vasopressor and anti arrhythmics Flashcards
(99 cards)
1
Q
Medications used to raise blood pressure in cases of hypotension
o Medications that constrict blood vessels, raising blood pressure
o Used primarily in shock and critical care settings to manage hypotension
o Increase systemic vascular resistance (SVR) and/or cardiac output to improve perfusion to vital organs
A
vasopressors
2
Q
Drugs used to treat abnormal heart rhythms (arrhythmias)
o Aim to restore normal sinus rhythm, control heart rate, or prevent arrhythmia recurrence
A
anti-arrhythmics
3
Q
ability or property of muscle to shorten, or become reduced
in size, or develop increased tension
A
contractility
4
Q
influencing the contractility of muscular tissue (strength of
contraction)
A
inotropic
5
Q
drug causing constriction of blood vessels
A
vasopressor
6
Q
affecting the rate of rhythmic movements such as the
heartbeat (rate of contraction)
A
Chronotropic
7
Q
process of sodium excretion in the urine through the action of the kidneys
A
natriuresis
8
Q
amount of venous return to the ventricle
A
preload
9
Q
exert effect through α-1, β-1, & β-2
A
catecholamines
10
Q
enhanced myocardial contractility
A
B-1 stimulation
11
Q
vasodilation in vascular smooth muscle cells through
increased intracellular Ca2+ uptake
A
B-2 stimulation
12
Q
smooth muscle contraction and an increase in systemic
vascular resistance
A
α-1 Stimulation
13
Q
renal vasodilation through dopaminergic receptors in the kidney
A
D-1 and D-2 Stimulation
14
Q
First-line for septic shock
A
Norepinephrine (Levophed)
15
Q
Used in anaphylaxis and advanced cardiac life support (ACLS)
A
Epinephrine:
16
Q
Used for various shock states, with dose-dependent effects
A
dopamine
17
Q
Often adjunct in septic shock
A
vasopressin
18
Q
Pure α1 agonist, used in hypotension with a low heart rate
A
Phenylephrine
19
Q
inotropes
A
Dobutamine
Milrinone
20
Q
Preferred vasopressor in septic shock and ACLS post-ROSC
A
Norepinephrine (NE) (levophed)
21
Q
MOA:
o Large ↑ vasoconstriction and modest ↑ in CO
o Potent α-1 agonist effect (vasoconstriction) with modest β-1 agonist effect (increase
HR and contractility)
o Reflex bradycardia usually occurs in response to the ↑ MAP
A
Norepinephrine (NE) (levophed)
22
Q
ADR of Norepinephrine (NE) (levophed)
A
Prolonged NE infusion can cause direct cardiac toxicity
Arrhythmias, bradycardia, peripheral (digital) ischemia, HTN with non-selective BB
23
Q
Indications:
* Treatment of anaphylaxis, ACLS (asystole/PEA, pulseless VT/VF)
* 2nd-line agent in septic shock (after NE), management of hypotension after coronary artery bypast graft surgery (CABG)
A
Epinephrine (Epi) (Adrenaline)
24
Q
MOA:
* Potent β-1 agonist (cardiac stimulation) and moderate β-2 (bronchodilation) and α-1 agonists
o β effects > @ low doses
o α-1 effects > @ higher doses (vasoconstriction)
A
Epinephrine (Epi) (Adrenaline)
25
Effects:
* Low doses: ↑ CO and ↓ PVR
* β-1 inotropic and chronotropic effects
* β-2 and α-1 effects offset
* High doses: ↑ PVR and ↑ CO (alpha predominates at higher doses)
Epinephrine (Epi) (Adrenaline)
26
ADR of Epinephrine (Epi) (Adrenaline)
ADRs:
* Ventricular arrhythmias
* Severe HTN resulting in cerebrovascular hemorrhage
* Cardiac ischemia
* Sudden cardiac death
High and prolonged doses can cause direct cardiac toxicity
27
Indications: hemodynamic support and inotropic support in advanced heart failure
dopamine
28
MOA:
* Variety of effects depending on the dose
* Low dose (dopamine receptors)
* Moderate dose (beta-1)
