Exam 1 Flashcards
primary goal of pre hospital mgmt
move pt to location that will provide definitive treatment
priorities in trauma situation (5) pre hospital
- Maintain airway
- Ensure adequate ventilation
- Control external bleeding and prevent shock
- Maintain spine immobilization
- Transport to appropriate facility
golden hour
first hour following trauma
what is the responsibility of the EMTs
stabilizing and resuscitating
3 Ts
Triage, treatment, transport
primary goal of in hospital mgmt
adhering to trauma Care protocol to allow for efficient ID of life threatening conditions
D2N
door to needle
TPA
60 minutes
D2B
door to balloon
PTI
90 minutes
3 things to diagnose STEMI
chest pain
EKG changes
elevated cardiac biomarkers (troponin, CK-MB)
what EKG changes do you see for ischemia
Can have ST depression and/or T wave inversion
what does ST elevation indicate
injury
QRS does not come back to baseline
what does Q wave indicate
infarct = death of tissue
usually happens in hours
what population may not complain of chest pain
diabetics
how to avoid ST elevation?
thrombolytic (TPA, alteplase)
how to know if a thrombolytic works?
ST will go back down
what is CABG?
Coronary artery bypass grafting
Healthy artery or vein is grafted to the blocked coronary artery –> One end is attached to the aorta with the other end attached to the block coronary distal to the occlusion → bypasses blocked portion of artery allowing blood flow to the cardiac tissue
why would you do a PCI vs. CABG?
PCI is for one area in one vessel
CBG - may be better for someone with weak heart that needs revascularization
normal troponin level
0.04
what is troponin?
Cardiac troponin I and T are proteins expressed exclusively in the heart, are a specific marker or muscle damage
Can be elevated within 4 hours of injury and can stay elevated for 10 days
what is creatine kinase
general marker of cellular injury
Released from cells in brain, skeletal muscle, and cardiac tissues after muscle damage has occurred
what is CK-MB and when does it show up
CK isoenzyme marker specific to cardiac tissue
When myocardial damage occurs, CK-MB is released from cells
Can show up 3-36 hours
what does ACS include
unstable angina, NSTEMI, STEMI
what does telemetry show
rate and rhythm only
when did triage start
Triage started in 1854 during Crimea war - Florence Nightingale
when/where/who created first US Clinical shock trauma unit
1961, Baltimore, R. Adams Crowley
who is R. Adams Crowley
father of the golden hour
when/where first civilian trauma unit
1966, Cook County, Chicago
where 3 levels of trauma were first identified
what did the 1966 highway safety act say
Said each state must include emergency medicine services as part of highway safety
Mobile intensive care unit EMS
what is the emergency medical services act
1973
15 components
Most important: identifies what type of emergency care an ED must have if designated as a trauma center
Trauma nurse certification course
what is included in primary survey during in hospital mgmt
Airway management
Breathing
Circulation
D - identify disability that is obvious to you (broken bone), neuro assessment
Exposure - measure to completely undress patient so that obvious and potential injuries
what is part of the tertiary survey (and ex)
Includes variables that will compact trauma
Ex: Pt over 75 or w/ substance abuse issue has a greater risk of not doing as well
5 priorities in hospital mgmt
primary survey
secondary survey
tertiary survey
fluid resuscitation
damage control/definitive care
ESI
emergency severity index, a five level system
ESI level 1
Presents with a life threatening condition at a resuscitation level
First is worst, most severe
ESI level 2
needs attention quickly, assessed by a nurse in 15 minutes
Examples: unstable, listless child, significant dehydration, severe pain
ESI level 3
urgent, has the potential to progress, assessed in 30 minutes.
