UW Notes - 7 - Cardiology Arranged
UW Notes - 7 - Cardiology Arranged
UW Notes - 7 - Cardiology Arranged
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❖ Cardiac looping
❖ Embryological abnormalities:
- Failure of apoptosis → syndactyly
- Failure of fusion → hypospadias
- Failure of obliteration → branchial cleft cyst
- Failure of proliferation of endocardial cushion → membranous VSD
- Failure of conotruncal septation → Truncus arteriosus
❖ Atria
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❖ Embryonic circulation
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❖ Paradoxical embolism:
• Can occur in ASD, VSD, PFO, large pulmonary AV malformation
• ASD: fixed splitting of S2, functional PS, TS
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CVS ANATOMY
277
❖ Anatomy of the heart & Trans-Esophageal ECHO (TEE)
❖ What are the structures best visualized by Trans Esophageal ECHO, anteriorly
& posteriorly?
- Anterior → LA, atrial septum, mitral valve
- Posterior → descending aorta
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❖ Penetrating from front
- Aortic arch lie behind sternum >>> rare injury if stab
- Penetrating stab in the 2nd intercostal space left sternal >> Pulmonary
trunk could be injured.
- Penetrating stab in the mid- and lower left sternal border >> right ventricle
injury + pneumothorax (pleural injury … not lung injury)
❖ Penetrating from back
- Penetrating stab to the back immediately to the right of vertebral column
>> injures IVC
- Penetrating stab to the back immediately to the left of vertebral column >>
injures descending aorta
❖ Aortic dissection:
- Stanford A: flap originates in the sinotubular junction (in the proximal part
of the ascending Aorta before the origin of the brachiocephalic artery)
- Stanford B: flap originates close to the origin of the left subclavian artery
- Swollen arm + swollen face on one side>> unilateral brachiocephalic vein
obs.
- Swollen arm + swollen face on both sides>> SVC obstruction.
- Swollen arm alone >> axillary or subclavian vein obs.
❖ What is the origin of the AV nodal artery? It usually arise from the dominant
artery either RCA & LCX
❖ To maintain the blood flow inside the circulation, the arterial flow must be
equal to venous flow, exception is bronchial circulation (bronchial circuit), <
5% of total circulation
❖ SA node :
o Site of earliest electric activity in the normal sinus rhythm
o Compact subepicardial structure → specialized pacemaker, site at the
junction of SCV with RA
❖ Atrial fibrillation
- If atrial fibrillation is not permanent (occur in attacks and recurrent) >>
radiofrequency ablation at the pulmonary vein ostia in the left atrium can
be used (pulmonary vein isolation)
- If AV node fail to control the ventricular rate in permanent Atrial
fibrillation >> radiofrequency ablation of the AV node is done.
- Site of AV node: endocardial surface of the RA near the insertion of the
septal leaflet of the tricuspid valve & orifice of the coronary sinus
- Atrial fibrillation >> systemic thromboembolism … the most common site
of thrombus formation is the left atrial appendage
❖ Site of ablation in Atrial flutter: the isthmus between IVC & tricuspid annulus
❖
❖ Coronary blood flow and its difference from other muscles:
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o Blood flow is mainly during diastole:
▪ LV → severe pressure (130/10), severe ↓↓ in dyastolic flow to
myocardium
▪ RV → much lower pressure (25/5), relatively constant blood flow
throughout cardiac cycle
o Very high oxygen extraction ratio → resting myocardium extract 60 – 75%
from arterial O2 → so the venous return of heart “coronary sinus”
is the most deoxygenated blood in body
o ↑↑ myocardial O2 needs can only be achieved by ↑↑ coronary blood flow
(by adenosine, NO2) as it has already max. O2 extraction
Prolonged QT interval is mainly due to repolarization defect → prolonged
T-wave, and slowed repolarization
❖ Mention the main limiting factor of myocardium perfusion:
• During systole, due to ↑↑ Tension & pressure > aortic pressure → no
coronary blood flow during systole
• Main coronary blood supply occurs during diastole, ↑↑ HR will ↓↓
diastole time → ↓↓ time available for max. coronary blood flow
❖ Coronary grafts :
o Occlusion of LAD only ➔ the best graft is left internal mammary
artery → superior patency rate
o Multiple occlusion or non-LAD ➔ GSV is usually used
▪ Anatomy of GSV : 3-4 cm infero-lateral to the pubic tubercle,
access is done from medial leg or at femoral triangle
▪ Deep circumflex iliac vessels → parallel & superior to the
inguinal ligament
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❖ Causes of coronary sinus dilatation seen on Echo:
1) Pulmonary hypertension
2) TAPVD
3) Persistent left SVC (drain into coronary sinus)
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CVS PHYSIOLOGY
278
❖ Fick’ principle for COP measurement:
• Rate of O2 consumption = COP X (A-V O2 content)
• Used to determine COP using Swan Ganz catheter
• Arterial O2 content → ABG, Venous O2 content → catheter in PA.
