U World

Thursday, 26 February 2015 1:46 am

1. Teratogens and cardiac malformations:

a. Lithium for Bipolar in mom causes Ebsteins anomaly in foetus
b. GDM: macrosomia + hypertrophic cardiomyopathy
c. Alcohol: Foetal alcohol syndrome (midfacial anomalies, growth retardation, mental
retardation)

2. Sudden deceleration injury:

a. Rupture of the aorta at the aortic isthmus (held by the ligamentum arteriosum; less
mobile)
i. Abdominal pain
ii. Chest pain
iii. Difficulty breathing
b. Rupture may also involve the ascending aorta (not as common)
i. Hemopericardium
ii. AV disruption

3. Aorta anterior to and to the right of the pulmonary artery is diagnostic of transposition of
great arteries (It's quite obvious really: Failure of neural crest cell migration

4. ECG physiology:
a. Ventricular response in AF depends on the AV node refractory period
i. Narrow QRS
ii. Irregularly irregular R-R
b. Bundle branch conductivity - determines duration of QRS

5. Catheter placement:
a. Hand washing ensures central lines are not infected
i. Staph aureus
ii. Staph epidermidis (coagulase negative)
b. Use subclavian
c. Catheter replacement doesn’t really work
d. Antibiotic prophylaxis doesn’t work

6. Amyloidosis
a. Localised amyloidosis list of precursor proteins:
i. Senile cerebral - A beta
ii. Thyroid - Calcitonin
iii. Pancreatic islets - Amylin
iv. Heart - ANP
v. Pituitary - Prolactin

7. Acute LVF:
a. Dyspnea
b. Tachypnea
c. CXR findings:
i. Cardiomegaly; LVH (RVF would show RVH)
ii. Alveolar edema / batwing
iii. Kerley B lines
iv. Blunt costophrenic angles (effusion)
1) COPD - Flat diaphgragm
d. 3rd heart sound due to increased LV end systolic volumes

8. Atherosclerosis:
a. Endothelial injury activates platelets
i. Release of PDGF, and increased expression of VCAM-1 on endothelium
ii. PDGF from endothelium + platelets + infiltrating macrophages (monocytes that
emigrate)
1) Migration of smooth muscle cells into intima from the media
2) Proliferation of smooth muscle cells
a) Reactive intimal hyperplasia
iii. TGF-Beta
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 iii. TGF-Beta
1) Chemotactic for SMC
2) Induces interstitial collagen production
b. Smooth muscle cells synthesize the fibrous cap, not fibroblasts
c. When coronary arterial occlusion >75% it can may cause angina of effort

9. Left lateral decubitus position:

a. Diastolic S4 sound (gallop) #important
b. Seen in high atrial pressure due to LVH

10. Complications of MI
a. Day 1 : Cardiogenic shock, arrhythmias
b. Day 1 - 3 : Pericarditis
i. Serofibrinous
ii. Localised: over the necrotic myocardium
iii. Rx: Aspirin, and short lived
c. Day 3 - 14 : Ventricular free wall rupture, cardiac tamponade
d. 2 weeks: Dressler's pericarditis
i. New pericardial, pleural effusions
ii. Autoimmune, diffuse involvement
iii. Fever, pleuritis, leukocytosis
iv. Responds to Aspirin, NSAIDS, Glucocorticoids

11. Sharp pleuritic pain radiating to neck, worsened with swallowing; relieved by leaning forward -
phrenic nerve involvement (close to the heart, and irritated in pericarditis)

12. Conduction speed of atrial fibers is faster than that of ventricular fiber.
a. Know the anatomy; locations of these fibres/nodes/
b. Purkinje fastest
c. AV node slowest (causes a delay of 0.13 seconds) 0.05 m/s
d. SA node --> 1.1 m/s
e. Purkinje (and bundles of His) > Atrial > Ventricular > AV node

13. Skeletal muscle vs cardiac/smooth

a. Not dependent on ECF Calcium
b. RyR1 Ca++ channels open in the sarcoplasmic reticulum, leading to contraction
c. Hence resistant to CCB therapy

14. A change in O2 saturation while blood moves into the atria to the ventricles - VSD
a. 75% SpO2 = 45mm Hg O2
b. 96% SpO2 = 96 mm Hg O2

15. Phenoxybenzamine:
a. Non selective irreversible alpha 1 and 2 blocker.
b. Norepinephrine can't overcome blockade hence, Emax is reduced (efficacy is reduced)

16. CN- toxicity treatment

a. Precipitated by Sodium Nitroprusside
b. Signs:
i. Lactic acidosis
ii. Altered mental status
c. Treated by Sodium thiosulphate
i. Liver rhodanase normally transfers S to CN
ii. Sodium thiosulphate donates S to rhodanase

17. Hydrochlorothiazide - first line drug for essential hypertension

18. HOCM:
a. Asymmetrical septal hypertrophy + dynamic outflow obstruction
b. AD with variable expression
i. Mutation in beta-myosin heavy chains
c. Can lead to sudden death
d. Increased blood flow (increased preload) = less murmurs
e. Decreases blood flow (decreased preload) = more murmurs because of AV closure

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 19. Susceptibility to occlusion:
a. CNS > Heart > Kidney > Spleen > Liver

20. Atrial Myxoma:

a. Constitutional symptoms
b. Mid diastolic rumbling murmur (apex)
c. Pedunculated mass
d. Positional dyspnea

21. Staph epidermidis

a. Penicillin and Methicillin resistant
b. Vancomycin
c. Biofilm production

22. Effects of ageing on the heart (>65 years):

a. Lipofuscin pigment (intra cytoplasmic, perinuclear)
i. Doesn’t stain blue-black with Prussian blue (Potassium ferricyanide --> Fe
ferricyanide)
ii. Wear and tear pigment
iii. Due to lipid peroxidation (lipid polymers and protein-complexed phospholipids)
b. Increased collagen
c. Banana shaped septum, decreased base to apex diameter
d. Increased deposition of fibrous tissue
e. Seen in:
i. Ageing
ii. Cachexia
iii. Malnutrition

23. Collagen types

Dermis, bone, tendons, ligament, cornea, dentin, scar tissue Type 1
Cartilage, vitreous humour, nucleus pulposus Type 2
a.
Skin, Lungs, intestines, blood vessels, bone marrow, granulation tissue Type 3
Basement membrane Type 4

24. Cardiac Transplant - Acute rejection:

a. (1-4 weeks)
b. Paroxysmal nocturnal dyspnea
c. Dyspnea
d. Biopsy:
i. T-Lymphocytes
ii. Dense mononuclear infilterate

e. Eosinophils = Hypersensitivity myocarditis

f. Patchy necrosis + granulation tissue = hyperacute rejection
g. Scant inflammation and fibrosis = chronic rejection (months to years)

25. IV drug abusers infective endocarditis: right valves are affected; otherwise 90% are left sided

26. Subacute bacterial endocarditis + negative culture

a. Streptococcus bovis - Group D streptococcus (colon cancer patients)
b. Streptococcus viridans - Post tooth extraction
i. Produce insoluble extracellular dextrans from sucrose/glucose
ii. Dextrans help streptococci bind to fibrin
iii. Hence are able to colonize heart valves and dental enamel
1) Preexisting damage on heart valves lead to deposition of fibrin and platelets
2) Fibrin carrying strep --> hence colonization of previously damaged valves
c. Mitral vegitations present - HACEK, Bartonella, Histoplasma, Chlamydia, Coxiella
d. Known mitral stenosis, low grade fevers + negative culture - RF

27. Varicose veins:

a. Superficial veins involved
i. Don’t commonly embolise to the pulmonary arteries (unlike DVT)
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 i. Don’t commonly embolise to the pulmonary arteries (unlike DVT)
ii. Main complication is skin ulceration and infection
iii. Caused by incompetent veins
iv. Complications:
1) Stasis dermatitis
2) Painful thromboses
3) Skin ulcerations
4) Poor wound healing
5) Superficial infections

28. Proximal 2-3 cm of pulmonary veins have cardiac muscle, and function as sphincters during
systole.

29. Warfarin administration requires monitoring of PT/INR (maintain INR between 2 - 3.5)
a. Most common long term anticoagulant to prevent venous thrombosis and pulmonary
embolism.
b. Long term anticoagulant in aortic valve replacement
c. Blocks Vit K dependent gamma carboxylation of glutamate residues
i. II, VII, IX, X
d. Typically longer onset of action (long half lives of clotting factors)
e. Factor VII has the shortest half life hence deficiency is seen first

30. Heparins - aPTT

a. Route of administration - sc / iv
b. Acute management of venous thrombosis (since warfarin takes a while to start working)
c. Acute management in the immediate post operative period

