Ch. 29, 31, 32 Flashcards
1
Q
valvular heart disease is categorized into
A
- mitral stenosis
- mitral regurgitation (insufficiency)
- aortic stenosis
- aortic regurgitation (insufficiency)
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
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
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
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
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)
7
Q
clinical manifestations of cardiac valvular disease
A
- fatigue & activity level
- dyspnea
- palpitations, angina
- arrhythmia
- edema
- heart sounds
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
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
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)
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
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
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
14
Q
diagnostic assessment for endocarditis
A
- positive blood cultures
- NEW regurgitation murmur
- evidence of endocardial involvement by echocardiography (patient teaching for echo)
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
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
17
Q
dressler’s syndrome
A
type of pericarditis after trauma, surgery, MI
18
Q
post-pericardiotomy syndrome
A
type of pericarditis that occurs after CABG
19
Q
chronic constrictive pericarditis
A
- “chronic” meaning it happens often to the patient
- tissue is stiff
- constricts the heart
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
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
22
Q
pericardial effusion puts patients at risk for
A
cardiac tamponade: where fluid is blocking the heart from moving (“tamponing”)
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
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
25
emergency care of cardiac tamponade
- 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
26
shock defined is
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
27
mean arterial pressure is determined by
- 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
28
mean arterial pressure is
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
29
early signs of shock
- map < 10mmHg from baseline
- effective compensation O2 to vital organs
- increased HR
30
compensatory signs of shock
- map < 10-15mmHg from baseline
- increased renin and ADH
- vasoconstriction
- decreased pulse pressure
- increased HR
- decreased pH
- restless
- apprehensive
31
progressive signs of shock
- map < 20mmHg from baseline
- tissue/organ hypoxia
- decreased UO (oliguria)
- weak rapid pulse
- decreased pH
- sensory neural changes
32
refractory signs of shock
- excessive cell/organ damage
- multisystem organ failure
- low pH
33
classifications of shock
- hypovolemic
- cardiogenic
- distributive
- obstructive
34
hypovolemic shock occurs when
LOW circulating BLOOD VOLUME causes a mean arterial pressure decrease
- the body's O2 needs are not met
- problem: fluid loss
35
hypovolemic shock is commonly caused by
"hole in the tank"
- shot/stabbed
- hemorrhage- PPH, child birth
- internal bleeding
- stomach ulcer perforates
- dehydration
- vomiting & diarrhea
36
cardiogenic shock occurs when
the actual heart muscle is unhealthy
- direct pump failure
- decreased CO
- decreased map
- problem: no fluid loss, pump is broken/failed
37
cardiogenic shock is commonly caused by
- MI is #1 cause
38
distributive shock occurs when
blood volume is not lost but is distributed to the interstitial tissues where it cannot circulate and deliver O2
39
distributive shock is commonly caused by
- 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)
40
neural-induced distributive shock
caused by head trauma, anesthesia
41
chemical-induced distributive shock
caused by sepsis, anaphylaxis, capillary leak
*septic shock
42
obstructive shock occurs when
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
43
examples of obstructive shock
- pericarditis
- cardiac tamponade* biggest cause of obstructive shock
- pulmonary HTN
- tension pneumothorax*
44
stages of shock
1. initial (early)
2. nonprogressive (compensatory)
3. progressive (intermediate)
4. refractory (late/irreversible)
45
initial (early) stage of shock
- 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
46
nonprogressive (compensatory) stage of shock
- 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
47
progressive (intermediate) stage of shock
- 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
48
refractory (late/irreversible) stage of shock
- 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
49
what can prevent shock from progressing past the nonprogressive stage?
stopping conditions that started shock and supportive interventions
50
conditions causing shock need to be corrected within ____ (timeframe) of the onset of the progressive stage of shock
within 1 hour
51
how can infection lead to septic shock
local infection --> systemic inflammatory response syndrome (early sepsis) --> systemic infection + SIRS --> organ failure (severe sepsis) --> MODS (septic shock)
52
pathophysiology of sepsis
infection that causes tissue damage, organ failure, and death if not treated promptly
53
septic shock is a subset of sepsis, including
- SIRS: overreaction- full-body inflammatory response, puts body into distributive response
- MODS: multi-organ dysfunction syndrome
54
SIRS sx
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
55
MODS
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
56
Sepsis-3 defines sepsis as
a life-threatening organ dysfunction brought on by dysregulated response to infection
57
septic shock is a term used to describe
a subset of sepsis
- circulatory, cellular, and metabolic abnormalities substantially increase the risk of death over that associated with sepsis alone
58
infection is usually accompanied by
inflammation
59
can inflammation occur without invasion of organisms?
