Coronary Artery Diseases
Risk Factors
 Traditional -↑ LDL, HTN, smoking. - ↓HDL, obesity, DM, - age >45♂, >55♀, - FH of premature CHD < 55 ♂, < 65 ♀, - others; hyperuricemia, CRF. Stress, personality.  Non traditional; Lp(a) , homocysteine , PAI-1, fibrinogen, cytokines, CRP, apo B , small dense LDL, visceral obesity , fasting hyperinsulinemia, microalbuminuria. NB; Effect of smoking; - ↑ Bl viscosity, ↑ carboxyHb, & Hct. - ↑ plat adh/agg, - ↓HDL. Leading to  ischemic stroke, SA Hge, CAD, HTN, AA, thromboembolism.

Protective factors; 1- ↓cholesterol in diet. 2- ↑HDL by; estrogen, exercise, alcohol. Effect of Estrogen. 1. ↑HDL, ↓LDL, ↓Lpa. 2. ↓LDL coronary uptake 3. ↓coagulation factors. 4. ↑insulin sensitivity. Beneficial effect of small amount of alcohol; ↑HDL, ↑ insulin sensitivity, anti-thrombotic (↑TPA), anti-plat (↑PC/ tx), anti-oxidant (flavinoids & polyphenolin red wine).

Normal adult 12-lead ECG

1)Hyperacute T

2)Raised ST

3)Q wave, T inversion

4)Q wave, inverted T

5)Q wave

Cardiac enzymes;
Enzyme Onset (hs) peak Return(day)

CPK-MB Troponin LDH

4 3 10

18 24 24

2 10 14

 CPK-MB ratio>2.5% of total CPK,  new rise infarction extension.  Troponin; - most sensitive, more specific than CPK. - indicator of severity. - n=<0.4 ng/ml. - false +verenal, PE, myocarditis baseline & 12 hs after.

 Angina pectoris;
transient attacks of chest pain caused by myocardial ischemia. It is a symptom of CAD. Ccc by burning,or boring substernal pressure or heaviness. Precipitated by exertion, stress, cold. Releived by rest, nitroglycerine. ECG; subendocardial ischemia= *transient ST depression in ant, inf or all leads ) during the attack. *sometimes T wave inversion.

 Prinzmetal angina;
- non infarction ischemia due to coronary artery spasm leading to transient transmural ischemia. - Atypical angina due to; ST elevation not depression, occur at rest or at night. - Rt coronary. - ¾ patients coronary atherosclerosis. - ECG; transient ST elevation, without Q or t wave inversion.

 Subendocardial infarction;
- ECG; non Q wave infarction= NSTEMI= persistent ST depression &/or T wave inversion.
 Transmural infarction - ECG; STEMI = Q wave infarction = 1) Hypercute T, 2) ST elevation & reciprocal ST depression 3) Q wave, 4) T wave inversion.

NB; - ECG may be normal in acute MI especially early infarction. - it is better to say Q or non-Q infarction. Diagnosis of recent MI - ↑enzymes + (sympt.
or ST)
or – postmortum pathological finding.

Diagnosis of Full thickness MI =
+ akinetic area or scar on ECHO .

Acute anterior myocardial infarction ST elevation in the anterior leads V1 - 6, I and aVL reciprocal ST depression in the inferior leads

Old anterior MI

Non-infarction transmural ischemia. (Prinzmetal angina) transient ST elevation

Q wave infarction transmural infarction Hypercute T, ST elevation, Q wave, T wave inversion.

Myocardial ischemia Non-infarction subendocardial ischemia (classic angina) Transient ST depression non Q wave infarction subendocardial infarction persistent ST depression &/or T wave inversion without path Q

DD of ST changes
 Raised ST; - transmural infarction (>2 □ in chest leads, >1 □ in limb leads), with evolutional changes & reciprocal depression. - prinzmetal angina; transient without evolutional changes or reciprocal depression. - early repolarization pattern; young, stable ST elevation without evolutional changes or reciprocal depression. - pericarditis; special pattern, in all leads. - LBBB; with characteristic QS pattern in V1,2 & notched R in V5,6. - Depressed ST; - angina. - LVH with strain. - non-Q MI=NSTEMI= subendocardial infarction. - reciprocal depression in transmural infarction. - digitalis; scooping of ST-T. - Post. Wall infarction.

DD of T wave inversion
Normally in avR, V1. Ischemia. Ventricular strain pattern. Pericarditis. Subarachnoid Hge (deep, wide + prolonged QT, U wave), may be due autonomic dysf. BBB. Ventricular Pacemaker.

Stable angina;
- signs (+/- S4, MR). - Management.; - ECG during the attack, transient ST depression &/or T wave inversion. - TTT During the attacknitroglycerine tab, 0.4 mg not more than 3 tab. - Exercise Stress test, if normal ECG in between the attacks; *The test is stopped if the patient develop angina, fatigue, diagnostic ST changes, *+ve results = failed ↑or ↓BP, ischemic ECG changes. * if early + ve results angio. If achieve 9 min medical ttt (BB, CCB, aspirin 150mg, exercise). - Thallium stress, to increase the diagnostic accuracy of Exercise Stress test, - coronary angio, indication; - unsettled diagnosis. - refractory to medical ttt. - suspect Lt main stem or 3 vessels dis. - pt > 40 yrs before valve replacement. *if proximal stenosis  dilatation by PTCA (may need repeated procedure). *CABG is done if - restenosis after PTCA. - severe 3 vs - severe Lt main stem. - DM + 2 vs.

Unstable angina.
 angina is said to be unstable if;
- accelerated (severe, frequent, longer). - at rest. - post MI, PTCA, CABG.  TTT ; 1. Medical; Aspirin (or clopidogril), Heparin (or

LMWH),GP IIb IIIa(absiximab, tirofiban), nitroglycerin (PO or IV), BB.( during the attack), . 2. early percutaneous coronary intervention (PCI), with or without stenting, is recommended in all except low risk patients. 3. In low risk patients discharge with outpatient stress testing within 72 hours. 4. After dischargeBB, Aspirin, nitrates, lipid lowering, ACEI.

NSTEMI= Non Q wave infarction= subendocardial infarction ;
- ECG; persistent ST depression &/or T wave inversion. - evidence indicates that subendocardial infarction may have as bad long term prognosis as transmural infarction with higher 1 yr mortality. - should be investigated early & aggressively. - TTT; GP IIb IIIa. - no benefit from thrombolysis.

 -

Syndrome X; Middle aged female presented with atypical chest pain. May be related to estrogen deficiency. Due to small vessel disease or Lt ventricular dysfunction. ↓ST on exercise test. Normal angio. TTT; medical ttt, Laser percutaneous transmyocardial revascularization; = Laser holes in the epicardium to form channels connected to vent cavities, benefit in distal dis e.g. DM.

 Rt coronary supplies the inferior (diaphragmatic) portion of the HT.  LAD supplies septum & most LT ventricle.  LT circumflex supplies the lateral wall of Lt ventricle.  Frequency of occlusion; LAD, RCA, Lt circumflex.

Transmural Myocardial infarction
Definition; ischemia & necrosis of a portion of the entire thickness of the LT ventricular wall. ECG changes; - Acute phase; Hypercute T, ST elevation + reciprocal depression. - Evolving phase; Q wave,T wave inversion.

Localization of infarction;
Anterior wall infarction; - anteroseptal; in V1,2. - Strictly ant= in v3,4. - Anterolateral; in V5,6.

Acute anterior myocardial infarction ST elevation in the anterior leads V1 - 6, I and aVL reciprocal ST depression in the inferior leads

 Complications of anterior wall Infarction; 1 - septal perforation & VSD.---- lt vent failure. 2- cardiac rupture (tamponade). 3- vent aneurysm;
- double apex, - persistent ↑ ST without reciprocal depression. - complication; 1.VT-  syncope , 2.thromboembolism, 3. rupture . - TTT: warfarin for 3-6 ms, surgery if significant dec in COP.

