Test 2 Flashcards
H’s and T’s
Hypovalemia Hypoxia Hydrogen Ion (acidosis) Hyper/Hypokalemia Hypothermia
Tablets Tamponade Tension Pneumothorax Thrombosis-coronary (MI) Thrombosis-Pulmonary (PE)
Hypovalemia
Low blood vol-fixed by fluids
Hydrogen Ion
Check if its acidosis/ or metabolic… fix with bicarb when acidosis
Hyper/Hypokalemia
Hyperkalemia-fixed with albuterol
Hypokalemia- fixed with potassium
Tablets-overdose
Find antidote and fix with Narcan
Tamponade
Cardiac, Relieve pressure around heart (squeeze)
Tension Pneumothorax
fix with chest tube/ needle
Thrombosis-coronary
MI- clut buster
PCI-Stent-relieve block, angioplasty-open up, see block
Thrombosis-Pulmonary
PE- Clot buster
Remove clot
PVC
Premature Ventricular Contraction- Normal Irritability of the heart that starts in ventricle, outside of the normal path of conduction and bounces through ventricle= wide QRS, no Pwave
PVC rate, Rhythm, P wave, QRS
Rate- dependent upon underlying rhythm
Rhythm- irregular because of PVC
P wave- No p wave is associated with the PVC
QRS- Greater than 0.12 seconds that is wide and bizarre
When is PVC a problem
When it is frequent and is symptomatic
PVC is caused by stress
Run of 3
Run of v. tach: loses C.O.
Happens every 2? Bigemity
Every 3? Trigemity
Ventricular Tachycardia
-Three Consecutive PVC’s is considered a “run” of ventricular tachycardia
-Ventricular Rate= 100-250 bpm
-Ventricular rhythm essentially regular
-QRS > 0.12 seconds
-Ventricular tach without a pulse is an emergent situation. BLS should be initiated as soon as possible and the pt defibrillated
DONT DELAY SHOCKING
Vent. Tach. shocking
Can have with or without pulse
With pulse-Can cardiovert
Without pulse- Defib/ CPR 2 min then check/ push meds= restore CO
Monomorphic V. tach.
All coming through the same ventirucle
Polymorphic V. tach.
Twisting of points
V. tach common causes/ problems
- MI
- Myocardial Ischemia
- Pt may become severely hypotensive to the point of syncope
- Cardiac output may deteriorate significantly causing the pt to become unresponsive
- Serious arrhythmia, often leading to ventricle fibrillation
Treatment of V. tach.
Follow pulseless ventricular tachycardia/ Ventricular fibrillation ACLS algorithm
Goal: return spontanious, then look at causes
Torsade De Pointes
Polymorphic Ventricular Tachycardia (PVC)
“twisting of points”
Caused by multiple things
-Drugs including: antidepressants, antidysrhythmics, eating disorders, and electrolyte imbalances
-Treated with mg sulfate (in crash cart)
Torsade De Pointes think
Magnesium!! important in muscle contraction
Ventricular Fibrillation
- Quivering of the ventricles with no beat producing rhythm
- Rhythm is chaotic with no pattern or regularity
- There is no CO or BP!!
- Pt becomes unconscious, no pulse
- Without tx the pt will die in minutes
- Nothing can be identified
Vent. Fibrillation tx
Follow pulseless ventricular tachycardia/ ventricular fibrillation ACLS algorithm
Compare asystole and PEA, SHOCK ASAP
Asystole
- Complete absense of electrical and mech activity
- no cardiac output
- Flatline: used to determine clinical death
- must confirm in two leads
Tx: Follow asystole/ PEA ACLS algorithm
Remove monitors
Can only do CPR and EPI
PEA
Pulseless Electrical Activity
Connected to Asystole
-Electrical Pattern that is seen on EKG or rhythm strip, bud does not produce a pulse
CAB
Circulation- most important
Airway
Breathing
check PETCO
Compressions should be performed at a rate of
at least 100bpm and atleast two inches deep on an adult. It is recommended to rotate the compressor every two min while heart rhythm is checked.