* High dose (alpha-1)
* Most often used as a 2nd-line alternative to NE in patients with
absolute or relative bradycardia and a low risk of tachyarrhythmias
* Severe hypotension cardiogenic shock
dopamine
29
Low-dose: (1-5 mcg/kg/minute): Dopaminergic (D1 and D2
stimulation) dopamine
↑ renal blood flow and urine output (direct effects on renal tubules)
30
Intermediate-dose: (5-10 mcg/kg/minute): β-1 stimulation dopamine
↑ HR, cardiac contractility, and CO (positive inotropic + chronotropic
effects)
31
High-dose: (>10 mcg/kg/minute) α-1 activity dominates + some β-1 activity dopamine
Vasoconstriction, ↑ BP + ↑ HR,
cardiac contractility, and CO
32
Dopamine
ADRs
* Severe hypertension (especially in pts on nonselective β-blockers)
* Ventricular arrhythmias
* Cardiac ischemia
* Tissue ischemia/gangrene (high doses or due to tissue extravasation)
33
Indications: diabetes insipidus, esophageal variceal bleeding, and vasodilatory shock
* Precise role in vasodilatory shock not fully defined
* Primarily used as a 2nd-line agent in refractory vasodilatory shock (usually septic shock )
* Also used to reduce dose of 1st-line agent
Vasopressin (ADH = antidiuretic hormone)
34
MOA:
* Stimulates V1 (agonist = constriction of vascular smooth muscle) and V2
receptors (water reabsorption in renal collecting duct)
* Causes less direct coronary and cerebral vasoconstriction than
catecholamines
* Increased systemic vascular resistance and mean arterial blood pressure— may see HR and CO decrease in response (PNS engages and increases vagal tone = less ADH
Vasopressin (ADH = antidiuretic hormone)
35
Vasopressin (ADH = antidiuretic hormone)
ADRs:
* Arrhythmias
* Hypertension
* Decreased CO
* Cardiac ischemia
* Severe peripheral vasoconstriction causing ischemia (especially skin)
* Rebound hypotension following withdrawal
* Hyponatremia
36
Indications: (FYI): hyperdynamic sepsis, anesthesia-induced
hypotension
phenylephrine
37
MOA:
* Vasoconstriction with minimal cardiac inotropy or chronotropy (alpha-1 selective agonist)
* Potential disadvantage: may ↓ stroke volume, so reserved for pts in whom NE is contraindicated due to arrhythmias or who have failed other therapies
Not recommended for septic shock except in the following circumstances: 1) when
norepinephrine (preferred first-line agent) is associated with serious arrhythmias; 2)
when cardiac output is known to be high and BP persistently low; or 3) used as salvage therapy when the combination of vasopressor/inotropic agents and low-dose vasopressin fail to achieve target mean arterial pressure (MAP)
phenylephrine
38
Clinical use:
* Septic shock (NE)
* Cardiogenic shock (NE + dopamine)
* Anaphylaxis (Epi)
* HOTN with bradycardia
vasopressor summary
39
vasopressor ADR
* Tachycardia, arrhythmias
* Peripheral ischemia
* HTN
Monitoring: continuous BP monitoring, urine output, titrate based on clinical
response
40
Indications:
* Medically refractory heart failure and cardiogenic shock (low cardiac output)
* Can be given for palliative measures for end-stage HF, cardiogenic shock, short-term bridge to
transplant
* Also used in ACLS (post-ROSC) and cardiac stress echo
dobutamine
41
MOA:
* Primarily β-1 agonist, some β-2 and α-1 agonism
* Potent inotrope: ↑ Contractility, HR, and CO
* NOT a vasopressor, but an inotrope that causes vasodilation (↓SVR)
* Vasodilation at normal doses
* Vasoconstriction progressively dominates at higher infusion rates
* Significantly ↑ myocardial oxygen consumption (stress test)
* Tolerance can develop after just a few days of therapy
