Vasopressors + antirrhythmics Flashcards
CABG
coronary artery bypass grafting
APD
action potential duration
NSR
normal sinus rhythm
ERP
effective refractory period
What are medications that raise BP in cases of hypotension?
vasopressors –> constrict blood vessels, used in shock and critical care, increase SVR and CO
What are medications that treat abnormal heart rhythms?
anti-arrhythmics
catecholamiens vs D1 and D2
catecholamines - SNS w/ adrenergic receptors
D1 and D2 = renal vasodilation w/ dopaminergic receptors in kidney
What is first line for septic shock
vasopressor - norepinephrine (levophed)
What is used in anaphylaxis and ACLS?
vasopressor - epinephrine
What is used for various shock states w/ dose dependent effects?
vasopressor - dopamine
What is used in adjunt in septic shock?
vasopressor - vasopressin
What is used in hypotension w/ low HR?
, vasopressor - phenylephrine, pure a1 agonist
What are ex of inotropes?
dobutamine and milrinone
What’s the MOA of norepinephrine (levophed)
large increase of vasoconstriction and modest increase of CO
potent a-1 effect, modest B-1 effect
reflex bradychardia occurs w/ increase of MAP
prolonged infusion = direct cardiac toxicity
What are ADRs of norepinephrine (levophed)?
arrhythmias, bradycardia, peripheral (digital) ischemia, HTN w/ non-selective BB?
What are indications of epinephrine (adrenaline)?
treatment of anaphylaxis, ACLS (asystole/PEA, pulseless VT/VF), 2nd line in septic shock, management of HOTN after CABG
What’s the MOA of epinephrine?
potent B-1 agonist (cardiac stimulant) and moderate B-2 agonist (bronchodilation) and alpha 1 agonist
B effects > @ low doses
a effects > @ higher doses (vasoconstriction)
What are some effects of epinephrine (adrenaline)
low: high CO and low PVR
b-1 inotropic + chronotropic effects
B-2 and a-1 can offset
high: high CO and high PVR
What are ADRs of epinephrine?
ventricular arrythmias, severe HTN resulting in hemorrhage, cardiac ischemia, sudden death
What are indications for dopamine?
hemodynamic support + inotropic support in advanced HF
What’s the MOA of dopamine?
low - dopamine receptors
moderate - beta 1
high - alpha 1
often used as 2nd line to NE in patients w/ bradycardia and low risk of tachyarrythmias
severe hypotension cardiogenic shock
What are effects of dopamine?
low dose - dopaminergic (D1/D2 stimulation) to increase renal blood flow + urine output
intermediate - B-1 stimulation, high HR, CO, contractility (both ino and chrono)
high - vasoconstriction, high BP + HR, CO, contractility (a1 dominates)
What are ADRs of dopamine?
severe HTN (esp w/ nonselective beta blockers)
ventricular arrythmias
cardiac ischemia
tissue ischemia/gangrene in high doses
What are indications for ADH (vasopressin)?
diabetes inspidus, esophageal variceal bleeding, vasodilatory shock (2nd line), also can reduce dose of 1st line agent
What’s the MOA of ADH?
stimulates V1 and V2 receptors, less coronary cerebral vasoconstriction, increases systemic resistance and mean ABP, which could lower HR and CO
What are ADRs of ADH?
arrythmias, HTN, low CO, cardiac ischemia, severe peripheral vasoconstriction, rebound HOTN, hyponatremia
What’s the MOA of phenylephrine?
vasoconstriction w/ minimal inotrophy or chronotrophy
may lower stroke volume, so reserved for pts in who norepinephrine is contraindicated due to arrythmias or failed other therapies
When is phenylephrine recommended?
Not recommended septic shock UNLESS
1) when NE is associated w/ serious arrythmias
2) when CO is known to be high and BP low
3) salvage therapy when combo fail to achieve target MAP
what are ADRs of phenylephrine?
reflex bradycardia, HTN (nonselective BB), severe peripheral and visceral vasoconstriction tissue necrosis w/ extravasation (central line preferred)
In summary what are the clinical uses of vasopressors?
septic shock (NE)
cardiogenic shock (NE + dopamine)
anaphylaxis (epi)
HOTN w/ bradycardia
What are ADRs of vasopressors
tachycardia, arrythmias, peripheral ischemia, HTN
continuous BP monitoring, UO, titrate based on response
What are the indications for dobutamine?
