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NU 360 > Ch. 29, 31, 32 > Flashcards

Ch. 29, 31, 32 Flashcards

1
Q

valvular heart disease is categorized into

A
  • mitral stenosis
  • mitral regurgitation (insufficiency)
  • aortic stenosis
  • aortic regurgitation (insufficiency)
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2
Q

mitral valve stenosis

A
  • narrowed mitral valve
  • stiff and narrow valve opening (calcium build-up, rheumatic heart disease- tissue is hard and stiff)
  • rheumatic fever is major (#1) cause
  • left ventricle is not being filled, heart has to work harder
  • systemic effect- not adequate blood flow
  • people end up needing mitral valve replacement
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3
Q

mitral regurgitation

A
  • mitral valve leafets do not meet, allowing backflow of blood into atrium during systole
  • floppy
  • valve tissue doesn’t work as well anymore
  • floppy flaps are not a good gate
  • mitral valve has trouble holding the blood in the left ventricle to go into the aorta
  • blood is going into aorta but also going back into atrium
  • decreased CO results
  • present with SOB, tired, fatigued
  • surgical repair, valve replacment
  • scale of how bad it is
  • can hear the regurg murmur with stethescope
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4
Q

aortic stenosis

A
  • narrowed aortic valve, reduces efficient blood flow from the left
  • stiff and narrow valve opening (calcium build-up, rheumatic heart disease- tissue is hard and stiff) ventricle of the aorta
  • cardiac muscle gets floppy and functions worse (tired) when it has to work harder- decreased CO
  • present with SOB, fatigue, chest pain
  • surgical repair or replacement indicated
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5
Q

aortic regurgitation

A
  • aortic valve does not close, blood leaks backward
  • valve tissue doesn’t work as well anymore
  • floppy flaps are not a good gate
  • blood into aorta but also back into left ventricle
  • presents with SOB, fatigue
  • can happen over time, gradual systems
  • regurg murmur can be heard
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6
Q

cardiac valvular assessment includes

A
  • onset: when did it start?
  • PMH
  • clinical manifestations (s/sx)- can listen APETM with stethoscope to listen for regurg murmur
  • diagnostic tests (echocardiogram- gold standard, needed to make a definitive dx)
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7
Q

clinical manifestations of cardiac valvular disease

A
  • fatigue & activity level
  • dyspnea
  • palpitations, angina
  • arrhythmia
  • edema
  • heart sounds
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8
Q

non-surgical nursing management of cardiac valvular diseases

A
  • drug therapy: diuretics, beta blockers, digoxin
  • management of a-fib (patients with valvular disease are prone to a-fib)
  • anticoagulation (b/c prone to blood clots)
  • REST w/ limited activity (take breaks w/ stairs, dont be training for a marathon)
  • prophylactic antibiotic
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9
Q

drug therapy for cardiac valvular disease

A
  • diuretics: if patient has edema, dont want extra fluid in the body to make body work harder
  • beta blockers: want a lower BP so heart is not working so hard to push through the pressure
  • digoxin
  • prophylactic antibiotic: people with valve disease are put on these to prevent endocarditis; damaged valves have an affinity for bacteria traveling to those damaged valves, ie dentist
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10
Q

surgical nursing management of cardiac valvular diseases

A
  • reparative procedures: balloon valvuloplasty- stick balloon into stenotic valve to squish valve open; not permanent fix- buys time
  • invasive surgical procedures
  • reconstruction: replacement- mechanical or biological valve (cow/pig used to be used, mechanical more often now)
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11
Q

ineffective endocarditis is a

A

microbial infection involving the endocardium (where the valves are)
- an acute problem
- vegetation grows on valves, lettuce in the way

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12
Q

ineffective endocarditis occurs primarily in patients who

A
  • abuse IV drugs * common
  • has had a valve replacement(s) - bacteria clings to something “foreign”
  • experienced systemic infections
  • structural defects
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13
Q

clinical manifestations of endocarditis

A
  • murmur
  • heart failure (not good pump, decreased CO)
  • arterial embolism (vegetation breaks loose): splenic infarction, neurologic changes
  • petechiae* (pinpoint red spots)
  • splinter hemorrhages in nail beds*
  • chest pain, muscle aches, joint pain
  • flu-like sick
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14
Q

diagnostic assessment for endocarditis

A
  • positive blood cultures
  • NEW regurgitation murmur
  • evidence of endocardial involvement by echocardiography (patient teaching for echo)
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15
Q

nursing management of endocarditis

A
  • rest
  • antimicrobials- IV for 4-6 weeks (long-term IV antibiotics)
  • PICC placement (probably in arm)
  • before d/c: home care involvement?, teaching for PICC care
  • good oral hygiene
  • monitor for effective therapy/recurrence endocarditis
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16
Q

pericarditis is

A

inflammation or alteration of the pericardium, the membranous sac that encloses the heart

