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Authors: Marc Sabatine
Tags: Medical, Internal Medicine
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ventricles → ↑ systemic venous pressures • Venous return is limited only after early rapid filling phase; ∴ rapid ↓ in RA pressure with atrial relaxation and opening of tricuspid valve and prominent x and y descents • Kussmaul sign: JVP does not decrease with inspiration (↑ venous return with inspiration but negative intrathoracic pressure not transmitted to heart because of rigid pericardium) Clinical manifestations ( NEJM 2011;364:1350)
• Right-sided > left-sided heart failure (systemic congestion > pulmonary congestion) Physical exam
• ↑ JVP with prominent y descent , Kussmaul sign (Ddx: tricuspid stenosis, acute cor pulmonale, RV failure and RV infarct, RCMP) • Hepatosplenomegaly, ascites, peripheral edema. Consider on Ddx of idiopathic cirrhosis.
• PMI usually not palpable, pericardial knock , usually no pulsus paradoxus Diagnostic studies
• ECG: nonspecific, AF common (up to 33%) in advanced cases • CXR: calcification (MTb most common), esp. in lateral view (although not specific) • Echocardiogram: ± thickened pericardium, “ septal bounce ” = abrupt displacement of septum during rapid filling in early diastole • Cardiac catheterization
atria: Ms or Ws (prominent x and y descents)
ventricles: dip-and-plateau or square-root sign (rapid ↓ pressure at onset of diastole, rapid ↑ to early plateau)
discordance between LV & RV pressure peaks during respiratory cycle ( Circ 1996;93:2007)
• CT or MRI : thickened pericardium (>4 mm; Se ~80%), w/ tethering ( Circ 2011;123:e418) Treatment
• Diuresis for intravascular volume overload; surgical pericardiectomy in advanced cases • ? MRI able to predict reversibility with anti-inflammatory agents ( Circ 2011;124:1830)
HYPERTENSION
BP should be determined by making ≥2 measurements separated by >2 min. Confirm stage 1 w/in 2 mo; can Rx stage 2 immediately.
Epidemiology ( JAMA 2003;290:199 & 2010;303:2043)
• Prevalence 30% in U.S. adults; >68 million affected (29% in whites, 33.5% in blacks) • Only 50% of patients with dx of HTN have adequate BP control Etiologies
• Essential (95%): onset 25–55 y;FHx. Unclear mechanism but ? additive microvasc
renal injury over time w/ contribution of hyperactive sympathetics ( NEJM 2002;346:913).
↑ Age → ↓ arterial compliance → syst HTN. Genetics also involved ( Nat ure 2011;478:103).
• Secondary : Consider if Pt <20 or >50 y or if sudden onset, severe, refractory HTN
Standard workup
• Goals: (1) identify CV risk factors or other diseases that would modify prognosis or Rx;
(2) reveal 2° causes of hypertension; (3) assess for target-organ damage
• History: CAD, HF, TIA/CVA, PAD, DM, renal insufficiency, sleep apnea, preeclampsia;FHx for HTN; diet, Na intake, smoking, alcohol, prescription and OTC meds, OCP
• Physical exam: ✓ BP in both arms ; funduscopic exam, cardiac (LVH, murmurs), vascular (bruits, radial-femoral delay), abdominal (masses or bruits), neuro exam • Testing: K, BUN, Cr, Ca, glc, Hct, U/A, lipids, TSH, urinary albumin:creatinine (if ↑ Cr, DM, peripheral edema), ? renin, ECG (for LVH), CXR, TTE (eval for valve abnl, LVH) Complications of HTN
• Each ↑ 20 mmHg SBP or 10 mmHg DBP → 2 × ↑ CV complications ( Lancet 2002;360:1903) • Neurologic: TIA/CVA , ruptured aneurysms, vascular dementia • Retinopathy: stage I = arteriolar narrowing; II = copper-wiring, AV nicking; III = hemorrhages and exudates; IV = papilledema • Cardiac: CAD , LVH , HF, AF
• Vascular: aortic dissection, aortic aneurysm (HTN = key risk factor for aneurysms) • Renal: proteinuria, renal failure Treatment ( Lancet 2012;380:591)
• Goal: <140/90 mmHg; if DM or CKD goal is <130/80 mmHg (nb, in DM, target of <120 does not ↓ CV risk & ↑ adverse events; NEJM 2010;362:1575) • Treatment results in 50% ↓ HF, 40% ↓ stroke, 20–25% ↓ MI ( Lancet 2000;356:1955); benefits of Rx’ing stage II HTN extend to Pts >80 y, goal BP <150/80 ( NEJM 2008;358:1887) • Lifestyle
• Right-sided > left-sided heart failure (systemic congestion > pulmonary congestion) Physical exam
• ↑ JVP with prominent y descent , Kussmaul sign (Ddx: tricuspid stenosis, acute cor pulmonale, RV failure and RV infarct, RCMP) • Hepatosplenomegaly, ascites, peripheral edema. Consider on Ddx of idiopathic cirrhosis.
