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- Exam Findings
- Atherosclerosis
- Hyperlipidemia
EchocardiographyNormal EF roughly 55% McConnell’s sign: reduced RV function with apical sparing (suggestive of PE) Detect intracardiac shunt with agitated saline bubbles General Circulatory Disturbances Edema Hypothermia Hypovolemia Shock CHF Hypertension Cor Pulmonale ACLS Edema Ddx: CHF, renal disease, inflammation, various drugs, hypothyroid, exogenous estrogen, thiamine (B1) deficiency Effects: hypovolemia, hydrocephalus, pulmonary edema anasarca (severe edema) / chronic passive congestion of lungs (hemosiderin, brown induration) / chronic passive congestion of liver (nutmeg liver) and spleen (splenomegaly) Hypovolemia Free Water Deficit: 0.6* • weight (kg) •| current Na ----------- - 1 140
*0.5 if female Shock stage I compensated stage II tissue hypoperfusion / dilated arterioles, fall in urinary output, DIC ? stage III cell and organ injury / decreased CO from hypoxia or pancreatic myocardial depressant factor / ATN (kidney) / ischemic encephalopathy / hemorrhage, necrosis in heart (zonal lesions, bands) / Phases 1) brain and CVS changes 2) renal dysfunction (2-6 days) 3) diuretic phase (renal tubules recover fxn) hypovolemic replace with saline/ringer’s cardiogenic this is due to left ventricular failure (MI, cardiomyopathy, etc) consider Swann-Ganz catheter to maintain wedge of ? 17 Consider ongoing occlusion: coronary reperfusion with PTCA
With LV failure: consider intraaortic balloon pump placement to increase coronary flow (increased diastolic pressure) and decrease afterload / can also use left-ventricular assist device (LVAD) (risk of infection, thrombosis, mechanical pump failure) Septic shock decreased SVR / goal is to maintain preload of ?>higher than normal consider Swann-Ganz catheter IVF: saline or lactated ringer’s to maintain wedge Pressors: dopamine, dobutamine, levafed Course: Capillary leak combined with a catabolic state will decrease albumin and cause 3rd spacing of fluid / pre-renal state will occur as renal arteries constrict as the body diverts blood to brain and other organs / after recovery, there will be a diuresis as fluid re-enters circulation and renal tubules are somewhat leaky may be associated with DIC Congestive Heart Failure (CHF) [NEJM] Systolic dysfunction (pump failure) all systolic also has some diastolic failure Diastolic dysfunction (impaired filling) can have isolated diastolic failure Note: RHF usually from LHF or cor pulmonale (RHF alone can actually cause pulmonary edema from pleural venous drainage) Causes: myocardial injury (see cardiomyopathies), chronic overload (AS, HTN), chronic volume overload (MR, other), infiltrative (amyloid, HC, other)Systolic dysfunction Framingham Criteria Clinical diagnosis of CHF can be made with at least one major and two minor Major: PND, neck vein distension, JVP, rales, cardiomegaly, acute pulmonary edema, S3 gallop, positive hepatojugular reflex, weight loss > 4.5 kg with 5 days treatment Minor: peripheral edema, night cough, DOE, hepatomegaly, pleural effusion, reduced VC (↓ ⅓) NYHA Functional Classification I – no limitation during ordinary physical activity II – slight limitation of physical activity. Develops fatigue or dyspnea with moderate exertion. III – marked limitation of physical activity. Even light activity produces symptoms. IV – symptoms at rest. Any activity causes worsening. Exam FindingsElevated JVP Pulmonary edema (see other) Orthopnea LV failure or inflow obstruction causes raised PCWP and dyspnea Paroxysmal nocturnal dyspnea (PND) similar phenomenon that occurs after several hours of recumbency (similar findings with pulmonary disease) Leg Swelling Pulsus alternans S3 Lab findings (biomarkers in heart failure) pro-inflammatory CRP FAS TNF, IL1,6,18 oxidative stress