For MRCP Preparation

1. C V S

2. 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.

3. 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).

4. Normal adult 12-lead ECG

5. 1
)
Hyperacute T
2
)
Raised ST
4
)
Q wave, inverted T
3
)
Q wave, T inversion
5
)
Q wave

6. Cardiac enzymes
;
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.
Enzyme
Onset (hs)
peak
Return(day)
CPK-MB
4
18
2
Troponin
3
24
10
LDH
10
24
14

7. definitions
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.

8.  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.

9. 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 .

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

11. Old anterior MI

12. Myocardial ischemia
Non-infarction
subendocardial ischemia
(classic angina)
Transient ST depression
Non-infarction
transmural ischemia.
(Prinzmetal angina)
transient ST elevation
non Q wave infarction
subendocardial infarction
persistent ST depression
&/or T wave inversion
without path Q
Q wave infarction
transmural infarction
Hypercute T, ST elevation, Q wave,
T wave inversion.

13. 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.

14. 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.

15. 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.

16. 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.

17. 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.

18.  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.

19. coronaries
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.

20. 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.

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

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

23. 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.
6- Mobitz II.
7- BBB.

24. 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.

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

26. 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.

27. 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.

28. 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

29. 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.

30. inf-post-lat

31. 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.

32. 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.

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

34. 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.

35. Thrombolysis
 Contraindications;
1) Absolute;
- active internal, uncontrolled ext. bleeding.
- suspected Aortic dissection.
- uncontrolled BP > 200/100.
- head trauma < 2w, stroke< 2 m.
- cranial or abd neoplasm.
- pregnancy.
2) 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

36. 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.

37. 3
)
PTCA
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 - stents
- NSTMI - unstable angina

38. 4
)
CABG
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.

39. 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.

40. 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.

41. 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.

42. Myocardial diseases

43. Myocarditis
Infective
Non- 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
-Rheumatic
-CT dis; SLE,
Rheumatoid,
myocarditis
recurrent
refractory VT.
-Drugs;
adriamycin,
chloroquine,
phenothiazine,
lithium, sulfa,
paracetamol.
-irradiation

44. Myocarditis
DCM
History
-Young
-Acute onset
-Prodrome (fever, flu like,arthralgia)
-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
ttt
Avoid BB, digitalis

45. Cardiomyopathies
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.

46. 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

47. 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.
(
HCM
)

48. (
HCM
)
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.

49. (
HCM
)
 Management;
1. Avoid volume depletion
2. avoid intense physical exertion and competitive sport.
3. Treatment of dyspnea and chest pain generally begins
with medical therapy.  negative inotropic agent;
- verapamil or
- beta blocker, +/- disopyramide,
- cautious addition of a diuretic,
4. If medical therapy fails  non-pharmacologic therapy;
surgical myectomy or alcohol septal ablation.
5. Prophylaxis for endocarditis.

50. 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=

51. 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.

52. Pericardial diseases

53. Pericarditis
Infective
Non- Infective ( T U M O R)
*Viral
Coxsakie.
*Bacterial
Strept, staph, TB.
-TB, trauma.
-Uremia
-Malignancy, medication (those causing SLE as
hydralazine, procainamide, INH), MI
-Other infections, viral , bacterial .
-Rheumatic fever, rheumatoid &Other CT,
radiation, recurrent
Types
1- acute dry= fibrinous.
2- associated with pericardial effusion;
serous CT.
serofibrinous  T U M O R
hgic TB, tumors, trauma
3- constrictive.

54. Pericarditis

55. Constrictive pericarditis (TB)
 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.

56. 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.

57. Restrictive CM
Constrictive P
P.effusion/tampon
Neck veins
Common; ↑JVP, Deep X & Y
Y obliterated
palpation
Systolic bulge
Systolic retraction
Impalpable apex
auscultatio
n
S3 gallop, TR +/-MR (cardiomyopathy as
Ht failure)
Pericardial knock
(as S3 due to catching effect
of pericardium on the relaxing
ventricle)
Distant Ht sounds
liver
Common; congested non pulsating
CXR
Ht failure without cardiomegaly
pericardial calcification
Flask shaped
cardiomegaly
ECG
Common; AF
Catheter
- Difference bet 2 ventricle
LT VEDP > RT
-Difference of pressure in the chamber
during cardiac cycle
-Less
-Less
ECHO
Common; normal systolic function
Confirmed
by
biopsy
CT, MRI
ECHO

58. Endocardial diseases

59. 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
minor
1-carditis
fever
2- arthritis
arthralgia
3- chorea
CRP, ESR
4-erythema marginatum
↑PR
5- SC nodules (non tender,
on knee, elbow, spine)
Previous RF

60.  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.

61. Endocarditis
Causes of endocarditis
Infective
Non- 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)
-Rheumatic
-Lebmansac
endocarditis
-Carcinoid
-Marantic

62. IEC
 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,,.

63. 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).

64. 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.

65. 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.
 People at risk are;
1. Acquired valvular HD with stenosis or regurge.
2. Valve replacement.
3. structural congenital HD except isolated ASD, fully repaired VSD
or PDA, closure devices that are judged to be endothelialised.
4. HCM
5. Previous IEC.