Examples: acute abdominal pain, chest pain without diaphoresis
ESI level 4
less urgent, less potential for deterioration, needs to be assessed within an hour
Examples: burning on urination, elevated temp less than 101 degrees
ESI level 5
no acute problem
Examples: suture removal, medication renewal
what is part of RN triage assessment (5)
-history of presenting complaint
-pertinent medical history
-physical assessment
-vital signs with orthostatics, pulse ox
- current meds, allergies
orthostatics
BP lying, sitting, and standing with a minute b/w each reading
what does a + orthostatic mean
Positive orthostatics if greater than 10% difference
What would you look for? HR will go up and BP will go down
5 nursing interventions in triage
Fever medications as per protocol
All lacerations must be dressed
All suspected fractures need to be immobilized
Antihypertensive medications as per protocol
Pain medications as per protocol
possible causes of unconscious patient (7)
head and neck trauma,
drug/ETOH overdose,
meningitis,
metabolic conditions like hypoglycemia,
cardiac arrest,
toxins,
acute stroke
clinical manifestations of unconscious patient
unarguable, altered neuro assessment and vital signs, pupillary changes, involuntary movements
how to tx unconscious patient
NARCAN and glucose
LOC: alert and oriented
Name, where they are, month/date/year, why are they in the hospital
LOC: lethargic
Drowsy but will follow simple commands and makes sense
LOC: obtunded
Arousable with stimulation, can follow simple commands
LOC: stuporous
Hard to arouse, inconsistently following commands, limited spontaneous movements
LOC: semi comatose
Movements are purposeful when stimulated but not following commands or speaking coherently
LOC: comatose
Patient may respond with reflexive posturing
Can still be breathing on their own and maintain BP and HR
Light vs deep coma
level 1 trauma center
serves a region
level 2 trauma center
serves a community
level 3 trauma center
Stabilizes and transfers to trauma center
level 4 trauma center
is a clinic that serves as an entry into the system
blunt trauma
w/o penetration of skin- don’t know extent of injury
Common with MVAs, sports injuries, falls
CT scan is most valuable tool
penetrating trauma
Injury from moving object that interrupts the skin
Firearms, knives, etc.
Can’t tell extent of internal damage
Do not remove whatever is there - it is removed in OR
what age is injury rate the highest
15-24 y.o
is trauma more common in males or females
2.5x higher for males than females - more likely
is incidence of trauma higher in rural or urban areas
rural areas
is incidence of trauma higher in low income or high income areas
low income
3 mediators of injury response
Underlying medical conditions
Drug ingestion
Age related variances
what is AVPU
baseline evaluation of patient’s neurological status
A-V-P-U
A = alert
V = response to voice
P = response to pain
U = unresponsive
warning signs for airway
Stridor
A crowing noise on inspiration
Gurgling
Hoarseness
3 interventions for airway
c-spine immobilization
Jaw thrust maneuver
endotracheal intubation
purpose / dangers of removing all clothing (e- exposure)
Purpose: allow entire body to be examined for evidence of trauma
Important: preserve forensic evidence
Danger: hypothermia
automaticity
ability to spontaneously generate an electrical impulse
conductivity
transmission of electrical impulse to another cardiac cell
excitability
ability to respond to electrical impulse
contractility
ability to contract after impulse is received
rhythmicity
ability to send impulses in a regular, paced manner
refractory period
cells’ inability to respond to another impulse during a certain time in the cardiac cycle
conduction system transmission steps
SA node → AV node → into ventricles through Purkinje fibers and right and left bundles
which comes first: electrical or mechanical activity
electrical
CO equation
HR x SV
what is SV
Stroke volume = blood ejected from LV after ventricular contraction
normal CO for healthy adult
4-8L per minute
SA node intrinsic rate
60-100 bpm
AV node intrinsic rate
40-60bpm
ventricle intrinsic rate
20-40 bpm
purpose of EKG
register heart’s electrical activity
used to diagnose/look for ischemia and infarct
P wave
Positive deflection that appears in the beginning of the normal EKG complex
Represents atrial depolarization
QRS complex
3 different waves, represents ventricular depolarization
Q wave
an initial negative deflection
Q represents pathology
If you see a Q - means MI
R wave
positive deflection
S wave
any subsequent negative deflection
T wave
Positive deflection following QRS complex
Represents ventricular repolarization
Have to have T wave in order to stimulate the heart cells and start depolarization all over again
P-R interval
- Measured from the beginning of P wave to beginning of QRS
- Normal - 0.12 - 0.20 seconds
- Represents length of time for impulse from SA node to get through atria and to AV node to start ventricular depolarization
QRS complex
Measured from the beginning of the Q (or R if there is no Q) to the end of the S
Start from beginning of deflection
Normal is 0.05 - 0.11 seconds
-reflects the amount of time for ventricles to depolarize
what if the QRS is longer than .12 seconds?