4- thromboembolism in 1/3 cases. 5- dressler $= post cardiotomy $
↑ESR, fever, anemia, pericardial eff, anticardiac ms ab ttt=NSAIDs, steroids.

Mobitz II. 7- BBB.

inf. Infarction
 inferior (diaphragmatic) portion of the LT ventricle.  Changes in lead II, III, AVF.  Due to occlusion of RT coronary & less commonly Lt circum.

Complications of inf. Infarction;
- Papillary ms dysfunction (rupture is rare). - conduction abn; CHB, Mobitz I (SAN is supplied by RCA in 60%). - RT vent infarction.  fluid & thrombolysis. - Posterior wall inf.

Acute inferior myocardial infarction
ST elevation in the inferior leads II, III and aVF reciprocal ST depression in the anterior leads

 Papillary ms dysfunction ( with Inf. MI); - in 0.1% of MI. - 80% the post. Papillary ms (supplied by RT coronary, so more common with Inf. MI. - several days after MI. - TTT; emergency MVR. - Prognosis; 24 hs survival = 25% with medical ttt, 50% with emergency MVR.

Posterior wall infarction
Posterior wall of the LT ventricle.  ECG; tall R, ST depression & tall +ve T in V1,2. May extend to the lateral or inferior wall (postero-inferior). Due to occlusion of RT coronary.

Acute posterior myocardial infarction
(hyperacute) the mirror image of acute injury in leads V1 - 3 (fully evolved) tall R wave, tall upright T wave in leads V1 -3 usually associated with inferior and/or lateral wall MI

RV infarction;
- in 1/3 of inferior infarction. - ↓BP, congested neck, clear lung bases. - diag.; ECG ↑ ST in V1, V3R, V4R,V5R. - confirmed; ECHO, coronary angio, thallium scan. - TTT= monitor by PCWP, IV fluid, thrombolysis but never nitroprusside or VD.


NB; * Cause of Post-MI VT; - scar EPS & ablation. - ischemia angio & thallium. if associated with LVEF < 40%ICD. * Indications for temporary pacing post MI (for 2 wks ) - ant wall & CHB or new BBB. - inf wall & CHB if HD unstable.
- if no sinus rhythm within 2 wks permanent pacing.

Shock after MI;
1 - RV infarctionfluids. 2- VSD Vs. papillary ms rupture (severe MR)  ECHO & IABP. 3- LV extensive infarction or re-infarction (loss of > 40% of LV) IABP. 4- free wall rupture (fatal) & tamponade.

 PCWP = Lt atrial pressure = LVDP. Post MI LVF MR VSD Tamponade RVI CVP ↑ N N ↑ ↑ PCWP ↑ ↑↑ ↑↑ ↑ ↓

Management of transmural infarction 1) Thrombolysis
Indication ( pain & ECG) - pain < 12 hs + ↑ ST in 2 leads. - pain + new BBB. Most benefit; - early 1 hr. - poor LVF or syst BP < 100. - high ↑ ST. - large ant. infarction.

 1) Contraindications; Absolute;
- active internal, uncontrolled ext. bleeding. - suspected Aortic dissection. - uncontrolled BP > 200/100. - head trauma < 2w, stroke< 2 m. - cranial or abd neoplasm. - pregnancy. Relative; - CPR > ½ hr probable IC thrombus e.g. (AF+MS)


Complications - reperfusion arrhythmia within 2 hs.

-Hge. NB; - 1ry angioplasty is better than thrombolysis, preferred if HD unstable

2) Drugs which decrease mortality in MI;
1) Aspirin (not dypyridamol).
2) thrombolytics/ angioplasty. 3) BB (FU with PR < 0.24, HR >45, SBP > 100)3 doses of 5 mg metoprolol 4) ACEI esp. CHF, EF< 40%, cardiomegaly. 5) Statin ( ↓ mortality & recurrence) even with

average cholesterol prior to discharge.
- LV function is the prognosticator post MI. NB: - nitrate ↓ morbidity not mortality. - DHP CCBs inc.CVS risk after MI. - In type II DM, must be kept on insulin infusion for 24 hs then SC for 3 months  ↓ mortality.

 Indication; - discrete lesion. - proximal. - non calcified . - non-occluded - short history of angina.  Complication; 1) acute occlusion. 2) restenosis. * for stent restenosis (for high risk patients as DM).  drug eluting stents + GP IIbIIIa + aspirin + clopidogril for 1 m .  GP IIbIIIa used in; - high risk PTCA - NSTMI - stents - unstable angina

 Indication; - symptomatic LT main stem dis. - symptomatic proximal 3 vs dis. - 2 vs including LAD.  Most benefit; moderately impaired LVF.  Complication; 1) mortality: < 2% , 10% for 2ry procedure. 2)periop. Graft occlusion; 10% esp venous grafts. ( art. Grafts have higher patency). 3) post cardiotomy $ up to 6 m after.

5) Laser percutaneous transmyocardial revascularization; = Laser holes in the epicardium to form channels connected to vent cavities, benefit in distal dis e.g. DM. 6) Elective balloon pump insertion; - cardiogenic shock - VSD - papillary ms rupture.

Post MI rehabilitation

1 month abstinence from sex & driving. 2 months off work.

Abstinence from driving after revascularisation - 1 m for ordinary driver - 3 m for vocational drivers. - Loss of license after ICD.

perioperative cardiac complication
 cardiac complication are the most common cause of perioperative mortality & morbidity esp. after vascular surgery. Investigations;  So if high risk of ischemia (history of CAD)coronary angio.  If intermediate risk ( DM, PVD) dipyridamol thalium scan or dopamine stress ECHO ( both are equivalent, NPP > 95%.  if low risk exercise stress test. TTT;  Perioperative BB ↓risk of morbidity by 50% & recommended for high & intermediate risk.  Temporary pacing for trifascicular block.

Myocardial diseases

Infective *Viral Coxsakie, ECHO, mumps, measles, influenza, EBV, HIV, adeno, rubella, robeola. *Bacterial TB, brucella, Hemophilus. * spirochital;leptospirosis, borellia burgdorferi *Fungal (aspergillus, histoplasmosis) *parasitic; trypanosomes cruzi, trichinosis, toxoplasma, amoeba, malaria Non- Infective -Rheumatic -CT dis; SLE, Rheumatoid, myocarditis recurrent refractory VT. -Drugs; adriamycin, chloroquine, phenothiazine, lithium, sulfa, paracetamol. -irradiation

Myocarditis History -Young -Acute onset -Prodrome (fever, flu like,arthralgia)

DCM -Older - chronic

Investigation -Neutrophilia -↑viral Ab titre e.g. cox B titre1:160. -CXR; Slight cardiomegaly. -ECG; episodic VT, HB, ST/T.

-ve -ve - CXR; Huge cardiomegaly


Avoid BB, digitalis

These are conditions that;  1ry affect Ht muscle.  Of unknown etiology.  Characterised by myocardial dysfunction  After exclusion of - volume & pressure overload. - IsHD - pericardial disease. NB; ischemic CM= IsHD that has no other manifestations as angina or MI but only present with Ht failure.

Hypertrophic cardiomyopathy (HCM)
 AD in 50%.  Mutation of ß myosin gene on chr 1, 11, 14, 15.  Bimodal 1st peak 2nd decade. 2nd peak 4-6 decade.  LV outlet obstruction occur in late systole.  Associations; - Friedreich ataxia. - WPW. - pheochromocytoma  Symptoms; - exertional dyspnea - chest pain. - palpitation. - syncope. - sudden death VT (dt acc. Path- associated AF) massive infarction outflow obst

Signs;  general, - prominent a wave in neck veins  Local, palpdouble apical impulse (S4), LS thrill. auscmurmur; late or pansystolic over LSE or apex more than A1, not over carotid dt outflow obst & MR. ↑ by obst e.g. digitalis, inotropics, ↓volume e.g. standing, valsalva, diuretics, VD as nitrates. ↓ by squatting, hand grip.

