Cardiology Flashcards
Stable Bradycardia Treatment
Monitor and observe
Unstable Bradycardia Treatment
Atropine (1st line)
Others: Epi, Dopamine, Transcutaneous Pacing
Shockable Rhythms
1) V-Fib
2) Pulseless V-Tach
Unstable Tachycardia Treatment
SYNCHRONIZED Cardioversion
Stable Tachycardia (Wide QRS) Treatment
Amiodarone (1st line)
Others: Lidocaine, Procainamide
Stable Tachycardia (Narrow QRS) Treatment
Adenosine (1st)
Then, Beta-blocker, CCB
Acute A-Fib Treatment
Beta-blocker or CCB
WPW Treatment
Procainamide preferred (avoid AV nodal blockers)
AV Nodal Blockers
ABCD= Adenosine Beta Blockers CCB Digoxin
Normal PR interval
0.12 - 0.2
Normal QRS time
<0.12 sec (if normal, there is no bundle branch block*)
Anterior Leads
V1-V4
Lateral Leads
I, aVL, V5, V6
Anterolateral leads
I, aVL, V4-V6
Inferior Leads
II, III, aVF
Posterior Leads
ST DEPRESSIONS in V1-V2
Causes of Left Axis Deviation
LBBB LVH Inferior MI Elevated Diaphragm (pregnancy, obesity) Left anterior hemiblock WPW
Causes of Right Axis Deviation
RVH
Lateral MI
COPD
Left posterior hemiblock
Normal Sinus Rhythm Determination
Every P-wave followed by QRS
P waves are positive/upright in I, II, and aVF
P waves are negative in aVR
Rate is 60-100
Sick Sinus Syndrome (What is it?/Caused by?)
Combination of sinus arrest with alternativing paroxysms of atrial tachyarrhythmias & bradyarrhythmias
Caused by sinoatrial node disease and corrective cardiac surgery
Sick Sinus Syndrome Management
+/- permanent pacemaker if symptomatic
If brady alternating with v-tach –> permanent pacemaker with automatic implantable cardioverter-defibrillator
First Degree AV Block Definition
Constant, prolonged PR-Interval (>0.20 sec)
QRS follows every P wave
First Degree AV Block Treatment
None, observation
Second Degree AV Block Type I Definition
Mobitz I (Wenckebach): Progressive PRI lengthening --> Dropped QRS
Second Degree AV Block Type I Treatment
Symptomatic –> Atropine (treat like brady)
Asymptomatic –> Observation +/- cardiac consult
Second Degree AV Block Type II Definition
Mobitz II:
Constant/Prolonged PRI –> Dropped QRS
Second Degree AV Block Type II Treatment
Atropine or temporary pacing
Progression to 3rd degree block is common so permanent pacemaker is the definitive treatment!
Which heart block is most likely to progress to 3rd degree
Mobitz II
Third Degree AV Block Definition
AV dissociation: P waves NOT related to QRS
Third Degree AV Block Treatment
Acute: Temporary pacing –> PPM
Definitive: PPM
Atrial Flutter Management
Stable: Vagal, B-blocker, or CCB
Unstable: Synchronized cardioversion
Definitive: Radiofrequency ablation
*Anticoagulation similar to A-Fib
Most common chronic arrhythmia
A-Fib
Stable A-Fib Management
RATE CONTROL (preferred in symptomatic Afib)
- B-blocker (metoprolol*, esmolol)
- CCB (diltiazem*, verapamil (nondihydropyridines))
- Digoxin +/- in elderly (preferred rate control in patients with hypotension or CHF)
RHYTHM CONTROL (may be used in younger patients with lone AFib)
- Direct current (synchronized) cardioversion (DCC) is preferred over pharmacologics; DCC can be done if AF present for <48 hours OR after 3-4 weeks of anticoagulation and TEE shows no atrial thrombi
- Pharm control: Ilbutilide, Flecainide, Sotalol, Amiodarone
- Radiofrequency ablation
Stable A-Fib Management in patient with hypotension or CHF
Digoxin
Unstable A-Fib Management
DCC
A-Fib Anticoagulation Risk Stratification
CHA2DS2-VASc Score:
- CHF - 1 point
- HTN - 1 point
- Age(2) >75 - 2 points
- DM - 1 point
- Stroke, TIA, Thrombus - 2 points
- Vascular disease (prior MI, aortic plaque, PAD) - 1 point
- Age 65-74 - 1 point
- Sex (female) - 1 point
Max Score: 9; 2 or more is high risk, 1 is low risk
High risk: chronic oral anticoagulation recommended
Low risk: clinical judgment
Anticoagulation options
NOACs (now preferred over warfarin)
Warfarin
