Cardiology Flashcards
Vector directions for standard EKG limb leads
I = R arm to L arm II = R arm to L foot III = L arm to L foot
Where to place precordial leads?
V1 = R 4th ICS adjacent to sternum V2 = L 4th ICS adjacent to sternum V4 = L 5th ICS in MCL V6 = L 6h ICS in MAL
When current direction has a component vector in the SAME direction as a lead, ECG deflection is … ?
Other cases?
Positive
Negative if vice versa
Net deflection of 0 if perpendicular to current
Which EKG leads are usually most positive?
II, I
aVF
V4, V5, V6
Normal time intervals on EKG for QRS complex, PR interval, and QT interval?
Issues if abnormal?
QRS (begin Q to end S) less than 120ms (3 small boxes) = for determining heart blocks
PR (begin P to begin Q) less than 200ms (1 big box)
QT (begin Q to end T) less than 500ms (2.5 big boxes) = may be lengthened by some drugs
How do you estimate HR from an EKG?
300 / (number of big boxes per cycle)
Describe these common rhythms:
AFib
Atrial flutter
Junctional rhythm
AFib: No P-waves seen, gravely baseline, irregular rate
Atrial flutter: Sawtooth baseline from fast atrial cycling
Junctional: AV source causes (-) depolarization of atria
QRS axis:
Normally aVF and I are … ?
If L deviation, aVF and I are … ?
If R deviation, aVF and I are … ?
Normal: Both (+)
L deviation: aVF (-) and I (+)
R deviation: aVF (+) and I (-)
Left anterior fascicular block occurs when … ?
QRS axis deflection is larger than -30deg (90deg from II)
Anatomically impossible -> Electrical abnormality
Right bundle branch block
Right conductive branch from AV node is not conducting, so current flows from LV to RV more slowly via muscle to cause RV contraction.
Since R side is delayed, the QRS widens to over 120ms, and the terminal QRS will be (+) in V1 and (-) in V6
A repolarization T wave of opposite magnitude follows the QRS in each lead
Left bundle branch block
Left conductive branches from AV node not conducting, so current flows from RV to LV more slowly via muscle to cause LV contraction.
Since L side is delayed, the QRS widens to over 120ms, and the terminal QRS will be (-) in V1 and (+) in V6, although for LBBB the wide QRS may be the only obvious change
A repolarization T wave of opposite magnitude follows the QRS in each lead
How to determine QRS width?
Find the greatest width on any lead
1st degree AV block definition, severity
Fixed PR prolongation (over 200ms), but number of P-waves = number of QRS complexes
Benign
2nd degree AV block Type I definition, severity
Gradual PR prolongation due to AV nodal disease; PR increases until a QRS is dropped
Usually benign
2nd degree AV block Type II definition, severity
Unpredictable AV block with dropped QRS at unpredictable intervals, wide QRS complexes
Needs a pacemaker
3rd degree AV block definition
P-wave and QRS happen at independent rates
Trifascicular block
1st degree AV block + LAFB + RBBB
2:1 AV conduction block appearance
P-waves occur at twice the rate of QRS, every other P-wave may occur during and be hidden by the QRS
Most common cause for a pause in contraction
Nonconducted atrial contraction
Left posterior fascicular block appearance
May cause a right axis deviation, but is rare and often not detectable
ECG progression of a STEMI, treatment
Hyperacute giant T-waves -> ST elevation -> Q-wave development, diminished R-waves -> ST normalization and T-wave inversion -> T normalization
Persistent ST elevation = LV aneurysm
Take to cath lab immediately
NSTEMI treatment
Give nitrates, heparin, O2, aspirin immediately
Check troponin
This is transient damage, but unstable. Take to the cath lab within 24h or ASAP if it progresses
Determining dominance of heart
Does posterior descending artery come from L or RCA?
Inferior ECG leads
II, III, aVF
Anteroseptal ECG leads
V1, V2
Anterior ECG leads
V3-V5
Lateral ECG leads
I, aVL, V6
Anterior MI due to occlusion of what vessel?
LAD
Lateral MI due to occlusion of what vessel?
Proximal L circumflex artery
Inferior MI due to occlusion of what vessel?
R circumflex OR distal L circumflex artery including posterior descending artery (determine dominance)
Inferior AND lateral MI due to occlusion of what vessel?