• PMI usually not palpable, pericardial knock , usually no pulsus paradoxus Diagnostic studies
• ECG: nonspecific, AF common (up to 33%) in advanced cases • CXR: calcification (MTb most common), esp. in lateral view (although not specific) • Echocardiogram: ± thickened pericardium, “ septal bounce ” = abrupt displacement of septum during rapid filling in early diastole • Cardiac catheterization
atria: Ms or Ws (prominent x and y descents)
ventricles: dip-and-plateau or square-root sign (rapid ↓ pressure at onset of diastole, rapid ↑ to early plateau)
discordance between LV & RV pressure peaks during respiratory cycle ( Circ 1996;93:2007)
• CT or MRI : thickened pericardium (>4 mm; Se ~80%), w/ tethering ( Circ 2011;123:e418) Treatment
• Diuresis for intravascular volume overload; surgical pericardiectomy in advanced cases • ? MRI able to predict reversibility with anti-inflammatory agents ( Circ 2011;124:1830)
HYPERTENSION
BP should be determined by making ≥2 measurements separated by >2 min. Confirm stage 1 w/in 2 mo; can Rx stage 2 immediately.
Epidemiology ( JAMA 2003;290:199 & 2010;303:2043)
• Prevalence 30% in U.S. adults; >68 million affected (29% in whites, 33.5% in blacks) • Only 50% of patients with dx of HTN have adequate BP control Etiologies
• Essential (95%): onset 25–55 y;FHx. Unclear mechanism but ? additive microvasc
renal injury over time w/ contribution of hyperactive sympathetics ( NEJM 2002;346:913).
↑ Age → ↓ arterial compliance → syst HTN. Genetics also involved ( Nat ure 2011;478:103).
• Secondary : Consider if Pt <20 or >50 y or if sudden onset, severe, refractory HTN
Standard workup
• Goals: (1) identify CV risk factors or other diseases that would modify prognosis or Rx;
(2) reveal 2° causes of hypertension; (3) assess for target-organ damage
• History: CAD, HF, TIA/CVA, PAD, DM, renal insufficiency, sleep apnea, preeclampsia;FHx for HTN; diet, Na intake, smoking, alcohol, prescription and OTC meds, OCP
• Physical exam: ✓ BP in both arms ; funduscopic exam, cardiac (LVH, murmurs), vascular (bruits, radial-femoral delay), abdominal (masses or bruits), neuro exam • Testing: K, BUN, Cr, Ca, glc, Hct, U/A, lipids, TSH, urinary albumin:creatinine (if ↑ Cr, DM, peripheral edema), ? renin, ECG (for LVH), CXR, TTE (eval for valve abnl, LVH) Complications of HTN
• Each ↑ 20 mmHg SBP or 10 mmHg DBP → 2 × ↑ CV complications ( Lancet 2002;360:1903) • Neurologic: TIA/CVA , ruptured aneurysms, vascular dementia • Retinopathy: stage I = arteriolar narrowing; II = copper-wiring, AV nicking; III = hemorrhages and exudates; IV = papilledema • Cardiac: CAD , LVH , HF, AF
• Vascular: aortic dissection, aortic aneurysm (HTN = key risk factor for aneurysms) • Renal: proteinuria, renal failure Treatment ( Lancet 2012;380:591)
• Goal: <140/90 mmHg; if DM or CKD goal is <130/80 mmHg (nb, in DM, target of <120 does not ↓ CV risk & ↑ adverse events; NEJM 2010;362:1575) • Treatment results in 50% ↓ HF, 40% ↓ stroke, 20–25% ↓ MI ( Lancet 2000;356:1955); benefits of Rx’ing stage II HTN extend to Pts >80 y, goal BP <150/80 ( NEJM 2008;358:1887) • Lifestyle
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