Palpitation

i
syncope

ii i
i

cardiactamponade
stable angina Pem

GERD
2 Pneumothorax Esophagial rupture

m
_ant
t

s i

iffy imdb.it acidosis

Anemia

PAabnormal awareness Renalfailure

of heartbeat palpitation
give
Palpitation if presented with syncope or presyncopy and interact
withdaily life it should be evaluatedand managed
if no symptoms it known as benign such
that occur duringexcertion
i
resyncope ThePeriod ofdizzinessthatPrecide
theloss of consousness a

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insideheart
drug Mcat

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andthisarterythen givePostdescendingartery in 85 ofPeople andthosecalledrightdominance
7s of People theirpostdescendingarteryoriginatefromleftcoronarythosecalled leftdominance
There are

other 7S ofpeoplethierartery originatefrom both Rightandleftcoronary co dominant

AMODE
IS ANNODE

oro.rsmis
 IAD Firstly ECG GOLDEN TEST MENORMAL1123.5 5.5 ma1dL

Psudohyperkalemia falseelevated K levels canbe excluded bydo ECGsince Produce

No changes in ECG in compared toTrue K andthisoccuredaringbloodtransfusionduetoruptureRBC K
Extracardiac manifestations monitored by Eco
1 Intracranial Pressure
2 Electrolytelevels
2
3 Drugeffects

ji
maximum sympathetic Effect on cardiac ratecandemonstrated by 220 Age Normal maximum
do excersizeand every 3 min we increase velocity Heart rate
excersize eco
maximus activity of heart monitorHeart
rate
off thedevice usedin
accordingaboveformula 220
age test
normal activity of Heartwithout ischemic change e

I
indicate in Angina present
the sensitivity of thistest near to 66 77
Binifit in Patientsof episodic angina
compensated heartfailure and episodic Palpitation especial
4

iii iii
physicallyunfit
acute coronary syndrom doefforts
nighfalsenigative

Diagnosis of ischemia
thIII Enzymatic

in myocarditis wehave general cardiac muscle inflammation so Troponin

released greaterthanthat in case of ischemia
I begin to rise 12 hr after ischemia and reach the maximumafter 24 36 hr
In caseof conginital Av Block The body adapt tothis condition so if do
excersitetherate will increase as occure in normal Person
while in case of aquired AVBloc
No increase in rate with excersize
episodic ischemia
I Excersize ECG use
Presyncope espicially in athletics

Atrial naturitic Peptide ProAND creatinine kinase notonly from cardiacorig

Decrease sympathetic tone

Renalfunctiontest
I butalso from skeletal muscle release
alsothereisothertypefrombrain
kidneymay impaired in heartfailureduetodecreasecardiacoutput
Liverfunctiontest Livermaycirrhoseddue to congestiveheartfailure Right
side
Thyroid hormones effect on heartrate
LipidProfile riskforischemicheartdisease
 i
ESR highin Rfever

ambulatory ECG for episodic attack such midnight palpitation or syncope

Lung my pleuraleffusion Pulmonary up ward

EDEMA encephalizatio
pneumonea de failure
compensateheart

bedside use for structural ABNORMALITIES

Ecocardiogram by t.gg
functional
Eco doppler for heamodynamic assising 2 whenthereare veto
resurgeinvalves see
anylesionsuchstenosisor
PharmacologicalExcer
Eco stress by use of Doputamin rather Than Exersize as in Eco

se the viability of cardiactissue befordo

revascularization
I MRI to
Andformassivethrombus tumoraorticanatomyanddisection

moai i ax

Ls ElectroPhysiology study Diagnostic vesiulize Ectopicfo

L therabatic
byelectrodesinsidetheheartbycatheter DoAblasion

Myocardial Perfusion test By use of Tichinatium

for tissue availabitty available tissue have have affinityfor

SCARED tissue Not take it

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tian
4 invasive
a a a swim as wwwsi wa y a mi mi nos at 5in as cat s on s
CT angiography givepatientcontrast andseecoronaryvessel
Furoscopy
byCTscanwhenthecontrast reachtoit
ct calisium scoring Tomakesurethere no atherosclerosis
or calsification Testfornigative predictarevalueown

Tissuedopier
É at 8 y poppier si p i s i Ost ti is w put It 11 w owe Dopplers
Assistant prof. Dr: Sami Al-Obaidy
Cardiology 1
Thyrotoxicosis

friggin
Anemia
Paget Heart failure low out Put
Definition:
Is clinical syndrome in which the cardiac output and body metabolic demand are not meet together.
this diseases
many
Classification of heart failure
A. Right-sided heart failure: systemic congestion → generalized edema
B. Left-sided heart failure: pulmonary congestion → pulmonary edema
C. both side heart failure (biventricular failure): systemic and pulmonary congestion backward
Pressure
Other classification of heart failure: accordingtophysiology
Systolic heart failure:
failure duetorespiratoryfailure
 is HF with reduce ejection fraction, the problem is with contractility
 filling ability is intact
Diastolic heart failure:
 Ventricular muscles become stiff and unable to to fill.
 is HF with preserved ejection fraction (contractility or pushing ability is intact)
to
classificationaccording anatomy
T If accordingtocauses nonischemic
ischemic

Epidemiology:
1. Prevalence of heart failure in population is around 1% in those below 60 years old while the
percentage increase to 10% in those above 80 years old (so the HF is increasing with increase
age)
Éa
2. 50% of untreated heart failure will die within 2 weeks due to pump failure or malignant
arrhythmia
3. Most common cause of death in hear failure is due to arrhythmias.
Etiology of heart failure:
É

C
especially if mildor
moderate
1. Reduced ventricular contractility
 Myocardial infarction es
 Myocarditis/cardiomyopathy
2. Ventricular outflow obstruction (pressure overload)
 Hypertension, aortic stenosis, pulmonary hypertension, pulmonary valve stenosis HOCM
3. Ventricular inflow obstruction
 Mitral stenosis & Tricuspid stenosis
4. Ventricular volume overload so someamountstayinheart notfromexogenousSource
 Mitral & aortic regurgitation
 Ventricular septal defect (VSD) & Atrial septal defect (ASD)
5. Arrhythmia Tach bfilling toco
brady rate toco
6. Diastolic dysfunction
 Constrictive pericarditis, restrictive cardiomyopathy
 Cardiac tamponade, left ventricular hypertrophy and fibrosis
duetoAortic stenosis Written by: Mustafa Abdul-Fattah
or Hypertension
Assistant prof. Dr: Sami Al-Obaidy
Cardiology 2

T.FI j f4g
ioti'diningejection
f riction
systolicHF
Pathogenesis of heart failure
Starling law: cardiac output is linear relationship with preload and contractility, while reverse
relationship with afterload
 Cardiac output ∝ pre-load T
trimmer'etionfictionis5o andabove

 Cardiac output ∝ contractility 50 Ef Preserved EF diastolicHf

1
 Cardiac output ∝
𝑎𝑓𝑡𝑒𝑟−𝑙𝑜𝑎𝑑 yo so Ef midrange
Neuro-hormonal modulation: teducedff

Heart failure causes activation of two systems: systolicH.f1m

belowhot.tt
1. RAAS activation
2. Sympathetic nervous system (SNS) activation
Activation of the RAAS
Causes vasoconstriction and sodium and water retention. This is primarily mediated by angiotensin
II, a potent constrictor of arterioles, in both the kidney and the systemic circulation.
Activation of the SNS:
 Also occurs and can initially sustain cardiac output through increased myocardial contractility
and heart rate.
 Prolonged sympathetic stimulation has negative effects, however, causing cardiac myocyte
apoptosis, cardiac hypertrophy and focal myocardial necrosis.
 Sympathetic stimulation also contributes to vasoconstriction and predisposes to arrhythmias.
Sodium and water retention is further enhanced by the release of aldosterone, endothelin-1 (a
potent vasoconstrictor peptide with marked effects on the renal vasculature)
 and, in severe heart failure, vasopressin (antidiuretic hormone, ADH). Natriuretic peptides are
released from the atria in response to atrial dilatation and compensate to an extent for the
sodium-conserving effect of aldosterone, but this mechanism is overwhelmed in heart failure.
N.B:
1. Inhibition of neuro-hurmonal modulation is basis for modern treatment of heart failure
2. Inhibition of neuro-hormonal modulation is best treatment of HF because, it is improve the
prognosis.
Inhibition of RAAS & SNS:
1. Beta blockers: (inhibit sympathetic stimulation and renin secretion)
2. ACEI and ARB (inhibit angiotensin) notgivenwithbeer creatinine
3. Spironolactone: is aldosterone antagonist agent
goodfort