L circumflex artery MI in L dominant heart occluding distal posterior descending artery
Infective endocarditis definition, causes
Microbial infection of endocardium, which may include valves and chordae tendinae
Caused by Staph aureus, Staph epidermidis from prosthetics, and various Strep species, including S. bovis in elderly (perform colonoscopy)
Also caused by ‘HACEK’ - Haemophillus, Actinobacillus, Cardiobacterium hominis, Eikenella, Kingella
Bartonella from flea bite
Infective endocarditis risk factors
Poor dental hygiene IV drug use Dialysis Indwelling catheters Diabetes mellitus Prosthetic valves
Infective endocarditis signs and symptoms
Systemic: Fever, weight loss, fatigue, night sweats, septic shock
Skin: Petechiae, conjunctival and splinter hemorrhages, Osler nodes (pain, subcu on fingers and toes, SUBACUTE), Janeway lesions (no pain, palms and soles, ACUTE)
Heart failure, heart murmur
Splenomegaly
Roth spots (hemorrhage w/pale center) on fundoscopy
Perivalvular abscesses cause … ?
Valve dysfunction (murmurs), heart block, stroke
Infective endocarditis diagnosis
2 Major / 1 M + 3 m / 5 minor
Major:
Lab evidence from 2 + blood cultures (1 + for Coxiella burnetti)
Endocardial involvment on transthoracic or -esophageal echo (TTE/TEE)
New valvular regurgitation, esp. mitral
Minor:
Predisposing heart condition
Fever
Vascular phenomenon (Emboli, mycotic aneurysm, hemorrhages)
Immunologic phenomenon (Glomerulonephritis, Osler node, +RF)
Positive blood culture
Infective endocarditis treatment
2-6w IV abx
If G+ and penicillin-sensitive, use PCN/Ampicillin + Aminoglycoside (usually gentamicin)
If G+ and not PCN-sensitive, use Vancomycin + Aminoglycoside
Do not use anticoagulation treatment: Doesn’t prevent embolism and ups bleeding risk
Libman-Sacks endocarditis associated with what?
SLE
Carcinoid syndrome associated with what finding?
Flushed skin
What murmurs increase with inspiration?
Which with expiration?
Inspiration = RS murmurs increased Expiration = LS murmurs increased
Likely CXR findings with tricuspid regurgitation
Cavitary lesions and pulmonary edema from congestion
Uses of TTE and TEE
For detecting endocarditis of native (TTE) and prosthetic (TEE) valves
Indications for endocarditis prophylaxis
Patient has: Prosthetic valve, heart transplant recipient, previous endocarditis history, or uncorrected cyanotic heart disease
Patient is undergoing: Dental work w/ bleeding or tonsillectomy/adenoidectomy
Right-sided heart failure causes what?
Systemic veinous congestion -> Anasarca
Left-sided heart failure causes what?
Pulmonary veinous congestion -> Pulmonary edema
AND decreased ejection and systemic perfusion
Mainstay diagnostic tool for valvular disease?
Echos - TTE or TEE
Causes of tricuspid stenosis
Rheumatic fever = w/regurgitation and MV stenosis, no calcification)
Carcinoid scarring = endocardial fibrosis causes decreases movement, causes combined stenosis and regurgitation
Congenital = Ebstein’s anomaly (TV pulled down into RV), atresia
Tricuspid stenosis symptoms
Fatigue, dyspnea
Forward failure = low CO, up RAA
Backward failure = anasarca
TV stenosis findings
Mid-diastolic murmur over L lower sternal border
Increases w/ inspiration (RS)
Hepatomegaly w/o pulsations
Anasarca
TV stenosis labs
CXR shows large RA, no pulmonary artery enlargement, and clear lungs (Pathognomonic triad)
EKG shows large p-waves unless AFib present
TV regurgitation causes
Rheumatic fever, endocarditis, trauma, carcinoid, myxoma
Functional causes from MV regurgitation (majority)
Congenital = Ebstein’s anomaly
TV regurgitation findings
Dyspnea, AFib Pansystolic murmur, increases w/ inspiration (RS) Hepatomegaly w/ pulsations JVD Anasarca
TV treatment
Observe mild-mod cases
Medical treatment for functional disease caused by left-sided lesion
Ring valvuloplasty/repair for severe disease
Commissurotomy to treat congenital/rheumatic stenosis
Replacement in infective, carcinoid, calcified stenosis
Ross procedure
Remove pulmonary valve as an autograft to replace an aortic valve in children to avoid future heart surgery
Mitral stenosis symptoms
Down CO, LA hypertrophy, Pulmonary hypertension and edema
Cough, hemoptysis, dyspnea on exertion
MV stenosis findings
LV normal or small