Dual antiplatelet therapy (ex. Aspirin + Clopidogrel) –> reserved for patients who cannot be treated with anticoagulation
Types of NOACs
Dabigatran (direct thrombin inhibitor)
Rivaroxaban, Apixaban, Edoxaban (factor Xa inhibitors)
Anticoagulation preference in A-Fib
NOACs
Warfarin Indications for A-Fib
Preferred in patients with severe chronic kidney disease, contraindications to NOAC (HIV patients on protease inhibitor therapy, patients on CP450 inducing antiepileptic meds), patient preference, cost
INR goal for A-Fib
2-3
Long QT Syndrome Etiology
Congenital
Acquired (macrolides, TCAs, electrolyte abnormalities)
Long QT Clinical Manifestations
Recurrent syncope (Get EKG in ALL Syncope)
Ventricular arrhythmias
Sudden cardiac death
Management of Long QT Syndrome
Discontinue offending drugs and correct electrolyte abnormality
Implantable cardiodefibrillator is definitive for congenital or recurrent ventricular arrhythmias
Paroxysmal SVT (PSVT) EKG
HR > 100
Rhythm usually regular with narrow QRS
P waves hard to discern
PSVT Management
Stable (Narrow complex):
Vagal Maneuvers
Adenosine (1st line medical treatment)
AV nodal blockers (B-blockers, CCB)
Stable (Wide Complex):
Antiarrhythmics (amiodarone, procainamide if WPW)
Unstable:
DCC
Definitive:
Radiofrequency ablation
Wandering atrial pacemaker (WAP) vs Multifocal atrial tachycardia (MAT) EKG
WAP:
HR < 100
3 or more p wave morphologies
MAT:
HR > 100
3 or more p wave morphologies
What condition is MAT associated with?
Severe COPD
Tx for WAP and MAT
CCB or B-blocker if LV function preserved
Stable WPW management
Vagal, antiarrhythmics (procainamide preferred)
Unstable WPW Management
DCC
Definitive WPW management
Radioablation
Junctional Rhythm EKG
P waves inverted (if present) or not seen
Narrow QRS
Regular Rhythm
HR 40-60 bpm (reflecting intrinsic rate of AV junction)
Accelerated junctional rhythm EKG
HR 60-100 w/out pwaves (or inverted if present)
Junctional tachycardia
HR >100 w/out pwaves (or inverted if present)
MC rhythm seen with digitalis toxicity
Junctional rhythms
PVC management
No treatment usually needed
MC cause of V-tach
Prolonged QT
MC cause of Torsades
Hypomagnesemia
Other: Hypokalemia, prolonged QT, V-tach
Stable Vtach treatment
Antiarrhythmics (Amiodarone*, lidocaine, procainamide)
Unstable Vtach w/ a pulse
Synchronized cardioversion
Vtach w/out pulse
Defibrillation (UNsynchronized cardioversion) + CPR (treat as VFib)
Torsades treatment
IV magnesium
Correct any electrolyte abnormalities
VFib treatment
Defibrillation + CPR
Pulseless electrical activity (PEA) definition
Organized rhythm on monitor, but patient does not have a palpable pulse (electrical activity is not coupled with mechanical contraction)
PEA treatment
CPR + Epinephrine + Check for shockable rhythm every 2 minutes
Asystole treatment
CPR + Epinephrine + Check for shockable rhythm every 2 minutes
Increased JVP + crackles/rales in lungs
CHF
Increased JVP + normal pulm exam
Pericardial tamponade
Increased JVP + decreased breath sounds
Tension pneumothorax
Causes of ST Depression
ST depression usually = ISCHEMIA
May be benign (upsloping)
Which ST depressions are pathologic
Horizontal and downsloping
Which ST elevations are pathologic
Convex down (most likely ischemic)
Which ST elevations may be benign
Concave up
Etiologies of ST elevation
- Acute MI
- LVH
- LBBB
- Acute Pericarditis
- Early repolarization abnormalities
- Coronary artery vasopasm/prinzmetal angina/cocaine
- Brugada syndrome
Early repolarization abnormalities EKG
DIFFUSE CONCAVE ST elevations
Large T waves
Tall QRS voltage
Fishook (slurring/notching) at the j point
Acute pericarditis EKG
- DIFFUSE CONCAVE ST elevations in the precordial leads (V1-V6)
- PR depressions in the same leads with the ST elevations
- Lead aVR: ST depression and PR elevation (opposite of precordial leads)
- NO reciprocal changes
Brugada Syndrome EKG
- RBB pattern (often incomplete) in V1-V3
