Cardiology
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| 🇬🇧 | 🇬🇧 |
| What are the disorders in PR interval? | Short PR (WPW syndrome - accessory pathway conducting impulse without AV delay called delta-wave) |
| What is an EKG? | Representation of the electrical events in the cardiac events Each event has a distinct wave form Gives an insight into pathophysiology |
| What can be identified by EKGs? | Arrythmias, Myocardial ischemia and infarction, pericarditis, chamber hypertrophy, electrolyte disturbances (hyper/hypokalemia), drug toxicity (digoxin prolongs QT interval) |
| What are the pacemakers of the heart? | SA node (dominant pacemaker, rate 60-100 bpm) AV node (back up, 40-60 bpm) Ventricular cells (back up, 20-45 bpm) |
| What is the standard calibration of EKG? | 25mm/s, 0.1 mV/mm If an electrical impulse is going towards the electrode appears positive, if away appears negative. |
| What do each EKG wave refer to? | P wave: atrial depolarization QRS: Ventricular depolarization (and atrial repolarization) T wave: Ventricular repolarization |
| What are the EKG leads? | They measure difference in potential between two points, either unipolar or bipolar. 12 leads, 6 limb leads (3 std and 3 augmented) and 6 precordial leads |
| What are the std limb leads and where are they installed? | Right arm, left leg and left arm Lead I (bipolar, RA to LA 0 degrees) Lead II (bipolar RA to LL +60 degrees) Lead III (Bipolar LA to LL +120 degrees) |
| What are the augmented limb leads and where are they installed? | AVR (unipolar, -150 degrees at right arm) aVL (unipolar, -30 degrees at left arm) aVF (unipolar, +90 degrees at left leg) |
| Where are precordial leads installed? | V1 right lower sternum, V2 left lower sternum (septal pulse) V3 between V2 and V4, V4 midclavicular (anterior pulse) V5 between V4 and V6, V6 midaxillary (Lateral pulse) |
| What are right and posterior leads? | Right placement like left for dextrocardia Posterior leads (3 cords under the scapulae. |
| What are the 10 rules of EKG? | 1-PR interval between 3-5 little squares (120-200 ms) 2-QRS less than 3 little square (110 ms) 3-QRS positive in leads I and II 4- QRS and T waves have same direction in limb leads 5-aVR all negative 6-R and S grow from V1 to V4 And S disappears in V6 7-ST segment starts isoelectric except V1 and V2 8-P wave upright in I, II and V2-V6 9-No Q or small Q I,II, v2-v6 (1 little square) 10-T wave upright in I, II, V2-V6 |
| How is the P wave? | Always positive in I and II and negative in aVR <3 squares duration and 2.5 amplitude Biphasic in V1, best seen in lead II Biphasic (first phase is for right atrial contraction and second is for left atrial contraction) |
| What are the disorders in P wave? | P Pulmonale (right atrial enlargement, pointed p wave and tall >2.5 squares) P Mitrale (left atrial enlargement, bifid p wave) |
| What is PR interval? | It is from the beginning of P till the beginning of QRS Represents atrial depolarization + delay in AV junction which allows time for atria to contract fully before ventricular contraction. |
| What are the disorders in PR interval? | Short PR (WPW syndrome - accessory pathway conducting impulse without AV delay called delta-wave) Long PR (First degree heart block (AV block)) |
| What are QRS complexes characteristics? | Q wave nonpatho in I,III, aVL, V5 and V6. R wave in V6 smaller than V5 S wave depth not more than 30mm Patho Q wave if >25% of R wave ampitude |
| What are the pathologies in QRS wave? | Right Ventricular Hypertrophy (V1 less positive R and V6 less negative) Left Ventricular Hypertrophy (V1 more negative and V6 more positive, Sokolow and Lyon criteria: R >11-13mm) Tall R (Right BBB, posterior MI, Type A WPW syndrome, RVH) |
| What is the ST segment? | Between end to QRS and Beginning of T, isoelectric, considered elevated or depressed by 1 mm Elevated in case of Acute MI (AMI_ |
| What is the T wave? | Asymmetrical, less that 2/3 of R amplitude follows QRS axis direction |
| What is an abnormal T wave? | Abnormal T waves are symmetrical, tall, peaked, biphasic or inverted. |
| How is the QT interval? | It is the duration of depolarization and repolarization. As heart rate increase, QT decrease, should be between 0.35 and 0.45 s and shouldn't exceed more than half of RR interval |