• Rate of O2 consumption → detected by O2 meter by easuring rate of
disappearance of O2 in exhaled air
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❖ Cardiovascular Effects of Adrenergic Drugs
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280
❖ Non-Drug Variables and Effects – maximum velocity of shortening
- when a skeletal muscle contracts, its maximum velocity of shortening is
indirectly/inversely proportional to the afterload attached to the fiber,
- maximal contractile shortening velocity increases as afterload decreases,
- whereas the greatest velocity of shortening occurs when there is no
afterload
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• except at their ostia
❖ Which change in
• Anaphylaxis, as VR ↓↓, COP ↑↑ due to ↓↓ TPR & to maintain BP
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❖ Which change in
• Chronic anemia lead to mildly ↑↑ VR (due t low blood viscosity), ↑↑ COP
due to ↓↓ TPR & to meet the needed COP
• In such curves, change sin TPR & blood volume affect both curves
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• Chronic AV fistula ➔ ↑↑ COP (↑ height of CO curve), ↓↓ TPR (↑↑ CO &
VR curve), ↑↑ MAP (↑↑ VR on X-axis (PSFP ))
❖ During exercise; ↑↑ sympathetic flow→ vasoconstriction of BV except for the
exercising muscles → shift of the blood to the muscles, blood (↑VR), but TPR ↓
due to vasodilatation (in response to local metabolites
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❖ Pressure-Volume Loop
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❖ Diastolic heart failure:
• Normal EF, normal LVEDV with ↑↑ LVEDP
• LVEDP determined by blood volume in LV & compliance
• Caused by ↓↓ compliance (e.g. amyloidosis), ↓↓ relaxation (ischemia)
• Notice the difference between ↑↑ preload curve & ↑↑ contractility curve
❖ Diastolic dysfunction:
• Due to ↓↓ compliance of the ventricle == ↑↑ pressure inside the ventricle for given
volume → shift the pressure volume curve to the upper side.
• ↓↓ compliance → ↑↑ end diastolic pressure at same level of end diastolic volume
➔ higher LVED pressure → transmit the pressure to the lug cause pulmonary
edema
❖ ↑↑ preload, ↓↓ after load >>> AV fistula
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❖ Cardiac Cycle
- In tracing the cardiac cycle, first detect where is the systole & diastole, plot
the vales that open and closed then answer
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❖ Tracing of aortic stenosis (how to detect the pathology in left heart
catheterization)
1) Determine the points where the mitral & aortic valve open & close
2) Determine where is the systole & diastole
3) Notice the pressure of the LV, aorta (normally SBP at both are equal)
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❖ What are the physiological changes occur in response to standing:
1) ↓↓ VR to the heart → ↓↓ ventricular filling → ↓↓ COP
2) ↓↓ BP → compensatory baroreceptor reflex → ↑↑ sympathetic tone → ↑↑
HR, vasoconstriction, contractility
4 phases of Valsalva:
1.) Phase 1: onset of straining with increased intrathoracic pressure, heart rate
doesn’t change, but BP rises,
2.) Phase 2: decreased venous return and consequent reduction in stroke volume
and pulse pressure as straining continues, HR increases and BP drops,
3.) Phase 3: release of straining decreases intrathoracic pressure and normalizes
pulmonary blood flow,
4.) Phase 4: BP overshoots in normal heart with return of heart rate to baseline,
Phase 2 used to distinguish fixed LV outflow obstruction (e.g. valvular Aortic Stenosis),
from dynamic obstruction (e.g. Hypertrophic Cardiomyopathy, Mitral Valve
Prolapse): valvular Aortic Stenosis murmurs decrease due to decreased venous
return and blood flow through the heart, however this decreased blood flow means
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less room in the LV, so Mitral Valve Prolapse (MVP) and Hypertrophic
Cardiomyopathy (HOCM) murmurs get louder, with earlier onset of the
click/murmur in MVP,
Phase 4 can be used to distinguish right-sided murmurs (return to normal immediately
after stopping Valsalva) from left-sided murmurs (require 5-10 cycles to return to
normal)
❖ Why patients with MVP on squatting lead to disappearance of the murmur,
late click
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❖ Why AF is more prevalent in AS?
• AS cause LV concentric hypertrophy → ↑↑ LV EDP → this pressure will be
transmitted to the LA → dilatation of the LA → more AF will occur in
response to this dilatation.
• AF indicate more severe AS
❖ Why AF in cases of severe aortic stenosis lead inevitably to acute LV failure?