Invest;  ECHO- Asymetrical septal hypertrophy 60%
concentric 30%, apical 10% - septum/post wall>1.5. - >30% LV outflow gradient - obliteration of LV cavity. - systolic ant. Motion of mitral valve leaflet.  Catheterbanana or spade like LV.  Poor prognostic features; - young age < 30 yrs. - FH of sudden death. - syncopal sympt. - LVH > 3 cm. - VT on Holter ECG. - hypotension on peak exercise test. NB; no correlation with outflow tract obst gradient.

 1. 2. 3. Management; Avoid volume depletion avoid intense physical exertion and competitive sport. Treatment of dyspnea and chest pain generally begins with medical therapy.  negative inotropic agent; - verapamil or - beta blocker, +/- disopyramide, - cautious addition of a diuretic, If medical therapy fails  non-pharmacologic therapy; surgical myectomy or alcohol septal ablation. Prophylaxis for endocarditis.

4. 5.

Dilated cardiomyopathies (DCM)
♂, Causes;  Alcohol.  Nutritional; thiamine, selenium, ↓Ca, ↓P.  Endocrinal; hypo &, DM, acromegaly.  Metabolic; glycogen storage diseases.  Infiltrative; hemochromatosis.  Toxic; cocaine, adriamycin.  Peripartum.  Viral, cox, HIV.  autoimmune,; SLE, Sclero. C/P; biventricular failure. ECG biventricular ++ ; LBBB , poor R prog., +/- AF. Catheter; ↓CO, ↑EDP in both vent. TTT; antifailure= ACEI, digoxin. anticoag= AF, mural thrombosis. antiarrhyth=

Restrictive CM
 Causes; - myocardial= idiopathic, amyloidosis, sarcoidosis, scleroderma, hemochromatosis, glycogen storage, Gaucher. - Endomyocardial =fibrosis, hyperesinophilic S, carcinoid, malignancy, irradiation, toxin-related.  Sympt; SVC, PVC, low COP, AF.  Signs; steep x, y. pulsus paradoxus, AF.  TTT; antifailure + anticoag + ttt of etiology.

Pericardial diseases

Infective *Viral Coxsakie. *Bacterial Strept, staph, TB. Non- Infective ( T U M O R) -TB, trauma. -Uremia -Malignancy, medication (those causing SLE as hydralazine, procainamide, INH), MI -Other infections, viral , bacterial . -Rheumatic fever, rheumatoid &Other CT, radiation, recurrent

1- acute dry= fibrinous. 2- associated with pericardial effusion; serous CT. serofibrinous  T U M O R hgic TB, tumors, trauma 3- constrictive.


Constrictive pericarditis
   -


Causes = T U M O R without ( medications, MI, RF). Symptoms; Rt vent failure (cachexia, ascites, hepatomegaly, oedema, ↑JVP) + dyspnea, AF due to atrial enlargement. Signs; X, y descent deep . Kaussmaul sign (inspiratory filling of neck v). Impalpable apex. Pericardial knock. AF. Ascites precox. CXR; pericardial calcification. ECHO; thick bright pericardium, biatrial enlargement, normal systolic function, poor diastolic function, ↓peak systolic & diastolic values during inspiration. ECG; ↓PR (early & specific), ↑ST, inverted T.

• •
• •

CT scan , pericardial rim of calcification.

pericardial effusion
 Types; 1) serous; transudateoedematous states. Exudate hypothyroid, CT, viral, TB, malignancy. 2) hgic; TB, tumors, trauma, CRF + heparin on HD. 3) bloody; ruptured aneurysm, dissecting AA, MI. 4) chylous; lymphedema .

• • • • •

Signs; ↑JVP, pulsus paradoxus, loss of y descent dt atrial compression, Ewart sign= bronchial breathing at Lt lung base dt compression of lingual lobe. CXR; globular cardiomegaly( flask shaped). ECG; electrical alternans, electromechanical dissociation in tamponade. TTT; drainage or pericardial window in chronic cases.

Restrictive CM
Neck veins palpation auscultatio n Systolic bulge S3 gallop, TR +/-MR (cardiomyopathy as Ht failure)

Constrictive P
Common; ↑JVP, Deep X & Y Systolic retraction Pericardial knock (as S3 due to catching effect of pericardium on the relaxing ventricle)

Y obliterated Impalpable apex Distant Ht sounds

liver CXR ECG Catheter

Common; congested non pulsating Ht failure without cardiomegaly Common; AF - Difference bet 2 ventricle LT VEDP > RT -Difference of pressure in the chamber during cardiac cycle -Less pericardial calcification Flask shaped cardiomegaly


ECHO Confirmed by biopsy

Common; normal systolic function CT, MRI ECHO

Endocardial diseases

Rheumatic Fever
 Diagnosis; evidence of recent strept infection (↑ASOT >250 adult or 333 children, scarlet fever, +ve throat swap, other antistrep Ab) + 2 Major or 1M & 2m criteria.
Major 1-carditis 2- arthritis 3- chorea 4-erythema marginatum 5- SC nodules (non tender, on knee, elbow, spine) minor fever arthralgia CRP, ESR ↑PR Previous RF

 Prophylaxis from recurrence;
1- TTT of strep infection with penicillin. 2-long term long lasting penicillin (Benzathine penicillin 1.2 million unit IM/month (erythromycin/12 hr if penicillin allergy) till - 25 yrs or - 30 yrs if RHD or - 5 yrs after the last attack.

 Treatment;
1. Benzathine penicillin 1.2 million unit/wk IM for 3 wks or oral penicillin 500 mg/6 hrs for 10 days. 2. Salicylates (5-6 g/d) for 6 wks e.g. indomethazin, diclofenac. or steroids 50 mg/d for 4 wks if intolerance to salicylates.  FU with ESR.

 Causes of endocarditis
Infective *Bacterial -Strept viridans (subacute), fecalis (=enterococci after urinary cath) bovis (colorectal cancer) -Staph aureus (skin, drug abuse, acute), albus (cardiac surgery), epidermidis ( valve replacement) -Pseudomonus. -Hemophillus (HACEK, ceftrioxone very effective) * Ricketsia, coxsiella (=Q fever) *Chlamydia *Fungal (candida, aspergillus) Non- Infective -Rheumatic -Lebmansac endocarditis -Carcinoid -Marantic

 IEC; 40% no valve lesion. 10%IV drug, cong, prothetic 50% strept viridans  Signs of IEC; - toxic manifestation + clubbing, subconj Hge, - spleen, soft small palpable ( -ve in renal, old, debilitated, HT failure), - cardiac( varying murmur, new murmur, conduction defect, dt abscess formation, Ht failure, infarction dt emboli0. - Thromboembolic ; *acute septic emboli pyemia, mycotic aneurysm in the brain subarachnoid Hge *SBE infarctions e.g. CNS, mesenteric, - renal, infarction, CRAO ,UL, LL. Immunological Kidney focal proliferative , MPGN. - skin, osler nodes ( tender, cutaneous), splinter He,, Janway spots. - eye; Roth spots,,.

 Poor prognostic factors. - staph, - culture neg. , - proth.valve, - low complement.  Indications for surgery - relapses, - septic emboli, - septal abscess, - fungal, - large vegetations, - extensive valve incompetence.  FU by CRP (ESR fall slowly).

Medical ttt till culture results. Pen G 2-4 mill U/4h + gentamycin 1 mg/kg/8h + nafcillin or oxacillin 1.5 g IV/4h Medical ttt after C& S; Strep benzyl pen (or vanco) + low dose genta. Staph. Flucloxacillin (or vanco) Rickettsia -> Rifampicin + doxycyclin. Pseudomonus carbinicillin 10 g/d + genta 240mg Medical ttt in special situations; Penicillin hypersensitivity vancomycin 15 mg/kg/12hr.

