| ¡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
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| ¡óHF Tx: |
Acute: MONL(nitrate, lasix)
Chronic: BDDE (beta blocker, digoxin, diuretics, ACEI)
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| ¡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)
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| ¡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
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| ¡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)
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| ¡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
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| ¡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.
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| ¡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.
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| ¡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. |
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