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Cardiovascular [a bunch of images] General Circulatory HTN, Edema, Thrombosis, PE, DIC, Shock, CHF, Cor Pulmonale General Metabolic hyperlipidemia, atherosclerosis (PVD) Ischemic ANGINA, MI (myocardial infarction) Cardiomyopathies dilated, restrictive, HOCM Arrhythmias bradycardia, heart block, atrial fibrillation, atrial flutter, SVT MAT, VT, prolonged QT, torsades de pointes Valvular AS, MS, AR, MR, TR, Rheumatic Fever antibiotic prophylaxis Aortic Aneurysm Aortic Dissection Endocarditis Myocarditis Pericardial Disease pericardial effusions, acute pericarditis, infectious pericarditis, Dressler’s, uremic, restrictive pericarditis, cardiac tamponade Cardiac Tumors, Cardiac Malformations [cardiac pre-op][cardiac physiology][cardiac physical exam][EKG reading] [cardiac labs] Cardiac PhysiologySingle Cardiac Cycle [see diagram] Jugular Venous Pulses [see diagram] Swan-Ganz catheter [interpretation of values] Radiology of the Heart in Cecil’s at MDconsult (great pictures) Fick equation CO = (O2 consumption) / (AO2% - VO2%)(Hg)(1.36)(10) Cardiac Physical Exam Systolic murmurs [see diagram] Diastolic murmurs [see diagram] Low-Pitched Sounds Bell S3, S4, MS, AR (Austin-Flint) High-Pitched Sounds Diaphragm everything else
S1 increased (↑) LVH (muscle), MS S1 decreased (↓) LVH (collagen), LV dilatation/dysfunction, some MR, AR, prolonged PR, LBBB Note: mechanisms can be way too complex and you’ll make yourself crazy; just refer to this S2 (normally S2 splitting increases with inspiration due to increase venous return and RVEF; it follows that inspiration will increase most right-sided murmurs/gallops) abnormally increased split S2 Delayed RV (electrical): incomplete RBB, pacemaker, PVC Delayed RV (mechanical): VSD (if LR flow), pulmonic stenosis, severe pulmonary edema (↑ impedance) Shortened LV ejection time:, MR
fixed split S2 ASD (explanation; why not variable? RV already ~max overloaded; and L/R atrial pressures equalized so no net Δ in LV/RV output with inspiration—unlike VSD) mild pulmonary HTN RVF
paradoxically split S2 (decreases with expiration) usually from delayed A2 due to electrical (complete LBB (1st), RV PVC) or mechanical (AS, HOCM, acute ischemia, myocarditis, CHF) S3 AR, TR, MR / don’t confuse with “tumor plop” S4 stiff ventricle (various causes) / it can’t happen during Afib Jugular Venous Pulsations (JVP) [diagram] “dip and plateau” or “square root” sign constrictive pericarditis Kussmaul’s sign constrictive pericarditis Prominent y descent constrictive pericarditis Large V wave TR Canon a wave AV dissociation Pericardial effusion r/o tamponade (pulsus paradoxus, undulating pulses) elevated venous pressure Borderline – expiration/inspiration 105/94 Electrical alternans or alternating voltage big pericardial effusions from TB and tumor [< 5 mm leads 1-aVF] / can also be from AV fistula in lungs/coronary vessels Treatment: pericardial window / can also obliterate pericardial space with nitrogen mustards, talc, tetracycline to prevent recurrence Pulsus paradoxus > 10 mmHg fall in SBP during inspiration / occurs in 95% of cardiac tamponade (as well as disorders involving intrathoracic pressure changes, such as COPD) / 4 mechanisms septal shift/pressure, RV enlargement (prevents filling of LV) tensing of pericardium (impairs cardiac output) increased capacitance of pulmonary capillary bed (decreases LV filling) decreased afterload (negative intrathoracic pressure, this is normal) Tilt Table Testing Decreased preload stimulates Bezal Jarisch reflex / catecholamines can be used to enhance this reflex / hold vasoactive drugs for 5 half-lives before / endpoint is pre-syncope w/ hypotension or bradycardia Reading EKG’s [Vectorial diagram of Limb Leads] EKGs of the Major Arrhythmias [tutorial with pictures] Method for EKG reading: heart rate / heart rhythm / intervals / axis deviation / hypertrophy EKG reading in myocardial ischemia For ECG changes associated with electrolyte disturbances (see lytes) [potassium ECG] Definitions: If the QRS complex begins with a negative deflection, it is called a Q wave 1st positive deflection is R wave a negative deflection following an R wave is an S wave T waves are positive because the ventricles repolarize from epicardium to endocardium (opposite of contraction) Heart Rate Each small box is 0.1 mV and 0.04 seconds / one large