#DAVIDSON_REVIEW

#CARDIOLOGY_1

Cardiology থেকে প্রায় ১৫ টা প্রশ্ন থাকে।৭/৮ Anatomy & Physiology related. Cardiology basic
একটা পোস্ট দেওয়া আছে।কিছুটা কভার হবে। ডেভিডসন থেকে কি পড়া লাগবে সেগুলো পোস্ট গুলোতে
কিছুটা রিভিউ করবো ইং শা আল্লাহ্।

N.B. Davodson Anatomy & physiology ভাল করে বুঝে পড়বেন।তাহলে অনেক প্রশ্ন কমন না থাকলেও
বুঝে উওর দিতে পারবেন।মুখস্থ করে গেলে পরিক্ষায় না পারার সম্ভাবনা অনেক বেশি।😥😥

### Page 442 -460

Anatomy & Physiology ********

Box 16.1 *****
Box 16.2 *** (MCQ IN JAN 20)
Box 16.3 **
Fig 16.9 **
Fig 16.17 **
Box 16.7 *****
Fig 16.20 **
Box 16.8 *****
Box 16.9 ***** (MCQ IN JAN 20)
Box 16.11 **
Fig 16.23 **

Page 442
+ Just read the figure

Page 443
** Common abnormalities of apex beat

Anatomy important :

*** Atria and ventricles are separated by annulus fibrosus, which forms the skeleton for AV
valves and electrically insulates atria from ventricles.

***** On left, the cardiac silhouette is formed by the aortic arch, the pulmonary trunk,left
atrial appendage and LV.

***** On right,silhouette is formed by RA and superior and inferior venae cavae, and RV.

* LAD gives supply anterior part of the septum (septal perforators) and the anterior, lateral
and apical walls of LV.

* CX gives marginal branches that supply lateral, posterior and inferior segments of the LV.

** Posterior descending artery is a branch of RCA in approximately 90% of people

(dominant right system) and by CX in remainder (dominant left system).

***** RCA supplies SA node in about 60% of individuals and AV node in about 90%.

***** Proximal occlusion of RCA therefore often results in sinus bradycardia and may also
cause AV nodal block.

***** Occlusion of left main coronary artery is usually fatal.

*** Annulus fibrosus forms a conduction barrier between atria and ventricles, and only
pathway through it is the AV node.

** Under resting conditions, vagal inhibitory activity predominates and heart rate is slow.
Adrenergic stimulation, associated with exercise, emotional stress, fever and so on, causes the
heart rate to increase. In disease states, the nerve supply to the heart may be affected.

PHYSIOLOGY

* The basic unit of contraction is the sarcomere which is aligned to those of adjacent
myofibrils, giving a striated appearance due to Z-lines

* Actin filaments are attached at right angles to the Z-lines and interdigitate with thicker
parallel myosin filaments.

* Thin filaments - Actin,Troponin, Tropomyosin. Thick filament - Myosin

* Troponin T binds to tropomyosin

** Enlargement of the heart seen in heart failure is due to slippage of the myofibrils and
adjacent cells rather than lengthening of sarcomere.

*** ANP - vasodilator,reducing blood pressure (BP), and diuretic by promoting renal
excretion of water and sodium.

** Neprilysin - an enzyme present in circulation,produced by kidney and other tissues,breaks

down ANP, BNP and other proteins,acts as a vasoconstrictor,a therapeutic target in patients
with heart failure.

*** Central arteries, such as aorta, are predominantly composed of elastic tissue with little or
no vascular smooth muscle cells.

** It prevents excessive rises in systolic BP while sustaining diastolic BP, thereby reducing
cardiac afterload and maintaining coronary perfusion.

** These benefits are lost with progressive arterial stiffening, which occurs with ageing and
advanced renal disease. .

*** Predominant effect of sympathetic stimulation in coronary arteries is vasodilatation.

* Parasympathetic timulation also causes modest dilatation of normal coronary arteries.

*** Narrowing or stenosis in a coronary artery does not limit flow, even during exercise,
until cross-sectional area of the vessel is reduced by at least 70%.

Box 16.1
+ Inspiration & expiration e change আলাদা করে পড়তে হবে
+ বক্সের নিচে ২ টা লাইন ***

INVESTIGATION

* ECG is the main test used in the diagnosis of myocardial ischaemia and infarction. .

* PR interval largely reflects the duration of AV nodal conduction.

* Injury to left or right bundle branch delays ventricular depolarisation, widening the QRS
complex.
* Selective injury of one of the left fascicles (hemiblock) affects the electrical axis.

* Repolarisation is slower and spreads from the epicardium to the endocardium.

* QT interval represents the total duration of ventricular depolarisation and repolarisation

* Lead I records the signal between the right (negative) and left (positive) arms.
Lead II records the signal between the right arm (negative) and left leg (positive).

* Lead III records the signal between the left arm (negative) and left leg (positive). average
vector of ventricular

*** Normal cardiac axis lies between −30° and +90°.

*** Leads V1 and V2 lie approximately over the RV, V3 and V4 over the interventricular
septum, and V5 and V6 over the LV.

** Exercise ECG Test is considered positive if angina occurs, BP falls or fails to increase, or
if there are ST segment shifts of more than 1 mm.

***** Stress testing is contraindicated in the presence of acute coronary syndrome,

decompensated heart failure and severe hypertension.

*** BNP is secreted by the LV,elevated in conditions associated with LV systolic

dysfunction.

*** NT-proBNP is measured inpreference to BNP since it has a longer half-life for the
diagnosis of LV dysfunction and to assess prognosis and response to therapy in patients with
heart failure

BOX 16.2
+ MCQ
+ কোন Condition এ কোন change হয়?
Ex - Tall P in rt atrial enlargement

***** [ ] TROPONIN I increased in

CARDIAC
• MI, Myocarditis
• Pulmonary embolism
• Pulmonary oedema
• Cardiac surgery, trauma
• Tachyarrhythmia
• Aortic dissection

NON CARDIAC
• Septic shock
• Prolonged hypotension
• ESRD
• Burn
• Stroke,SAH

ANP
• Secreted by both atrium (Rt>Lt)
• Degraded by endopeptidase
• Promotes Na excretion, antagonize angiotensin 2, aldosterone,lower BP
BNP
• Diuretic and natriuretic
• Vasodilator
• Suppress sympathetic and RAA system

• Most information is given by a postero-anterior (PA) projection taken in full inspiration

• Lt atrial dilatation - prominence of lt atrial appendage,appearance of a straight lt heart

border, a double cardiac shadow to rt of sternum, and widening of angle of carina (bifurcation
of the trachea).

• Normal resting systolic flow velocity across aortic valve is approximately 1 m/s.

• TOE under light sedation & positioning it behind LA

*** Useful for - Lt atrial appendage, pulmonary veins, thoracic aorta and interatrial septum,
especially if the patient is overweight or has obstructive airway disease

*** TOE particularly valuable for prosthetic (especially mitral) valve dysfunction,
ASD,aortic dissection,infective endocarditis (vegetations too small for TTE) & systemic
embolism (intracardiac thrombus or masses).

• Contrast CT are very useful for aortic dissection,pulmonary embolism.

• Redistribution of contrast, so-called delayed enhancement, can be used to identify

myocardial scarring and fibrosis,a particular strength of cardiac MRI

• An electrophysiology study (EPS) is most commonly performed to evaluate patients for

catheter ablation

• Chest pain on effort is the hallmark of angina pectoris

•In patients with chest pain where exercise ECG is normal but there is a suspicion of CAD,
CT coronary angiography should be performed

PALPITATIONS

• Unusually erratic, fast, slow or forceful heart beat, or even chest pain or breathlessness.

