CARDIOLOGY
Antithrombotic Therapies
Anticoagulants: for Vitamin K antagonists Warfarin (Coumadin) -Impairs hepatic synthesis of thrombin, 7, 9, and 10
treatment of venous -Interferes with both clotting and anticoagulation = need to use another med for first 5 days of therapy
clots or risk of such -Must consume consistent vit K
as factor V Leiden -Pregnancy X
disorder, other -Monitor with INR and PT twice weekly until stable, then every 4-6 weeks
clotting disorders, Jantoven -Rarely used, usually only if there is a warfarin allergy
post PE, post DVT
Marvan
Waran
Anisindione (Miradon)
Heparin -IV or injection
-Short half-life of 1 hour
-Monitored with aPTT, platelets for HIT
-Protamine antidote
LMWH Ardeparin (Normiflo) -Inhibit factors 10a and thrombin
Dalteparin (Fragmin) -Injections can be done at home
Danaparoid (Orgarin) -Useful as bridge therapy from warfarin prior to surgery
Enoxaparin (Lovenox) -Monitor aPTT and watch platelets initially for HIT, then no monitoring needed once goal is reached?
Tinzaparin (Innohep) -Safe in pregnancy
Heparinoids Fondaparinux (Arixtra) -Direct 10a inhibitor
Rivaroxaban (Xarelto) -Only anticoagulant that does not affect thrombin
Direct thrombin Dabigatran (Pradaxa) -Monitor aPTT
inhibitors Lepirudin (Refludan)
Bivalirudin (Angiomax)
Antiplatelets: used COX inhibitors Aspirin -Blocks thromboxane A-2 = only 1 platelet pathway blocked = weak antiplatelet
for arterial clots or -Only NSAID where antiplatelet activity lasts for days rather than hours
risk of such as ADP receptor inhibitors Ticlopidine (Ticlid) -No monitoring needed
stroke, TIA, -May ease migraines
atherosclerosis, Clopidogrel (Plavix) -Needs monitoring during initiation due to risk of blood count abnormalities
CAD, MI, angina, Ticagrelor (Brilinta)
PVD, post PCI, post Prasugrel (Effient)
CABG, a-fib PPD inhibitors Cilostazol (Pletal) -Contraindicated in CHF
-May be useful in PVD as it widens leg arteries
-Pregnancy X
Glycoprotein IIB/IIIA Abciximab (ReoPro) -IV only
inhibitors Eptifibatide (Integrilin)
Tirofiban (Aggrastat)
Defibrotide
Adenosine reuptake Dipyridamole (Persantine) -Strong treatments for prevention of recurrent stroke
inhibitors
1
, CARDIOMYOPATHIES
-A group of diseases of the myocardium associated with mechanical or electrical dysfunction that usually exhibit ventricular hypertrophy or dilation
-Current major society definitions of cardiomyopathies exclude heart disease secondary to CV disorders such as HTN, CAD, or valvular disease
-Etiologies may be genetic, inflammatory, metabolic, toxic, or idiopathic
Type Info Signs & Symptoms Workup Management Prognosis
Dilated Cardiomyopathy: -Common etiologies: viral, -CHF -Treat CHF symptoms
dilation and impaired contraction genetic, alcoholism -Arrhythmias -ICDs
of one or both ventricles -Systolic dysfunction -Sudden death -Eval for transplant
-Exercise intolerance
-Fatigue or weakness
-Dyspnea
Hypertrophic Cardiomyopathy: -Caused by genetic mutations -Varied presentation, may be asymptomatic -Differential: athlete’s -β-blockers to reduce O2 -Annual
disorganized hypertrophy of left -Diastolic dysfunction -CHF heart (physiologic LVH), demand mortality of 1%
ventricle and occasionally right -Usually asymptomatic until -DOE: the most common sx HTN, aortic stenosis -CCB to reduce -May progress
ventricle childhood or adolescence -Orthopnea and PND -Valsalva will increase contractility and improve to dilated
-Athletes with underlying -Exertional chest pain HCM murmur and diastolic relaxation cardiomyopathy
HOCM at greater risk for lethal -Atypical chest pain decrease aortic stenosis -Pacer or AICD
arrhythmia during exertion -Syncope and presyncope murmur -Surgical myectomy,
-May have abnormal SAM -Palpitations -EKG: prominent Q mitral valve surgery, or
movement of mitral valve -Postural hypotension waves, P wave ethanol ablation to
-Fatigue abnormalities, LAD destroy thickened
-Edema -Echo septum
-Arrhythmias -Holter monitor
-Harsh crescendo systolic murmur ± mitral -Exercise stress test
regurg -Screen relatives
-S4
-Displaced apical impulse or thrill
-Sudden death
-Stroke
Restrictive Cardiomyopathy: -Etiologies: scleroderma, -R CHF as pulmonary pressures must increase to -Differential: constrictive
diastolic dysfunction normal amyloidosis, genetic, HOCM, deliver blood pericarditis
contractility but rigid and stiff DM, chemo, HIV
ventricular walls -Uncommon in US
Arrhythmogenic Right -Genetic cause -Ventricular arrhythmias
Ventricular
Cardiomyopathy/Dysplasia: RV