  • can be caused by surgery, infection, trauma (anything that irritates the pericardial lining and causes an inflammatory response
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17
Q

dressler’s syndrome

A

type of pericarditis after trauma, surgery, MI

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18
Q

post-pericardiotomy syndrome

A

type of pericarditis that occurs after CABG

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19
Q

chronic constrictive pericarditis

A
  • “chronic” meaning it happens often to the patient
  • tissue is stiff
  • constricts the heart
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20
Q

clinical manifestations for pericarditis

A
  • substernal precordial (chest) pain radiating to left side of the neck, shoulder, or back
  • grating, oppressive pain, aggravated by (deep) breathing, coughing, swallowing
  • **pain worsened by the supine position; relieved when the patient sits up and leans forward ** classic sx
  • pericardial friction rub
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21
Q

nursing management of pericarditis

A

pain management: NSAIDs (anti-inflammatories), antibiotics if bacterial cause suspected
- pericardiectomy if chronic pericarditis- cut a chunk of pericardium off to allow the heart so it cant constrict the heart anymore (you can live without your pericardium)
- prevent pericardial effusion

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22
Q

pericardial effusion puts patients at risk for

A

cardiac tamponade: where fluid is blocking the heart from moving (“tamponing”)

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23
Q

clinical findings with cardiac tamponade

A
  • JVD- jugular venous distention
  • paradoxical pulse (feel)
  • decreased CO, perfusion is bad
  • muffled heart sounds
  • circulatory collapse
  • look bad and going into shock- looks like on death’s door, evident there is a problem
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24
Q

pericardial tamponade

A
  • **very dangerous!
  • fluid is built up in the pericardium- not allowing movement
  • need to do pericardiocentiusis - life saving procedure to suck fluid out with needle or catheter
  • no medications will fix the problem until the fluid is removed from the pericardial space
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25
Q

emergency care of cardiac tamponade

A
  • increase fluid volume bc we need to increase BP, but still have to decrease fluid around the heart - DON’T INCREASE RAPIDLY
  • hemodynamic monitoring
  • pericardiocentesis- take fluid out with needle/catheter
  • pericardial window- cut a chunk of pericardium out
  • pericardiectomy
  • if patient was otherwise healthy, once fluid is removed, heart can move/pump normally and CO will increase/return to normal
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26
Q

shock defined is

A

any problem impairing oxygen delivery to tissues and organs can precipitate shock
- oxygenation and tissue perfusion needs are not met*
- syndrome; whole body response*
- leads to life threatening emergency
- widespread abnormal cellular metabolism

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27
Q

mean arterial pressure is determined by

A
  • blood volume
  • effectiveness of the heart as a pump (cardiac output)
  • resistance of the system to blood flow
  • relative distribution of blood between arterial and venous blood vessels
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28
Q

mean arterial pressure is

A

the pressure inside our artery system that keeps our body perfused with blood
- normal is 70-100
- more specific than taking BP
- higher MAP when blood is thick
- lower MAP when blood is thin
- MAP determines level of patient is in

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29
Q

early signs of shock

A
  • map < 10mmHg from baseline
  • effective compensation O2 to vital organs
  • increased HR
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30
Q

compensatory signs of shock

A
  • map < 10-15mmHg from baseline
  • increased renin and ADH
  • vasoconstriction
  • decreased pulse pressure
  • increased HR
  • decreased pH
  • restless
  • apprehensive
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31
Q

progressive signs of shock

A
  • map < 20mmHg from baseline
  • tissue/organ hypoxia
  • decreased UO (oliguria)
  • weak rapid pulse
  • decreased pH
  • sensory neural changes
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32
Q

refractory signs of shock

A
  • excessive cell/organ damage
  • multisystem organ failure
  • low pH
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33
Q

classifications of shock

A
  • hypovolemic
  • cardiogenic
  • distributive
  • obstructive
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34
Q

hypovolemic shock occurs when

A

LOW circulating BLOOD VOLUME causes a mean arterial pressure decrease
- the body’s O2 needs are not met