31. SVC forms behind the first costal cartilage, Descending aorta echo = rotate TEE posteriorly
32. Valve findings:
a. Aortic regurgitation:
i. Early diastolic crecendo murmur
ii. Amyl nitrite reduces preload >> Reduces murmur
b. HOCM - increases while standing (reduced preload)
c. AS - decreases while standing (reduced preload)
d. Non splitting murmur (ASD)
e. Wide S1 splitting - mitral stenosis/bundle branch block
f. Mitral / tricuspid stenois - diastolic murmur with presystolic accentuation Tyrosine is essential in PKU, since mcc is
deficiency of phenylalanine hydroxylase.
33. Anterior uveitis: (Enzyme that converts Phe to Tyr)
a. HLA-B27 linked diseases
b. Lyme disease Asparagine formed from aspartate
c. Syphilis (Asparagine synthetase; Glutamine as
d. Herpes virus amino donor). Essential for rapidly
dividing tumour cells that cant produce
34. Beta 1 selective blockers - no hyperkalemia its own Asparagine.
a. Hyperkalemia is a beta 2 blockade effect due to blockade of insulin release >> 1. Asparaginase >> lysis of tumour
hyperkalemia cells

35. Decreased preload = decreased end diastolic volume

36. Decreased afterload = decreased end systolic pressure
37. Jesus christ all these heart sounds

38. Severe MR = S3 gallop (diastolic component may also be indicative); intensity of murmur isnt
very useful
a. S3 = high ventricular filling rate during mid diastole
b. Pulmonary edema (if acute)
c. Functional MR - improves with diuretics --> Decrease in LV size decreases size of mitral
valve annulus
i. Holosystolic murmur at the heart apex
ii. Maximum intensity at the beginning of systole
d. Calcific Mitral annulus - doesn’t decrease in size
e. MR due to chordae rupture - doesn’t magically go away with drug therapy

39. Beta blockers decrease mortality in patients with acute coronary syndrome; watch out for
exacerbation of asthma / COPD due to B2 blockade causing bronchoconstriction
a. Acute increase in TPR (B2 blockade) but that’s transient
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 a. Acute increase in TPR (B2 blockade) but that’s transient
b. Contraindicated in asthma / COPD

40. Renin is inhibited by (B1 receptors on JG cells) B1 selective beta blockers; reduces ATII,
Aldosterone; useful in hypertension
a. But - plasma renin levels have little to do with antihypertensive efficacy of beta blockers.
Main mechanism of action is negative chronotropic and inotropic effect
b. Basically YMMV

41. B2 receptor mediated vasodilation in muscular vessels (increases blood flow during exercise);
Epinephrine
42. Beta blockers - good for reducing reflex tachycardia when administering vasodilators; more
effective that non-DHP CCB's too.
a. Beta blocker + non-DHP --> Significantly reduced heart rate (sinus bradycardia)
i. Depressed AV node, contraction
ii. Bradycardia + Hypotension
b. Other drugs that will reduce heart rate:
i. Digoxin
Sturge-Weber syndrome :
ii. Pilocarpine / Rivastigmine
1. Encephalotrigeminal angiomatosis
iii. Amiodarone & Sotalol
2. Skull radio-opacities tram track
calcifications
43. Glucagon:
3. Nevus flammaeus
a. Directly acts on Gs proteins on cardiac myocytes
b. Increases intracellular cAMP
c. Bypasses beta receptors, hence useful in beta blocker overdose
i. Reverses the following - bradycardia, hypotension, CVS collapse

44. Defective neural crest cell migration:

a. TOF
b. Transposition of great arteries
c. Truncus arteriosus
45. Abnormal primitive heart tube looping:
a. Severely misplaced inflow and outflow tracts

46. Left atrial dilation (due to eg Mitral stenosis):

a. Dysphagia
b. Hoarseness of voice (recurrent laryngeal nerve impingement and neurapraxia) Ortner
syndrome

47. Most common cause of death post MI = Cardiogenic shock

48. Recurrent laryngeal nerve:
a. Right - loops below the right subclavian artery
b. Left - Loops below the aortic arch

49. Dose calculations:

a. Maintenance dose = Plasma conc x (CL / bioavailability)
b. Loading dose = (Plasma conc / Bioavailability) x Vd
c. Half life = Vd x 0.7/CL

50. Cilostazol and Dipyramidol:

a. Increasing cAMP alters platelet function
b. Treatment for peripheral artery disease ?
c. PDE 3 inhibition
i. Vasodilatory and anti platelet
ii. Aspirin can aslo perform the same functions, however it is a less effective
vasodilator

51. Rupture of free ventricular wall - 3 to 7 days post MI

a. Previous MI's may actually be protective because of fibrosis
b. Rupture more likely if patients first MI

52. Erythema nodosum:

a. Violaceous painful subcutaneous nodules appearing on the legs
b. S. aureus, Coccidiomycoses, Histoplasmosis, Blastomycosis, Chlamydia
c. Crohns disease
d. Sarcoidosis
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 d. Sarcoidosis

53. Homocysteine is substrate for both methionine and cysteine synthesis

a. S - adenosyl homocysteine (SAM, methyl donor) >> Homocysteine >> Methionine (via
methionine synthase)
b. In homocystenuria; mcc is cystathione beta synthetase defect
c. Requires B6 (Pyridoxine)
d. Cystathione >> Cysteine (via cystathionase)
i. Cysteine hence becomes an essential amino acid in homocysteinuria
e. Complete deficiency of cystathione beta synthetase:
i. Premature atheroscleorosis
ii. Osteoporosis
iii. Mental retardation
iv. Ectopia lentis

54. Management of digoxin toxicity:

a. Charcoal (GI decontaminant); more for suicides
b. Serum potassium management (decrease):
i. Insulin
ii. Kayexalate: Sodium polystyrene (cationic exchange resin)
iii. Digibind

cAMP cGMP
55.
4 protein subunits Receptor + guanylyl cyclase in single protein
a. cGMP:
i. Transmembrane receptor - ANP
ii. Free cytosolic receptor - NO
b. Increased cGMP - Increased Myosin Light chain phosphatase >> Relaxation

56. FA = produce more ATP than glucose, but uses more O2 per ATP than glucose

57. Holosystolic murmur - atrioventricular valve regurgitations; VSD

a. Palpable systolic thrill

58. Crecendo-Decrecendo: Aortic stenosis; Decrecendo ending before S1: Pulmonary

regurgitation

59. Action potentials:

a. Purkinje cells + Cardiomyocytes = Phase 0 1 2 3 4 ; 0 - Na current
b. Conducting fibres = Phase 0 3 4; 0 - Ca current

60. Hereditary hemorrhagic Telangiectasias:

a. AD
b. Osler-Weber-Rendu syndrome
c. Severe nosebleeds
d. GI bleeding
e. Hematuria
f. Pink spider like lesions, oral/nasal mucosa, GI mucosa, urinary tract, face, arms

61. Endocardial cushion defect + flat face + epicanthal folds

a. Downs Syndrome
b. Meiotic non-dysjunction of Chr 21; Trisomy 21.

62. Kussmaul's signs:

a. Paradoxical increase in JVP during inspiration
b. Causes:
i. Chronic constrictive pericarditis
ii. Restrictive cardiomyopathy
iii. Severe RHF
iv. Tricuspid stenosis
v. Cardiac tamponade [rare]

63. Pulsus Paradoxus:

a. Decrease in sbp by >10 mm Hg during inspiration
b. Causes:
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 b. Causes:
i. Pericarditis
1) CT may show thickening and calcification of the pericardium
2) Progressive dyspnea, edema, ascites
3) Also see Kussmaul's sign: paradoxical increase in jvp during inspiration
4) Rapid y descent that is steeper and deeper during inspiration
a) Causes:
i) TB
ii) Irradiation
iii) Previous cardiac surgery
ii. Cardiac tamponade
1) Cardiac tamponade - Can lead to bulging of the intraventricular septum
when the ventricular free wall is prevented from expanding. Inspiration
leads to increased RV preload --> septum bulges into LV --> Decreased LV
filling. Hence pulsus paradoxus
2) Drop in arterial pressure >10mmHg during inspiration
3) Force is sufficient to cause collapse of atria (diastolic)
iii. Croup
iv. Asthma
v. Obstructive sleep apnea
64. Pericardial knock - present in constrictive pericarditis; can be confused for opening snap of MS
65. Development of the sinus venosus:
a. Left side -
i. Common cardinal vein --> Oblique vein of RA and coronary sinus
ii. Proximal part of left vitelline vein --> obliterates
1) Distally - anastomotic vessels formed around the duodenum --> Portal vein
2) Hepatic sinusoids

iii. Left umbilical vein is left:

1) Proximal part obliterates
2) Distal part carries blood from placenta to liver and ductus venosus
3) After birth:
a) Ligamentum teres hepatis (umblical vein)
b) Ligamentum venosum (ductus venosus)
i) Used for central venous access via the umbilical vein in neonates
ii) Ductus venosus closes in about 1 week (functionally closes in a
few hours after birth though)
b. Right side -
i. Right common cardinal vein & ACA --> SVC
1) Anastomosis btw anterior cardinal veins --> brachiocephalic vein
ii. Right umbilical vein --> obliterates

iii. Right vitelline vein --> IVC

Defect LV-EDP LV-Systolic Pressure Wedge Pressure

Mitral stenosis - - ⇈
Aortic stenosis ↑ ⇈ ↑
66.
Dilated cardiomyopathy ↑ ⇊ ↑
Restrictive cardiomyopathy ⇈ - ↑
Cardiac tamponade ↑ ↑

67. Anti arrhythmic ECG site of action:

a. QT prolongation - Phase 3 effect
i. Quinidine (Group 1A)
ii. Sotalol (Group 3)

b. PR prolongation - Phase 4 effect; no nodal effects

i. Beta blockers (Group 2)
ii. CCB
iii. Caused by slowing conduction velocity in AV bundle
1) Useful in atrial arrhythmias

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 68. Sildenafil + Nitrate = Solid hypotension
a. Sildenafil is a PDE5 inhibitor and leads to an increase in cGMP levels.
i. In fact any PDE inhibitor (milrinone even) will cause peripheral vasodialtion
b. Engorgement of the corpus cavernosa (upper two circles)

69. Angiotensin II - Gq
70. ADH:
a. V1 - Gq
b. V2 - Gs

71. NBTE - Marantic endocarditis

a. Sterile vegetations, non destructive on valve cusps; no inflammation
b. Associated with cancers
c. Caused by hypercoagulability
i. Mucinous adenocarcinomas (mucin --> procoagulant)
ii. Similar pathophysiology to Trousseaus phenomenon
72. Metastasis to the heart:
a. Pericardium
b. Myocardium

73. Patients with noncoronary atherosclerotic disease, diabetes, or chronic kidney disease are at
the same risk for MI / Stroke as patients with known heart disease. Coronary disease --> mcc of
death in diabetics.

74. Atrial fibrillation:

a. Common in patients with severe aortic stenosis, long standing hypertension,
hyperthyroidism
b. Excessive alcohol intake 'holiday heart syndrome"
c. Decreases the preload into the heart
d. ECG findings:
i. Absent P waves
ii. Varying R-R intervals; irregularly irregular rhythm
iii. Narrow QRS
iv. F waves (squiggles)
e.

75. Spironolactone inhibits action of aldosterone, and hence prevents cardiac remodeling and
fibrosis that way. Hence increases overall survival [RALES trial, significant reduction in
mortality in CHF III and IV; spironolactone + standard therapy]

76. Diseases causing myocardial fibrosis:

a. Dermatomyositis
b. Muscular dystrophy
c. Sarcoidosis
d. Scleroderma

77. CHF treatment - Spironolactone or epleronone (less toxic)

a. Spironolactone toxicities:
i. Gynaecomastia is a common side effect [structurally similar to steroids]
ii. Decreased libido
iii. Impotence
iv. Hyperkalemia

78. Cystic medial necrosis:

a. Myxomatous degeneration of the tunica media
i. Fragmentation of elastic tissue
ii. Replacement of elastic + muscular components by small cleft like spaces filled with
amorphous extracellular matrix
iii. Inhibition of lysyl oxidase
1) Oxidative deamination of Tropocollagen
2) Fucks up collagen and elastin
3) Can be inhibited by beta aminopropionitrile
b. Associated with:
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 b. Associated with:
i. Large dose of baclofen
ii. Marfans disease
iii. Beta aminoproionitirle - Angiolathyrism
1) Mimics marfans disease
c. Aortic dissections and aortic valve incompetence
d. Mitral valve prolapse (mid systolic click)
i. Increase in preload --> Moves it closer to S2
ii. Decrease in preload --> Moves it closer to S1

79. Mitral valve prolapse:

a. Most common cause of native valve bacterial endocarditis in the 15 - 60 age group

80. Small arteries / arterioles - CCB and alpha blockers

81. Precapillary sphincter -
a. Norepinephrine
b. Epinephrine
c. Histamine:
i. Dilates
ii. Low O2
iii. High CO2; decreased pH

82. Ventricular and outflow tract maximum pressures are almost equal

83. Cardiac Output + Venous Return curves

a. Anaphylaxis:
i. Venous and arteriolar dilation; increased permeability of mainly veins (thinner).
ii. Drop in venous return + increased cardiac contractility

b. Increase in TPR - reduces the slope of both Venous return and CO curves
i. Veins - decreases the amount of arterial blood entering veins; venous return
decreases
ii. Arteries - increases afterload, which decreases SV = Decreased CO.

c. Arteriovenous fistula
i. Acute - only decrease in TPR (since arterioles are bypassed)
ii. Chronic
1) Decreased TPR
2) Increased CO (due to sympathetic overdrive and renal fluid retention?)
3) Increased Psf and Venous return

84. AV fistula:
a. Congenital
b. Acquired -
i. Secondary to penetrating injury
ii. Dialysis
c. Pulsatile mass with a constant bruit

85. Antiarrhythmics:
a. Sodium channel blockade effect:
i. Ic > Ia > Ib
b. Class Ia
i. Moderate Na channel blockade effect
ii. Extend the AP duration
c. Class Ib
i. Very weak Na blockade
1) More selective for ischemia induced ventricular arrhythmias
ii. Associate and dissociate rapidly from Na channels
iii. Reduces AP
d. Class Ic
i. Most potent effect
ii. Strongest Na channel blockade
1) Can promote arrhythmias; speed on conduction slowed more than the ERP
iii. Slowest dissociation from the channels
iv. AP duration stays same

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 86. Plaque rupture can cause acute coronary syndrome
a. Plaque stability influenced by strength of fibrin cap
b. Macrophages in atheroma --> Release MMP
c. Increased inflammation can lead to MMP overdrive (metalloproteinase)
i. Predisposes to plaque rupture
ii. Can be reduced to some extent by statins
d. More lipid rich core --> Increased risk of rupture
e. Ostial location (at root of aorta) has nothing much to do with this

f. Slowly developing stenosis allows for collaterals to develop; hence no necrosis or

ischemia with almost total occlusion.

87. Hypoxia leads to decreased ATP synthesis

a. Decreased activity of membrane ion pumps
b. Intracellular increase in Na+ and Ca++
i. Increase in water attraction; hence cellular swelling
ii. Net solute gain
iii. Mitochondrial activation

88. Temporal arteritis

a. Granulomatous (tunica media) + fragmentation of internal elastic lamina
b. Segmental involvement
i. Biopsy may not always show inflammation
c. Patients older than 50
d. Inflammatory condition affects the wall of large vessels
e. Sudden monocular vision loss:
i. May be transient or permanent
ii. Painless
f. Headache:
i. Focal pain and tenderness (scalp tenderness while combing)
ii. Pain nodularity and thick to palpation over the temporal area
g. Craniofacial pain syndromes:
i. Pain during mastication, tongue pain (claudication)
h. Polymylagia rheumatica
i. Neck, torso, shoulder, and pelvic girdle pain and morning stiffness
ii. Fatigue, fever, weight loss
iii. Normal CK
i. Diagnosis: Increased ESR + Biopsy findings
i. Treat early to prevent vision loss, don’t wait for confirmation
j. Treatment = Corticosteroids

89. Takayasu arteritis

a. Medial granuloma formation, affects the arch of the aorta
b. Younger age group than Giant cell arteritis
i. Females < 40 (vs Giant cell arteritis > 60)
c. May also affect major branches
i. Coronaries
ii. Renal arteries
d. Reduced pulses in the upper extremities (pulseless disease)
e. Cold / numb fingers

90. Infective endocarditis:

a. Doesn’t usually affect the aortic valve because of the relatively higher blood flow
b. Janeway lesions
i. Macular
ii. Painless microemboli (from cardiac valve vegetations) to the palms and soles
iii. Subcutaneous hemorrhage
iv. Bacteria, neutrophils, necrotic tissue
c. Osler nodes
i. Painful papulopustules in the pulp of fingers and toes

91. Microscopic polyangitis (Leukocytoclastic vasculitis)

a. Necrotising vasculitis + Fibrinoid necrosis
b. Similar lesions to PAN; however in PAN, vessels are in all stages of infection
c. Affects small vessels
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 c. Affects small vessels

92. Internal thoracic artery and veins are between the trasversus thoracis and internal intercostal
muscle.

93. Pulmonary trunk may be pierced by penetrating injury to 2nd intercostal space at left sternal
border

94. IVC injury --> Stab to the back, just to the right of the vertebral bodies
95. Restrictive cardiomyopathy:
a. Sarcoidosis
b. Amyloidosis
c. Radiation damage
d. Hemochromatosis

