Acute Cardiac Flashcards
Digoxin Mechanism of Action
Sodium-Potassium ATPase blocker leading to inhibition of SNS and decreases automacity of AV node
Digoxin indications
Atrial fibrillation and heart failure
Control ventricular rate in patients with prolonged atrial fibrillation
Digoxin Adverse Drug Effects
Arrhythmias
Nausea and vomiting
Yellow/green visual auras
Types of Vasodilators and Examples

Hydralazine Indications and Mechanism of Action
Acute antihypertensive (IV)
4th line agent for chronic HTN
Used in conjunction with nitrates as chronic therapy in HFrEF
Mechanism of action is unknown, somehow cause smooth muscle relaxation resulting in arteriolar vasodilation
Minoxidil Indications and Mechanism of Action
4th line agent for chronic HTN
Increases Potassium channel activity in smooth muscle leading to membrane hyperpolarization and relaxation and arteriolar vasodilation
Minoxidil Adverse Effects
Hair growth
Calcium Channel Blockers Indications
Angina
Coronary artery spasm
HTN
Supraventricular arrhythmia (action at AV node—Verapamil, Diltiazem)
**No benefit in heart failure**
Nitrates Mechanism of Action
Mostly venodilation, some arteriolar dilation in coronary beds
Causes arteriolar dilation in face (flushing)
Decreases preload and at higher doses afterload
Sodium Nitroprusside Indications
Drug of choice for HTN emergency
Acute decompensated HF
Decreases both preload and afterload
Central α2 agonists Adverse Effects
Sedation
Rebound HTN with abrupt discontinuation
Diuretic drug classes and examples

Classes of antiarrythmic agents
▪Class I—Na + channel blockers
▪Class II—Beta-adrenergic receptor blockers
▪Class III—K + channel blockers
▪Class IV-Ca 2+ channel blockers
Quinidine Mechanism of Action
Blocks transmitter release from the vagus nerve
Can increase conduction velocity through the AV node
Quinidine Adverse Effects
Nausea, light headedness, headache, tinitis
Drug interaction with dixogen can lead to toxicity, need to monitor K+
Procainamide Indications
Supraventricular and ventricular arrhythmias
Conversion of new onset Afib to NSR,
Decrease likelihood of re-entry arrhythmias in acute MI
Can be used for VT—but not preferred drug
**Avoid with hyperkalemia (toxicity)
Procainamide Adverse Effects
Reversible SLE with chronic use
Prolonged QT
Torsades de pointes

Lidocaine Mechanism of Action and Indications
Alters the ventricular action potential by blocking Na+ channels which causes Na+ channels to remain open or inactive longer.
Can shorten repolarization, but DOES NOT prolong QT interval
Indicaitons: emergency ventricular arrhythmias, VT and PVC in stable patients
Lidocaine Adverse Effects
▪Slurred speech, tinnitus, hearing impairment, seizures, muscle twitching
▪Altered mental status, confusion
▪Blurred vision
▪Heart blocks
▪Altered AV conduction
Mexiletine Mechanism of Action and Indications
Blocks Na+ channels thereby altering ventricular action potential
DOES NOT prolong QT interval and it lacks vagolytic side effects
Indications: emergency ventricular arrhythmias
Mexiletine Adverse Effects
Nausea and tremor
Take with food to reduce side effects
Flecainide Indications and Contraindications
Indications: SVT, Atrial fibrillationn, PVC
Contraindications: structural heart disease and post MI
Should only be given to patients with normal EF
Flecainide Adverse Effects
Dizziness, headache, visual distrubance
Propafenone Mechanism of Action and Indications
Sodium channel blocker (most potent) with weak beta blocking activity
Indications: SVT, Atrial fibrillation, PVC
Should only be given to patients with normal EF
Propafenone Adverse Effects
Dizziness, disturbance in taste
Beta 1 vs Beta 2 receptors