  • problem: fluid loss
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35
Q

hypovolemic shock is commonly caused by

A

“hole in the tank”
- shot/stabbed
- hemorrhage- PPH, child birth
- internal bleeding
- stomach ulcer perforates
- dehydration
- vomiting & diarrhea

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36
Q

cardiogenic shock occurs when

A

the actual heart muscle is unhealthy
- direct pump failure
- decreased CO
- decreased map

  • problem: no fluid loss, pump is broken/failed
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37
Q

cardiogenic shock is commonly caused by

A
  • MI is #1 cause
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38
Q

distributive shock occurs when

A

blood volume is not lost but is distributed to the interstitial tissues where it cannot circulate and deliver O2

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39
Q

distributive shock is commonly caused by

A
  • loss of sympathetic tone
  • vasodilation
  • pooling of blood in venous and capillary beds
  • capillary leak
  • problem: tank got bigger, not enough juice to keep up pressure; vessels are more permeable, so fluid leaks out of vessels into tissues (looks swollen/edematous)
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40
Q

neural-induced distributive shock

A

caused by head trauma, anesthesia

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41
Q

chemical-induced distributive shock

A

caused by sepsis, anaphylaxis, capillary leak
*septic shock

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42
Q

obstructive shock occurs when

A

heart is normal, but conditions outside the heart prevent either adequate fillings of the heart or adequate contraction of the healthy heart muscle

  • problem: something is blocking the pump so it cannot work effectively
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43
Q

examples of obstructive shock

A
  • pericarditis
  • cardiac tamponade* biggest cause of obstructive shock
  • pulmonary HTN
  • tension pneumothorax*
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44
Q

stages of shock

A
  1. initial (early)
  2. nonprogressive (compensatory)
  3. progressive (intermediate)
  4. refractory (late/irreversible)
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45
Q

initial (early) stage of shock

A
  • baseline MAP decreased by less than 10 mmHg*
  • HR and RR: very subtle* increase
  • DBP: start coming up to fight
  • production of lactic acid increases*
  • adaptive responses
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46
Q

nonprogressive (compensatory) stage of shock

A
  • MAP decreased by 10-15 mmHg
  • HR increases; SBP decreases (narrowing pulse pressure); O2 Sat: decreased
  • renal system: UO decreases
  • tissue hypoxia in non-vital organs: fingers and toes
  • acidosis and hyperkalemia: acid goes into cell and pushes potassium out of cell into blood= hyperkalemia
  • cool extremities: cold, purpley fingers
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47
Q

progressive (intermediate) stage of shock

A
  • sustained decreased in MAP of more than 20 mmHg from baseline
  • vitals: HR, RR, increase; BP decreases
  • labs: K+ increase; Ph increase; Lactic Acid increase
  • life-threatening emergency
  • immediate interventions are needed
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48
Q

refractory (late/irreversible) stage of shock

A
  • too much cell death and tissue damage result from too little oxygen reaching the tissues
  • body cant respond effectively to interventions, and shock continues
  • unconsciousness, non-palpable pulses
  • cool, mottled skin
  • respirations: slow and shallow, low O2 sat
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49
Q

what can prevent shock from progressing past the nonprogressive stage?

A

stopping conditions that started shock and supportive interventions

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50
Q

conditions causing shock need to be corrected within ____ (timeframe) of the onset of the progressive stage of shock

A

within 1 hour

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51
Q

how can infection lead to septic shock

A

local infection –> systemic inflammatory response syndrome (early sepsis) –> systemic infection + SIRS –> organ failure (severe sepsis) –> MODS (septic shock)

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52
Q

pathophysiology of sepsis

A

infection that causes tissue damage, organ failure, and death if not treated promptly

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53
Q

septic shock is a subset of sepsis, including

A
  • SIRS: overreaction- full-body inflammatory response, puts body into distributive response
  • MODS: multi-organ dysfunction syndrome
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54
Q

SIRS sx

A

systemic inflammatory response syndrome- any 2 of the following sx: **
- temp < 96.8 or >101 F
- RR > 20/min
- hyperglycemic (non-diabetic): stress & cortisol release increases blood sugar
- HR > 90 bpm
- acute AMS (altered mental status)
- WBC < 4 or > 12

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55
Q

MODS

A

multi-organ dysfunction syndrome- the organs die

  • sequence of cell damage caused by massive release of toxic metabolites and enzymes
  • metabolites are released from dead cells
  • microthrombi form
  • myocardial depressant factor from the ischemic pancreas
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56
Q

Sepsis-3 defines sepsis as

A

a life-threatening organ dysfunction brought on by dysregulated response to infection

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57
Q

septic shock is a term used to describe

A

a subset of sepsis
- circulatory, cellular, and metabolic abnormalities substantially increase the risk of death over that associated with sepsis alone

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58
Q

infection is usually accompanied by

A

inflammation

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59
Q

can inflammation occur without invasion of organisms?