Written by: Mustafa Abdul-Fattah

Assistant prof. Dr: Sami Al-Obaidy
Cardiology 3

Beneficial neuro-hormonal axis in heart failure: AHinute SNS

 Atrial natriuric peptide (ANB): are family of hormones cause reduction in extracellular fluid
volume by increasing sodium excretion from kidney.
 Neprilysin inhibit this pathway above so we used neprilysin inhibitor in order to obtain this
benefit.
a
 Neprilysim inhibitor: sacubitril Presentation
Hit due
withno clinical
byNH
to compensation
Clinical features: most common presentation of patient with HF is acute on chronic
medulal
good P
Acute case: Fortcase so since no chamberchangesoccuryet
presentation occure
so acute respiratory tobad
Signs of pulmonary congestion
agetationanddistress auxity duetosins
 dyspnea, paroxysmal nocturnal dyspnea, orthopnea,
 exertional cough
 pallor, cyanosis, tachycardia, cold extremities
SE fine end inspiratory basal crepitation: indicate that the congestion reach alveolar level
 may be associated with wheezing (cardiac asthma): indicate severe congestion reach bronchial
level
ThreadyPulse
‫ ويسوي‬bronchial level ‫ من يزيد راح يوصل لل‬fine crepitation ‫ يسوي‬alveoli ‫ اذا وصل ال‬congestion ‫ال‬
genicshock s sametimeduetosnsitshypertension
Lowpressure cardio wheezing
Chronic case:
1. Generalized pitting edema (leg, ascites, sacral if the patient continuously in sitting position, ..)
2. Congested neck vein
3. general fatiguability: ‫يتعب المريض بسرعة‬
4. oliguria
5. GIT: dyspepsia, Malabsorption
6. Liver: enlarged, soft, tender

i
Causes of acute on chronic presentation: At
1. Stop administration of medication & non-compliance to diet (these most common causes)
2. Infection
3. Iatrogenic:

iii iii
 calcium channel blockers has (-ve inotropic effect)
i ii
 steroid: causes sodium & water retention
4. Physical or emotional stress me
5. Pregnancy & delivery inflammatorycondition
so PILTNF
6. Anemia of
atrophy muscles
occuredueto
mediatorsofchronic inflammation
7. arrythmias dueto aminannine disuseatrophy
badPromos
nightlosspresence isvery

Patient with It f
Jundice is one of the Earily Presentation ofWritten by: Mustafa Abdul-Fattah
 Assistant prof. Dr: Sami Al-Obaidy
Cardiology 4

Complication of HF:
1. Renal failure: due to low renal perfusion & and drug toxcicity
2. liver congestion splenomegaly
3. Mesentery ischemia stasisofbloodsoThrombo Embolicstate Pulmonary
ectably4. arrhythmia i commonest cause of death
tach 5. DVT: due to bed siting stasis Thromboembolic
6. weight gain png
7. sudden death yyqgy.gg
8. urea and electrolytes disturbances gg
gym anything
9. stroke af
to nightloss
cardiaccatchacsia i
N.B: organ failure is syndrome and for every syndrome there are causes and there is precipitating cause
bring the patient acutely.
‫ الي جاب المريض‬ischemic heart disease ‫ على سبيل المثال ال‬cause ‫ ال‬syndrome ‫ هو‬HF ‫ يعني عدنا ال‬
Investigations: ifmorethannoonah itscardiaccause
as
azotemia
vena
pere ratherthanresin
1. Blood: CBC, liver and renal and thyroid function tests, tropin, ANP, potassium arrethmia
2. ECG: (arrhythmia, ischemia, champer enlargement) and ur
follow
diagnostic prognostic

3. Chest x-ray: (pleura, cor pulmonale), cardiomegaly upwardencephalization of pulmonary vessels Carly Bline
nitrate angle
costanrenic septal line
4. Echo: (blood flow, follow-up) is the gold standard method in heart failure
sqtegoge.si statial
and discategorizeite functionrationoccurrence
III nation
standers edema
Acute pulmonary edema
Tandaownaair.su
Clinical signs:
1. Pallor 2. Dyspnea 3. Cyanosis respiratory distress
n
Treatment of pulmonary edema:
forpatientthatagetated
gymorinine
1. setting position preload
a
2. high flow O2: through I.Vy cannula or face mas
3. or continuous positive airway pressure: if high flow oxygen is not adequate CPAP my
4. loop diuretic: furosemide 50-100 mg I.V
bitcoin
ischemic
5. glyceryl trinitrate (angesid) ay
6. positive inotropic drugs (dobutamine):
 if the patient not respond to management above
 especially if the patient is hypotensive
7. intra-aortic pallon pump to increase cardiac output: if the pharmacological measures is fails

8 Su nitroglecrine if systole morethantoo

Written by: Mustafa Abdul-Fattah

 Assistant prof. Dr: Sami Al-Obaidy
Cardiology 5

Treatment of chronic case of HF:

1. General measures: education
 avoid salt in diet
 weight reduction
 vaccination (influenza, pneumococcal) to avoid infection
 avoid alcohol ve inotropic steroidsof naretention
B. Pharmacological therapy: anthetimeyoushouldknowvolumestate t sacral
1. Diuretics Wow shouldloss o s I kgday
wow aa
 Loop: furosemide, torsamide, bumetanide, ethacrynic acid. thinaciding
notthick descinding
stat  Thiazide: chlorothiazide, hydrochlorothiazide, metolazone, indapamide
wanted
Times  K sparing (mineralocorticoids): spironolactone, eplerenone,
Side effects of diuretics:
 Loop: hypocalcemia, Hyponatremia, hypokalemia, ototoxicity hyperare coming lycemia

 Thiazide: hyper GLUC (glucose, lipid, uric acid, calcemia) H

Goat
 K sparing: hyperkalemia, spironolactone causes gynecomastia retaincarather thanotherelectrolyte
2. Angiotensin Converting Enzyme Inhibitors: Trained h oe patient
a ctivityofanti
enzymatic androgenic properties bykeepfunctionof
 Captopril, enalopril, quinapril spductase
 are venodilators and arteriodilators
 Beneficial in prognosis becauses they block neuro-hurmonal axis.
 Contraindication in renal failure patient
 Side effects of ACEIs: CAPTOPRIL
Cough, Angioedema, Pregnancy proplem, Taste change, Others (rash, fatigue), Proteinuria,
Renal failure, Increased potassium (hyperkalemia), Low blood pressure (hypotension)
3. Angiotension II Receptor Blockers:
 Losartan, valsartan, candesartan, eprosartan, telmisartan
 are venodilators and arteriodilators
 Beneficial in prognosis becauses they block neuro-hurmonal axis.
 Contraindication in renal failure patient
 Side effects of ARBs: LOSARTAN
Low blood pressure (hypotension), Others (fatigue, headache, dizzines), Allergic reaction,
Raised potassium (hyperkalemia), Teratogenic, Acute renal failure, Nasal congestion
4. Atrial Natriuric Peptide
 There is no atrial natriuric peptide as a drug so we block neplyrysin that causes degradation of
ANP
 Sacubatril is neprilysin inhibitor I
angioedema a
 Entersto is sacubatril + valsartan, more beneficial becauses plus sacubatril it contain ARB
a em
0  Neprilysi causes degradation of ANP

