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NURS 2500 > Class 21: Ischemic Heart Disease > Flashcards

Class 21: Ischemic Heart Disease Flashcards

1
Q

describe the filling of the heart muscle during systole & diastole

A
  • systole = surface coronary arteries filled
  • diastole = blood from surface flows deep into muscle

therefore, diastole is when heart muscle is actually nourished

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2
Q

when occurs if the left main coronary artery is blocked

A
  • reminder: left main splits into circumflex & LAD

- blockage = decreased blood supply & devasting

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3
Q

when does the heart muscle receive blood? why?

A
  • during diastole
  • due to high pressures during systole
  • also due to aortic recoil which aids perfusion into coronary arteries
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4
Q

what is the aortic recoil

A
  • bulging of aorta at the end of systole
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5
Q

what happens to the coronary arteries when heart rate or metabolic rate increases?

A
  • smooth muscle in arterioles supply the heart muscle (coronary arteries) relax
    = vasodilation & increased blood flow
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6
Q

what is the local dilation of the coronary arteries caused by?

A
  • metabolites produced by the heart muscle workload
  • B-adrenergic stimulation (SNS)
  • release of NO from the vascular endothelium
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7
Q

how does increased heart rate affect diastole

A
  • decreases the diastolic time more than systolic

= decreased perfusion time of coronary arteries = ischemia

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8
Q

what are the effects of increased HR on demand, metabolic waste, and filling time? what do these cause?

A
  • increased demands
  • increased metabolic waste = vasodilation
  • decreased filling time
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9
Q

what is the most common form of heart disease

A
  • coronary heart disease

aka ischemic heart disease

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10
Q

what is the most common cause of CAD

A

athersclerosis

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11
Q

what is athersclerosis

A
  • formation of fatty, fibrous mass (atheroma) = plaque

- within the wall of an artery

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12
Q

when does plaque formation usually begin

A
  • around age 20
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13
Q

when does athersclerosis become symptomatic

A
  • usually asymptomatic until vessel is 75% blocked
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14
Q

what happens when the vessel is 75% blocked?

A

= symptoms

- signs of ischemia, particularly during times of exertion when metabolic demand in higher

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15
Q

what is the difference between partial and full blockage of an artery

A
  • partial = may only cause ischemia = sub lethal

- full blockage for >20 min = necrosis = lethal

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16
Q

what happens if we have partial blockage of the coronary arteries for a long period of time

A
  • go from sublethal to lethal
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17
Q

describe the healing of necorsis tissue

how does this effect our goal?

A
  • never heals

= want to keep necrosis as small as possible

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18
Q

describe the zones of injury

what is our goal of treatment?

A
  • have lethal/necrosis surrounded by sublethal injury

- want to save area of sublethal ischemia

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19
Q

what is collateral circulation

A
  • additional arterial connection that form around a blockage
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20
Q

what influences our ability for collaterial circulation

A
  1. genetic predisposition

2. chronic ischemia

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21
Q

describe collateral circulation with rapid arterial acclusion

A
  • no time for development of collateral circulation
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22
Q

how do we compensate with acute ischemia

A
  • anerobic metabolism
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23
Q

how might CAD manifest as.. (5)

how predictable is each?

A
  • chronic stable angina = most predictable
  • acute coronary syndrome = least predictable
  • cardiac arrythmia
  • HF
  • sudden cardiac death
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24
Q

what is acute coronary syndrome divide into

A
  1. unstable angina

2. acute myocardial infarction

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25
Q

what are two types of MI

A
  1. stemi

2. nonstemi

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26
Q

what does typical myocardial O2 supply & demand look like

A
  • normally should be able to supply as much O2 as needed
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27
Q

how does supply and demand change with CAD

A
  • supply decreases due to blockage

- demand increases during activity

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28
Q

what are the goals of antianginal treatment

A
  • increase supply by removing blockage or using vasodilator

- decrease demand thru rest, decreasing HR, decreasing afterload to push against

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29
Q

what determines myocardial O2 demand

A
  • HR
  • contractility
  • afterload
  • preload
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30
Q

describe the improtant of balance of HR

A
  • want enough for perfusion

- but not so much you cant fill ventricles (decrease diastolic time) or feed heart