• Recurrent but short-lived bouts of an irregular heart beat are usually due to atrial or
ventricular extrasystoles (ectopic beats).

• Episodes of a pounding, forceful and relatively fast (90–120/ min) heart beat are a common
manifestation of anxiety.

• These may also reflect a hyperdynamic circulation, such as anaemia, pregnancy and
thyrotoxicosis, and can occur in some forms of valve disease such as aortic regurgitation.

• Discrete bouts of a very rapid (over 120/min) heart beat - a paroxysmal supraventricular or
ventricular tachycardia

• In contrast, AF typically present with irregular and usually rapid palpitation.

• Palpitation associated with pre-syncope or syncope may reflect more serious structural or
electrical disease and should be investigated without delay
Box 16.7
+ MCQ
+ Structural / Non structural seperately পড়তে হবে

Fig 16.20
+ Reversible cause *** (4H 4 T)

Box 16.8
+ Both SBA & MCQ
+ Timing, Mechanism,
Variable features *********

*** Benign murmurs do not occur in diastole and systolic murmurs that radiate or are
associated with a thrill are almost always pathological

Box 16.11
+ MCQ
+ সব পড়তে হবে।

** Continuous murmur
• PDA (Machinery ***) (SBA)
• Bruit from arterial shunt,venous hump
• Pericardial friction rub

#DAVIDSON_REVIEW
#CARDIOLOGY_2

(আমি বিভিন্ন সাজেশন থেকে এবং আমার কাছে যা ইম্পরট্যান্ট মনে হয়েছে সেগুলো দেওয়ার চেষ্টা করেছি।
পারলে এর বাইরেও পড়বেন এবং অবশ্যই কন্সেপ্ট ক্লিয়ার রাখবেন।একেবারেই যদি না বুঝতে পারেন কিছুটা
মুখস্থ করবেন😐😐)

### Page 461 - 482

Heart failure ***

Box 16.12 **
Box 16.13 *
Box 26.14 (drugs only)
Fig 26.26 *****
Fig 26.27 A *
Box 16.15 ***
Box 16.16 (Vaccination)
Box 16.19 *****
Box 16.20 **
Atrial fibrillation ***
Box 16.21 *****
Box 16.23 **
Box 16.25 **********
Box 16.26 **********
Atrioventricular block *****
Box 16.27 ***
Box 16.28 ***
Fig 16 51 *****
Box 16.29 *****
Box 16.30 (Amiodarone side effects *****)
Box 16.32 *
Box 16.33 *****
HEART FAILURE

+ Scenario based question for SBA

+ Complications
+ Drugs used in HF
+ Side effects of drugs used in HF

Important

*** Ventricular dysfunction is the most common cause of heart failure

** High output failure

• Arteriovenous shunt
• Beri beri
• Severe anemia
• Thyrotoxicosis

** A ‘gallop’ rhythm, with a third heart sound, is heard quite early in the development of
acute left-sided heart failure

***** A new systolic murmur may signify acute mitral regurgitation or ventricular septal
rupture (SBA)

*** Complications - Name only

***** HYPONATRAEMIA IS A FEATURE OF SEVERE HEART FAILURE AND IS A

POOR PROGNOSTIC SIGN.

** Sudden death occurs in up to 50% of patients with heart failure and is most probably due
to ventricular fibrillation.

** Neprilysin inhibitor - Mx of resitant heart failure

** B blocker :
• When initiated in standard doses β-blockers may precipitate acute-on-chronic heart failure,
but when given in small incremental doses they can increase ejection fraction, improve
symptoms, reduce the frequency of hospitalisation and reduce mortality

• Beta-blockers are more effective at reducing mortality than ACE inhibitors

*** CARDIAC TRANSPLANTATION

** Coronary artery disease and dilated cardiomyopathy are the most common indications

***** Contraindicated in pulmonary vascular disease due to long-standing left heart failure,
complex congenital heart disease such as Eisenmenger’s syndrome, or primary pulmonary
hypertension

** Heart–lung transplantation can be successful in patients with Eisenmenger’s syndrome,

and lung transplantation has been used for primary pulmonary hypertension.

IMPROVE MORTALITY IN CHF

• ACEi
• Spironolactone
• B blocker
• Hydralazine with nitrate
Box 16.12
+ Cause & Examples

Box 16.15
+ Only headline & effect

ATRIAL FLUTTER

• Rate is approximately 300/min, and is usually associated with 2 : 1, 3 : 1 or 4 : 1 AV block.

• ECG shows saw-tooth flutter waves .

• Carotid sinus pressure or iv adenosine may help to diagnosis by temporarily increasing the
degree of AV block and revealing flutter waves

• Digoxin, β-blockers or verapamil is often successful in controlling the ventricular rate.

• Class Ic anti-arrhythmic drugs such as flecainide are contraindicated.

• Catheter ablation - highly effective, offering > 90% chance of complete cure, and treatment
of choice for patients with persistent symptoms

ATRIAL FIBRILLATION

** ATRIAL FIBRILLATION (AF) IS THE MOST COMMON SUSTAINED CARDIAC

ARRHYTHMIA.

** Ectopic beats arising from conducting tissue in the pulmonary veins or from diseased
atrial tissue.

• Atria beat rapidly but in an uncoordinated and ineffective manner.

*** The ECG shows NORMAL BUT IRREGULAR QRS COMPLEXES. NO P WAVES but
the baseline may show irregular fibrillation waves.

• Paroxysmal (self-terminate within 7 d), persistent (>7 d) or permanent (Can't be terminated.

Rx goal - Rate & rhythm control)

• Typical presentation is with palpitation, breathlessness and fatigue.

• Occasional attacks of AF that are well tolerated do not necessarily require treatment.

*** Beta-blockers - first-line therapy. MOST EFFECTIVE - AMIODARONE

***** Rhythm control:-

• < 48 hr - Immediate cardioversion

• Stable patients without structural heart

disease - IV flecainide.

• In structural or IHD - IV amiodarone

• DC cardioversion is an alternative treatment

• 48 hours or longer or doubt about its duration, DC cardioversion after anticoagulation for 4
weeks. Anticoagulation should be maintained for at least 3 months following cardioversion.
• Amiodarone is used to reduce the risk of recurrence.

• Catheter ablation is less effective treatment than for paroxysmal AF.

Rate control :-

** β-blockers,rate-limiting CCB (verapamil or diltiazem) & Digoxin

• Combination therapy with digoxin and a β-blocker can help with rate control but calcium
channel antagonists should not be used with β-blockers because of the risk of bradycardia.

Thromboprophylaxis:-

*** Warfarin therapy adjusted to a target INR of 2.0–3.0.

• Aspirin should not be used since it has little or no effect on embolic stroke and is associated
with significant bleeding risk

Box 16.23
+ Parameter with score porte hobe
+ Scenario তে parameter দেওয়া থাকবে scoring করে দেখতে হবে anticoagulant দিতে হবে কিনা।
+ প্রশ্নে অপশন থাকবে warfarin দিব কি দিব না

SUPRAVENTRICULAR TACHYCARDIA

• Usually NARROW-COMPLEX TACHYCARDIAS

• Three principal types - atrioventricular nodal re-entrant tachycardia (AVNRT),

atrioventricular re-entrant tachycardia (AVRT) and atrial tachycardia.

AVRT

• An abnormal band of conducting tissue that connects the atria and ventricles.

*** Premature ventricular activation via the pathway shortens the PR interval and produces a
‘slurred’ initial deflection of QRS complex, called a delta wave

*** When associated with symptoms, the condition is known as Wolff–Parkinson–White

syndrome.

• Carotid sinus pressure or intravenous adenosine can terminate tachycardia.