Beta Blockers Adverse Effects
Hypotension
Bradycardia
AV block
Suppress hypoglycemia symptoms
First Generation Beta Blockers
Propranolol
Nonselective: Beta 1 and Beta 2
Second Generation Beta Blockers
Atenolol, Metoprolol
Relatively selective for Beta 1
Third Generation Beta Blockers
Labetolol, Carvedilol
Selective for Beta 1
Also cause vasodilation
Potassium Channel Blockers Examples
Amiodarone, Ibutelide, Dofetilide, Sotalol
Ibutelide Indications and Adverse Effect
Indications: atrial fibrillation and flutter
Adverse Effect: Prolonged QT–> Torsades de Pointes
Do NOT give to patients with pre-existing prolonged QT
Dofetilide Indications and Adverse Effects
Indicated only in Afib or Aflutter to NSR, can be used with depressed EF
Adverse effects: prolonged QT–> torsades de pointes
Sotalol Mechanism of Action and Indications
Mixed class II and III
▪Non-selectively antagonizes β-receptors (Class II action)
▪Blocks K+ channels (Class III action)
Indications: atrial fibrillation/flutter, severe ventricular arrhythmias
Sotalol Adverse Effects
Remember it has both class II and class III
Class II: fatigue, bradycardia
Class III: Torsades de Pointes
Amiodarone Class and Mechanism of Action
Mainly Class III but also acts as Class I, II, IV arrhythmic
Alteration of lipid membrane in which ion channels and receptors are located
Amiodarone Indications
▪Preferred drug for hemodynamically unstable ventricular tachycardia or fibrillation
▪Highly effective in prevention of recurrent parxosymal atrial fibrillation or flutter
▪Preferred drug in ACLS VT/VF algorithm
Amiodarone Adverse Effects
▪Bradycardia, AV block, HF
▪Pulmonary fibrosis
▪Hepatic failure
▪Thyroid dysfunction
▪Corneal microdeposits
▪Photosensitivity
▪Blue-gray skin
▪Neutropenia

Verapamil and Diltiazem Mechanism of Action
Calcium Channel Blockers: Class IV antiarrhythmic agents
Slow AP upstroke in AV nodal cells, leading to slowed conduction velocity through AV node
Verapamil and Diltiazem Indications and Adverse Effects
Used for treating paroxysmal SVT
Increases plasma digoxin level by competing with Digoxin for renal excretion
Administration of IV Verapamil in patients taking β-blockers can precipitate severe heart failure
Adenosine Adverse Effects
Very short half life (less than 10 seconds)
Bronchoconstriction, CP, flushing, excessive SA or AV nodal inhibition
Magnesium Indications
Replacement therapy, Digoxin toxicity
Drug of Choice for Torsades de Pointes
Vassopressor Definition
Agent that causes vascular constriction
Inotrope Definition
Agent that affects force of heart’s contraction
Chronotrope Definition
Agent that increases heart rate by affecting the electrical system and neuronal stimulation to the heart
Domotrope Definition
Agent that increases the conduction speed in the heart and AV node
Lusitrope Definition
Agent that increases diastolic relaxation
Bathmotropy Definition
Refers to myocardial excitability
Which receptors are vasoactive?
▪Catecholamine receptors
▪Dopamine receptors
▪Vasopressin receptors
▪Angiotensin II receptors
Catecholamine Receptors
Alpha 1 vs Alpha 2

Catecholamine Receptors
Beta 1 vs Beta 2 vs Beta 3

Dopamine Recpeptors
Promotes vasodilation
Promotes diuresis (because of vasodilation of renal arteries)
Vassopressin Recpetors

Angiotensin II (type I) receptors
Promotes vasoconstriction
Promotes aldosterone production
Promotes vasopressin release
Decreases renal blood flow
Phenylephrine Mechanism of Action
Works by stimulating alpha-1 adrenergic receptors in peripheral vasculature
Norepinephrine Mechanism of Action
Potent alpha-adrenergic agonist, with mild beta agonism
Acts as a potent vasoconstrictor, risk for tissue necrosis
Epinephrine Receptor Responses
Agonist for all types of adrenergic receptors
▪Lower concentrations—beta effects predominate
▪Increasing doses—alpha 1 agonism present
Dobutamine Mechanism of Action
Preferentially activates beta 1 receptors with 3 times more affinity than beta 2 receptors
Also has mild alpha agonist activity
Isoprotorenol Mechanism of Action
▪Synthetic non-selective beta-agonist
▪Increases inotropy
▪More chronotropic effect than Dobutamine
▪Less selective beta 2 agonism
▪No alpha activity
Dopamine Mechanism of Action
Acts directly on dopamine receptors in renal, mesenteric and coronary vascular beds causing vasoconstriction
Hemodynamic effects due to conversion into NE and Epi