square is 0.2 seconds (5 small boxes of 0.04) HR is 300/# of large boxes in RR interval [ex., 4 large boxes between R waves 300/4 or 75 bpm or just count # of large squares from 1,2,3,4,5,6 corresponds to 300, 150, 100, 75, 60, 50 Heart Rhythm Regular? Are P waves present? In sinus rhythm, P waves should be upright in lead II (unless reversal of leads or dextracardia) Are P waves related to QRS? [sinus arrhythmia v. multifocal atrial tachycardia v. atrial fibrillation v. ventricular arrhythmias etc.] Intervals PR interval [0.12 to 0.21] becomes shorter as HR increases QRS Axis Extreme left axis (-90 to -180°) Right-axis deviation in presence of LBBB (+90 to +180°)
RBBB: >140 msec QRS Morphology QT interval normal is less than ½ RR interval with HR < 100 Prolonged QT interval QTc – corrected for heart rate / women > men / can be a sign of ischemia (lack of ATP and reduced inward K current) / can cause torsades de pointes Prolonged QT: class Ia and III agents, sotalol, amiodarone, TCA’s, phenothiazines, ketoconazole, quinolones, erythromycin, clarithromycin, antiemetics, antipsychotics, pentamidine, hypomagnesemia, hypokalemia, hypocalcemia, hyperthyroid, hypothyroid, intracranial bleeds, congenital long QT Shortened QT: hypercalcemia, digitalis (scooping) Tip: regarding intracellular electrolytes (K, Ca, Mg) ↑ Elevations shorten ↓ QT interval ↓ Depressions prolong ↑ QT interval Voltage low voltage is any 3 limb leads < 15 mm or any one precordial lead < 10 mm Causes: pericardial effusion/tamponade, emphysema, obesity Axis [vectorial diagram of limb leads] Calculate Axis If lead I and II /aVF are both positive 0 to 90 and normal axis (down and to the left) If lead I is positive and II/aVF is negative LAD If lead I is negative and II/aVF is positive RAD Note: axis can also be determined by finding the isoelectric deflection (i.e., shortest QRS) (axis is perpendicular to that vector) Frontal planes: axis deviation (I, II/AVF) Horizontal planes: axis rotation (V1-6)
LAD LVH, LBBB, LAFB RAD RVH, RBBB, LPFB, RV strain (pulmonary HTN, PE), emphysema / may be normal in children, young adults Note: mean QRS tends to point away from infarct, toward hypertrophy Hypertrophy LVH sum of deepest S in V1 or V2 and tallest R in V5 or V6 is > 35 mm (in patients > 35 yrs) R in aVL > 12 mm (strain pattern) R in V6 > 25-35 mm Note: may see asymmetrical or inverted T in V5 or V6 (strain pattern ~ ST ↓ with upward hump in middle) Criteria for LVH (sensitivity/specificity) RaVL + SV3 > 28 mm (men) (40/95) or RaVL + SV3 > 20 mm (women) SV1 + RV5 or RV6 > 35 mm (30/95) RV5 or RV6 >/= 25 mm (20/95) RaVL > 11 mm (20/95) RVH right atrial enlargement, right axis deviation, incomplete RBBB, low voltage, tall R wave in V1, persistent precordial S waves, right ventricular strain Criteria for RVH (sensitivity/specificity) Limb lead criteria R in I S2 S2 S3 (45/75) Precordial lead criteria R/S ratio in V1 > 1 (30/100) R wave height in V1 > 0.7 mV (30/100) S wave depth in V1 < 0.2 mV (20/100) R/S ratio in V5 or V6 < 1.0 (10/100) QR in V1 (-/100) QRS axis > + 90 degrees (15/100) P wave amplitude > 0.25 mV in II, III, aVF, V1 , or V2 (20/100) LAE (P-mitrale) broad, notched (M-shaped) P waves in mitral leads (I, II, aVL) or deep terminal negative component to P in lead V1 (biphasic V1 is the most specific criterion) / causes include MS, HTN RAE (P-pulmonale) P waves are prominent V1 or > 2.5 mm in any limb lead (tall, peaked in II) EKG segments [anterior heart] [posterior heart] Q waves Septal depolarization normally moves from R to L causing small downward deflection in V6 Significant Q waves > 1 mm wide or > ⅓ QRS amplitude (measured from top to bottom) / can start early in MI or in ensuing weeks Small, insignificant Q waves normal is < 0.04 seconds in I, aVL and V1-6 / < 0.025 in II and < 0.030 in aVF small “septal Q’s” commonly seen in lateral leads (I, aVL, V4, V5, or V6) mid-septal depolarization (from LBB) moving L to R medium to large Q waves may be normal in aVR if not lead placement Q in V2 could be lead placement, LVH, LBB, pulmonary disease downgoing delta waves in II, III, aVF can mimic Q waves large (deep, broad) Q’s in I and III may occur in HOCM R waves R in V1, V2 with posterior MI (see below) Intrinsicoid deflection > 50 mm with some LVH Delta wave with WPW, large R in I with LBBB and LAFB, large R in inferior leads with LPFB R wave