• Catheter ablation is first-line treatment in symptomatic patients and is nearly always

curative.

• Digoxin and verapamil should not be used.

VENTRICULAR TACHYCARDIA (SBA)

• Associated with extensive ventricular disease, impaired LV function and ventricular

aneurysm,ventricular fibrillation.

• Palpitation or symptoms of low cardiac output, including dyspnoea, lightheadedness and

syncope.

*** ECG shows tachycardia and broad, abnormal QRS complexes, rate > 120/min.
• Difficult to distinguish VT from SVT with bundle branch block or pre-excitation (WPW
syndrome) on ECG

*** When there is doubt, it is safer to manage the problem as VT.

• Patients recovering from MI sometimes have periods of idioventricular rhythm (‘slow’ VT)
- reflect reperfusion of the infarct territory and may be a good sign.

• They are usually self-limiting and asymptomatic, and do not require treatment.

***** Synchronised DC cardioversion - Rx of choice if systolic BP < 90 mmHg.(Also in

chest pain/HF/HR >150 /min) (SBA)

***** If arrhythmia is well tolerated iv amiodarone may be given as a bolus, followed by a

continuous infusion. (SBA)

• If fail to amiodarone - DC cardioversion

• Class Ic anti-arrhythmic drugs should not be used for prevention of VT in patients with
coronary artery disease or heart failure.

• In patients with poor LV function or where VT is associated with haemodynamic

compromise,use of an implantable cardiac defibrillator is recommended.

• Treatment of choice for VT occurring in a normal heart is catheter ablation, which often can
be curative.

• VERAPAMIL should not be used in VT

TORSADES DE POINTES

• ECG will usually show a prolonged QT interval (> 0.44 sec in men, > 0.46 sec in women).
• More common in women

***** IV magnesium should be given in all cases.

• Brugada syndrome may present with polymorphic VT or sudden death.

• Characterised by a defect in sodium channel function and an abnormal ECG (right bundle
branch block and ST elevation in V1 and V2 but not usually prolongation of the QT interval).

• Rx is an implantable defibrillator.

FIRST-DEGREE ATRIOVENTRICULAR BLOCK

• AV conduction is delayed and so the PR interval is prolonged (> 0.20 sec)

SECOND-DEGREE AV BLOCK

• progressive lengthening of successive PR intervals, culminating in a dropped beat.

• The cycle then repeats itself. This is known as the Wenckebach phenomenon and is usually
due to impaired conduction in the AV node itself.

*** The phenomenon may be physiological and is sometimes observed at rest or during sleep
in athletic young adults with high vagal tone.
• In Mobitz type II PR interval remains constant but some P waves are not conducted. This is
usually caused by disease of the His–Purkinje system and carries a risk of asystole.

***** THIRD-DEGREE ATRIOVENTRICULAR BLOCK (SBA)

• Escape rhythm arising in the AV node or bundle of His (narrow QRS complexes) or the
distal Purkinje tissues (broad QRS complexes).

• Complete AV block produces a slow (25–50/min), regular pulse that does not vary with
exercise, except in the case of congenital complete AV block.

***** There is usually a compensatory increase in stroke volume, producing a large-volume

pulse.

***** Cannon waves may be visible in the neck and intensity of the first heart sound varies
due to the loss of AV synchrony.

• The typical presentation is with recurrent syncope or ‘StokesAdams’ attacks.

• There is pallor and a death-like appearance during the attack, but when the heart starts
beating again there is a characteristic flush.

• A permanent pacemaker is usually indicated in asymptomatic Mobitz type II or third-degree

AV heart block.

Fig 16.51
+ SA node & AV node *****
+ others are also important 😅

Box 16.29
+ VVI & difficult but you have to read the whole box with effect on action potential 😐😐

Box 16.30
+ Very tough.
+ Name & Use
+ Amiodarone side effect *****
+ Atropine, adenosine side effect *

#DAVIDSON_REVIEW_23rd
#CARDIOLOGY_3

(আজকের টপিক এর মধ্যে Acute coronary syndrome বাদে গুরুত্বপূর্ণ খুব বেশি নাই।কাল থেকে ইং শা
আল্লাহ্ যে টপিক গুলো দিব সেগুলো খুবই গুরুত্বপূর্ণ। Cardiology চ্যাপ্টার এর প্রথম এবং শেষের অংশ বেশি
গুরুত্বপূর্ণ। শেষের দিক থেকে পড়া শুরু করাটা ভাল)

Page 483-504

Box 16.35 ***

Box 16.38 ***
Angina pectoris ***
Box 16.39 **
Box 16.41 *
Acute coronary syndrome **********
Box 16.48 **
Box 16.49 ***
Box 16.50 ***
Box 16.51 ***
Fig 16.70 **
Box 16.52 ***
Peripheral arterial disease *
Box 16.57 ***
Box 16.58 **

Box 16.35
+ Both SBA & MCQ

Box 16.38
+ SBA & MCQ
+ Q: Factors affecting oxygen demand / coronary blood flow?
+ Coronary blood flow occurs mainly in diastole

ANGINA PECTORIS
+ Syndrome X ***
+ Anti anginal drug *****

Important:

*** Atherosclerosis is by far the most common cause of angina pectoris.

*** Typical angina on effort, objective evidence of myocardial ischaemia on stress testing,
and normal coronary arteries on angiography,more common in women,good prognosis,may
respond to anti anginal therapy - Syndrome x

• The first-line investigation is an exercise ECG.

** Planar or downsloping ST segment depression of 1 mm or more is indicative of ischaemia.

Up-sloping ST depression is less specific.

*** All patients with angina secondary to CAD should receive antiplatelet therapy.

• Similarly, all patients should be prescribed a statin, even if cholesterol is normal.

• It is conventional to start therapy with sublingual glyceryl trinitrate (GTN) and a β-blocker,
and then add a calcium channel antagonist or a long-acting nitrate if needed.

*** Nitrates -
• venous and arteriolar dilatation.

• They help angina by lowering preload and afterload, which reduces myocardial oxygen
demand, and by increasing myocardial oxygen supply through coronary vasodilatation.

• Beta-blockers lower myocardial oxygen demand by reducing heart rate, BP and myocardial
contractility

• Beta-blockers should not be withdrawn abruptly, as rebound effects may precipitate

dangerous arrhythmias, worsening angina or MI.

• Calcium channel antagonists - These drugs lower myocardial oxygen demand by reducing
BP and myocardial contractility.

• Since dihydropyridine calcium antagonists, such as nifedipine and amlodipine, may cause a
reflex tachycardia, it is best to use them in combination with a β-blocker.
** In contrast, verapamil and diltiazem can be used as monotherapy because they slow SA
node firing, inhibit conduction through the AV node and tend to cause bradycardia.

*** Calcium channel antagonists reduce myocardial contractility and must be used with care
in patients with poor LV function.

*** Coronary artery bypass grafting

• Internal mammary artery
• Radial artery
• Saphenous vein

ACUTE CORONARY SYNDROME

+ SBA & MCQ
+ Clinical feature ***
+ Pericarditis,Dressler syndrome,Ventrcular septal rupture
+ ECG *****
+ Cardiac biomarkers ***
+ Reperfusion therapy ***

Important :
• Unstable angina - new-onset or rapidly worsening angina (crescendo angina), angina on
minimal exertion or angina at rest in absence of myocardial damage.

• MI differs from unstable angina, since there is evidence of myocardial necrosis.

• Adverse prognostic factors include recurrent ischaemia, extensive ECG changes at rest or
during pain, raised troponin I or T levels, arrhythmias and haemodynamic complications
(hypotension, mitral regurgitation).