- ST elevation in V1-V3 (often downsloping)
- Twave inversions in V1 and V2 +/- S wave in lateral leads
Demographic group associated with Brugada
Asian males
Brugada syndrome cause and manifestations
Genetic disorder associated with syncope, sudden cardiac death
Most common arrhythmia with brugada
Ventricular arrhythmias
Brugada management
AICD to prevent death from V Fib
When are left sided murmurs best heard in regards to breathing?
End expiration
When are right sided murmurs best heard in regards to breathing?
End inspiration
What does inspiration do to stroke volume
Decreases, but CO stays the same due to an increase in HR
Gold standard test for diagnosing CAD, PAD, renal artery stenosis, and AAA
Angiography
Most useful test to diagnose heart failure
Echocardiogram
Biggest risk factor for CAD
Diabetes
Most important modifiable risk factor for CAD
Smoking
How much of the lumen is occluded to cause symptomatic CAD?
> 70%
Class I Angina
Angina only with unusually strenuous activity. No limitations of activity.
Class II Angina
Angina with more prolonged or rigorous activity. Slight limitation of physical activity.
Class III Angina
Angina with usual daily activity. Marked limitation of physical activity.
Class IV Angina
Angina at rest. Often unable to carry out any physical activity.
Levine’s Sign
Clenched fist over chest
Classic angina description
Substernal chest pain brought on by exertion/anxiety (sometimes radiating to arm/jaw) and relieved with rest/nitroglycerin (predictable pattern)
Classic EKG finding for angina
ST depression (horizontal or downward) if LVH present = increase in adverse outcomes
Most useful noninvasive screening tool for angina
Stress Testing
Angina definitive management
- Percutaneous Transluminal Coronary Angioplasty
2. CABG
Indication for percutaneous transluminal coronary angioplasty
1 or 2 vessel disease NOT involving the left main coronary artery and in whome ventricular function is normal/near normal.
CABG indications
Left main coronary artery disease
Symptomatic or critical (>70%) stenotic 3-vessel disease
Decreased left ventricular ejection fraction (<40%)
Medical management of angina
- Nitrates
- B-Blockers
- CCB
- Aspirin
1st line drug for chronic management of angina
B-Blockers
Contraindication to nitrates
SBP <90
RV infarct
Use of sildenafil & other PDE-5 inhibitors
UA/NSTEMI EKG
ST depressions &/or T-wave inversions = Subtotal occlusion (EKG may be normal)
STEMI EKG
ST elevations in two or more consecutive leads = Total occlusion
UA vs NSTEMI
Cardiac enzymes elevated in NSTEMI (EKG may be the same)
Patients with “silent MI”
Women, elderly, diabetics, & obese
Symptoms of atypical MI
abdominal pain, jaw pain, or dyspnea WITHOUT chest pain
Inferior MI physical exam findings
Chest pain + bradycardia +/- S4
Progression of EKG changes in STEMI
Hyperacute (peaked) T-waves –>
ST elevations –>
Q waves –>
T wave inversions
Pathologic Q-wave definition
Q wave > 0.03 sec & 0.1 mv deep
Q wave depth at least 25% of associated R wave
Most sensitive and specific cardiac marker
Troponin
Other causes of increased troponin
Renal failure
Advanced heart failure
Acute PE
CVA
Management of STEMI
- Reperfusion therapy (most important) - PCI or thrombolytics
- Antithrombotics - Asprin, Heparin
- Adjuntive therapy - B-Blockers, ACE, Nitrates, Morphine
PCI indication in STEMI
Best w/in 3 hours of sx onset (esp w/in 90 min)
PCI is superior to thrombolytics
Thrombolytic indication in STEMI
PCI is not an option/unable to get PCI early
CI of Betablockers in STEMI
HR <50 SBP <100 Decompensated CHF 2nd/3rd degree heart block Severe asthma/COPD Shock Cocaine induced MI
CI of ACE Inhibitors in STEMI
Renal failure
SBP <100
AMI protocol for ACS
EKG w/in 10 min
Door to thrombolytics w/in 30 min
Door to PCI w/in 90 min
STEMI AMI protocol
B-Blockers Nitro Asprin Heparin ACEI Reperfusion!!!