Effects of Vasopressin
Increased free water resorption from collecting tubules in kidney
Vasoconstriction of peripheral vasculature
Which antihypertensives should you give with HF?
ACEI, BB, ARB, AA, Thiazide
Which antihypertensives should you give post MI?
ACEI, BB, AA
Which antihypertensives should you give with high CVD risk?
Thiazide, ACEI, BB, CCB
Which antihypertensives should you give with diabetes?
Thiazide, ACEI, ARB, CCB
Which antihypertensives should you give with CKD?
ACEI, ARB
Which antihypertensives should you give for recurrent stroke prevention?
Thiazide, ACEI
Relative contraindications for antihypertensive therapy
▪Hyperkalemia: Aldosterone Antagonists not good
▪Bradycardia: BB not recommended
▪Uncontrolled Asthma: BB not recommended
▪ESRD: HCTZ does not work
Pharm agent for atrial fibrillation rate control
BB, CCB, Digoxin
Also need antithrombotic therapy (warfain or aspirin 325)
Pharm agent for atrial fibrillation rhythm control
▪Flecainide, Propafenone (Class IC): Structurally normal hearts, younger patients
▪Amiodarone, Dofetilide, Sotalol (Class III): Structurally abnormal hearts or nomal hearts. Dose adjust Dofetilideand Sotalol for GFR. Monitor QTc.
▪Amiodarone: Usually used for older patients (risk of lung, liver, thyroid toxicities)
▪Ibutilide (Class III): IV; used for acute cardioversion
Pharm agent for atrial flutter rate control
BB, CCB, Digoxin
Pharm agent for atrial flutter rhythm control
Catheter ablation of the “Isthmus” in the right atrium
Pharm agents AVNRT
Acute: Adenosine, BB, CCB
Chronic: AV nodal blocking agent—BB, CCB, Digoxin can all be used
BB are by far the most commonly used
Ablation of slow pathway also option
Pharm agents AVRT
Acute: Narrow complex—>Adenosine. If wide complex, be careful that it is not VT
▪Slowing down AV node conduction—very dangerous
▪AV nodal blockers can be used in conjunction with Flecainide or Propafenone for rhythm control in AVRT
Pharm agents Monomorphic VT
Amiodarone (III)—Acute or Chronic setting
Sotalol also useful (Class III)
Lidocaine (IB) IV in acute MI (second line to Amiodarone)
Beta-blockers
Chronic Rx: Usually adjuncts to defibrillators—reduce shocks
Flecainide and Propafenone are Contraindicated (Class IC)
Class IA drugs are rarely used
Torsades de Pointes
▪Magnesium
▪Isoproterenol
▪Overdrive pacing
▪Shock
Angina Therapies
▪Anti-ischemic agents: Beta blockers, CCB, Nitrates
▪Anti-platelet agents: Aspirin, Clopidogrel or Thienopyridine if ASA intolerant
▪Lipid lowering therapy: Statin for LDLc < 100 or <70 mg/dL
▪Consider ACE-I or ARB for beneficial effect of CAD progression
What is MONA?
Morphine, oxygen, nitrate, aspirin
Given for acute STEMI
Acute STEMI management
- MONA
- Beta Blocker
- Reperfusion: PCI or thrombolytic
- Antithrombotics
Chronic STEMI/NSTEMI Management
▪Aspirin
▪Clopidogrel or other thienopyridine
▪For dual antiplatelet for any stent
▪For indication of NSTEMI or STEMI itself
▪Statin regardless of lipid level
▪BB
▪ACEI or ARB
Acute Decompensated HF management
- Diuresis
- Vasodilators
- Uptitrate HF meds
- Inotropes
Chronic HFrEF management
▪Beta-blockers
▪ACEI or ARB
▪Diuretic (usually loop)
▪Aldosterone antagonist—Class II or III Sx, ~ EF < 35%
▪Hydralazine + Nitrate—use also in patients who can’t tolerate ACEI or ARBs
▪Digoxin— helps reduce hospitalization
Chronic HFpEF management
▪Volume Control
▪BP control
Lipid lowering therapies
Statins are first line
Secondline (contraversial): colesevelam, niacin, ezetimibe
Elevated triglyceride management
Check for DM and hypothyroidism
If trigylcerides over 500: start fibrates and omega 3 fatty acids d/t risk for pancreatitis
Cardiac output =
Heart rate x Stroke volume