Auscultatory triad = apical diastolic rumble, loud S1, opening snap
CXR shows large LA, normal heart size, and straight L heart border
MV calcified on imaging
Engorged pulmonary lymphatics (Kerley’s lines)
MV stenosis cause
Rheumatic disease -> Fibrosis, calcification
MV stenosis treatment
Observation/medical - keep up w/ echos, use anticoagulation if thrombus or AFib if asymptomatic
Percutaneous balloon commissurotomy if minimal calcification, mild disease, and no LA thrombus
Open commissurotomy or replacement with severe stenosis
Repair is rare due to fibrosis
Pulmonary HTN reverses post-op
MV regurgitation causes
Rheumatic Infective endocarditis Secondary to MI, cardiomyopathies, LV aneurysm CT diseases Myxoma Prolapse Trauma Papillary muscle rupture/dysfunction
MV regurgitation findings
Loud pansystolic murmur transmitting to axilla
Up LA and pulm vein pressure
Fatigue, dyspnea, AFib, palpitations
LA hypertrophy
If acute due to ruptured muscle post MI, pulm edema due to inability of LA to compensate
MV treatment
Observe mild disease w/ echos for thrombi
Medical - diuresis to reduce afterload, anticoagulation, maybe b-blockers
Surgery - repair/annuloplasty for symptomatic severe cases, replacement if repair impossible
Acute cases require urgent surgery
Aortic stenosis causes
Degeneration/Calcification - most common, may block conduction with lots of Ca
Congenitally bicuspid valve
Rheumatic w/ MV disease
Aortic stenosis pathology
Up afterload, concentric LV hypertrophy (wall only) that depends on atrial contraction to fill; AFib with this is bad
LV hypertrophy can lead to LV failure as increased muscle increases O2 demands -> ischemia, microinfarcts -> failure
Most common fatal valve lesion
Aortic stenosis findings
Angina, syncope, CHF, sudden death
May be asymptomatic for years, but then malignant once sx develop
Systolic ejection murmur at R 2nd ICS radiating to carotids
EKG shows LVH, maybe blocks like R/LBBB, AVB, AFib
CXR shows valve calcification, aortic enlargement
Aortic stenosis treatment
Observe mild-mod disease
Medical - control HTN, arrhythmias
Surgery if severe for valve replacement
Aortic regurgitation causes
Degenerative calcified AV, mixed AS/AR Rheumatic Bacterial endocarditis Congenital RA, AnkSp Marfan's Aortic dissection Trauma VSD involving valve leaflets Myxoma
Aortic regurgitation pathology
AR causes LV volume overload -> massive LV dilatation, eccentric hypertrophy (up chamber size and wall thickness) -> LV failure
Decreased diastolic coronary flow from regurg -> May get angina with normal coronaries
Aortic regurgitation symptoms
Dyspnea, angina
May be asymptomatic until LV dysfunction and impending CHF
Widened pulse pressure
Blowing diastolic murmur
Austin-Flint murmur from turbulent flow against MV heard at apex
Water hammer pulse = bounding, forceful peripherally
Quincke’s pulse = pulsating nail beds
De Musset’s sign = head bobbing w/ cardiac cycle
Duroziez’s = sys/diastolic murmur of femoral aa
Traube’s = pistol shot sound over large aa
Aortic regurgitation labs
LVH, pulmonary edema, regurgitant jet on echo, enlarged ascending aorta
Aortic regurgitation treatment
Surgical comparison to AS?
Observe mild-mod w/ serial echos
Medical - reduce afterload by diuresis, treat HTN
Surgery to replace valve if severe, repair occasionally; May need to replace ascending aorta
AR patients do worse than AS patients post-op in general
When to place a pacemaker in CHF?
When EF below 30% with MI OR 35% w/o improvement of chronic condition despite Rx
CHF treatments (general, daily Rx, refractory Rx)
Diuretics, vasodilators, inotropes
General treatments: Limit Na+, monitor weight for rapid gain, vaccinations to stop infxn ACE inhibitors b-blockers Spironolactone Hydralazine Diuretics Digoxin Pacemaker / resynchronization
Refractory treatments:
Dobutamine, milrinone for inotropic support
LV assist device - assists pumping
Cardiac transplant
Heart failure definition
Syndrome from structural or functional cardiac disorders impairing heart’s ability to fill with or eject blood
Reasons for acute CHF decompensation
Dietary or medication noncompliance
Inappropriate medications
Don’t seek care
Acute ischemia, HTN, arrhythmias
Backward failure causes ?