MPO, others neurohormones Renin, ATII, aldosterone, endothelin, others myocyte injury troponins, light chain kinases, CKMB, others myocyte stress BNP, NTProBNP, others Treatment of CHF (stages I-IV): I – ACE inhibitors II – ACE inhibitors + salt restriction + diuretics +/- B-blockers (metoprolol, carvedilol) III – add inotropic agents and vasodilators IV – add aortic balloon pump or cardiac transplantation Note: if cannot tolerate ACEI, isosorbide dinitrate + hydralazine has proven mortality benefit over placebo (Imdur alone has not been proven as of 3/07) Plus: Anticoagulants with atrial fibrillation or other risk factors for thrombus formation (such as very low EF with severe hypokinesis)welling Anti-arrhythmia agents vs. AICD Some patients may need anti-arrhythmia agents for chronic atrial fibrillation (B-blockers are safest and might be useful) Some studies favor AICD’s (+/- sotalol) over anti-arrhythmia agents alone for severe CHF with high-risk of ventricular tachycardia Cardiac resynchronization therapy (CRT) or biventricular pacing may decrease mortality by decreasing sympathetic activation; consider for moderate to severe HF The intra-aortic balloon pump (IABP) is positioned in the aorta with its tip distal to the left subclavian artery. Balloon inflation is synchronous with the cardiac cycle and occurs during diastole. The hemodynamic consequences of balloon counterpulsation are decreased myocardial oxygen demand and improved coronary blood flow. Additionally, significant preload and afterload reduction occurs, resulting in improved cardiac output. Severe aorto-iliac atherosclerosis and aortic valve insufficiency are relative contraindications to intra-aortic balloon pump placement. Ventricular assist devices (VADs) require surgical implantation and are indicated for patients with severe HF after cardiac surgery, in patients who have intractable cardiogenic shock after acute MI, and in patients who deteriorate while awaiting cardiac transplantation. Currently available devices vary with regard to degree of mechanical hemolysis, intensity of anticoagulation required, and the difficulty of implantation. Therefore, the decision to institute VAD circulatory support must be made in consultation with a cardiac surgeon experienced in this procedure. Prognosis: 75% five-year survival with transplant peak oxygen uptake of 20 mL/min/kg is associated with a good 1-year prognosis Physiology of CHF Vasoconstriction / Salt-retention Left ventricle, carotid sinus, aortic arch, renal afferent increased ADH, renin Brain-derived natriuretic peptide (BNP) promotes diuresis Sympathetic System B1 and B2 are uncoupled (B1 ↑ HR, B2 ↑ TPR) NE causes myocyte hypertrophy, direct myocyte toxicity / NE (over 4.7 nmol/L) carries poor prognosis Treatment: B-blockers may ↑ survival by counteracting NE affects (may also have anti-oxidant properties), ↑ diastolic filling time (via slowing HR) / biventricular pacing Renin-angiotensin system No escape from renal sodium retention / combination of NE and ATII stimulation increases Na transport in proximal tubule and decreases delivery to distal tubule (which helps explain lack of escape phenomenon in CHF, unlike Conn’s syndrome) / resistance to atrial natriuretic peptide may result from decreased distal delivery of Na ACE inhibitors and ATII blockers also reduce mitogenic effect on cardiac muscle (which would crowd capillaries and decrease blood delivery) / they may actually reverse LVH ATII receptors may stimulate thirst despite hyponatremia Treatment: ACE inhibitors and spironolactone both reduce mortality ADH (AVP) System ADH V2 receptors in collecting duct principal cells AC aquaporin-2 translocation and production ADH V1 receptors constrict vascular smooth muscle Baroreceptors override atrial receptors (Henry-Gauer atrial reflex) Endothelial hormones Endothelin Prostacyclin and PGE2 counteracts (afferent?) renal vasoconstriction NSAIDS can precipitate acute renal failure in severe CHF Endothelin receptor antagonist BQ-123 (in development) may also counteract vasoconstriction Diastolic Dysfunction Inadequate filling during diastole / can be due to variety of causes Treatment depends on cause
