Pharm Cardiology Exam 1 Flashcards
Most common first line Medication
Ace inhibitor
-Pril
Most common side effects for Ace
Cough
Angioedema
Types of diuretics
Loop
Osmotic
K+ Sparring
Thiazides
MOA of Loop Diuretics
Inhibit the Na / K / Cl transporter at the thick ascending loop of Henle
MOA of Osmotic diuretics
Promote osmotic diuresis
MOA of K+ Sparring Diuretics
Antagonize the actions of aldosterone to affect Na+/K+ exchange
MOA of Thiazide diuretics
Inhibit reabsorption by Na+/Cl transporter at distal tubule
Common Loop Diuretics
Bumetanide
Furosemide
Torsemide
Common osmotic diuretics
Mannitol
Glucose
Common K+ sparring Diuretics
Spironolactone
Eplerenone
Common Thiazide diuretics
HCTZ
Metolazone
Acetazolamide location of action
PCT
Pulls sodium bicarb out of tubule
Osmotic diuretic location of action
Pulls H2O out of
PCT
descending loop
Collecting duct
Location of action of loop diuretics
Thick ascending loop of henle
Pulls K+, CA2+, Mg2+, NA+
out of tubule
Thiazide location of action
Proximal tubule/ descending loop
DCT
Pulls NaCl out of tubule
Location of action of aldosterone antagonists
Collecting duct
Pulls NaCl out of Collecting duct
Beta Blocker
Non selective
B1 & B2
Nadolol
Propranolol
Timolol
Sotalol
Beta Blockers
Cardio selective
B1
Atenolol Metoprolol Esmolol Betaxolol Bisprolol Nebivolol
Beta Blockers
Mixed
A1 & B1 & B2
Carvedilol
Labetalol
Beta Blockers
Mortality benefit for HFrEF
Carvedilol
Metoprolol Succinate
Bisoprolol
Beta Blockers
With ISA
Acebutolol
Pindolol
(Associated with less resting bradycardia)
Contraindications for beta blockers
Asthma
Liver disease
Calcium channel blockers
2 types
Dihydropyridine
-dipines
Non dihydropyridine
Calcium Channel Blockers
Dihydropyridines
-dipines
Amlodipine Felodipine Nicardipine Nifedipine Nimodipine
Calcium Channel Blockers
Non Dihydropyridines
Di-Ver
Diltiazem
Verapamil
Common side effects of Calcium Channel Blockers
Dizzy HA Edema (pedal edema) Constipation Facial redness Gingival overgrowth Altered HR
Digoxin
+ Ionotrope (increased contraction)
- Chronotrope (slows heart rate)
- dromotrope (decreased AV node conduction)
For SVT , afib/aflut, cardiogenic shock and HF
Cardiac glycoside
Antidote is digibind
Therapeutic range is 0.5-2
monitor for toxicity
S/S of tox = N/V, dysrhythmias, vision changes (yellow/green hue & halos)
Vasodilators
Nitroglycerine
Sodium nitroprusside
Unstable angina tx
Always treat as if having an MI
Stable angina Tx
Manage dyslipidemia
Stain (improves mortality)
Antiplatelet
ASA
Beta blocker
Slow the heart, allow for increased ventricular filling and reduce oxygen demand
Calcium channel blocker
Reduce afterload and contractility and dilate coronary arteries (not nifedipine due to reflex tachycardia)
Nitroglycerine
Decrease preload, dilate cornary arteries (Acute or chronic use)
PCI/CABG
Most common adverse reaction to statin is
Increased LFT’s
Check AST/ALT and AP at baseline
High intensity statins
Atorvastatin
Rosuvastatin
LDL Goal is <70
Preferred Med for initial treatment and prevention of anginal symptoms
Beta Blockers
Calcium channel blockers and long acting nitrates are alternatives if Beta Blockers are contraindicated
Angina Treatments
Lifestyle mods Sublingual Nitro Long acting Nitrates (isosorbide mononitrate) Beta Blockers ACE (for unstable and s/s of HF) CCB (considered alternative to BB)
Angina treatment
with Beta blockers effects
HR / BP / MOA
Decrease in HR
Decrease in BP
Decreased Pump function
Angina treatment
with Calcium Channel Blockers
HR / BP / MOA
Decrease in HR
Decrease in BP
Decreased Pump function + vasodilation
Angina treatment
with Nitrates
HR / BP / MOA
Increased HR
Decreased BP
Vasodilation
Angina treatment
with Ranolazine (ranexa)
HR / BP / MOA
No change in HR
No change in BP
Reduces Cardiac Stiffness
Ranolazine
Ranexa
Chronic stable angina
can be used with BB, nitrates, CCB, ACE, ARB, Anti platelet and lipid lowering therapies.