progression transition should occur between V2 and V4; LVH may change vector of conduction such that R wave progression seems poor (yet not ischemic); poor R wave progression is c/w prior anteroseptal infarct; early R wave progression can be sign of prior inferior infarct S waves V6 with RBBB Large S in inferior leads with LAFB Large S in lateral leads with LPFB T wave changes [diagram] – cannot definitively localize MI’s subepicardial ischemia (inverted, symmetric), subendocardial ischemia (peaked) hyperacute MI (tall, peaked, may have associated ST ↑ and/or Q’s) RBBB, LVH, RVH (septal leads), LBBB (lateral leads) hyperkalemia (peaked, also with widened QRS, prolonged PR, sine wave) [ECG] hypokalemia (may have flat, inverted T) pericarditis (inverted), intracranial hemorrhage (ICH) Note: can be normal in limb leads, but usually pathological in V2 to V6 Wellen’s T waves – deep, symmetric TWI (usu. early precordial leads) may occur in significant left main or proximal LAD ST segment changes [diagram] shape more important than size of changes / J point is the beginning of the ST segment / ST segment changes tell you where the injury is because the injured tissue remains depolarized when surrounding tissue is repolarized / diffuse ST elevations with chest pain [table] ventricular aneurysm: can produce baseline ST elevations pericarditis: ST elevations are flat or concave (often entire QT segment) ST elevation Diffuse: pericarditis, myocarditis, cerebral hemorrhage, others Localized: transmural ischemia, MI, wall motion disorder (e.g. aneurysm), others
subendocardial ischemia (e.g. angina) ST ↓ V1, V2 with posterior MI (flip and invert EKG to see posterior ST ∆’s) reciprocal changes with ST elevation MI’s (note:) LVH, LV strain with repolarization (inverted T’s) hypokalemia digoxin toxicity U waves (+) > 1 mm / caused by class Ia drugs, hypokalemia [pic], hypomagnesemia, CNS disease (TU fusion waves) [pic], LQTS (+/-) [pic] / predisposes to torsades de pointes (-) HTN, AV valvular disease, RVH, major ischemia, 60% of anterior MI, 30% of inferior MI, 30% of angina ECG changes suggestive of MI ST changes: convex suggests infarction (concave could be pericarditis, other) ST ↑ > 2 mm in 2 contiguous (by grouping) precordial leads ST ↑ > 1 mm in 2 contiguous (by grouping) limb leads > 1 mm ↓ in at least 2 contiguous leads suggests ongoing ischemia (subendothelial infarct, positive stress test) or digoxin effect In presence of LBBB: cannot exclude MI but MI very likely if: ST ↑ > 1 mm concordant with QRS (in same direction as QRS) ST ↑ > 5 mm discordant (not in same direction as QRS) ST ↓ > 1 mm in V1, V2 or V3 Indication for thrombolysis: > 2 mm ST elevation in 2 limb leads, new onset LBBB Contraindications include SBP > 180 (at any time, despite what happens after BP meds) Reciprocal changes suggest ischemia (where to look) Inferior ST depression, T inversion anterior leads Anterior ST depression, T inversion inferior lateral Lateral ST depression, T inversion inferior, anterior Localization of infarct Which artery is/was occluded I, aVL (high lateral) – L circumflex V1- V4 (anteroseptal) – LAD (see below) V5- V6 (lateral) – L circumflex II, III, aVF (inferior) – RCA (85%), L circumflex (15%) Note: minimal ST changes and inverted T waves in II, III, aVF common with circumflex a. occlusion ⅓ of inferior MI involve right ventricle / get right sided ECG if inferior leads involved, because right ventricular MI requires much different treatment! (see treatment of MI and avoid nitrates) Anterior Vs. Posterior MI V2 is most reliable for determining anterior vs. posterior (it lies in the A-P vectorial plane through LV) Don’t confuse anterior sub-endocardial MI with posterior MI acute posterior MI (would be mirror of anterior MI) V1-V2 w/ large R wave, ST depression LAD occlusion Scenario A (wrap-around LAD) V3 V4 ST II, III, AVF ST Scenario B V1V2 ST II, III, AVF may be normal 2o to cancellation of vectorial forces I, AVL, ST if affecting high diagonal Scenario C ST I, AVL, V1-6 ST II, II, AVF
PCWP > LVEDP in MS, LA myxoma, pulmonary venous obstruction, patient on PEEP PCWP < LVEDP with “stiff” left ventricle ( > 25 mm Hg) Cardiac output [3.5 to 7 L/min] Cardiac index [2.4 to 4 L/m2] SVR [900-1300 dynes/sec/cm-5] PVR [155-255 dynes/sec/cm-5] Download 3.95 Mb. Share with your friends:
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