wall replaced with fibrous tissue
Unclassified Cardiomyopathies -Includes stress-induced
cardiomyopathy and left
ventricular noncompaction
2
, ARRHYTHMIAS AND CONDUCTION DISORDERS
Atrioventricular Block
Type Signs & Symptoms/Info/Workup Management EKG
First degree -Asymptomatic -Treat reversible
-EKG showing lengthened PR interval causes such as
-Determine site of block using EKG ischemia, increased
findings, atropine, exercise, or vagal vagal tone, or meds
maneuvers -Pacemaker usually not
recommended
Second Wenckebach -Typically asymptomatic -Treat reversible
degree (Mobitz type I) -EKG shows progressive PR causes such as
prolongation for several beats prior to ischemia, increased
nonconducted P wave vagal tone, or meds
-Beats classically occur in ratios of 3:2, -Pacemaker if there is
4:3, or 5:4 symptomatic
-Can be a result of inferior MI bradycardia
Mobitz type II -May be asymptomatic or have signs of -Treat reversible
hypoperfusion or HF causes such as
-PR interval remains unchanged prior to ischemia, increased
a nonconducted P wave vagal tone, or meds
-Most patients will
require a pacemaker
Third degree -May have dizziness, presyncope,
syncope, v-tach, v-fib, worsening HF, or
angina
-P waves don’t correlate to QRS
-Escape rhythm takes over for QRS
(junctional or ventricular)
3
, Bundle Branch Block
-Occurs when block in left or right BB delays depolarization Differential Workup
to a ventricle -Any BBB: ventricular rhythm or ventricular pacing -RBBB: if asymptomatic and no other evidence of cardiac
-Variation is “intermittent Mobitz” where there is a RBBB or -RBBB: Brugada syndrome disease, no further w/u indicated
LBBB plus intermittent BBB of opposite side can progress -LBBB needs further w/u for cardiac cause
to 3° AV block BBB and acute MI
-LBBB interferes with dx of ventricular hypertrophy, myocardial Management
Causes ischemia, and acute MI because of associated Q waves (early -Permanent pacemaker insertion for symptomatic BBB or
-Structural heart disease: cor pulmonale, pulmonary ventricular depolarization is affected) as well as ST changes progression to AV block
embolism, MI or ischemia (both branches receives blood (ventricular repolarization is affected)
supply from LAD), myocarditis, HTN, congenital heart -RBBB usually does not interfere with dx of Q wave MI (early Prognosis
disease ventricular depolarization is not affected) but can inflict ST -LBBB in older individuals associated with increased mortality
-Iatrogenic: R heart cath, ethanol ablation segment changes
EKG
-Joined QRS’s or “rabbit ears”
-May have accompanying ST or T wave change due to altered sequence of
repolarization
-RBBB will be prominent on R heart leads (V1 and V2)
-LBBB will be prominent on L heart leads (V5 and V6)
Sick Sinus Syndrome
-A combination of unhealthy SA that stops pacing Signs & Symptoms Management
intermittently + unresponsive supraventricular foci -Lightheadedness -May eventually need pacemaker
-Seen in the elderly with heart disease and in kids with -Presyncope or syncope
congenital and acquired heart disease after corrective -DOE Workup
cardiac surgery -Worsening angina -Appears as sinus bradycardia
-Palpitations -May also see intermittent SVT
Causes bradycardia-tachycardia syndrome
-SA node tissue becomes replaced with fibrous tissue
-Compromised blood supply to SA node
(atherosclerosis, inflammation, emboli)
-Lyme disease
-Drugs causing depressed SA node function: β-blocker,
clonidine, methyldopa, digitalis, Li, amiodarone
4
Antithrombotic Therapies
Anticoagulants: for Vitamin K antagonists Warfarin (Coumadin) -Impairs hepatic synthesis of thrombin, 7, 9, and 10
treatment of venous -Interferes with both clotting and anticoagulation = need to use another med for first 5 days of therapy
clots or risk of such -Must consume consistent vit K
as factor V Leiden -Pregnancy X
disorder, other -Monitor with INR and PT twice weekly until stable, then every 4-6 weeks
clotting disorders, Jantoven -Rarely used, usually only if there is a warfarin allergy
post PE, post DVT
Marvan
Waran
Anisindione (Miradon)
Heparin -IV or injection
-Short half-life of 1 hour
-Monitored with aPTT, platelets for HIT
-Protamine antidote
LMWH Ardeparin (Normiflo) -Inhibit factors 10a and thrombin
Dalteparin (Fragmin) -Injections can be done at home
Danaparoid (Orgarin) -Useful as bridge therapy from warfarin prior to surgery
Enoxaparin (Lovenox) -Monitor aPTT and watch platelets initially for HIT, then no monitoring needed once goal is reached?