A

yes

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60
Q

segmented neutrophils

A

(mature WBCs)
- not active infection, something else is going on

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61
Q

banded neutrophils

A

(less mature WBCs) “baby bands”
- we know there is an active infection going on
- left-shift
- immature WBCs trying to respond to infection

62
Q

SIRS nursing interventions

A

prioritize - O2 and antibiotics
- 100% O2
- collect lactate levels and blood cultures BEFORE antibiotics
- hypotension management or if high lactic acid level (give lots of IVFs)
- broad-spectrum antibiotics within 1 hour of dx; don’t need to wait for labs
- treat fever if needed
- hyperglycemia (sugar) management: insulin
- if in shock: may need to give vasoconstrictor- dopamine, epinephrine

63
Q

MODS first occurs in the

A

liver, heart, brain, and kidney

64
Q

how can sepsis be prevented? (primary prevention)

A
  • avoid trauma and hemorrhage
  • use proper safety equipment
  • seat belts
  • awareness of hazards in home/workplace
65
Q

secondary prevention of sepsis

A
  • assess for early s/sx ( catch it early )
  • patient teaching/education
66
Q

physical assessment of shock

A
  • CNS changes
  • respiratory changes
  • CV changes
  • skin changes
  • renal and urinary changes
  • MS changes
67
Q

hypovolemic shock labs

A

low: pH, PaO2
high: PaCO2, lactic acid, K+
high or low: H&H

68
Q

septic shock labs

A

low: segmented neutrophils
high: lactic acid, WBC (or normal), banded neutrophils (L-shift)

69
Q

hypoxia occurs during shock due to

A

hypovolemia

70
Q

inadequate perfusion occurs during shock due to

A

active fluid volume loss and hypotension

71
Q

anxiety occurs during shock due to

A

potential for death and decreased cerebral perfusion

72
Q

decreased cognition occurs during shock due to

A

decreased cerebral perfusion

73
Q

management of hypovolemic shock

A
  • IV access and fluids
  • oxygen
  • position
  • medications
  • treat underlying cause
74
Q

cardiogenic shock labs

A
  • high troponin (because it is probably caused by an MI)
75
Q

management of septic; cardiogenic; distributive shock

A
  • septic: give antibiotics
  • cardiogenic: give dysrhythmics
  • distributive: plug hole and replace
76
Q

drug therapy to treat shock

A

vasoconstrictors:
- dopamine
- epinephrine
- norepinephrine
- phenylephrine

agents enhancing contractility & myocardial perfusion

77
Q

coronary artery disease includes/causes

A
  • chronic stable angina
  • acute coronary syndromes: unstable angina and AMI

(the arteries that go to the heart)

78
Q

ischemia

A

insufficient oxygen supply to meet the requirements of the myocardium

79
Q

infarction

A

necrosis or cell death that occurs when severe ischemia is prolonged and decreased perfusion causes irreversible damage to the tissue

80
Q

chronic stable angina pectoris

A

temporary imbalance between the coronary artery’s ability to supply oxygen and the cardiac muscle’s demand for oxygen
- Imbalance of supply and demand of O2
- stable is predictable- we know what causes/helps it

81
Q

if ischemia is limited in duration (timing) and does not cause damage to the myocardial tissue, it can subside with

A

rest and SL NTG (nitroglycerin)
- can take up to 3 nitro (check BP + re-evalute chest pain between every nitro)

82
Q

what is referred to as the “strangling of the chest?”

A

chronic stable angina pectoris

83
Q

patients who present with either unstable angina or an acute myocardial infarction have (hint: category of syndromes)

A

an acute coronary artery syndrome

84
Q

what causes acute coronary artery syndromes?