UA or NSTEMI AMI Protocol
B-Blockers Nitro Asprin Heparin NO emergent reperfusion or ACEI (unlike STEMI)
Cocaine Induced MI AMI protocol
Aspirin Nitro Heparin Anxiolytics (*AVOID B-Blockers b/c of vasospasm)
Dressler syndrome
Post-MI pericarditis +
Fever +
Pulmonary infiltrates
Prinzmetal Angina Tx
CCBs (drug of choice)
Nitrates as needed
Prinzmetal Angina EKG
Transient ST elevations that resolve with CCBs or nitro
Prinzmetal Angina clinical manifestations
CP, usually NONexertional and occurring at rest
Absolute contraindications to thrombolytics in ACS
Previous intracranial hemorrhage Non-hemorrhagic stroke w/in 6 months Closed head/facial trauma w/in 3 months Intracranial neoplasm, aneurysm, AVM Active internal bleeding Suspected aortic dissection
MC cause of heart failure
CAD
MC cause of R-sided HF
L-sided HF
Also, pulmonary disease, mitral stenosis
Systolic vs Diastolic HF
Systolic:
- Decreased EF
- +/- S3 gallop
- Most common form of HF
- Etiologies: Post-MI, DILATED cardiomyopathy, myocarditis
Diastolic:
- Normal/Increased EF
- +/- S4 gallop
- Normal cardiac size (stiff/noncompliant ventricle)
- Etiologies: HTN, LVH, elderly, valvular heart disease, cardiomyopathies, constrictive pericarditis
Classifying of HF
Class I - No symptoms, no limitation during ordinary physical activity
Class II - Mild symptoms, slight limitation of activity
Class III - Sxs cause marked limitation in activity
Class IV - Symptoms present at rest
MC sx of L-sided HF
Dyspnea
Cheyne-Stokes breathing
Associated with L-side HF
Deeper, faster breathing w/ gradual decrease & periods of apnea
R-sided HF physical exam
Peripheral edema
JVD
GI/hepatic congestion: anorexia, n/v, HSM, RUQ tenderness, hepatojugular reflex
Diagnosis of HF
Echo (most useful)
CXR (esp useful in congestive HF)
BNP
CXR findings with HF
Cephalization of flow –> Kerley B lines –> Butterfly pattern –> cardiomegaly
Pleural effusions –> pulmonary edema
Initial management of HF
ACE + Diuretic (for sxs) –> Add beta blockers as needed
Best 2 meds for decreasing mortality of HF
ACE > Beta-blockers
Management of acute pulmonary edema/CHF
LMNOP:
Lasix, Morphine, Nitro, Oxygen, Position (place upright)
2 MC causes of pericarditis
Idiopathic
Viral
MC Viral causes of pericarditis
Enteroviruses-Coxsackie; Echovirus
Drugs that cause pericarditis
Procainamide
INH
Hydralazine
Clinical manifestations of pericarditis
3 P’s:
- Pleuritic CP
- Persistent CP
- Postural CP (worse supine, relieved sitting forward)
Physical:
Pericardial friction rub (best heard at end expiration while upright and leaning forward
Pericarditis diagnostics
EKG: DIFFUSE ST elevations in precordial leads (concave up in V1-V6)
Echo: Assesses complications (effusion/tamponade)
Pericarditis management
Aspirin/NSAIDs x 7-14 days
Colchicine (2nd line)
+/- steroids if sxs >48 hours refractory to 1st line meds
Pericardial effusion EKG
Low voltage QRS
Electrical alternans
Management of pericardial effusion
Observation if small & no tamponade
+/- Pericardiocentesis if tamponade or large
Knuckle sign
Lead aVR: PR elevation with ST depression reflects atrial injury in acute pericarditis