Prothetic valve- vancomycin 15 mg/kg/12hr. - gentamycin 1 mg/kg/8h for 2 wks. - Rifampicin 300 mg/8 hrs. Rt sided; - 50% staph, 15% pseudom, - diagnosed with transthoracic ECHO, - flucloxacillin (vanco or teicoplanin) + gentamycin for 2 wks. - no valve replacement if pulm septic emboli.
2-6 months Post operative (staph, 85% MRSA)  vancomycin.

Antibiotic prophylaxis
   NICE guidelines 2008 recommended that Antibiotic prophylaxis is no longer offered routinely for defined inteventional procedure. Antibiotic prophylaxis has not been proven to be effective & there is no clear association between episodes of IEC & interventional procedures. Benefits of antibiotic prophylaxis must be weighed against the adverse effects for the patients & the risk of developing antibiotic resistance.

1. 2. 3. 4. 5.

People at risk are;
Acquired valvular HD with stenosis or regurge. Valve replacement. structural congenital HD except isolated ASD, fully repaired VSD or PDA, closure devices that are judged to be endothelialised. HCM Previous IEC.

 -

Advice people at risk about; Good oral hygiene. Symptoms of IEC. Risks of invasive procedures Why ab prophylaxis is no longer indicated. Do not offer ab prophylaxis for; - All dental procedure. except…. - Upper & lower GIT, respiratory, genitourinary. - Do not offer chlorhexidine mouth wash before dental procedures. - Investigate & treat any episode of infection. - Offer ab that cover organisms causing IEC for those pts undergoing procedures at a site where there is a suspected infection.

Antibiotic prophylaxis

not indicated for; - cardiac cath - diagnostic upper GI endoscopy. - large secondum ASD. - MVP without regurge. - after 6 month of valve repair. - TEE.
indicated for; -- all surgery. - rigid bronchoscopy. - therapeutic upper GI endoscopy.


Upper (e.g. dental)
BeforeAmox 2 g oral or 1 g IV 1 hr After genta 1.5 mg/kg IV + 500 mg oral amox 6 hr if general anathesia. Lower (colonoscopy and biopsy) Amox 1 g IV + genta 1.5 mg/kg IV + Amox 1g oral 6 hrs

 50% -Myxomas * 2ries from breast & lung  But tumor that most commonly metastasis to the heart= melanoma.  Atrial myxoma; - interatrial septum, LT atrium. - ♀. - sympt.constitutional (IL-6fever, clubbing) systemic embolism. postural syncope. - signsMS , early diastolic plop (murmur). PHT, sinus rhythm. - invest; ↑ WCC., ↑ESR in 60%, ↑IG (hypergammaglobulinemia) . - diag.=TEE, avoid catheter. - TTT= surgical resection without delay ( rapidly growing, & embolize)

Cardiac tumors

Valvular Diseases
MS Normal valve area average =4.5 cm, MS<2cm, tight MS<1cm. MR AR AS 2.5 cm, AS<0.7 cm, severe AS<0.5




-Rh, -cong 2- functional; - Austin flint (with AR). Cary comb(Rh carditis - MR, VSD, PDA. - tumors

1-organic; 1- organic; -Rh chronic -Cong marfan -Rh -syphilis, RA, -Cong e.g. Ank. Sp. Marfan, MVP -Acute; IEC, -Ischemic dissecting aneurysm Acute (infarction, IEC, post valvotomy)


1- organic; -Rh -Cong valv; bicuspid suprav; wiliam, coarct subv; HCM calcific; 2- functional; Hemic HTN AR

MS Symptoms 1- PVC 2-Low COP 3-SVC

MR 1-palpitation 2- PVC 3- Low COP



1-palpitation 1-Angina 2- angina 2-syncope(Low 3-PVC dt LVF COP) 3-dyspnea(PVC)

Signs 1- general

- Malar flush

Peripheral signs e.g. corrigan, DeMussey, waterhummer pulse, Duroziez, Hill’s


-Palpable S1 -Loud S1,OS, -Loud S2 -Mid-diastolic rumbling murmur.

Soft S1 Early soft

Soft blowing blowing diast murmur pansystolic murmur

Soft S2 Harsh ejection systolic murmur at A1





Signs of severity

-OS near S2 -long murmur -PH, loud S2, PR, RV heave, TR - ECHO; M area <1cm -Cath; PCWP>25. pr gr>15. COP<2.5L/min/m2.


-Thrill -LV++ -S3 -Func MS

-LVF -Peripheral signs - S3. -Long murmur -Funct MS (austin flint)

-Syncope, LVF

-Pulsus T&P -Low pulse pr, low BP -Thrill -Single soft A2, reversed splitting -S3,S4 -Long murmur -ECHO; V area<0.5 SP gr>60
symptoms Severe AS

Indication for surgical interventi on

Severe symptoms Severe MS Thromboembolism despite adequate anticoag inr=2.5-3.5)

Severe symp Severe MR ECHO; EF<60%,

symptoms Severe AR -ECHO; EF<50%, AV root>50mm, LVESD>50mm

TTT 1- Prophylaxis from IEC. 2- diuretics 3- ttt of AF 4-+/-surgery Silent MS; 1-lutembacher (+ASD) 2-PH 3-RVF Calcified 1-soft S! 2-no OS NB; huge Lt atrum in MR, AF in MS

1- Prophylaxis from IEC. 2-ttt of AF 3-VD 4-+/-surgery Predominant MI in Double M; 1-soft S1 2-S3 3-displaced hypertrophied apex S1+ MR; 1-MS 2-post. Leaflet

-If asymtomatic FU with ECHO. -surgery

-surgery - No role for medical ttt


without surgery, sudden death 73%. in Asympt. Adult, sudden death3-5%. child, sudden death in 6-9%. Complications (S Death, CHB, calcific emboli, CAD in 50% of severe AS)

Bicuspid AV - Most common cong HT - Sporadic, familial in 10%. - calcify with age AS. - Surgery is likely to be required. Aortic sclerosis - Only localized murmur - No LVH - Normal pulse volume Cause of AS according to the age; <60yrs Rh, cong >60yrs + calcified valve.

 Causes; - organic; Rh, cong (Ebstein anomaly), IEC, carcinoid. - Functional; RVF.

Symptoms; palp, SVC, low COP.  Signs; general cyanoecterous, prominent V, absent X, ascites precox. local  pansystolic murmur to the Lt of the sternum, carvello sign(↑murmur by inspiration). PS  Causes - organic cong (fallot).. - Functional; ASD, hemic , PHT.

Prothetic valve  Types 1. Mechanical valve; adv; durable. disadv; lifelong anticoagulation. NB; INR target for AV= 2-3, for MV=2.5-3.5. 2. Tissue valve (porcine, homograft) indications; old age. adv; no anticoagulation. disadv; calcify with restenosis, replaced after 5-10 yrs.  Indications; 1. Severe AS, AI, MI. 2. MS in the following conditions; - MV score >8 (according to mobility, thickness, calc., subvalvular apparatus. - associated MR 2/4. - Lt atrial thrombus.  Signs; MV prothesis; metalic S1, metalic OS+ systolic murm+/-diastolic murmur. AV prothesis; metalic S2, metalic E click + systolic murmur only. NB; any early diastolic mrmur at AV area malfunctioning V. tissue valves does not produce metalic sounds.

 Complications; - infection; mortality 60%. early ½-1 y staph epidermidis. later fungal. if↑ PR septal abcess. - dehescencesurgery. - hemolysis. - thromboembolism.
 Anticoagulation + surgery; - stop warfarin & give heparin/6h, 3 days before. - stop heparin 6 h before till 24 h after major surgery or to 6 h after minor surgery.  Anticoagulation + pregnancy; - 1st tri.heparin, 2nd warfarin, 3rdheparin, lactationwarfarin. - warfarinfetal hge teratogenic 5-30% acc. To dose; mental R, optic A, nasal hypoplasia, chondrodysplasia.