| What are the U waves? | • U wave related to afterdepolarizations which follow repolarization • U waves are small, round, symmetrical and positive in lead II, with amplitude < 2 mm • U wave direction is the same as T wave • More prominent at slow heart rates |
| How to calculate HR using 300s rule? | Count big boxes between RR, divide 300 by the number of boxes |
| How to calculate HR using 10s rule? | Count all the waves in the display under and multiply by 6 (for waves that are irregular) |
| What is the QRS axis? | It represents the overall direction of the hearts electrical activity. abnormalities hint at ventricular enlargements and conduction blocks. Normal axis is between -30 deg and +90 deg |
| What are the abnormal QRS axis? | -30 , -90 this is Left axis deviation +90 , +180 this is right axis deviation +180 , -90 this is indeterminate axis |
| What is the quadrant approach to get the QRS axis? | See Leads I (0 degree) and aVF (+90 degree). If both positive -->normal If Lead I negative and aVF positive --> RAD If both negative -->indeterminate If Lead I positive and aVF negative --> check Lead II if Positive normal if negative LAD |
| What is the equiphasic approach to get the QRS axis? | Check the most equiphasic QRS among the limb leads, QRS is the lead 90 degrees away from the most equiphasic, it can be positive or negative |
| What are the bradyarrhythmias? | Sinus Bradycardia, Junctional Rhythm, SA block, AV block |
| Describe the sinus bradycardia. | All appears regular (QRS, PR...) but we have a long PP interval. There appears to be a problem in SA conduction of impulse (commonly sick sinus syndrome - low battery) |
| Describe the junctional rhythm. | No P wave, electrical impulse is done by the AV node not the SA, QRS normal. May be caused by hypokalemia, MI, digitalis toxicity... |
| What is the SA block? | Sudden absence of a complete cardiac cycle after being normal with a regular rhythm. Occurs for athletes, digitalis toxicity, hypokalemia, sick sinus syndrome. What happens is that the sinus impulse is blocked within the SA node Irregular and unpredictable |
| How many types of AV blocks are present? | First Degree Second Degree (mobitz type 1 and type 2) Third Degree |
| How is the first degree AV block? | It is a delay in conduction, prolonged but constant PR interval Associated with Carditis, digitalis, beta blockers, ischemia, AV/ junctional disease |
| How is the second degree AV block? | Intermittent conduction failure in AV, blocked by AV node, two mobitz types |
| How is mobitz type 1 AV block? | Classic AV Wenckebach: PR gradually increases untill there is a pause RR decreases until the pause occurs then RR after pause is longer than RR before the pause. |
| How is mobitz type 2 AV block? | Sign of bilateral bundle branch block, normal/prolonged PR interval but at some point there is a pause (no QRS after a P) |
| How is the third degree heart block? | Complete dissociation of a rhythm, SA node fires alone and AV fires alone, cause bradycardia (RR interval increases -->45 bpm) |
| How to see a pacemaker on EKG? | Spikes at the Q |
| What is AV dissociation? | Non conducted PACs and QRS escapes |
| What are the problems causing arrhythmias? | Problems in • Sinus node • Atrial cells • AV junction • Ventricular cells |
| What SA node problems cause arrhythmias? | Fast firing (sinus tachycardia- may be caused by stress) or slow firing (sinus bradycardia) |
| What atrial cell problems cause arrhythmias? | Premature atrial contractions (if they fire occasionally from a focus) Atrial flutter (if the fire continuously in a looping circuit) |
| What AV junctional problems cause arrhythmias? | Paroxysmal supraventricular tachycardia by continous looping circuit firing AV junctional block by blocking impulses from SA node |
| How does premature atrial contraction appear on EKG? | Ectopic P waves appearing occasionally with a different contour (biphasic) with a normal sinus rhythm (NSR) |
| What are the supraventricular arrythmias? | • Atrial Fibrillation • Atrial Flutter • Paroxysmal Supraventricular Tachycardia |
| What is atrial fibrillation? | It is a deviation from NSR, no normal P wave due to no normal atrial depolarization (impulses are not from sinus node) chaotic atrial activity Many P waves appear before conduting a QRS wave Commonly affects elderly >80 yrs |
| What are the ventricular arrhythmias? | • Ventricular Tachycardia • Ventricular Fibrillation |