Beck’s Triad
Associated with tamponade:
- Muffled heart sounds
- JVD
- Hypotension
MC symptom of constrictive pericarditis
Dyspnea
Kussmaul’s sign
Increased JVD during inspiration associated with constrictive pericarditis and restrictive cardiomyopathy
Heart sound associated with constrictive pericarditis
Pericardial knock: high pitched 3rd heart sound due to sudden cessation of ventricular filling
Treatment of constrictive pericarditis
Pericardiectomy (definitive treatment)
Diuretics for symptomatic control
MC cause of myocarditis
Viral infection (enterovirus (esp. coxsackie))
Others: Bacteria (rickettsial, chagas, diptheria); Fungal; Parasitic; Scorpion envenomation; SLE, rheumatic fever, rheumatoid arthritis, Kawasaki Meds Uremia
Meds associated with myocarditis
Clozapine***
Methyldopa, tetracycline, penicllin, isoniazid, etc.
Classic CXR with myocarditis
Cardiomegaly (may be normal)
Gold standard of diagnosing myocarditis
Endomyocardial biopsy
Management of myocarditis
- Supportive (mainstay) - diuretics, ACE I, inotropic drugs (dopamine, dobutamine, milrinone)
- Beta blockers not used in management of peds patients
- IVIG may be helpful in some patients
MC cause of dilated cardiomyopathy
Idiopathic (50%)
Apical left ventricular ballooning following stress
Takotsubo Cardiomyopathy
MC cause of restrictive cardiomyopathy
Amyloidosis
Others: Sarcoidosis, idiopathic myocardial fibrosis
Treatment of restrictive cardiomyopathy
No specific treatment, treat underlying cause
MC initial complaint of hypertrophic cardiomyopathy
Dyspnea
Hypertrophic cardiomyopathy murmur
Harsh systolic crescendo-decresendo murmur: best heart @ LLSB (similar to AS)
Decreased murmur intensity with INCREASED venous return (squatting, lying suping)
Increased intensity with DECREASED venous return
Rheumatic Fever diagnostic criteria
JONES criteria
JONES criteria for Rheumatic Fever
Major criteria (2 pts):
- Joint (migratory polyarthritis)
- Oh my heart (active carditis)
- Nodules (subcutaneous)
- Erythema marginatum
- Sydenham’s chorea
Minor criteria (1 pt):
- Fever >101.3
- Arthralgia
- Increased ESR/CRP/leukocytosis
- Prolonged PR on EKG
PLUS supporting evidence of recent GAS infection
MC valve affected by Rheumatic fever
Mitral (75%-80%)
Aortic (30%)
Rheumatic fever management
- Aspirin x 2-6 weeks with taper +/- steroids
2. Pen G (erythromycin if PCN-allergic)
Fixed split of S2
Left to Right shunts (ASD, VSD) or
Delayed pulmonary closure (pulmonary HTN, mitral regurgitation)
Physiologic split of S2
Inspiration splits S2 into A2 followed by P2
Systolic ejection click
Mitral valve prolapse
Diastolic opening snap
Mitral valve stenosis
MC valve affected by Rheumatic fever
Mitral (75%-80%)
Aortic (30%)
Rheumatic fever management
- Aspirin x 2-6 weeks with taper +/- steroids
2. Pen G (erythromycin if PCN-allergic)
Fixed split of S2
Left to Right shunts (ASD, VSD) or
Delayed pulmonary closure (pulmonary HTN, mitral regurgitation)
Physiologic split of S2
Inspiration splits S2 into A2 followed by P2
Systolic ejection click
Mitral valve prolapse
Diastolic opening snap
Mitral valve stenosis