 Associations; - WPW, ASD, PDA, LA myxoma. -CT disorders. pseudoxanthoma, osteogenesis imperfecta, Marfan, - Symptoms; palpitation, pain due to stress ischemia of papillae.  Signs; - midsystolic click ↑by squating, - midsystolic murmur ↑by standing .  Complications; - long QT, arrhysthmias, death. - rupture of chordae. - embolism. - neurosis.  ECG;depressed ST, T inversion in inferior leads, long QT,  ECHO; systolic posterior motion of 1 or2 leaflet, mainly post. Leaflet).  Treatment; - BB for palpitation, pain. - anticoag for embolic manifest. - prophylaxis of IEC if audible murmur or thick leaflets. - valve repair (not for the click only).

Pulmonary hypertension
 Mean P pressure =20mmHg,  Mean P pressure=pulm. Diastolic pressure+1/3 pulm puls pressure  PH = mean PP> 30 mmHg  C/P; inspection; Pulm. pulsation. palpation; palpable P2, auscultation, 2 sounds= P2, S4; 2 murmur = PS, PR (graham steel), 1 click= ejection systolic at Pulm.area.

Causes; A) 2ry PH
- Passive; MVD, const p, restrictive CM, Lt atrial myx. - Hyperkinetic; ASD, VSD - reactive=VC e.g. high altitude, COPD. - obliterative= sclerosis, fibrosis (EAO e.g. B). - obstructive = embolic ,vasculitis , Bilarz.  TTT of PH; 1-Digoxin (even in sinus rhythm) 2-diuretic in RVF 3-Ttt of the cause,

B) 1ry PH (<1% of all cases) - Def; mean PAP>25 at rest without any cause. - Female /male = 2:1. - 1/10 may be familial, other possible causes; CT dis, vasculitis, HIV, drugs as appetite suppressor (fenfluramine). - CXR; dilated proximal artery & pruned (very small diameter) peripheral. - Median survival if untreated = 3 yrs. - Management; 1-Do 1st PFTs, ECHO, immunologic markers, V/Q scan, Rt catheter & VD test with adenosine or inhaled NO if dec. in PAP without ↓COP CaCB if no  SC pump of epoprostenol

2-avoid pregnancy, exercise. 3-Digoxin (even in sinus rhythm) 4-diuretic in RVF 5-O2 6-Anticoag 7- surgery; - HL transplant if; RVF, PASP>60 mmhg, expected 2 yr survival <50%. - atrial septostomy in no resting hypoxia.

Congenital heart diseases
without shunt Acyanotic -AS -coarctation - dextrocardia + shunt (potentially cyanotic) Mixed blood -ASD, VSD, PDA -Coarctation of Aorta -Fallot -Ebstein -Complete transposition of great vessels


-P atresia -Severe PS -Hypoplastic Lt Ht

NB: - Most common cong HT= biscuspid AV. - Most common isolated cong HT= VSD ((30%) - Most common cong in adult = ASD.

 Most common cong in adult.  Complication; Paradoxical embolism-> stroke in young.  Associated; - fetal alcohol S, Down S , cong rubella, Noonan

 Types; - 70% Osteum secondum - ass with MVP (10-20%) - RT vent dilatation  RBBB + RAD - 15% Osteum Primum - ass with MI, TI , VSD - - affect conduction system RBBB, LAD - picked early in childhood. - 15% sinus venosus - defect in upper septum - ass with anomalous pul venous drainage.

 Signs; -P; fixed splitting of S2, functional PS (ejection systolic murmur). - Lt parasternal heave. - PS. - in OP (MI, TI, VSD).  Invest.; - ECG; biatrial enlargement, RBBB, RAD. - ECHO; paradoxal septal motion (bidirectional movement through the defect), septal defect. - CXR; pulmonary plethora. - catheter; step up O2 in RT atrium(mean increased oxygen concentration in the RT atrium), PH, ↑RVP. NB; Best is TEE.  TTT; - antibiotic prophylaxis from IEC only in O Primum. - indication for surgery; ↑ pulm/systolic flow ratio > 1.5/1 - may be closed with a prothetic patch through cardiac catheter.

Patent foramen oval; - 25% of population. - slit- like dehiscence in fossa oval. - unlike ASD; no equalization of pressure between 2 atria. - like ASD; Paradoxical embolism.

Holt-oram S - Rare S; ASD, triphalyngeal thumb, absent upper arm. - AD.
Lutembacher S.  ASD + Rh MS silent MS(ASD decreased the load over the stenosed mitral area ,so no early diastolic murmer of MS)

 Types; 1. Muscular (Roger’s dis); small defect.... close 2. Membranous; most common is memb., 30-50% spont. Closure. Signs; apex; hyperdynamic Palpable P2, parasternal thrill Auscult; inc. P2, parasternal pansystolic murmur; if eisenmenger murmur & thrill disappear, signs of PH +/- RVF.  NB; VSD↓ COP.  TTT; antibiotic prophylaxis from IEC (high risk) surgery at 3-6 yrs if pulm/systolic flow ratio > 1.5.

• -

 Causes; - prematurity - cong rubella  Most common distal to LT subclav.  Signs; - general; peripheral signs of AI. - local; Lt infraclav thrill, enlarged lt Ht. ausc, Lt infraclav machinary mur. if eisenmenger diff cyanosis in LL, mur become short & soft. PH.  TTT; - Premature infantindomethacin (90% closure). - antibiotic prophylaxis

 Sign; -general; clubbing, cyanosis, ↑ V wave dt TR. -local; Palp P2, Rt vent heave. ausc; ↓ pansyst murm & flow mur., PR (graham steel).

• Catheter; ↑RA, RV, PA pressures.
Complications; - RVF, - hemoptysis, - cerebral embolism, abscess, - polythythemia, thrombosis, gout, - IEC (rare)

• TTT; - medical for HT F.
- Ht lung transplantation




  -


-PS -RVH -Overridding aorta -VSD

ASD + F4

Cyanotic spill=hypoxic syncope= ↑PS,↓periph resistance. Signs; general; cyanosis, squatting, clubbing, stunded growth local; RV heave, PS murmur. inversly related to pulm gradient, single loud A2.

 Invest; - CXR; pulm oligemia, coeur en sabot - ECG; RVH.  Complications;

-IEC, -polythythemia, thrombosis, gout.
-paradoxical embolism, cerebral abcess. -Vent arrhysthmia.  TTT; blalock operation (BL from Lt subclav a to P) weak radial pulse.

NB; Ebstein anomaly; - Maternal intake of lithium in 1st trimester. - Cyanotic. - pulmonary atresia,TR, - ASD, Rt to lt shunt

 2 - 5 times more common in males.  Most common distal to LT subclav.  Symptoms; - in infants Ht failure. - adult UL; shoulder pain, headache, HTN, epistaxis. LL; cold, intermittent claudications, weakness.  Signs. - general; HTN, radiofemoral delay or absent femoral pulse - Local; ins/palp; suzman sign= visible, palp interscapular collateral pulsation. auscul; - HTN; ↑ A2, S4 , A ejection click, AS , -Lt interscapular late syst mur. - syst or continuous mur of collaterals over the back.

 Invest; - CXR; - Roesler sign; 3-8 rib notching - - Ba swallow; reversed 3 or E sign of oesophagus.  Association; cardiac; - Bicuspid AV - PDA - mitral V dis. extra cardiac; - Berry’s aneurysm - renal abn. - Turner S.
 Complications; - IEC - dissecting AA

- subarachnoid Hge

- LVH.

 TTT - surgical resection at 4-6 yrs. - balloon angioplasty if recurrent. - antibiotic prophylaxis & ttt of HTN.