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31
Q

describe the importance of balance of contraction

A
  • want enough to have a good SV

- but not so much force that workload/demand is too high (= O2 consumption)

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32
Q

describe the importance of balance of preload

A
  • want enough to fill the heart
  • but not so much that it is overloaded w volume = effect function
    ex. think of when have too much food in mouth
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33
Q

describe the importance of balanced afterload

A
  • want enough for good bp and perfusion

- but not so much its hard to push against

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34
Q

what does decreased contractility cause

A 
= decreased SV
= decreased CO
= decreased bp
= symptoms of hypotension 
ex. lightheaded, weak legs, pre syncope, syncope, angina
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35
Q

how long does it take for heart cells to stop contarcting vs die

A
  • starts contracting within several minutes after total occlusion
  • die after 20 min
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36
Q

cardiac ischemia may result in.. (5 things)

A
  1. diastolic dysfunction
  2. systolic dysfunction
  3. electrical dysfunction
  4. angina
  5. MI = cardiac muscle death
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37
Q

describe diastolic dysfunction

A
  • ischemic muscle becomes stiff
    = reduced relaxation, stretch, and filliing
    = reduced preload, reduced SV, reduced CO & BP
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38
Q

describe systolic dysfunction

A
  • failure of heart to properly contract

= reduced SV, CO, and BP

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39
Q

describe electrical disturbances in the heart due to cardiac ischemia

A
  • conduction moves around the ischemic tissue or heart muscle is irritabloe
    = ECG changes, irregular or ineffective pumping
  • tachy or brady can alter CO
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40
Q

how does tachycardia alter CO

A
  • increased HR = decreased filling = decreased feeding = increased O2 demand = increased workload
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41
Q

how does bradycardia alter CO

A
  • decreased HR = decreased CO = decreased BP
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42
Q

what is angina pectoris

A
  • chest pain
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43
Q

what causes angina

A
  • reversible myocardial ischemia
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44
Q

does angina always have symptoms?

A
  • no, may be silent but that is unusual
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45
Q

how can angina be described

A
  • pressure
  • clenching
  • elephant on chest
  • aching
  • heaviness
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46
Q

does angina change with position or breathing? how can we differentiate between pleuritic & muscle pain

A
  • no it does not

- pleuritic & muscle pain changes w respiration

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47
Q

what symptom is associated with angina that is important to identify? how can we tell?

A
  • may experience indigestion or burning quality

= give antacid

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48
Q

is ST depression common or uncommon with angina

A
  • common
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49
Q

what respiratory symptom is associated with angina? why?

A
  • SOB/dyspnea
    1. compensation
    2. from pulmonary edema
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50
Q

why might pulmonary edema occur with myocardial dysfunction

A
  • occurs from systolic dysfunction

= failure to move blood forward = back up of fluid & pressure in lungs = pulmonary edema

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51
Q

describe the effects of pulmonary edema

A

= decreased gas exchange

= SOB and decreased O2 sats, increased RR, cough

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52
Q

describe the referred pain of angina

A
  • midsternal
  • down both arms
  • left shoulder
  • lower jaw
  • neck
  • intrascapular
  • epigastric
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53
Q

describe the characteristics of stable angina

A
  • reproducable = happens every time I ___, i get angina = can expect it everytime you do it
  • intermittent = only during exertion
  • caused by increased exertion
  • can have it for years = chronic
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54
Q

how long does the feeling of angina occur during stable angina

A
  • brief = 3-5 min
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55
Q

how is stable angina relieved

A
  • rest and/or

- nitroglycerine (vasodilator)

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56
Q

what is the #1 way to reduce demand on the heart

A
  • rest!
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57
Q

what causes stable angina

A
  • advanced plaque that is highly fibrotic & contains little lipid
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58
Q

describe the pattern of angina during stable angina

A
  • similar pattern of onset, duration, and intensity of symptoms
    “my usual angina”
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59
Q

what is seen on ECG during stable angina

A
  • transient ST depression
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60
Q

describe use of nitroglycerin

A
  • rescue med

- can also take before the activity that causes angina

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61
Q

how is stable angina controlled

A
  • usually w meds

- BUT not cured, will still be limit in activity

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62
Q

what is another name for stable angina

A
  • effort or exertional angina

- can significanty reduce a persons daily functioning

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63
Q

what stage of atherosclerosis is present in stable angina

A
  • fibrous plaque
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64
Q

what is prinzmetal’s angina

A
  • variant angina
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65
Q

what causes prinzmetal’s angina? when does it occur?

