Internal Medicine¡Gcardiology
¡óArterial pulse pulsus parvus: AS, MS
pulsus tardus: AS
pulsus bisferiens: AR, HCM
pulsus alterans: severe LV dysfunction
pulsus paradoxus: pericardial tamponade, COPD(exaggerated inspiratory fall > 10mmHg SBP)
Bounding pulse: PDA
¡@
¡óHF Tx: Acute: MONL(nitrate, lasix)
Chronic: BDDE (beta blocker, digoxin, diuretics, ACEI)
¡@
¡óPTCA: success rate :95%
restenosis in 6 mo :30-45%
angina in 1 yr :25%
Stent: restenosis in 6 mo :10-30%¡÷¡÷TX: Aspirin+ Ticlopidine(neutropenia, aplastic anemia)
¡@
¡óTIMI grade after t-PA grade 0: failure
grade 3: succeed
¡óCardiac enzymes Troponin I: late, but remain 7-14 days, prognostic index
Myoglobin: earliest
¡óEKG exercise EKG: ST depression (upsloping type: > 1.5mm)
angina EKG: ST elevation

Hyperkalemia: tenting T, wide QRS, PR prolong, loss of P

¡óRheumatic Heart in Taiwan ¡÷Jones Criteria for rheumatic fever:
carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules
¡÷MR> MR&AR > AR....
¡÷TX: Prednisolone, Aspirin, Penicillin prophylaxis
¡@
¡óMS: ¡÷most RHD
¡÷2/3 female (Menstration!!)
¡÷hemoptysis, PE, Af
¡÷S1¡ô¡ô, opening snap
¡óvalsalva maneuver ¡÷MOST valvular hearts attenuate, except 1.MVP & 2. Hypertrophic obstructive cardiomyopathy
¡óQT prolongation (> 500ms) 1.Hypo-calcemia
2.Antiarrhythmia IA, III
¡óDuke clinical criteria for Infective endocarditis Requires the presence of :
Two major criteria or
One major and three minor criteria or
Five minor criteria

1. Major criteria
Positive blood cultures
Evidence of endocardial involvement

2. Minor criteria
Predisposing heart condition or intravenous drug abuse
Fever (>38.0 deg C)
Vascular phenomenon
¡÷Major arterial emboli
¡÷Septic pulmonary infarcts
¡÷Mycotic aneurysm
¡÷Intracranial haemorrhage
¡÷Conjunctival haemorrhages
Immunological phenomenon
¡÷Glomerulonephritis
¡÷Osler's nodes
¡÷Roth spots
Microbiological evidence (but less than major criteria)
Echocardiographic findings (but not meeting major criteria)
¡@
¡óatrial natriuretic peptide (ANP), and B-type natriuretic peptide (BNP). BNP, in particular, produces selective afferent arteriolar vasodilation and inhibits sodium reabsorption in the proximal convoluted tubule. BNP inhibits renin and aldosterone release and, possibly, adrenergic activation as well. Both ANP and BNP are elevated in chronic heart failure. BNP, in particular, has potentially important diagnostic, therapeutic, and prognostic implications.
¡óSinus of Valsalva: ¡÷The portion of the aortic root just distal to the aortic valve containing the coronary ostia.
¡÷Aneurysms of the Sinus of Valsalva
congenital: Marfan's syndrome, Ehlers-Danlos syndrome, VSD type I
acquired: mycotic aneurysms secondary to infective endocarditis of the aortic valve
¡@
¡óDC shock Afib: 350-500/min¡÷DC 100-200J
AF:250-350/min¡÷DC 50J
¡óAtrial fib ¡÷1. Rate control is the goal 2. Convert rhythm 3. Anticoagulant
¡÷prehospital care includes administration of diltiazem(Herbesser, Ca blocker, Class IV)
¡÷initial energy of 200 J or greater is recommended for electrical cardioversion in unstable pt (ie, those with chest pain, shortness of breath, altered level of consciousness, AMI)
¡÷In patients without ventricular preexcitation, rate is controlled most effectively with IV verapamil, diltiazem(Herbesser), or beta-adrenergic blockers. (Class II)
¡÷Beta-blockers are especially effective in the presence of thyrotoxicosis and increased sympathetic tone or in patients with myocardial ischemia/AMI.
¡÷Other antiarrhythmic drugs : procainamide, disopyramide(IA), propafenone, flecainide(IC), amiodarone, sotalol(III)
¡÷Class IB contraindicated
¡÷Echocardiography or transesophageal echocardiography (TEE): identifying valvular disease, pericardial fluid, LV dysfunction and, most importantly, clots in the atria, which may place patient at embolic risk after cardioversion.
¡@
¡óSVT ¡÷vagal maneuvers can be very helpful in the acute setting.
¡÷In the infant, it is worthwhile to apply a plastic bag containing ice cubes and water to the face for 25-30 seconds to induce the diving reflex, a vagal stimulus. Other vagal maneuvers can be attempted, such as breathholding or Valsalva maneuver.
¡÷the next step is to administer medication. The drug of choice is adenosine. Use of esmolol, a short-acting beta-blocker, also has been successful.
¡÷Perform electrical cardioversion if patients have a deteriorating condition or if there is no response to the initial attempts of conversion.
¡÷Esophageal overdrive atrial pacing is also quite safe and effective in converting to sinus rhythm.
¡÷Drugs used for long-term therapy that have some effect in AV node reentrant tachycardia include digoxin, beta-blockers, and verapamil. Avoid intravenous verapamil use in infants because of its negative inotropic effects and avoid its use in combination with beta-blockers.
¡@
¡óMarfan syndrome ¡÷caused by mutations in the fibrillin-1 (FBN1) gene located on chromosome 15q21.1. The gene encodes the glycoprotein fibrillin, a major building block of microfibrils, which constitute the structural components of the suspensory ligament of the lens and serve as substrates for elastin in the aorta and other connective tissues. Abnormalities involving microfibrils weaken the aortic wall. Progressive aortic dilatation and eventual aortic dissection occur because of tension caused by left ventricular ejection impulses. Likewise, deficient fibrillin deposition leads to reduced structural integrity of the lens zonules, ligaments, lung airways, and spinal dura.