Differential diagnosis
 1. 2. 3.  1. 2.  1.  1. Of systolic murmur over the apex; MI AS, PS (propagated from above). VSD (all over the precordium) Of diastolic murmur over the apex; MS AI Of systolic murmur over the A1; AS (with all its causes; organic, functional) Of systolic murmur over the P; PS (organic, functional).

 1. 2. 3. 4. 5.

Of Lt parasternal systolic murmur Posterior leaflet MI. TI VSD Subval. AS (HCM) Subvalv. PS.

Pressure in cardiac chambers;
Values in mmHg


15-30 /0-6

90-140 /4-12

120 (90-140) /80 (60-90) 25 (15-30) /10 (8-15)

Vascular diseases

Invest; - venous duplex rarely venogram - ankle-brachial pressure index +/arteriogram to detect ischemia which could contraindicates compression. TTT; - recent DVT  anticoagulation. - old DVT ttt of oedema, infection, compression after exclusion of ischemia.

C/P; 1.

Massive pulm embolism&Submassive pulm embolism - when > 50% of pulm vascular area is obstructed ↑ PAP. - retrosternal pain, dyspnea, shock, cyanosis, Rt sided failure. 2. Pulm infarction; uncommon, must have occlusion of bronchial vs & airways cough, hemoptysis, fever, jaundice, signs of atelectasis, rub, effusion. 3. Chronic pulm HTN; recurrent small pulm emboli no symptoms, cor pulmonale, recurrent episodes of dyspnea, fever, arrhythmias. NB; V/Q scan; - v=xenon, Q= macroaggregated albumin.(no iodine used.) - can be done during pregnancy (perfusion only is adequate). - sens =98%, specificity = 40% so if –ve virtually exclude PE. - in COPD & emphesema  matched defects. D Dimer ↑ in  PE, sepsis, MI, DIC.

 1. 2. 3.

Invest; D Dimer ↑ (non specific), good –ve no PE except if ↑ clinical suspicion. CT angio; only show large artery, same sens & specificity as VQ & angio. ECG; an S1, Q3, T3 pattern
sinus tachycardia T wave inversion in leads V1 - V3 RBBB, RAD, poor R progression. ABG; low or normal PCO2, hypoxia, resp. alkalosis..DD; acute severe asthma but PEFR is normal. V/Q; mismatch, not adequate if basal consolidation shown. Pulm angio; gold standard. Diagnosis; ↑clinical probability + ↑ V/Q mismatch diagnostic. ↓clinical probability + ↓ V/Q mismatch  exclude. If any other investigate more.

5. 6.  1. 2. 3.

Ttt; anticoag for high & moderate clinical probability; - heparin  5-10,000 unit IV bolus then 1000 IU/h (adjusted to keep PTT = 1.5-2.5 for 5 days at least or stop when INR = 2-3. (or twice daily SC LMWH).

Acute pulmonary embolus
ECG; The following, often transient, changes may be seen in a large pulmonary embolus;  an S1 Q3 T3 pattern  sinus tachycardia  T wave inversion in leads V1 - V3  Right Bundle Branch Block  low amplitude deflections

Acute pulmonary embolus

TTT;  Massive pulm embolism - TTT of DVT - Thrombolysis (or embolectomy) 2. Submassive - Anticoagulation - ttt of Rt sided HT failure. 3. Chronic recurrent; - Anticoagulation - IVC filters. NB; in pulm septic emboli; # thrombolysis for PE & surgery for the valve for IEC.

 1. TTT; Anticoagulation; LMWH twice daily SC. Or heparin 5-10.000 u IVbolus then 1300 u/h adjusted to keep PTT=1.5-2.5 times for at least 5 days & stopped when INR=2-3 Warfarin for 3-6 months. 6 wks if post poerative PE. 1 yr or lifelong if recurrent. 2. Thrombolysis; - indications; collapse dt massive embolism. - contraindicated if septic emboli as in RT sided IEC in drug abusers. - done through a peripheral vein to pulm artery, as effective as embolectomy (which is rarely done now). 3. IVC filters; - indications; when anticoagulation is # or failed (=continuous showers of emboli)

NB; Shock
With ↑ PCWP= -LVF -Temponade -MS

With ↓ PCWP= -RV infarction -PE -Hypovolemia -Septic shock

Aortic aneurysm
Causes; 1. 2.  Atherosclerosis (commonest). Congenital; - cystic medial necrosis (Marfan, Ehler Danlos ) - osteogenesis imperfecta. - repair of coarct in Turner. 3. Trauma. 4. Inflammatory; - infectious; Mycotic (IEC), syphilis, TB. - Non- infectious; rheumatoid arthritis, takayasu, Giant cell sero-ve, Behcet, Reiter, ankylosing S. Site of Atherosclerotic aneurysm; 75% abdominal, 25% thoracic. Site of dissection; 2/3 ascending A, 1/5 descending.

 

C/P;  1. Thoracic; asympt, mediastinal compression, signs; supresternal pulsation. 2. Abdominal; asympt, majority below renal arteries, signs; abd mass, peripheral ischemia.  Prognosis; Mortality rates; 3% in elective excision. 18% in emergency excision. 50% in acute rupture.  TTT; 1. If < 5 cm, asymtomatic annual U/S, BB to achieve HT rate < 60b/min, optimal BP control. 2. If > 5 cm abd or > 6 cm thoracic, rapidly expanding, symptomatic, A thrombosis & peripheral embolism surgical excision. NB; in Marfan operate if > 5 cm thoracic.

Aortic dissection
   1. 2. 3.
 1. 2.  1. 2. 3. 4.

Type A= ascending. Type B= descending. Causes; cystic medial necrosis. HTN (70%) Atherosclerosis Congenital; coarct, bicuspid AV, Turner, Noonan.
Sympt; Sudden severe chest pain radiate to the back. Vasovagal manifestations. Signs; HTN Loss of arterial pulse. Occlusion of important vs (stroke, paraparesis) Compression (mediastinal S).

Complications of ascending; AR, inferior MI, pericardial
effusion, carotid dissection, ↓subclavian pulse.

1. 2. 3. 4. 5.  1. 2. CXR; wide mediastinum. TOE (most imp); for diagnosis, severity of AR, LV function, pericardial effusion. CT does not identify site of tear, AR, coronary involvement. MRI does not allow monitoring, # if prothesis. Coronary angio to assess the need for concomitant CABG.

TTT; Early; releive pain, Na nitroprusside & BB to ↓syst BP<120, ↓ cardiac contractility ↓shear stress of Aorta. Later; Ascending surgery. Descending -surgery if; impending rupture, compress major Vs, uncontrolled pain, continuing dissection, Marfan/ Aortic root> 5cm. - medical ttt with BB, CaCB & CT/6months if old dissection>2wks, stable, isolated arch, uncomplicated descending.

Classification of hypertension
Classification According of BP level:  Normal <120/80  Prehypertension 120/80 – 139/89  Hypertension >140/90

Staging Hypertension:  Stage 1: 140-159/90-99  Stage 2 :> 160/100 Isolated systolic hypertension:  Grade 1 140-145/ < 80  Grade 2 > 160/ < 80

Causes of hypertension

Renovascular Reno-parenchymal Glomerulonephritis Collagen Disease, Henoch-Schonlein Purpura, Chronic Nephritis

Hyperaldosteronism Pheochromocytoma Hypo/Hyperthyroidism Cushing


See HTN in pregnancy

Drugs Diet

Contraceptive pills Corticosteroids Mineralcorticoids Sympathomimetics -nasal decongestants -appetite suppressants Phenothiazine Antidepressants Cyclosporine Erthropiotin

Licorice Tyramine rich food Salty food

Standing BP should be taking in:
• First visit evaluation. • Elderly patients above 60 years. • Diabetic patients. • Patients with postural symptoms. • Patients on potent VD or large doses of diuretics.

Standing BP should be measured 2 minutes after standing.