• Patients with severe AS can ↑↑ LV wall thickness → ↓↓ LV complicance &
impaired end diastolic volume, making the atrial contraction related filling
of the LV is a good proportion of the LV EDV → so in AF, loss of this atrial
contraction → rapid loss of the LV preload → more ↓↓ COP → acute failure
❖ Bicuspid aortic valve (QID: 2106)→ asymptomatic patient, with soft systolic
ejection crescendo-decrescendo murmur best heard at A1 (right sternal
border), with ejection click
❖ Mitral stenosis:
o Opening snap (OS): heard shortly after S2 … during opening of the mitral
valve.
o After mitral valve opening (during rapid filling of the LV) there is abrupt
halt of the MV opening due to fusion → result in opening snap.
❖ Mitral stenosis & RF
o > 99% of MS are due to RF with 10 – 20 years latency period (MS appear at
4th – 5th decade)
o In isolated MS: diastolic LV pressure is normal or decreased.
o ↑↑ LV pressure suggest combined aortic disease (co-exist in 25%) mostly AS & AR
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❖ The most reliable indicator of severity of MS is duration between S2 (A2
component) & opening snap, mean tans-valvular pressure gradient
Mitral Regurgitation
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causes:
1.) Chronic RF/Infective Endocarditis,
2.) Chordae Tendineae Rupture,
3.) Mitral Valve Prolapse,
4.) Ischemic Heart Disease: post MI,
presents with dyspnea, orthopnea, fatigue, symptoms occur if regurgitation develops
acutely or if atria can no longer compensate in chronic disease
Tricuspid Regurgitation –
systolic murmur, retrograde blood flow into RA that occurs throughout systole,
similar to Mitral Regurgitation/Insufficiency, but softer due to lower pressure in
pulmonic circuit,
causes:
1.) Carcinoid Heart Disease: symptoms begin when GI tumor metastasizes to liver
(any hormones produced distal to liver in venous system metabolized by MAO in
lungs), produces 5-HT which fibroses tricuspid and pulmonary valves,
2.) IV Drug Use: results in right heart endocarditis (S. aureus), presents with pulsatile
liver due to increased venous pressures behind the right heart
❖ Describe carcinoid heart disease:
• ↑↑ serotonin → stimulate fibroblast, finrinogenesis ➔ plaque like
endocardial deposits of fibrous tissue → tricuspid regurgitation &
pulmonary valvopathy → RSHF
• Normal
Notice the difference between the SBP & DBP in the aorta
• Aortic regurge
- Loss of diacrotic notch
- Steep decline in aortic pressure → ↑↑ PP
Murmur will be heared immediately after closure of aortic valve (early
diastolic) just after closure of aortic valve
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• Mitral regurge
- Murmur heard at the opening of the aortic valve
Notice the markedly ↑↑ LA pressure → early & large V wave in the LA tracing
• Aortic stenosis
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• Mitral stenosis
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Pacemaker action potential
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❖ Arrhythmia Physiology – mechanism of arrhythmias:
DISORDERS OF IMPULSE FORMATION:
1.) Increased Automaticity: largely due to genetic alterations of membrane
channels,
2.) Triggered Afterdepolarizations: either early (EADs) or delayed (DADs),
- Early Afterdepolarization (EAD): triggered by spontaneous SR Ca2+ release or
delayed Phase 3 repolarization (because membrane stays closer to threshold
longer), caused by acute MI, β adrenergic activity, or Digitalis/Digoxin
toxicity, typically may lead to VTAC and Torsades de Pointes,
- Delayed Afterdepolarization (DAD): triggered by long QT syndrome drugs, more
likely to occur with bradycardic conditions,
DISORDERS OF IMPULSE CONDUCTION: some sort of
3.) Block or 4.) Reentry Pathway: area where split occurs in a conduction pathway
with a fast and slow half of the loop, slow half conducts signal slowly enough that
by the time the signal rejoins the fast half at the end of the split, the fast half is
no longer refractory, causing slow loop to reactivate it – this happens over and
over, caused by genetic influences (either acting alone or with some
environmental insult), ischemia, acidosis, high sympathetic activity, drug
(Digitalis/Digoxin) toxicity, electrolyte imbalance (esp. K+ and Ca2+), myocyte
damage due to MI,
TYPES OF ANTIARRHYTHMICS:
1.) RATE control Drugs (Class 2 and 4 Antiarrhythmics): slows HR in tachycardic
patients, usually patients who are severely bradycardic do not take drugs, they
get a pacemaker,
2.) RHYTHM control Drugs (Class 1 and 3 Antiarrhythmics): regulates rhythm to
make it more even rather than trying to slow it down or speed it up (though they
may do either in the process of regulating it), acts by prolonging QT interval (time
between atrial and ventricular depolarization)
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❖ Atrial fibrillation :
o ECG : low amplitude fibrillary waves may exist
o Most common site of focus is pulmonary veins
o Atrial HR → due to ↓↓ ERF & incinc conductivity of the atria
o Ventricular response → dependant on the ERF of the AV Node,
most of the atrial pulstions never reach the ventricles.
o Ventricular myocyte ERF is not an obstacle as it may reach HR up to
300 beat / min.