* Adrenergic receptors become desensitized and downregulated
dobutamine
42
Dobutamine
ADRs:
Tachycardia
* Cardiac ischemia
* Proarrhythmic (Atrial Fibrillation, Ventricular Tachycardia)
* *can occur at any dose*
43
Phosphodiesterase-3 Enzyme (PDE) inhibitor
Indications: Inotropic support in heart failure or in heart transplant recipients
* VERY useful if adrenergic receptors are downregulated or
desensitized (usually in chronic HF or after chronic β-agonist
administration)
* Recommended inotrope if patient is not on a beta blocker and not
hypotensive
Milrinone
44
MOA:
* Potent inotrope and vasodilator: ↑ Contractility and vasodilation
* Effects similar to those of dobutamine but with a lower incidence of dysrhythmias
* Vasodilatory effects limit use in hypotensive pts
Milrinone
45
Depolarization: voltage gated Na channels open
phase 0
46
initial repolarization:
- voltage gated Na channels close
- voltage gated K channels begin to open
phase 1
47
Plateu:
- voltage gated Ca channels open
- K efflux continues
- myocytes contraction
Phase 2
48
Rapid repolarization:
- voltage gated Ca channels close
- slow voltage gated K channels open
phase 3
49
resting permeability
- High K permeability
phase 4
50
what medication is used at phase 0
Class 1: Na channel blocker
51
what medication is used at phase 2
class 4: Ca channel blocker
52
what medication is used at phase 3
class 3: K channel blocker
53
what medication is used at phase 4
class 2: beta blocker
54
the relative refractory period coincides with what wave
T wave
55
* Ia = Disopyramide (Norpace), Quinidine, Procainamide (Pronestyl)
* Ib = Lidocaine (Xylocaine), Mexiletine (Mexitil, fast dissociation)
* Ic = Flecainide (Tambocor), Propafenone (Rhythmol, slow
dissociation)
Class I: Na+ channel blockers
56
Metoprolol (Toprol), Atenolol (slow HR and
conduction)
Class II: β-blockers
57
Amiodarone (Cordarone, Pacerone),
Dofetilide (Tikosyn, prolong action potential), Ibutilide (Corvert), Sotalol
(Betapace
Class III: K+ channel blockers
58
Diltiazem
(Cardizem), Verapamil (Calan) (slow AV conduction
Class IV: non-dihydropyridine calcium channel blocker
59
* Drugs are characterized by ability to block sodium entry into
the cell during depolarization
* This decreases the rate of rise of phase 0 of the action potential
* These drugs also suppress automaticity of the Purkinje fibers
and bundle of His
Sodium Channel Blockers
Class I drugs are sodium channel blocker
60
* Drugs: Quinidine, Procainamide,
Disopyramide
* MOA: Slow the rate of rise of phase 0 by
prolonging duration of action potential and
increases the effective refractory period of
the ventricle
* Large block of both open Na & K Channels at
normal heart rates, hence both QRS & QT
affected
Class Ia Drugs
61
Indications: Treatment of ventricular and atrial arrhythmias in patients without a history
of ischemic heart disease
ADRs:
* Increased arrhythmias including torsades
* Hypotension
* Tinnitus, headache
* lupus-like syndrome***
Quinidine: used primarily for malaria, but not arrhythmias due to ADRs, proarrhythmic &
better drug options available
Procainamide: Hypotension common with IV
Class Ia Drugs
62
Drugs: Lidocaine (IV), Mexiletine (PO)
MOA: shorten action potential duration (APD) and refractory period of the Purkinje fibers
* These drugs decrease the duration of action potential during phase 0 depolarization in the Purkinje fibers (conducting fibers in the heart) and ventricular muscles**
* High affinity for open & inactivated Na channels
