Acute Coronary Syndrome Flashcards
1
Q
For 12 Lead EKG, just note that how many leads are actually being placed ?
A
6
2
Q
what is at the fifth intercostal space at the midclavicular line ?
A
apical pulse
3
Q
what is the function of an EKG?
A
electrical activity/conduction that is going through the heart at the moment
4
Q
what is the most useful EKG?
A
having a baseline EKG, usually starting at 50 years old because if you have chest pain coming in at an older age, then compare the baseline and today of having chest pain
5
Q
does a normal EKG means that your heart is perfect?
yes or no and why ?
A
no
it just shows that a the very moment, a normal electrical conduction is being sent through your heart
6
Q
how long is the EKG strip?seconds wise?
A
6 second
7
Q
having a 6 second EKG strip, if the heart is normal, what can you estimate?
A
a pulse
multiple this by 10
8
Q
what does the P wave mean?
A
atrial depolarization
9
Q
what does the QRS complex mean?
A
ventricular depolarization
10
Q
what does T wave mean?
A
ventricular repolarization
11
Q
can we tell where in the heart a heart attack is happening through an EKG?
yes or no and why ?
A
yes
we can see through an EKG that if the person if having a heart attack, the respected lead will show abnormality in that certain section of the heart
12
Q
what is ischemia ?
A
when there is not enough oxygen getting into your heart ; doesn’t mean you have tissue death currently unless
we dont fix it, there will be tissue death
13
Q
what conditions have ischemia issues ? (3)
A
acute coronary syndrome
heart attack
unstable angina
14
Q
what are we doing to see in ischemia on an EKG?
A
ST-segment depression & T wave inversion
ST-segment depression is significant if it is at least 1mm ( one small box ) below the isoelectric line
15
Q
does ST-segment depression and T wave inversion for ischemia ever go back to normal and if it can, how can it?
A
it can change back to normal when we fix the adequate blood flow and oxygen back to the myocardium
( heart )
16
Q
If there is an injury( usually necrosis is going on) to the heart, what can we see in an EKG?
A
ST-segment elevation occurs
- significant if >1mm above the isoelectric line
17
Q
ST-segment elevation happens when there is damage/injury to the heart, what do most people call it when looking at the EKG?
A
tombstones
18
Q
if we treat the injury of the heart causing ST-segment elevation promptly and effectively, what are we avoiding?
A
infarction
19
Q
if the injury of the heart causing ST-segment elevation has absence of _____markers confirms that ____didnt happen
A
serum cardiac markers
no infarction didn’t happen
20
Q
Sometimes with ST-segment elevation we can have pathologic Q wave, what does it mean ?
A
there is probably ischemia to the cardiac muscle
21
Q
How do we know when an infarction is happening or has happened in the EKG?
A
Physiologic Q wave is the first negative deflection following the P wave
22
Q
What is acute coronary syndrome ?
A
Prolonged Ischemia to the heart muscle, that may or not been reversible ;
not reversible immediately
23
Q
Acute coronary syndrome is a underbelly term that covers what two subjects?
A
Unstable & stable angina
myocardial infarction
24
Q
what are some characteristic of stable angina ?
A
narrowing but not completely blocked of the blood flow
25
if someone has stable angina when do they feel the pain ?
when they are moving around
26
what happens when someone who has stable angina stops moving around ?
the pain stops
27
what is so great about stable angina?
its reproducible, every time they walk they will have chest pain but once they stop walking, get rids of the pain
28
what is unstable angina ?
not a complete blockage, but enough blockage that when a patient has high need of oxygen, oxygen and blood flow is not being able to pass through
29
I know I am in the middle of this flashcards, but a good review back to what we were learning was
ischemia on an EKG looks like ?
injury on an EKG looks like ?
infarction on an EKG looks like ?
sometimes after an ST-segment elevation happens, what can occur?