66. 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.

67. 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.
regimen
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

68. Cardiac tumors
 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)

69. Valvular Diseases
MS
MR
AR
AS
Normal
valve
area
average =4.5 cm,
MS<2cm, tight MS<1cm.
2.5 cm,
AS<0.7 cm, severe AS<0.5
Causes
1- organic;
-Rh,
-cong
2- functional;
- Austin flint (with AR).
Cary comb(Rh carditis
- MR, VSD, PDA.
- tumors
1-organic;
chronic
-Rh
-Cong e.g.
Marfan, MVP
-Ischemic
Acute
(infarction, IEC,
post valvotomy)
functional;
-LVF
-HCM
1- organic;
-Rh
-Cong marfan
-syphilis, RA,
Ank. Sp.
-Acute; IEC,
dissecting
aneurysm
1- organic;
-Rh
-Cong
valv; bicuspid
suprav; wiliam,
coarct
subv; HCM
calcific;
2- functional;
Hemic
HTN
AR

70. MS
MR
AR
AS
Symptoms
1- PVC
2-Low COP
3-SVC
1-palpitation
2- PVC
3- Low COP
1-palpitation
2- angina
3-PVC dt LVF
1-Angina
2-syncope(Low
COP)
3-dyspnea(PVC)
Signs
1- general
- Malar flush
Peripheral
signs e.g.
corrigan,
DeMussey,
water-
hummer
pulse,
Duroziez,
Hill’s
2-local
-Palpable S1
-Loud S1,OS,
-Loud S2
-Mid-diastolic
rumbling murmur.
Soft S1
Soft blowing
pansystolic
murmur
Early soft
blowing diast
murmur
Soft S2
Harsh ejection
systolic murmur at
A1

71. MS
MR
AR
AS
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.
-PH,
-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
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
symptoms
Severe AS

72. MS
MR
AR
AS
TTT
1- Prophylaxis from
IEC.
2- diuretics
3- ttt of AF
4-+/-surgery
1- Prophylaxis
from IEC.
2-ttt of AF
3-VD
4-+/-surgery
-If asymtomatic
FU with ECHO.
-surgery
-surgery
- No role for
medical ttt
NB;
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
Predominant MI
in Double M;
1-soft S1
2-S3
3-displaced
hypertrophied
apex
S1+ MR;
1-MS
2-post. Leaflet
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)

73. 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.

74. TR
 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.

75. 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.

76.  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.

77. MVP
 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).

78. 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.

79. 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,

80. 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.

81. Congenital heart diseases
 NB:
- Most common cong HT= biscuspid AV.
- Most common isolated cong HT= VSD ((30%)
- Most common cong in adult = ASD.
without shunt
+ shunt
Acyanotic
-AS
-coarctation
- dextrocardia
(potentially cyanotic)
Mixed blood
-ASD, VSD, PDA
-Coarctation of Aorta
cyanotic
-P atresia
-Severe PS
-Hypoplastic Lt Ht
-Fallot
-Ebstein
-Complete transposition
of great vessels

82. 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.

83.  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.

84. 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)

85. VSD
 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.

86. PDA
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

87. Eisenmenger
 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

88. Fallot
 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.
F3
F4
F5
-ASD
-PS
-RVH
-PS
-RVH
-Overridding aorta
-VSD
ASD
+ F4

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

90. Coarctation
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.

91.  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.

92. Differential diagnosis
 Of systolic murmur over the apex;
1. MI
2. AS, PS (propagated from above).
3. VSD (all over the precordium)
 Of diastolic murmur over the apex;
1. MS
2. AI
 Of systolic murmur over the A1;
1. AS (with all its causes; organic, functional)
 Of systolic murmur over the P;
1. PS (organic, functional).
 Of Lt parasternal systolic murmur
1. Posterior leaflet MI.
2. TI
3. VSD
4. Subval. AS (HCM)
5. Subvalv. PS.

93. Pressure in cardiac chambers
;
Values in mmHg
0-6
4-12
15-30
/
0-6
90-140
/
4-12
25
(
15-30
)
/
10
(
8-15
)
120
(
90-140
)
/
80
(
60-90
)

94. Vascular diseases

95. DVT
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.

96. PE

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.

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

98. 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

99. Acute pulmonary embolus

100. PE
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.

101. PE
 TTT;
1. 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)

102. NB; Shock
With ↑ PCWP=
-LVF
-Temponade
-MS
With ↓ PCWP=
-RV infarction
-PE
-Hypovolemia
-Septic shock

103. Aortic aneurysm

Causes
;
1. Atherosclerosis (commonest).
2. 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.

104. 
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.

105. Aortic dissection
 Type A= ascending.
 Type B= descending.
 Causes; cystic medial necrosis.
1. HTN (70%)
2. Atherosclerosis
3. Congenital; coarct, bicuspid AV, Turner, Noonan.
 Sympt;
1. Sudden severe chest pain radiate to the back.
2. Vasovagal manifestations.
 Signs;
1. HTN
2. Loss of arterial pulse.
3. Occlusion of important vs (stroke, paraparesis)
4. Compression (mediastinal S).
 Complications of ascending; AR, inferior MI, pericardial
effusion, carotid dissection, ↓subclavian pulse.