A
  • due to coronary artery spasm
  • may be response to a stimulant
  • occur at rest
  • may occur with or without CAD
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66
Q

what stimulants might cause prinzmetal’s angina

A
  • cocaine
  • extreme cold
  • extreme stress
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67
Q

is prinzmetal’s angina common? what might people have a history of?

A
  • rare

- hx of migraine, raynaud’s syndrome

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68
Q

what might cause chronic stable angina to progress to acute coronary syndrome

A
  • increased lesion size & blockage

- increased complication leison w clot

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69
Q

describe management of stable angina vs acute coronary sybdrom

A
  • stable = manage at home

- acute = go to hospital or ER

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70
Q

what does acute coronary syndrome split intoo

A
  • unstable angina & nonstemi MI

- stemi MI

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71
Q

what is the difference between unstable angina & nonstemi MI

A
  • unstable = no necrosis

- non stemi = necrosis

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72
Q

describe the thickness of necrosis in stemi vs nonstemi

A
  • nonstemi = partial thickeness = <100% blockage

- stemi = full thickness = ~100% blockage

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73
Q

what causes acute coronary syndrome

A
  • develops when myocardial ischemia is prolonged & not immediately reversible
    = not stable angina
  • typically when a coronary artery is >90% occluded
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74
Q

how does the size of artery impact the amount of dysfunction

A
  • bigger with more branches = more muscle deprived = greater injury = greater dysfunction
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75
Q

what is the difference between MI and angina

A
  • angina = no cardiac death = reversible

- MI = cardiac death = no reversible

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76
Q

what causes unstable angina?

A
  • complicated lesion
  • rapid change from stable to ustable
    = rupture of plaque with coronary vasoconstriction & thrombus formation
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77
Q

what allows unstable angina to resolve

A
  • followed by spontaneous thrombolysis
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78
Q

does unstable angina require hospitalization?

A
  • yes requires immediate hospitalization
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79
Q

what are the manifestations of unstable angina

A
  • chest pain
  • dyspnea
  • reduced cardiac output may occur bc of systolic dysfunction
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80
Q

how does systolic dysfuction cause decreased CO

A
  • decreased contraction/stunned = decreased CO & BP
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81
Q

why might dyspnea occur with unstable angina

A
  • due to myocardial dysfunction and pulmonary edema
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82
Q

how long does chest pain last during unstable angina? how is it relieved?

A
  • symptoms last up to 20 min

- not relieved by nitro or rest

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83
Q

what happens if chest pain goes on longer than 20 min during unstable angina

A

= likely get necrosis = MI

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84
Q

what is a big difference between stable & unstable angina

A
  • stable = relived by rest & nitro, and caused by exertion
  • unstable = may occur at rest & require less exertion, not promptly relieved by nitro but once was
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85
Q

describe angina during unstable angina

A
  • develops w less exertion
  • can develop at rest or during sleep
  • not promptly relieved by nitro but once was
  • gradually worsen over days
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86
Q

describe the changes in biomarkers during unstable angina

A
  • remain normal or are minimally elevated
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87
Q

what are cardiac biomarkers

A
  • contents spilled by myocytes when they die

- can be measured in the blood

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88
Q

how can biomarkers distinguish MI vs angina

A
  • MI = significant rise in biomarkers

- angina = no or little death = normal biomarkers

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89
Q

what happens if myocardial ischemia is brief during unstable angina

A
  • ventricular dysfunction is reversible
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90
Q

what happens if ischemia is persistent but less than 30 min during ustable angina

A
  • ventricle may become stunned

= mild decrease in ventricular function that can last for weeks

91
Q

what happens if blood flow is not restore for 40-60 min during unstable angina

A
  • cardiac cells begin to die = permanent myocardial dysfunction
92
Q

how come during unstable angina it takes 40-60 min for cell death and not 20 min?

A
  • if cell is completely deprived of O2 takes 20 min

- with unstable angina, usually still some blood flow = >20 min for cell death

93
Q

what is myocardial infarction

A
  • nercrotic death of cardiac muscle from prolonged ischemia (20-60 min)
94
Q

is an MI irreversible?