Written by: Mustafa Abdul-Fattah

Assistant prof. Dr: Sami Al-Obaidy
Cardiology 6

5. Combination of hydralazine & Isordil dinitrate:

 Used to treat HF in patient with renal failure rather than ACEIs & ARBs.
bidet
 Isordil dinitrate act on venous side causing venodilation
 Hydralazine act on arterial side causing arteriodilation
 When we used them in combination, we obtain the same action of ACEIs/ARBs without
harmful effect on the kidney

ACEIs & ARBs ‫ هذه الخاصية متوفرة بال‬arteriodilation ‫ و‬venodilation ‫ نحتاج دواء يسوي‬HF ‫بمريض ال‬
‫( راح‬hydralazine & isordil) ‫ لذلك استخدمنا ال‬Renal failure ‫ الي عندة‬HF ‫ولكن منكدر نعالج بيها مريض ال‬
kidney ‫ الي نحتاجه بدون التأثير على ال‬ARBs & ACEIs ‫يسوون نفس شغل ال‬
Mad Af c BlakeyT EE
6. Beta- Blockers: starttopatient withneareavolumicstate s sopreventthe congestion
 carvidilor, bisoprilol, metaprolol succinate (only these 3 B-Blockers are success in HF)
 Improve prognosis becauses block sympathetic system, decrease remodeling and hypertrophy
and apoptosis of myocardial cells.
 We start beta-blocker as a small doses then we do titration-up every 12 weeks interval.
7. Ivabradine:
 decrease heart rate by acting on funny channel in SA node,
 This drug reduce heart rate without effect on blood pressure because its action is on SA node.
 The drug has the effect of beta-blocker but without reduce the blood pressure and without
-ve inotropic effect
 used in patient that is contraindicated for Beta-Blockers
 May be used in combination with beta-blockers if we used the BB in maximum dose and the
heart rate still high.
 used in fluid overload patient
 not useful in atrial fibrillation
8. Digoxin:
 Used in HF especially severe cases of HF
 Beneficial in Atrial Fibrillation.
 It useful in symptoms control and decrease hospitalization but not improve prognosis
(does not reduce the mortility) Arrythmogenicdrug since low index
9. Amidarone:
 only effective in treatment of symptomatic arrhythmia (atrial & ventricular arrythmias)

Thyroid dearrangement
since it's structure has Iodine
i
m sodain glucose co transport inhibitor
il Ad on b ooooconvertfrom anaerobictoaerobic
with utsside asdiuretic

Written by: Mustafa Abdul-Fattah

Assistant prof. Dr: Sami Al-Obaidy
Cardiology 7

C. device therapy: revascularization

1. Implantable cardiac defibrillation:
 indicated in patient with symptomatic ventricular arrhythmia
 Makes DC shock into the heart that restore cardiac rhythm.
 This improve prognosis
2. percutaneous catheter intervention
3. Resynchronisation therapy (benefit in left bundle branch blocker)
4. heart transplantation (limit therapy due to decrease facilities)
5. ventricular assist devices: transplant blood from ventricle to major blood vessels to relieve
the load on the heart
Arrhythmias
Definition: is disturbance of electrical rhythm of the heart
Either tachy or brady arrhythmias
Initiation of impulse: SA → AV → purkinjes fibers → ventricles
Impulse can be initiated in all heart tissue but due to dominancy of SA node, it is suppress other
impulses.
‫ اقوى‬SA node ‫ بس الن ال‬impulse ‫ بي يكدر يولد‬muscle fiber ‫ يعني كل‬automaticity ‫ عندة خاصية ال‬heart ‫ ال‬
atrial ‫ راح ال‬impulse ‫ او صارت بي مشكلة ال‬SA ‫كهربائية تطلع من عندة فراح يغطي على البقية يعني اذا وخرنا ال‬
.. ‫ يستلم المهمة وهكذا‬tissue
1. SA is 60-100 beat/min
2. Atrial tissue is 50-70
3. AV node 50 zoo
4. His purkinji system 30-50
5. Ventricles around 30
N.B:
 His purkinji fibers are the speedest than all tissue fibers of the heart (thier velocity 2-4 m/s)
 While SA node is slowest of heart tissue (its velocity < 0.01 m/s)
Disorders:
1. SA node disorders:
 sinus tachycardia
 sinus bradycardia
 sick sinus syndrome

Written by: Mustafa Abdul-Fattah

 Assistant prof. Dr: Sami Al-Obaidy
Cardiology 15

Common causes of LBBB:

0
1. coronary artery syndrome (IHD)
2. hypertension
3. valvular diseases (especially aortic valve) because LBBB lies just below aortic valve.
4. cardiomyopathy
Ischemic heart disease
Epidemiology:
 Prevalence of IHD increase nowadays even in younger age group.
 10% of general population are suffer from ischemic heart disease
MBADHEART othersymptomssuch intermitantclaudication
Risk factors: sometimespresentwith
 Atherosclerosis is patchy process occur normally in early in life but can accelerated by certain
factors:
F s notfam
 Cardinal risk factors (smoking, hypertension, hypercholesterolemia, DM, family history) I
 Other risk factors: age, sex (pre-menopausal women has more protection from atherosclerosis
than post-menopausal women), obesity, hemostatic factors, decrease physical activity, alcohol,
ettime
connective tissue diseases (APS, SLE), diet rich in lipid hormonalreplacementtherapypostmenoposalused is
notprotective
Causes:
1. Atherosclerosis is the most common cause of IHD
t.is ago
inside
pressure pressure

2
are.si pressure mean
coronary
arterial

2. Non-atherosclerosis causes of IHD:

Troponine  vasospasm
Him
I  connective tissue diseases (vasculitis)
 anemia
 aortic stenosis
way  hypertrophy obstructive cardiomyopathy (HOCM) so compress coronary artery
andit'sselfneed more supply
Pathogenesis:
 Pathogenesis of IHD is usually caused by atherosclerosis:
 Lipid deposition in tunica intima → macrophages try to engulf these lipid particle → when the
macrophages engulf lipid particles, they will become lipid laden macrophages → this causes
restriction of macrophages motility → macrophages also release inflammatory mediators that
causes attraction of other inflammatory cell (such as fibroblast) → fibroblast produce collagen
fibers → these complex of macrophages & inflammatory cell, atherosclerosis and collagen
fibers causes what is called atherosclerotic plaque → this causes narrowing of the blood
vessels thus decrease tissue perfusion.
 Usually atherosclerosis is asymptomatic, but once increase in size, it becomes symptomatic in
70% of cases, this what is called stable angina or chronic coronary syndrome.
WBBpothumin

 In case of stable angina, the patient is asymptomatic unless he exposed to exertion such as
heavy exercise, stress, cold weather, heavy meal.

inversion

are
Written by: Mustafa Abdul-Fattah
 Assistant prof. Dr: Sami Al-Obaidy
Cardiology
stEÉÉ 16

 While Acute Coronary Syndrome or unstableX angina: the atherosclerotic plaque is ruptured
or become ulcerated this lead to platelet aggregation and thrombus formation if this thrombus
causes:
1. Complete occlusion: this causes STEMI angina (ST elevation-MI)
2. Partial occlusion: this causes non-STEMI angina OR a Differbytroponinff

 In STEMI there is tissue damage → so there is troponin release (+ve) of mi unstably t.mn
Management of IHD: ivtissueaus non
1. Primary Prevention: by avoiding the risk factors
a
2. Secondary prevention: by screening
3. Pharmacological treatment ix es w Gus
Chronic coronary syndrome (Angina pectoris):
 Imbalanced between blood supply and cardiac load
 Syndrome (x): is typical anginal symptoms and positive ECG finding but normal coronary
angiography (example of non-atherosclerotic IHD)
 Worm up angina: pain at rest resolve when walking because during walking collaterals will
opened
Clinical presentation: examination
of
1. Pain
i
stableangina
lessthantomin
 retrosternal pain y morethanthat acutecoronarysyndrome
YI underlyingcausesuch
AS aortic

fijjjjjjj
stenosis

 heavy or burning, squeezing in nature complicationsuch

Hf
 radiate to the arm, jaw, neck, back
 inferior MI radiate to epigastrium atherosclerosis
established

 associated with nausea, vomiting and sweating

a
2. Signs aviaries nurses intemitantandication

 Anemia
 Signs of thyrotoxicosis
bruit
 hypertension
carotid j
 Signs of cause (aortic stenosis,…)
 Signs of other atherosclerosis (cerebrovascular, ..)
signsofresult
Investigations:
edema pulmonaryedema
hypotenios body