Class Ib Drugs
63
Indications: treatment of ventricular arrhythmias (ventricular tachycardia,
ventricular fibrillation, and ventricular ectopy)
* Lidocaine: 2nd-line (vs Amiodarone) to terminate VTach and prevent VFib after defibrillation
* Used only in a hospital/EMS setting (IV only)
* Ineffective against atrial arrhythmias
ADRs: Central nervous system (CNS): confusion, change in vision,
drowsiness
Class Ib Drugs
64
Drugs: Propafenone, Flecainide
MOA: greatest effect on the early
depolarization; less of an effect on the refractory period of the ventricle
* Blocks open Na channels & very slow unbinding during diastole, QRS markedly prolonged during NSR
- wide QRS
Class Ic Drugs
65
Indications:
* Supraventricular arrhythmias in patients without structural heart
disease
* Also useful in chronic suppression of ventricular arrhythmias
ADRs: Better tolerated than Ia and Ib
* Increased arrhythmias
* CNS (dizziness, visual disturbances, headache) Increased mortality in patients with MI, can worsen H
Class Ic Drugs
66
Drugs: Propranolol, Atenolol, Esmolol, Metoprolol
MOA: cardiac β-1 receptor blockade and reduction in cAMP
* Results in a modest reduction of both sodium and calcium currents
and suppression of abnormal pacemakers
* Rhythm stabilization MOA is unknown
* Results in cardiac membrane stabilization**
* Conduction through SA and AV nodes is slowed and the
refractory period is increased**
Class II Drugs: Beta Blocker
67
Indications:
* Prevent re-infarction & sudden death in patients with heart failure or myocardial infarction
* Treat exercise-induced arrhythmias
* Prevent occurrence of AV node reentry (e.g. patients with paroxysmal supraventricular tachycardia)
* Control ventricular rate in patients with supraventricular tachyarrhythmias by
increasing the AV node effective refractory period
ADRs: Bronchospasm, cardiac depression, AV block**, hypotension
Class II Drugs
68
Drugs: Amiodarone, Sotalol, Dofetilide, Ibutilide
MOA:
* Prolong/delay repolarization**
* Sometimes designated as potassium channel blockers, actually delay K efflux
* Drugs show complex pharmacological properties
* Classified together because all prolong APD without altering phase 0 depolarization or the resting membrane potential
Prolong QT (Amiodarone the least)
Sotalol also BB
Class III Drugs: Potassium Channel Blocker
69
Indications:
* Amiodarone: Drug of choice for acute treatment of ACLS VT and VF; slow ventricular rate and convert AF
* Atrial Fibrillation
* Safe in concomitant heart failure***: amiodarone and dofetilide
ADRs:
* QT prolongation, Torsades de pointes ****
Amiodarone and Dofetalide are the only two antiarrhythmics shown to not increase mortality with long term use in patients with structural heart damage
(post MI, HFrEF)
Class III Drugs
70
toxicity of amiodarone (GI) adverse effects
nausea, vomiting
71
toxicity of amiodarone (Pulmonary) adverse effects
pulmonary fibrosis
72
toxicity of amiodarone (endocrine) adverse effects
hyperthyroidism, hypothyroidism
73
toxicity of amiodarone (opthalmologic) adverse effects
corneal microdeposits
74
toxicity of amiodarone (hepatic) adverse effects
hepatotoxicity
75
half life of amiodarone
52 days
76
what to check at baseline before amioderane
* PFT, CXR, thyroid panel, lipid profile, EKG, eye exam, CBC, BMP,
neuro and dermatologic exams
* BMP watching for K+ and Mg++ when on an antiarrhythmic to avoid
QT prolongation
o K+ goal 4, Mg++ goal 2
77
what does amiodarone inhibit
CYP3A4, 2C9, 1A2, 2D6, and p-glycoprotein