Contra:
Liver cirrhosis
Warnings:
Not for acute angina or Diabetes
Adverse:
Prolonged QT, Dizziness, headache, constipation, nausea
Ranolazine (Ranexa)
MOA
Inhibits the late inward sodium current
Prevents diastolic stiffness and thereby preserves myocardial blood flow.
Vasospastic angina (Prinzmetal)
Calcium channel blocker
Start with diltiazem
Sublingual nitro
in an attempt to decrease the frequency of myocardial infarction and life threatening arrhythmia
Nonselective beta blockers
such as propranolol should be avoided
ACS encompasses
STEMI, NSTEMI, Unstable angina
Unstable angina treatment
Reduce progression to Acute MI
Antiplatelet - ASA
Beta blockers
ACE
Statin
Revascularization
Absolute contraindications to thrombolytics
Known intracranial neoplasm Active internal bleeding Suspected aortic dissection Recent head trauma History of Hemorrhagic CVA Major surgery or trauma <2 weeks
C B D T S S
Cocaine related ACS
Benzos
Lorazepam 2-4 mg IV q 15 mins
as needed to relive symptoms
DO NOT GIVE BB
Nitroglycerine
Acute relief of angina
Acute prophylaxis of angina
Dose: 0.4mg tab
1 tab sublingual at onset, q 5mins x 3
(max=3 tabs in 15mins)
Contraindications:
Severe anemia, Increased ICP, TBI, Cerebral hemorrhage, Acute circulatory failure or shock. PDE-5 use.
Interactions:
PDE-5
Adverse reactions:
HA, dizzy, paresthesia, vertigo, weakness, palpitations, postural hypotension, syncope
Beta blockers
Improves symptoms by decreasing HR and contractility
Decrease myocardial oxygen consumption
Increase ventricular diastolic filling
Decrease cardiac output gradient
Metoprolol Tartate
Lopressor (immediate release)
Cardioselective Beta blockers
For use in stabilized patients after MI to reduce mortality
Contra:
All Heart blocks, BP under 100, HR under 45
Moderate/Severe cardiac failure
Warning:
Avoid abrupt discontinuation in ischemic heart disease
Adverse reactions:
Fatigue, dizzy, depression, hypotension (discontinue), bronchospasm, heart block
Fibrinolytics
Thrombolytics
Alteplase Reteplase Tenecteplase Streptokinase Anistreplase
Alteplase
Treatment of acute myocardial infarction to reduce mortality and the incidence of heart failure
Interactions:
Increased risk of bleeding with anti-coags, anti platelets. Angioedema risk with ACE
Adverse:
Bleeding (fatal)
Antiplatelet drugs
Cox inhibitors
ASA
ADP inhibitor Clopidogrel Ticlopidine Prasugrel Ticagrelor
GP IIB/IIIA inhibitor
Abciximab
Eptifibatide
Tirofiban
Anti coagulants
Vitamin K antagonists
Warfarin
Thrombin inhibitors (direct) Dabigatran Argatroban Hirudin Bivalidurin
Thrombin Inhibitors (indirect) Heparin Enoxaparin Dalteparin Tinzeparin -Xabans
GP IIB / IIIA antagonists
Abciximab (irreversible)
Eptifibatide (reversible)
Tirofiban (reversible)
HFrEF
The goals of management is to reduce morbidity
(including reducing symptoms, improving health-related quality of life and functional status, and decreasing the risk of hospitalization),
and to reduce mortality.
