test 3 Flashcards
what is cardiac cycle caused by
electrical (caused by automaticity) (1st)
mechanical (muscular) (2nd)
2 phases of electrical activity
depolarization= active (contract)= systole
repolarization= resting =diastole
two mechanical responses
systole
diastole
systole
contraction
diastole
resting or filling phase
sino atrial node (SA)
rate of 60-100 bpm
depolarization begins
atrial contraction
AV node
40-60 bpm
delays impulse to ventricles; allows for filling
backup pacemaker for SA node
Bundle of His
20-40 bpm
electrical conduction pathway
- SA node
- AV node
- Bundle of His
- Bundle Branches (L and R)
- Purkinje fibers
what consist of Autonomic Nervous System
sympathetic nervous system
parasympathetic nervous system
parasympathetic nervous system
acetylcholine
decreased HR, decreased contractility, vasodilation
sympathetic nervous system
epinephrine and norepinephrine
increased HR, increased contractility, vasoconstriction
difference between 15 lead and 12 lead
12 lead is only on the front where 15 has 3 on the back
cardiac monitoring
continuous monitoring via 3 lead or 5 lead
skin prep, lead placement and appropriate lead selection are very important
ECG graph paper
vertical= measures amplitude
horizontal= measures time
1 box is 0.04 secs
P wave
atrial depolarization
normally indicates firing of SA node
shouldn’t exceed 3 boxes high
PR interval
Atrial depolarization/delay in AV node
beginning of P wave to beginning of QRS complex
should be anywhere from .12 to .20 secs
shorter interval- impulse from AV junction
Longer interval= first degree AV block
QRS complex
ventricular depolarization
0.06 to 0.10 secs
if wide its a slowed conduction
ST segment
look for depression or elevation.
elevation- MI
depression- ischemia, reciprocal changes, digoxin
QT interval
beginning of QRS complex to end of T wave
0.32 to 0.50 secs
U wave
not normally seen
PP intervals (atrial)
is regular when distance between PP intervals is equal
RR intervals (ventricles)
is regular when distance between RR intervals is equal
normal sinus rhythm
60-100 bpm
sinus tachy
100-150
causes- hyperthyroidism, hypovolemia, heart failure, anemia, stimulants, fever, sympathetic responses
assess for symptoms of low cardiac output
sinus bradycardia
less than 60 bpm
causes- vagal, drugs, ischemia, diseases of the nodes, ICP, hypoxemia, and athletes (normal)
what causes atrial dysrhythmias
increased automaticity in the atrium
causes- stress, electrolyte imbalance, hypoxia, atrial injury, digitalis toxicity, hypothermia, hyperthyroidism, alcohol, pericarditis
premature atrial contraction
early beats initiated by atrium
noncompensatory pause
Afib
erratic impulse formation in atria
no discernible P wave
irreg vent rate
high risk for emboli
A flutter
sawtooth patterns
supraventricular tachycardia
rate 150/160-250
regular rate, P waves may or may not be present
PR interval 0.12-0.20
QRS 0.10 secs or less
ventricular dysrhythmias
impulses initiated from lower portion of the heart
depolarization occurs leading to abnormally wide QRS complex
ectopic and escape beats
common causes- MI, low K or Mg, hypoxia, acid-base imbalances
ventricular Tachycardia
rapid life threatening, rate can be 150-250. ACLS will most likely be needed
torsades de pointws
Med emergency. Caused by prolonged QT interval and is often caused by Mag deficiency. Treated as pulseless Vtach
characterized by the presence of both positive and negative complexes that move above and below the isoelectric line. This lethal dysrhythmia
V fib
Life threatening. Immediate treatment needed
asystole
flat line
check leads and pt
pulseless elecrtical activity
has rhythm but no pulse. Caused By Hs and Ts. Must treat cause
AV blocks
block of conduction from atria to ventricles
4 types- first degree, second (morbitz type 1 and 2), third degree (complete)
Cardiac pacemakers
deliver an electrical current to stimulate depolarization
can pace atrium, ventricle or both
method of pacing: cardiac pacemaker
transcutaneous- emergency
transvenous
epicardial
what to know when taking care of pt w pacemaker
rate
mode
electrical output (mA)
sensitivity
sense-pace indicator
AV interval
automaticity
the ability of certain cardiac cells to spontaneously generate electrical impulses, leading to heart contractions without external stimulation.