there is some sort of pathology that is making the time it takes to get the ventricles ready to contract much longer (i.e. bundle branch block)
what is the QT interval
Measured from beginning of the Q to the end of the T wave
Indicates the total time interval from the beginning of depolarization and end of repolarization
normal is < .44 seconds
ST segment
Beginning of the end of the S to the beginning of the T
It is not measured but the shape and location are evaluated
elevated in STEMI
normal sinus rhythm characteristics
- P, QRS, T
- P - P equal
- R - R equal
- PR interval is between .10 and - .20
- QRS complex b/w .05-.11
- HR is between 60-100 bpm
sinus brady characteristics
P, QRS, T
P - P is equal
R - R is equal
PR interval is between .12-.20 seconds
QRS complex between .05.-.11 seconds
HR is below 60, usually between 40-60 bpm
causes of sinus brady
Well trained athlete
Sleep
Increased ICP
Medications - BBs, CCBs
Vagal stimulation
Ischemia from an anterior wall MI
symptoms of sinus brady
hypoperfusion s/s
Dizziness
Cold, clammy skin
diaphoresis
tx for sinus brady
atropine 0.5 mg IV bolus followed by 3-5 minute wait, NS in between, and then another dose (3 times total)
If it doesn’t work - pacing
sinus tachy characteristics
P, QRS, T
P - P is equal
R - R is equal
PR interval is between .12-.20 seconds
QRS complex between .05.-.11 seconds
HR: 100-140, usually not greater than 160
Gradual onset and gradual resolution
causes of sinus tachy
Anxiety, fear
Pain
Fever
Certain meds (Bronchodilators)
Drugs (crack, cocaine)
Shock
Heart failure (heart rate will increase in a compensatory way)
s/s of sinus tachy
Chest pain - because heart is filling in diastole
nursing interventions for sinus tachy
Monitor vital signs
Check blood pressure
Treat underlying cause
If symptomatic w/ ST of greater than 150 bpm - should give adenosine 6 mg IV, then 12 mg IV, then 12 mg IV (3 doses)
-If that doesn’t work → cardioversion
sinus arrhythmia characteristics
P, QRS, T
P - p are unequal
R- R are unequal
P-R interval within normal limits
QRS complex within normal limits
HR = 60-100 bpm
nursing interventions for sinus arrhythmia
Normal variation that occurs with the respiratory cycle
Monitor vital signs
Rate should have no greater difference than 10%
Least serious rhythm disturbance
premature atrial contractions
characteristics of PACs
P, QRS, T wave
P - P = except for premature beat
R - R = except for premature beat
P-R interval is normal
QRS complex normal
Ventricular rate = 60-100 bpm
what are PACs
ectopic beats that occur within the context of other rhythms
unifocal PACs
If they come from one atrial pacemaker cell
multifocal PACs
Come from multiple atrial pacemaker cells
couplet
two PACS together
frequent PACs
more than 6 per minute
bigeminy PACs
every other beat is a PAC
trigeminy
PAC falling every 3rd beat
short burst PACs
6 in a row
4 causes of PAC
- Can be caused by excessive caffeine, stress, fatigue
- Can also occur in the presence of organic heart disease