*** ACS almost always occurs in patients who have atherosclerosis.

*** Chest pain at rest is the cardinal symptom but breathlessness, vomiting and collapse are
also common features.

*** Painless or ‘silent’ MI may also occur and is particularly common in older patients or
DM.

*** Vomiting and sinus bradycardia are particularly common in inferior MI.

• Risk of arrhythmia can be minimised by adequate pain relief, rest and the correction of
hypokalaemia.

• Patients with dynamic ECG changes and ongoing pain should be treated with intravenous
glycoprotein IIb/IIIa receptor antagonists.

• Pericarditis is particularly common on the second and third days.

• Patient may recognise a different pain, even though at the same site,positional and tends to
be worse or sometimes present only on inspiration.

*** Opiate-based analgesia should be used. NSAIDs and steroid may increase risk of
aneurysm and myocardial rupture in early recovery period, and should be avoided.

*** Dressler’s syndrome - persistent fever, pericarditis and pleurisy - probably due to
autoimmunity. Occur a few weeks or even months after MI & often subside after few days.
Rx - high-dose aspirin, NSAIDs or glucocorticoids
• Papillary muscle rupture typically presents with acute pulmonary oedema and shock.

• Examination - a pansystolic murmur due to MR and 3rd heart sound but murmur may be
quiet or absent in severe MR

*** Ventricular septum rupture - sudden haemodynamic deterioration + a new and loud
pansystolic murmur radiating to rt sternal border

** ACE inhibitor and mineralocorticoid receptor antagonist therapies reduce late ventricular
remodelling

• Initial ECG may be normal or non-diagnostic in one-third of cases

*** Earliest ECG change is usually ST-segment deviation

• Proximal occlusion of a major coronary artery - ST-segment elevation (or new bundle
branch block) > diminution in size of R wave & in transmural infarction , development of a Q
wave > T wave invertion (persists after ST segment has returned to normal).

• Non-ST segment elevation - partial occlusion of a major vessel or complete occlusion of a

minor vessel - unstable angina or partial-thickness (subendocardial) MI.

• Usually associated with ST-segment depression and T-wave changes.

• In presence of infarction,some loss of R waves in absence of Q waves.

*** Anteroseptal - V1 to V4, Anterolateral - V4 to V6,aVL and I, Inferior - II, III and aVF,

• Infarction of posterior wall of the LV - ST depression and a tall R wave V1–V4.

• Unstable angina - no detectable rise in troponin. MI - rise in troponin T,I and other cardiac
enzymes

*** Troponins T and I increase within 3–6 hours, peak at about 36 hours and remain elevated
for up to 2 weeks.

• Lipids should be measured within 24 hours as there is often a transient fall in cholesterol in
the 3 months following infarction.

• Echocardiography is normally performed before discharge from hospital

• No complications and angiography not required - patient can be mobilised from the 2nd day
and discharged after 2–3 days.

• Low-risk patients without spontaneous angina - exercise tolerance test approximately 4

weeks after ACS

• IV opiates (morphine sulphate or diamorphine) & antiemetics (metoclopramide) - relief

pain

***** Immediate reperfusion with PCI - if ECG shows new BBB or characteristic ST-
segment elevation in two contiguous leads of 1 mm/> in limb leads or 2 mm/> in chest leads.

*** Rx of choice within 12 hours of symptom onset - PCI

• If PCI cannot be performed within 120 min and thrombolysis is contraindicated PCI should
be performed as soon as possible.
• PCI should be considered within first 24 hours, even if they have reperfused spontaneously
or with thrombolytic therapy

• Coronary artery patency is restored in over 95% of patients undergoing PCI.

*** PCI confers no immediate mortality benefit in non-ST segment elevation ACS

• If primary PCI cannot be achieved in a timely manner,thrombolytic therapy should be

administered.

• Although survival advantage is not as good as primary PCI mortality is reduced

• Benefit of thrombolytic therapy is greatest within first 12 hours and especially first 2 hours.

• Modern thrombolytic agents - tenecteplase (TNK) and reteplase (rPA). Treatment should be
withheld if there is a significant risk of serious bleeding

• All patients should receive therapy with HMG CoA reductase enzyme inhibitors (statins)
after ACS

• Smoking cessation- improve mortality

• Necrotic muscle of an acute MI takes 4–6 wks to be replaced with fibrous tissue & so
restrict physical activities during this period.

*** ICDs prevent sudden cardiac death LV impairment (ejection fraction ≤ 30%) after MI.
• Early death is usually due to an arrhythmia and is independent of the extent of MI.

*** Prognosis is worse for anterior than for inferior infarcts.

Box 16.51
+ Secondary prevention drug ***

Extra.
*** Cardiac biomarker গুলা পড়ে রাখবেন।

#DAVIDSON_REVIEW_23RD
#CARDIOLOGY_4

### Page 505-517

N.B: আজকের সবগুলা টপিক ই অনেক গুরুত্বপূর্ণ পরীক্ষার জন্য।

Aortic aneurysm ***

Aortic dissection *****
Box 16.62 ***
Fig 16.72 **
Box 16.63 *****
Box 16.65 *****
Fig 16.76 *****
Box 16.66 *****
Box 16.71 *
Box 16.72 **********
Box 16.73 ***
Box 16.74 ***
Fig 16.79 *
Fig 16.80 ***
Box 16.75 *****
Box 16.76 ***
Rheumatic fever ***

AORTIC ANEURYSM
+ SBA (Mentioned below)

Important:

*** Most common site - infrarenal AA (SBA)

** Suprarenal AA & descending thoracic aorta may be affected but ascending aorta is usually
spared.

*** Most common cause - atherosclerosis (SBA)

** Marfan’s syndrome - associated with aortic aneurysm and aortic dissection

** Thoracic aneurysms - acute severe chest pain. Other - aortic regurgitation,stridor,

hoarseness and superior vena cava syndrome.

* Usual age at presentation is 65–75 years for elective and 75–85 years for emergency.

* ULTRASOUND is the best way of establishing diagnosis of an abdominal aneurysm and of

FOLLOWING UP (SBA) asymptomatic patients

*** CT provides more accurate information (SBA).

* Standard pre-operative investigation but not suitable for surveillance.

• Repair if symptomatic or AAA max 5.5 cm in diameter or distal embolisation

*** Open AAA repair has been treatment of choice in both elective & emergency (SBA)

** In Marfan’s syndrome - Β-BLOCKERS reduces rate of aortic dilatation & risk of rupture

AORTIC DISSECTION
+ SBA
+ Mainly scenario thake (READ C/F carefully)
+ Dx,Inv of choice,Rx of choice *****

Important:

** Peak incidence - 6th and 7th decades bt CAN OCCUR IN YOUNGER PATIENTS WITH
MARFAN’S SYNDROME, PREGNANCY OR TRAUMA.

* Multiple tears or entry points are common.

** Aortic disease and hypertension - most important aetiological factors

• Classified type A (2/3) and type B involving or sparing ascending aorta respectively.
Involvement AA - anterior chest pain & DA - intrascapular back pain.

*** Pain - tearing & very abrupt in onset, collapse is common. Unless major
haemorrhage,patient is invariably hypertensive. (SBA Scenario)
** There may be asymmetry of the brachial, carotid or femoral pulses and signs of aortic
regurgitation.

• Occlusion may cause MI , Stroke, Paraplegia, mesenteric infarction with an acute

abdomen,renal failure & acute limb ischaemia.

*** Investigations of choice are CT or MR angiography (SBA)

• Chest X-ray - characteristically shows broadening of upper mediastinum and distortion of

the aortic ‘knuckle’, pleural effusion.

• Initial Mx - pain control and antihypertensive.