when do codes occur
cardiac arrest
resp arrest
life threatening dysthymia’s causing loss of consciousness
when to call a rapid
change in pt conditions such as:
HR, BP
RR, o2 sat
mental status
Urinary output
lab values
what do rapid response teams decrease
cardiac arrest
critical care length of stay
incidence of acute illness
they do not reduce mortality rate
types of nurses in a code
primary nurse- knows patient
secondary- gives meds, get equipment
teritary- records events
nurse supervisor- traffic control, secures ICU bed if needed
equipment needed for code
crash cart
backboard
monitor/defibrilator, pacemaker
bag valve mask device
airway supplies/suction
meds
IV supplies
NG tube
BP cuff
sequence of events: BLS
Advanced directives
airway open
breathing
circulation- compressions
technique to open airway
head tilt/chin lift
rate of air ml/min for ACLS
15 mL/min
ACLS
advanced cardiac life support
additional certification
uses early defibrillation and AED
what meds can be delivered through endotracheal tube (ETT) if needed
lidocaine
epinephrine
vasopressin
treatment of V-fib and pulseless V tach
ABCD, initiate CPR
shock-CPR-shock-CPR
consider antidysrthymic drugs. Amiodarone is drug of choice
ensure IV access
pulseless electrical activity (PEA)
Rhythm without pulse
airway, o2, intubate, IV access
treat cause
med= epinephrine
ABCD with circulation
causes of pulseless electrical activity
hypoxia
hypovolemia
hypothermia
H+ ions (acidosis)
hypokalemia or hyperkalemia
tablets (OD)
Tamponade
tension pneumothorax
thrombosis (coronary or pulmonary)
treatment of asystole
ABCD with CPR
Airway, o2, intubate, IV access
confirm with multiple leads
treat cause
pacemaker
epinephrine
treatment of symptomatic bradycardia
ABCD with car
airway, o2, IV access
atropine if conscious. could also use epinephrine or dopamine
transcutaneous pacing (very painful. only used if emergency)
NO lidocaine
unstable tachycardia
ABCD
airway, o2, IV access
sedation
cardioversion
cardioversion
electric current, much lower joules then defib. (60 joules)
synchronized delivery on R wave.
used for symptomatic tachycardia.
defibrillation
primary treatment for V Fib and pulseless V tach. Used when there is no pulse
electric current- 200-360 joules
completely depolarizes the heart. allows for resumption of the rhythm.
everything must be clear before shock
may cause skin burns (ensure good contact with skin)
continue CPR after and reassess
transcutaneous cardiac pacing
for symptomatic bradycardia
sedation and analgesics may be needed
Meds may be used in code
o2
epinephrine
vasopressin
atropine
amiodarone
lidocaine
adenosine
magnesiun
dopamine
what o2 percent to give during arrest
100%
epinephrine
potent vasoconstrictor
typically given 1mg IV push but can also be given intraosseous or ETT.
continuous infusion may also be done
used in V fib, Pulseless V tach, asystole, PEA
Vasopressin
vasoconstriction
may be as effective as epinephrine
atropine
for symptomatic brady.
Given IV push, can be given through ETT.
decreases vagal tone= increases HR
Amiodarone
for VT and VF
reduces membrane excitability
can be given IV/IO in cardiac arrest
lidocaine
antidysrhythmic
surpasses ventricular ectopy
can be IV/IO/ETT
adenosine
for SVT
slows conduction through AV node
rapid IV push
magnesium
used for refractory VF, torsades de pointes.
only if known deficiency of Mg
sodium bicarb
treatment of metabolic acidosis
Dopamine
for symptomatic hypotension
vasoconstrictor- increases bp
continuous drip
documentation of arrest
Write everything- order of events, med (doses, time, etc), time when things are done, vitals, Pt responses, team members present
postresusication goals
optimize cardiopulmonary function
transport to critical care unit
determine cause of arrest
post CPR interventions
12 lead ECG
neuro exams
arterial line
indwelling Cath for hourly output
monitor BG
interventions if pt comatose after CPR
Head CT, EEG
Therapeutic hypothermia
For fever from brain injury increases the level of neurological damage post CPR
lower body temp is associated with better recovery. Must have continous EEG.