Forward failure causes ?
Backward = congestion, needs vasodilators and diuresis Forward = poor perfusion, needs inotropes
Signs of L-sided CHF
Low CO -> RAA and SNS activation -> fluid retention (up preload) and vasoconstriction (up afterload) -> Up LV end-diastolic P ->
Pulmonary edema and high PV pressure
Patient uses accessory muscles for breathing (like COPD)
Rales
Hemoptysis
Paroxysmal nocturnal dyspnea, orthopnea
Signs of R-sided CHF
Dilated liver veins
JVD
Pitting edema, weight gain, fatigue
Causes of HF
Coronary atherosclerosis (about 1/2) HTN DM Valvular disease Alcohol Infection
HF diagnosis
Clinical exam
Echo
BNP levels up when RV/RA pressures up
CXR: cardiomegaly, vascular engorgement, Kerley B lines, pleural effusion
Ejection fraction and heart failure
Normal over 50%
Mild less than 50%
Moderate less than 40%
Severe less than 30%
Pericardium description
Double-layered fibroelastic sac w/ 15-50mL plasma ultrafiltrate filling it
Causes of pericarditis
Idiopathic - most common
Infection - bacterial (TB/from HIV, pneumococcus, strep, staph, legionella), viral (coxsackie A/B, echo, mumps, adeno, HIV), fungal (histo, coccidio, candida, blasto)
Radiation
Neoplasm
Trauma
Autoimmune - SLE (drug associated w/ procainamide, isoniazid, hydralazine)
Metabolic - hypothyroidism or uremia
Cardiac - early infarction pericarditis, post-cardiac injury (Dressler’s), myocarditis, dissecting aortic aneurysm
Pericarditis pathology
Usually serous fluid accumulation or exudate due to infection, may cause adhesions
Pericarditis signs
Sharp, stabbing chest pain unrelated to exertion that’s worst laying flat
Pericardial friction rub, ECG changes, pericardial effusion, fatigue, dyspnea, may have fever
Pericarditis evaluation - ECG and CXR
ECG shows inflammation of epicardium, not epicardium (electrically inert) = DIFFUSE ST-elevation and PR-depression, later duffuse T-inversions w/ normal STs and PRs; Also sinus tachycardia
Normal CXR
Acute pericarditis complications
Pericardial effusion and tamponade
Constrictive pericarditis (late stage)
Relapse
Acute pericarditis DDx
ACS, myocarditis, aortic dissection
Pleurisy, pneumonia, PE, pneumothorax
MSK or esophageal pain
Pericarditis treatments
Idiopathic and viral: NSAIDs, colchicine
Post-acute MI: Aspirin, colchicine (avoid NSAIDs to allow scar formation)
Glucocorticoids, esp. for autoimmune
Causes of pericardial effusion
Acute pericarditis
Radiation, malignancy
Cardiac perforation
Hypothyroidism CT disease Post-MI/heart surgery Chronic renal failure Aortic dissection
Signs of pericardial effusion
Electrical alternans on ECG w/ sinus tach, low voltage
CXR shows new grossly enlarged heart
CHF symptoms w/ clear lungs = Edema, JVD
Pericardial tamponade pathology
Pericardial fluid increases pressure, impedes diastolic filling of LV/RV -> SV, CO, BP down; HR up
Pulsus paradoxus and its mechanism
Fall of systolic BP of at least 10mm w/ inspiration
Inspiration normally ups RV inflow, but w/ fluid compression, septum shifts and LV volume downed
Pericardial tamponade findings
Sinus tach
Tachypnea
Hypotension, narrow pulse pressure, pulsus paradoxus
JVD w/ loss of Y-descent
Edema
ECG w/electrical alternanas and low voltage
EMERGENCY - perform pericardiocentesis
Constrictive pericarditis pathophys, causes, signs, findings
Pericardial scarring -> Encasement, impaired diastolic filling of ventricles
Idiopathic, viral, cardiac surgery, radiation
‘Dip and Plateau’/’Square root’ sign on ECG
Unexplained R heart failure - may be misdiagnosed as cirrhosis
JVD, prominent x and y descents, pericardial knock, Kussmaul’s, anasarca
CXR shows pericardial calcification or thickening
Low voltage ECG w/ ST and T changes
Kussmaul’s sign?