*** Rx - Type A - iv Labetalol + surgery. Type B - Usually medically

* Aim of medical Mx - maintain MAP of 60–75 mmHg

*** First-line therapy - β-blockers (Labetalol very useful due to additional @ block) (SBA)

• Alternative - rate limiting CCB (Verapamil,Diltiazem)

• Na nitroprusside & hydralazine shouldn't be used alone(increases LV ejection)

BOX 16.63
+ For MCQ

Remember:
+ Hypertension (80%)
+ Pregnancy 3rd trimester

MARFAN SYNDROME
+ Clinical features *****
+ যেকোন জায়গায় লাগতে পারে 😉😉

Box 16.65
+ MCQ
+ Endocrine cause *****
+ Drugs *** ( Not given in the box)

Fig 16.76 & Box 16.66

+ According to grade ( feature)
+ Diabetic retinopathy r sathe compare kore niben

Important

***** Hard’ exudates (small, white, dense deposits of lipid) and microaneurysms (‘dot’
haemorrhages) are more characteristic of diabetic retinopathy

******
Adverse effects & contraindications of following drugs are VVI
(Read from any pharmacology guide)
• Thiazide
• Loop diuretic
• ACEi
• ARB
• Bblocker
• Statin
• Ca channel blocker

Box 16.72 (SBA IN JAN 2020)

+ VVVVVI
+ SBA & MCQ
+ সব লাগবে বিশেষ করে Contraindication

Remember
***** Isolated systolic HTN - CCB & Tiazide (SBA)

Accelerated HTN
+ Reading

ARF
+ MCQ & SBA
+ Scenario based question (C/F vlo kore pprte hobe)

Important
• ARF usually affects children and young adults between the ages of 5 & 15 yrs.

• Cross-react with cardiac myosin and sarcolemmal membrane proteins.

• Histologically, fibrinoid degeneration is seen in the collagen of connective tissues.

*** Aschoff nodules are pathognomonic and occur only in the heart. (SBA)

* They are composed of multinucleated giant cells surrounded by macrophages and T

lymphocytes, and are not seen until the subacute or chronic phases of rheumatic carditis.

** A presumptive diagnosis can be made without evidence of preceding streptococcal

infection in cases of isolated chorea or pancarditis

*** A soft systolic murmur due to mitral regurgitation is very common.

*** A soft mid-diastolic murmur (the Carey Coombs murmur) is typically due to valvulitis,
with nodules forming on the mitral valve leaflets.

*** Aortic regurgitation occurs in 50% of cases but the tricuspid and pulmonary valves are
rarely involved.

** Arthritis is the most common major manifestation - acute painful, asymmetric and
migratory inflammation of the large joints typically affects the knees, ankles, elbows and
wrists.

*** Aspirin - a response within 24 hours helps confirm the diagnosis

** Glucocorticoids in carditis & severe arthritis

Box 16.75
+ Major & Minor alada kore porte hbe

Box 17.76
+ MCQ
+ ECG findings ***
*** Remember both first & 2nd degree AV block found in ARF but only first degree is
included in jones criteria

#DAVIDSON_REVIEW_23RD
#CARDIOLOGY 5

### Page 517 - 527

Box 16.77 **********

Box 16.79 ***
Box 16.80 ***
Box 16.81 **********
Box 16.83 *
Box 16.84 ***
Box 16.85 **********
Fig 16.84 ***
Box 16.88 *****
Box 16.89 *********
Box 16.91 ***
MS,MR,AS,AR *****
TS,TR ***
PS,PR *
Prosthetic valve *

MITRAL STENOSIS

• MS is almost always rheumatic in origin

• Mitral valve orifice is normally about 5 cm2 in diastole but can be reduced to < 1 cm2 in
severe mitral stenosis.

• The patient is usually asymptomatic until the orifice is < 2 cm2.

• Effort-related dyspnoea is usually the dominant symptom

*** An opening snap may be audible and MOVES CLOSER TO THE SECOND SOUND
(S2) as the stenosis becomes more severe and left atrial pressure rises (SBA)

*** Turbulent flow produces the characteristic low-pitched MID DIASTOLIC MURMUR
and sometimes a thrill.

** The murmur is accentuated by exercise and during atrial systole (pre-systolic

accentuation)

**Inv - Doppler ECHO

Box 16.77
+ Symptoms & signs name porlei hobe
+ Auscultation ***

Box 16.79
+ SBA & MCQ

MITRAL REGURGITATION

*** Most common - Mitral valve prolapse due to degenerative myxomatous (SBA)
** Dilated cardiomyopathy & heart failure from CAD are common causes of so-called
‘functional’ MR

• Chronic MR - symptom complex of MS but acute MR - acute pulmonary oedema

• The regurgitant jet causes an apical systolic murmur which radiates into the axilla and may
be accompanied by a thrill. Increased forward flow through the mitral valve causes a LOUD
THIRD HEART SOUND and even a short mid-diastolic murmur.

*** Apex beat - displaced, thrusting

*** Fig 16.83 murmur

AORTIC STENOSIS

** Three cardinal symptoms are angina, breathlessness and syncope

• Murmur is often likened to a saw cutting wood and may (especially in older patients) have a
musical quality like the ‘mew’ of a seagull.

***** Slow rising carotid pulse (SBA)

*** Narrow pulse pressure

***Apex beat - Discrete,heaving (Ref: page 443)

• Rx - Surgery if symptomatic or aortic valve gradient >50 mmHg. Asymptomatic -

observation

Fig 16.84

** Ejection systolic murmur radiates to right upper sternal edge, suprasternal notch and
carotids

** An ejection click (EC) may be present in young patients with a bicuspid aortic valve but
not in older patients with calcified valves.

Aortic stenosis may lead to left ventricular hypertrophy with a FOURTH SOUND at the apex
and post-stenotic dilatation of the aortic arch

Box 16.88
+ MCQ & SBA

Box 16.89
+ VVI
+ Murmur *****
+ No need to memorise the name of sign
+ Apex beat - thrusting (Page 443)

AORTIC REGURGITATION

• Until the onset of breathlessness, the only symptom may be an awareness of the heart beat

• Paroxysmal nocturnal dyspnoea is sometimes the first symptom

• Regurgitant jet causes fluttering of the mitral valve and, if severe, causes partial closure of
the anterior mitral leaflet, leading to functional mitral stenosis and a soft mid-diastolic
(AUSTIN FLINT) MURMUR.

*** Large-volume or ‘collapsing’ pulse (SBA)

*** Low diastolic and increased pulse pressure (SBA)

N.B Last two point are differentiating between AS & AR

TRICUSPID STENOSIS

• Tricuspid stenosis is usually rheumatic in origin.

*** The main clinical feature is a RAISED JVP WITH A PROMINENT A WAVE, AND A
SLOW Y descent due to the loss of normal rapid right ventricular filling. (SBA)

** A mid-diastolic murmur, best heard at the lower left or right sternal edge, HIGHER-
PITCHED THAN THE MURMUR OF MITRAL STENOSIS AND IS INCREASED BY
INSPIRATION.

• Right heart failure causes hepatomegaly with presystolic pulsation , ascites and peripheral
oedema.

TRICUSPID REGURGITATION

• TR is - most frequently functional,as a result of Rt ventricular dilatation due to Rt HF or

biventricular failure.

*** The most prominent sign is a ‘GIANT’ V WAVE in the jugular venous pulse (a cv wave
replaces the normal x descent). (SBA)

• Other features include a PANSYSTOLIC MURMUR at the left sternal edge and a
PULSATILE LIVER.

• Valves damaged by endocarditis do not usually need to be replaced. Those with rheumatic
damage may require valve replacement.