- Increasing PACs can often be one of the initial signs of HF
- low K+
Paroxysmal Atrial Tachycardia (PAT) characteristics
Sudden onset w/ sudden stop
Abnormal P wave
Rapid heart rate
P, QRS, T wave
P - P are equal
R - R = equal
PR interval = normal
QRS complex = normal
Ventricular rate from 160/180-220/250 bpm
causes of PAT
Emotional stress
Physical fatigue
Stimulants
Organic heart disease, especially in those that involves pressure changes in the heart
why can PAT precipitate HF
Because it is beating so fast
blood from ventricles can lead back into atria and back into pulmonary systems
symptoms of PAT
Palpitations
Vertigo
Precordial pain
Anxiety
Signs of decreased CO
tx of PAT
if stable - CA channel blockers (CCBs), Adenosine (6 mg, 12 mg, 12 mg)
unstable - Cardioversion
less common - Increase vagal tone - Carotid sinus massage, Valsalva maneuver
Sedation
AE of amiodarone
Liver, thyroid, pulmonary toxicity
atrial flutter characteristics
Absent P wave → not SA node, atria takes over
QRS complex
T wave
Sawtooth waves = F, flutter, waves
F-F is equal
R is R is equal usually
No P-R interval
QRS complex is normal
Ventricular rate and atrial rate are not the same
8 causes of atrial flutter
-Rapid, strong ectopic impulse in the atria beats fast, from 250- 350 times per minute
-The AV node acts as a gatekeeper
-Rheumatic Heart Disease
-Mitral Heart Disease
-Pericarditis
-Cor Pulmonale
-Thyroid disease
-CHF, AMI
nursing interventions for atrial flutter
Monitor BP
If hemodynamically stable → vigilant observation
If hemodynamically unstable → digitalis, beta blockers
Lastly - cardioversion
*Danger in atrial flutter is the loss of the atrial kick
how to determine atrial rate
Number of boxes between one f wave and divide into 1500
atrial fibrillation characteristics
Absent P wave
QRS complex present
T waves present
P wave not present, instead small “f” fibrillatory waves - cannot plot of the “f”s
R-R totally irregular
No PR interval
QRS complex is normal
VR and AR totally different
Chaotic atrial activity 350-1000 bpm
controlled a fib
< 100 bpm
uncontrolled a fib
> 100 bpm
No time to fill → decreased CO – also blood moving backwards through pulmonary vein → into capillaries and alveoli (crackles produced)
causes of a fib
-Rheumatic Heart Disease
-Mitral Heart Disease
-Pericarditis
-Cor Pulmonale
-Thyroid disease
-CHF, AMI
-seen after coronary artery bypass surgery and chest trauma
-Common rhythm disturbance in the elderly
tx for atrial fib
If a common rhythm disturbance in a hemodynamically stable patient → might be no treatment
Digitalis, CCBs, BBs
Cardioversion if unstable
danger of a fib
reduced CO, thrombus formation leading to stroke
Blood hangs out in atria → predisposed to clotting, thrombus formation → can lead to stroke
PVC characteristics
P, QRS complex, T wave
P-P is equal, except for premature beat
R-R is equal, except for premature beat
P-R interval is normal
QRS complex is normal - Will be wide and bizarre
PVCs can occur in any ventricular rate
Are ectopic beats that occur in context of other rhythms.