ST-segment depression and T wave inversion
ST-segment elevation occurs
Physiologic Q wave is the first negative deflection following the P wave
Pathologic Q wave
30
when someone has unstable angina, when do they feel the pain ?
at rest
31
does unstable angina ever go away ?
nope, it takes longer to go away, and even become more frequent
32
what is myocardial infarction ?
heart attack
33
you can have 2 types of myocardial infarction, which are?
unstable angina and non-st segment elevation myocardial infarction ( NSTEMI )
ST-segment-elevation myocardial infarction (STEMI)
34
which one is worse, stemi or nonstemi and why?
stemi
- complete blockage
35
is stemi an emergency and why so?
yes because perfusion is completely blocked!!
36
is nstemi an urgency and why?
yes because its not completely blocked but like some things are going through
37
To re-emphaise
NSTEMI VS STEMI
which is worse ?
which one is urgency ?
which one is emergency ?
Which one is total blockage?
Which one is narrowing ?
STEMI
NSTEMI
STEMI
STEMI
NSTEMI
38
What is the goal for patients of STEMI?
they are back in the Cath lab for revascularzation within 30mins when they walked in the door to the ER
39
presentation of chest pain
of stem vs NSTEMI
ST elevations they are more likely to be a what?
ST segment depression and T wave inversion, they are more likely to be what?
STEMI ( tombstones! )
UA or NSTEMI
40
If ST-segment depression and T wave inversion is present or not for NSTEMI, what else can we use to evaluate ?
Serum cardiac biomarkers
41
Dr. Brooks mentions how labs are not always going to come back quick for patients in critical care, it's very important to always assume the worst and treat it like it's the worst thing happening.
Lets think outside the box here, lets see the patient walks into the ER and complains about left sided Chest pain, what other than heart attack can it be ?
Heart failure
anxiety
pulmonary embolism
Pneumothorax
Pneumonia
Bronchitisis
Stress ulcers
GERD
Muscle pain
42
What are some questions we are going to ask patients when they have chest pain ?
describe the pain
do you smoking
shortness of breath
do you have a cough
when was the last time you ate
palpitations
any medications
any movement with pain
43
usually in the ER, patients who come in, we have standing labs and medications for patients who come in with Chest pain.
what are some times we are going to do ?
lab wise ? (4)
medication wise ? (2)
troponin levels = heart attack
potassium levels
vital signs
EKG
aspirin and nitroglycerin
44
what does aspirin do for patients who have chest pain ?
describe the patho
if you are having narrowing in your blood, the aspirin will help thin your platelets and prevent clumping so its easier for the blood to get through that narrow artery
45
most of the time patients who have stable angina, so the angina that happens when you are moving and stops at rest can develop ____?
unstable angina
46
to re-emphaize again, what Is unstable angina ?
chest pain that occurs at rest with an increase frequency, duration or less effort to cause than stable angina patterns
47
unstable angina can be the first clinical sign of what?
CAD
48
most of the time patients who have unstable angina have pain durations of longer than ?
10 minutes
49
what does unstable angina show on the EKG and mean?
ST depression and T wave inversion
meaning there is some ischemic changes, so lack of blood flow and oxygen is being able to make it through to the heart
50
does unstable angina need immediate treatment?
yes
51
is unstable angina predictable ?
nope
52
Something very important to restate again is that when patients come into the ER and says they were having Chest pain like yesterday and request and EKG, what happens ?
however what if they are having Chest pain now, what can we see on the EKG?
nothing will show, remember EKG shows the electrical conduction that is being sent to your heart at this VERY MOMENT.
- so if the patient says it happen yesterday the EKG will be normal
so if they are having chest pain now, the EKG will be able to pick it up
53
to restate again, what does myocardial infarction (MI), heart attack mean?
result of abrupt stoppage of blood flow through a coronary artery with a thrombus caused by platelet aggregation
causing irreversible myocardial cell death ( necrosis )
short
when there is no blood getting to the heart
54
what are some examples of patients causing/getting an myocardial infarction ?
anemia
losing a lot of blood
high cholesterol
hypertension
family history
heart failure
obesity
males, elderly
55
its very important to know that most of the time women are less likely to develop a heart attack at a young age for what reason ?
estrogen is protective of the heart!