| How is ventricular tachycardia? | Deviation from NSR, impulse originates from ventricles so no P waves and many conseqeutive QRS waves |
| How is ventricular fibrillation? | Completely abnormal low QRS with no P wave |
| What are bundle branch blocks? | Stopping of conduction either at right bb or left bb, appears at the QRS complex. QRS widens and changes morphology |
| How is RBBB? | In V1 and V2 appears as rabbit ears (goes first to the right ventricle starts impulse then blocked so it becomes negative, then left bundle conducts so it goes back to positive) |
| How is LBBB? | Wide and deep negative S wave |
| What are the lab findings of TTE in AR? | TTE is used to Describe valve anatomy, quantify aortic regurgitation, evaluate its mechanisms, define the morphology of the aorta, and determine the feasibility of valve-sparing aortic surgery or valve repair. at 4 levels annulus, sinuses of Valsalva, sinotubular junction, and tubular ascending aorta early detects change in LV size and function |
| What are the aortic valve diseases? | Aortic stenosis and Aortic regurgitation. |
| What are the etiologies causing aortic stenosis? | Congenital (Bicuspid -most common heart valve defect, or Unicuspid valve) Degenerative Calcification Rheumatic Fever Radiation |
| How is the pathogenesis of AS? | Degenerative calcification of aortic cusps occurring on a substrate of congenital defect, chronic deterioration (trileaflet) and previous rheumatic inflammation It is not a passive process, features include vascular atherosclerosis, endothelial dysfunction, lipid accumulation, inflammatory cell activation, cytokine release and upregulation of signaling pathways. |
| How is the progression towards AS? | Risk factors include (genetics, older age, male sex, comorbidities, smoking, increased serum phosphate) this will lead initially into aortic sclerosis (by stress or inflammation preceding lipid inflitrates and myofibroblast differentiation) Then this will lead to aortic stenosis, first with progressive disease (by oxidative stress, increased Angiotensin II), then finally leads to aortic obstruction (hydroxyapatite nodules and cartilage and bone formation) with age |
| What are risk factors associated with development and progression of calcific AS? | High LDL, Lpa, DM, smoking, chronic kidney disease, metabolic syndrome |
| How is the pathophysiology of AS? | Obstructing LV outflow causes pressure gradient between aorta and LV, resulting in mean systolic pressure gradient >40 mmHg (between aorta and LV) with normal CO or aortic orifice area <1cm2. (leading to increased blood velocity through the valve |
| What are the complications associated with calcified aortic valve? | Pulmonary HTN, diastolic dysfunction, reduced LV systolic function, LV hypertrophy, myocardial fibrosis, reduction coronary flow reserve. |
| What is the natural history of AS? | Valve area decrease 0.1-0.3 cm2/year, systolic pressure gradient increases 10-15 mmHg/year, we can't predict rate of progression, average survival after symptoms is 2-3 years. severe AS can cause sudden death (rarely without any prior symptoms) |
| What are the symptoms of AS? | Rarely clinical if aortic valve >1cm2. Three cardinal symptoms are exertional dyspnea, angina pectoris and syncope |
| What are the physical findings if AS? | Regular rhythm, normal systemic arterial pressure, thrill or shudder palpable over carotid arteries (left). Systolic ejection murmur (after S1) increases intensity to reach a peak in middle of ejection, low pitched, rough and loudest at heart base (second right intercostal space) (grade III/VI |
| How is the initial evaluation of AS? | Pt with physical findings should undergo ECG, chest X ray. |
| What are the findings in TTE of AS? | ECG confirms it, assesses valve calcifications, LV functioning, wall thickness, and detects other valve disease. |
| What are the classifications of severity of AS? | Mild (10-20 mm area>1.2 cm2) Moderate (>20mm, area<1.2 cm2) Severe (>40mm, <1cm2) |
| What are serial testings of AS (follow up)? | ECG (if severe every 1 year, if moderate every 2 year, if mild every 5 years) ECG should be done whenever there is a change in clinical findings. |
| What are the indications of cardiac catherterization? | Recommended before any surgery, in pt with: history of CVD, suspected MI, LV systolic dysfunction, Men>40 and postmenopause, CVD risk factors, secondary MR. |
