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CS Block II Cardio
Second half
| Question | Answer |
|---|---|
| Pericarditis: acute | Most common pericardial disease; <6wks, fibrinous, serous; painful |
| Pericarditis: subacute | 6wks - 6 months; effusive, constrictive |
| Pericardidtis: chronic | >6wks; adhesive, effusive, constrictive |
| Pericarditis etiologies | Infectious, non-infectious, hypersensitivity/autoimmunity |
| Infectious pericarditis: viral | Coxsackievirus A&B, echovirus, mumps, adenovirus, HIV, hepatitis, Epstein-barr |
| Infectious pericarditis: bacterial | Pneumococcus, strep, staph, Neisseria, Legionella, Tuberculosis |
| Infectious pericarditis: fungal | Histoplasmosis, blastomycosis, coccidiodomycosis, candida, assorted mushrooms |
| Other infectious pericarditis | Syphilis, protozoans, parasites |
| Non-infectious pericarditis | Trauma, post-irradiation, acute MI (**Dressler’s syndrome), uremia (crystals), primary tumors, metastatic tumors, myxedema (rare dt hypothyroidism); aortic dissection |
| *Acute Pericarditis (idiopathic, viral, T-U-M-O-R) | T (tumor, trauma), U (uremia), M (myocardial infarction - **Dressler’s), O (other infxns: bacterial, fungal, TB), R (RA, autoimmune disorders, scleroderma, polyarteritis nodosa, lupus, Radiation) |
| Hypersensitivity/Autoimmune causes of Pericarditis | Rheumatic fever; collagen vascular diseases (SLE, RA, scleroderma, Wegener’s granuloma); drug-induced (hydralazine, phenytoin, procainamide, isoniazid, minoxidil, anticoagulants); Postcardiac injury (Dressler’s syndrome, postpericardiotomy, posttraumatic) |
| Pericardial Diseases: | Acute pericarditis, pericardial effusion (dt acute pericarditis; inc pericardial fluid), cardiac tamponade (obstruction produced by effusion), constrictive pericarditis (dt chronic pericarditis; rare; scar tissue in pericardial space) |
| *Presentation of Acute Pericarditis | sudden onset severe chest pain waxes/wanes w/movement (*worse lying supine; better sitting up and leaning forward); worse w/deep breathing/cough; pain radiates along ligamentous attachments (retrosternal, neck, L shoulder/arm), fever dt inflam/virus |
| *Differential for Acute Pericarditis | acute MI or other acute coronary event; pulmonary embolism; aortic dissection; pneumothorax; pneumonia, pericardial effusion/cardiac tamponade |
| *Diagnostic key findings for Acute Pericarditis | *pericardial friction rub* (high-pitched, scratching, grating heart sounds when pt is sitting;* ECG is most IMPORTANT tool (widespread concave ST elevations at 2-3 limb leads & V2-V6; serology inconclusive (usu elev WBC/ESR) |
| Chronic Relapsing acute Pericarditis | ~25% of acute idiopathic cases; at risk for constrictive pericarditis; longer prednisone taper? Consider pericardiectomy |
| Bacterial Pericarditis | Rare; intrathoracic spread of pneumonia/empyema/endocarditis; usu missed b/c lack of typical findings…usu fatal |
| Acute Pericarditis Dx & Tx | viral/idiopathic if CP worsens w/motion; cardiac rub on auscultation; characteristic ECG; neg cardiac enzymes, no evidence of TUMOR, HIV, effusion, tamponade; negative echo; expect full recovery in 1-4wks w/bedrest & anti-inflamm; rule out TB w/skin test |
| Tuberculosis Pericarditis | <8% of pulmonary cases; presents w/typical TB signs (night sweats, wt loss); Dx w/sputum or bronchoscopy + pericardial biopsy |
| Uremic Pericarditis | Usu in pts w/uremia from end-stage renal Dx who are undergoing chronic hemodialysis |
| **Post-AMI Pericarditis (Dressler’s Syndrome) | <15% of AMI pts develop w/in 3 months; cause not clear; presents w/fever, sharp pain, friction rub; rely on Hx, ECG, labs to rule out new AMI; Tx bedrest, ASA, NSAIDs |
| Chronic Constrictive Pericarditis | Confused w/restrictive cardiomyopathy dt similar presentation w/JVD Kussmaul’s sign that inc w/inspiration; sustained venous pressure (peripheral edema, hepatomegaly, ascites) |
| How to differentiate constrictive pericarditis from chronic constrictive pericarditis | Hearing a diastolic (pericardial) knock 3rd heart sound, but no other murmurs |
| Pericardiocentesis | Subxiphoid puncture to avoid major epicardial vessels; guidewire, flexible catheter drains fluid |