Wide, bizarre, early beats
causes of PVCs (7)
Caffeine, smoking, stress
Sudden fear
Hypokalemia
Digitalis toxicity
Hypoxia
Myocardial ischemia
Acute Myocardial infarction (AMI)
tx for PVCs
Occasional require no treatment - Check K and O2 stat, Seen with hypokalemia
(Rule on cardiac units: Keep K above 4 and Mg above 2 to avoid rhythm)
Treat those with acute MI (most common rhythm disturbance) if systematic or sustained
Treat with amiodarone (150 mg IV over 10 mins bolus then drip), lidocaine rarely used (is neurotoxic)
unifocal PVCs
If they come from one ventricular pacemaker cell
multifocal PVCs
Come from multiple ventricular pacemaker cells
two PVCs in a row
couplet
3 PVCs in a row
triplet or three beat run of VT
PVC ever other beat
bigeminy
trigeminy PVC
PVC falling every 3rd beat
salvo
short burst = 4 in a row - nonsustained ventricular tachy
V Tach characteristics
Deadly rhythm
100-250 beats per minute
Only wide, bizarre looking complexes
QRS complex is greater than .12 seconds and wide and weird looking
tx for v tach
Patient is awake and alert with adequate vital signs → amiodarone - 150 mg IV bolus over 10 minutes
Might add BB to prevent from coming back
If patient has inadequate vital signs and is not awake → treat with defib/cardioversion
what is ventricular fibrillation also called
sudden cardiac death
characteristics of ventricular fibrillation
Deadly rhythm
Rhythm does not generate a pulse
Completely uncoordinated electrical activity without any discernible complexes
All waves are fibrillatory waves
tx for ventricular fibrillation
Defibrillate
CPR
Defibrillate
CPR, epinephrine 3-5 mins
Defibrillate
Continue with CPR, ACLS protocol
Second drug of choice = amiodarone
what is cardioversion
Delivers a shock that is synchronized w/ heart’s activity
defibrillation
Indicated in pulseless ventricular tachycardia and ventricular fibrillation
Shock delivered
Be prepared to deliver subsequent shocks per ACLS protocol
Biphasic defibrillators use less current so there is less damage to the heart
asystole characteristics
Cardiac standstill/flatliner
Rhythm is associated with death
Less than 5bpm
No complexes associated with this rhythm
when is asystole seen
head trauma and significant drug abuse
tx for asystole
intubate
resusitate
look for reversible causes
Hs of asystole reversible causes
hypovolemia,
hypoxia,
hydrogen ions (acidosis, DKA),
hypo or hyperkalemia,
hypothermia
Ts of asystole reversible causes
tension pneumothorax,
cardiac tamponade,
toxins,
pulmonary thrombosis (embolus),
coronary thrombosis (acute MI with blood clot)
3 goals of treatment for patient with CAD
- reduce symptoms
- improve quality of life
- improve survival
5 cardiac risk factors
Family history - under age of 60
DM
HTN
Dyslipidemia
smoking/tobacco use history
what is S1
Closure of the mitral and tricuspid valves
Beginning of systole
what is s2
Closure of aortic and pulmonic valves
Beginning of diastole
where is chest pain usually?
usually in the front of the chest (retrosternal) but can also be in the upper abdomen, neck, jaw, left arm or left shoulder.
where does chest pain radiate?
neck
jaw
back
left or right arm
if chest pain is due to ischemia, what might it feel like
tight and crushing
s3
happens in heart failure
cadence of a galloping horse
*innocent in children and young adults but never over 30
s4
occurs before the 1st
is abnormal
occurs with ventricular hypertrophy, coronary heart disease, dilated cardiomyopathy, hyperdynamic circulation, arrhythmia and heart block.
what does an electrocardiogram (EKG) record
-Records electrical impulses traveling through the heart
-Detects abnormal conduction
-Identifies dysrhythmia
-Detects left ventricular enlargement
-Diagnostic for acute MI
what labs are drawn for a cardiac patient
-troponin
-K+
-BUN
-creatinine
-CBC
-H&H
-coags (INR, aPTT, PTT especially if on anticoags)
-lipids
-BNP
troponin
Cardiac troponin I and T are proteins expressed exclusively in the heart, are a specific marker or muscle damage
Can elevated within 4 hours of injury and can stay elevated for 10 days
what is creatinine kinase
Released from cells in brain, skeletal muscle, and cardiac tissues after muscle damage has occurred
what is CK-MB
CK isoenzyme marker specific to cardiac tissue
When myocardial damage occurs, CK-MB is release from cells
Can show up 3-36 hours
what can a chest XR show
Visualizes vascular and cardiac shapes
Evaluates size,
pulmonary congestion,
pleural and pericardial effusions,
position of central lines
what is the gold standard for evaluating coronary artery lumen
cardiac catheterization (angiography)
Hemodynamic monitoring
Arterial, central venous, and pulmonary artery catheters
nursing responsibilities with catheters
Check all connections to be certain they are tight
Assess circulation to the cannulated limb
Inspect skin color, temperature, capillary refill and distant pulses, motor function and sensation of the cannulated limb
Monitor wave forms
what is the normal wedge pressure (pulmonary artery occlusion pressure)
8-12 mm hg
what does it mean if the wedge pressure is over 18
systolic dysfunction d/t MI damage
what does the wedge pressure measure
LV end diastolic pressure
indicator of LV function
how do crackles develop?