Remember:
*** Dilated cardiomyopathy causes MR not AR.
*** But AR leads to LV dilation

Box 16.91
+ MCQ
*** Associated with ebstein's anomaly
*** Common in IV drug abuser

PULMONARY STENOSIS

• Occur in carcinoid syndrome but is usually congenital

*** Ejection systolic murmur, loudest at the left upper sternum and radiating towards the left
shoulder.

*** PROMINENT a WAVES in the jugular pulse.

N.B. Pls read other causes of prominent a wave

PULMONARY REGURGITATION

*** GRAHAM STEELL murmur

PROSTHETIC VALVE

** All generate prosthetic sounds or clicks on auscultation

** All mechanical valves require long-term anticoagulation

** Biological valves are less durable than mechanical valves

• They are more durable in the aortic position and in older patients, so are particularly
appropriate for patients over 65 undergoing aortic valve replacement.

#DAVIDSON_REVIEW_23RD
#CARDIOLOGY 6

### Page 527 - 544

।।।আজকের পোস্টের সব টপিক অনেক অনেক বেশি গুরুত্বপূর্ণ।।। পোস্ট টাও এক্টু বড়।।।

N.B: CAPITAL letter এ লেখা গুলো অনেক ইম্পর্ট্যান্ট।

নিচে (*********) দেওয়া ৪ টা টপিক আছে।খুবই ভাল করে পড়বেন। এখান থেকে মোটামুটি শিউর প্রশ্ন
আসেই।

Infective endocarditis (**********)

Box 16.93 *
Box 16.94 ** (Only name)
Fig 16.89 (*********)
Box 16.95 ***
Box 16.97 ***
Box 16.98 *****
PDA **
COA **
ASD **
VSD **
TOF ***
Box 16.104 ***
Dilated cardiomyopathy *
Hypertrophic cardiomyopathy (**********)
Box 16.105 (**********)
Box 16.106 ***
Acute pericarditis *****
Box 16.108 ***
Chronic constrictive pericarditis (**********)
Box 16.109 (*********)
Cardiac temponade (**********)
Box 16 110 (*********)

INFECTIVE ENDOCARDITIS
+ SBA
+ Scenario based or from important line
+ Question : Dx, Inv,Rx

Important :
• The most common causes of infective endocarditis are streptococci and staphylococci

• S. aureus can cause endocarditis in a previously normal heart

*** STAPHYLOCOCCAL endocarditis of the TRICUSPID VALVE is a common

complication of INTRAVENOUS DRUG USE

*** Patients who are found to have endocarditis caused by STREP. GALLOLYTICUS
should undergo COLONOSCOPY, since this organism is associated with LARGE-BOWEL
MALIGNANCY. (SBA)

*** S. aureus - most common cause of acute endocarditis (SBA)

*** Post-operative endocarditis - most common organisms are coagulase-negative

staphylococci such as Staph. epidermidis (SBA)

• Streptococci and Enterococci - subacute endocarditis

*** In Q fever endocarditis due to Coxiella burnetii - HISTORY OF CONTACT WITH

FARM ANIMAL + AORTIC VALVE is usually affected +/- hepatitis, pneumonia and
purpura. Life-long antibiotic therapy may be required.

• Brucella endocarditis - history of contact with goats or cattle and often affects the aortic
valve.

• Subacute endocarditis - persistent fever, unusual tiredness, night sweats or weight loss, or
develops new signs of valve dysfunction or heart failure, purpura and petechial haemorrhages
in the skin and mucous membranes, and splinter haemorrhages under the fingernails or
toenails. Osler’s nodes. Digital clubbing is a late sign. The spleen is frequently palpable.

*** Acute endocarditis - severe febrile illness with PROMINENT AND CHANGING
HEART MURMURS and petechiae. (SBA)

• Embolic events are common, and cardiac or renal failure may develop rapidly.
Echocardiography - Abscesses

• Post-operative endocarditis - unexplained fever in a patient who has had heart valve surgery

*** INV: Trans-oesophageal echocardiography (TOE), Microbiological Culture.

• CBC - (+)WBC,CRP,ESR,normocytic normochromic anaemia. Urine R/E - Protein,RBC.

ECG - AV block

• In subacute - antibiotic treatment should ideally be withheld until the results of blood
cultures are available. If empirical - amoxicillin with or without gentamicin

*** In acute - vancomycin and gentamicin (SBA)

*** Suspected prosthetic valve endocarditis - vancomycin and gentamicin plus rifampicin
orally (SBA)

• Poor prognostic factors - S. aureus infection,Culture (-) endocarditis,low complement

level,Prosthetic valve

Fig 16.89
+ VVVVVI for SBA & MCQ
Remember:
+ Digital clubbing & Splenomegaly - long standing endocarditis only

Box 16.97 & 98

+ MCQ & SBA

CONGENITAL HEART DISEASE

*** Maternal rubella infection - Persistent ductus arteriosus, pulmonary valvular and/or
artery stenosis, and atrial septal defect.

** Maternal alcohol misuse - septal defects

*** Maternal lupus erythematosus - congenital complete heart block (SBA)

*** In the neonate, the most common cause is transposition of the great arteries (SBA)

*** In older children, cyanosis is usually the consequence of a ventricular septal defect
combined with severe pulmonary stenosis (as in tetralogy of Fallot) or with pulmonary
vascular disease (Eisenmenger’s syndrome).

*** Cyanosis in Eisenmenger’s syndrome may be more apparent in feet & toes than in upper
part of the body - differential cyanosis. Common Cause - VSD,ASD,PDA (But not TOF).
Particular risk in vasodilation, anaesthesia & pregnancy.

PATENT DUCTUS ARTERIOSUS

*** CONTINUOUS ‘MACHINERY’ MURMUR is with late systolic accentuation, maximal

in second left intercostal space below clavicle (SBA)

*** Large volume,pounding,collapsing pulse

** Wide pulse pressure

• If ductus is structurally intact a prostaglandin synthetase inhibitor (indometacin or

ibuprofen) may be used in first week of life to induce closure

COARCTATION OF THE AORTA

*** Associated with - Bicuspid aortic valve, Berry aneurysms,Turner's syndrome,

Neurofibromatosis

** Acquired (rare) - trauma or Takayasu’s disease.

• Narrowing occurs where the ductus arteriosus joins the aorta, at the isthmus just below the
origin of the left subclavian artery.

*** HEADACHES may occur from HTN proximal to coarctation, and occasionally
WEAKNESS OR CRAMPS IN LEGS may result from decreased circulation. FEMORAL
PULSES - WEAK AND DELAYED in comparison with the radial pulse. (SBA Scenario)

• A systolic murmur is usually heard posteriorly, over the coarctation

• There may also be an ejection click and systolic murmur in the aortic area due to a bicuspid
aortic valve
• Collaterals form - involve the periscapular, internal mammary and intercostal arteries, result
in localised bruits.
*** Inv of choice - MRI (SBA)

ATRIAL SEPTAL DEFECT

*** MOSTLY OSTIUM SECUNDUM DEFECTS, involving the fossa ovalis that, in utero,
was the foramen ovale (SBA)

• Ostium primum defects result from a defect in the atrioventricular septum and are
associated with a ‘cleft mitral valve’ (split anterior leaflet)

*** WIDE, FIXED SPLITTING OF THE SECOND HEART SOUND,systolic flow murmur
over pulmonary valve (SBA)

• ECG - RBBB +/- Rt axis deviation

• With a ‘primum’ defect, there is also left axis deviation

*** Inv : TOE

• In 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

VENTRICULAR SEPTAL DEFECT

• MOST COMMON CONGENITAL CARDIAC DEFECT (SBA)

** Mostly PERIMEMBRANOUS occurring at the junction of membranous & muscular

portions of septum

** Produces a PANSYSTOLIC MURMUR, usually heard best at the LEFT STERNAL

EDGE but radiating ALL OVER THE PRECORDIUM

*** Small defect often produces a loud murmur (maladie de Roger). Conversely, a large
defect produces a softer murmur

• In addition to the murmur, there is prominent parasternal pulsation, tachypnoea and

indrawing of the lower ribs on inspiration.

