Cardio Flashcards
QT prolonging meds
some risky meds can prolong QT - sotalol, risperidone (antipsychotics), macrolides, chloroquine, protease inhibitors (-navir), quinidine (class 1a, also class III), thiazides
Romano-Ward Syndrome
congenital long QT syndrome
- AD, pure cardiac phenotype
Jervell and Lange-Nielsen syndrome
congenital long QT syndrome
- AR, sensorineural deafness
ANP/BNP mechanism of diuresis
causes vasodilation and decreased Na reabsorption in renal collecting tubule
- constricts efferent arterial and dilates afferent via cGMP
nesiritide
recombinant form of BNP for treatment of heart failure
Cushing reaction
- triad of HTN, bradycardia and resp depression
- mediated by baroreceptors
- increased ICP –> constricts arterioles –> cerebral ischemia and reflex sympathetic increase in perfusion pressure –> increased stretch, –> baro-receptor induced bradycardia
aortic arch baroreceptors
respond ONLY to increased BP
carotid baroreceptors
respond to increased and decreased BP
peripheral chemoreceptors
stimulated by dec PO2, inc PCO2, and dec pH
central chemoreceptors
stimualted by inc PCO2, dec pH only
Monckeberg (medial calcific sclerosis)
uncommon calcification in the media of the arteries, esp radial/ulnar
- usually benign “pipestem” arteries on xray
- does not obstruct blood flow, intima not involved
arteriolosclerosis
common - two types
- hyaline: thickening of small arteries in HTN or diabetes
- hyperplastic: “onion-skinning” in severe HTN, can cause acute renal failure with “flea bitten” appearance
atherosclerosis mechanism and location
- endothelial cell dysfunction –> macrophage and LDL accumulation –> foam cell formation –> fatty streaks –> smooth muscle cell migration (PDGF and FGF), proliferation and ECM deposition –> fibrous plaque –> complex atheromas
- abdominal aorta > coronary arter > pop >carotid
variant angina (Prinzmetal)
- angina at rest due to coronary vasospasm with transient ST elevation
- triggers: tobacco, cocaine, triptans
- treat with CCBs, nitrates, smoking cessation
coronary steal syndrome
- distal to coronary stenosis, vessels are maximally dilated at baseline, so the addition of vasodilator (dipyridamole, rgadenoson) dilates normal vessels and shunts to well perfused areas –> decreased flow and ischemia of the post-stenotic region
MI (0-4hr)
minimal change on light microscope
- complications include: arrhythmia, HF, cardiogenic shock and death
MI (4-12hr)
- light microscope: early coagulative necrosis, release of necrotic cell content into blood, edema, hemorrhage, wavy fibers
- complications include: arrhythmia, HF, cardiogenic shock, death
MI (12-24hr)
- light microscope: neutrophil migration starts. reperfusion injury may cause contraction bands (due to free radical damage), early coagulative necrosis
- complications include: arrhythmia, HF, cardiogenic shock, death
MI (1-3days)
- light microscope: extensive coagulative necrosis, tissue surrounding the infarct shows acute inflammation with neutrophils
- complications include: fibrinous pericarditis
MI (3 - 14 days)
- light microscope: macrophages, then granulation tissue at margins
- complications include: free wall rupture –> tamponade. papillary muscle rupture –> MR. intraventricular septal rupture due to macrophage-mediated structural degradation. LV pseudoaneurysm.
MI (2 weeks - several months)
- light microscope: contracted scar complete (collagen deposition)
- complications include: Dressler syndrome, HF, arrthymias, true ventricular aneurysm (dyskinesia)