56
just to split it up and be able to match, you are going to see which ones are which
STEMI vs NSTEMI
occlusive thrombus
Non-occlusive thrombus
PCI within 12-72hours
ST elevations
Emergency
urgency
PCI or trhombolytic 30-90mins
ST depression and T wave inversion
STEMI
NSTEMI
NSTMI
STEMI
STEMI
NSTEMI
STEMI
NSTEMI
57
its important to know that if the hospital doesn't have a Cath lab, if there is a Cath lab that is ______away the patient will be transported.
however if there is not the next thing to do is give the patient ____
120minutes (2hours)
thrombolytic ( clot busting medication )
58
what is the first line of treatment for STEMI?
cardiac Cath and putting in a stent to help improve blood flow (perfusion)
59
what is the first line of treatment of NSTEMI?
Cath lab within 3 days, depending on things are going, remember this is urgent but not emergency
60
what are the 3 main coronary arteries?
right coronary artery
left anterior descending coronary artery
circumflex coronary artery
61
what are the 4 consequences of total artery occlusion?
O2 and glucose deprivation
heart muscle hypoxic within 10 secs
anaerobic metabolism -> lactic acid -> cellular death
heart cells only viable for 20mins then damage is irreversible
62
something I want to emphasize a lot on, your heart cells are only alive for ____ if you do now reperfused the body within that time frame, permentaly damage will happen as a consequence of total artery occlusion
20 minutes
if reperfused, aerobic metabolism and contractility restored and cellular repair will begin
63
what is the side effect of hypertension ?
how does this apply to myocardial infarction ?
left sided ventricular hypertrophy
so your body is already struggling to get blood through the small artery, so your perfusion will be decreased, putting you at a higher risk of developing a myocardial infarction
cardiac output is decreased !!
64
what is the time Frame that myocardial infarction can happen in ?
takes hours to a few days for a myocardial infarction to occur
65
what is the first step of the evolution of a myocardial infarction pathophysiology?
ischemia goes from inner to outer layers of the heart and necrosis can occur
66
what is the time frame of full occlusion of necrosis ?
what is the time frame of partical occlusion of necrosis?
4-6hours
up to 12 hours
67
how is Myocardial infarction described by ?
location
68
severity of myocardial infarction is influenced by ?
collateral circulation
the reason why this is important is because as mentioned in the next flashcards, your body will compensate by making collateral circulation, so the more you have these "side roads" the less likely you are to develop permenanet damage because its taking the small vessels instead of the really huge vessels
69
what is collateral circulation?
when you have heart disease, you typically have some form of narrowing or blockage.
your body will try to grow new vessels and expand to other sides of the heart in order to be able to perfuse well.
she uses a great anagram here
normally you drive on i66 highway, however lets say its 8am with massive traffic, this is your blockage, so what you think will be better is taking the side roads to be able to get to school faster to avoid that traffic.
70
additional notes regarding this
women are typically often ___and have worse ___
underrated
outcomes
71
what is the MAIN/classical clinical manifestations of pain of cardiac?
1 then 4 apart of it
crushing chest pain that is left sided or substernal and radiates to the left arm and jaw, accompanied by nausea, sweating, dizziness and shortness of breath.