Lack of inspiratory decline in JVP = opposite of normal
Constrictive pericarditis treatment
Diuretics, pericardial stripping
Chronic ischemic heart disease risk factors
(Same as atherosclerosis)
Age, FH, DM, HTN, smoking, cholesterol, obesity, lack of exercise
Metabolic syndrome
Any 3 of:
HTN, abdominal obesity, low HDL, high triglycerides, high fasting glucose
Manifestations of coronary artery disease
Chronic stable angina Unstable angina MI CHF Sudden cardiac death Silent ischemia
Typical angina features vs atypical angina
Substernal pain, brought on by exertion/stress, relieved by rest/NTG
Atypical missing one or more of these
Chest pain DDx
Coronary artery disease, myocardial ischemia
Aortic dissection (sudden, bad pain, unequal pulse), hematoma
Pericarditis (Sharp, worse with inspiration)
PE (sudden dyspnea), pneumonia, pneumothorax, pleurisy
Esophageal spasm, inflam, or stricture; GERD (burning w/ meals)
Anxiety
Musculoskeletal (fleeting, reproduced w/ palpation)
Non-atherosclerotic coronary artery diseases
Coronary vasospasm - Prinzmetal angina Anomalous coronary arteries Coronary arteritis Coronary dissection Myocardial bridge (myocardium crosses one of coronary arteries) Coronary embolization
When to perform a stress test (or any test)?
When a positive or negative test result will determine the therapy the patient will receive
Evaluation of ischemic heart disease
Confirm the diagnosis of CAD
Assess functional limitations due to symptoms
Assess modifiable risk factors
Assess the ischemic burden - how much muscle, how many vessels, how severe - can you revascularize?
Assess LV function
Bad prognostic ST changes in stress tests
Worse signs: Greater magnitude, earlier timing, longer duration, more leads involved
When to do stress imaging w/o exercise
Patient can't exercise, has an abnormal ECG, or known CAD Use dobutamine (ino-/chronotropic) or adenosine (coronary vasodilatation -> relative hypoperfusion of stenosed artery)
Stress imaging findings indicative of high risk
Wall motion abnormalities in multiple coronary territories
Large wall motion abnormalities in single territory
LV dysfunction (low EF)
When to do cardiac catheterization?
In patients with stenosis AND ischemia
W/o ischemia, don’t catheterize = medical therapy
Ischemic heart disease management
Aspirin Sublingual NTG as needed Lipid lowering therapy Healthy lifestyle Activity as dictated by symptoms Report symptom changes immediately
Risks for STEMI
Age over 65y At least 3 CAD risks ST-deviation on ECG at admission Prior coronary stenosis over 50% At least 2 angina episodes in last 24h Elevated cardiac markers Aspirin use in last 7d
- If ECG shows ST-elevation or new LBBB or true posterior MI, then … ?
- If ECG shows ST-depression or T-inversion?
- This is a STEMI
2. Are troponins raised? YES = NSTEMI, NO = Unstable angina
T-inversion globally in leads may be a sign of what?
Intracranial hemorrhage
STEMIs vs NSTEMIs and risk of death
STEMI patients are more likely to die in hospital
NSTEMI patients are more likely to die after being sent home inappropriately
Nitrates mechanism, use, CIs
Up NO formation -> Up guanylate cyclase activity -> Up cGMP -> Vascular smooth muscle relaxation
For angina control
CI if on phosphodiesterase inhibitors (Viagra) or RV infarction (Hypotension, JVD, but clear lungs; ST-elev in R leads)
Beta-blockers mechanism, use, CIs, ones to avoid
Decrease O2 demand (Down HR, Afterload, contractility) -> Down O2 deficit
Use in all patients w/ ACS unless CI (hypotension, bronchospasm, bradycardia, coronary spasm)
Avoid b-blockers w/ ISA (partial agonists)
Aspirin substitutes?
Clopidogrel (Plavix)
Prasugrel - not as often used b/c of bleeding risk
Ticagrelor
Heparin
Low MW heparin is better than unfractionated heparin for reducing risk in ACS
GP IIb/IIIa inhibitors
Abciximab, intelligrin