Investigations (1st . visit & annually)

Urine exam proteinuria

Blood K+ Bl.sugar Lipid S.Creatinine Uric acid HB



Hypertension Treatment
 Life style modification

 Stage 1: (140-159 / 90-99)
 Start with thiazide or in special situations you can start with ACEI , ARB , BB ,CCB .

 Stage 2:≥ 160/100
 Two drugs combinations

 If patient with diabetes or chronic kidney disease you start with 2 or more antihypertensive drugs to achieve goal BP  After 1 month if target BP is not reached: reach optimum doses or add additional drug  Inadequate response to antihypertensive drugs
 BP < 10/5 after 15 days therapy

Resistant Hypertension
•Office blood pressure >140/90 or 130/80 mm Hg in patients with diabetes or chronic kidney disease

•Patient prescribed 3 or more antihypertensive medications at optimal doses, including if possible a diuretic

Premature beats - loud S1. - TTT;  reassure if no sympt, young, not frequent, not multifocal, no structural HT dis.  if not or failed  BB.

Supraventricular tachy; Atrial rate 150-250. Types; 1) Atrial tachy (repeated abn. P) 2) MAT - 3 diff P - HR >100. - COPD due to hypoxia. - TTT= verapamil & TTT of COPD. - NB; digoxin ≠ (arrythmogenic) unless AF.


3) Reenterant tachy ; a) AVNRT - reenterant in or around AVN. - sudden onset- offset. - P wave inverted, just before or after or burried. - TTT; adenosine, carotid sinus massage terminate it. b) AVRT (in WPW) 1- orthodromic ( retrograde through acc path)Narrow complex. 2- antidromic ( retrograde through AVN) wide complex + delta wave. - P wave inverted & some time after complex. - TTT; amiodarone ( BB, flecainide) - NB; digoxin & verapamil ≠.



Incisional tachy - PAT. - scar of corrected ASD. - gradual onset. - TTT= propafenone. Wondering atrial pacemaker; - as MAT but rate =95. - physiological.

♂, non familial. Types A tall R in V1 dt LT path. ECG ( short PR, delta wave, broad complex. Associations ( MVP, HCM, EBstein, thyrotoxicosis). TTT; Radiofrequency ablation if asymp no TTT, can participate in competitive sports.  Ttt of Complications; - treat narrow complex tachycardia (rate is usually 190) with vagal stimulation, cardioversion, verapamil or adenosine- same as any SVT. * AVRT orthadenosine. *AVRT antidromicamiodarone, flecainide, BB.      - But never treat Acute AF or A flutter with digoxin, verapamil or BB. ( may lead to VT through acc path) DC or lignocaine or procainamide. but digitalis, verapamil, adenosine, are ≠.


Rt pathway activate from Rt to Lt from ant to post -ve in V1


Lt pathway activate from Lt to Rt from post to ant  +ve in V1


Atrial flutter
A. Rate=250-350. NB; Regular tachy 150/min, narrow complex  A.flutter 2 :1 untill proved otherwise.  Best seen in inferior leads.  Uncover by adenosine or massage.  TTT; - DC ( most likely arrhyth. To respond) - Class III ( Ibutilide, amiodarone, sotalol)= medical cardioversion  60 % sinus. - DC + Ibutilide  100%. - Radiofrequency ablation 90%.  Low risk of thromboembolism but anticoag if prolonged.

 A. Rate=400-600.  Most common, ↑ with age.  C/P ( varing S1, absent a, pulsus deficit> 10, ↑ with exercise .  Causes; - MVD, LA > 4.5 cm. - IsHD, HTN, LVH, - ASD, SSS, WPW, a myxoma - myocarditis, const. peri., - PE, pneumonia, hypoxia, br. carcinoma. - thyrot, alcohol, coffee - lone, idiopathic

 TTT;
- Paroxysmal if young event monitoring. if old patient, previous TIA anticoag, INR=2-2.5 + sotalol or amiodarone.

ttt of the attack stable
Old> 1 y
Anticoag + digoxin
Atria > 5 cm Anticoag + digoxin > 2 days

TTE atria< 5 cm < 2 days Cardioversion without anticoag No thrombus
Cardioversion without anticoag then anticoag


Anticoag 3 wks Cardioversion then anticoag 3 wks


Anticoag 6 wks then repeat

AF  Anticoag 3 wks before & after cardioversion.  after cardioversion Anticoag (most imp) + amiodarone or sotalol.  Propranolol or verapamil instead of digoxin in young or hyperdynamic unless Ht failure.  rate control is better than rhythm.  rhythm control ↑ mortality.  Pt with slow AF without TTT tend to be chronic.

 Risk factors for recurrence after cardioversion = indication for digoxin & anticoag. - long duration > 1 y. - Lt atrium > 5cm - old age > 75 y - Rh MVD - LV impairment.  Risk factors for thromboembolism.(5-7% annually); - Rh MVD - DM, HTN - LV impairment, Lt atrium enlargement. - previous CVA/TIA. if anyanticoag at all ages(↓risk to 1.6%) If not acc to the age(<65 = aspirin, 65-75= aspirin or warfarin, >75= warfarin)  Digoxin level ↑by – erythromycin, thiazides, amiodarone, verapamil, quinidine.  Digoxin ≠ in AVB, WPW, HCM, MAT, constrict. Cardio, myocarditis, prior to elective cardioversion.

1) Monomorphic  Causes ( acute MI, DCM, chronic CAD, HCM, myocarditis.  Signs (regular pulse, 160, variable S1dt variable AVV position, abn splitting).  TTT;
if unstable DC. if stableIV amiodarone (of choice) or lignocaine. if recurrent  pacing. if post-arrest  ICD.

Monomorphic VT

Features favoring VT
 Concordance.  P waves.  Capture & fusion beats.  Very broad > 3.5 □. +  History of IsHD.  Variable S1, no decrease in rate with carotid sinus masage or adenosine.  Must be ttt as VT.

Non-sustained VT

if chronic recurrent


not sustained ttt only if poor LVF & structural HT dis VT induced by exercise test

Poor LV funct. ICD

Good funct amiodarone + BB Or EPS + radiofreq ablation

VT induced by EPS

ICD +/- amiodarone

BB +/- amiodarone

NB; - if not sure VT/SVT with aberration adenosine diagnostic dose (↓SVT) & TTT as VT. - Sustained VT=> 3 runs of V beats<30 sec. - CCBs are absolutely ≠  ↓ BP. Do not ever use verapamil in wide complex tachy in the emergency setting (30% of those with V tac rapidly deteriorate)

Avoid verapamil with;
1. 2. 3. AF or a flutter in WPW. Wide complex tachy With BB.

 1. 2. 3. 4. 5. 6. 7.

OK verapamil with; AF or a flutter in healthy HT. MAT PSVT (2nd choice ater adenosine) WPW with narrow complex tachy symptomatic ttt of HCM Severe concentric LVH HTN.

2) Polymorphic (Torsade de points):  Causes - ↓ K, ↓Mg, ↓Ca, hypothyroid, hypothermia. -TCA, antipsychotics (phenothiazines) - clarithro, erythro, quinolones, cotrimoxasole, Ketoconasole, pentamidine. - antiarr; amiodarone, sotalol, class 1a. - IsHD, cong long QT S.  TTT 1- avoid or withdraw class Ia, c, III. 2- IV MG 1 gm or K channel opener. 3- BB ( not sotalol) IV in cong. Forms 4- temporary pacing & isoprenaline ( prevent brady & hence VT).  2ry prevention. 1) congBB & permanent pacing. ICD if life threatening arrhyth while on BB, FH od death in young. Lt stellate gangliectomy. 2) acquired ttt of the cause.  NB; Torsade de points is resistant to DC. -amiodarorone & class I a, c are ≠.

Torsade De pointes

 SSS.  WPW  AV block; - signs ( weak S1, variable in CHB, abn splitting, regular a wave, +/- prolonged V wave) - TTT; 1) atropine, isoprenaline. 2) ttt of the cause. 3) temporary pacing. 4) permanent pacing ( Mobitz II, CHB with wide complex. -NB; LT BBB is almost always associated with HT disease.