96. Anthracyclines: Doxorubicin, Daunorubicin, epirubicin, idarubicin - Cause ROS generation -->
Dilated cardiomyopathy - Systolic failure
a. CHF Symptoms:
i. Dyspnea on exertion
ii. Orthopnea
iii. Peripheral edema
b. Presents many months after discontinuing drug
c. Swelling of sarcoplasmic reticulum
d. Loss of cardiomyocytes
e. Prevention:
i. Dexrazoxane - Fe chelating agent (decreases ROS formation)

97. Other causes of dilated cardiomyopathy (DCM); systolic dysfunction

a. Viral myocarditis
b. Alcohol toxicity
c. Diphtheria

98. Right ventricular overload will lead to widening of S2 split (increased ejection time)

99. Unilateral swelling of leg - vein / lymphatic occlusion

100. tPA is also used for acute clot lysis in PE and arterial thrombosis aside from MI

101. Fibrinolytics are DOC for post MI reperfusion; ST elevation

a. Act on recently formed fibrin plugs
b. tPA, reteplase, tenecteplase
c. They act only on bound fibrin; no systemic activation
d. Contraindications:
i. Hemorrhagic stroke
ii. Ischemic stroke history
iii. Internal bleeding
iv. Blood pressure > 180/110
v. Dissecting aneurysm
e. Reperfusion arrhythmias:
i. After restoration of blood flow after clot lysis in MI
ii. Benign arrhythmias, don’t predispose to mortality

102. Fibrinolytics are also used for pulmonary embolism, and arterial thrombosis

103. Polyarteritis nodosa (PAN)

a. Segmental, transmural, necrotising inflammation of medium sized arteries
i. Fibrinoid necrosis - eosinophilic deposits (immune complexes, complement,
proteins)
ii. All stages of acute/chronic inflammation (vs microscopic polyangitis)
b. Associated with HBV infection
c. Leads to focal aneurysms
i. Renal - hematuria
ii. GIT - bloody diarrhoea
iii. Skin -ischemic ulcer
iv. Testicle - Testicular pain
v. Spares pulmonary arteries
d. Symptoms:
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 d. Symptoms:
i. Fever
ii. Abdominal pain
iii. Peripheral neuropathy
iv. Weakness and weight loss

104. Tetrology of Fallot (TOF)

a. Keep in mind the SVR/PVR ratio (pulm vascular resistance)
i. PVR is a product of the pulmonary infundibular stenosis
b. Squatting increases systemic vascular resistance:
i. ↑ in afterload --> ↑ blood goes into pulmonary circulation; improving dyspnea
ii. Increases LV work load too

105. Differential cyanosis:

a. PDA (patent ductus arteriosus)
i. S2 split with inspiration
ii. Machine like murmur best heard left infraclavicular region
iii. Remember - ductus arteriosus is the derivative of the 6th aortic arch (left)
b. Cyanosis of lower extremities but not of the whole body
c. Reduced SpO2 in the distal aorta; spike in PaO2 in the pulmonary artery
d. Left to right shunt
i. Initially doesn’t cause hypoxemia
ii. Can progress to full blown Eisenmengers (late onsent cyanosis; total cyanosis)
iii. Frequent respiratory infections
e. Rx:
i. Indomethacin or ibuprofen (younger patients)
ii. Surgical ligation / percutaneous occlusion (older patients)

106. Acute rheumatic fever:

a. Antecedent pharyngitis; not caused by skin infection (strep)
b. Structural homology between antigenic determinants (epitopes) on GAS - M protein -
and human cardiac tissue (ARF), CNS (sydenham chorea), cutaneous tissues (rash etc)
c. B and T cells are activated and become autoreactive
d. Early treatment with penicillin to prevent

107. Coronary artery aneurysms - Kawasaki disease

a. More common in patients of Asian ethnicity
b. Medium sized artery vasculitis
c. Diagnosis:
i. Fever >5 days [must; remainder any 4]
ii. Periungual desquamation, Palmoplantar erythema
iii. Mucositis - strawberry tongue
iv. Cervical lymphadenopathy
v. Bilateral non-exudative conjunctivitis
vi. Edema + swelling
vii. Erythema / rash on extremities that spreads centripetally
d. Don’t confuse with scarlet fever (which also has strawberry tongue and rash; that’s
caused by strep, and predisposes to PSGN)

108. Scarlet fever:

a. GAS - pyrogenic exotoxin mediated
b. Associated with streptococcal pharyngitis
i. Incubation period: 1-5 days
ii. Erythematous + swollen pharynx (lymph nodes)
iii. Covered with gray-white exudates
iv. Strawberry tongue (vs Kawasaki disease which has a distinctive bilateral
conjunctival injection and absence of pharyngitis)
c. RASH appearance:
i. Scarlet spots (blotchy rash) on neck / armpits / groin
ii. Sandpaper like rash; spreads to trunk and becomes confluent
iii. Circumoral pallor (other disease - erythema infectiousum also has circumoral
pallor)
iv. Desquamation
1) Armpits
2) Groin
3) Tips of fingers and toes
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 3) Tips of fingers and toes
d. Complications
i. Acute rheumatic fever
ii. PSGN

109. Dihydropyridines - causes peripheral vasodilation, has little action on the heart - watch out for
reflex tachycardia

110. Verapamil and Diltiazem - Rate control for Atrial fibrillation (Slows AV conduction)
a. Constipation/nausea
b. Flushing
c. Hypotension

111. Second line drug for AF: Digoxin

112. Pulsus alterans:

a. Beat to beat variation in the magnitude of the pulse pressure; regular cardiac rhythm
b. Sign of LV dysfunction

113. Dicrotic pulse: Two peaks in the pulse (systole + diastole); extremely low systolic output

114. Hyperkinetic pulse: rapid ejection of a large stroke volume against decreased afterload [figure
this out later?]
a. PDA
b. AV fistula (dialysis one)

115. Statins for CVS risk

a. In patients with a normal HDL profile, use of statins to lower LDL is indicated for
preventing cardiovascular events
i. Raising HDL doesn’t improve CVS outcomes; Niacin is therefore useless
ii. LDL reduced by 20-25%; increased clearance by increased LDL receptor expression
1) Hence decreases circulating Apo B100 (its present on LDL and VLDL)

b. Indicated for secondary prevention in all patients of atherosclerotic cardiovascular

disease regardless of baseline lipid levels
c. Omega 3 fatty acids - slightly increases HDL, and slightly decreases TG; does nothing for
CVS side effects

116. Group IB antiarrhythmics - most selective to ischemic myocardial tissue

a. Because ischemic tissue:
i. Depolarised / rapidly depolarising
b. Lidocaine
c. Used to treat post MI Ventricular arrhythmias (DOC is amiodarone)

117. Group IA drugs - for areas of normal automaticity

118. Adenosine - PSVT; Digoxin - AF

a. Adenosine has a half life of 10s, acts instantly. Converts PSVT to normal rhythm.
b. Digoxin
i. prolongs AV nodal conduction (Vagal parasympathetics)
ii. Increases contractility
iii. QT interval shortening
c. Treat digoxin toxicity with Potassium replacement (only if accompanied by hypokalemia)
d. Digibind (Fab protein) also useful

119. Adenosine toxicities:

a. Flushing
b. Chest burning (bronchospasm)
c. Hypotension & high grade AV block

120. Verapamil - inhibits AV nodal conduction:

a. Acts from the interior side of the Ca channel
b. Useful for supraventricular arrhythmias
c. Can really screw you over if you have a ventricular arrhythmia
d. Side effects:
i. Constipation
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 i. Constipation
ii. Gingival hyperplasia

121. Rheumatic heart disease:

a. Listen to murmurs over the heart apex
i. Mitral valve regurgitation Initial lesion (First few decades) - [HOLOSYSTOLIC
MURMUR] - Be confident with sounds.
ii. Mitral stenosis (chronic) Later lesion (Middle age) - Due to fibrosis of the valve
leaflets
1) OPENING SNAP; right after S2 BEGINNING OF DIASTOLE
2) Diastolic rumble murmur

b. Congenital diseases, degenerative calcinosis both cause regurgitation not stenosis

c. Commissural fusion may be present
d. Thickening
e. Atrial enlargement --> Mural thromboses --> Embolic stroke

122. Infective endocarditis:

a. Destruction of leaflets rather than fibrosis
b. Mitral regurgitation
c. Can cause septic infarcts and strokes

123. Mitral regurgitation - increased regurgitant flow with increased afterload [logical, think about
it]. Hence arterial vasodilators and beta blockers can help (Reduces afterload), surgery
definitive treatment.