| Chronic Constrictive Pericarditis | Formation of scar tissue in pericardial cavity following healing of acute or chronic relapsing pericarditis; can be calcified, idiopathic, cardiac surgery, TB, radiation, autoimmune disorders |
| Chronic constrictive pericarditis lab visualization | MRI or CT scans are most sensitive/specific for thickening; CXR can show pericardial calcification |
| Chronic constrictive pericarditis treatment | Pericardial resection (pericardectomy or cardiac decortication); full improvement can take months |
| Acute pericarditis summary | Positional pain, friction rub, widespread ST elevations, treat w/anti-inflammatories |
| Pericardial effusion summary | Part of the continuum btw pericarditis and tamponade; may require pericardiocentesis |
| Cardiac tamponade summary | Increased venous pressure, pulsus paradoxus, diagnostic echocardiogram, treat w/pericardiocentesis |
| Constrictive pericarditis | Signs of right heart failure, diastolic knock, Kussmaul’s sign, diagnostic CT or MRI, treat w/pericardiectomy |
| Acute Endocarditis | Most common endocarditis, febrile, erratic spiking fevers, rapid damage to heart, seeds extracardiac sites via blood, progresses to death w/in wks, usu a/w IVDA; 10/100,000 per yr |
| Subacute Endocarditis | Indolent course, rarely febrile, rarely damaging, rarely spread by blood; gradual progression; rarely causes death unless a/w major embolism/ruptured mycotic aneurysm |
| Populations at risk for endocarditis | Abnormal/damaged heart valves, prosthetic valves, intravascular appliances (ex: indwelling catheters, elderly, IVDA |
| 4 Bugs a/w endocarditis | Streptococcus (native valve & long-term prosthetic valves); Pneumococci (community acquired native valves); Enterococci (nosocomial native & prosthetic valves); Staphylococci (IVDA |
| Other bugs a/w endocarditis | Gram-negative bacilli; HACEK group (fastidious G-neg coccobacilli); Candids; polymicrobial |
| Clinical Features of Endocarditis | Fever, chills, sweats, anorexia, wt loss, new heart murmur, worsening murmur, arterial emboli, splenomegaly, petechiae |
| Peripheral manifestations of endocarditis: Janeway Lesion | Flat, painless bluish/purplish lesion on palms or soles; CLASSIC dt bacterial embolis spit out by heart valve and gets stuck in skin |
| Peripheral manifestations of endocarditis: Roth Spots | Small erythematous rings dt bacterial emboli from infected valve |
| Peripheral manifestations of endocarditis: others | Petechiae and splinter hemorrhages on nails |
| Peripheral manifestations of endocarditis: Osler’s Nodes | Painful, red, raised nodules (differentiate from Janeway lesion); usu on sides of fingers/toes or thenar/hypothenar eminences |
| Clinical Criteria for Dx of Infective Endocarditis (IE): Major | 1. Positive blood culture for typical microbe from 2 separate draws OR persistently positive cultures; 2. evidence of endocardial involvement (pos echo w/oscillating intracardiac mass/abscess/partial detachment of prosthetic valve, new valve regurgitation |
| Clinical Criteria for Dx of Infective Endocarditis: Minor | 1. predisposing heart dx or IVDA; 2. Fever >100.4F; 3. Vascular phenomena; 4. Microbiologic evidence not meeting major criterion; 5. Consistent echo results not meeting major criterion |
| Common treatment regimens: Penicillin-sensitive Strep bovis or Strep viridans | Penicillin G, IV q6h for 4wks OR Penicillin G q6h + Gentamycin q8h for 2wks OR Ceftriaxone IV or IM 1qd for 4wks |
| Common treatment regimens: Relatively penicillin-resistant S. bovis or viridans | Penicillin G + Gentamyxin OR Vancomycin |
| Methicillin-sensitive staphylococci w/o prosthesis | Nafcillin + Gentamycin OR 1st generation cephalosporin |
| Methicillin-resistant staphylococci w/o prosthesis | Vancomycin |
| Methicillin-sensitive staphylococci in uncomplicated tricuspid endocarditis | Nafcillin + Gentamycin |
| Methicillin-resistant staphylococci w/prosthesis | Vancomycin + Gentamycin OR Vancomycin + Rifampin |
| Myocarditis | Any inflammation or degeneration of the heart; usu diagnosed from autopsy! Endomycardial biopsy may provide greater insight into pathogenesis/etiology/treatment |