72
most of the time clinical manifestation of pain happens during what point of day and for how long ?
early morning and greater than 20mins
73
if a patient has diabetes, what is the most important thing to know about them when regarding cardiac?
they can have cardiac neuropathy, they won't even feel a heart attack/ chest pain
74
lets talk about the SNS stimulation that occurs when patients are having a heart attack
what are we going to see
skin wise?
and why is the skin like this ^
- explain the patho behind and apply it to skin
skin: ashy, clammy and cold to the touch
because of vasoconstriction of peripheral blood vessels. the body is going to be in a flight or fight mode so everything is going to constrict and focus on the core of your body, your organs, so blood is not going to go into your hands and feet as much as your chest area, so thats why your skin around your feet and hands will be presented that way
75
SNS Stimulation
fight or flight remember that ^
the patient is going to be nervous, they are going to be in a flight mode, what do you think the body will be do?
sweat
76
lastly again SNS stimulation, your body is in that state of fight or flight, what do you think your heart rate and blood pressure are going to be at?
increased/ high levels
77
to recap, what are the 4 things happening in the SNS stimulation?
diaphoresis - sweating
increased HR and BP
vasoconstriction of peripheral blood vessels
skin : ashen, clammy and cold to the touch
78
lets talk about the cardiovascular response to when a patient is having an heart attack.
what do you think is happening to the heart rate and blood pressure? (2 things to note here)
and why?
from previous knowledge, we know its going to be in that fight or flight state, so high bp and hr, however, it can only compensate for so long, so it'll then drop
so increase hr and bp
then drop in hr and bp
the reason is because the body can only compensate for so much before it tires out and gives up
79
the cardiovascular response, every single lecture we talk about the best way to assess for perfusion in the body, what is the first thing that is going to be given out or the first sign that perfusion is bad?
decreased in urine output, renal perfusion will be gone
80
cardiovascular respones to a heart attack, what can you be hear in patients who are having left ventricular dysfunction ?
explain the patho behind this
crackles
the patient will not have good blood flow so the blood will back into the lungs, that is why we will be able to hear crackles and patient will be complaining of shortness of breathe
81
cardiovascular respones
what are some physical signs we are going to be able to see on a patient who is having a myocardial infarction ?(3)
jugular venous distention
hepatic engorgement
peierphal edema
82
lastly what type of murmur do you think will be occurring in our patient who is having a cardiovascular response to a heart attack?
holosystolic
(s3 or s4 murmur )
83
to recap what are the 5 main things we need to remember for when the patient who is having a myocardial infarction that is happening during a cardiovascular response?
4th point is the physical signs ( there are 3 signs to remember )
hr and bp will be increased at first then it will decreased
lack of renal perfusion = no urine
crackles being heard because of the back of blood flow into the lungs
( patient will be complaining of shortness of breath)
jugular venous distention, hepatic engorment, peripheral edema
abnormal heart sounds, holosystolic
84
something to note jugular venous distention, hepatic engorment, peripheral edema, typically are associated with what ?
right sided heart failure
85
its pretty obvious that when a patient is having a myocardial infarction is going to be vomiting, but can you tell me the patho behind this?
vasovagal reflex
the vagus nerve runs through the heart, so when you're having this heart attack, this vagus nerve is being irritated causing this nausea and sweating
86
another obvious thing that is happening with these patients is a fever, what temp can the fever get to when the patient is in a myocardial infarction ?
explain the patho behind this ?
100.4F (38C) in the first 24-48 hours and can go up to 4-5days
low- grade fever for a couple of days
myocardial infarction causes a systemic inflammatory process which is caused by all the heart cell death that a heart attack brings to the body, so its only normal you're body Is going to try to fight it off by a fever
87
now that the myocardial infarction has happened, what does the body do first when it comes to the healing process after a heart attack?
inflammatory process
88
can you explain the patho to me behind the inflammatory process of the healing stages after a heart attack?
within 24 hours, leukocytes, your white blood cells, will go into the area of cell death and release enzymes in order to clean up the body.
89
necrotic tissues is removed by the ___day resulting in a thin wall of the heart
4th
90
10-14 days after an MI, scar tissue is still going to be ?
weak
91
its important to note that the heart muscle is vulnerable to stress after having a heart attack so what are we going to do as a nurse to help prevent this for patients?
monitor activity level
92
by how many weeks does post heart attack is scar tissue is replacing necrotic tissue ?