124. Congenital QT syndromes

a. (Jervell and Lange-Nielsen) - QT prolongation and neurosensory deafness
i. AR
b. Romano Ward syndrome - AD, no deafness
c. Delayed rectifier (Ik) current:
i. Increased risk of Torsades de pointes and sudden cardiac death

125. Cardiac output/Blood flow for left and right heart = same (both rest and exercise)

126. Pericytes around capillaries regulate the blood flow into that vascular bed

127. Myocardial infiltration:

a. Acute rheumatic fever:
i. Aschoff bodies (interstitial granulomas)
ii. Mononuclear infiltrate + scattered multinucleated giant cells
iii. Anitschkow cells abundant cytoplasm, round to ovoid nucleus, slender chromatin
ribbons
1) Coalesce into Aschoff giant cells
b. Viral myocarditis:
i. Interstitial Lymphocytic infiltrate
c. Hypersensitivity myocarditis:
i. Interstitial Eosinophilic + mononuclear cells
ii. Drug induced or something
d. Trypanosoma cruzi:
i. Intracellular T. cruzi pathogen
ii. Distention of individual myofibres
e. Diptheria myocarditis:
i. Interstitial pleomorphic macrophage involvement
ii. No Aschoff type granulomas

128. Trachea is a good landmark in CT images:

a. Black (air)
b. Anteriorly - Great vessels
c. Posteriorly - Esophagus (no visible lumen)

129. Monckebergs medial calcific sclerosis - calcific deposits in tunica media muscular arteries;
age >50; asymptomatic because no luminal narrowing

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 130. Cyanotic heart diseases (5 T's):
a. TOF
b. Tricuspid atresia
c. Transpositon of great vessels
d. Truncus arteriosus
e. Total anomalous pulmonary venous return

f. PDA - isn't really cyanotic; may cause differential cyanosis (later in life)

131. Post MI sudden cardiac death (within an hour of MI):

a. Caused by ventricular arrhythmia
i. Ischemic tissue is electrically unstable
b. AF isn't really fatal
c. Ventricular failure:
i. Usually develops gradually as the infarct extends
ii. Death during hospital stay

132. Ventricular mural thrombosis:

a. 48 hours post MI
b. >2 weeks post MI; true ventricular aneurysm (increases risk of mural thrombosis)

133. Bifurcation of the carotid:

a. C4, inferior to hyoid bone
b. Site contains chemoreceptors

134. Tricyclic antidepressants (TCA) and arrhythmia:

a. Quinidine like effects on cardiac conduction; inhibition of fast sodium channels
b. QRS and QT prolongation
c. TREAT WITH NaHCO3
i. Why? No fucking idea

135. SVC syndrome -bilateral edema of body and engorgement of veins of face; mcc is malginancy
136. Jugular venous pulse (jvp)
a Right atrial contraction Prominent - RVH, Tricuspid
stenosis, pulmonary
hypertension
Absent - AF
c Bulging of tricuspid valve during RV
contraction
a.
x Atrial relaxation
v Gushing in of blood into atria during late
systole, early diastole
y Passive emptying of RA after tricuspid opens Deep in pericarditis
in diastole
b. Giant c-v wave: No x descent; Tricuspid regurgitation

137. Aortic arches

First Meckels cartilage Maxillary artery
Second Reicherts cartilage Stapedial artery, hyoid artery maybe?
Third Common carotid + internal carotid artery
a.
Fourth Superior laryngeal nerve (X) Left: Aortic arch; Right: Proximal subclavian
Fifth
Sixth Recurrent laryngeal nerve (X) Pulmonary arteries, ductus arteriosis

138. Nitrate bioavailability:

a. Nitroglycerin (high first pass; sublingual)
b. Isosorbide dinitrate (first pass glucuronidation)
c. Isosorbide mononitrate (active component of Isosorbide dinitrate; 100% bioaval PO)

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 d. Amyl nitrite - inhaled, not used anymore
e. Sodium nitroprusside - iv only; hypertensive emergency, causes cyanide toxicity

139. Carotid massage and valsalva:

a. Increases pressure; leading to increased baroreceptor firing
b. This leads to increase in parasympathetic outflow
i. Prolongs the AV node refractory period
ii. Hence useful in PSVT (supraventricular tachycardia)
iii. Decreases heart rate and cardiac output
c. PSVT pharmacological treatment - Adenosine
d. Remember:
i. Carotid baroreceptors (carotid sinus; above the bifurcation) - CN IX
(Glossopharyngeal)
ii. Aortic baroreceptors - CN X (Vagus)
iii. Both terminate in the NTS

140. Baroreceptor firing decreases in low pressure states

a. Increase in heart rate and sympathetic outflow

141. CABG
a. Single LAD - Internal mammary artery
b. Multiple coronary arteries - Great saphenous veins
i. Accessed at the medial leg, or at it's point of termination in the femoral triangle of
the upper thigh

142. Popliteal artery aneurysms are common

143. Popliteal artery is more likely to be damaged than the tibial nerve or whatever in a posterior
tibial displacement or any other traction force.
a. The artery is deep in the popliteal fossa
b. The artery is tightly fixed proximal and distal to the popliteal fossa by: adductor magnus
and the soleus muscles.
c. Tibial nerve - doesn’t pass through the adductor magnus (vs artery)

144. Cocaine can precipitate angina and MI by causing reuptake inhibition of NE

a. CVS stimulation
b. CNS stimulation
c. Mydriasis

145. Adenosine and NO - local autoregulation of coronary blood flow

a. Both are vasodilators
b. Acts on A1 receptors on cardiac cells
c. Causes a transient conduction delay through AV node; used for PSVT termination

146. Nitric oxide (NO):

a. Synthesised by eNOS from Arginine
b. Released in response to neurotransmitters (Ach and NE)
i. Coronaries
ii. Large arteries
iii. Pre arteriolar vessels
c. Released in response to pulsatile stretch and flow shear stress near coronaries
d. cGMP --> MLC(PO4) phosphatase mechanism

147. Wide fixed splitting of S2

a. ASD
b. No murmur as such, but may be associated with pulmonary ejection murmur, TR and PR
c. Left to right shunt between LA and RA
i. Won't lead to cyanosis (vs right to left)
ii. This increases the pulmonary blood flow; can cause pulmonary artery medial
hypertrophy
1) Chronic pulmonary hypertension --> Permanent pulmonary vascular sclerosis
2) Concentric laminar intimal fibrosis, thickening of endothelium and smooth
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 2) Concentric laminar intimal fibrosis, thickening of endothelium and smooth
muscle too
iii. Pulmonary resistance > Systemic vascular resistance
iv. Leads to Eisenmenger syndrome
1) Heart wont tolerate ASD repair at this stage because the pressures have
inverted.
2) Mucosal cyanosis + finger clubbing
d. Right atrium also does enlarge, but it is not irreversible and can revert to normal once
corrected.
e. PaO2 -->
f. How to prevent Eisenmenger?
i. Close the ASD surgically

148. When analysing murmurs:

a. First - Systolic or diastolic
b. Second - How does it change with respiration

149. Gallop heart sounds:

Normal Abnormal
Third Ventricular gallop; Kids Age > 40
(S3) after S2 Young adults Heart failure (Dilated)
Rapid filling of Pregnancy
ventricles High output (anemias)
Restrictive cardiomyopathy

Fourth Atrial gallop; right Healthy older adults Concentric ventricular

a. (S4) after S3, but before hypertrophy (long standing
S1 hypertension)

Acute MI
Reduced ventricular
compliance:
- Aortic stenosis
- Hypertensive heart disease
- HOCM

150. Long standing hypertension; hypertensive heart disease:

a. Left ventricular hypertrophy (LVH)
i. S4 heart sound; best heard with the bell of the steth in the left lateral decubitus
position
ii. Increases with increase in preload (expiration; also closer to chest wall)
iii. Diastolic dysfunction
1) Increased LVEDP (to compensate for decreased compliance)
2) Normal EDV (compensated by above)
3) Normal EF
b. Decompensation
i. Appearance of pulmonary edema, dyspnea
c. Calcifications of aortic and mitral valves
i. Endothelial and fibroblast death due to chronic hemodynamic stress or
atherosclerosis
ii. Release of degradation products into valve interstitium--> Calcification of leaflets
and annulus
iii. Progression:
1) Aortic sclerosis
2) Calcific aortic stenosis

151. Calcific aortic stenosis:

a. Most common cause of aortic stenosis in people >65 years of age
b. Puslus parvus et tardus
c. Crescendo-decrescendo systolic murmur

152. Hypokalemia
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 152. Hypokalemia
a. ECG findings:
i. ST depression
ii. T wave flattening
iii. Prominent U waves
b. Premature atrial / ventricular contractions
c. VT / VF (profound hypokalemia)