medically refractory heart and failure and cardiogenic shock (Low CO), also pallative for end stage HF, cardiogenic shock, shor-term bridge to transplant
ACLS and echo
What’s the MOA of dobutamine?
primarily B-1 agonist, potent inotrope with high contractility, HR, CO
What are ADRs of dobutamine?
tachycardia, cardiac ischemia, proarrythmic that can occur at any dose
What does milrinone do?
phosphodieterase-3 enzyme inhibitor
What’s the recommended inotrope if patient is not on a beta blocker or not hypotensive?
milrinone
What’s milrinone’s MOA?
potent inotrope and vasodilator; increasing contractility and vasodilation
What are ADRS of milrinone?
proarrythmic (torsades de points), hypotension, cardiac ischemia
What are class I antiarrhythmics?
Na+ channel blockers
What are class I a antiarrhythmics?
disopyramide (norpace), quinidine, procainamide (pronestyl)
What are class Ib antiarrhythmics?
lidocaine (xylocaine), mexiletine (mexitil, fast dissociation)
What are class Ic antiarrhythmics?
flecainide (tambocor), propafenone (rhythmol, slow dissociation)
What are class II antiarrhythmics?
beta blockers
What are examples of beta blockers?
metoprolol (toprol), atenolol (slow HR and conduction)
What are class III antiarrhythmics?
K+ channel blockers
What are examples of K+ channel blockers?
amiodarone (cordarone, pacerone), dofetilide (tikosyn, prolong action potential), ibutilide (corvert), sotalol (betapace)
What are class IV antiarrhythmics?
non-dihydropyridine CCBs
What are examples of class IV antiarrhythmics?
Diltiazem (cardizem), verapamil (Calan, slow AV conduction)
What are class V antiarrhythmics?
adenosine (adenocard), digoxin (digitalis, lanoxin) paroxysmal SVT
What’s the general MOA of class I antiarrhythmics?
block sodium entry into cell during depolarization – decreases rate of rise of phase 0 of action potential, also suppressing automaticity of Purkinje fibers + bundle of His
What’s the MOA of class Ia drugs?
slow rate of rise of phase 0 by prolonging duration of AP and increasing effective refractory period – QRS and QT are affected, whole shift
What class are these drugs: quinidine, procainamide, disopyramide?
class Ia drugs
What class of drugs are indicated by: treatment of ventricular and atrial arrhythmias in patients w/o hx of ischemic heart disease?
class Ia drugs
What are ADRs of Class Ia drugs?
increased arrhythmias including torsades, hypotension, tinnitus, headache, vision changes, thrombocytopenia, lupus-like syndrome**
Is quinidine used in arrhythmias?
no - only for malaria bc of ADRs
What’s common with procainamide IV?
hypotension
What class are these drugs: lidocaine (IV), mexiletine (PO)?
class Ib drugs
What’s the MOA of class 1b drugs?
shorten action potential duration and refractory period of Purkinje fibers – decrease duration of AP during phase 0 depolarization AND ventricular muscles
What are the indications of class 1b drugs?
tx of ventricular arrhythmias (ventricular tachycardia, ventricular fibrillation, ventricular ectopy)
What is lidocaine 2nd line to?
terminate v tach and vfib after defribillation (amiodarone is better) and only used in hospital/EMS setting and ineffective against atrial arrythmias
What are ADRS of class 1b drugs?
CNS: confusion, vision change, drowsiness
What class are these drugs: propafenone, flecainide
class 1c drugs
What’s the MOA of class 1c drugs?
greatest effect on early depolarization and less on refractory period – blocks open Na channels + slow unbinding during diastole, QRS markedly prolonged during NSR
What is this indicative of: supraventricular arrhythmias in patients WITHOUT structural heart disease, chronic suppression of ventricular arrhythmias?
class 1c drugs
What are ADRs of class 1c?
better tolerated, increased arrythmias, CNS, increased mortality in patients w/ MI, CHF
class 1a
complete shift
class 1b
shorten AP
class 1c
normal durations, longer depolarization, earliest and greatest effect on early depolarization
What are these types of drugs: propanolol, atenolol, esmolol, metoprolol?
beta blockers
What’s the MOA of beta blockers?
step 4 of conduction
cardiac B-1 receptor blockade + reduction in cAMP – results in modest reduction of Na and Ca currents + suppression of abnormal pacemakers –> cardiac membrane stabilization
conduction through SA and AV nodes = slowed –> refractory period is increased
PR interval is increased
What are these indications of:
- prevent re-infarction + sudden death in patients w/ HF or MI
- treat exercise-induced arrythmias
- prevent occurence of AV node reentry
- control ventricular rate in patients w/ supraventricular tachyarrythmias by increasing AV node refractory period
beta blockers
What are ADRs of beta blockers?
bronchospasm, cardiac depression, AV block, hypotension
What type of drug are these; amiodarone, sotalol, dofetilide, ibutilide?
potassium channel blockers
What’s the MOA of class 3 drugs, potassium channel blockers?
step 3 of cardiac depolarization
Prolong/delay repolarization
can prolong QT, and solatol is also a BB!