- remember its not as good as healthy tissue from the start
6 weeks
93
what is scar tissue made out of ?
collagen matrix
94
what is the most common finding after the healing process is done that the body will do to try to compensate?
typically left ventricular hypertrophy
or some type of hypertrophy
95
every single cell in your heart as the ability to ?
generate electricity impulse for the heart
automatsitiy
96
how does dysrhythmias come by for patients ?
remember every single cell in the heart has the ability to create electricity, so there is this one little cell and is like, fuck it im doing my own thing, and creates dysrhythmias and doesn't want to listen to our sa node
97
what is the biggest complication of heart attack, typically the reason why post patients end up dying?
dysrthymias
- ventricular tachycardia and ventricular fibrillation
98
how does dysrhythmias happen after a heart attack for patients ?
remember every single heart cell can create an electrical conduction, however after a heart attack, the dead cells are just sitting there with the normal happy cells, so now the normal happy feels are unhappy because they got a dead cell next to them, so thats how dysrhythmias occurs
99
what are other complications that can occur of myocardial infarction? 6
and explain each one
heart failure
- piece of a big ventricular doesn't work so the heart has to work harder
cariogenic shock
- heart stops working, no blood pressure or heart rate
papillary muscles dysfunction or rupture
- mitral valve doesn't work so no blood flow
left vencitrular aneurysm
- wall is thin and can rupture
pericarditis
- inflammation of pericardium
Dressler syndrome
100
what is an anagram to help me remember the 7 complications of myocardial infarction ?
dj
heart
cares (about)
poor
left
peri
dressler
101
how do we treat the pericarditis ?
high dose of aspirin
102
what is dressler syndrome ?
treatment?
pericarditis and fever that develops 1-8 weeks after an heart attack
high dose of aspirin
103
what are some main clinical manifestation of dressler syndrome?
pericardial friction rub
chest pain
104
what are some diagnostic studies for acute coronary syndrome, stable/unstable angina and myocardial infarction?
12-lead ECG
health history
serum cardiac biomarkers
( serial troponin levels )
105
if we know a patient is going or having a heart attack we do troponin levels, but how do we know this ?
increase of troponin 4-6 hours after onset of MI
peaks at 10-24hours
106
troponin levels will return back to normal/baseline after ?
10-14 days
107
biomarkers will be negative for ?
biomarkers will be positive for ?
unstable angina
NSTEMI
108
its important to note that there are other diseases that can cause patents to have increased troponin levels like having a pulmonary embolism, but what's important behind this ?
we take a baseline, lets they are at 12 which is high!
if we retake it and its still 12, its there baseline and nothing to worry about
but if that 12 goes to like 14, we know its a heart attack because it isn't normal
109
why do we sit the patient up during any chest pain ?
expanding their airway/lungs
110
why do we give oxygen to patients, even though they have a blockage and it isn't going to help?
we are just making sure that the blood in their body has oxygen even if the small event that some blood is going through
111
ANY TIME AN EMERGENCY WE WANT THE PATIENT TO HAVE WHAT!!???
2 LARGE BORE IVS
112
what is a on site medication patients with chest pain will be given typically in the er? (2)
nitroglycerin
( vasodilator, be able to perfused )
aspirin
(chew It up)
113
what should nitroglycerin do to the blood pressure and is a normal !?
drop in blood pressure
114
if a patient has nitroglycerin at home, what do we tell them and when do we tell them to call 911?
you take a max of 2 nitroglycerin, if it doesn't help, you call 911
115
why do we give them patients morphine for myocardial infarction ?
it helps vasodilates, remember it helps with pain so it'll be easier for them to breathe and ignore the pain, and itll help vasodilator all those vessels that are constricted
116
and why do we even give statin to patients who are having UA,NSTEMI, STEMI?
it isn't going to do anything during the moment but however, it'll prevent future blockages
117
what were the 4 medications we are going to first treat a patient with when entering the er?
aspirin
nitroglycerin
morphine
statin
118
notes ; most of this has been covered in past flashcards but just read this out loud to relearn and emphasize on
acute care for ST depression or T wave inevrsion (NSTEMI)
- admit to the icu/tele unit
- monitor vs and pulse ox
- continuous ecg
- 12 ecg
- heparin or lovenox
- PCI within 12-72 hours
- bed rest until recovery
119
even though I mentioned this before, if a patient is having a STEMI, so a ST elevation, an emergency, what is the fist treatment?