Use bladder Cath to monitor temp
control shivering with IV sedatives, analgesics, neuromuscular blockade meds
REWARM slowly after 24 hours
complications of ther hypothermia
bleeding
infection
metabolic and electrolyte disturbances
hyperglycemia
hemodynamic monitoring studies the relationship of:
blood flow
o2 delivery
tissue perfusion
heart rate
goal of hemodynamic monitoring
assess the patient and provide therapies to optimize o2 delivery and tissue perfusion
cardiac output
volume of blood ejected from heart/min
heart rate + stroke volume= cardiac output
normal Cardiac output
4-8 L/min
low = body doesn’t have enough blood/fluid.
high= vise versa
ejection fraction
fraction of blood ejected with each beat
normal ejection fraction
60-70%
low in HF pts. may be around 20%
contractility
force of ventricular contraction.
how well the heart is pumping
digoxin is a med that can help this
systemic vascular resistance
peripheral vascular resistance. diameter of blood vessels.
what is arterial BP
cardiac output + SVR
afterload
pressure or resistance against flow
it is related to lumen size and viscosity
preload
degree of muscle fiber stretch before systole- volume of blood in ventricle prior to contraction
increased stretch= increased volume
vasodilators
nitroglycerin, hydralazine
vasoconstrictors
vasopressin, epinephrine, atropine
noninvasive hemodynamic monitoring modalities
BP cuff
jugular venous pressure
serum lactate levels
invasive hemodynamic monitoring modalities
arterial BP
pulmonary artery BP
right arterial pressure
components of invasive hemodynamic monitoring system
invasive catheter
noncompliant pressure tubing
transducer and stepcocks
flush system
bedside monitor
arterial pressure monitor indications and complications
treat hemodynamic instability
assess efficacy of vasoactive meds
obtain frequent blood samples
complications: could fall out and cause person to bleed to death, infection.
hold pressure for 15 mins when out.
Central venous pressure (CVP)
Catheter in superior or inferior vena cava. triple lumen.
normal value or right arterial pressure (RAP) and central venous pressure (CVP)
2-6 mm Hg
low= not enough pressure
high= too much pressure
nursing interventions RAP/CVP
zero it
PT position 0-60 degrees
monitor for comp- puncture, dysrhythmias, pneumothorax, infection
what does RAP/CVP assess
RV preload or right vent end diastolic pressure
direct measurement of pressure in right atrium
pulmonary artery pressure
normal level is 8-12
created by Dr Swan and Ganz
insertion of pulmonary artery cath
proper position of pt- tredelenburg position, towel roll between shoulder blades
Monitor waveforms
confirm placement with chest x-ray, check for puncture
norepinephrine like drugs
epinephrine, norepinephrine, vasopressin, atropine
acetylcholine like drugs
nitroglycerin, beta blockers, hydralazine
coronary artery disease
progressive narrowing of arteries due to atherosclerosis
diagnosed by cardiac enzymes, EKG
management- aspirin, lower lipids
angina
3 types
chest pain/discomfort caused by imbalance in myocardial o2 supply and demand
decrease pain, find out cause.
MI
ischemia with myocardial cell death
STEMI vs NSTEMI
ST elevation vs no ST elevation
MI s/s
chest pain
pale and diaphoretic
dyspnea
syncope
n/v
dysrhythmias
shoulder blade/arm pain
flu like symptoms
diagnosis of MI
12 lead EKG
elevated troponin, elevated CK-MB
Complication of MI
dysrhythmias
HF
Rupture
pericarditis
cardiogenic
complications of CABG
dysthymias
impaired contractility
MI
pericardial temponade
resp insufficiency
pain
emboli
death
post CABG management
assess for adequate cardiac output
airway management- vent
circulation
goal of HF treatment
improve pump function
remove fluid
reduce cardiac workload/o2 damage
improve gas exchange
flash pulmonary edema
HF complication
pink frothy sputum
hypoxemia
dyspnea
cyanosis
lassix needs to be given immediately
4 types of aortic aneurysm
flase
fusiform
saccular
dissecting
aortic dissection
tear of inner layer of aorta
s/s- sudden sharp, severe chest pain
usually by the time it presents its too late
management- surgical intervention, control BP