patient with systolic dysfunction that leads to poor cardiac outputs and low BP bc of decreased volumes being pumped into systemic circulation..The blood ends up going “backwards” into pulm circulation, causing fluid build up in alveoli = crackles
why are we concerned with MI?
Sets someone up for arrhythmia
Damages muscle → loses systolic function
what does an echo measure?
structures of heart, valvular dysfunction/disease, wall thickness, and pressures in chambers
what is normal ejection fraction
65-75%
what does an EF of 40% indicate
myocardial dysfunction
what does an EF of 30 indicate
may need automatic defibrillator to avoid v tach or v fib
what does EF of 20 indicate
severe
Medications: positive inotropes, ACE, or ARBs
what does EF of 10 indicate
critically ill, will be referred for transplant
what causes increased o2 demand
-increased HR
-contractility
-BP
-preload = venous return
-afterload
what is o2 supply
-coronary artery patency
-diastolic pressure
-diastolic time / filling time
- o2 extraction (hb, saO2)
how to measure preload
Measure central venous pressure in superior or inferior vena cava
how to increase preload
fluid, blood products
what is afterload
pressure heart has to squeeze against to eject blood from heart
how to manipulate afterload
Decrease afterload w/ nitroglycerin, relax vessel walls with ACE inhibitors, ARBs, diuretics
First line = diuretics
what are two types of stents
BMS (bare metal)
DES (drug eluting)
what are DES stents
emits chemotherapeutic agent in vessel to decrease scar tissue formation
Need to be on anti platelet therapy for longer than BES (1 year vs 3 months)
what is dual antiplatelet therapy
aspirin + clopidogrel/ticagrelor
two options for reperfusion therapies
PCI or fibrinolytics
contraindications for fibrinolytics/thrombolytics
recent stroke within 3 months
on anticoags
5 types of PCI procedures
-balloon
-laser
-directional atherectomy
-rotational atherectomy
-stenting
nursing interventions: pre-PCI
Cardiac monitor, BP, and pulse oximetry
O2 if indicated
Premedicate w/ PPI, benadryl and IV solumedrol
VS before procedure
Nursing assessment
Explain the procedure
Verify NPO status
Check labs- INR, any kidney injury?
Verify allergies
Informed consent (nurse should witness)
IV assess
nursing interventions - peri PCI
Continuous VS, O2, LOC, and cardiac rhythm monitoring
Alert physician of any changes
Be prepared for CPR/ACLS
Emergency equipment and medications nearby
nursing intervention: post PCI
Monitor VS and rhythm
Check catheterization site –radial or femoral
Check distal pulses
Post EKG for changes
Keep extremity straight
Maintain IV infusion per physician’s order/protocol
Supplemental O2 as needed
Encourage PO fluids – kidney fx?
Check coagulation studies before sheath removal
2 complications post arterial stick
pseudoaneurysm (PSA)
arteriovenous fistula
what will a bruit sound like with a PSA
turbulent flow, swishing sound - will be pulsatile b/c with arterial flow
More common with femoral sticks
what will a bruit sound like with AVF
Bruit - continuous sound - flow is continuous
what must occur prior to procedure
time out
-Verify right patient
Verify right procedure
Verify consent signed and matches procedure
Verify right laterality
Verify labs
Verify premedications
indications for CABG
Older
More advanced CAD
Impaired LV function
Previous CABG surgery
what vein is used for CABG
saphenous
avg life of bypass graft
10 years
epicardial temporary pacing
temporary pacing wires are placed on the epicardial surface of the heart and brought out of the chest wall.