Emergency PCI
120
what happens if the patent with a STEMI can not receive a PCI?
thrombolytic therapy is the second choice
121
what is the goal standard time that you have to save a patent life with a STEMI?
30mins but in the powerpoint it says 90mins
122
what will stop you from giving a patient thrombolytic medications ?
hemorrhagic stroke
bleeding
perforated ulcer
surgery
123
if your patient started bleeding after you give them thromoblytic therapy, what are you going to see?
internal bleeding
drop in blood pressure
change in your level of consciousness !!!
blood in the urine
increase heart rate
blood at the iv site
124
why Is change in level of consciousness the biggest/first symptom of patients bleeding after receiving thromblytic medications ?
because no blood is being going to the head
125
notes
what are some complications fo PCI
- dissection or rupture of artery
- abrupt artery closure
- failure to cross blockage
- extended infarct
126
what is the criteria for a patient to receive thrombolytic therapy for a myocardial infarction and a PCI is not avaliable?
(3)
chest pain less than 12 hours
and 12 lead shows STEMI
no absolute contraindications
127
remember if there are any invasive procedures, so like putting a cath in for urine, you may want To do that first before you give ____ to prevent further ____
thrombolytic therapy
bleeding
128
how do we know thromboluytic therapy worked for a patient with myocardial infarction ? (3)
ST segment returns to baseline
no chest pain
reperfussion dysrhythmias
- so like think about how when you sit on your hand and it falls asleep but once you change position, it goes back to normal, its like that
129
what is our major concern with thrombolytic therapy?
reocclusion
130
how do we prevent reocclusion from happening to our patients?
IV heparin
131
once again, what is our biggest complication after a thrombolytic therapy ?
bleeding
132
what type of diet will these patients after heart attacks ?
low salt, low saturated, low fat and low cholesterol
133
she mentions an anagram to help remember what the main interventions are for myocardial infraction which is and stands for
?
mona
morphine
oxygen
nitroglycerin
aspirin
134
what are the big drugs we are going to be giving to patients with acute coronary syndrome ?(8)
IV nitroglycerin
morphine
beta blockers
ace inhibitors & arbs
antidysrthymic drugs
lipid-lowering drugs
aldosterone antagonist
stool softeners
135
what does nitroglycerin do ?
what is its biggest side effect?
vasodilator
hypotension
136
what does morphine do ?
what is the biggest side effect?
vasodilator and decrease pain
respiratory depression
137
what does beta blockers do?
biggest side effect?
decrease oxygen demand by decreasing heart rate and blood pressure
bradycardia
138
what does ace inhibitor and arbs do ?
biggest side effect?
prevent ventricular hypertrophy(remodeling )
hyperkalemia
139
what does lipid lowering (statins) do?
biggest side effect?
decrease plaque development
increase LFT
140
what does aldosterone antagonist do (spironolactone)?
biggest side effect?
decrease mortaliity
monitor potassium
141
what does stool softener do ?