| What are the Abx prophylaxis that should be taken? | Should be considered for high-risk procedures, pt with prosthetic valves, pt with infective endocarditis, standard invasive procedure measures, considered in dental procedures... |
| What is the medical treatment of AS? | Asymptomatics don't have any medication, symptomatics need surgery not medication Most patients with moderate or severe AS should be advised to restrict physical activity |
| How is aortic valve replacement? | Recommended for severe AS, asymptomatic with severe AS and systolic LV dysfunction or demonstrable symptoms on exercise testing |
| What are the modes of interventions of AS? | We have two choices (surgical and transcatheter intervention) choice is according to clinical, anatomical, procedural team factors and risks and benifits ratio. Low-risk young pt <75 yrs or unsuitable for TAVI transfemoral (SAVR) Older pt, high risk pt unsuitable for surgery (TAVI) remaining pt both procedures are recommended SAVR recommended also for severe AS undergoing CABG or surgical intervention on ascending aorta |
| What are the etiologies of aortic regurgitation? | Valvular (congenital (bicuspid), endocarditis, myxoma, RF, traumatic, syphilis, SpA) Root disease (aortic dissection, cystic medial degeneration, Marfan's, non-familial aneurysm, bicuspid aortic valve) Aortitis HTN |
| How is the pathophysiology of aortic regurgitation? | Causes myocardial ischemia by decreased consumption, decreased stroke volume, decreased diastolic pressure, and left ventricular volume. |
| What is the natural history of AG? | 3/4 of pt are men, but primary valvular AR associated rheumatic mitral valve disease. Acute AR seen in infective endocarditis, aortic dissection, and trauma. |
| Talk about acute AR. | LV cannot dilate and maintain SV, diastolic pressire of LV then rises with elevation of LA and PA wedge pressure, causing pulmonary edema and cardiogenic shock. |
| Talk about chronic AR. | May be asymptomatic for 10-15 years, associated with exertional dyspnea, diminished cardiac reserve, orthopnea, paroxysmal nocturnal dyspnea, and excessive diaphoresis. Also angina pain could occur, even in younger patients, and may develop at rest or at motion. |
| What are the physical findings in severe AR? | Widened arterial PP of systolic and diastolic pressure, displaced LV laterally and inferiorly, a diastolic thrill may be palpable along left sternal border in thin-chested people, and a systolic thrill in suprasternal notch and towards carotid arteries. Aortic valve closure sound (A2) is absent. High-pitched decrescendo diastolic murmur heard best in third intercostal space along left sternal border. |
| What are the physical findings in mild AR? | Brief murmur holodiastolic (increases with severity) Mid-systolic ejection murmur audible in isolated AR heard at heart base transmitted along carotid artery. Austin-flint murmur (third murmur soft low pitched diastolic murmur, sometimes heard in AR) |
| What are the lab findings of TTE in AR? | TTE is used to Describe valve anatomy, quantify aortic regurgitation, evaluate its mechanisms, define the morphology of the aorta, and determine the feasibility of valve-sparing aortic surgery or valve repair. at 4 levels annulus, sinuses of Valsalva, sinotubular junction, and tubular ascending aorta early detects change in LV size and function |
| What are other lab findings seen for AR? | TEE CMR should be used to quantify the regurgitant fraction when echocardiographic measurements are equivocal or discordant with clinical findings CCT is recommended to assess the maximum diameter at four levels in patients with aortic dilatation |
| What are the measures taken before deciding treatment options? | Keep in mind that chronic AR pt don't have symptoms unless exists myocardial dysfunction and when delayed too long surgery doesn't restore LV function. so chronic AR need follow up and ECG done every 6-12 months if operation is necessary at optimal time (after LV dysfunction and prior to development of severe symptoms) |
| What are the operations done for AR? | It can be deferred as long as the pt is asymptomatic with normal LV function without severe chamber dilation. AVR indicated for severe AR symptomatic individuals irrespective of LV function. Operation should be carried out in asymptomatic pt with severe AR and progressive LV dysfunction. |