• Non congenital - Post MI

TETRALOGY OF FALLOT

*** Most common cause of cyanosis in infancy after the first year of life

• Abnormal development of bulbar septum that separates ascending aorta & pulmonary artery

• Children - cyanosed but not in neonate because it is only when right ventricular pressure
rises to equal or exceed left ventricular pressure that a large right-to-left shunt develops

• In older children, Fallot’s spells are uncommon but cyanosis becomes increasingly
apparent, with stunting of growth, digital clubbing and polycythaemia

*** The most characteristic feature is the combination of cyanosis with a loud ejection
systolic murmur in the pulmonary area (as for pulmonary stenosis)
• Primary surgical correction may be undertaken prior to the age of 5 years

• Palliation in the form of a Blalock–Taussig shunt - anastomosis between the pulmonary

artery and subclavian artery

MYOCARDITIS

*** Viral infections are the most common causes, such as Coxsackie and influenza A and B

* Myocarditis has been reported as a cause of sudden and unexpected death in young athletes.

Box 16.104
+ MCQ

HYPERTROPHIC CARDIOMYOPATHY
+ SBA
+ Scenario (Sudden death of young athletes *****)

IMPORTANT

*** Most common form of cardiomyopathy, most common cause of sudden death in young
athletes (SBA)

*** AUTOSOMAL DOMINANT,high degree of penetrance and variable expression

*** Beta-myosin heavy-chain mutations - elaborate ventricular hypertrophy - most common

(SBA)

* Septal hypertrophy - dynamic left ventricular outflow tract obstruction (HOCM) and MR
due to abnormal systolic anterior motion of anterior mitral valve leaflet - ECHO findings

*** S/S similar to aortic stenosis, except that ARTERIAL PULSE IS JERKY (SBA)

• Degree of hypertrophy is usually greater than in physiological hypertrophy and pattern is

asymmetrical

• Rx - Amiodarone,Beta-blockers,CCB & disopyramide (ABCD). Myectomy/Ablation by

alcohol solution to relieve obstruction. Risk of sudden death - ICD

*** Digoxin /inotropes and vasodilators/nitrates should be avoided

*** Signs of outflow tract obstruction (murmur/jerky pulse) may be augmented by standing
up (reduced venous return),inotrope and vasodilator, Valsalva maneuver,reduced by squatting

DILATED CARDIOMYOPATHY

*** Left ventricular mass is increased but wall thickness is normal or reduced

• Dilatation of the valve rings can lead to functional mitral and tricuspid incompetence

*** Autosomal dominant trait

• Mutations affect proteins in the cytoskeleton of the myocytes, such as dystrophin, lamin A
and C, emerin and metavinculin

• Many are also associated with abnormalities of skeletal muscle Conversely, most of the X-
linked inherited skeletal muscular dystrophies, such as Becker and Duchenne
• Arrhythmia, thromboembolism and sudden death may occur at any stage;

RESTRICTIVE CARDIOMYOPATHY

*** Amyloidosis is the most common cause (SBA)

TAKOTSUBO CARDIOMYOPATHY

*** Takotsubo CardiomyopathyIn terms of both symptoms and the ECG, the condition
mimics acute ST elevation acute coronary syndrome

• Dx is usually made at coronary angiography

*** Echocardiography shows characteristic ‘APICAL BALLOONING’ of the LV

*** The normal pericardial sac contains about 50 mL of fluid, similar to lymph, which
lubricates the surface of the heart

ACUTE PERICARDITIS

+ SBA (Scenario/Important line)

Important

*** Chest pain - retrosternal,radiates to shoulders and neck,aggravated by deep

breathing,movement,a change of position,exercise and swallowing (Scenario)

*** PERICARDIAL FRICTION RUB - a high-pitched, superficial scratching or crunching

noise,DIAGNOSTIC OF PERICARDITIS (SBA)

*** Widespread ST elevation with upward concavity.

*** PR depression - specific of acute pericarditis (SBA)

• Later,may be T-wave inversion, particularly due to myocarditis

• Rx:- Aspirin / Indometacin,Prednisolone/Colchicine

CCP

+ SBA (Small heart***** & MCQ)

• Thickening, fibrosis and calcification of the pericardium

*** Tuberculous pericarditis(common), haemopericardium, viral pericarditis, rheumatoid

arthritis and purulent pericarditis

*** The symptoms and signs of systemic venous congestion are the hallmarks of constrictive
pericarditis (SBA)

*** AF is common and there is often dramatic ascites and hepatomegaly

*** Breathlessness is not a prominent symptom

*** Should be suspected in any patient with unexplained right heart failure and a small heart.

*** Loud early third heart sound or ‘PERICARDIAL KNOCK’.

*** Elevated JVP with a rapid y descent (SBA)

Box 16.109
+ MCQ & SBA

CARDIAC TAMPONADE

*** Electrical alternans

Box 16.110
+ MCQ & SBA

CCP & Cardiac temponade এর scenario তে প্রায়ই প্যাচ লাগে।ভাল করে পড়বেন। নিচের কিছু Clue
খেয়াল রাখবেন।

CCP
*** Small heart
* Ascites
* Hepatomegaly

Cardic Temponade
*** Electrical alternans
* Tachycardia, Hypotension

#CARDIOLOGY_BASIC
N.B: I won't say it's enough 😅😅 but it be helpful in sha ALLAH. I made this note during my
preparation but couldn't share..Any suggestion or correction will be appreciated..🙂
[Source: Davidson,Genesis sheet,Wikimedia]
Please pray for me so that i can help you & others 😊😊

[ ] DEVELOPMENT OF HEART:-

ATRIUM

• Trabeculated part of both atrium - primitive atrium.

• Smooth part of right atrium - Sinus venosus (Rt horn)
• Smooth part of left atrium - Pulmonary veins

VENTRICLE

• Trabeculated part of right ventricle - Proximal dilated bulbus cordis

• Trabeculated part of left ventricle - Primitive ventricle
• Smooth part of both ventricle - Conus cordis (middle 1/3 of bulbus cordis)
AORTA / PULMONARY TRUNK:-
• Truncus arteriosus - Distal 1/3 of bulbus cordis

CORONARY SINUS & OBLIQUE VEIN OF LEFT ATRIUM:-

• Body and Lt horn of Sinus venosus

### Spiral septum is responsible for triple relation of ascending aorta and pulmonary trunk.
### Pericardium encloses heart and root of great vessels except inferior vena cava.