Advanced airways are important because
providing ventilation and compressions becomes simultaneous
Breathing- avoid
excessive ventilation (one breath every 6 seconds after an advanced airway has been placed) Excessive= increase pressure in chest
Cardioversion vs. Defibrillation
Both deliver an electrical shock to the heart, in joules, in hopes of restoring adequately perfused conduction
External Defibrillator
Can also perform cardioversion, external heart pacing-transcutaneously shocking or pacing(capture to see NRG is strong enough), synchronizing
Defibrillation
Delivery of a uniform current of sufficient intensity to depolarize ventricular cells and terminate the abnormal heart rhythm
- Momentary asystole provides opportunity for SA node to regain control
- Also called unsynchronized counter shock
- Monophasic 360 or biphasic 200
Rhythms that we defibrillate
Pulseless V. tach and V. Fib
AED
Automated External Defibrillation
- Voice prompted
- Looks at rhythm, QRS width, rate, and amplitude
- Safety checks for false signals: poor/ loose electrode contact, radio transmissions
Cardioversion
- Synchronized to deliver a shock during ventricular depolarization or on the “R” wave.
- MUST HAVE A QRS
- Shock attempts to restore normal sinus rhythm
- Can also give drugs to reduce symptoms, otherwise shock
Cardioversion rhythms
SVT! Unstable tachycardia, Unstable A. flutter or A. Fib, High ventricular rate= 150bpm or more
- No CPR , patient is awake and having symptoms
goal: restore ventricular rate
Routes of Delivery
IV= Intravenous
IO= Intra-osseous
Endotracheal
IO
- Infusing medication, fluids, and blood products into the bone marrow cavity which intern enters venous circulation
- Any medication that can be administered IV can be administered IO (same dose)
Endotracheal meds
Medication is absorbed by the lungs and carried into circulation
- Unreliable
- Double dose and bag for circulation (optimal dose unknown)
Approved ETT drugs
NAVEL N: Naloxone/ narcan- reverse opiates A: Atropine- Symptomatic Brady V: Vasopressing- Potent vasoconstrictor E: Epinephrine- Given Q 2-3 min, PRN L: Lidocaine- Antiarrythmia
(plus mycomyst, combivent, duo, ect)
Drugs that have dose changes as increased
Amiodarone and Adenosine
RES Q-POD
Improves cardiac output by improving venous return during chest recoil- creates a vacuum like effect in chest
- also has a light that flashes to guide ventilation: keeps from hyperventilating
- If pt is resuscitated successful, the Res Q POD must be removed (immediately after ROSC)
- Aka impedence threshhold device
- Can be used with ETT and BVM
How does hyperventilating impede resuscitation efforts
reduces cardiac output inhibit
PETCO
End Tidal CO2
- Reflects perfusion efforts during CPR- circulation not ventilation
- If end tidal CO2 drops below 10mmhg, improve compressions or switch compressors
- At 40mmhg; ROSC
- Keep at 10-20 during CPR atleast
- Measured during exhalation
STEMI
ST elevated myocardial infarction
- PROTOCOL; EKG within 10 minutes of ED admission
- TX: Fibrolytics or percutaneous coronary intervention (PCI) (angioplasty, stenting): 90 minutes
- MONA
Fibrolytic Tx of STEMI
-No catheterization lab within distance
-break down of fibrin clots
-tx with fibrolytics increases risk of bleeding out
ex.
Retavase, Streptokinase, Tissue Plasminogen activator (tPA)
They break of clots, risk of bleeding out
TX for suspected MI
MONA
M: Morphine- Helps pain, reduces stress
O: Oxygen- Treat hypoxemia, low dose 1-4lpm, maintain SpO2 (too much=coronary vasoconstriction)
N: Nitroglycerin- tx angina (chest pain), cause vaso coronary dilation be careful of low BP
A: Aspirin- doesnt bust clots, helps stop continue of formation
STROKE
Cerebral Vascular Accident (CVA)
-You must find out if it is caused by a clot or hemorrhage
-treatment with fibrolytics
-timely tx extremely important: within 3 hours- stroke fibrolytic check list
Signs and symptoms? CT right away rule out head bleed
STEMI= 90 min
Clot
Occlusion of vessel
Hemorrhage
burst of vessel
Cardiovert at
50Joules- any tach
Adenosin
SVT IV Access 6mg followed by rapid flush of saline 12 mg rapid flush No compressions
Epinephrine
1mg every 3-5 minutes followed by CPR
PEA, Pulseless vtach,
Amiodarone
300mg
150mg ETT
Pulseless Vtach
Continue CPR
TPA
Fibrolytic
given within 3 hrs of CVA: stroke, busts clot not blood thinner
Atropine
Bradycardia
0.5mg every 3-5 minutes, Max 3mg
no compressions
Chewable Aspirin
STEMI
160-320 mg
STEMI Intervention and outcome
Repurfusion- 90 minutes