A

atherosclerotic plaque in coronary artery ruptures, resulting in platelet aggregation, thrombus formation, or vasoconstriction

85
Q

unstable angina pectoris

A
  • new on-set angina, or
  • previously stable angina now with pain at rest, or
  • variant (prinzmetal’s) angina
  • we don’t know what is causing it (random) or what will relieve it
  • red flag that MI may happen
86
Q

time is muscle meaning:

A

don’t want to sit on symptoms because you want to save as much of the heart as possible
- longer time = more muscle damage

87
Q

variant (prinzmetal’s) angina results from

A

spasm of coronary arteries usually at rest

88
Q

pre-infarction angina refers to

A

chest pain that occurs days or weeks prior to an AMI

89
Q

patients with unstable angina pectoris may present with

A

ST changes on 12-lead EKG

  • NO changes in troponin levels
90
Q

most serious acute coronary syndrome

A

myocardial infarction

91
Q

MI occurs when

A

the myocardial tissue is abruptly or severely deprived of oxygen

  • occlusion of blood flow (blocked from heart)
  • necrosis (muscle dying)
  • hypoxia (O2 not getting to cardiac tissue)
  • ventricular remodeling (ventricle scars, not reversible)
92
Q

MI is divided by the ACC/AHA into (categories)

A
  • non-ST MI (NSTEMI)
  • ST elevation MI (STEMI)
93
Q

non-ST MI (NSTEMI)

A
  • ST segment is either depressed or T is inverted
  • draw cardiac enzymes- need to look at troponin level
  • assess patient for clinical presentation (see): hx of smoking, diabetes, gray in color, SOB, sweating
  • same sx as STEMI, but it shows up different on EKG
94
Q

ST elevation MI (STEMI)

A
  • ST segment on EKG is elevated
  • measured in mm
  • “tombstone” ST wave
95
Q

non-modifiable risk factors for MI

A
  • age
  • gender (females with abdominal obesity and metabolic syndrome are at risk)
  • hereditary (family hx, ethnic background)
96
Q

modifiable risk factors for MI

A
  • elevated serum cholesterol
  • elevated triglycerides
  • large waist size
  • cigarette smoking
  • hypertension
  • impaired glucose tolerance
  • obesity/overweight
  • physical inactivity
  • stress
  • alcohol
97
Q

average age of first MI

A

female: 72 years old
male: 65 years old

98
Q

acute coronary syndrome: assessment

A

history: if sx present, skip for now and start interventions
physical assessment: rapid assessment crucial; always put on 12-lead EKG if they have chest pain
psychosocial assessment: coping mechanisms, calm patient, be therapeutic but also while moving/intervening

99
Q

ACS s/sx: angina

A
  • precipitated by exertion/stress
  • substernal C/P radiate to L arm
  • relieved by Nitro
  • lasts < 15 min
100
Q

ACS s/sx: MI

A
  • occurs w/out cause
  • substernal C/P radiate to L arm and ___
  • pain relieved by MONA
  • lasts > 30 min (ongoing, nitro wont get rid of it)
  • associated symptoms
101
Q

chest pain assessment: STEMI

A
  • chest pain
  • suspected acute coronary syndrome
  • HAS ST elevation
102
Q

chest pain assessment: NSTEMI

A
  • chest pain
  • suspected acute coronary syndrome
  • DOES NOT HAVE ST elevation
  • positive NSTE-ACS
103
Q

chest pain assessment: unstable angina

A
  • chest pain
  • suspected acute coronary syndrome
  • DOES NOT HAVE ST elevation
  • negative NSTE-ACS
104
Q

ACS nursing assessment includes

A
  • pain
  • cardiac rhythm
  • pulses
  • vitals
  • skin
105
Q

EKG changes with ACS: full wall thickness, myocardial infarction

A
  • ST elevation (STEMI)
  • new Q wave, ST normalizes
  • Q wave often disappears
106
Q

EKG changes with ACS: partial or small area, myocardial wall infarction

A
  • ST depression (NSTEMI)
  • no Q wave, ST normalizes
107
Q

EKG changes with ACS: angina (stable or unstable), no myocardial wall injury

A
  • ST depression
  • no changes in EKG
108
Q

lab assessment with ACS

A

troponin T and troponin I
- normal T 0-0.4, normal I < 0.03
- should not have any number (unless renal failure)

cholesterol (not acute) - do patient teaching/get it after the MI

109
Q

imaging assessments with ACS

A
  • 12-lead EKG: STEMI vs NSTEMI
  • stress test: adenosine MIBI/Exercise (*not in acute period)
  • Echo: wall motion, used after the MI to determine the damage to the heart structure in real time
  • cardiac catheterization
110
Q