What are indications for amiodarone?
DOC for acute treatment of ACLSVT and VF, slow ventricular rate + convert AF
What PCB class 3 drugs are safe in concomitant HF?
amiodarone and dofetilide
What are ADRs of PCB/class 3 drugs?
QT prolongation, torsades de points
What two antiarrhythmics are shown to not increase mortality w/ long term use in patients w/ structural heart damage?
amiodarone and dofetalide
What are adverse effects of amiodarone?
N/V, pulmonary fibrosis, hyper/hypothyroidism, corneal microdeposits, hepatotoxicity
Can reactions be delayed in amiodarone?
yes - half life is 52 days
What baseline do you need to chec for amiodarone?
PFT, CXR, thyroid panel, lipid profile, EKG, eye exam, CBC, BMP, neuro, derm
BMP - watching K+ and Mg2+ when on antiarrhythmic to avoid QT prolongation!
What is your goal for K and Mg in amiodarone monitoring?
4 for K, 2 for Mg
What are the two big drugs that interact with amidarone?
warfarin and digoxin, cyclosporine, phenytoin, statins– amiodarone inhibits 3A4, 1A2, 2D6, p-glycoprotein
What class of antiarrhythmics are diltiazem and verapamil?
calcium channel blockers in group 4
What’s the MOA of group 4 CCBs?
slow conduction through AV node and increase effective refractory period in AV node, blocking calcium in phase 0 and 2 of cardiac cycle, slowing conduction + prolong refractory period
prolongs PR interval
What does this indicate: more effective against atrial than ventricular arrythmias, rate control in atrial fibrillation?
class IV - CCBs
what are ADRs of CCBs/class 4?
cardiac - negative inotrope, AV node block, sinus arrest
non-cardiac - peripheral vasodilation, constipation
REVIEW: What’s the MOA of class I antiarrhythmics?
block sodium channels to slow depolarization during aP
REVIEW: What’s the MOA of class II antiarrhythmics?
block beta-adrenergic receptors to reduce HR and conduction velocity
REVIEW: What’s the MOA of class III antiarrhythmics?
block potassium channels, prolong repolarization, increase refractory period
REVIEW: What’s the MOA of class IV antiarrhythmics?
block calcium channels, slow AV node conduction, decrease HR
REVIEW: What’s the use of class I antiarrhythmics?
ventricular arrythmias and atrial fibrillation (1a, 1c)
REVIEW: What’s the use of class II antiarrhythmics?
afib, ventricular arrythmias, post-MI
REVIEW: What’s the use of class III antiarrhythmics?
atrial and ventricular arrythmias, especially when others fail
REVIEW: What’s the use of class IV antiarrhythmics?
afib and atrial flutter
What must be corrected before initiation of antiarrhythmics?
K, Mg, Ca
Can antiarrhythmics make some worse?
yes
Do antiarrhythmics interact with other drugs?
yes
What’s the MOA of adenosine?
stimulates adenosine receptors (a1) and decreases automaticity and AV node conduction – restoring normal sinus rhythm
What are indications of adenosine?
paroxysmal SVT (acute)
What are ADRs of adenosine?
flushing, dyspnea, AV nodal block, arrhythmia (PAC, PVC, afib)
What’s the MOA of digoxin?
inhibits Na/K ATPase pump, increasing contraction, slowing conduction
Does not control HR in exercise
Digoxin is ___ for AF or HF
2nd-3rd line
What are ADRs of digoxin?
N/V, visual disturbances, AV block (drug level monitoring is required)! narrow therapeutic index
What do these drugs work on:
- BBs
-CCBs
- adenosine
- digoxin
-antiarrhythmics (all except 1b)
AV nodal blocking drugs
What do these drugs do:
- antiarrhtmics 1A, III
- tricyclic antidepressants
- quinolones
- phenothiazines
-haloperidol (haldol)
- ondansteron (zofran)
QT prolonging drugs