| What is the indication for surgery in AR? | Symptomatic pt, asymptomatic pt with LVESD >50 mm/ >25 mm/m2 BSA (small body size pt) or resting LVESD<50%, and symptomatic and asymptomatic pt with severe aortic regurgitation undergoing CABG or surgery of ascending aorta/other valve |
| When is aortic root/tubular ascending aortic aneurysm recommended? | Valve-sparing aortic root replacement is recom- mended in young patients with aortic root dila- tion, if performed in experienced centres and durable results are expected Ascending aortic surgery is recommended in patients with Marfan syndrome who have aortic root disease with a maximal ascending aortic diameter ≥50 mm. |
| What is cardiogenic shock? | Common cause of mortality with challenging management. It is caused by severe impairment of myocardial performance resulting in diminished CO, end-organ hypoperfusion and hypoxia. Clinically presents as hypotension with end-organ hypoperfusion features Acute MI accounts for 81% of CS |
| What are the characteristics of CS? | Systemic hypoperfusion due to CO depression (Cardiac index <2.2), sustained systolic hypotension despite elevated filling pressure (PCWP>18 mmHg) (SBP <90 for 30 mins) Evidence of end-organ hypoperfusion (urine output <30ml/h, cool extremities, altered mental status) In hospital mortality of >50% |
| What are etiologies causing CS? | AMI/ ischemia (LV failure, ventricular septal rupture, papillary muscle ruputure, ventricular free wall rupture, other conditions) Hemorrhage (infection, excessive vasodilator meds, prior valvular disease, hyperglycemia/ketoacidosis) Severe valvular disease (AS/MS, aortic regurgitation/ mitral regurg) Toxic (b-blockers/ calcium channel antagonist overload) RV failure, bradyarrhythmias (refractory), pericardial tamponade, post-cardiac arrest, post-cardiotomy, cardiomyopathy, takotsubo, hypertrophic cardiomyopathy... |
| How is the epidemiology of CS? | 5-10% of AMI cases will complicate to CS causing death (leading cause of AMI death) STEMI (ST elevation MI) is associated with 2x risk to get CS than non STEMI (NSTEMI) |
| How is the presentation of CS? | Pt commonly present with cool extremities and signs of pulmonary cogenstion (Cold and wet presentation (reduced cardiac index, increased vascular resistance, and increased PCWP)) Pt may also present Cold and dry (reduced CI, increased resistance but normal PCWP- euvolumic (were exposed to previous MI or CKD)) Wet and warm (also could occur, systemic inflammatory response syndrome in conjugation with MI with higher degree of mortality and sepsis, pt have reduced CI, low-normal vascular resistance, elevated PCWP |
| How is typical pt profile in CS? | Old, female, Prior MI, diabetic, anterior MI location, extensive coronary artery stenosis If it was caused by first inferior MI, we should look for any mechanical cause |
| When is the timing of CS? | 1/4 on admission, 1/4 rapidly after it (within 6h of MI), 1/4 later on first day Onset may be due to reinfarction, infarct expansion or mechanical complication |
| How is the dx of a CS? | Clinical (dyspnea, paleness, altered mental status, weak rapid pulse, or bradycardia due to high-grade heart block, hypotension with narrow PP, tachypnea, cheyen-stokes respirations, jugular vein distention, oligouria (maybe) Labs (leukocytosis (left shift), urea and creatinine rise, liver hypoperfusion elevates liver proteins, lactic acid elevated, ABG (hypoxemia and acidosis, maybe compensated by respiratory alkalosis), cardiac markers (CPK, MB, Troponin I and T elevated)) ECG (Anterior infarct (more than half), ST depression (left main stenosis cause), AMI with LV failure (Q wave / ST elevation, LBBB) CXR (pulmonary vascular congestion and pulmonary edema (only third of pts), normal Heart size (may be enlarged in first MI) TTE (sees severity and dx (shunts, PE, dissection) Left heart catheter (may be done)) |
| How is the treatment of CS? | Depends on the clinical signs, tx of arrhythmias. hypovolemia (administer fluid, transfusion, vasopressors...) low output CS (check pressure (if HTN ->give nitroglycerin, if normal give dobutamine, if low give NE/dopamine) acute pulmonary edema (check BP, if high give ACE inhibitors (short acting)) We can also use intraaortic baloon pump/ reperfusion/ revascularization. |