Tinzaparin (Innohep) -Safe in pregnancy
Heparinoids Fondaparinux (Arixtra) -Direct 10a inhibitor
Rivaroxaban (Xarelto) -Only anticoagulant that does not affect thrombin
Direct thrombin Dabigatran (Pradaxa) -Monitor aPTT
inhibitors Lepirudin (Refludan)
Bivalirudin (Angiomax)
Antiplatelets: used COX inhibitors Aspirin -Blocks thromboxane A-2 = only 1 platelet pathway blocked = weak antiplatelet
for arterial clots or -Only NSAID where antiplatelet activity lasts for days rather than hours
risk of such as ADP receptor inhibitors Ticlopidine (Ticlid) -No monitoring needed
stroke, TIA, -May ease migraines
atherosclerosis, Clopidogrel (Plavix) -Needs monitoring during initiation due to risk of blood count abnormalities
CAD, MI, angina, Ticagrelor (Brilinta)
PVD, post PCI, post Prasugrel (Effient)
CABG, a-fib PPD inhibitors Cilostazol (Pletal) -Contraindicated in CHF
-May be useful in PVD as it widens leg arteries
-Pregnancy X
Glycoprotein IIB/IIIA Abciximab (ReoPro) -IV only
inhibitors Eptifibatide (Integrilin)
Tirofiban (Aggrastat)
Defibrotide
Adenosine reuptake Dipyridamole (Persantine) -Strong treatments for prevention of recurrent stroke
inhibitors
1
, CARDIOMYOPATHIES
-A group of diseases of the myocardium associated with mechanical or electrical dysfunction that usually exhibit ventricular hypertrophy or dilation
-Current major society definitions of cardiomyopathies exclude heart disease secondary to CV disorders such as HTN, CAD, or valvular disease
-Etiologies may be genetic, inflammatory, metabolic, toxic, or idiopathic
Type Info Signs & Symptoms Workup Management Prognosis
Dilated Cardiomyopathy: -Common etiologies: viral, -CHF -Treat CHF symptoms
dilation and impaired contraction genetic, alcoholism -Arrhythmias -ICDs
of one or both ventricles -Systolic dysfunction -Sudden death -Eval for transplant
-Exercise intolerance
-Fatigue or weakness
-Dyspnea
Hypertrophic Cardiomyopathy: -Caused by genetic mutations -Varied presentation, may be asymptomatic -Differential: athlete’s -β-blockers to reduce O2 -Annual
disorganized hypertrophy of left -Diastolic dysfunction -CHF heart (physiologic LVH), demand mortality of 1%
ventricle and occasionally right -Usually asymptomatic until -DOE: the most common sx HTN, aortic stenosis -CCB to reduce -May progress
ventricle childhood or adolescence -Orthopnea and PND -Valsalva will increase contractility and improve to dilated
-Athletes with underlying -Exertional chest pain HCM murmur and diastolic relaxation cardiomyopathy
HOCM at greater risk for lethal -Atypical chest pain decrease aortic stenosis -Pacer or AICD
arrhythmia during exertion -Syncope and presyncope murmur -Surgical myectomy,
-May have abnormal SAM -Palpitations -EKG: prominent Q mitral valve surgery, or
movement of mitral valve -Postural hypotension waves, P wave ethanol ablation to
-Fatigue abnormalities, LAD destroy thickened
-Edema -Echo septum
-Arrhythmias -Holter monitor
-Harsh crescendo systolic murmur ± mitral -Exercise stress test
regurg -Screen relatives
-S4
-Displaced apical impulse or thrill
-Sudden death
-Stroke
Restrictive Cardiomyopathy: -Etiologies: scleroderma, -R CHF as pulmonary pressures must increase to -Differential: constrictive
diastolic dysfunction normal amyloidosis, genetic, HOCM, deliver blood pericarditis
contractility but rigid and stiff DM, chemo, HIV
ventricular walls -Uncommon in US
Arrhythmogenic Right -Genetic cause -Ventricular arrhythmias
Ventricular
Cardiomyopathy/Dysplasia: RV