❖ Atrial fibrillation :
Pulmonary veins → are the commonest origin of AF
Left atrial appendage (LAA) → is the commonest site of thrombosis in AF
patients
• LAA is sac like structure in the LA, contribute to 90% of thrombosis of LAA
associated with non-valvular AF → can lead to embolism
❖ Biventricular Pacemaker – fed through subclavian vein into SVC, then into RA,
then RV (if only 2 leads), if 3 leads, 3rd is fed through coronary sinus, then
advanced into lateral venous tributary to pace LV
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❖ Lightning Injury
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❖ Reading of Swan Ganz catheter & how to locate the site of the catheter:
• The catheter is introduced through subclavian / IJV.
• Once reached SVC → venous pattern appear with small amplitude
oscillation
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• When introduced to the RA → unchanged as SVC
• Introduced to RV → sudden rise of the systolic pressure with pulsatile
waveform, diastolic pressure is just below the RA pressure.
• Once it pass the pulmonary valve → sudden rise of the diastolic pressure
with no change in the systolic pressure (due to capillary resistance,
backward transmission of the LA)
• When the catheter tip is lodged inside the vein → venous type waveform
appear
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CVS PATHOLOGY
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3) Reversal of shunt & late cyanosis (Eisenmenger syndrome )
4) Differential cyanosis , as blood distal to left subclavian artery is
unoxiginated from PDA
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❖ Cardiovascular Associations of Congenital Disorders
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❖ fibromuscular dysplasia (FMD)
o FMD typically occurs in women age <55.
o Characteristic pathology findings of fibromuscular webs alternating with
aneurysmal dilation and loss of the internal elastic lamina, is consistent
with fibromuscular dysplasia (FMD).
o Angiography (ie, percutaneous, CT, MRI) is diagnostic and typically
demonstrates a string-of-beads appearance in multifocal disease.
o FMD can involve any artery but most commonly the renal, cerebral (eg,
carotid, ertebral), and visceral arteries.
o Up to 80% of patients develop renal artery stenosis, which limits renal
perfusion and leads to activation of the renin-angiotensin-aldosterone
system.
o Other presentations are related to locations of the dysplastic artery;
cerebrovascular involvement (ie, headache, stroke, aneurysm rupture),
mesenteric ischemia, or extremity claudication may be seen … This young
woman with recent-onset hypertension died of an intracranial
hemorrhage, likely from a ruptured aneurysm.
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❖ Types of xanthomas:
1) Eruptive xanthoma → yellow papules appears when TGs or cholesterol ↑↑
2) Tuberous & tendinous → Achilles tendon & extensor finger tendons
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3) Plane xanthomas → liner lesions in skin folds associated with primary
biliary cirrhosis
4) Xanthelasma → peri-orbital palques, 50% with normal cholesterol level
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Arteriosclerosis – hardening of arteries, with arterial wall thickening and loss of
elasticity
Arteriolosclerosis – common, affects small arteries and arterioles
Atherosclerosis (Peripheral Artery Disease) – very common, disease of elastic arteries
and large- and medium-sized muscular arteries
❖ Mention the steps of development of atherosclerosis:
1) Endothelial inury → endothelial cell dysfunction
2) Monocyte & lymphocyte migration into the intima → GFs
3) Platelets adhesion with the exposed collagen
4) GFs – smooth muscle cells migration (fibrous cap)
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5) LDL cholesterol deposition in the intima
❖ Atherosclerosis
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❖ Describe the cystic medial
degeneration, its clinical importance.
• It is characterized by myxomatous
degeneration of the media with
pooling of proteoglycans in the
medial layer
• It is characterized by
fragmentation of elastic tissue
(baset weave pattern)
• These fragmentations make cleft like
spaces in the media filled with ECM
matrix.
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❖ Dissecting aortic aneurysm :
• Stanford A : flap begin at the sino-tubular junction
• Stanford B : flap begin close to left subclavian artery
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❖ Acute cornonary syndrome pathophysiology:
• Atherosclerotic plaques are usually asymptomatic except > 70% luminal
stenosis
• ACS occur due to plaque rupture → the likelihood of plaque rupture
is related to plaque stability rather than plaque size or degree
of luminal stenosis
• Plaque instability → depend on the mechanical strength of the fibrous cap
(thin cap are unstable, more risk of rupture)
• Thin cap fibroatheromas → large necrotic core covered by thin fibrous
cap, due to ↑↑↑ activity of macrophage metalloproteinases
• While ↑↑ stability usually occur by lysyl oxidase
❖ Vasospastic angina :
o Occur at rest, night time.
o Triggered by: + amphetamines
o Ergotamines act as vasoconstriction due to its action on α receptors (partial
agonist) and serotonin receptors
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❖ What is the factor that determine whether the plaque cause necrosis or not.