yes
60
segmented neutrophils
(mature WBCs)
- not active infection, something else is going on
61
banded neutrophils
(less mature WBCs) "baby bands"
- we know there is an active infection going on
- left-shift
- immature WBCs trying to respond to infection
62
SIRS nursing interventions
*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
MODS first occurs in the
liver, heart, brain, and kidney
64
how can sepsis be prevented? (primary prevention)
- avoid trauma and hemorrhage
- use proper safety equipment
- seat belts
- awareness of hazards in home/workplace
65
secondary prevention of sepsis
- assess for early s/sx ( catch it early )
- patient teaching/education
66
physical assessment of shock
- CNS changes
- respiratory changes
- CV changes
- skin changes
- renal and urinary changes
- MS changes
67
hypovolemic shock labs
low: pH, PaO2
high: PaCO2, lactic acid, K+
high or low: H&H
68
septic shock labs
low: segmented neutrophils
high: lactic acid, WBC (or normal), banded neutrophils (L-shift)
69
hypoxia occurs during shock due to
hypovolemia
70
inadequate perfusion occurs during shock due to
active fluid volume loss and hypotension
71
anxiety occurs during shock due to
potential for death and decreased cerebral perfusion
72
decreased cognition occurs during shock due to
decreased cerebral perfusion
73
management of hypovolemic shock
- IV access and fluids
- oxygen
- position
- medications
- treat underlying cause
74
cardiogenic shock labs
- high troponin (because it is probably caused by an MI)
75
management of septic; cardiogenic; distributive shock
- septic: give antibiotics
- cardiogenic: give dysrhythmics
- distributive: plug hole and replace
76
drug therapy to treat shock
vasoconstrictors:
- dopamine
- epinephrine
- norepinephrine
- phenylephrine
agents enhancing contractility & myocardial perfusion
77
coronary artery disease includes/causes
- chronic stable angina
- acute coronary syndromes: unstable angina and AMI
(the arteries that go to the heart)
78
ischemia
insufficient oxygen supply to meet the requirements of the myocardium
79
infarction
necrosis or cell death that occurs when severe ischemia is prolonged and decreased perfusion causes irreversible damage to the tissue
80
chronic stable angina pectoris
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
if ischemia is limited in duration (timing) and does not cause damage to the myocardial tissue, it can subside with
rest and SL NTG (nitroglycerin)
- can take up to 3 nitro (check BP + re-evalute chest pain between every nitro)
82
what is referred to as the "strangling of the chest?"
chronic stable angina pectoris
83
patients who present with either unstable angina or an acute myocardial infarction have (hint: category of syndromes)
an acute coronary artery syndrome
84
what causes acute coronary artery syndromes?
atherosclerotic plaque in coronary artery ruptures, resulting in platelet aggregation, thrombus formation, or vasoconstriction
85
unstable angina pectoris
- 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
time is muscle meaning:
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
variant (prinzmetal's) angina results from
spasm of coronary arteries usually at rest
88
pre-infarction angina refers to
chest pain that occurs days or weeks prior to an AMI
89
patients with unstable angina pectoris may present with
ST changes on 12-lead EKG
- NO changes in troponin levels
90
most serious acute coronary syndrome
myocardial infarction
91
MI occurs when
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
MI is divided by the ACC/AHA into (categories)
- non-ST MI (NSTEMI)
- ST elevation MI (STEMI)
93
non-ST MI (NSTEMI)
- 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
ST elevation MI (STEMI)
- ST segment on EKG is elevated
- measured in mm
- "tombstone" ST wave
95
non-modifiable risk factors for MI
- age
- gender (females with abdominal obesity and metabolic syndrome are at risk)
- hereditary (family hx, ethnic background)
96
modifiable risk factors for MI
- elevated serum cholesterol
- elevated triglycerides
- large waist size
- cigarette smoking
- hypertension
- impaired glucose tolerance
- obesity/overweight
- physical inactivity
- stress
- alcohol
97
average age of first MI
female: 72 years old
male: 65 years old
98
acute coronary syndrome: assessment
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
ACS s/sx: angina
- precipitated by exertion/stress
- substernal C/P radiate to L arm
- relieved by Nitro
- lasts < 15 min
100
ACS s/sx: MI
- 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
chest pain assessment: STEMI
- chest pain
- suspected acute coronary syndrome
- HAS ST elevation
102
chest pain assessment: NSTEMI
- chest pain
- suspected acute coronary syndrome
- DOES NOT HAVE ST elevation
- positive NSTE-ACS
103
chest pain assessment: unstable angina
- chest pain
- suspected acute coronary syndrome
- DOES NOT HAVE ST elevation
- negative NSTE-ACS
104
ACS nursing assessment includes
- pain
- cardiac rhythm
- pulses
- vitals
- skin
105
EKG changes with ACS: full wall thickness, myocardial infarction
- ST elevation (STEMI)
- new Q wave, ST normalizes
- Q wave often disappears
106
EKG changes with ACS: partial or small area, myocardial wall infarction