ACS analysis: acute pain due to

A

imbalance between myocardial oxygen supply and demand

111
Q

ACS analysis: decreased myocardial tissue perfusion due to

A

interruption of arterial blood flow

112
Q

ACS analysis: potential for dysrhythmias due to

A

ischemia and ventricular irritability

113
Q

ACS analysis: potential for heart failure due to

A

left ventricular dysfunction

114
Q

treatment plan approach to ACS

A
  • manage acute pain
  • increase myocardial tissue perfusion
  • ID and manage dysrhythmias
115
Q

ACS: acute pain interventions

A
  • provide pain relief modalities, drug therapy
  • decrease myocardial oxygen demand
  • increase myocardial oxygen supply
116
Q

immediate treatment of an MI (hint acronym)

A

“MONA” (generally speaking; does not need to be given in this order)
- morphine - pain, relax vessels, anxiety (patient specific, if BP supports it)
- oxygen - only if O2 Sat is below 94%
- nitroglycerine - if BP supports it (higher, not if <100 SBP), not every patient gets nitro
- ASA (aspirin)** - prevents clot from getting bigger; NOT for pain (contraindicated with active bleeding, allergy to ASA)

117
Q

nitroglycerin: tunnel rate

A

bigger is better
- need an open, wide tunnel to all better access

118
Q

nitroglycerin quick release

A
  • sublingual tablets
  • translingual spray
119
Q

nitroglycerin slow release

A
  • nitro-bid (patch)- remember to take the old one off
  • nitro ointments
  • sustained release tablets
120
Q

what to watch for with any kind of nitroglycerin

A
  • severe hypotension***
  • tachycardia
  • dizziness
  • headache
  • syncope (fainting)
  • DON’T GIVE WITHOUT GLOVES ON
121
Q

interventions for ineffective tissue perfusion r/t interruption of arterial blood flow (with ACS)

A
  • drug therapy (ASA, thrombolytic agents “clot busters”)
  • restoration of perfusion to the injured area often limits the amount of MI exertion and improves left ventricular function
  • complete sustained reperfusion of coronary arteries in the first few hours after an MI has decreased mortality

clot buster OR cath lab (cath lab is priority if accessible)

122
Q

heparin for ACS

A
  • drip based on weight
  • check PTT
  • protamine sulfate (antidote)
  • enoxaprin (lovenox)

does not break up clot, prevents it from getting bigger

123
Q

antidote for heparin

A

protamine sulfate
- makes patient clot

124
Q

thrombolytic therapy is used if ___ not available

A

if PCI/PTCA is not available

125
Q

ACS: thrombolytic therapy- what do fibrinolytics do?

A

fibrinolytics dissolve thrombi in the coronary arteries and restore myocardial blood flow
- tissue plasminogen activator (t-PA)
- reteplase
- tenecteplase

meds that end in “-ase” break up clots/clot busters

126
Q

pain relief and myocardial oxygen requirements are done through

A

preload and afterload reduction

127
Q

medications for ACS (hint: list, 8)

A
  • glycoprotein (GP) IIB/IIa inhibitors (cath lab meds, help w/ platelet aggregation)
    • abciximab
    • eptifibatide
    • tirofiban
  • once a day beta-adrenergic blocking agents (beta blockers)
  • angio-tensin converting enzyme inhibitors or angiotensin receptor blockers (ACE inhibitors or ARBs)
  • calcium channel blockers (CCBs)
  • antiplatelets: clopidogrel
  • ranolazine
  • statins
128
Q

percutaneous transluminal coronary angioplasty (aka PTCA/PCI)

A

done in cath lab
1. balloon-tipped catheter is positioned in the artery
2. uninflated balloon is centered in the obstruction
3. balloon is inflated, which flattens plaque against the artery wall
4. balloon is removed and the artery is left unoccluded

129
Q

percutaneous transluminal coronary angioplasty: meds

A
  • before procedure: clopidogrel
  • after procedure: IV heparin
  • IV or intracoronary nitroglycerin or diltiazem
  • possible IV GP IIb/IIa inhibitors
  • long-term therapy, antiplatelet therapy, beta blocker, ACE inhibitor, or ARB
130
Q

PTCA with stent

A

wire mesh stent widens the artery like the balloon but the stent stays in, holding plaque against artery wall and leaving open artery

