cards Flashcards
wide splitting
exaggeration of normal split: split on expiration, and incr on inhalation. 2/2 delay in RV emptying (pulmonic stenosis, RBBB)
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
CO
SV*HR = (rate of O2 consumption)/ (arterial O2 - venous O2)
Ohm’s law
MAP = CO*TPR
MAP
⅔ diastolic pressure + ⅓ systolic pressure
fixed split
pulmonic closure delayed regardless of breathing
2/2 ASD
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)
cardiac AP vs skeletal AP
- plateau (from calcium influx). Contraction of myocyte is triggered by this influx of Ca
- nodal cells depolarize spontaneously due to funny current (slow, inward Na/K mixed current)
- Cardiac myocytes electrically coupled by gap junctions
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
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
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
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
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
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)
amiodarone
Class III. but has class I, II, III, and IV effects because it alters lipid membrane
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
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
hyperkinetic pulse
rapid ejection of large stroke volume against decr afterload. Exercise or high-output conditions eg PDA, AV fistula
Mg
torsades and dig toxicity
layers of artery
intima – endothelial cells sitting on BM
media – smooth muscle
adventitia – connective tissue
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
Takayasu’s arteritis
large vessel vasculitis
asian females
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)
Kawasaki dz
medium vessel vasculitis: muscular arteries supplying organs
kids
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
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
microscopic polyangiitis
small vessel vasculitis: arterioles, capillaries, venules lung and kidney no granulomas p-ANCA Tx: cyclophosphamide, corticosteroids relapses common
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)
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
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 **
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 **
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.
Liebman-Sacks endocarditis
SLE
sterile
both sides of mitral valve
results in MR
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)