Why do we use these for patients who have had a heart attack?
aid with pooping
To prevent stressing/straining the heart too much during any constipation, plus other medication they will be on will be causing them to be constipated
142
what is an anagram to help remember all the drug therapy for the coronary artery syndrome ?
nitro
morphine
betters
Anthonys
anti
lowering
amazon
sells
143
what are some subjective data we might want to ask when discussing to a patient when they are having any medical issues?
this is nursing assessment stuff
health history
- family history
- cad/chest pain/angina
- valve disease
- hypertension, diabetes
medications
history of present illness
144
why are we going to ask about any associated symptoms, give examples and to why ?
think about the poop story and how it applies here
straining at stool
chest pain
stress
depression
heartburn
straining can decrease your heart rate because the interadominal pressure when trying to poop will stimulate your vagus nerve and that runs by your heart and when irritated, they become bradycardia and hypotensive
145
next is our objective assessment, what are some general things we will see with our patients?
anxious
fearful
cool, clammy, pale skin
146
what are the 4 cardiovascular nursing assessment things we will sometimes find on a patient ?
tachycardia or bradycarida
pulses alternans
pulse deficit
dysrhymias
147
what is pulses alternans?
alternating weak and strong beats
148
what is pulse deficit mean?
you can hear the heartbeat at the apical pulse, however to any other peripheral pulse, like radial, you can't feel the pulse
149
since know knowing what pulse deficit mean, what does it tells us now about their cardiac output?
its very dimisihed because the body doesn't have enough force or volume to pump the blood to the peripheral pulse
150
why do you have decreased cardiac output after a heart attack ?
because the heart is now having thin scar tissue and it doesn't work effectively, especially when one part of the ventricular isn't gonna work so its going to cause left hypertrophy
151
note
planning
immediate goals
- pain relief
- quick and appropriate treatment
- preservation of heart muscle
goals during hospitalization
- effective coping with illness-associated anxiety
- participation in a rehabilitation plan
- reduce risk factors
pain
- nitroglycerin
- morphine
- oxygen
monitoring
- ecg, v-fib, PVCS, vt and st segment
- physical assessment, vs, I and o, 02
rest and comfort
- bed rest and gradual increase in activity to promote relaxation
152
notes
nursing management
anxiety
- explore fears and concerns, provide education
emotional and behavioral reactions
- psychosocial responses support systems
patient teaching
- assess literacy and learning needs, consider timing
153
additional medication, when a patient who is having a heart attack, comes into the er and says, oh im on erectial dysfunction medications, what are you going to do as a nurse?
you're probably not going to hold off on the nitroglycerin cause It will help them, but MONITOR THE HELL OUT OF THEIR BLOOD PRESSURE, the risk of hypotension is INTENSE.
154
how do we manage and patient education for physical activity?
gradual increase of physical activity
brushing their teeth, taking shower without symptoms
then move them to the walking in the hallway
155
what type of maneuver do we want patients to avoid when after having a heart attack ?
why and describe it
valsalva maneuver
- when you are baring down on the abdomen when trying to poop, we really try out best to avoid this because it can decrease your heart rate
156
after a heart attack we send everyone to what and why?
cardiac rehabilitation
its a good way to restore optimal function
157
when can we tell patients to have sex again ? (2)
typically 7-10days post heart attack
or when a patient can climb stairs or walk briskly
158
what would be the hopes or evaluation after a mi ?
maintaining stable signs
having relief of pain and shortness of breathe
report reduced anxiety
achieve relatistc program activity
159
what is sudden cardiac death (SCD)?
abrupt, unexpected death from cardiac causes ; occurs within 1 hour of symptom onset
160
what are the most common causes for sudden cardiac death? (3)
coronary artery disease
structural heart diseases
conductions distrubances ( dysrhythmias )
161
what is the difference between a myocardial infarction and sudden cardiac death?
heart attack is a progressive
then sudden cardiac death is talking -> death
162
what are the 2 dysrhythmias that a patient would have when after heaving a heart attack ?
ventricular tachycardia
ventricular fibrillation
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what does ventricular tachycardia mean ?
ventricles are pumping way too fast
- but your atria and other parts are beating normally
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what happens to your cardiac output when you have ventricular tachycardia?
decreases because there isn't time for your ventriculars to fill up and pump out blood to the rest of the body
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how many PVCS are in a ventricular tachycardia ?
3
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what is a PVCS?
an additional heart beat
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what are the 2 types of ventricular tachycardia that can be described on an EKG?
monomorphic
polymorphic
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what is monomorphic ventricular tachycardia?