control heart rate and increase relaxation with B-blockers (1st), Ca channel blockers (2nd) normalize any arrhythmias (i.e. atrial fibrillation, atrial flutter) Cor Pulmonale Hypotension Cardiovascular Orthostatic hypotension (see Ddx) Postural orthostatic tachycardia syndrome (POTS) Young females, light-headed, palpitations, weakness, tremulousness upon standing / fatigue, sleep disturbance / heat and exercise worsens / ⅓ with abnormalities of autonomic function testing Pulmonary HTN and RV dysfunction vasoconstriction (ex. CF) primary idiopathic part of autoimmune disease (scleroderma) chronic pulmonary embolism parenchymal (sarcoidosis, ILD) obesity hypoventilation syndrome ECG: peaked P waves in II, III, aVF (RA enlargement), deep S in V6 with ST changes (RVH), R-axis deviation, RBBB occurs in 15% of patients CXR: edema (if pleural effusion, think more of LV failure instead) Treatment: treat pulmonary HTN (see other) Hypertension [see pulmonary hypertension] Definitions > 140/90 (stage I) >160/100 (stage II) essential HT 90% of HTN / genetics, environment / older age, except blacks malignant HT (5%) 50% essential, 50% secondary (10% renal, 40% endocrine, vascular, neurogenic (rare)) Secondary causes Renal parenchymal (chronic pyelonephritis, glomerulonephritis, APKD) Tubular interstitial (reflux and analgesic) Endocrine: hyperthyroidism, primary aldosteronism, Cushing’s syndrome, pheochromocytoma, acromegaly, oral contraceptives Other: pain!, hypervolemia (posttransfusion, renal failure), hypercalcemia, drugs (steroids, TCAs, sympathomimetics, NSAIDs, cocaine), coarctation of aorta, vasculitis, renovascular hypertension (RAS), fibromuscular dysplasia Clues to renovascular HTN: epigastric or flank bruits, accelerated or malignant HTN, < 35 or > 55, sudden development or worsening, concomitant poor renal function, refractory to anti-HTN meds, extensive occlusive disease in peripheral circulation (including CAD/CVA) Complications cardiac hypertrophy heart failure, MI vascular aortic dissection hyaline arteriolosclerosis: retinal, renal disease arteriolosclerosis: MI, CVA, renal failure fibroelastic hyperplasia retinal changes grade III retinal changes (hemorrhages, cotton wool spots, hard exudates) grade IV retinal changes (papilledema)
Goal is to reduce BP by 10-15% or diastolic 110 Organ dysfunction usually at > 130 diastolic
Avoid B-blockers with asthma, CHF (depends), peripheral vascular disease, theoretical risk of increasing sugars with DM or hyperlipidemia (nobody really worries about that) Avoid diuretics with gout (impairs urate excretion) With pregnancy, ACE contraindicated (fetal kidney agenesis) and diuretics risky; use aldomet or hydralazine HTN emergency – must lower BP in < 1 hr Causes: malignant HTN, associated with MI, flash pulmonary edema, ARF, intracranial events, post-operative bleeding, eclampsia, pheochromocytoma) SZ, coma, death MRI: posterior leukoencephalopathy (parietooccipital regions) can be missed on CT Cerebral blood flow autoregulation maintains MAP 60-120 (curve shifts to right in chronic HTN; which is why BP must not be lowered > 25% over ~1 hr, especially in presence of neurological effects) HTN urgency – must lower BP in < 24 hrs Causes: accelerated HTN, associated with CHF, stable angina, TIA, peri-operative Pre-eclampsia and Eclampsia (Toxemia of Pregnancy) Presentation: headache, epigastric pain, visual disturbances, swelling Criteria: hypertension (systolic > 140 or +30, diastolic > 90 or +15), proteinuria, edema Complications: placental ischemia, hypertension, DIC, seizures (true eclampsia) 6% of pregnancies / often last trimester (20 wks to 6 wks post-partum) / Risk factors: hydatidiform moles, age extremes Mechanism: angiotensin hypersensitivity may result from decreased PGE synthesis Treatment: IV MgSO4 or BZ for seizures Screening: neurokinin B test under development / maternal serum inhibin A concentration is elevated in established preeclampsia (early indicator of risk?) Treatment for HTN emergency/urgency