The rate of arterial occlusion, if the plaque developed slowly over time, it give
the coronaries the time to develop collaterals around point of occlusion. While
in rapidly developing plaque, no time for collateral circulation.
❖ Describe the L/M changes of cardiac cells after MI in 0 -4 hr, 4 – 12, 12 – 24,
1- 5 days, 5 – 10 days, 10 – 14, 2 weeks – 2 months
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❖ Describe process of myocardial hibernation: reduction of the
myocardial metabolism an function in case of myocardial ischemia to match
the new low level of O2, to prevent myocardial necrosis. It include ↓↓
responsiveness to Ca, sympathetic control ➔ ↓↓ contractility & LVEF, t is
reversible by reperfusion.
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❖ Collagen in different stages of myocardial infarction
o Type III collagen → seen after 7 days after MI but eventually replaced by
type I
o Type I collagen → most abundant in mature scar tissue
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❖ Evolving ECG changes seen in transmural MI:
1) Hyperacute T wave (1st sign) → due to localized hyperkalemia
2) ST elevation → follow the T-changes within minutes to hours.
3) Deep Q wave → appear within days
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❖ Pathogenesis & Clinical picture , incidence of fibrinous pericarditis post MI:
• Clinical picture : sharp, pleuritic chest pain, +/- ↑↑ with swallowing →
posterior pericardium, +/- radiate to the neck → inf. Pericardium, +/- low
grade fever → inflammatory
• Incidence : 10 – 20% of STEMI, in 2 – 4 days
• Pathogenesis: nflammation localized to the region of the pericardium
overlying the necrotic myocardial segment , usullay short lived & treated by
aspirin
❖ Pathogenesis, incidence of Dressler syndrome:
• Incidence: < 4% of patients, occur from 1 week to few months
• Pathogenesis: MI expose antigen → provoke autoimmune generalized
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serositis (pleuritis, pericarditis), usually respond to aspirin / steroids
❖ Atheromatous plaques in coronary arteries don’t produce
symptoms unless there are 75% luminal stenosis.
❖ Previous MI lead to ↓↓ risk of free wall rupture due to presence of fibrotic
scar, multiple collaterals which ↓ burden of the infarciton
❖ What is the type & character of reperfusion arrhythmia: Benign and not
associated with ↑↑ mortality, the commonest of them is acclereated
idioventricular (AIVR) rhythm
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❖ Hypertrophic cardiomyopathy :
o Commonest cause of SCD in athletes < 35 (33% in autopsy)
o Mostly asymptomatic → +/- dyspnea, fatigue, chain pain
o Histologically :
▪ Myocyte hypertrophy
▪ Muscular disarray of the muscle fibers (pic. 1)
▪ Abnormally looking myocytes. (pic. 2)
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❖ Renin produced by juxta-glomerular apparatus, ACE enzyme present in small
pulmonary arteries
❖ Heart failure cells (occur in LV failure) occurs due to alveolar hemorrhage →
macrophage digest blood → hemosiderin → hemosiderin / iron (any
where) detected by perussian blue stain (not exclusively in hemochromatosis)
❖ Cardiogenic shock → ↓↓ LV filling → ↓↓ PCWP due to LA atrium.
❖ Pheocromatocytoma may lead to orthostatic hypotension due to ↓↓ plasma
volume
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❖ Mention the immunological & vascular manifestations of infective
endocarditis
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❖ Difference between Janeway lesions, Osler nodules:
• Janeway lesions: nontender macular, erythematous lesions on palm &
sole. Due to septic emboli → consists of microabscesses
• Osler nodules: tender, violaceous nodules typically located in the pulp of
fingers and toes. Due to immune complex deposition in the skin
Endocarditis
Risk factors include history of right heart disease, valvular heart disease, IV drug use,
immunosuppression, prosthetic valve, ASD/VSD
Types:
1.) Acute Endocarditis:
- caused by S. aureus (high virulence),
- large vegetations occur on healthy or damaged valves, esp. from Mitral Valve
Prolapse (most common predisposing condition) or Rheumatic Heart Disease,
- associated with IV drug users,
- presents with fever and rapid degradation of heart tissue,
2.) Subacute Bacterial Endocarditis:
- slower onset with less severe symptoms,
- caused by Enterococcus (GI/GU surgery), S. viridans (oral/dental surgery, low
virulence), S. epidermidis (prosthetic valves), S. bovis (gallolyticus, Ulcerative