¡÷Major criteria include the following:

1. Pectus excavatum requiring surgery or pectus carinatum
2. Reduced upper-to-lower body segment ratio (0.85 vs 0.93) or arm span-to-height ratio greater than 1.05: Arms and legs may be unusually long in proportion to torso.
3. Positive wrist (Walker) and thumb (Steinberg) signs: Two simple maneuvers may help demonstrate arachnodactyly. First, the thumb sign is positive if the thumb, when completely opposed within the clenched hand, projects beyond the ulnar border. Second, the wrist sign is positive if the distal phalanges of the first and fifth digits of one hand overlap when wrapped around the opposite wrist.
4. Scoliosis greater than 20? More than 60% of patients have scoliosis. Progression is more likely with curvature greater than 20?in growing patients.
5. Reduced extension of the elbows (<170?
6. Medial displacement of the medial malleolus, resulting in pes planus
7. Protrusio acetabula (intrapelvic protrusion of the acetabulum) of any degree (ascertained on radiograph): Prevalence is about 50%.

¡÷Minor criteria are as follows:

Pectus excavatum of moderate severity
Scoliosis less than 20?
Thoracic lordosis
Joint hypermobility
Highly arched palate
Dental crowding
Typical facies (dolichocephaly, malar hypoplasia, enophthalmos, retrognathia, down-slanting palpebral fissures)
¡óHMG Co-A reductase: Hepatic, Muscular(Myositis,rhabdomyolysis,ARF), Grapefruit juice(Cyp3A4)
¡@
¡óBile acid Resin: Raising (TG)
¡óApo CII Deficiency Apolipoprotein C-II is present as a peripheral apoprotein of chylomicrons, very low density lipoproteins (VLDLs), and intermediate density lipoproteins (IDLs). Apolipoprotein C-II activates lipoprotein lipase to hydrolyze triglycerides in the chylomicrons, VLDLs, and IDLs to release free fatty acids for cellular absorption. When the apoprotein is absent, lipoprotein lipase activity is compromised. This results in high triglyceride and chylomicron levels. LDL and HDL levels are abnormally low. The risk of atherosclerosis does not change significantly.
¡@ ¡@
¡@ ¡@


Hosted by www.Geocities.ws

1