2nd Degree AV Block, Type I

LBBB and 2nd degree AV Block, Mobitz Type II

 CHB; - causes; 1) cong, unknown cause, minority due to maternal AID with anti Ro permanent pacing. 2) acquired; RCA dis or extensive ant MI temporary & rarely permanent pacing. NB: - most common cause of permanent pacing. - mortality 50% at 1 year esp. if age> 80y or non rheumatic.

1. bradycardia. 2.sinuatrial block. 3. sinus node arrest. 4. Tachybrady syndrome. 5. AF.

 Nomenclature; 1st letter= chamber paced (V, A, D). 2nd letter= chamber sensed (V, A, D). 3 rd letter= pacemaker response to sensed impulse (T, I, T/I=atrially triggered, vent inhibited)  Uses of temporary pacing. 1) brady asystole, hemodynamic unstable, severe not responding to drug, post MI CHB, 2nd degree HB. 2) Tachy overdrive termination e.g.A flutter, VT prevention e.g. torsade. 3) before cardiac intervention to high risk ( LBBB, RCA angioplasty) vascular surgery, preop to trifascicular. 4) Post MI with trifascicular or RBBB+ LAH or LPH.

 Uses of permanent pacing; 1) brady; - SSS ( symptomatic S arrest > 3 sec or asymptomatic S arrest > 5 sec)AAI. - chr AV block, post AV ablation DDD or VVI. - syncope  DDD or VVI. - post cardiac transplant 2) others; HCM, DCM, long QT.  NB; most common pacemaker is DDD; most physiologic & provides better exercise tolerance. DDD maintain AV synchrony, + rate responsive models (R) if young energetics for Chronotropic incompetence.Most clinicians use DDD, unless the pt is in chronic slow AF - AAI are used e.g. in symptomatic sinus brady. -

 Pacemaker S;
- with VVI. - short of breath at rest, relieved with exertion. - ECG= retrograde P. - TTT= DDD.

 Pacing in ant. MI; any except MOBITZ1 - 2nd or CHB. - new bifascicular. - new RBBB with preexisting 1st, LAH, LPH. - in LBBB with preexisting 1st AVB.  Pacing in Ht failure cardiac resynchronization therapy =CRT= bivent.or multisite pacing. if - EF<35% with optimal drug therapy.

Overdrive pacing. Indications; - cardiac arrest dt VF,VT. - sustained VT + LVEF< 40% - non sustained VT + LVEF< 40% + syncope or post MI. - long QT; post arrest or FH of sudden death.

Antiarrhysmic drugs:
Class Class I A
Quinidine Disopyramide procainamide

(- ) Na channels ↑ AP

A, V, acc



Lignocaine Phenytoin Mexiletin
Flecainide propafenone Propranolol Atenolol Amiodarone Sotalol Ibutilide verapamil Adenosine digoxin

(- ) Na channels ↓ AP
(- ) Na channels No effect on AP BB


Monomorph VT

C Class II

A, V, acc nodes

AF Stress, thyroid, sinus, cong long QT, VT AF, A flutter AVRT+ wpw VT SVT, MAT SVT, diag of flutter

Class III

(- )Na, Ca, K channels ↑ plateau (- )Ca channels K opener, no(-) inotrop.

A, acc ,V

Class IV Others

AV node AV node

Adenosine  Short acting.  IV, 6-12 mg  Uses (diag diff bet VT & SVT, therapy SVT)  Enhanced by disopyramide & inhibited by theophyllin.  Side effect; chest pain, bronkospasm, flushing, hypotension. Amiodarone  Side effects. most common after oral neurotoxicity, most common after IV hypotension. Lung toxicity (1-10%) IPF, ARDS, BOOP, pl effusion. others; hepatitis, throiditis, optic neuritis, corneal opacities, photosensitivity, ↑digoxin & anticoag level, ↑ PR, ↑QRS, ↑QT esp with 1a.  ≠ in Torsade de points. NB; no prophylactic use of lignocaine after MI ↑ mortality.

HT failure
 EF= 50-70%.  5 ys survival; 65% if EF<40. 95% if EF>50.  Causes of High COP failure.  Diastolic HF; - preserved syst. function ( >40%). - ischemia. - transient in MI , permanent in restrictive cardiomyopathy & Vent Hypertrophy.  Systolic HF; EF< 40%.

1) 2) 3) 4) Physical activity. Diet. Exercise. VD;

NB; ACEI ↓ mortality & hospitalization. of no benefit in – RVF. - obstructive valve lesion. - ≠ in HCM. 5) Digoxin- ↓renin, symp, hospital but not ↓ mortality. - used in Syst HF, S3, severe CHF. - ≠ AVB, asymtomatic HF, acute MI.

6)Diuretics e.g. spironolactone ↓ mortality & hospitalization & symptoms.
used in severe CHF.

7) BB ( Meto, Biso, Carvi)  ↓ mortality & hospitalization & symptoms.
not used in volume overloaded patients.

Definition; sudden transient loss of conscious dt cerebral ischemia. A) Neurocardiogenic 1) Vasovagaltilt table test, never biting tongue. 2) situational ( cough, micturition). 3) carotid sinus syndrome carotid sinus massage, ttt=DDD or sympathomimetic, fludro. 4) Pyschgenic (panic, hysteria). NB; carotid sinus massage; - 5 sec massage Rt then lt 30 sec apart while pt supine, if – ve repeat in upright. - +ve= >3 sec asystole, ↓ SBP > 50mmHg. - # in carotid bruit, recent MI (3 m), recent stroke (3m), previous VT.

B) Orthostatic hypotension 30% of syncope in elderly. Definition;
↑ HR> 30b/min, ↓SBP>20mmHg, ↓DBP>10mmHg after 3min up. (n= ↑ HR =10 b/min, ↓SBP=3mmHg, ↑DBP= 5mmHg,stabilize in 45 sec.)

causes; - hypovolemia. - drugs; anti HTN, diuretics. - addisson. - autonomic dysf. - HF or stenotic lesions. tilt table test, TTT; non pharmacological; avoid heavy meals, alcohol, postural training. pharmacological; sympathomimetics, MAOI-A, fludro.

C) Neurological e.g. Migraine, hyperventilation, vertebrobasilar TIA. D) Cardiac disorders at rest e.g. arrhyth, MI. exertional= mechanical obst e.g. AS, MS, HCM, dissection,PE, PS, PH, temponade. positional, ball & valve thrombus, myxomas.

 Normally.  Kussmaul’s sign.  Absent HJR.  Absent & giant a wave.  Canon a; regular, irregular, regular but not constant.  Absent x, steep x.  Absent Y, rapid y.  Temponade compress ventricles, constrictive P compress atria.

Cardiac examination
Apex;  Heaving, thrusting/hyperdynamic, Tapping.  Dyskinetic/displaced, diffuse.  Double apex, pericardial knock.  Parasternal heave, palpable S3.

Diastolic shock. S1; loud, soft, split, variable.
NB; PAC has long PR & loud S1 as it is premature=short diastole.

S2; loud, soft, wide split, fixed split, reversed split or single S2. NB;wide split, soft S2=PS. narrow split, loud S2=PH. wide split, loud S2=ASD.

Murmurs Systolic murmurs over Apex, A, P. Diatolic murmurs over Apex, A2. Continuous murmurs. NB; all murmurs ↓ by standing exept MVP & HCM. - Effect of respiration.

HT transplantation
 Survival; 80% at 1 yr. 75% at 3 yrs. 505 at 10 yrs  Complications; - accelerated coronary small vs dis. - lymphoma, skin cancer - CRF dt cyclosporin.  Indications; 44% CHD, CM, myocarditis. NB; in myocarditis, transplantion does not worse the prognosis but may recur in the transplant.

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