153. Carvedilol (beta blocker, with alpha blocker) - Improves all cause mortality in CHF

154. False aneurysm

a. Blood collects in a connective tissue sac outside the vessel tunica
b. True aneurysm - all 3 layers out pouch
c. Dissection - blood between the tunica media and tunica intima

155. Lutembacher syndrome

a. ASD + MV obstruction with continuous murmur

156. Alpha agonism --> increases sytolic and diastolic bp; decreased renal and splanchnic blood flow
157. Norepinephrine may be useful in shock

158. Aortic regurgitation due to tertiary syphilis

a. Decrescendo murmur
b. FTA-ABS [+]
c. Brassy cough - left recurrent laryngeal nerve stretched by the dilated aorta
d. Endarteritis and obliteration of the vasa vasorum
i. Ischemia and weakening of the adventitia
ii. Intense plasma cell infiltrate
iii. Aneurysmal dilation of the aortic ring
1) MR

159. Measuring cardiac output

a. CO = O2 consumption / arteriovenous O2 difference
b. CO = 135 x BSA / [(13 x Hb) x (SaO2 - SvO2)]

160. P/V graph for atria:

a. Check for compliance of the atria
b. Large compliance:
i. Chronic mitral regurg that has developed over time
1) Myxomatous degeneration of MV
2) MVP
ii. Leading to adaptive dilation of the LA
1) Atrial fibrillation
2) Atrial mural thrombosis
c. Small (near normal) compliance:
i. Acute MR
1) Spontaneous rupture of chordae
2) Infective endocarditis
3) Chordal rupture
4) Ischemia / rupture of papillary muscle
5) Prosthetic valve failure
ii. Can lead to acute pulmonary edema because pressures are high in the atria
iii. More prone to pulmonary hypertension

161. Pulmonary artery hypertension leads to RHF, (elevated RH pressures) which can lead to
coronary sinus dilation. Coronary sinus dilation is not a normal finding, and is dilated by any
factor that causes atrial dilation

162. Coronary artery disease --> reduced drainage into coronary sinus

163. Amiodarone:
a. Class III antiarrhythmic
b. Prolongs QT; but has a much lower likelihood of causing Torsades de pointes
i. Less QT dispersion, whatever the hell that means
c. Drug of choice for post MI Ventricular fibrillation
d. Toxicity:
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 d. Toxicity:
i. Blue gray discoloration of skin
ii. Photosensitivity
iii. Pulmonary fibrosis
iv. Thyroid dysfunction

164. Procainamide - increased risk of torsades (QT prolongation; IA)

a. 283pg FA for more
165. Infective endocarditis:
a. Valvular scarring and damage is a risk factor for infective endocarditis
b. Fibrin and platelet deposition at site of bacterial colonization --> vegetations

166. Cocaine
a. Reuptake inhibitor
i. Hypertension
ii. Tachycardia
iii. Mydriasis
iv. CNS activation
b. Vasoconstrictor
i. MI, Coronary artery vasospasm
ii. Intranasal use --> Mucosal atrophy, nasal septal perforation

167. Heart blocks

a. Complete 3rd degree heart block:
i. SA node --> Atria
ii. AV node --> Fires the ventricles; QRS is narrow
b. The P wave and QRS waves are totally out of sync
c. QRS will be prolonged and wide when:
i. Impulses are generated below the AV node
ii. Purkinje system, ventricles etc
d. Mobitz type II and 3rd degree heart blocks may be the result of transmural septal
ischemia

168. Causes of PDA

a. Prematurity
b. Patent ductus arteriosis
c. Congenital rubella
d. Turners syndrome with bicuspid aortic valve

169. Cushings syndrome and SLE - Increase the risk of coronary artery disease
170. Atropine - treats bradycardia

171. RCA - gives off the posterior descending artery in 90% of the population; 10% LCX
a. Right dominant circulation
b. AVF, II, III - ST elevations + Sinus node dysfunction (bradycardia) = RCA thrombosis
i. Rx Bradycardia:
1) Atropine (inhibits Vagal influence)
a) Toxicities - Can precipitate acute angle glaucoma in pts with shallow
anterior chambers

172. Anticholinergic drugs - reduce pain & prevents adhesions of iridocyclitis (uveitis)
173. Coronaries:
a. LCX - runs between the left atrium and ventricle (AV groove, kinda close to the rear of
the heart)
b. LAD - runs in the anterior interventricular groove
c. Remember the heart apex is tilted

174. Capillary hemangioma (juvenile strawberry hemangioma)

a. Very common benign congenital vascular tumour
b. Thin walled loose aggregate of capillaries
c. May be multiple;
i. Skin, subcutaneous tissue, oral mucous membranes, lips
ii. Compressible plaques; dusky if deeper
iii. Initially increase in size, then regress
d. Most begin to fade by 1-3 years of age and then fade completely by age 7

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 175. Cherry hemangioma
a. Benign vascular proliferation in adults; present in the papillary dermis
b. Don’t regress

176. Thromboangiitis obliterans (Buerger's disease)

a. Heavy smokers, young age of onset
b. Nicotine antigens, smoke antigens whatever

177. Urokinase
a. Treatment for myocardial infarction and pulmonary embolism
b. Plasminogen --> Plasmin; Plasmin degrades Fibrin into its degradation products

178. Concentric hypertrophy of LV:

a. Increased afterload
b. Chronic hypertensive heart disease
c. Aortic stenosis
d. High voltage ECG

179. Restrictive cardiomyopathy --> mcc of death is CHF that develops due to it
a. Decreased ventricular compliance (dV/dP)
180. Eccentric hypertrophy of LV in Mitral regurgitation
a. Because increased regurgitant flow during systole = amount of blood returning to the LV
during diastole
b. Volume overload

181. Hypertrophic cardiomyopathy - important cause of VF in individuals <30 and mcc of sudden
cardiac death in young athletes.
a. Massive cardiac hypertrophy
b. Septal involvement
c. Normal coronaries

182. Friedreich ataxia - hypertrophic cardiomyopathy

183. Alpha 1 selective agonists - Don’t cause much reflex tachycardia (wha?)
184. Adult type aortic coarctation:
a. Post-ductal coarctation
b. Hypertension in head + upper extremities
i. LVF
ii. Berry aneurysms - rupture due to htn
iii. Aortic aneurysms
c. Hypoperfusion in lower extremities
i. Low exercise tolerance / muscle weakness
d. Large palpable intercostal vessels
i. Sign of development of collateral circulation
ii. Notching of ribs

185. Sydenham chorea

a. Restlessness and purposeless movements; 3 mo post sore throat
b. Mcc acquired chorea in childhood
i. Autoimmune reaction involving anti-streptococcal antibodies to basal ganglia
c. Hyperkinetic defect

186. Maintaining cardiac output in aortic regurgitation

a. Increased EDV due to regurgitant blood - Increases Preload
i. Heart rate increases transiently, then comes back to normal as heart adapts to
volume overload
ii. Increased ventricular stroke volume
b. Afterload is already high; medical stabilization of acute AR might need to be reduced
with vasodilators + inotrope (to ensure CO is maintained)
i. Vasodilation - Decreases afterload; hence improves stroke volume
c. Eccentric hypertrophy

187. Place filter in the IVC in patients with DVT treatment complications (GIT bleeds)
a. Renal veins join IVC at L1/L2
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 a. Renal veins join IVC at L1/L2
b. Common iliac veins merge to become IVC at L4

188. Ticlopidine and clopidogrel

a. Useful in treating and preventing ischemic stroke, acute coronary syndrome, peripheral
vascular disease
i. Very useful in patients allergic to aspirin
b. ADP receptor blockers (prevents platelet activation/aggregation/binding)
c. Ticlopidine
i. Neutropenia (1% of patients)
ii. ITP
iii. Regularly measure complete blood counts

189. Heparin, Abciximab and other GpIIb/IIIa antagonists --> Thrombocytopenia

a. Abciximab given during angioplasty in patients with acute coronary syndrome
190. Amlodipine - DHP Calcium channel blocker; tox - peripheral edema and reflex tachycardia

191. SERCA channels in the cardiac musculature:

a. Calcium channels in the cardiac SER

192. Splinter hemorrhages:

a. Subungual flame shaped embolic hemorrhages
b. Sign of infective endocarditis

193. Pathogenesis of left heart failure causing right heart failure:

a. Increased pressure in systemic circulation (hypertension) --> Increased pressure in the LA
and pulmonary veins.
b. Pulmonary venous congestion --> endothelial damage; which leads to decreased
production of NO and increased endothelin.
c. Vascular remodeling:
i. Smooth muscle cell hypertrophy (medial hypertrophy)
ii. Collagen and elastase deposition (intimal thickening and fibrosis)
iii. Not as severe as idiopathic pulmonary hypertension
1) Partially reversible if LV dysfunction / MV is repaired
d. Loss of compliance
e. Remember: LHF causes RHF; via pulmonary venous congestion
f. Associate this entire point with MS; ie MS can lead to all of this