Arteriosclerosis Pathological Types Senile sclerosis insidious / aging Monckeberg’s medial calcification / wear and tear lesion? Atherosclerosis see below Arteriolosclerosis hyaline benign HT, DM / slow, stenosis / plasma proteins, thick BM hyperplastic malignant HT / flea-bitten kidney transplant accelerated 2 to 5-10 yrs Atherosclerosisabdominal aorta > coronary > popliteal > carotid Pathology: diffuse intimal thickening (normal aging) / gelatinous lesions (focal edema) / microthrombi / fatty streaks (normal aging) Causes: by hyperlipidemia (diet, DM, gout), chronic HTN, smoking, Fabry’s, elevated homocysteine Markers: CRP is associated with increased risk / other markers are associated but not useful for screening: homocysteine, lipoprotein A, plasminogen activator factor 1 / C. pneumoniae and CMV also implicated Coronary Artery Disease (see other) Peripheral Vascular Disease [NEJM] Presentation: < 20% report typical symptoms of intermittent claudication / leg fatigue, difficulty walking, other atypical leg pain Exam findings: cyanosis (with dependent rubor), decreased temperature, atrophic changes (shiny skin, thick nails, absence of hair), decreased pulses / ulceration usu. toes, heels, anterior shin and extended over malleoli Risk factors: smoking, diabetes, HTN, hyperhomocysteinemia, hyperlipidemia Diagnosis: [table] ankle-brachial index (ABI) > 1.0 normal / 0.41 to 0.9 intermediate / < 0.40 critical ultrasound – limited compression of calcified vessels, operator dependent MRA/CTA – usual considerations angiography – good because could also do stenting at same time Ddx [table]: Buerger’s disease, fibromuscular dysplasia, Takayasu’s, acute arterial occlusion, compartment syndrome, venous congestion, spinal stenosis Treatment: reduce contributing factors (smoking, DM, etc) smoking cessation reduces related/CAD mortality 50% / exercise (as tolerated re: possible CAD) actually helps Medical therapy cilostazol – phosphodiesterase type 3 inhibitor vasodilation + mild anti-platelet activity / shown to increase walking distance 50% pentoxifylline (Trental) immunomodulator people doubt efficacy ASA or plavix more to prevent MI and CVA Note: other vasodilators (CA blockers, a-blockers, hydralazine) may worsen symptoms by decreasing perfusion to affected area Surgery: critical leg ischemia, persistent foot pain at rest, non-healing ulcers, disabling claudication PTA (PCI) versus bypass / must take several factors into decision [table] Leriche syndrome claudication in buttock, buttock atrophy and impotence in men due to aortoiliac occlusive disease / treat with bypass Acute arterial occlusion embolic or in situ / consider source / consider HIT Ab Treatment: heparin (to prevent propagation), limb placed below horizontal plane without pressure, urgent vascular consult Hyperlipidemiadiagnose based on FH, blood tests (cholesterol not changed by fasting, TG are decreased) Friedwald formula: LDL chol = total - (HDL chol + TG/5) / 100 - 139 (mild) / >139 (severe) Note: very severe hyperlipidemia can affect platelets causing elevated ESR CARE trial no benefit shown for lowering LDL < 125 mg/dL in post-MI patients HPS trials simvastatin reduced coronary or vascular events by 33% (regardless of lipid levels) SSSS trial simvastatin reduced MI (55%), mortality (43%) VA-HDLIT 24% reduction in stroke/MI with gemfibrozil and LDL > 140 and HDL < 40 Combination of statin and fibrate is promising; fibrate alone probably not as good as statin alone