QRS complexes that are the same in shape, size and directions
( usually 1 part in the heart is causing problems )
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what is polymorphic ventricular tachycardia ?
QRS complexes gradually change back and forth from one shape, size and direction to another over a series of beats
( usually multiple part in the heart is causing problems )
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ventricular tachycardia
sustained
non-sustained
seconds wise ?
more than 30secs
less than 30secs
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if the ventricular tachycardia is non-sustained, so less than 30seconds and doesn't come back, what do we do ?
and what if it is sustained for more than 30 seconds?
its not too big of an issue, but monitor
intervention is needed
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you have 2 types of ventricular tachycardia, remember this isn't what can be described on the EKG, just in general?
stable
unstable
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what is stable ventricular tachycardia?
can be treated with ? (2)
patient has a pulse
(cardiac output is adequate)
antidysrhytmic medication
cardio version
( shock but not to much voltage )
( adenisne for example )
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what is unstable ventricular tachycardia ?
do what after?
medications ? (2)
patient is pulseless
CPR, rapid defibrillation
vasopressors and antidysrhytmics
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test question
what to do stable vs unstable v-tach?
stable
give them antidysrthymic medication
and if that doesn't work go to cardioversion
( which is a small shock )
unstable
do cpr until we can shock them
and then treat with vasopressutes and antidysrthymics
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how do we usually treat ventricular tachycardia, like what are we trying to really look for
and give an example to what can cause v-tach?
precipitating causes that cause a patient to go into v-tach
example being hypoxia, drugs, CNS disorder, electrolyte imbalances, CAD, and honesty dont even need a heart disease
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remember we just reviewed that sustained v-tach can cause severe decrease in cardiac output because the ventricular are not being able to fully fill up with blood and pump It out to the rest of the body
what symptoms do you think we would see in a patient with severe sustained v-tachy? (4)
hypotension
- remember there is no blood going to the rest of the body
pulmonary edema
- blood being backed up because it can't push it all back in
decrease cerebral blood flow
- again no blood moving period
cardiopulomonary arrest
- unstable v-tachy if untreated really
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what is ventricular fibrillation?
what was the example she gave for this ?
ventricles contract very quickly and without coordination
fish out of water, literally doing nothing but just flopping without coordination
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are ventricles able to pump blood in ventricular fibrillation ?
nothing, its a huge significant decrease in cardiac output and perfusion
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how is our patient going to look like during ventricular fibrillation ?
pulseless and apniec
unresponsive
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what is the immediate treatment behind ventricular fibrillation ?
CPR and defribilation
( additional with drug therapy like epinephrine and vasopressin )
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to recap
how do we treat stable v-tach?
how do we treat unstable v-tachy?
how do we treat v-fib?
antidysrhtymics
and if those dont work
cardio version
cpr, defribillation
antidhyrthmics
then
vasopressors to keep up the blood pressure
cpr, defrillation
then vasopressors and epinephrine
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if you happen to live through a sudden cardiac death, what is the sad part for this?
its more likely for you to get it again
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more than likely when patients get a sudden cardiac death, what do we put in them ?
ICD, its a small shock that the defrilbator will detect that you are in heart pumping long
implanted cardio defibrillator
( you can get shock if you have a patient have an ICD, when it goes off when you touch a patient, pretty interesting )
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what are some symptoms we can see before a patient has a sudden cardiac death ?
angina
palpitations
dizziness
lightheadness
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if they dont want an ICD, what can they do as well for sudden cardiac death ?
amiodarone
- cardioverter defrillator
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notes
diagnostics workup for sudden cardiac death
- PCI, Cardiac catherziation, telemetry, biomarkers
adaptation
- driving restrictions
- role reversal
- change in occupation
- brush with death is often the term
- or a ticking time bomb because you never know when its going to happen again
address their anxiety, anger and depression and provide emotional support for these patients