  • stent is closed when entering artery, then opens and expands to hold artery open
131
Q

nursing management post-PTCA

A
  • patient will probably be on blood thinners: stent puts patient at risk for blood clotting
  • post-cath, nurse is worried about bleeding risk
  • constant reassessment
  • check the extremity on other side of poke to make sure blood flow is normal and reaching peripherals
132
Q

leading cause of death in most patients with an MI who die before hospitalized is due to

A

dysrhythmias
aka “re-entry dysrhythmias” progressing to PVCs to v-tach/v-fib

133
Q

in-hospital interventions for dysrhythmias post MI

A
  • identify the dysrhythmia
  • assess hemodynamic status
  • treat with antidysrhythmics
  • evaluate for discomfort
134
Q

cardiogenic shock post-MI: clinical findings

A
  • > 40% of L ventricle is necrotic
  • HR: low (?)
  • BP: low (?)
  • UO: decreased (?)
  • cold, clammy skin
  • poor peripheral pulses
  • agitation, restlessness, confusion
  • pulmonary congestion
  • tachypnea
  • continuing chest discomfort
135
Q

medical management of cardiogenic shock post-MI

A
  • pain relief and decreased myocardial oxygen requirements through preload and afterload
  • drug therapy: inatrope, epinephrine, dopamine, anything that makes the heart squeeze harder
  • intra-aortic balloon pump: machine, pumps the heart, temporary fix
  • immediate reperfusion
136
Q

two methods of CABG

A
  • saphenous vein grafts
  • internal mammary artery graft
137
Q

CABG: saphenous vein grafts

A

bypassing the coronary artery d/t complete bloackage and using the saphenous vein to make a new road

138
Q

CABG: internal mammary artery graft

A

bypassing the coronary artery d/t complete blockage and using the mammary artery to make a new road

139
Q

CABG pre-op patient teaching

A
  • splint chest with pillow C&DB - frequent cough and deep breathing
  • arm and leg exercises
  • report any pain to nurse
  • analgesics for pain/pain management
  • anxiety and coping
140
Q

CABG intra-operative: patient has (equipment)

A
  • intubated
  • on bypass pump (some done off pump)
  • heart arrested –> graft done
  • chest tubes
  • pacer wires
  • foley catheter
141
Q

CABG post-op management

A
  • manage fluids and lytes
  • manage BP: hypotension/hypertension
  • cardiac tamponade
  • bleeding
  • hypothermia
  • change in level of consciousness
  • VS monitoring
  • incision site: clean, dry intact
  • chest incision site: clean, dry, intact
142
Q

discharge teaching post-MI

A
  • medications: beta blockers, ARB/ACE, ASA/plavix, statin, nitro SL prn
  • exercise
  • no smoking
  • diet
  • follow-up appointments
143
Q

expected patient outcomes post-MI (during evaluation)

A

patient will
- state pain is relieved
- have adequate myocardial perfusion
- be free of complications, ie dysrhythmias, heart failure

144
Q

atherosclerosis

A

fat build up in the arteries

145
Q

arteriosclerosis

A

hardening of the arteries

146
Q

LAD blockage

A

left anterior descending artery blocked means that the left ventricle gets no blood = dying heart

147
Q

nitroglycerin

A
  • can give up to 3 doses at a time
  • HA is common s/e (this is expected)
  • hypotension - check BP between every dose
  • given for chronic stable angina pectoris
148
Q

ACS focused assessment

A
  • pain: L shldr + jaw
  • cardiac rhythm
  • cardiac history
  • pulses
  • vitals
  • skin: cold, clammy, gray, dusky, pale
  • fatigue (big under-looked sx in women)
    *know that people present differently
149
Q

why give adenosine to patient during stress test?

A
  • adenosine will mimic what happens to the heart during exercise
  • the patient is on a monitor, not painful
150
Q

what do we worry about with a patient on a thombolytic?

A

worry about bleeding w/ thrombolytics

151
Q

hypovolemic shock interventions

A
  • stop the cause
  • replace the fluid (blood/plasma/IV fluids LR/isotonic solutions)
  • antiemetics/antidiarrheals
152
Q

cardiogenic shock interventions

A
  • intra-arterial balloon pump
  • inotropic drugs: epi, dopamine (these drugs cause vasoconstriction)
  • extra fluids to increase BP

NU 360 (12 decks)

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