A
  • irreversible dysfunction = scar
95
Q

what causes an MI

A
  • plaque rupture followed by occlusive thrombus formation

NOTE: with unstable angina it is followed by spotaneous thrombolysis but not in MI

96
Q

what are two kinds of MI

A
  1. non STEMI

2. STEMI

97
Q

how long does it take for MI to be complete? how long until most cell death has occured?

A
  • 12 hours to complete

- most cell death in first 6 hr

98
Q

describe the progression of necrotic tissue

A
  • begins on the endocardial (inside) and progresses to the pericardial (outside)
99
Q

why does necrotic tissue first form on the inside?

A
  • bc outer vessels travel to inner layers = furthest away from blood supply
100
Q

what is a transmural infarction

A
  • involves full thickness of ventricle

= STEMI

101
Q

what is a subendocardial infarction

A
  • only inner portion of ventricle has died

= non-STEMI

102
Q

does angina or IHD always preced MI? why or why not?

A
  • rupture-prone plaques can be less than 50% occlusive = no a history of angina does not always preced
103
Q

what are manifestations of MI

A
  • angina
  • dyspnea, orthopnea
  • increased JVP & leg edema (decreased CO = “back up fluid”
  • syncope, presyncope (decreased CO)
  • ashen, cold, clammy (with decreased bp)
  • reflex tachy with decreased bp = SNS stim
  • N&V (from pain)
  • brady if inferior infarct = PSNS
  • small temp rise from necrosis
  • ECG changes
  • elevated cardiac biomarkers
104
Q

how might angina differ during an MI vs unstale angina

A
  • more severe & lasts longer

- can also be silent

105
Q

why might you get N&V with MI? where is this most common?

A
  • if injury stimulated vagus nerve = triggers PSNS = lowered HR
  • most common with injury to inferior aspect to heart bc its where the nerve runs
  • N&V also from pain
106
Q

why do we get elevated biomarkers in blood with MI

A
  • when muscle cells die from necrosis, contents spill into the blood
107
Q

what are diagnostic studies for a MI

A
  • ECG –> see ST changes
  • serum cardiac markers
  • angiography
108
Q

what can you see with an angiography

A
  • direct picture of vessels
109
Q

what are the 3 cardiac biomarkers

A
  1. troponin
  2. CK-MB
  3. myoglobin
110
Q

what is the preferred cardiac biomarker

A

troponin

111
Q

why is troponin the preferred biomarker

A
  • rises fast & early = early detection
  • stays elevated for long period of time = helpful if pt delays coming to hosputal
  • can see elevation up to 2 days later
112
Q

what is a con to the biomarker myoglobin

A
  • not specific to heart muscle
113
Q

what is a con to CK-MB

A
  • does not go up quick = not good early indicator
114
Q

why do we get a small increase in temp during a MI

A
  • necrosis = tissue injury = inflammation = infiltration of macrophages
115
Q

how come we get scar formation w MI

A
  • cardiac cells cannot regenerate = scar tissue formation
116
Q

what does the scar formation during MI cause

A
  • cannot contract = permanent ventricular dysfunction
117
Q

what does the amount of dysfunction depend on

A
  • size of scar tissue
118
Q

how does scar tissue effect conduction? how does this show during a transmural MI?

A
  • scar tissue is not excitable = no electrical conduction

- transmural MI = permanent change in ECG = pathological Q

119
Q

describe the change in Q wave seen in a transmural MI

A
  • pathological Q –> deep.wide Q
120
Q

describe SNS stimulation during & after an MI

A
  • during: SNS stim = keep heart pumping

- after: too much SNS stim may aggrevate an injured or healing heart

121
Q

describe the use of beta blockers post MI

A
  • prevent overstimulation of heart & reduce HR/contracility
  • helps the heart rest
  • reduces the risk of life-threatening arrythmias
122
Q

what are complications of a MI (5)

A
  1. arrythmias
  2. acute HF or cardiogenic shock
  3. pericarditis, effusion, myocardial rupture
  4. mural thrombosis & embolism
  5. valve disorders
123
Q

what arrythmias may occur with MI

A
  • atrial & ventricular rhythmns that result in tachy, brady, or AV conduction blocks
  • cardiac arrest rhythmns such as VT or VF
  • disrupted conduction or SNS or PSNS overstim
124
Q

what do VT and VF require?

