secrete ___

A

BNP; ANP

196
Q

The gold-standard for confirmation/quantification of level of HF is ___

A

serum level BNP

197
Q

Healthy male serum BNP level:

A

50pg/mL

198
Q

S/S of cariogenic shock are generally related to ___

A

decreased perfusion + compensatory responnses

199
Q
Normal ABG values
pH:
pO2:
sO2:
pCo2:
HCO3:
A
7.35-7.45
80-100mmHg
97-100%
34-45mmHg
22-26mEq/mL
200
Q

If pCO2 is abnormal, the pH imbalance is ___ in nature

if HCO3 is abnormal, the pH imbalance is ___ in nature

A

respiratory

metabolic

201
Q

Respiratory acidosis is a state of ___

A

low pH caused by inhibition of normal breathing pattern

202
Q

Decreased RR causes:

A

hypercapnia (retention of CO2

203
Q

Respiratory acidosis is typically caused by some degree of __

A

hypoventilation

204
Q

Typical ABG findings of respiratory acidosis

A

low pH
low pO2
high pCO2
normal HCO3

205
Q

Increased depth or rate of breathing causes:

A

CO2 blow off > alkalosis

206
Q

The kidneys attempt to compensate for respiratory alkalosis by:

A

decreasing HCO3 production
or
increasing excretion os HCO3

207
Q

State of low pH caused by accumulation of acids in the body

A

metabolic acidosis

208
Q

HCO3 levels will be ___ in metabolic acidosis

A

low

209
Q

Normal breathing should be ___

A

passive

210
Q

Subjective feeling of not getting enough air

A

dyspnea

211
Q

DOE

A

dyspnea on exertion

212
Q

dyspnea upon lying down

A

orthopnea

213
Q

Usually related to increased preload when lying down + compromised LV unable to pump effectively

A

Orthopnea

214
Q

Waking suddenly and feeling SOB

A

paroxysmal nocturnal dyspnea (PND)

215
Q

RR < 12/min

A

hypoventilation

216
Q

RR > 20/min

A

tachypnea/hyperventilation

217
Q

Shallow breathing

A

hypopnea

218
Q

increased depth of breathing

A

hyperpnea

219
Q

absence of breathing

A

apnea

220
Q

Purulent sputum usually indicates ___

A

infection

221
Q

Accessory muscle use during exhalation due to difficulty breathing =

A

respiratory distress

222
Q

When a PT can no longer breathe adequately on their own

A

respiratory failure

223
Q

Restrictive lung dz generally refers to dz processes related to ___

A

difficulty w/ inhalation

224
Q

V/Q ratio means:

A

liters of air breathed in per minute/# liters of blood available for gas exchange in one minute

225
Q

Normal V/Q ratio:

A

0.8 (4/5)

226
Q

Low VQ disorders are caused by

A

inability to get the normal amount of air from the atmosphere to the blood

227
Q

High VQ disorders are caused by:

A

difficulty w/ perfusion

228
Q

In low VQ disorders, low V=

A

less ventilation (can’t get air from atmosphere to blood)

229
Q

Low VQ disorders include restrictions in the: (4)

A

chest wall
airway
Pleura
lung tissue

230
Q

Chest wall restrictions can include:

A

physical deformity or neuromuscular weakness

231
Q

airway restrictions can include:

A

foreign bodies, tumors

inflammation

232
Q

Most dz that cause inflammation of the larynx and bronchi are caused by:

A

viruses

233
Q

Inflammation of the larynx, trachea, and bronchi typically seen inn young children

A

croup

234
Q

Pleural restrictions include:

A

pleural effusion, pneumothorax

235
Q

irritation/inflammation of the pleural space that causes fluid buildup

A

pleural effusion

236
Q

S/S of pleural effusion

A

chills, fever (infection related)
pleuritic pain w/ movement
shallow respirations

237
Q

Presence of air in pleural space caused bay rupture in pleura

A

pneumothorax

238
Q

Pneumothorax disrupts the ___

A

normal negative pressure environment

239
Q

Pneumothorax caused by outside trauma

A

open pneumothorax

240
Q

Pneumothorax caused by internal trauma

A

closed pneumo

241
Q

Lung tissue restriction is caused by __

A

pneumonia

242
Q

Pneumonia is an infection of the ___

A

lower respiratory tract

243
Q

Pneumonia can be caused by:

A

viruses
bacteria
parasites
fungi

244
Q

3 types of pneumonia

A

Community acquired
Hospital acquired (nosocomial)
Aspiration

245
Q

Organisms that cause CAP are usually ___

A

less virulent

246
Q

Nosocomial pneumonia is typically caused by __

A

virulent microbes like pseudomonas

247
Q

Inhalation of foreign substance into lungs that results in inflammation of lung tissue

A

aspiration pneumonia

248
Q

Aspiration pneumonia usually effects:

A

ppl with debilitations or depressed/absent gag, cough, or swallowing reflexes

249
Q

Collapse of portions of lung tissue

A

atelectasis

250
Q

Atelectasis is caused by:

A

accumulation of inflammatory/infectious debris that accumulates in alveoli

251
Q

Excess water in alveoli

A

pulmonary edema

252
Q

Noncardiogenic pulmonary edema is caused by:

A

injury to capillary endothelium from external sources

253
Q

Pathology of pulmonary edema:

A

capillary endothelium injured by external source > increased capillary permeability, disruption of surfactant production > fluids/proteins shift from capillaries into alveoli

254
Q

S/S of pulmonary edema

A

pink, frothy sputum
inspiratory crackles
hypoxemia
Dyspnea

255
Q

Lung cancer arises from __

A

respiratory epithelium

256
Q

Pathology of lung cancer

A

carcinogens from smoking cause genetic abnormalities in bronchial cells > carcinoma in situ > invasive carcinoma

257
Q

High VQ disorders involve restriction of:

A

blood vessels in the lungs

258
Q

Most common cause of High VQ ratio

A

pulmonary embolism

259
Q

Virchow’s triad:

A
endothelial injury
Hypercoagulability
Venous stasis (DVT)
260
Q

High VQ ratio in PE is caused by:

A

lower O2 saturation of blood returning to the LV

261
Q

Obstructive pulmonary dz results in:

A

difficulty w/ exhalation

262
Q

S/S of obstructive pulmonary disorders

A

Accessory muscle use
Prolonged expiratory phase
Dyspnea

263
Q

Common types of obstructive pulmonary dz

A

Asthma
Bronchitis and Emphysema
Cystic fibrosis

264
Q

Chronic inflammatory disorder caused by bronchial hypersensitivity to stimuli

A

Asthma

265
Q

Pathology of asthma

A

Inhaled irritants > inflammatory mediators > vasodilation and swelling

spasm and constriction of bronchi

266
Q

Collective term for emphysema and chronic bronchitis

A

COPD

267
Q

S/S of COPD

A

prolonged expiration
accessory muscle use
chronically low PF made worse by exacerbation

268
Q

Basic pathology of emphysema

A

Inhalation of irritants > airway inflammation > alveolocapillary membrane and walls between clusters destroyed > alveoli stiff and hyper inflated > loss of elastic recoil > air becomes trapped in alveoli and exhalation becomes harder

269
Q

Emphysemics live in a chronic state of ___

A

hyperventilation > respiratory alkalosis

270
Q

Hypersecretion of mucous and chronic productive cough for > 3 months for > 2 consecutive years

A

chronic bronchitis

271
Q

Hypoxemia in chronic bronchitis is caused by:

A

mucous plugs in bronchial walls

272
Q

PTs with chronic bronchitis are typically in a state of chronic ___ due to ___

A

hypercapnia (>45); inability to exchange gases

273
Q

Enlargement of the prostate gland tissues

A

Benign prostatic hyperplasia

274
Q

S/S of BPH

A

Varying degrees of urinary flow obstruction
Urgency, delayed start of flow
Decreased flow
Urine retention

275
Q

TX for BPH

A

TURP

Transurethral resection of prostate

276
Q

Malignant neoplasm of the prostate

A

prostate cancer

277
Q

Risk factors for Prostate cancer

A

Age >50
family Hx
diet high in saturated fat
high T levels

278
Q

Cancer most common in males age 15-35

A

testicular cancer

279
Q

Inflammation of the

a. prostate
b. urethra

A

prostatitis

urethritis

280
Q

Female flow related problems of the uterus

A

dysmenorrhea, amenorrhea, endometriosis

281
Q

More painful, higher than normal volume of bleeding than normal menstruation

A

dysmenorrhea

282
Q

Absence of menses (can be sign of start of menopause)

A

amenorrhea

283
Q

Presence of functioning endometrium outside of the uterus

A

Endometriosis

284
Q

pathology of Endometriosis

A

sloughed off endometrium travels to the abdominal cavity thru the Fallopian tube > tissue reacts to menstrual hormones by proliferating & bleeding as if still in the uterus

285
Q

S/S of endometriosis

A

dyspareunia,dysmenorrhea, pelvic pain

286
Q

1 cause of cancer deaths in females

A

ovarian cancer

287
Q

early S/S of ovarian cancer

A

bloating, mild abdominal pain, constipation

288
Q

S/S of abdominal metastasis ovarian cancer

A

abdominal pain, ascites, dyspepsia, committing, alterations in BMs

289
Q

Infection of the female reproductive tract

A

pelvic inflammatory disease

290
Q

PID can cause:

A

infertility

291
Q

UTIs are most commonly caused by __

A

E. coli

292
Q

UTI involving the urinary bladder

A

cystitis

293
Q

UTI involving only the kidneys

A

pyelonephritis

294
Q

STI that causes urethritis in males, PID in females

A

Chalmydia

295
Q

STI that is easily treated in early stages, but left untreated may become systemic and evolve

A

Syphilis

296
Q

Not an STI:

HSV1 - HSV2

A

HSV1

297
Q

STI that invades the genital area and spreads to the perineum and anus

A

HSV2 “genital herpes”

298
Q

Anything that interferes with flow of urine from the kidneys to the urethral meatus

A

Obstructive disorders of the urological system

299
Q

Enlargement of and pressure on the renal pelvis due to pathologic accumulation of fluid