194. Idiopathic pulmonary artery hypertension

a. Endothelial dysfunction (idiopathic)
i. Even in other forms of pulmonary hypertension, the first event is pulmonary
endothelial dysfunction - embolus, cardiac defects, collagen vascular disease,
ii. Progressive proliferation of endothelial cells, smooth muscle cells
iii. Concentric laminar intimal fibrosis
b. Younger age group (30s)
c. Narrowing of pulmonary vascular bed; resultant RVH (Rt axis deviation too)
i. Further increase in pulm. artery pressure [afterload]
ii. Further exacerbation of hypertrophy
d. Clinical features:
i. Shortness of breath, dyspnea
ii. Angina
iii. Peripheral edema
iv. Increased S2 (P2 component)
v. Systolic ejection murmur ?
vi. Right ventricular heave
1) Parasternal heave - basically a precordial impulse that is palpable [physical
examination finding]
vii. Death within a few years of decompensation

195. Pulm artery hypertension causes:

a. Hereditary
b. LHF
c. Chronic hypoxia (COPD, obstructive sleep apnea)
d. Chronic thromboembolism [decreases parallel circulation, increases resistance]
e. HIV

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 196. Hypoxia induced pulmonary artery vasoconstriction seen in COPD
197. Inflammatory vascular disease - Wegener's granulomatosis, Churg strauss (eosinophilic
granulomatosis with polyangitis)

198. Cheyne-stokes breathing:

a. Cyclical breahting + apnea due to overcompensation [feedback gain]
b. Seen in: Congestive heart failure and advanced neurological disease (respiratory center
Hypoperfusion)

199. Management of acute hypertensive emergency

a. Intravenous management to bring down bp over minutes/hours to minimize target
organ damage.
b. Fenoldopam:
i. Selective D1 agonist; no action on alpha or beta receptors
ii. Reduces systemic vascular resistance (vasodilation)
iii. Increases renal perfusion and increases sodium and water excretion
1) Useful in patients with hypertensive emergencies + renal insufficiency

c. Diazoxide and Hydralazine

i. Not safe for aortic dissection + hypertensive emergency
ii. Cause significant reflex tachycardia
d. Sodium nitroprusside
i. Quick + short duration of action
ii. Can precipitate cyanide toxicity
e. Esmolol
i. Immediate onset of action
ii. Short acting beta 1 receptor antagonist
1) Decreases heart rate + CO
2) Decreases hypertension
f. Nicardipine
i. Causes some tachycardia
ii. Longer half life than other drugs

200. Orthopnea
a. Supine dyspnea that is relieved by sitting up; specific sign of LHF
b. LHF progresses to:
i. Pulmonary interstitial edema, widening of alveolar septa
ii. Intra alveolar accumulation

201. Cardiac asthma - exercise induced wheezing in LHF. Exercise = increased venous return to the
heart, but failing heart cant increase CO appropriately. Hence pulmonary pressures rise.
a. Not a specific sign
b. Seen in COPD and Asthma

202. Aortic stenosis

a. Congenital bicuspid valve --> calcification in 50s [you may get endocarditis, but that’s
rare]
b. Calcification of normal valve
i. Occurs at a greater age > 65
c. Rheumatic heart disease

203. Chronic heavy alcohol intake - prolonged QT

204. B1 selective beta blockers - MAAE (Metoprolol, Acetabulol, Atenolol, Esmolol)

205. Non selective beta blockers + ACE inhibitors --> Hyperkalemia

206. Isoproterenol - b2 agonism can cause increased blood flow in skeletal muscles, renal and
mesenteric vascular beds. Not useful for increasing perfusion in the skin though.

207. Diagnosis of congenital heart diseases - ECHO

208. Adjust dose of Digoxin in the elderly, since renal function decreases with age and can lead to
digoxin toxicity.
a. Only a 1/3 of the drug is actually protein bound (so protein binding isn't really a big deal)
b. Not accompanied by increase in creatinine; since muscle mass also falls with age
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 b. Not accompanied by increase in creatinine; since muscle mass also falls with age
c. Muscle mass - lean body weight (important for dosing calculations of digoxin; just not as
important as renal function)
d. Symptoms:
i. Changes in colour vision [neurological sign]
ii. Fatigue and weakness [hyperkalemia]
iii. Delirium
iv. Diarrhoea, nausea, vomiting
v. Arrhythmias

209. Q = P x R ; Flow = Pressure x Resistance

210. Isoproterenol - increases cardiac contractility (b1) and decreases peripheral venous resistance
(b2) at low doses; [understand the axes of the graph and then figure out if effect increasing or
decreasing with x]

211. Labetalol (alpha + beta blocker)

a. Vasoconstriction (increased PVR)
b. Decrease in contractility (b1 blockade)

212. Intermittent claudication (muscle pain with exercise that remits with rest)
a. Result of atherosclerosis of large arteries, fixed stenotic atheromatous plaques that
bulge into the arterial lumen
i. Blood flow to muscle cant increase during exercise
b. Pain relieved by resting; exacerbated by minimal exercise (ischemic muscle pain)
c. Thigh claudication:
i. Ipsilateral external iliac artery or common femoral artery
ii. Common femoral and profunda femoris artery

213. Isolated systolic hypertension

a. Common form of hypertension in the elderly
b. First line in non-diabetics and non CHF patients
i. Thiazide diuretics
ii. DHP Calcium channel blockers
c. In diabetics - Use ACE inhibitors; anti proteinuric effect.
i. ACE inhibitors don’t cause pedal edema, it may however cause angioedema and
hyperkalemia
ii. ACE inhibitors are useful in CHF as it inhibits the AT-II mediated myocardial
hypertrophy and remodeling.

214. Amlodipine side effects -Flushing & Bilateral ankle swelling

215. Familial hypercholesterolemia

a. AD
b. LDL receptor defect

216. Familial dysbetalipoproteinemia (Type III)

a. Apo E3/E4 deficiency
b. Reduced chylomicron remnant, and VLDL uptake
c. Symptoms:
i. Palmar xanthomas
ii. Premature coronary and peripheral vascular disease

217. Chylomicrons - synthesized on the RER and the Golgi apparatus of the small intestinal
enterocytes with Apo B48.
218. LCAT - Esterifies cholesterol

219. Nitrates (sublingually administered)

a. Nitroglycerin
i. Stimulate guanylyl cyclase to convert GTP into cGMP
ii. Decreased MLCK activity, increased MLC-PO4 phosphatase activity
b. Main mechanism of relief during angina:
i. Venodilation --> Decreased cardiac preload
1) Reduced ESV (since less volume enters ventricle due to decreased EDV and
compensatory increase in contractility)
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Cardiology Page 23
 compensatory increase in contractility)
2) Compensatory increase in heart rate
ii. Hence reduces myocardial oxygen demand (reduced stroke work etc)
c. High doses can lead to reduced coronary flow due to a decrease in systemic arteriolar
vasodilation.
i. Main arteriolar dilators are not however nitrates; they are ACE inhibs, ARB, CCBs
d. Long acting nitrates can cause tolerance development
i. Prevented by off-dosage during the night time (cardiac work load is the least when
sleeping)

220. Remember diastole --> Coronary vessel perfusion. Increase in diastolic pressure increases
afterload --> Increases cardiac work and increases O2 demand

221. Dobutamine increases myocardial oxygen demand (increases B1 mediated contraction + heart
rate)
a. Hard question that tested on specific knowledge of stuff
b. Dobutamine can also increase conduction velocity; causes arrhythmias

222. During systole: subendocardial myocardium is the least perfused because:

a. Coronary arteries compressed by contracting myocardium
b. Open aortic valve partially obstructs coronary blood flow

223. Coronary circulation is maximum during diastole, also in stress, the increase in adenosine
vasodilates the coronaries

224. Coronary vessel dilators:

a. Dipyrimadole
b. Causes coronary steal syndrome
i. Cardiac vessels are already maximally dilated in an attempt to perfuse ischemic
area of the heart
ii. Dipyrimadole will instead cause dilation of surrounding vessels, further depleting
the ischemia part of its blood supply.