ACE MOA (Chart)
Stops angiotensin I from converting to angiotensin II
Renin inhibitors (Chart)
Stops renin from converting to angiotensin I
Spironolactone MOA (Chart)
Helps stop cardiac remodeling
Beta Blocker MOA (Chart)
Helps stop cardiac remodeling
Suppress renin secretion
Digoxin MOA (Chart)
Increases cardiac output
improves CO and decreases HF (ionotropics)
Diuretics MOA (Chart)
Decrease NA+ and H2O retention
Vasodilators MOA (Chart)
Decreases vasoconstriction
AT1 receptor antagonists (ARB) (MOA) (Chart)
Decrease cardiac remodeling
Inhibits angiotensin from converting to aldosterone
Decreases vasoconstriction
MOA of ACE Inhibitors (-prils)
inhibit the activity of angiotensin-converting enzyme
Stops angiotensin I from becoming angiotensin II
There by decreasing the formation of angiotensin II, a vasoconstrictor, and increase the level of bradykinin, a peptide vasodilator
Causes relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart
MOA of ARB (-sartans)
Drugs that bind to and inhibit the angiotensin II receptor type 1 (AT1)
and thereby
block the arteriolar contraction and sodium retention effects of renin–angiotensin system
Angiotensin receptor neprilysin inhibitor
ARNI
Sacubitril / valsartan
Entresto
Inhibit BNP breakdown
What medications raise levels of kinins which may have beneficial hemodynamic effects but also increase the risk of angioedema and dry cough.
ACE inhibitor and ARNI (but not single agent ARB)
Angiotensin receptor neprilysin inhibitor
ACE and ARB MOA in HF
Vasodilation
Reduce cardiac preload and afterload which improves systolic function and CO
Facilitate salt and water excretion by complex effects on the kidneys (attenuation of aldosterone effect)
ACE inhibitors and ARBS reduce LVH, Myocardial fibrosis and stiffness
Lisinopril
Reduce symptoms of systolic HF
Contraindications
History of ACE associated or other angioedema
Warning:
Fetal Toxicity
Adverse reactions
HA, cough, angioedema, dizzy, hypotension, chest pain, hyperkalemia, renal impairment
Valsartan
HF (NYHA class II-IV) Reduce cardiovascular mortality in stable post MI patients with LV failure or dysfunction
Contra:
Concomitant aliskiren in patients with diabetes
Warning:
Fetal toxicity
Adverse:
Dizzy, hypotension, diarrhea, arthralgia, back pain, fatigue, hyperkalemia
Beta blockers that improve mortality in HFrEF
Carvedilol (coreg) Metoprolol Succinate (Toprol XL) Bisoprolol fumerate (Zebeta)
Carvedilol
Non-cardioselective BB / Alpha 1 blocker (Coreg)
Mild to severe heart failure, increase survivability and reduce hospitalization risk.
Reduce post MI mortality with left ventricular EF <40%
Contraindications
Cardiogenic shock, decompensated HF,
Asthma with bronchospasms, 2nd/3rd degree AV blocks, sick sinus syndrome, severe bradycardia (unless paced)
Adverse:
dizzy, edema, hypotension, syncope, bradycardia, AV block
Aldosterone antagonists
Spironolactone
Eplerenone
(K+ sparring)
Aldosterone antagonist MOA
mineralocorticoids
Has diuretic and blood pressure lowering effects, raises serum potassium concentration via reduced urinary potassium loss
Side effects:
spironolactone has anti-androgen effects such as erectile dysfunction and gynecomastia in men
(use eplerenone in men)
Spironolactone
K+ sparring diuretic
NYHA class III–IV HF and reduced ejection fraction to increase survival, manage edema, and reduce the need for hospitalization for HF, when used in addition to standard therapy.
Contra:
Hyperkalemia, Addison’s disease, concomitant eplerenone
Warnings:
Hyperkalemia in renal patients
Interactions:
Severe hyperkalemia with K+ supplements
Adverse:
Gynecomastia, GI upset, Hyperkalemia
Sacubitril / Valsartan (entresto)
Neprilysin inhibitor + angiotensin II receptor blocker
Dose: 49mg/51mg BID (initial)
To reduce risk of cardiovascular death and hospitalization for heart failure in patients with chronic heart failure (NYHA Class II–IV) and reduced ejection fraction; usually given with other therapies, in place of an ACEI or other ARB. To treat symptomatic heart failure with systemic left ventricular systolic dysfunction in children aged ≥1 year.