1. ECG, if ECG normal we do exercise ECG:

 ECG changes: down sloping ST-segment depression and T-wave inversion
g
 Normal ECG does not rule out ischemic hear diseases
2. troponin
3. myocardial perfusion scanning
4. stress Echo Nophysicalworkneeded butdubatamininjection
5. CT coronary angiography: improve the diagnosis, determine extension of disease and guide
Ingaragistrangtagedforischemiabajusts
treatment strategy.

fness s4heartsound ups

tach
Reflex
Rfd
Bradydue
Written by: Mustafa Abdul-Fattah
bloodsupplyabashed
 o
Assistant prof. Dr: Sami Al-Obaidy
Cardiology 17

Triggers of angina:
1. Heavy exercise & emotional sress
2. Heavy meals
3. Cold exposure
4. Lying flat (nocturnal angina) less common bit
er deca usangina
Classification of angina
t.is
physicalabilityislimit high
risk

Liang
1. class I: only during physical activity init
2. class II: mild limitation 3vesseldiscus n
3. class III: moderate limitation
4. class IV (angina arrest): severe limitation (inability to perform any physical activity)
Management of angina:
1. General measures:
 Need time for explanation and education the patient.
 Reassurance
 Advise him to avoid risk factors or controlling the risk factor (DM & HTN) or
2. Pharmacological therapy: shianotient
cut
a) low dose aspirin (life-long) 75 t Statin atom the arid is
profile norma
rosovastain
astatin so even
u
Fb) clopidogril: used as alternative drug than aspirin in patient with peptic ulcer & asthma
Acute c) sub-lingual nitroglycerine: which relieve chest pain. wi thenminutes
d) Anti-anginal drugs: nitratefreeperiodadvised us tolerance suithydrasarenathatnitratewaroncanbeabolishedsosgivetime reform
to it
1. Nitrates:
 isosorbide dinitrate, nitroglycerin
soo
soo  Has direct relaxant effect on vascular smooth muscles thus dilation of coronary vessels
g which improve oxygen supply to myocardium.
 This drug reduce pre-load and after-load
 Side effect: headache, hypotension, rash, flushing I AND sonocompliance
2. Beta-Blockers: running bitempora e
 Metoprolol, bisoprolol, atenolol
 Reduce cardiac demand by reducing myocardial work, increase time of coronary filling.
3. CCB:
 verabamil and deltiazm, amlodipine, clevidipine, nicardipine, niomdipine
 Usually we use non-hydrodipridine (verabamil & deltiazm) because these agents do not
causes reflux tachycardia.
 side effect: edema, hypotension, headache, flushing, dizziness, verapamil causes
constipation

Written by: Mustafa Abdul-Fattah

 Assistant prof. Dr: Sami Al-Obaidy
Cardiology 18

ur
L
angiogram

Other newly drugs:nonnarmacasiamana

coronary
4cg have
sitelessthan I
should

1. K channel activator (nicorandil): both arterial and venous side dilators tolerance
or
am orto
2. funny channel eactivator (ivabradine): decrease heart rate (when BB is contraindicated)heart contra
rate
3. decrease vascular tone (rauolazine) sanone usedwitless
substitution
withnoeffect
onbioodp re.me
n Therapy usedasaddon or tags
nachannelmocker
Prognosis: is related to number of vessels occlusion, if single occlusion and good LV function 5
years survival is 90% while if multiple vessels occlusion the 5 years survival is less than 30%.
Acute coronary syndrome tu function
ofcourse
Include unstable angina, NON-STEMI and STEMI
mine troponineve
Pathogenesis tosotoofPatientthat
changescan
occur

I
everydayPractice
Rupture or ulceration of atheromatous plaque
not toleratethestent
Clinical presentation: someabnormalityin thelast
month if vesselcoronaryarterybipass grafti
duetosomeinflammatory
c ause
cascade
we use
systemiceffect
1. pain ca by
 at rest nuanyinoninvasiisbetter
 Retrosternal
 squeezing
 radiate to epigastrium and left jaw and inner aspect of the left arm, throat, back
 associated with nausea, vomiting, sweating, dyspnea
gene
am 2. pallor, anxious patient (I feel death)
3. palpitation fate of thrombusthatformed
o i i
tal 4. hypotension lysis witherfew days
5. tachycardia
6. low grade fever
recon
7. apex beat displaced
8. third heart sound
9. basal crepitation
10. Painless or silent myocardial infarction: occur in DM patient & elderly.

I
If patient of acute coronary syndrome develop atrial fibrillation we should think about:
sudden death
1. LV systolic dysfunction
2. Pericarditis
3. Extensive ischemia (from ventricle to atrium)
box artides weuseatropine
inischemia rightcoronaryartery Heart
brador
sinus taint

ectoras
yep s anot onlongterm s's
effect
accelerated idioventricularrythen from
arise ventricle
to minimizethearretamiasweshouldkeeppatientat freeof
rest painelectrolite inrange.essoanti

Written by: Mustafa Abdul-Fattah

 Assistant prof. Dr: Sami Al-Obaidy
Cardiology 19

Complications of Acute Coronary Syndrome:

1. sudden death duetoarrythmia
2. Acute heart failure
3. Recurrent angina : angina with ACS
Any patient receive thrombolytic therapy should be catheterized within 24h to remove resident
atherosclerotic plaque (emboli, thrombus)
4. Pericarditis: or
directs is localized retrosternal pain exacerbated with inspiration relieved by lying forward frection
Tay  avoiding NSAID or analgesia in pericarditis to avoid myocardial rupture rub

than
 Dressler syndrome: late or chronic pericarditis develop after 21 days from MI
more (autoimmune)
day
 Corticosteroids or aspirin used to treat patient with pericarditis
 Colchicine sometimes used to treat acute pericarditis. yy
5. Papillary muscle rupture lead to Mitral Regurge → pansystolic murmur (fine) (the patient
develop Lt. sided heart failure) → pulmonary congestion
6. ventricular septal rupture → pansystolic murmur (harsh) clear murmur (the patient develop
Rt. Sided heart failure) → systemic congestion
7. ventricular rupture: very fatal may lead to death Temponastroup sound
hypotension

8. ventricular remodeling: scarredareabeing surroundedby hypertrophiedtisshiert

 early use of small dose of ACEI or ARB or spironolactone are useful to prevent ventricular
remodeling
Iaitov
cost.ie
9. ventricular aneurysm:
 is develop in 10 % of patient
 In ventricular aneurysm, there is paradoxical movement lead to stagnant blood and thus
thrombus formation. saclikedilitation
 In the presence of ventricular aneurysm, ST segment remaining elevated
 Some times we do aneurysmectomy.
10. Embolization (LV) that goes to systemic circulation, that lead to (stroke, ischemic limb,..)
tissuetosonsthosegenerateerectait
11. Arrhythmias: usually ventricular arrhythmia
Investigation atleasttwosequentialleadPresentlocally while thatof
1. ECG: leadsmorethanzsmanseauire PE
if j.t
chest
m is son
 should be done within 10 minute It tn
 The important findings are hyper acute T-wave, ST elevation, Q-wave start to present, T-
wave start to invert, ST-segment start to return to normal.
 New LBBB w
re
 T-wave, Q-wave may be persist inverted (other finding return to normal)
antistantasan 
g Antero-septal MI: V1-V4
at circa Antero-lateral MI: lead I, aVL, V4, V5, V6
coronary

right  Inferior MI: lead II, lead III, aVF

c oronareya

Written by: Mustafa Abdul-Fattah

 Assistant prof. Dr: Sami Al-Obaidy
Cardiology 20

2. serum troponin:
 Negative in unstable angina
 In STEMI, it is positive (it start to increase 3-6 hrs, peak level occur after 36 hrs and
remain elevated up to 2 weeks after myocardial infarction. (more troponin mean more
muscle damage)
3. Echo 4. Cardiac catheterization: for diagnostic and therapeutic purpose.
Treatment: one

