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1


wide splitting


exaggeration of normal split: split on expiration, and incr on inhalation. 2/2 delay in RV emptying (pulmonic stenosis, RBBB)

2


JVP


v wave = slow incr 2/2 atrial filling against closed Valve
y descent = blood flow from atrium to ventricle after opened valve
a wave = Atrial kick
c wave = RV Contraction and bulging of TV
x descent = atrial relaxation and downward displacement of TV during ventricular contraction

3

CO

SV*HR = (rate of O2 consumption)/ (arterial O2 - venous O2)

4

Ohm’s law

MAP = CO*TPR

5

MAP


⅔ diastolic pressure + ⅓ systolic pressure

6

fixed split

pulmonic closure delayed regardless of breathing
2/2 ASD

7

paradoxical split


delayed A2, so split on inspiration. on expiration, P2 comes later and no longer split
2/2 delayed LV emptying (aortic stenosis, LBBB)

8

cardiac AP vs skeletal AP

1.plateau (from calcium influx). Contraction of myocyte is triggered by this influx of Ca
2.nodal cells depolarize spontaneously due to funny current (slow, inward Na/K mixed current)
3. Cardiac myocytes electrically coupled by gap junctions

9


pacemaker potential

Phase 0 upstroke = Vgated Ca channels (vs Na channels in muscle). slower upstroke → AV delay. Fast v-gated Na channels are permanently inactivated b/c resting potential is less negative than in muscle
Phase 1 initial repol and phase 2 plateau are absent
Phase 3 repol is inactivation of Ca and activation of K
Phase 4 slow depol is If from mixed Na/K inward current. Slope determines heart rate. sympathetic activation → incr If channels open → incr HR

10

Class Ia antiarrhythmics


Quinidine, Procainamide, Disopyramidine.
Na+ channel blockers
decr slope of phase 0 and phase 3
state dependent! incr threshold for firing in abnormal pacemaker cells.
incr AP duraction, incr ERP, incr QT
Reentrant/ectopic SVT, VT
Hyperkalemia causes incr toxicity.
Quinidine: cinchoism--headache, tinnitus.
Procainamide: reversible SLE-like syndrome
disopyramide: heart failure.
All have thrombocytopenia, torsades

11

Class Ib antiarrhythmics

Lidocaine, Mexiletine, Tocainide
Na+ channel blockers
decr slope of phase 0 and incr slope ofphase 3
state dependent! incr threshold for firing in abnormal pacemaker cells.
decr AP duration.
Preferentially affect ischemic or depolarized purkinje/ventricular tissue.
Ventricular arrhythmias, especially post-MI, and digitalis toxicity
Hyper-K incr toxicity
Local anesthetic effects, CNS stimulation/depression, CV depression

12

Class Ic antiarrhythmics

Flecainide, propafenone
Na+ channel blockers
decr slope of phase 0 and no change to slope of phase 3
state dependent! incr threshold for firing in abnormal pacemaker cells.
No effect on AP duration
Vtach progressing to VF, intractible SVT. Last resort.
contraindicated post-MI and in pts with structural heart dz
Hyperkalemia incr toxicity
proarrhythmic, esp post-MI. Significant prolongation of ERP of AV node

13

Class II antiarrhythmics


beta blockers
metoprolol, propranolol, esmolol, atenolol, timolol
Decrease SA/AV node activity by decr cAMP, decr Ca current.
Suppress abnormal pacemakers by decr slope of phase 4
Incr PR interval (AV node)
Esmolol -- short acting
VT, SVT, rate control
Toxicity: impotence, asthma, bradycardia, AV block, CHF, sedation. May mask signs of hypoglycemia
Metoprolol -- dyslipidemia. Treat OD with glucagon.
Propranolol -- exacerbates vasospasm in prinzmetal’s angina

14

Class II antiarrhythmics

K channel blockers
amiodarone, ibutilide, dofetilide, sotalol
incr AP duration, incr ERP. decr slope of phase 3
Used when other drugs fail. incr QT interval
Toxicity:
sotalol -- torsades
ibutilide -- torsades
amiodarone -- pulm fibrosis, hepatotoxicity, hypo/hyperthyroidism (iodine), corneal deposits, skin deposits (blue/gray), photodermatitis, neuro effects, constipation. (Check PFTs, LFTs, TFTs)

15

amiodarone

Class III. but has class I, II, III, and IV effects because it alters lipid membrane