Contra:
History of angioedema, Concomitant ACE or aliskiren use.
Warning
Fetal toxicity
Adverse
Hypotension, hyperkalemia, cough, angioedema, renal failure
Vasodilators Doses
Hydralazine
Hydralazine
(25-50mg TID-QID)
(Target=300mg QD)
Vasodilators Doses Isosorbide dinitrate (ISDN)
Isosorbide dinitrate
(20-30mg TID-QID)
(target=120mg QD)
Isosorbide dinitrate and hydralazine
Indications
Bidil
The combined use ofhydralazineand nitrates reduces cardiac afterload and preload, and may also enhance nitric oxide bioavailability.
Indicated when
ACE and ARBS are contraindicated (i.e. renal failure)
Systolic dysfunction
Acute episodes of CHF (via preload and afterload reduction)
Indicated for black patients
Digoxin side effects
Dizzy HA Blurred vision Yellow or green vision AV / SA block PR prolongation ST Depression Diarrhea
Digoxin MOA
Inhibits the NA+ K+ ATPase pump
Digoxin indications
Severe systolic dysfunction
Used as an inotrope (does not reduce mortality but does reduce hospitalizations)
Positive pressure ventilation
Digoxin
Cardiac Glycoside
Mild-to-moderate heart failure (with a diuretic and an ACE inhibitor when possible). Increase myocardial contractility in pediatrics with heart failure
Contra
V-Fib
Dilated cardiomyopathy
Most common type 95%
Common cause = ETOH
Diagnostics
Chest X ray for cardiomegaly
Echo for LV dilation and dysfunction
(high diastolic pressures with low CO)
Treatment:
Treat underlying cause or offending agent
Hypertrophic cardiomyopathy
Massive septum hypertrophy
small left ventricle
diastolic dysfunction
Usually autosomal dominant, genetic or chronic hypertension
Diagnostics
Echo
LVH, asymmetrical septal hypertrophy, small LV, diastolic dysfunction
Positive iontropes
Dopamine dobutamine epi/norepi Digoxin PDE inhibitors (milrinone) Glucagon Insulin Amiodarone
Negative iontropes
Beta Blockers
Calcium channel blockers
Class 1A antiarrhythmics (Quinidine, procainamide)
Class 1C antiarrhythmics (flecainide)
If the patient has contraindications to a beta blocker (eg, reactive airway disease) in Hypertrophic cardiomyopathy
Monotherapy with a nondihydropyridine calcium channel blocker can be considered
or,
in the appropriate patient, proceeding directly to combination therapy with an atrioventricular nodal blocking agent anddisopyramide.
Beta blocker treatment for patients with left ventricular dysfunction
Start at very low doses and gradually increase if lower doses are well tolerated
Start as soon as LV dysfunction is diagnosed
Calcium channel blocker drugs
Dihydropyridines -dipines Amlodipine Felodipine Nicardipine Nifedipine Nimodipine
Non dihydropyridines
“di-ver”
Di - Diltiazem
Ver - Verapamil
Calcium channel blocker drugs
Dihydropyridines
-dipines Amlodipine Felodipine Nicardipine Nifedipine Nimodipine
Calcium channel blocker drugs
Non dihydropyridines
“di-ver”
Di - Diltiazem
Ver - Verapamil
Calcium channel blocker drugs
Non dihydropyridines
“di-ver”
Di - Diltiazem
Ver - Verapamil
Verapamil
CCB
Non dihydropyridine
Contraindications
Severe left ventricular (LV) dysfunction or LV dysfunction treated with β-blockers.
Moderate to severe heart failure. Hypotension. Cardiogenic shock. Sick sinus syndrome, 2nd- or3rd-degree AV block,
Diltiazem
Cardizem
CCB
Non dihydropyridine
Vasospastic or chronic unstable angina
Contra
sick sinus syndrome, 2nd- or3rd-degree AV block (unless paced), hypotension
Adverse
Edema, HA, fatigue, dizzy, asthenia, 1st degree AV block, bradycardia
disopyramide indications
use in combination with BB or CCB
Negative inotrope (for CHF and CM)
Anti-arrhythmic
disopyramide contraindications
Cardiogenic shock.