1. General measures: avoid (smoking + fatty diet + heavy exercise + alcohol)

2. MONASHAB:
 Morphine (or any analgesia),
 Oxygen,
 Nitrate, enzyu
 Antiplatelet (clopidogrel usually used, aspirin), ECO
 Statin, Eck
 Heparin (or other anti-coagulant),
 ACEI or ARB,
 Beta blockers Cabo
or
3. Early re-perfusion: for STEMI and high risky patient: by thrombolytic + PCI
Tonsteminatament
Patient indicated to give thrombolytic: ageis
markerstroponin
coasts
1. ST elevation with/without Newly LBBB smite.sn
risk
pain
anemic
coronavisualize
2. Chest pain less than 12 hrs aspirin

Contraindication of thrombolytic drugs: enstable

1. Active GI bleeding
fE
ate 2. Previous subarachnoid or intra-cerebral hemorrhage as I us that soy willdie
oil3. Recent surgery or Trauma
4. Pregnancy
wetook
5. Uncontrolled hypertension
Prognosis of ACS: catheter
ti
 depend on:
1. Related to the extent of residual myocardial ischemia
CABG
2. Degree of myocardial damage
3. Ventricular arrhythmias
 25% of cases will die within few minutes if not receive appropriate medical care.
 40% of cases will die within one month if not receive appropriate medical care.
 Patients with unstable angina have 50% of mortaliaty rate as compared to MI patient.
 Early death is usually due to arrhythmia
Thrombolytic
St
 The prognosis is worse for anterior MI than inferior.
 Presence of LBBB and high serum troponin level indicate worse prognosis onlyfor

Written by: Mustafa Abdul-Fattah

Assistant prof. Dr: Sami Al-Obaidy
Cardiology 25

Management
1. If ascending aorta involved must immediate surgery
2. If descending aorta involved treated by medication Beta-Blockers or calcium channel blockers.

%5 ‫ كل ساعة تأخرها تقل فرصة النجاة بنسبة‬

Marfan’s syndrome
 Autosomal dominant inherited syndrome
 Connective tissue disorder (mechanical integrity of connective tissue will be lost) → laxity
 Occur in 0.2% of general population
 Pathogenesis: mutation of febrilin protein (an extra-celluar matrix protein)
 its presentation are aortic aneurysm & dissection, valvular disorders, pneumothorax,
musculoskeletal involvement, neuron involvement
Valvular heart disease:
1. Genetic Valvular Diseases:
 Such as Mitral Regurge that cause by mitral valve prolapse (mitral prolapse is commonest
congenital cause of mitral regurge) bicuspedAorta
2. Acquired:
 HOCM that cause mitral regurge
 Acute myocardial infarction adore Cordatendane rupture
Rheumatic fever:
 Is multi-systemic disease, usually affected children and adult between age of (5-50) years
 The incidence of rheumatic fever is decrease due to wide use of antibiotics.
 The incidence of RF is decrease with age increase
 More common in women (2/3) of cases.
 RF is the most common cause of Mitral valve disorders (90%) of cases, especially causes
mitral stenosis.
 Affect aortic valve in 50% of cases
 Usually affect endocardium and sometimes myocardium and even pericardium
 also affecting joint and skin
Pathogenesis of Rheumatic fever:
 It is not true or primary infection of the heart
 This infection trigger delayed autoimmune response (cross-reaction) in which antibodies
against group A, Beta hemolytic streptococci antigens will attack heart tissue (autoantibodies)

Written by: Mustafa Abdul-Fattah

Assistant prof. Dr: Sami Al-Obaidy
Cardiology 26
fibrenoid o
degeneration f
 Histological appearance: aschoff nodule seen only in heart tissue, which is fibrinoid
degeneration, composed of multi-nucleated giant cells surrounded by macrophages and T-
lymphocytes and usually not seen in acute cases.
Clinical presentation of rheumatic fever:
weeks
 Occur after 2 - 3 from the pharyngitis or sore throat
 fever, anorexia, lethargy
 Arthritis occur in about 75% of patient
 erythema marginatum
 sub-cutaneous nodules (skin involvement)
 Carditis (valvular, myocardial, pericardial symptoms)
 neurological manifestation after 6 months
5 Major criteria:
5 1. Carditis (endocarditis, myocarditis, pericarditis and sometimes pancarditis)
2. polyarthritis

Y
3. Sydenham chorea
4. Erythema marginatum (rarely to occur)
5. Sub-cutaneous nodules.
me
When there are 2 major criteria it is diagnostic of RF or 1 major plus 2 minor criteria → +RF
Cardiac involvement in RF (Carditis):
 If affect the endocardium → the presentation is valvular diseases AcuteBreathlessness
 If affect the myocardium → the presentation is heart failure Heartfailuresymptoms
 If affect the pericardium → the presentation is pericardial pain or effusion
 Aschoff nodules aggregate on mitral valve which causes stenosis → soft mid-diastolic murmur
(carey coombs murmur)
aortic
 Acute regurge occur in 50% of cases of RF
 Pulmonary valve and tricuspid valve are rarely involved in RF.
 If the pericardium are affected, we can hear pericardial fraction rub.
 ECG changes involve ST and T-wave (ST-segment depression and T-wave inversion)
 May be causes first & second-degree heart block and in some cases even causes third degree
heart block.
Arthritis:
 Arthritis in rheumatic fever are migratory process
 Affect joints of the lower limb more than the joint of upper limb
 Highly painful: due to inflammatory condition
 Prevalence of arthritis in acute RF is about 75%, in the order: knee > ankle > elbow > wrist

Written by: Mustafa Abdul-Fattah

Assistant prof. Dr: Sami Al-Obaidy
Cardiology 27

Skin involvement
A. Erythema marginatum:
 Rare presentation in rheumatic fever patient (<5%)
 Rash usually on the trunk or extremities, arranged in ring shape, its margin is red while the
center is clear
 Never to occur on the face
B. Sub-cutaneous nodules:
 Also rare (5-7%)
 Thin and painless
 Around 1-2 cm
 Delayed for 3 weeks to appear in RF
 Presence on extensor surface of the bone and tendons (usually in the arm & shin of the tibia)
 Usually help to confirm the diagnosis
 Usually associated with chronic cases on acute
Neurological involvement:
sydenham chorea:
 More common in female, occur in about 1/3 of cases
 is short repetitive movement (site vitus dance)
 snake-like tongue movement
 usually delayed after acute attack by 6 months
 is benign condition recover spontaneously after 2 months n
µ
 Those patients have chance about (25%) to get chronic rheumatic fever yo
Investigation: IFEcardiac
god
1. CBC, ESR, CRP
2. Anti-streptolysin O antibodies (ASOT) , throat soap: to detect streptococcus infection
3. Culture is not beneficial, it is only positive in 10-25% of cases ‫من يجون رايح األنفكشن‬
4. Echo: valvular involvement, myocardial and pericardial involvement
5. ECG (heart block, prolongation in PR-interval) 6. chest x-ray ➡ cardiomegaly
Treatment:
Arthritis
1. Bed rest since
2. Penicillin
 Given for 10 days to treat acute cases
 if allergic ➡ erythromycin or cephalosporin,
 Prophylaxis penicillin (benzathin penicillin), monthly injection for at least 5 years to
prevent recurrent attack of RF.