V wires on Left and Atrial wires typically on right.
Can be hooked up to a generator and pace the heart.
Demand pacing
demand is pacing that withholds a stimulus when generator senses an adequate intrinsic heart rate
asyncronous pacing
asynchronous is pacing at a set and fixed rate regardless of intrinsic activity of the heart
where are pacing wires placed
Right side - atrial pacing
Left side - ventricular pacing
what is the function of a water seal chamber of a pleurovac
prevents air going back to the patient; filled to -2 cm H2O which maintains a slight negative pleural pressure and prevents air entering the pleural space when off suction and on water seal.
what does the collection chamber of a pleurovac do
collects fluid with air passing through
indication for intra-aortic balloon pumping (4)
cardiogenic shock
MI
post op LV failure
unstable angina
when is the IABP balloon inflated and what is the result
diastole
increases blood flow to coronary arteries
when is the IABP balloon deflated and what is the result
balloon is deflated quickly as heart starts to squeeze → helps pull blood out of LV, decreases LV outflow resistance (afterload)
therapeutic effect of IABP (5)
increase CO
increase CA perfusion
increase aortic pressure (BP)
decrease myocardial o2 consumption
decrease cardiac afterload
how often to check IABP insertion site
hourly, note any oozing
nursing interventions IABP
- Palpate DP & PT pulses in affected leg hourly; mark the location of pulses & compare them to the other extremity
- Firmly secure the IABP & possibly restrain the affected extremity to maintain it in a straight position
- Keep HOB lower than 30 degrees
- Note any sudden decrease in urinary output or any differences in BP between both arms
- Maintain appropriate timing-trigger off of EKG or Aline
5 potential complications of IABP
- Distal extremity ischemia
- Balloon migration (toward the renal arteries with occlusion of those arteries or toward the aortic arch with occlusion of the subclavian arteries)
- Potential perforation of the aorta during insertion or with inadvertent patient movement
- Inappropriate timing causing hypotension & dysrhythmias
- Psychological consequences (anxiety, loss of control, & sleep alteration
what is the purpose of a ventricular assist device
It assists the patient’s own heart to pump blood throughout the body, decreasing the work of the left ventricle
what does a LVAD do
receives blood from the left ventricle and delivers it to the aorta
what does an RVAD do
receives blood from either the right atrium or right ventricle and delivers it to the pulmonary artery
pulsatile VAD
fills with blood, then pumps, and continues
non pulsatile VAD
whirling and continuous.
no palpable pulse
complications of acute STEMI (8)
-Rhythm disturbances (A fib, v tach)
-Cardiogenic shock - LV pump failure (Elevated PA pressure, elevated wedge pressure, Tachycardia)
-HF
-Pericarditis
-Embolisms
-Papillary muscle dysfunction
-Interventricular septal rupture
-Ventricular aneurysms
HFpEF
heart failure with preserved ejection fraction - diastolic dysfunction
HFrEF
heart failure with reduced ejection fraction - systolic dysfunction
what is BP an indirect measure of?
afterload
what would indicate an unstable patient
Rapid RR, diaphoresis, thready pulses, cool clammy skin, poor cap refill, neurologic impairment
max number of pts waiting in traige
5
main threat for circulation following trauma
hemorrhage
tx for hemorrhage
0.9% NS/LR
secondary survey
performed after the primary survey is complete and lifesaving interventions have been initiated. This survey identifies the other injuries that the primary survey did not assess along with pertinent information about the patient such as other comorbidities.
- assess vitals, pain
which tool to use to look at viability of heart tissue
MRI
when can fibrinolytics be given
within 30 minutes of arrival to hospital