2nd- or 3rd- degree AV block, unless paced.
QT prolongation
Hypertrophic cardiomyopathy treatment
Avoid strenuous exercise, sports, dehydration
Do not give diuretics, ACE, Vasodilators or positive inotropes
Screen 1st degree relative with EKG and Echo
Stress induced cardiomyopathy
transient regional left ventricular dysfunction in the absence of significant coronary artery disease
Causes may include
catecholamine excess, microvascular dysfunction, and multi-vessel coronary artery spasm
Generally a transient disorder managed with supportive therapy. Conservative treatment and resolution of physical or emotional stress usually results in rapid resolution of symptoms
Restrictive cardiomyopathy
Secondary / infiltrative causes include
Amyloidosis
Sarcoidosis
Treatment
Relieve congestive symptoms with loop diuretics
Antiarrhythmics Class 1a
Medications
Intermediate dissociation
Procainamide
Disopyramide
Quinidine
P D Q
Antiarrhythmics Class 1b
Medications
Rapid dissociation
Lidocaine
mexilitine
Antiarrhythmics Class 1c
Medications
slow dissociation
Propafenone
Flecainide
Antiarrhythmics Class IIa
Medications
(non selective)
Beta blockers
non selective
Carvedilol
propranolol
nadolol
Antiarrhythmics Class III
Medications
K+ channel blockers and openers
Antiarrhythmics Class IIIa
Medications
Voltage dependent K+ channel blockers
Amiodarone dronedarone dofetilide ibutilide sotalol
Antiarrhythmics Class IV
Medications
Ca2+ handling modulators
Antiarrhythmics Class IIa
Medications
(selective)
Beta Blockers
selective
atenolol bisoprolol betaxolol celiprolol esmolol metoprolol
Antiarrhythmics Class IVa
Medications
Surface membrane Ca2+ channel blockers
Diltiazem
verapamil
Antiarrhythmic drug class mneumonic
PDQ = Police department questions LM = Liquored man FP = For peeing BB = Behind building ADSID = After drinking scotch in dark DV = Dirty vehicle
Ia = procainamide, disopyramide, quinidine Ib = lidocaine, mexilitine Ic = Flecainide, propafenone II = Beta blockers III = Amiodarone, dronedarone, sotalol, ibutilide, dofetilide IV = Diltiazem, verapamil
Atropine
Mechanism of Action
inhibits the muscarinic actions of acetylcholine on structures innervated by postganglionic cholinergic nerves, and on smooth muscles, which respond to endogenous acetylcholine but are not so innervated
Atropine ACLS
Bradycardia
0.5mg IV q3-5min PRN
Heart block poem
1st degree
If the R is far from P,
then you have a first degree
Heart block poem
2nd degree type 1
Longer longer longer drop,
then you have a Wenkebach
Heart block poem
2nd degree type 2
If some P’s don’t get through,
then you have a Mobitz 2.
Pacemaker for you
Heart block poem
3rd degree
If the p’s and Q’s don’t agree,
then you have a 3rd degree
2 types of broad afib
Newly diagnosed Afib
decisions regarding anti-coag treatment, and rate and rhythm control strategies
Previously diagnosed and managed afib
Periodic assessments of the adequacy of treatment
TEE to check for clot in left atrial appendage
Don’t cardiovert if clot present (could dislodge)
Start on lovenox if clot present (reevaluate in 1 month)
New onset afib
prevention of systemic embolization
The choice between rhythm and rate control strategy, both of which may improve symptoms
Anti-coag therapy for nonvalvular afib patients
Warfarin dabigatran rivaroxaban apixaban edoxaban
Reduce the risk by almost 70% (embolization)
INR
International normalized ratio
therapeutic range usually between 2 and 3
Most patients who present with afib will require
slowing of ventricular rate to improve symptoms
(afib with RVR is really just uncontrolled afib)
Treatment then focuses on
normalizing ventricular rate (60-99bpm)
to decrease symptoms and restoring NSR
TEE
Treatment guided by the presence or absence of left atrial thrombus on TEE and the presence of HF
Patients with thrombus or at high risk of thrombus formation including history of a fib >48hrs should be treated with
Anticoagulants Heparin or lovenox and warfarin or dabigatran and rate control for 3-4 weeks before attempting cardiovert
Patients with afib and with no thrombus and at low risk for thrombus formation can be treated with
cardioversion once anticoagulation with heparin is established
Rate control of afib
In presence of HF
digoxin or amiodarone
In absence of HF
IV beta blockers (metoprolol, propranolol, or esmolol)
or
dihydropyridine Calcium channel blockers
Chronic rate control strategy in patients with afib
Generally use drugs that slow conduction across the AV node such as
Beta blockers
non-dihydropyridine calcium channel blockers or digoxin
Cardioversion of unstable patients with afib
For a patient who is hemodynamically unstable due to afib and is at low risk for thrombus and aspiration,
Urgent cardioversion is recommended
Cardioversion of stable patients with afib
Most patients with afib do not need emergent cardioversion.