Colitis or Colorectal Cancer),
- smaller vegetations occur on diseased or congenitally abnormal valves,
3.) Marantic Endocarditis:
- neoplastic syndrome (GI tract),
- sterile vegetations occur on valves due to increased coagulability caused by
increased mucin production (same process underlying Trousseau’s sign of
malignancy – different from the low calcium Trousseau’s sign),
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- may produce emboli to periphery,
4.) Libman-Sacks Endocarditis:
- caused by SLE (“SLE causes LSE”),
- usually asymptomatic, but may cause Mitral Insufficiency/Regurgitation,
5.) HACEK Organisms:
- Haemophilus, Aggregatibacter (formerly Actinobacillus), Cardiobacterium,
Eikenella, Kingella, all fastidious G⊖ organisms (e.g. Coxiella burnetii,
Bartonella),
- suspect if fever with a murmur, but negative blood cultures,
Duke Criteria:
1.) Blood Cultures: obtain 3 separated in time and location, multiple positive
cultures of the same organism strong evidence for endocarditis,
2.) Echocardiography: look for vegetations, not ruled out by negative echo,
3.) CXR: may reveal septic emboli in right sided endocarditis,
Treat with prolonged empiric antibiotic therapy (low-dose Penicillin or Vancomycin),
surgical valve replacement,
Complications include chordae tendineae rupture, emboli, glomerulonephritis,
suppurative pericarditis, intravascular infection that can spread to other organs
(watch for signs of neurologic, joint, and lung manifestations)
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Rheumatic Fever/Rheumatic Heart Disease (RHD)
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- Rheumatic Fever (RF) is a systemic immune process that may or may not lead to RHD,
- presentations (JONES criteria):
1.) Migratory Polyarthritis: no permanent damage, occurs at both large and small
joints,
2.) Endocarditis: most commonly affects high pressure valves first (sterile
vegetations at closure line of valve, mitral > aortic >> tricuspid), produces mitral
regurgitation or prolapse (early), or stenosis (late),
3.) Myocarditis: contains Aschoff bodies, which are granulomas surrounded by
reactive histiocytes called Anitschkow cells (enlarged macrophages with ovoid,
wavy, rod-like nucleus), pathognomonic for RHD),
4.) Pericarditis: friction rub,
5.) Erythema Marginatum,
6.) Subcutaneous Nodules: extensor surfaces,
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7.) Sydenham’s Chorea: involuntary movements of all muscles, late finding,
- serum shows elevated ESR and CRP,
- ECG shows leukocytosis-increased PR interval,
- ASO positive,
- positive throat culture,
- treat with Penicillin,
- acute morbidity most likely caused by pancarditis (inflammation of endocardium,
myocardium, and epicardium)
❖ Acute rheumatic fever :
o Syndeham Chorea :
▪ Hyperkinetic extra-pyramidal movement
▪ Commonest cause of acquired chorea of childhood
▪ Caused by delayed onset autoimmune reaction against basal ganglia
❖ Most acute morbidities & death from ACUTE rheumatic fever is due to
pancarditis → MR, myocarditis → Heart failure
❖ Pericarditis pain → severe middle or left chest pain that radiate to the neck &
trapezius ridge
❖ Acute pericarditis may cause fluid accumulation inside the pericardial cavity
→ cardiac tamponade
❖ Constrictive pericarditis show rapid Y descent that becomes deeper &
steeper during inspiration.
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❖ Histology of different causes of myocarditis:
• Acute rheumatic fever related myocarditis :
Interstitial fibrosis with central lymphocytes & macrophages +
scattered multi-nucleated giant cells ➔ Aschoff body (myocardial
granuloma)
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❖ Pulsus paradoxus technique (QID: 2099):
• During BP measurement; 1st Korotkoff sound is heared when SBP just <
cuff pressure.
• During expiration BP > BP during inspiration
• If you heared the 1st Korotkoff sound only dueing expiration (so SBP in
inspiration is lower), the first BP when you hear Korotkoff sound in both
inspiration & expiration (this correspond to BP) difference between two if
> 10 = pulsus paradoxus due to impaired filling of the RV → bowing of the
IVS to the LV cause its diameter to ↓↓
• Normally there is difference in IPP during inspiration ~ 2-5 mmHg, in COPD &
BA this drop is greatly exaggerated (commonest cause of pulsus paradoxus in
absence of pericardial disease)
❖ Cardiac tamponade :
o During LV expansion at diastole → fluid displaced ➔ prevent RA expansion
→ late diastolic collapse of the right atrium.