Familial HTG AD / TG combined AD / chol, TG broad beta (rare disorder) (85%) polygenic chol sporadic TG Secondary hyperlipidemia elevated cholesterol elevated TG (DM, other) Hypolipoproteinemia AR disorders Diabetes Mellitus (see endocrine) Drug-Induced: certain b-blockers, protease inhibitors Coronary Artery Disease [chest pain Ddx] [angina] [MI] 1st COD in US / 90% of cardiac deaths PDA to AV node – 90% L circumflex / 10% RCA Risk Factors: DM extremely important risk factor [annals] Family history (MI < 40 yrs) Smoking HIV Male, post-menopausal Age Hypercholesterolemia (LDL > 100 / HDL < 50 / TG > 170) Cocaine (vasospasm, promotes blood clotting) Obesity (BMI > 27) OCP/estrogens HTN
LVH Stress
Hyperthyroid Initial testing guidelines: Pt’s over 50 yrs old: LDL, smoking, fasting glucose ankle-brachial index can be checked in patients over 55-60 yrs old
low serum folate (required for homocysteine methionine) elevated CRP, homocysteine, ApoA, ApoB Physical Exam Retinal changes – AV nicking and/or copper-wire changes (HTN) S4 (HTN) Peripheral bruits Absent/decreased peripheral pulses
>1 mm ST depression (70/75) >2 mm ST depression (33/97) >3 mm ST depression (20/99) Perfusion scintigraphy Planar (83/88) SPECT (87/65) Echocardiography Exercise (85/76) Pharmacologic stress (86-96/66-95) Stress Test adenosine / sestamibi (MIBI) / dobutamine (less bronchoconstriction, better for COPD) Pt unable to exercise: can use persantine (vasodilates normal but not diseased vessels, inducing ischemia)
Bruce (fast) vs. Naughton (slower) Note: females tend to have less reliable results on graded stress tests (use of thallium/nuclear imaging improves specificity)
Symptomatic with occlusion of 50% diameter or 75% cross-sectional area EKG: may show ST depression, T wave flattening or inversion Diagnosis: stress test or other Treatment: ASA and other newer anti-platelets to limit aggregation Nitroglycerin SL or spray should work in 5-7 mins (if not, could be MI or other) coronary artery dilation improves blood flow to sub-endocardium venodilation reduces preload and wall tension Isosorbide dinitrate / mononitrate (Imdur) is taken during daytime / can use patch to protect against night time MI Note: tolerance develops to nitrates Side effects: hypotension, light-headedness, HA B-blockers reduce myocardial oxygen demands (try to avoid worsening CHF) Calcium channel blockers (Verapamil, Diltiazem) Coronary vasodilation, variable peripheral vasodilation can be used instead of B-blocker to reduce HR, BP and vasodilate [except in heart block, bradycardia, severe CHF (due to negative ionotrope/chronotrope activity] Unstable angina pre-MI (80%) / thrombus persists 15-20 mins (> 20 mins is MI) / chest discomfort at rest / decreased O2 delivery because plaque ruptures, thrombus formation / Biological factors: thromboxane, 5HT, ADP, platelet activating factor, tissue factor (endothelium/macrophage), endothelin (potent vasoconstrictor), free radicals – vasospasm, vasoconstriction mitogen – residual fibroproliferation - elevated troponin I or CRP is a poor prognostic sign
coronary artery spasm (causes similar EKG changes as STEMI) / majority of cases do have CAD and spasm occurs within 1 cm from lesion / RCA most common location / usu. younger age, do not have preceding stable angina and usu. risk factors Presentation: similar to ACS, often occurs in early morning (4-11am) / sudden cardiac death (30% of heart attacks, most common COD post-MI, V-fib)
Defect in coronary microcirculation / normal angiogram, abnormal stress test / excellent prognosis Download 3.95 Mb. Share with your friends:
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