[ ] BASE OF HEART
• Mainly by left atrium,partly by right atrium
• Opposite to T5-T8
[ ] BORDER OF HEART
• Upper - Both atrium, chiefly left atrium
• Inferior- Both ventricle, mainly right ventricle
• Right - Right ventricle
• Left - Left ventricle mainly + Left auricle

[ ] ARTERIAL FLOW
• Peripheral arterial elasticity
(maintain DBP in arteries and arterioles)
• Ventricular systole
• Recoil of the elastic aorta

[ ] VENOUS FLOW
• Suction during cardiac diastole
• Negative pressure during inspiration
• Contraction of external muscles
• Residual pressure from blood flow through the capillaries

[ ] CAPILLARIES
• Continuous / Somatic
Muscle tissue,Connective tissue,Nervous tissue, Exocrine gland
• Fenestrated / Visceral
Brain(choroid plexus),Intestine,Kidney, Endocrine glands
• Sinusoidal
Liver, Spleen,Bone marrow,Adrenal gland

### Most blood flow - Liver

### Most oxygen supply - Liver
### Most blood per 100g wt - Kidney
### Most oxygen per 100g wt - Heart

[ ] VASOCOACTIVE SUBSTANCE

LOCAL
VASOCONSTRICTOR
• (-) Temperature
VASODILATOR
• (+)Temperature,Adenosine,Lactate,K+, CO2
• (-) O2,PH

ENDOTHELIAL HORMONE
VASOCONSTRICTOR
• Endothelin - 1
• Thromboxane A2
• Serotonin
VASODILATOR
• NO
• Prostacyclin
• Kinin

CIRCULATING HORMONE
• Epinephrine ( Except liver and skeletal muscle)
• Norepinephrine
• Vasopressin
• Angiotensin 2
• AVP
• Neuropeptide Y
• Na - K ATPase inhibitors

VASODILATOR
• Epinephrine in liver and skeletal muscle
• Histamines
• Substance P
• ANP
• VIP
• CGRP @

[ ] TURBULENT FLOW DPENDS ON

Proportional to -
• Velocity
• Diameter of vessel
• Density of blood
Inversely to -
• Viscosity of blood

### Flow = Velocity × Area (r^4) × Pressure/ Viscosity × Length

[ ] CARDIOVASCULAR CHANGES DURING MODERATE EXERCISE

• Increase in - HR, Myocardial contractility,VR,SV,CO,SP,EDV,PP
• Decrease in - TPR,DP,ESV

[ ] DURING STANDING
• Increase in - FOC
• Decrease in - VR,CVP,SV,CO,BP
• No change in - HR,TPR

[ ] PULSE PRESSURE

WIDE IN
• Arteriosclerosis / Old age
• AR
• PDA,ASD
• Thyrotoxicosis, OSA
• Exercise

NARROW IN
• AS
• Cardiogenic shock
• Cardiac tamponade
• Heart failure
• ACS

# Adrenaline and thyroxin increases systolic pressure but decreases diastolic pressure.
# Baroreceptor - Unmyelinated, Encapsulated,Spray type nerve ending,in adventitia of
vessel,more sensitive to pulsatile pressure than constant pressure.
# Carotid sinusis more sensitive than aortic arches.
# About 70% ventricular filling occurs passively during atrial diastole.

[ ] PULSUS BISFERIENS/BIPHASIC PULSE

• Aortic stenosis
• Aortic regurgitation
• Hypertrophic cardiomyopathy
**** PULSUS ALTERNANS
• ALVF
• Aortic regurgitation

[ ] SECOND HEART SOUND (S2)

• Loud: hypertension
• Soft: AS
• Fixed split: ASD
• Reversed split: LBBB

[ ] THIRD HEART SOUND

• Mitral regurgitation
• Heart failure
• Chronic constrictive pericarditis
• Cardiac temponade
• Dilated cardiomyopathy
• ACS

**** FOURTH HEART SOUND

• HOCM
• Aortic stenosis
• Aortic regurgitation

[ ] JVP
RAISED JVP, NORMAL WAVEFORM
• Bradycardia
• Fluid overload
• Heart failure

**** LARGE 'a' WAVE (INCREASED ATRIAL CONTRACTION PRESSURE)

• Tricuspid stenosis
• Right heart failure
• Pulmonary hypertension

******* CANNON 'a' WAVE (ATRIA CONTRACTING AGAINST CLOSED TRICUSPID

VALVE)
• Third degree heart block (Irregular)
• Atrial flutter
• Premature atrial rhythm (or tachycardia)
• Ventricular ectopics
• Ventricular tachycardia

***** ABSENT 'a' WAVE (no UNIFOCAL ATRIAL DEPOLARISATION)

• Atrial fibrillation

***** LARGE 'v' WAVE (c–v WAVE)

• Tricuspid regurgitation

ABSENT x DESCENT
• Tricuspid regurgitation (sometimes 'x' wave is replaced by a positive wave)

***** PROMINENT 'x' DESCENT

• Cardiac tamponade

**** SLOW 'y' DESCENT

• Tricuspid stenosis
• Cardiac tamponade (may be absent)
****** PROMINENT & DEEP 'y' DESCENT
• Constrictive pericarditis

***** PARODOXICAL JVP (KUSSMAUL'S SIGN: JVP RISES WITH INSPIRATION,

DROPS WITH EXPIRATION)
• Pericardial effusion
• Constrictive pericarditis
• Pericardial tamponade

[ ] CARDIAC CYCLE

ATRIAL SYSTOLE
• First phase of cardiac cycle
• P wave in ECG, a wave in JVP
• Corresponding to last part of ventricular dilatation

VENTRICULAR SYSTOLE

1. ISOVOLUMETRIC CONTRACTION
• Begins with appearance QRS complex
• 1st heart sound due to closure of AV valve
• c wave in JVP & just after peak of c wave is x descent
2. RAPID EJECTION
3. SLOW EJECTION

VENTRICULAR DIASTOLE

1. PROTODIASTOLE
• Produces 2nd heart sound
2. ISOVOLUMETRIC RELAXATION
3. FIRST RAPID FILLING
• Third heart sound
• y descent in JVP
4. REDUCED FILLING PHASE
5. LAST RAPID FILLING PHASE
• Fourth heart sound
• Corresponding to atrial systole
• P wave in ECG

ATRIAL DIASTOLE
• 70% ventricular filling occurs passively in this phase

[ ] BOUNDING PULSE
• Anemia
• Thyrotoxicosis
• Aortic regurgitation
• Pregnancy
• Sepsis

[ ] CORONARY CIRCULATION

Rt. CORONARY ARTERY

• From anterior aortic sinus
• SA node in 60% & AV node in 90%
• Occlusion leads to bradycardia & AV conduction block
Lt. CORONARY ARTERY
• From left posterior aortic sinus
• Larger than RCA
• Occlusion leads to sudden death

### Veins having no valve

• Superior vena cava
• Pulmonary vein
• Portal vein
• Hepatic vein

###Cardiac dominance
• Right dominant : In 90% posterior interventricular branch atises from RCA
• Left dominant : In 10% arises from CX branch of LCA
# Depolarisation starts from SA node & repolarisation spreads from epicardium to
endocardium.
# SA node - Develops from rt side of embryo and suplied by rt vagus
# AV node - Develops from lt. Side of embryo and suplied by lt vagus
# Noradrenargic supply of heart is epicardial and predominantly vasodilator effect.
# Cholinergic supply is endocardial and causes modest vasodilation.

• Benign murmurs do not occur in diastole and systolic murmurs that radiate or are associated
with a thrill are almost always pathological

ECG IN HYPERKALEMIA
• Hyperacute T wave
• Wide QRS complex

ECG IN HYPOKALEMIA
• Prolonged PR interval
• Prolonged QT interval
• Presence of U wave
• Flat or absent or inverted T wave
• ST depression

ECG IN HYPOTHERMIA
• Bradycardia
• Atrial and ventricular arrhythmia
• First degree heart block
• Long QT interval
• J wave - small hump at the end of QRS

ECG IN ATHLETES (NORMAL)

• Sinus bradycardia
• Junctional rhythm
• First degree heart block
• Wenckebach phenomenon

ECG CHANGES AND ARTERY

• Anteroseptal / V1-V4 - LAD
• Inferior / II,III,aVF - RCA
• Anterolateral / V4-V6,I,aVL - LAD/CX
• Lateral / 1,aVL (+/-)V5-6 - CX
• Posterior / Tall R in V1-2 - CX/RCA