A
  • immediate defibrillation
125
Q

what is acute HF or cardiogenic shock

A
  • stunned heart = failure to pump adequate blood

= hypotension & hypoperfusion of all organs, particularly in the brain & kidneys

126
Q

what is pericarditis

A
  • inflammation to the pericardium
127
Q

what is a effusion of the heart

A
  • exudate fills the pericardial cavity
    = P on heart = tamponade
    = reduced output
128
Q

what is a myocardial rupture

A
  • ventricle can perforate = blood fill the pericardial cavity
129
Q

what causes mural thrombosis & embolism

A
  • stasis of the blood in the ventricle (due to stunning) = thrombus & embolism
  • the clots can be sent into cirulation = cerebral or pulmonary embolism
130
Q

what causes valve disorders

A
  • if necrosis occurs close to valve
131
Q

what is a valve disorder

A
  • damage to papillary muscle = A-V valve disorders (mitral & tricupsid)
132
Q

what is sudden cardiac death

A
  • immediate loss of CO = decreased bp = decreased perfusion = no pulse = death
133
Q

how does sudden cardiac death affect the brain

A

= loss of cerebral blood flow

= decreased LOC

134
Q

how long does it take death to occur after onset of a cardiac death

A
  • usually within 1 hr of symptom onset
135
Q

what are the highest predictors of sudden cardiac death

A
  • vent EF <30% (so bad CO)

- vent arrhythmia post MI (catecholamines)

136
Q

sudden cardiac death may the first sign of ________ in 25%

A
  • heart disease
137
Q

what are the fatal arrythmias

A
  • acute ventricular arrhythmias
    1. V tach
    2. V Fib
138
Q

what are other uncommon causes of sudden cardiac death

A
  • outflow obstruction

- extreme bradycardia

139
Q

what increases myocardial O2 demand?

A
  • physical activity
  • stress
  • SNS input
  • tachycardia
  • increased afterload
  • volume overload
  • cardiac hypertrophy & dilation
140
Q

what is cardiac hypertrophy

A

thickening of heart wall

141
Q

what is cardiac dilation

A
  • stretching of the heart
142
Q

how does cardiac hypertrophy & dilation increase myocardial O2 demand

A
  • cause cells to be insufficient & require O2
143
Q

what decreases myocardial O2 supply

A
  • CAD
  • hypovolemia
  • weakened heart muscle
  • arrythmias
  • cardiac injury/remodeling
  • valve disease
  • anemia
  • resp disease
144
Q

what is cardiac remodelling

A
  • dilation or hypertrophy
145
Q

how does anemia decrease O2 supply

A
  • decreased O2 carrying capacity
146
Q

how does valve disease cause decreased O2 supply

A
  • causes leakiness

- or stenosis

147
Q

how does resp disease cause decreased O2 supply

A

= decreased oxygenation

148
Q

what are anginal managment goals

A
  • minimize the frequenzy, duration, and intensity of anginal pain
149
Q

what is the goal of anginal therapy regarding functional capacity

A
  • improve or maintain functional capacity
150
Q

what do you hope to delay or prevent with anginal therapy

A
  • MI
  • cardiac remodelling
  • arrythmias
151
Q

what does cardiac remodelling lead to

A
  • HF
152
Q

what is the goal of anginal therapy regarding meds

A
  • minimize adverse effects
153
Q

what are common adverse effects with anginal drugs

A
  • bradycardia
  • hypotension
  • hypercalemia
    (due to over effect)
154
Q

what is included in non pharmacological management of angina

A
  • diet
  • lifestyle mod
  • treating underlying disorder
  • angioplasty
  • surgery
155
Q

what changes in diet can be included for management of angina

A

decrease intake of:

  • alcohol
  • cholestrol/sat fats
156
Q

describe lifestyle modifications for management of angina

A
  • exercise
  • weight management
  • smoking
157
Q

what underlying disorders can you treat to manage angina

A
  • DM
  • HTN
  • hyperlipidemia
158
Q

what is angioplasty

A
  • surgery to unblock a blood vessel
159
Q

what is a surgery done for angina

A

CABG –> redirection of blood around a blocked artery

160
Q

what does CABG stand for

A
  • coronary artery bypass graft
161
Q

why do we want to create moderate disease progression

A
  • allow time for collateral development
162
Q

what are antianginal drugs

A
  • drugs that target cardiac vessels and worload
163
Q

what is the therapeutic goal of antianginal drugs

A
  • increase supply to ischemic heart tissue

- decrease myocardial O2 demand & workload

164
Q

how can antianginal drugs increase O2 supply to ischemic tissue

A
  • dilate coronary arteries
165
Q

how can antianginal drugs decreased O2 demand & workload

A
  • slow HR
  • dilate veins in the body so the heart receievd less blood = decreased preload
  • cause heart to contract w less force = reduced contractility
  • dilating arterioles in the body to lower body pressue = reduced afterload
166
Q

what are the antianginal drug classes

A
  • nitrates/nitrites
  • beta-blockers
  • calcium channel blockers
  • antilipemics
  • antiplatelets, anticoagulants, thrombolytics
167
Q

what are 2 types of nitrates

A
  • nitroglycerine

- isosorbide dinitrate

168
Q

what is the MOA of nitrates

A
  • artificial NO donor
  • dilate veins in the body = decreased venous return = decreased preload = decreased workload
  • dilate coronary arteries = increased blood supply to myocardium
169
Q

what are nitrates used for

A
  • prevention & treatment of all types of angina
170
Q

what is an important consideration w nitrates

A
  • degrades in light = in brown bottle
171
Q

how can nitroglycerine be given (routes)? why is this important?

A
  • sl tablet
  • spray
  • transdermal
  • iv
    = no first pass effect
172
Q

what is the rescue med for angina

A
  • nitroglycerine
173
Q

explain how nitroglycerine is administeres

A
  • sit down –> to keep safe from decreased bp & decreases workload
  • first dose –> wait 5 min
  • if not gone then 2nd dose –> wait 5 min
  • if not gone then 3rd dose
174
Q

how many doses of nitro can you give in 15 min

A
  • 3
175
Q

what should you assess for an in-patient taking nitro

A
  • angina, BP (to keep safe from falls) and HR after each dose
176
Q

what should you do if the 3 rd dose of nitroglycerine does not work

A

= unstable angina or MI

- call ambulance

177
Q

what should you for a patient in the hospital taking nitroglycerine

A
  • return to bed or chair

- check vital signs between doses

178
Q

what are side effects of nitroglycerin

A
  • increased HR (reflex tachy)
  • decreased BP –> orthostatic
  • pounding headache (due to dilation of vessels in head)
  • dizziness
  • flushing
179
Q

describe headache associated w nitroglycerin

A
  • will go away after continued use

- due to vasodilation

180
Q

does tolerance develop with nitroglycerin?

A
  • yes if taking 24/7
181
Q

how can we prevent tolerance w nitro

A
  • nitrate holiday = nitrate free period
  • remove patch nitro patch at bedtime for 8 hrs
  • apply new patch in morning
182
Q

describe the difference in use of patch vs spray for nitro

A
  • patch = for maintenance

- spray = rescue

183
Q

why is it important to prevent nitro tolerance

A
  • would result in no effect of nitro spray if needed
184
Q

what drug does nitro have an interaction w ? why?

A
  • any other med w nitro in it –> viagra

- both dilate vessels = risk of dangerous drop in pressure & precipiate MI

185
Q

describe the use of nitro IV

A
  • used for urgent
  • hypertensive emergencies
    ex. bp control w perioperative HTN
186
Q

what are 2 types of beta blockers

A
  • metaprolol

- atenolo

187
Q

what is the action of beta blockers

A
  • decreased HR = decreased workload

- decreased contractility = decreased workload

188
Q

what is the MOA of beta blockers

A
  • selectively block beta adrenergic stimulation of the heart
189
Q

what are beta blcokers used for? what are they first line for?

A
  • decrease frequency of anginal attacks
  • 1st line for chronic angina –> so if do something, HR wont automatically go up too high
  • critical cardioprotective IHD med
190
Q

what is one consideration for pts taking beta blocker

A
  • bc HR is blocked from rising - must be carefulw ith exertional activity
191
Q

does tolerance occur with beta blockers?