225. Best indicator for mitral stenosis severity

a. Length of time between S2 and Opening Snap
b. Byproduct of increasing LA pressures
i. Increased LA pressures --> mitral valve will open more forcefully
c. Standard for MS diagnosis:
i. Mean transvalvular pressure gradients via 2D Doppler Echo
d. Dilation of the LA predisposes to thrombi, which can cause a stroke
e. Right sided S3 and S4 develops as LHF progresses to cause RHF. Very severe state.
i. Left sided S3 and S4 doesn’t happen because there is impaired left ventricular
filling because of MS.

f. LVEDP is normal or reduced in severe MS; if LVEDP is increased, it is a sign of a

dysfunctional aortic valve along with that --> Sign of Rheumatic heart disease

226. LDL receptors functions by receptor mediated endocytosis; (clathrin pits yada yada)
227. Accentuated P2 - Pulmonary hypertension; Accentuated S2 - Systemic hypertension

228. Peripheral artery disease

a. Thin shiny skin, hair loss, nail changes
b. Calf claudication (with pain during rest)
c. Prolonged venous filling time
d. Associated with Diabetes (especially if presenting with a foot ulcer / infection)

229. Aortic aneurysm:

a. Most likely predisposing cause is atherosclerosis, atheromas can progressively weaken
the underlying intima.
b. Other less common causes:
i. Medial degeneration
ii. Vasa vasorum obliteration (syphilis)
c. Fatty streaks --> Foam cells insudate into the intima as the endothelium becomes more
leaky
d. Diabetes can lead to atherosclerosis so keep that shit in mind
e. Clinical features:
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 e. Clinical features:
i. Vague abdominal discomfort (vs tearing chest/back pain of a dissection)
ii. Palpable pulsatile mass (vs dissection since hematoma may form)
f. Dx by USG

230. Aortic dissection:

a. Most important predisposing condition - hypertension
i. Leads to intimal tears
ii. Intimal tears then get filled with blood that collects as an intramural hematoma
b. Other risk factors:
i. Cystic medial degeneration

231. Remember that cardiac hypertrophy is because of increased mRNA synthesis for myosin/actin
(increased sarcomeres), more mitochondria etc. No increase in mitoses since there is no
hyperplasia

232. Systolic failure:

a. Impaired contractility
b. Increased LVEDP and LVEDV to compensate for loss of contractility

233. Beta blockers worsen Raynauds

234. Muscarinic receptors are present on the endothelium; on stimulation trigger the release of NO
(EDRF) --> Smooth muscle relaxation.

235. Cholinergic action on the heart:

a. M2 muscarinic receptors
b. Decreases contractility and conduction velocity
i. More in atria than ventricles (since ventricles are more richly supplied with
adrenergic receptors)

236. Milrinone - increases cardiac contractility by preventing the degradation of cAMP within the
myocytes [PDE-3 inhibitor]
a. Increased cAMP --> Calcium conductance increases

237. Wolf-Parkinson-White syndrome (WPW)

a. Causes sudden cardiac death
b. Accessory AV impulse conduction pathways anatomically distinct from the AV node

238. RVH - Either a result of lung disease, or primary pulmonary hypertension

239. ACE inhibitor therapy - causes characteristic dry cough [you know why]
a. ARBs don’t inhibit bradykinin degradation, hence don’t cause dry coughs

240. Atherosclerosis, neointimal hyperplasia, aneurysmal disease - shear stresses induced by

turbulent blood flow has something to do with these.

241. Fatty streaks are present in kids, may not always progress to atherosclerosis. But they will be
made of foam cells.

242. DCM causes

a. Idiopathic
b. Cardiotoxic substances (alcohol)
c. Peripartum state
d. Viral myocarditis
i. Lots of inflammatory interstitial infiltrate
e. Mitochondrial / cytoskeletal defects

243. Aortic regurgitation

a. Large pulse pressure (high systolic, low diastolic)
i. Waterhammer pulse
b. Head bobbing with carotid pulsations (de Musset); transfer of momentum from the large
LVSV
c. Intensity of murmur is highest when the pressure gradient between the aorta and LV is
maximum; (ie as soon as the aortic valve is supposed to close)
i. High pitched blowing decrescendo murmur
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 i. High pitched blowing decrescendo murmur
ii. Holodiastolic [best heard with the patient leaning forward @ left sternal border]

244. Cardiac pressure / volume curves

a. Increase in afterload:
i. Increases the peak of the curve at the top
ii. Decreases stroke volume

245. IV drug abusers

a. Right sided Valvular disease is common
i. Tricuspid regurgitation
1) Can cause RHF
2) Jugular venous distention, pulsatile hepatomegaly
3) Hepatojugular reflex, edema
ii. Murmur intensifies on inspiration
iii. Left lower sternal border
246. Mycotic aneurysm is rarely associated with fungal infection

247. Mitochondrial vacuolization is a sign of irreversible injury (permanent inability to generate

further ATP)
a. Simple mitochondrial swelling may still be reversible
b. Polysomal disaggregation (reversible)
c. Clumping + disaggregation of granular/fibrillar elements (reversible)

248. Cardiac tamponade

a. Key finding is an increased jugular venous distention (JVD)
b. Blood (trauma, dissection); acute
c. Puslus paradoxus
d. Viral pericarditis (after a respiratory infection) - acute
i. Serous pericardial effusion --> Tamponade
ii. Fibrinous pericarditis --> Pericardial friction rub
iii. Constrictive pericarditis takes years to happen (not acute); kussmaul's [+] and
Pericardial knock [+]
e. JVD + Hypotension + Muffled heart sounds = Beck's triad
i. Tachycardia too (similar picture in tension pneumothorax)
f. Pain over the trapezius ridge

249. ATP depletion in the myocytes, around the contractile elements occurs within 60s of ischemia;
leads to cessation of contractility.
a. Total ATP levels stay normal for the first few seconds
i. ATP --> AMP --> Adenosine (vasodilator)
b. If ischemia is reversed within 30 mins, the contractility impairment is reversed after
prolonged 'stunning'

250. Carcinoid heart disease:

a. Fibrosis of right heart valves; since Serotonin is inactivated distally by pulmonary
endothelial MAO
i. Tricuspid regurgitation
ii. Pulmonary stenosis
b. May evolve to restrictive cardiomyopathy

251. Calcium binding sarcoplasmic reticulum protein

a. Predisposes to ARVC (arrhythmogenic right ventricular cardiomyopathy)

252. Fibrates: Gemfibrozil

a. First line for hypertriglyceridemia
b. Acts via PPAR-alpha:
i. Upregulates capillary lipoprotein lipase
c. May supplement with omega-3-fatty acids (fish oil) which helps control triglycerides

253. Bile acid binding resins (cholestyramine) useful for treatment of cholesterol; interferes with
bile acid circulation and increases cholesterol excretion
254. Ezetimibe + statin = hepatotoxic
255. Antihyperlipidemics max effect:
Statins Decrease LDL Reduces atherosclerotic heart disease

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Cardiology Page 26
 a. Fibrates Decrease TG
Niacin Increase HDL

256. Cyanotic toe discoloration + renal failure after invasive vascular procedure
a. Atheroembolic disease of renal arteries
b. Cholesterol debris gets pushed from larger arteries into the smaller ones --> Ischemia of
the organs and tissues.
c. Other sites:
i. Livedo reticularis
ii. Cholesterol emboli on retinal examination
iii. Skin infarcts

257. Hibernating myocardium

a. Repetitive ischemia, or persistent hypoperfusion
b. Metabolism is reduced, but sufficient ATP is present to prevent contracture
i. Increased TNF and NOS (inhibitors of contraction)
c. REVERSED BY:
i. Revascularization with CABG or a balloon angioplasty
ii. Basically this is the opposite of reperfusion injury (heart recovers in hibernation,
after revascularisation)

258. Ischemic preconditioning - development of resistance to infarctions due to prior repetitive

non-lethal ischemia.

259. Ventricular remodeling - chronic change in mass, volume, shape & myocyte composition of the
heart. Usually adjacent to the ischemic dysfunctional myocardium.

260. DVT risk is high in patients who are undergoing hip/knee replacements and are non-
ambulatory:
a. Heparins (bind to ATIII & Xa)

261. Patent foramen ovale - is normal variant of human anatomy.

262. Fenestrated membranous interventricular septum - ABNORMAL

263. Ivabradine - slows heart rate by blocking sodium channels from the cytoplasmic side, prolongs
the Na+ funny current.
a. No effect on contractility
b. Decreases heart rate
c. Rx for HF with reduced ejection fraction

264. Coronary sinus blood - most deoxygenated blood in the body. Myocardial oxygen extraction
(75 - 90%) is the highest in the body.
a. Mixes with slightly less deoxy blood from the rest of the body at the RA before entering
the PA.

265. Pacemaker wires (3 leads): Enter the SVC

a. RA
b. RV
c. RA --> Coronary sinus --> lateral venous tributaries (for pacing the LV)

266. Unstable anginas - don’t get better with rest

267. Prinzmetal angina - ST elevations on ECG (transient transmural); Rx: CCB or nitroglycerin

268. No LM signs of coagulative necrosis MI before 4 hours

269. Increased sympathetic tone - increases both SBP and DBP

270. Minoxidil/Hydralazine - Edema and reflex tachycardia

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