Written by: Mustafa Abdul-Fattah

 Assistant prof. Dr: Sami Al-Obaidy
Cardiology 28

therabatic trialfordiagnosis
3. Aspirin givenas a responsingrapidlywith24

we
ediatric
 We give 6 divided doses until ESR return to normal, where the aspirin is stopped
 The patient of RF especially who has arthritis immediately respond to aspirin (within 24h)
me 1st8  maximum dose of aspirin is 8 mg/day
Rf
 aspirin is gastric irritant, so we give gastric protective agent
 side effect of aspirin: nausea, vomiting, tetanus, deafness, acidosis & tachypnea
4. Prednisolone
 not routinely used, we given if the patient not respond or contraindicated to aspirin.
 same principle of using aspirin
Infective endocarditis (IE) sometime there is Non infective endocarditissuchthatoccure inureme
or in libmansyndro
 70% of cases caused by streptococci and staphylococci.aurisus damagenormalvalvesince highvirula

used
Inf  Other organism (HACEK) H. influenza, Aggregatibacter, Cardiobacterium hominis, Eikenella
corrodens and Kingella
ost  Staph epidermidis is associated with prosthetic valve infection. Damageandvisitationpretent
common
theantibiotic fromreachingthe
useespiciany siteof bactrea
drug  Increasing in incidence of around 5-50 cases per 1000
users Can affect also native (intact) valve due to infection by purulent organism.
 Infective endocarditis occur in pre-existing endocardial damage then the infection (IE) causes
Herit vegetation then clinical manifestation of IE, except some organism such as staph. aureus

id
(purulent) which causes infection in native valve and did not need to pre-existing damage to
reptococcuscauses infection.

É
 Drug abuser develop infection in Rt side of the heart, lead to damage to tricuspid valve.
 Some congenital heart diseases especially ventricular septal defect also predispose to infective
endocarditis.
 VSD causes IE more than ASD due to high pressure gradient in ventricles (pressure in left
ventricle (140) is highly more than in right ventricle (20), while in atria pressure gradient
between left and right is almost equal, so tissue damage is little → IE is less in atria.
a
 Infection is characterized by vegetation, vegetation is composed from microorganism (strept,
staph, fungal), fibrin and platelet aggregation.
 Q fever endocarditis is caused by coxiella burnetii, and this organism plus to brucella causes
damage to aortic valve due to unknown cause.
 Rarely fungi can causes infective endocarditis especially in immunocompromised, cancer,
corticosteroid abuse patients and fungi infection is of poor prognosis.
24 of Prevous Rhumatic heartdisease damagevalve act as anidus for infection
Clinical presentation: insidetheheart valveex res embolization
urged formation septic
Pathology Et
ormaycausethrombus
o utsidetheheart autoimmuneglomerulonephritis vasculitis
 Presentation may be acute or sub-acute presentwithPainlesshe
maturea
 Depend on virulence of microorganism, prosthetic valve,.. while it Painful he maturemayberenal
infarctionduetothromboembolic phenomena
 There is no clear clue to diagnosis the (IE) while if patient of congenital heart disease or
valvular heart diseases is present with persistent fever in this status the first suspicion should be
infective endocarditis

Written by: Mustafa Abdul-Fattah

 Assistant prof. Dr: Sami Al-Obaidy
Cardiology 29



ind'Niddiddd'NTnd
Symptoms usually non-specific: fever, weight loss, night sweating,
In acute (IE) the patient present with severe febrile illness
Present

beginningofregurge
 May be presented with signs of valvular heart diseases sinceaftersudden
noenoughtimefor
accomidationtothisvd

ggg 
May be presented with signs & symptoms of acute heart failure (dyspnea, ..) overload
Sometimes develop thromboembolic manifestation in the (brain, kidneys, limbs, spleen,..)
 Petechial skin rash, splinter hemorrhage
 Osler’s nodes (painful),
 valvular dystrophy
 Elms
digital clubbing (late sign) her's Prefepreagretic



two
palpable splenomegaly in cases of coxiella & brucella
If affect tricuspid valve: TR and lead to hepatomegaly
presentation fromsimplefeverto lifethreateningpulmonary
Criteria forvary
diagnosis IE: edema
Major criteria:
1. Positive blood culture
2. Endocardial involvement: detect by echo or newly murmur (newly MR, AR)
Minor criteria: or change in quility of murmer
1. Pre-disposing valvular abnormalities so
2. I.V. drug abuse v set
3. Fever equal or more than 38 C
4. Embolic phenomena: (stroke, renal infarction,…) 3
5. Vascular phenomena: osler’s nodes I use PDA
6. Positive blood culture but not meet the major criteria.
Diagnosis of IE according to criteria above:
finite1. Presence of 2 major criteria is diagnostic am m atypical
2. Presence of 1 major criteria + 3 minor criteria is diagnostic
3. Presence of 5 minor criteria is diagnostic
Previously we takeblood duringepisode
ssities offeverbutnowdays it'snotused
becausetakerandomantibiotics sinceit'snottrue
Investigations: nigati
1. Blood culture & sensitivity (1st line): for diagnosis and also guide treatment
2. Trans-thoracic cardio-Echography (2nd line): show vegetation & valve damage & abscess tutu
formation.
si
1
3. Trans-esophageal Echo: more accurate than trans-thoracic Echo
4. Blood test blood of 20mi at

 ESR: high spenffive ihr intervalbetween

 Normocytic, normochromic anemia samples thenagain
 Leukocytosis do it after iz urtota
another 3samples
and
nigativeEchoorbloodculturebutnot bothNotexcludethe diagnosis sotheresultis 6samples
Written by: Mustafa Abdul-Fattah
Assistant prof. Dr: Sami Al-Obaidy
Cardiology 30

 CRP & other inflammatory markers

 Coagulase: in staph aureus, coagulase is positive while in staph epidermidis, coagulase is
negative
5. ECG:
 may show AV block especially in case of aortic root abscess. The Purkenti Justbelow
 benefit to detect if MI due to embolization the rootso theAbcess
6. Chest x-ray: show if there is cardiomegally can affectandcause
heart block
Management: (4-6 weeks) prosthetic valve needs 6 weeks while native needs 4 weeks
1. Empirical therapy: until the result of the culture
 Amoxicillin forstrepto we
Pincilline
useBenzyl
 Vancomycin we shouldchecktherenalfunction gentamycine
 Gentamycin or vancomycine
gentamycine
2. If the patient suspected prosthetic valve
 Vancomycin ForEnterococcus
 Gentamycin use Pincillin
 rifampicin Gentamicin

Prevention: É orVancomycin
Gentamycin
AB administrate as prophylaxis
Prosthitic
4 anomane For staph
Mitral valve:
Normal diameter 2-4 cm2, increase up to 5 cm2 in diastole. whilebiovalveadded fluclocissiline
Amoxillia gentamycin
Anystaph
Mitral stenosis
Causes: aiggiggy
1. Rheumatic fever (most common cause) (rheumatic and rheumatic and rheumatic and nothing than
rheumatic)
2. Very rare causes (SLE, CT disease, congenital).
Pathophysiology:
 In case of rheumatic fever the valve is calcified and fibrosed and the surface area will decrease
to less than 1 cm2
 Symptoms not appear until the surface area reduce to less than 2 cm2
Symptoms and sign:
1. Pulmonary congestion (orthopnea, SOB, cough, , hemoptysis, malor flush, fatigue, palpitation
secondary sinus tachycardia, later on pulmonary hypertension and LVH).
2. left atrial dilation (AF) that lead to atrial fibrillation
3. low cardiac output symptom ( headache, dizzy, blurred vision)
Written by: Mustafa Abdul-Fattah
 Assistant prof. Dr: Sami Al-Obaidy
Cardiology 30