o During diastole & inspiration → ↑↑↑ VR to the right atrium → RV ➔
expansion of the right ventricle ( cannot expand outward) so press on the IVS
cause bulge of the IVS to the LV → ↓↓ LV EDV → ↓↓ LV SV → SBP & pulse
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(pulsus paradoxus)
o Electrical alternans → occur in very large pericardial effusion
o Other causes of pulsus paradoxus : COPD, hypovolemic shock,
constrictive pericarditis
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Medium Vessel Vasculitides
- Kawasaki Disease (Mucocutaneous Lymph Node Syndrome)
- Polyarteritis Nodosa
- Raynaud Phenomenon
- Thromboangiitis Obliterans (Buerger Disease)
❖ Berger disease :
• Acute & chronic inflammation of medium & small sized vessels (mainly tibial
& radial) with extension of the inflammation to the surrounding
veins & nerves
• Clinical picture : Rest pain →nerve, Raynaud’s phenomena → artery,
thrombophlebitis → veins
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• More common in ́♂ < 35 years in Israel, Japan, India ≫ US & Europe
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Small Vessel Vasculitides without Immune Complexes
- Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss Syndrome)
- Granulomatosis with Polyangiitis (Wegener’s Granulomatosis)
- Microscopic Polyangiitis
- Primary Pauci-Immune Crescentic Glomerulonephritis – vasculitis limited to
kidney, “paucity” of antibodies, histologically indistinguishable from renal
involvement of Microscopic Polyangiitis or Granulomatosis with Polyangiitis, p-
ANCA (MPO-ANCA) antibodies (neutrophil myeloperoxidase)
❖ Clinical & laboratory features of Churg Strauss polyangitis:
- Eosinophilic granulomatosis with polyangitis
- Clinical picture:
• Late onset asthma, transient pulmonary nodules
• rhinosinusitis, PNS abnormalities
• Mono-neuritis multiplex , skin nodules → due to vasculitis of the
epineural vessels → nerve damge
- Lab : eosinophilia, P-ANCA
❖ Lacunar infarction:
• Form of ischemic stroke involving the small penetrating arterioles → deep
brain matter
• Cardiac embolism & atherosclerosis → medium & large size artery
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• Chronic hypertension → lipo-hyalinosis, micro-atheroma formation,
sclerosis of the vessel (hypertensive arteriolar sclerosis) →
progressive narrowing of the arteriolar lumen → thrombotic vessel
occlusion
• CT initially free due to small sized stroke.
• Clinical picture :
- Posterior limb of the IC → pure motor stroke, ataxia-hemiplegia
syndrome, very rarely cause pure sensory stroke
- Genu of the IC → Dysarthria – clumpsy hand syndrome
- VPL / VPM of the thalamus → pure sensory stroke
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❖ Left atrial myxoma:
• Clinical picture : the mass produce large amount of IL-6 which cause the
constitutional symptoms, cause valve obstruction by the myxoma so
the cardiovascular symptoms are positional, the mass ma be very large in
size with emboli, myxomas produce very large amounts of growth
factors → angiogenesis which lead to hemorrhage
• L/M: scattered cells with mucopolysaccarides, abnormal BV, bleeding
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CVS PHARMACOLOGY
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❖ hypertension (+)
• BPH → α 1 blockers
• CHF / CAD → β blocker
• Essential → HCTZ
• DM → ACE-I
• Prinzmetal angina / Raynaud’s disease → Dihydropyridine CCB (2nd line)
❖ ACE-I & ARBs are not only important in Heart failure due to ↓↓
hypertension, but it has independent effect to ↓↓ cardiac
remodeling
❖ Difference between rise in creatine level due to ACE-I or ARF due to ACE-I
• Rise in serum creatinine up to 30% within 2 – 5 days after ACE-I is
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common, stabilize after 2 – 3 weeks & reversible
• For patients dependent on efferent arterioles (e.g. RAS, AHF, CKD) →
ACE-I cause acute renal failure
❖ First dose hypotension in ACE-I :
• Hypotension is significant with ↑↑ renin as in ↓↓ volume (diuretics), Heart
failure
• Mechanism: use of ACE-I → significantly ↓↓ vasoconstriction effect of AT-II
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❖ Deverse effects of nitrites: headache, flushing hypotension, lightheadedness,
reflex tachycardia,
❖ Around the clock administration of nitrates will lead to rapid tolerance to the
drug, so nitrate free period must be provided every day, this period is
preferred to be at night (the patient is sleeping & least cardiac load)
❖ Nitroglycerin :
o Low doses → dilate veins, higher doses → + arterioles.
o Know the composition
❖ Additional actions of nitrate:
- mild ↓↓ in afterload die to systemic vasodilatation
- mild coronary vasodilatation
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❖ Mention the mechanism of action of milrinone, inamrinone
• Used in some cases of refractory Heart failure as inotropic agents
• PDE-3 inhibition → ↑↑↑ cAMP in (same as cilostasol, dipyridamole):
Cardiac cells →↑ Ca influx → ↑↑ contractility
Smooth muscle → systemic arterial & venous dilatation → ↓↓ BP
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❖ Statin therapy, obtain base line liver function tests before starting the therapy,
otherwise no routine monitoring is needed except symptoms appear.