106. 
Invest
;
1. CXR; wide mediastinum.
2. TOE (most imp); for diagnosis, severity of AR, LV function,
pericardial effusion.
3. CT does not identify site of tear, AR, coronary involvement.
4. MRI does not allow monitoring, # if prothesis.
5. Coronary angio to assess the need for concomitant CABG.
 TTT;
1. Early; releive pain, Na nitroprusside & BB to ↓syst BP<120, ↓
cardiac contractility ↓shear stress of Aorta.
2. 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.

108. 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

109. Essential
Endocrine
Hyperaldosteronism
Pheochromocytoma
Hypo/Hyperthyroidism
Cushing
Vascular
Coarctationn
Drugs
Pregnancy
See HTN in
pregnancy
Contraceptive pills
Corticosteroids
Mineralcorticoids
Sympathomimetics
-nasal decongestants
-appetite suppressants
Phenothiazine
Antidepressants
Cyclosporine
Erthropiotin
Licorice
Tyramine rich food
Salty food
Diet
Renal
Renovascular
Reno-parenchymal
Glomerulonephritis
Collagen Disease,
Henoch-Schonlein Purpura,
Chronic Nephritis
Causes of hypertension
Secondary

111. 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.

112. Blood
K+
Bl.sugar
Lipid
S.Creatinine
Uric acid
HB
ECG
Investigations (1st . visit & annually)
Fundus
Urine exam
proteinuria

113. 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

117. Resistant
Hypertension
•Office blood pressure >140/90 or 130/80 mm Hg in patients with
diabetes or chronic kidney disease
and
•Patient prescribed 3 or more antihypertensive medications at optimal
doses, including if possible a diuretic

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

121. 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.

122. MAT

123. 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 ≠.

124. AVNRT

125. AVRT

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

127. WPW
 ♂, 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 ≠.

128. Rt
LT
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

129. WPW

130. 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.

131. AF
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

132.  TTT;
- Paroxysmal
if young event monitoring.
if old patient, previous TIA anticoag, INR=2-2.5
+ sotalol or amiodarone.
ttt of the attack
stable unstable
DC
Old> 1 y recent
Anticoag + digoxin
TTE
Atria > 5 cm atria< 5 cm
Anticoag + digoxin
>
2
days <
2
days
Cardioversion
without anticoag
Anticoag 3 wks
Cardioversion
then anticoag 3 wks
TEE
thrombus No thrombus
Cardioversion without anticoag
then anticoag
Anticoag 6 wks
then repeat

133. 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.

134.  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.

135. VT
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.

136. Monomorphic VT

137. 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.

138. Non-sustained VT

139. 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)
if chronic recurrent
sustained
not sustained
ttt only if poor LVF
&
structural HT dis
Poor LV funct
.
ICD
Good funct
amiodarone + BB
Or EPS + radiofreq ablation
VT induced by EPS
VT induced by
exercise test
ICD
-/+
amiodarone
BB
-/+
amiodarone

140.  Avoid verapamil with;
1. AF or a flutter in WPW.
2. Wide complex tachy
3. With BB.
 OK verapamil with;
1. AF or a flutter in healthy HT.
2. MAT
3. PSVT (2nd
choice ater adenosine)
4. WPW with narrow complex tachy
5. symptomatic ttt of HCM
6. Severe concentric LVH
7. HTN.

141. VT
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 ≠.

142. Torsade De pointes

144. Bradyarrhysmias
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.

146. 2nd Degree AV Block, Type I

147. LBBB and 2nd degree AV Block,
Mobitz Type II

148. 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.

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

151. Pacemakers
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.

152.  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.
-

153. 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.

154. ICD
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.

155. Antiarrhysmic drugs:
Class
effect
site
use
Class I
A
Quinidine
Disopyramide
procainamide
(- ) Na channels
↑ AP
A, V, acc
WPW+ AF
B
Lignocaine
Phenytoin
Mexiletin
(- ) Na channels
↓ AP
V
Monomorph VT
C
Flecainide
propafenone
(- ) Na channels
No effect on AP
A, V, acc
AF
Class II
Propranolol
Atenolol
BB
nodes
Stress, thyroid,
sinus, cong long
QT, VT
Class III
Amiodarone
Sotalol
Ibutilide
(- )Na, Ca, K
channels
↑ plateau
A, acc ,V
AF, A flutter
AVRT+ wpw
VT
Class IV
verapamil
(- )Ca channels
AV node
SVT, MAT
Others
Adenosine
digoxin
K opener, no(-)
inotrop.
AV node
SVT, diag of
flutter

156. 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.

157. 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%.

158. TTT
1) Physical activity.
2) Diet.
3) Exercise.
4) 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.

159. Syncope
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.

160. 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.

161. 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.

162. JVP
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.

163. 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.

164. 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.

165. 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.