rate slowing will often improve symptoms
Best to defer cardioversion until anti-coag treatment with heparin is initiated.
For select stable patients, the restoration of sinus rhythm with either electrical or pharmacological cardioversion is necessary or reasonable
Most patients with whom cardioversion is chosen will need
the ventricular rate controlled and the need for anti-coag assessment prior to cardioversion
For patients with no structural heart disease
(including no evidence of CAD)
Flecainide or propafenone is the recommended pharmacological choice
Rhythm therapy in afib patients
Beta blockers are modestly effective in maintaining NSR and can be tried first in select patients.
(those without structural heart disease or who are concerned about proarrhythmic)
Compared to placebo
amiodarone, sotalol, dofetilide, dronedarone, fecainide, and propafenone are effective for the maintenance of sinus rhythm.
(maintenance rates at one year are significantly less than 75 %)
Amiodarone is consistently more effective than the other antiarrhythmic drugs
Rhythm therapy
in patients with no structural heart disease and no apparent risk for drug induced brady/tachycardia
flecainide or propafenone is recommended as the preferred antiarrhythmic
Amiodarone, dofetilide, dronedarone or sotalol may be used
For patients with HF Amiodarone is recommended.
Side effects of Amiodarone
T =
Thyroid = hyper or hypo (iodine in amiodarone)
2P =
Photosensitive (gray/blue skin discoloration when sun exposed)
Peripheral neuropathy = (shoulder, pelvic girdle)
2L =
Lung = Fibrosis (progressive and fatal) (most serious)
Liver = Liver damage
2C =
Cardiac depression = Decreased HR , decreased BP (usually due to IV)
Corneal micro deposits = (usually reversible or self correcting after drug is stopped)
Amiodarone
Class IIIa antiarrhythmic
Life threatening recurrent v fib
or hemodynamically unstable v tac
Contra:
Cardiogenic shock sick sinus syndrome, 2nd or 3rd degree block, bradycardia with syncope unless paced
Adverse:
Pulmonary fibrosis, thyroid, heart block, sinus bradycardia, corneal deposits, optic neuritis, photosensitivity, skin pigment, peripheral neuropathy
Base line test for amiodarone
All are done at base line and then……
LFT = q 6mo TSH = q 6mo Cr/electrolytes = PRN Chest x ray = annually Ophthalmic = PRN for symptoms PFT = Symptoms EKG = annually
A flutter treatment options
Control of the ventricular rate
beta blocker, calcium channel blocker
Reversion to normal sinus rhythm
Radiofrequency catheter ablation (preferred treatment)
SVT treatment options
If vagal maneuvers are ineffective
pharmacological therapy with an AV node blocking agent should be instituted.
(adenosine, verapamil, BB)
IV adenosine over IV verapamil initially due to its high efficacy and short half life.
If Adenosine is ineffective, use verapamil.