A

hydronephrosis

300
Q

Hydronephrosis is caused by:

A

retrograde flow of urine that cannot get past an obstruction

301
Q

Hydronephrosis can lead to:

A

infection and fibrosis within the kidney; decline in nephron function

302
Q

Types of urological obstructions (not gender specific)

A

Tumors
scarring from past problems
Neurogenic problems (paralysis)
Kidney stones

303
Q

Presence of kidney stones

A

lithiasis

304
Q

Risk factors for lithiasis

A
male gender
Gout
Dehydration
Dietary factors
Hypercalcemia caused by dz state
305
Q

Kidney stones form when urine becomes super saturated with:

A

calcium, uric acid, and other ions

306
Q

Volume of fluid filtered from the glomerular capillaries into the Bowmans capsule per minute

A

Glomerular filtration Rate (GFR)

307
Q

Clinically speaking, decreased GFR = ___

A

decreased UO

308
Q

Decreases in GFR increases the risk of ___

A

accumulation of wastes and water in the body

309
Q

Abbrupt (<48 hrs) oliguria and/or jump in serum creatinine

A

acute kidney injury

310
Q

2 possible outcomes of AKI

A

full recovery if caught and corrected early

Some degree of residual kidney problem if not caught early enough

311
Q

3 categories of AKI based on location

A

Prerenal AKI
Intrarenal AKI
Postrenal AKI

312
Q

Intrarenal AKI can lead to ___

A

acute tubular necrosis (ATN)

313
Q

S/S of prerenal AKI

A

S/S of decreased preload:
dry mucous membranes, dry mouth
and oliguria

314
Q

Causative factors of Prerenal AKI

A

decreased arterial blood flow to kidneys due to arterial vasoconstriction or trauma to aorta/renal arteries
and
hypotension/hypovolemia

315
Q

Occurs when a blockage occurs between the kidneys and the urethral meatus

A

post renal AKI

316
Q

Factors that can cause Postrenal AKI

A

obstruction from BPH
Uterine prolapse
Ureteral obstruction/calculi

317
Q

Intrarenal AKI can occur when:

A

post- or prerenal AKI are not fixed

Acutely diminished kidney function due to direct kidney tissue injury

318
Q

Pathology of infrarenal AKI

A

ischemia to nephron blood supply > tubule cells slough off and block urine flow > retrograde flow > hydronephrosis > ischemia, necrosis, malfunction

319
Q

Causative agents of ATN

A

direct trauma to nephrons by:

ischemia, hydronephrosis, nephrotoxic drugs, poison/toxins, renal infections

320
Q

S/S of intrarenal AKI

A

acute oliguria
high serum creatinine
Casts in urine

321
Q

Slow, negative effect on renal function from a slow, insidious problem or genetic disorder

A

Chronic kidney dz (CKD)

322
Q

Congenital Disorders that can cause CKD

A

PKD

323
Q

Acquired dz that can cause CKD

A

unresolved AKI
Atherosclerosis
diabetes mellitus
HTN

324
Q

Autoimmune dz that can cause CKD

A

glomerulonephritis

325
Q

2 divisions of CKD

A

fluid/solute balance impairment

Metabolic function impairment

326
Q

Pathology of glomerulonephritis

A

inflammatory process > glomerular capillaries become leaky > substances allowed into urine that aren’t supposed to be (RBCs, protein)

327
Q

post infectious glomerulonephritis is caused by

A

autoantibodies attached to the glomerular membrane, causing inflammation & leakiness

328
Q

high BUN and serum creatinine

A

Azotemia

329
Q

___ is almost always associated with renal dysfunction

A

high serum creatinine

330
Q

serum creatinine levels are high in renal dysfunction due to:

A

inability of impaired kidneys to excrete the normal amount into urine

331
Q

Azotemia + other S/S is called ___

A

uremia

332
Q

Precipitation of urea on skin, causing itching

A

pruritis

333
Q

Hyperkalemia/hypernatremia in CKD is due to:

A

unresponsiveness of DCT to aldosterone

334
Q

Sequela of Na+ and H2O retention in CKD

A

peripheral/pulmonary edema, HTN

335
Q

Neurological changes from toxic levels of urea in the blood

A

Uremic encephalopathy

336
Q

Inability to activate vitamin D in CKD is caused by

A

hypocalcemia

337
Q

because CKD PTs will usually be hypocalcemic, they will also be:

A

hyperphosphatemic

338
Q

pH imbalance seen in CKD

A

metabolic acidosis

339
Q

Dietary restriction for CKD patients should include

A

restrictions of Na, K, and H2O intake

340
Q

Dietary supplements that should be given to CKD patients:

A

vitamin D and calcium, phosphate-binding antacids, erythropoeietin

341
Q

Medications given to CKD patients should include

A

antihypertensives and non-potassium sparing diuretics

342
Q

___ is converted from ammonia by the liver

A

urea nitrogen

343
Q

Pathology of hyperkalemia/hypernatremia in CKD

A

DCT unresponsive to aldosterone > pathologic retention of solutes > increase in serum K+ and Na+