❖ Statin induced myopathy usually mild muscular pain, may cause ↑↑ CK &
rhabdomyolysis with concurrent use of fibrates (↓↓ clearance of statins), also
myopathy risk ↑↑ by use of niacin & ezetimibe (but to lesser extent)
myopathy is the most common adverse effect in statins
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❖ Lipid lowering drugs :
➢ Statins : ↓↓ hepatic cholesterol synthesis → ↑↑ LDL receptors on liver to ↑↑
uptake of LDL from blood
➢ Bile acid resin → ↑↑ bile salt synthesis → ↑↑ uptake of LDL from blood to ↑↑
hepatic cholesterol synthesis
➢ ↓↓ hepatic cholesterol synthesis → ↑inc HMG-CoA reductase ➔ Adding
statin to drugs further reduce LDL (synergistic effect)
o Fibrates :
▪ Actions
1) ↑↑ LPL
2) ↓↓ cholesterol 7 α hydroxylase → ↓↓ bile salt formation & ↑↑ cholesterol
excretion → ↑↑ precipitation of crytals → ↑inc GB stones
3) ↑↑ PPAR-γ
o Fish oil ➔ ↑↑ ω3 fatty acids → ↑↑ bile acid synthesis → ↓↓ cholesterol
saturation in bile → ↓↓ Gall stone formation
❖ side effects of bile acid resin:
• GI upset (diarrhea)
• ↓↓ absorption of nutrients & drugs
• ↑↑ hepatic production of triglycerides (# fibrates)
• ↑↑ VLDL in circulation
• These changes are side effects not related to mechanism of action of the
drug
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Fish Oil/Omega-3 Fatty Acids
o Mechanism: decreases VLDL and apolipoprotein B synthesis
o Treats: Triglycerides, HDL
o Side Effects: fishy taste
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❖ Digoxin toxicity :
• Although hypokalemia can precipitate digoxin toxicity, digoxin toxicity
cause ↑↑ potassium level.
• The most serious complication is cardiac arrhythmias (any type)
• AF – RVR → 1st line: BB, CCB. 2nd line: Digoxin (especially if there is
Heart failure)
❖ Digoxin as anti-arrhythmic drug:
o Used in Af/ AF RVR, although CCB, BB are better
o Due to para-sympatho-mimetic action ➔ a) enhance efferent vagal
ganglionic transmission b) sensitize arterial baro-receptors augment
afferent input
❖ Action of digoxin:
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❖ Mention the effect of antiarrhythmic drugs on QRS & QT duration
• Class IA → ↑↑ QRS duration (due to Na block), ↑↑ QT interval (moderate K
block)
• Class IB → no effect on QRS, QT (due to rapid dissociation)
• Class IC → ↑↑ QRS duration (strong blockage on Na), normal QT interval
• Class III → no effect on QRS, ↑↑ QT interval , ↑↑ AP duration
❖ Mention the effect of class IC on the AP duration?
• The drugs act mainly on the fast conducting pathways as it cause use
dependenace
• It cause ↑↑ QRS duration without changing the total AP duration
or QT interval
• So class 1C lengthen the duration of QRS in rate dependant manner
(normally in exercise, ↑↑ HR but the QRS duration slightly reduced)
❖ Why class IB is used mainly in post infarction arrhythmia:
- Class IB bind avidly to the inactivated Na channels, because normal cells
has short refractory period so they are dissociated so rapidly (no effect on
QRS in normal heart)
- Ischemic myocardium → less negative RMP → more to be depolarized →
inactivated fro longer period → more bind specifically- to the ischemic
tissues
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❖ Use dependence of anti-arrhythmic drugs :
• Anti-arrhythmic drugs bind to activated & inactivated Na channels,
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dissociate in resting state (state dependence).
• So tissues that more frequently depolarized (tachycardia) → more to be in
activated & inactivated state → more binding to drugs → more blockage
(use dependence)
• Class IB: have the weakest binding of class I drugs → dissociation of drugs
is so rapid ➔ little use dependence
More selective for ischemic myocardium → less negative RMP → take
more time in repolarization (more time to be in inactivated state) →
more drug binding → ischemia induced VTac
• Class IC: have the stongest binding → highest use dependenace → use to
terminate tachyarrhytmias
Class IC usage → excessive delay in conduction speed that promote
arrhythmia (especially in ischemic patients)
• Affection of Phase 0 depend on the use dependence → class IC > A > B in
case of phase 0 inhibition
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❖ Amiodarone is class III anti-arrhythmic rug cause prolongation
of QT interval → but very little risk of torsade des pointes (due to its
homogenous effect on ventricular repolarization)
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❖ Class IV anti-arrhythmic drugs (e.g. verapamil) → prevent recurrent nodal
arrhythmias (paroxysmal SVT) → block L-Ca channels in SA nodes (slowing
phase 0), block T-Ca channels (slowing phase IV)
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