If AVRT persists, use IV procainamide and BB (propranolol, metoprolol, esmolol)
Consider amiodarone
Adenosine
Contra
2nd/3rd block, sinus node disease unless paced, bronchoconstriction, asthma
Interactions
Adenosine may be potentiated by:
BB, cardiac glycosides (dig), CCB; use with caution
Adverse
Flushing, chest discomfort, dyspnea, head, neck, throat discomfort, gi discomfort, lightheadedness, dizziness, cardiac arrest, v tac, MI, bronchoconstriction, hypo or hyper tension, CVA, seizure, a fib
Adenosine dosage
6mg IV once
Then 12mg IV after 1-2 mins
repeat dose again once after 1-2 mins
Acute termination of orthodromic AVRT
unstable patients
Synchronized cardioversion
Acute termination of orthodromic AVRT stable patients (WPW)
1st line = Vagal 2nd = IV adenosine 3rd = IV verapamil or diltiazem Other = IV procainamide or IV BB Cardiovert if other therapies are ineffective or unfeasible.
Reversible causes of v tac
5 H’s
5 T’s
Hypovolemia Hypothermia Hypoxia Hydrogen ions (acidosis) Hypo/Hyperkalemia
Tension pneumo Tamponade Toxins Thrombus pulmonary Thrombus cardiac
Reversible causes of v tac
5 H’s
Hypovolemia Hypothermia Hypoxia Hydrogen ions (acidosis) Hypo/Hyperkalemia
Reversible causes of v tac
5 T’s
Tension pneumo Tamponade Toxins Thrombus pulmonary Thrombus cardiac
ACLS cardiac arrest meds
Epi IV/IO
1 mg q 3-5 min
Amiodarone IV/IO
1st dose = 300mg bolus
2nd dose - 150mg bolus
or
Lidocaine IV/IO
1st dose = 1.0 - 1.5 mg/kg
2nd dose = 0.5 - 0.75 mg/kg
Torsade’s (polymorphic v tac) treatment
IV Mag sulfate
1 to 2 grams IV over 15 mins
(can be followed by an infusion)
Polymorphic v tac other than torsade’s
Beta blockers if BP allows
metoprolol 5mg IV q 5mins, max of 15mg
IV amiodarone may prevent a recurrent episode
V fib Treatment
Amiodarone is the most commonly studied antiarrhythmic for prevention of SCD
Valvular diseases (aortic)
Surgery
Aortic regurgitation
For treatment of hypertension (SBP >140) in patients with chronic Aortic regurg,
vasodilators such as ACE inhibitors, ARBs, or dihydropyridine calcium channel blockers (eg,amlodipine) are favored
since they may reduce systolic blood pressure in this setting.
Tricuspid regurg
In symptomatic patients with severe Tricuspid regurg,
Diuretics are indicated
to treat volume overload and congestion
Tricuspid regurg and Right sided HF
Loop diuretics are typically used.
Aldosterone antagonists may provide additional benefit, particularly in those with hepatic congestion with secondary hyperaldosteronism.
Tricuspid regurg and Left sided HF
If heart failure due to left ventricular systolic dysfunction is present,
standard therapy, including beta-blockers and agents that inhibit the rennin-angiotensin-aldosterone system, are recommended.
Tricuspid stenosis
TX
In patients with severe Tricuspid stenosis
symptoms of systemic venous hypertension, including lower extremity edema and hepatic congestion,
are treated with loop diuretics.
Mitral regurgitation
Symptomatic patients with chronic primary MR (stage D) and left ventricular ejection fraction (LVEF) <60 percent who are awaiting valve surgery or who are not candidates for valve surgery
are treated with standard guideline-based medical therapy for heart failure with reduced ejection fraction (including angiotensin converting enzyme [ACE] inhibitor [or angiotensin II receptor blocker or angiotensin receptor-neprilysin inhibitor], beta blocker, diuretics, and possibly also mineralocorticoid receptor antagonist).
Mitral Stenosis
Long-term oral anticoagulation (with vitamin K antagonist; target International Normalized Ratio 2.5, range 2.0 to 3.0) (Warfarin)
in patients with mitral stenosis who have a prior embolic event, left atrial thrombus, or paroxysmal, persistent, or permanent atrial fibrillation (AF).
Mitral valve prolapse
Magnesium supplementation may benefit a subset of patients with symptoms and magnesium deficiency.
Beta blockers (i.e. propranolol) may be helpful in patients who present with hyperadrenergic symptoms such as tachycardia, palpitations, nervousness, and an exaggerated heart rate response to exercise.
Secondary prophylaxis for rheumatic heart disease
Pen G IM 1.2 million units q 21-28 days
Pen V oral 250mg BID