 CRP & other inflammatory markers

 Coagulase: in staph aureus, coagulase is positive while in staph epidermidis, coagulase is
negative
5. ECG:
 may show AV block especially in case of aortic root abscess.
 benefit to detect if MI due to embolization
6. Chest x-ray: show if there is cardiomegally
Management: (4-6 weeks) prosthetic valve needs 6 weeks while native needs 4 weeks
1. Empirical therapy: until the result of the culture
 Amoxicillin on
 Vancomycin
 Gentamycin
2. If the patient suspected prosthetic valve
 Vancomycin
 Gentamycin
 rifampicin
Prevention:
AB administrate as prophylaxis
Mitral valve:
Normal diameter 2-4 cm2, increase up to 5 cm2 in diastole.
Mitral stenosis
Causes:
1. Rheumatic fever (most common cause) (rheumatic and rheumatic and rheumatic and nothing than
rheumatic)
2. Very rare causes (SLE, CT disease, congenital). the
tocalcification
Pathophysiology: surfacearea y oamp
 In case of rheumatic fever the valve is calcified and fibrosed and the surface area will decrease
to less than 1 cm2
Jaasytmptomaticantilbecome
 Symptoms not appear until the surface area reduce to less than 2 cm2 less
than aem
Symptom is prominent during exercise ‫عراض‬%‫متر او اصعد درج تطلع ا‬٣٠٠ ‫ريض من امشي‬:‫يگلك ا‬
Symptoms and sign: Bcz filling of the heart is during diastiol ‫جهود والرياضة راح يزيد‬:‫ فا‬HR ‫ منا هو الصمام ضيق ومنا قل الوقت مال‬filling bcz
of increased HR
1. Pulmonary congestion (orthopnea, SOB, ftp.hestpain
cough, , hemoptysis, malor flush, fatigue, palpitation
secondary sinus tachycardia, later on pulmonary hypertension and LVH).

ta
on
increased
sincebodydemandincre
2. left atrial dilation (AF) that lead to atrial fibrillation soheartrateincreaseandtime
3. low cardiac output symptom ( headache, dizzy, blurred vision)
Csomeofthemc
o havefibroticatriumsomaintainthiersinusrythm Written by: Mustafa Abdul-Fattah
Assistant prof. Dr: Sami Al-Obaidy
Cardiology 31

4. Auscultation of MS : irregularlyirteguarrythm dueto atrialfib

 Load S1 but in advanced stage S1 lead to be faint
 Load S2 also due to secondary HTN
 Opening snap (normally opening of a valve not produce sound but in MS, it produce opening
snap)
 Mid-Diastolic Murmur ➡ rumble and PAS murmur.
 Basal and infiltrative crepitation due to HT.
Investigation:
1. ECG: show
 P-mitrale (bifid P-wave),
zit
fib  AF (absent P-wave, irregular irregularity of RR- interval, irregular base line)
 RVH (V1, V2, V3) omitraicalcificationcanseenon
X Ray
2. X-ray ( pulmonary congestion + pleural effusion, Lt atrial dilated, in advanced stage➡ LVH)
3. Echo: (gold standard in any valvular heart disease)
 calcified and thickening mitral valve
 reduce valve area
 Echo can measure pressure gradient: to estimate pulmonary hypertension
 enlarged left atrium
Management of MS:
1. Treatment of AF as explained previously:
2. Treatment of Pulmonary congestion by diuretics
sometimes Af is
It
if mildno treatmentneeded
compensated so wejust
control therate bydigoxin BB CCB
3. Surgical
a. Valve replacement
b. Balloon valvo-plasty
Indication of balloon valvo-plasty:
1. Significant symptomatic pt.
2. Isolated MS mm
3. Good sub valvular area and not calcified
4. Without LA thrombus (to avoid emboli)
Except these 4 above we made (valve R.T.)

Written by: Mustafa Abdul-Fattah

Assistant prof. Dr: Sami Al-Obaidy
Cardiology 32

Mitral regurgitation
 Incompetence of mitral valve
 Up to 4% percent of the women develop mitral valve prolapse
 Increase risk of emboli from cardiac origin
 Long-term prognosis is usually good (benign condition).
 Majority of patient of mitral valve prolapse not develop MR.
Causes:
1. Congenital: mitral valve prolapse (most common cause)
2. Rheumatic fever, infective endocarditis
3. Rupture in corda tempani in (ischemic heart diseases)
4. Dilatation of left ventricle due to any cause secondcomonc ause
Clinical features:
t imsismorethanthatata.r
1. Acute onset
Sudden severe pulmonary edema

Mee
2. Chronic onset
 Dilatation of left ventricle or dilatation of left atrium
 Gradually onset of pulmonary edema.
 fatigue
3. Pulse: large volume secondary to volume overload, irregular if there is (Atrial fibrillation)
4. displaced apex beat (forceful not sustained) secondary to cardiomegaly.
5. Right ventricular heave.
6. Auscultation:
n
 Soft S1, presence of S3
 If there is no regurge → just Mid-systolic click
 If there is regurge → Pan-systolic murmur radiated to the left
Éitzy
axilla (book-shape murmur)
 Basal crepitation
anpulmonate
Investigation:
1. ECG: AF + RVH
in
sittin
2. CXR: cardiomegaly + pulmonary edema
mr theenlargementinLA W

✔ 3. Echo:
 dilation of left ventricle and left atrium
secondary Itd
Primary dilatation and abnormal structure of mitral valve calcification
4. Heart catheterization
 Determine champer enlargement
 Determine if there is pulmonary hypertension
 If there is coronary heart diseases

Written by: Mustafa Abdul-Fattah

 Assistant prof. Dr: Sami Al-Obaidy
Cardiology 33

Management of Mitral regurgitation:

1. Diuretics Eighteen
LORNE
2. Vasodilators: Decrease regurged blood
3. Control rate with AF
4. Anticoagulants
5. Surgery: valve replacement therapy
Aortic Stenosis:
Causes of AS
1. Congenital: appear in infancy period and early childhood
2. Rheumatic fever: in adult (30-50) age
3. Bicuspid aortic valve: in elderly (50-60) age, present in up to 5% of population.
4. Degenerative calcification of the valve: 70 age or above
terly
Usually If the causes of AS is rheumatic fever, AS is associated with mitral stenosis
Fate of bicuspid aortic valve:
1. 1/3 of the cases persist long life and not develop aortic stenosis
2. 1/3 will develop aortic regurgitation
3. 1/3 will develop aortic stenosis
Clinical features:
1. May be asymptomatic which discovered accidently during routine physical examination.
2. Chest pain because the left ventricular hypertrophy → lead to ischemia (due to compression
and increase muscle demand) and ischemia causes chest pain
3. Dyspnea on effort, Syncope on effort, angina on effort
4. LCO: CNS manifestation
5. Episode of pulmonary edema and heart failure develop lately in the course of the disease.
6. May cause sudden death
Physical examination:
1. Pulse: small volume slow raising pulse (parvus tardus)
2. Apex beat is forceful sustained,
3. Auscultation
 S1 is normal, (soft weak S2 in severe cases and especially in calcified valve)
 Ejection (late) systolic murmur (crescendo and decrescendo) diamond shape
 in aortic & carotid areas and radiated to both carotid arteries
 the murmur is musical (seagull murmur)
 Gallavardin phenomenon: the murmur is listen elsewhere in the precordium

fi Regurge
Levelopmentopulmonaryoedema islate
Written by: Mustafa Abdul-Fattah
Assistant prof. Dr: Sami Al-Obaidy
Cardiology 34

Investigation:
1. ECG: LVH , LBBB mitral anti_az
2. CX-RAY: enlarge ventricle, calcified aortic valve
3. ECHO: calcified valve + LVH
4. Catheterization: to detect coronary artery diseases, therapeutic (balloon plasty).
Management: Once symptoms develops the
1. Asymptomatic patient: by regular follow-up life expectancy is 3 to 5 years
no more
2. Once symptom develop, the death is within 3-5 years, so we should manage by valve
replacement or if the patient does not tolerated the surgery, we do aortic ballon valvo-plasty
Aortic Regurgitation: ddÉT
surgery of replacement
Causes:
1. Congenital: bicuspid aortic valve (1/3)
2. Acquired:
A. disorders involve the aortic valve leaflets: (aortic valve itself)
 RF,
 IE,
 trauma, mjg
B. disorders involve the aortic root
 Marfan’s syndrome,
 Aortic dissection
 syphilis,
 aortic aneurysm,
 Ankylosing spondylitis
Clinical features:
Symptoms:
1. May be asymptomatic in mild cases
2. Shortness of breath
3. Palpitation
4. Angina chest pain
5. Paroxysmal nocturnal dyspnea
6. Peripheral edema
Sings:
1. Collapsing pulse
2. Widened pulse pressure (large volume)
3. Femoral brui
4. Quincke’s sign: increase pulsation of capillary nail bed
5. De Musset sign: nodding of the Head
6. Pulsatile pupil
Written by: Mustafa Abdul-Fattah
Assistant prof. Dr: Sami Al-Obaidy
Cardiology 35