- ST depression (NSTEMI)
- no Q wave, ST normalizes
107
EKG changes with ACS: angina (stable or unstable), no myocardial wall injury
- ST depression
- no changes in EKG
108
lab assessment with ACS
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
imaging assessments with ACS
- 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
ACS analysis: acute pain due to
imbalance between myocardial oxygen supply and demand
111
ACS analysis: decreased myocardial tissue perfusion due to
interruption of arterial blood flow
112
ACS analysis: potential for dysrhythmias due to
ischemia and ventricular irritability
113
ACS analysis: potential for heart failure due to
left ventricular dysfunction
114
treatment plan approach to ACS
- manage acute pain
- increase myocardial tissue perfusion
- ID and manage dysrhythmias
115
ACS: acute pain interventions
- provide pain relief modalities, drug therapy
- decrease myocardial oxygen demand
- increase myocardial oxygen supply
116
immediate treatment of an MI (hint acronym)
"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
nitroglycerin: tunnel rate
bigger is better
- need an open, wide tunnel to allow better access
118
nitroglycerin quick release
- sublingual tablets
- translingual spray
119
nitroglycerin slow release
- nitro-bid (patch)- remember to take the old one off
- nitro ointments
- sustained release tablets
120
what to watch for with any kind of nitroglycerin
- severe hypotension***
- tachycardia
- dizziness
- headache
- syncope (fainting)
- DON'T GIVE WITHOUT GLOVES ON
121
interventions for ineffective tissue perfusion r/t interruption of arterial blood flow (with ACS)
- 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
heparin for ACS
- drip based on weight
- check PTT
- protamine sulfate (antidote)
- enoxaprin (lovenox)
*does not break up clot, prevents it from getting bigger*
123
antidote for heparin
protamine sulfate
- makes patient clot
124
thrombolytic therapy is used if ___ not available
if PCI/PTCA is not available
125
ACS: thrombolytic therapy- what do fibrinolytics do?
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
pain relief and myocardial oxygen requirements are done through
preload and afterload reduction
127
medications for ACS (hint: list, 8)
- 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
percutaneous transluminal coronary angioplasty (aka PTCA/PCI)
**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
percutaneous transluminal coronary angioplasty: meds
- 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
PTCA with stent
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
nursing management post-PTCA
- 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
leading cause of death in most patients with an MI who die before hospitalized is due to
dysrhythmias
aka "re-entry dysrhythmias" progressing to PVCs to v-tach/v-fib
133
in-hospital interventions for dysrhythmias post MI
- identify the dysrhythmia
- assess hemodynamic status
- treat with antidysrhythmics
- evaluate for discomfort
134
cardiogenic shock post-MI: clinical findings
- > 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
medical management of cardiogenic shock post-MI
- 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
two methods of CABG
- saphenous vein grafts
- internal mammary artery graft
137
CABG: saphenous vein grafts
bypassing the coronary artery d/t complete bloackage and using the saphenous vein to make a new road
138
CABG: internal mammary artery graft
bypassing the coronary artery d/t complete blockage and using the mammary artery to make a new road
139
CABG pre-op patient teaching
- 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
CABG intra-operative: patient has (equipment)
- intubated
- on bypass pump (some done off pump)
- heart arrested --> graft done
- chest tubes
- pacer wires
- foley catheter
141
CABG post-op management
- 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
discharge teaching post-MI
- medications: beta blockers, ARB/ACE, ASA/plavix, statin, nitro SL prn
- exercise
- no smoking
- diet
- follow-up appointments
143
expected patient outcomes post-MI (during evaluation)
patient will
- state pain is relieved
- have adequate myocardial perfusion
- be free of complications, ie dysrhythmias, heart failure
144
atherosclerosis
fat build up in the arteries
145
arteriosclerosis
hardening of the arteries
146
LAD blockage
left anterior descending artery blocked means that the left ventricle gets no blood = dying heart
147
nitroglycerin
- 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
ACS focused assessment
- 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
why give adenosine to patient during stress test?
- adenosine will mimic what happens to the heart during exercise
- the patient is on a monitor, not painful
150
what do we worry about with a patient on a thombolytic?
worry about bleeding w/ thrombolytics
151
hypovolemic shock interventions
- stop the cause
- replace the fluid (blood/plasma/IV fluids LR/isotonic solutions)
- antiemetics/antidiarrheals
152
cardiogenic shock interventions
- intra-arterial balloon pump
- inotropic drugs: epi, dopamine (these drugs cause vasoconstriction)
- extra fluids to increase BP