78
Drug Interactions with Amiodarone
warfarin (reduce warfirn dose by 50%)
digoxin (reduce digoxin dose by 25-50%)
79
Drugs: Diltiazem and Verapamil
MOA: slow conduction through the AV node and increase the effective
refractory period in the AV node
* Block the slow inward calcium current during phases 0 and 2 of the
cardiac cycle
* Slowing the inward calcium current, slows conduction and prolongs effective refractory period
* Inhibits SA and AV nodes thus prolonging PR
Class IV: Calcium Channel Blockers
80
Indications: more effective against atrial than ventricular arrhythmias
* Rate control in atrial fibrillation
ADRs:
* Cardiac: negative inotrope, AV node block, sinus arrest
* Non-cardiac: peripheral vasodilation, constipation
Class IV Drugs
81
Block sodium channels to slow depolarization during action potentia
class 1
82
Block beta-adrenergic receptors to reduce heart rate and conduction
velocity
class 2
83
Block potassium channels, prolong repolarization, and increase the
refractory period
class 3
84
Block calcium channels, slow AV node conduction, and decrease heart rate
class 4
85
Used for ventricular arrhythmias (Ia, Ic) and atrial fibrillation (Ia, Ic)
class 1
86
Indicated for atrial fibrillation, ventricular arrhythmias, and post-myocardial
infarction
Class II (Beta-blockers
87
Used for atrial and ventricular arrhythmias, especially when
other drugs fail
Class III (Potassium channel blockers
88
Effective for atrial fibrillation and atrial flutter
Class IV (Calcium channel blockers
89
Class I:
Ia ADR
Quinidine (tinnitus, headache, vision changes, thrombocytopenia, lupus-like syndrome)
90
Class I:
Ib ADR
Lidocaine (CNS effects, confusion, seizures)
91
Class I:
Ic ADR
Flecainide (pro-arrhythmic, especially in structural heart disease)
92
Class II (Beta-blockers) ADR
Bradycardia, hypotension, bronchospasm
93
Class III (Potassium channel blockers) ADR
QT prolongation, Amiodarone: Pulmonary fibrosis,
thyroid abnormalities, hepatotoxicit
94
Class IV (Calcium channel blockers) ADR
Bradycardia, AV block, hypotension
95
special considerations for anti arrhythmics
* Electrolyte Imbalances: Potassium, magnesium, and calcium levels must be
corrected before initiation
* Pro-arrhythmic Effects: Some anti-arrhythmic medications can worsen arrhythmias
in certain patients
* Drug Interactions: Many anti-arrhythmic drugs interact with other medications (e.g.,
amiodarone with warfarin, statins)
96
MOA: Stimulates adenosine receptors (A1) in
heart, decreases automaticity and AV node
conduction
* Slows conduction time through the AV node,
interrupting the re-entry pathways through the
AV node, restoring normal sinus rhythm
Indications: paroxysmal SVT (acute)
* Half-life <10 seconds
ADR: Flushing, dyspnea, AV nodal block,
arrhythmia (can develop PACs, PVCs, Afib)
adenosine
97
MOA:
* Partially inhibits Na+/K+-ATPase pump, thus increases contraction
* Parasympathetic action in AV node = slows conduction
* Does not control heart rate during exercise
Indications: 2nd -3rd line for AF or heart failure
ADRs:
* Toxicity: N/V, visual disturbances (blurred vision/halos), AV block
(Drug level monitoring required!)
* Narrow Therapeutic Index
Digoxin
98
AV Nodal Blocking Drugs
* Beta-blockers
* Calcium channel blockers = Verapamil & diltiazem
* Adenosine
* Digoxin
* Antiarrhythmics
* All but class IB (lidocaine & mexiletine
99
QT-Prolonging Drugs
* Antiarrhythmics: 1A, III
* Tricyclic antidepressants
* Quinolones
* Phenothiazines
* Haloperidol (Haldol)
* Ondansetron (Zofran)