16

class IV antiarrhythmics

Ca channel blockers
verapamil, diltiazem
decr conduction velocity, incr ERP, incr PR. Prevention of nodal arrhythmias, especially SVT
Reduce contractility (decr phase 2), but allow body to retain adrenergic control, unlike beta blockers
Toxicity: constipation, flushing, edema, CHF, AV block

17

adenosine

incr K out of cells → hyperpolarization and decr Ca current. diagnosing/abolishing SVT. Very short acting.
Tox: flushing, hypotension, chest pain
Blocked by theophylline, caffeine

18

hyperkinetic pulse

rapid ejection of large stroke volume against decr afterload. Exercise or high-output conditions eg PDA, AV fistula

19

Mg

torsades and dig toxicity

20

layers of artery

intima -- endothelial cells sitting on BM
media -- smooth muscle
adventitia -- connective tissue

21

Temporal arteritis

large vessel vasculitis
branches of carotid (temporal → HA, ophthalmic → visual sx, jaw claudication)
ESR > 100, PMR
granulomatous inflammation with intimal fibrosis of vessel
Segmental lesions (need long bx, negative bx does not exclude dz)
Tx: corticosteroids. tx early to prevent blindness

22

Takayasu’s arteritis

large vessel vasculitis
asian females

23

polyarteritis nodosa

medium vessel vasculitis: muscular arteries supplying organs
necrotizing, segmental, spares lungs
HTN (renal), GI Sx (mesenteric) skin lesions
Transmural inflammation with fibrinoid necrosis (pink vessel wall) → massive fibrosis (nodosa)
associated with HBsAg positivity
immune complex mediated
Tx: steroids or cyclophosphamide (fatal if untreated)

24

Kawasaki dz

medium vessel vasculitis: muscular arteries supplying organs
kids

25

buerger’s dz (thromboangiitis obliterans)

medium vessel vasculitis: muscular arteries supplying organs
necrotizing vasculitis of digits
ulceration, gangrene, autoamputation
Reynaud’s
highly assoc with smoking
Tx: cessation

26


Wegner granulomatosis


small vessel vasculitis: arterioles, capillaries, venules
nasopharynx (septal perf, ulceration), lungs (b/l nodular infiltrates), kidneys (RPGN) (“C distribution)
Bx: large necrotizing granulomas with adjacent necrotizing vasculitis
c-ANCA
Tx: Cyclophosphamide, Corticosteroids

27


microscopic polyangiitis


small vessel vasculitis: arterioles, capillaries, venules
lung and kidney
no granulomas
p-ANCA
Tx: cyclophosphamide, corticosteroids
relapses common

28


Churg strauss

small vessel vasculitis: arterioles, capillaries, venules
lung, heart
asthma, peripheral eosinophilia (vs MPA)
p-ANCA
path: necrotizing granulomatous vasculitis with eos (vs GPA)

29


HSP


small vessel vasculitis: arterioles, capillaries, venules
palpable purpura (inflammation along with bleeding) in buttocks, legs
GI pain and bleeding
hematuria (IgA nephropathy)
follows upper respiratory tract infection
Tx: self limited, but can recur. steroids if severe

30


path atherosclerosis


Intimal plaque (necrotic lipid core) with fibromuscular cap
injury → Lipid enters intima → oxidation → macrophages form “fatty streak” → thickening, necrotic core → proliferation of SM and fibrosis → fibromuscular cap

SMC proliferation (derived from media) is responsible for intimal thickening **

31


atherosclerosis


Intimal plaque (necrotic lipid core) with fibromuscular cap
injury → Lipid enters intima → oxidation → macrophages form “fatty streak” → thickening, necrotic core → proliferation of SM and fibrosis → fibromuscular cap

SMC proliferation is responsible for intimal thickening **

32


phases of MI


1 wk -- granulation tissue (plump fibroblasts, collagen blood vessels). Gross: red border coming from outside (vascular)
>1 month -- fibrosis type I collagen. gross: white scar. aneurysm, mural thrombus, Dressler syndrome.

33


Liebman-Sacks endocarditis

SLE
sterile
both sides of mitral valve
results in MR

34

Class III antiarrhythmics

K channel blockers
amiodarone, ibutilide, dofetilide, sotalol
incr AP duration, incr ERP. decr slope of phase 3
Used when other drugs fail. incr QT interval
Toxicity:
sotalol -- torsades
ibutilide -- torsades
amiodarone -- pulm fibrosis, hepatotoxicity, hypo/hyperthyroidism (iodine), corneal deposits, skin deposits (blue/gray), photodermatitis, neuro effects, constipation. (Check PFTs, LFTs, TFTs)