Module 3 Flashcards
ACS management
ASA Clopidigrel Heparin Nitroglycerin IV opiods TNK
ASA/Clopidogrel
Antiplatelet ( stops aggregation)
Stops the clot from getting bigger
Heparin
Anticoagulation
Works on Thrombin (which acts like plastic wrap)
stops thrombin from sticking to platelets
Nitroglycerin
Reduces preload and afterload
DO NOT GIVE TO RT SIDED (Inferior) MI
because it drops the preload
IV opiods
decrease preload and stop SNS activations
TNK
fibrinolytic
clot buster
NSTEMI
ischemia/tissue damage but not death
STEMI
STevelvation MI- cell death/Infarct
Needs- fibrinolytic, PCI and maybe Defib
Key features of successful thrombolysis
Resolution of CP
Resolution of ST-segment elevations
Reperfusion arrhythmias
Cardiogenic shock
Pump problem
Causes of cardiogenic shock
MI coronary artery dissection chest trauma Infection ( pericarditis) tamponade arrhythmia pharmacological OD Mechanical valve
Cardiogenic shock symptoms
CP
Decreased cardiac output decreased BP Decreased LOC Cool extremities decreased urinary output
Pulmonary edema
Pulmonary crackles
Increased JVD
cardiogenic shock- Preload
INCREASED
compensation/consequence
Treatment:
Vasodilation- Nitro,
Diuretics- lasix
Opiods-morphine
cardiogenic shock- Afterload
INCREASED- increased SVR
this is compensation- the body feels the decreased cardiac output so it constructs vessels causing an increase in afterload
Treatment: Vasodilation- Nitroglycerine or Nitroprusside
cardiogenic shock- Contractility
DECREASES
This is the cause of cardiogenic shock
Treatment:
Increase contractility with positive inoptropes
Dobutamine, Milinone and Dopamine
cardiogenic shock- HR
INCREASED
this is compensation for decreased cardiac output
Treatment if needed - negative inotropes to decrease cardiac oxygen demand
Cardiogenic shock- Cardiac output
DECREASES
as a consequence
treatment: Intra aortic balloon pump
ST segment
reploarization of teh ventricles J point (measure 1.5 boxes over) to T wave
PR
< 0.2 seconds
Brady rhythms
> 50 bpm
decreased cardiac output
Pacemakers
SA node
AV node
Ventricles
SA node rate
60-100
AV node
AV node rate
40 -60
Ventricular rate
20-40
Ventricular rate
20-40
Things that slow the heart
Beta blockers
Vagus nerve
MI
hypoxia
Symptoms of brady cardia
Heart failure symptoms Decreased LOC hypotension/poor perfusion CP weakness/fatigue
Why do we give EPI
Alpha 1- vasoconstriction
Beta1- contractility
Beat 2 Bronchodilation
EPI dose
1mg Q 3-5 mins IV
Drug for brady rhythms
Atropine
Atropine
anticholinergic stops parasympathetic stops vagus nerve only works at atria 0.5-1mg Q3-5 mins ( max 3 mg)
Hs
Hypothermis Hypoxia Hydrogen Hypo/Hyperkalemia Hypovolemia
Ts
Tension pneumo Tamponade Toxins Thrombosis (pulm) Thrombosis (cardiac)
Reasons for PEA
No mechanical activity caused by
hypoxia- heart can contract
Hypovolemia- no preload
unstable tachycardia symptoms
CP >20 mins
SOB or new or worsening CHF
Low BP
Signs of shock
Synchronized cardioversion
For persistent unstable tachyarrhythmia
Shock on R
Consider sedation
Adenosine
Pauses conduction through the AV node
Only treats irritability/reentry near the AV node (party close to the border)
Does not work on Atrial irritability (doesn’t treat afib or flutter)
Antiarrhythmics
Procainamide (works on Na/CL)
Amioodarone (works on all channels)
1st 4 steps in a PEA arrest
CPR while putting pads on/monitor
rhythm check asap (if its shockable we need to know so we can intervene asap)
CPR x 2 mins- give epi 1mg while doing CPR
Rhythm check
CPRx2mins
ROSC - what to do next
Airway- intubate
Breathing-oxygenate
Circulation- BP low (pt has no vascular tone) give fluid bolus 1-2. start vasopressors. ECG
Differential diagnosis. labs, cath lab, SX, CXR
Disability (34-36 C) targeted temperature management
Keep afebrile x24h b/c we want to decrease O2 demand
aggressive
ROC infusion