A
  • no
192
Q

what can sudden discontinuation of beta blockers cause

A
  • may cause anginal attack

- rebound effect from HR no longer being reduced

193
Q

what else do beta blockers treat

A
  • treats HTN and angina = reduced incidence of Mi
194
Q

beta blockers are _______-

A

cardioprotective

195
Q

explain how beta blockers are also anti-arrythmic

A
  • after an MI, high levels of catecholamine irritate the heart = imbalance in supply & demand which can lead to arrythmias
  • beta blockers blcok the harmful effect of catecholamines = improve survival after MI
196
Q

how do we get side effects with beta blockers

A
  • over effect

- too big of drop in HR, BP etc.

197
Q

what are the two classes of calcium channel blockers

A
  1. vascular

2. cardiac

198
Q

what are cardiac CCBs known as

A

non-dihydropyridine

199
Q

what do cardiac CCBs do

A
  • dilate coronary arteries = increase supply
  • slow conduction velocity thru the heart to reduce HR
  • reduce vasospasm
  • treat arrythmias thru slowing conduction
200
Q

what are 2 types of cardiac CCB

A
  1. verapamil

2. diltiazem

201
Q

what is the MOA of cardiac CCBs

A
  • inhibit transport of Ca into myocardial cells = reduce conduction velocity
202
Q

how can cardiac CCBs treat variant angina

A
  • by reducing vasospasm
203
Q

describe the interaction between diltiazem and digozin

A
  • may increase digoxin levels
204
Q

what are adverse effects of cardiac CCBs

A
  • very safe
  • caution with other blockers
  • bradycardia
  • complete heart block
205
Q

what is the antidote fro complete heart block

A
  • ca chloride IV

- competes with blocking of Ca

206
Q

what are vascular CCBs

A
  • dihydropyridine
207
Q

what is the MOA of vascular CCBs

A
  • inhibit transport of Ca in smooth muscle cells
208
Q

what do vascular CCBs do

A
  • cause peripheral arterial vasodilation = decreased afterload = decreased workload
  • also helps with IHD
209
Q

what are 2 types of vascular CCBs

A
  • amlodipine

- nifedipine

210
Q

what are adverse effects of vascular CCBs

A
  • very safe

- r/t to vasodilation: headache, hypotension, dizziness, edema of ankles & feet

211
Q

what is a CXR

A
  • chest x-ray
  • can also look for cardiac remodelling
    = silhouette of heart
212
Q

what is an ECHO

A
  • ultrasound
  • can see chambers & muscle move
  • cardiac echocardiogram
  • can see valves, calculate EF
213
Q

what are the 2 main uses of ECGS

A
  • arrythmias

- cardiac ischemic/damage

214
Q

what is a MUGA scan

A
  • multigated acuistion scan

- used to get EF

215
Q

what is a cardiac MRI good for

A
  • soft tissue
  • no radiaition
  • calculate EF
216
Q

what is one important thing to look for on ECG

A
  • St elevation or not
217
Q

what is ejection fraction

A

“report card for heart”

218
Q

what is pulmonary edema? how can we see it?

A
  • fluid in the lung tissue

- can see on CXR

219
Q

what are basic cardiac diagnostic studies

A
  • 6 min walk test
  • stress/exercise test
  • angiogram
220
Q

what is a PCI

A
  • percutaneous coronary intervention
  • going into an artery thru the skin & go to area of blockage in heart
  • will inject dye & blow up balloon to crush plaque to the side
  • may also place stent (mesh) to prevent plaque from squishing back in, or pieces from breaking off
221
Q

what is revascularization? what 2 procedures are used for this?

A
  • restoration of perfusion
    1. PCI
    2. CABG
222
Q

what is a CABG

A
  • coronary artery bypass graft
223
Q

what does a CABG do

A
  • open heart surgery
  • use another blood vessel to divert blood flow around blockage
  • may reroute a blood vessel in heart
  • may harvest a vessel from leg
224
Q

what is a ventricular assist device

A
  • pump that will pump blood in heart
  • often temporary
  • for severe HF or heart disease, often while waiting for transplant

NURS 2500 (5 decks)

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