7. Pulse deficit
8. Apex beat: displaced forceful not sustained
9. Auscultation:
 early diastolic murmur (due to aortic regurge itself)
 mid diastolic murmur (soft)
 May be ejection systolic murmur (secondary to large volume flow over the aortic valve).
lo.Pulmonar
Investigation: ais_latesign
1. ECG : LVH
2. X-RAY : cardiomegaly, aortic root dilatation, root calcification
3. ECHO : show valve anatomy: root dilatation, valve leaflet, calcification in valve, vegetation
4. Catheterization
Management:
1. Treatment of underlying cause
2. Valve replacement 11lLWfwWi.L
ti t p
N.B: any patient undergo to valve replacement should be given life-long anti-coagulants especially if
the valve is mechanical while in tissue valve replacement, the anti-coagulant is given only for first 3
month then stopped.
Right-sided heart valves:
Tricuspid Stenosis:
TS is very rare condition, occur due to RF, carcinoid syndrome
Genital
Clinical feature:
1. Right sided-HF manifestation:
 raised JVP
 hepatic congestion,
 ascites
 peripheral edema
2. Auscultation:
Mid Diastolic Murmur (higher pitch in comparison to MS).
Investigation: same above
Treatment: usually valve replacement or bullon plasty

Written by: Mustafa Abdul-Fattah

Assistant prof. Dr: Sami Al-Obaidy
Cardiology 36

Tricuspid Regurgitation:
Causes:
m.ms

nIifjj1
1. Primary diseases:
 RF
 Congenital heart diseases: Epstein anomaly
2. Secondary diseases:
j
 RSHF

ii i
 Pulmonary HTN
 RT ventricle infarction
Pulmonary stenosis: is part of congenital HD
watacngenital
e
 Common causes: is congenital disorders (tetralogy of fallot)
 Ejection systolic murmur in the left intercostal space, usually associated with thrill
i_
Pulmonary regurge:
Commonly in case of pulmonary hypertension

Myocarditis:
Inflammation of myocardium,
Myocardial diseases:
B
Rare disorder, occur usually in young age group.
Causes
1. Infection:
a. bacterial infection: lyme disease, burgdorfer (broelia)
b. viral infection: HIV, adenovirus, coxsackie, influenza
c. parasitic infection: toxoplasma gonide
d. fungal: aspirgillus
2. Drugs and toxins: alcohol, cocaine, lithium,
Eat authracycline
3. Autoimmune: SLE, sclerosis, RA, sarcoidosis, hypersensitivity reaction to drugs (penicillin,..)
Presentation:
range from mild self-limiting to fulminant LV systolic dysfunction and pulmonary edema
1. sometime self-limiting disease just SOB, chest pain, fever and palpitation
2. fulminant myocarditis (LV systolic dysfunction): is sudden sever life threatening heart failure
3. In children can recover smoothly but develop chronic dilated cardiomyopathy after 10-20
years later.
4. acute myocarditis: dilated cardiomyopathy
5. chronic active myocarditis: long Hx of myocarditis (rare)

Written by: Mustafa Abdul-Fattah

Assistant prof. Dr: Sami Al-Obaidy
Cardiology 43

down syndrome Trisomy21 Associatedwithuse Asp

Treatment:

___SDe
1. Emergency pericardio-centesis
2. Surgical drainage sometimes we needed ooooeee
Congenital heart disease
Ventricular Septal Defect (VSD): g
Commonest cardiac congenital anomaly
Constitute 30% of Congenital Heart Diseases
Types Gasul Phenomena
1. Peri-membranous VSD: is near to the valve Themostcommon
2. Mid-muscular VSD: is far from the valve
3. Sub-arterial VSD
4. inlet VSD
Clinical features:
 Pan systolic murmur, maximal intensity in left parasternal area, associated with thrill
 May be associated with load S2 ON_N__t ago
on
Investigation: Echo
Treatment:
ioaE I i
j
1. surgical
stenosisthecondition becomebenignbecause
2. trans-catheter
3. in 8% may be closed with age
4. small VSD may be lift without treatment
called Gasul Phenomena
5. serial follow up
NN0N0
N F
NENNIIENNNN hi
Atrial septal defect (ASD):
sure difference
 fixed splitting S2 pductolowerPres
 ejection systolic murmur (does not give murmur itself but secondary to fluid overflow)
 Murmur in the pulmonary area
ANNENOTTENT
Toousuallydiag adults
differentiate between murmur of ASD & PS
wide, fixed splitting of the second heart sound: wide
because of delay in right ventricular ejection
(increased stroke volume and RBBB), and fixed
 Fixed splitting S2 (ASD) EMM.am
because the septal defect equalises left and right
atrial pressures throughout the respiratory cycle
 Thrill in pulmonary area (PS)
• a systolic flow murmur over the pulmonary valve. In
Types of ASD gearimium children with a large shunt, there may be a diastolic
flow murmur over the tricuspid valve. Unlike a mitral
flow murmur, this is usually high-pitched.
1. primum type: from side of the valve
2. secondum: in mid septum (not side of the heart)
08 we have A 5 4 1 digs.tt
marmara

Written by: Mustafa Abdul-Fattah

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tti
Assistant prof. Dr: Sami Al-Obaidy
Cardiology 44

Investigation: Echo is diagnostic

Treatment: trans-catheter occlusion of ASD, surgical treatment
___________ whhst
Coarctation of aortaFfFNTf__EEF__fTfff 3oyggyy ____ conbacwheeze
 narrowing of the aorta usually just distal to the left subclavian artery
 Brachio-femoral delay, radio-femoral delay

t
 Asymmetrical body built
 This narrowing result in systemic hypertension Nht Eisenmenger’s syndrome
 50% of cases associated with bicuspid aortic valve

i t
berry’ aneurysms of the cerebral circulation

ist
Treatment:
1. stenting
2. Surgery During fetal life, before the lungs begin to function, most of the blood from the
pulmonary artery passes through the ductus arteriosus into the aorta.
i
Persistencebe
and s hould closedshraeteraneuary
Patent Ductus Arteriosus of the ductus causes a continuous AV shunt from the aorta to the

Egging pulmonary artery since pressure in the aorta is higher than that in the pulmonary
circulation.

 Persistent of the Arteriosus ligament that should be obliterated after birth

 Present between left pulmonary artery and descending aorta


Continues machinary murmur best heard in pulmonary area
pulmonary hypertension
continuous ‘machinery’ murmur is heard with late systolic accentuation,

andeven RAF
maximal in the second left intercostal space below the clavicle. It is
TIseatt.to
gaordgtnhgp
Mate
Io
frequently accompanied by a thrill.
Pulses are increased in volume

 cyanosis of lower limb (late sign)

si.is dstandered
Treatment: prostaglandins inhibitors, catheterization, surgery
ANAANA IN A
E
ESID IFEco
andxrayshowrightventric
Tetralogy of Fallot (TOF): IDREE IN FILE
In early childhood in infancy or neonates
Clinical features EtatadedafWHbutHmmntN
Fehn of aorta need time todevelop
1. VSD

W
2. Pulmonary stenosis
3.
4.
over-riding of aorta
cor pulmonale
t
N.B: If there is ASD plus the 4 features of tetralogy of fallot, this congenital anomaly is called
Pentalogy of fallot:
Treatment: need multiple corrective surgeries.

The affected child may suddenly become increasingly

pts
.. ‫لتنسونا من الدعاء‬ cyanosed, often after feeding or a crying attack, and may
become apnoeic and unconscious. These attacks are called
‘Fallot’s spells’

Written by: Mustafa Abdul-Fattah