wall replaced with fibrous tissue
Unclassified Cardiomyopathies -Includes stress-induced
cardiomyopathy and left
ventricular noncompaction
2
, ARRHYTHMIAS AND CONDUCTION DISORDERS
Atrioventricular Block
Type Signs & Symptoms/Info/Workup Management EKG
First degree -Asymptomatic -Treat reversible
-EKG showing lengthened PR interval causes such as
-Determine site of block using EKG ischemia, increased
findings, atropine, exercise, or vagal vagal tone, or meds
maneuvers -Pacemaker usually not
recommended
Second Wenckebach -Typically asymptomatic -Treat reversible
degree (Mobitz type I) -EKG shows progressive PR causes such as
prolongation for several beats prior to ischemia, increased
nonconducted P wave vagal tone, or meds
-Beats classically occur in ratios of 3:2, -Pacemaker if there is
4:3, or 5:4 symptomatic
-Can be a result of inferior MI bradycardia
Mobitz type II -May be asymptomatic or have signs of -Treat reversible
hypoperfusion or HF causes such as
-PR interval remains unchanged prior to ischemia, increased
a nonconducted P wave vagal tone, or meds
-Most patients will
require a pacemaker
Third degree -May have dizziness, presyncope,
syncope, v-tach, v-fib, worsening HF, or
angina
-P waves don’t correlate to QRS
-Escape rhythm takes over for QRS
(junctional or ventricular)
3
, Bundle Branch Block
-Occurs when block in left or right BB delays depolarization Differential Workup
to a ventricle -Any BBB: ventricular rhythm or ventricular pacing -RBBB: if asymptomatic and no other evidence of cardiac
-Variation is “intermittent Mobitz” where there is a RBBB or -RBBB: Brugada syndrome disease, no further w/u indicated
LBBB plus intermittent BBB of opposite side can progress -LBBB needs further w/u for cardiac cause
to 3° AV block BBB and acute MI
-LBBB interferes with dx of ventricular hypertrophy, myocardial Management
Causes ischemia, and acute MI because of associated Q waves (early -Permanent pacemaker insertion for symptomatic BBB or
-Structural heart disease: cor pulmonale, pulmonary ventricular depolarization is affected) as well as ST changes progression to AV block
embolism, MI or ischemia (both branches receives blood (ventricular repolarization is affected)
supply from LAD), myocarditis, HTN, congenital heart -RBBB usually does not interfere with dx of Q wave MI (early Prognosis
disease ventricular depolarization is not affected) but can inflict ST -LBBB in older individuals associated with increased mortality
-Iatrogenic: R heart cath, ethanol ablation segment changes
EKG
-Joined QRS’s or “rabbit ears”
-May have accompanying ST or T wave change due to altered sequence of
repolarization
-RBBB will be prominent on R heart leads (V1 and V2)
-LBBB will be prominent on L heart leads (V5 and V6)
Sick Sinus Syndrome
-A combination of unhealthy SA that stops pacing Signs & Symptoms Management
intermittently + unresponsive supraventricular foci -Lightheadedness -May eventually need pacemaker
-Seen in the elderly with heart disease and in kids with -Presyncope or syncope
congenital and acquired heart disease after corrective -DOE Workup
cardiac surgery -Worsening angina -Appears as sinus bradycardia
-Palpitations -May also see intermittent SVT
Causes bradycardia-tachycardia syndrome
-SA node tissue becomes replaced with fibrous tissue
-Compromised blood supply to SA node
(atherosclerosis, inflammation, emboli)
-Lyme disease
-Drugs causing depressed SA node function: β-blocker,
clonidine, methyldopa, digitalis, Li, amiodarone
4