| Important causes of myocarditis | Infection (viral, bacterial, rickettsial, spirochetal, protozoan, metazoan, fungal); Toxic (anthracyclines, catecholamines, IL-2, IFN-a2); Hypersensitivity |
| Myocarditis: Viral infections | Cocksackie A&B, echo, influenza A&B, polio, herpes simplex, varicella zoster, Epstein-barr, cytomegalovirus, mumps, rubella, rubeola, vaccinia, coronavirus, rabies, hepatitis B, arbovirus, junin virus, HIV |
| Myocarditis: Bacterial | C. diptheriae, Salmonella typhi, b-hemolytic strep, N. meningitides, legionella pneumonophilia, listeria monocytogenes, campylobacter jejuni, coxiella burnetti (Q fever), Chlamydia trachomatis, mycoplasma pneumoniae, chlamydia psittaci, M. tuberculosis |
| Myocarditis: Rickettsial, Spirochetal, Protozoan, Metazoan | rickettsia rickettsii (rocky mountain), borrelia burdorferi (lyme); Trypanosoma cruzi (Chagas); Toxoplasma gondii; Trichinosis, Echinococcosis |
| Myocarditis: Fungal | Aspergillosis, blastomycosis, candidiasis, coccidioidomycosis, cryptococcosis, histoplasmosis, mucormycosis |
| Myocarditis: Drug-induced hypersensitivity | Antibiotics, anticonvulsants, antituberculars, anti-inflammatories, diuretics, others |
| Myocarditis: Clinical manifestations | Acute usu asymptomatic; 60% flu-like; 35% HF/CP; mimic acute MI w/ventricular dysfxn, ischemic CP; ECG: injury or Q-waves; syncope, palpitation w/AV block or ventricular arrhythmia; sudden death; systemic//pulmonary thromboembolic disease |
| Myocarditis: Blood studies | ESR: 60%; WBC elevation 25%; CK-MB elevation 12%; a 4-fold rise in IgG titer over 4-6wk period is required to document acute viral infxn; heart specific Ab are non-specific for myocarditis (also found in dilated cardiomyopathy) |
| Myocarditis: Echocardiography | Useful in managing pts w/acute myocarditis; LV systolic dysfxn common w/abnml segmental wall motion; LV size is usu nml; slight wall thickness; 15% ventricular thrombi |
| Myocarditis: Imaging studies | Gallium 67 for inflammation; Indium 111-antimyosin monoclonal antibody for injured myocardium |
| Myocarditis: diagnostic standard | Endomycardial biopsy! |
| Myocarditis: Treatment | Usu self-limited; manage LV dysfxn like other CHF/AV blocks; *caution: exercise may intensify inflammation; consider anticoagulant to prevent thromboemboli; temporary pacer for complete AV block |
| Cardiomyopathy | Primary disorder of heart muscle; not caused by inflammation; it manifests as CHF; classified by pathophysiology and clinical presentation |
| Dilated 1* Cardiomyopathy | Congestive/DCM; ventricular enlargement and systolic dysfxn; may look like pericardial effusion on CXR |
| Hypertrophic 1* Cardiomyopathy | HCM; inappropriate myocardial hypertrophy in absence of hypertension or aortic stenosis |
| Restrictive 1* Cardiomyopathy | Infiltrative; abnormal filling and diastolic function |
| Secondary Cardiomyopathies - specific heart muscle disease | Infectious, metabolic, systemic disease, familial, sensitivity, toxic |
| Idiopathic Dilated Cardiomyopathy | Dx of unknown etiology affecting myocardium w/LV dilation, hypertrophy, and fibrosis; <10/100,000/yr; middle aged; death dt progressive pump failure; 30% 5yr survival; dx may stabilize but rarely recover completely |
| Idiopathic Dilated Cardiomyopathy: Pathophysiology | Dec systolic fxn results in dec cardiac output; in advanced disease fibrosis develops, most pts deteriorate progressively despite treatment; dt combo of genetic, environmental, immunologic factors |
| Idiopathic Dilated Cardiomyopathy (IDC) Hx and Physical Findings | Sx of heart failure (dyspnea, orthopnea w/ Left HF); Peripheral edema (Right HF); fatigue and weakness (low CO); hypotension, tachycardia, tachypnea, JVD, 3rd/4th heart sounds?; tricuspid or mitral murmurs/regurgitation |
| DCM Cardiac Imaging | CXR (enlarged cardiac silhouette); ECG (LVH, BBB); echocardiogram, holter monitor, radionucleotide vetriculography |
| IDC Management | Treat CHF (salt restriction, diuretics, digitalis, antihypertensives); anticoagulants (dec risk of thromboembolism), pacemaker/cardioverter-defribrillator; cardiac transplant |
| Causes of DCM | Myocarditis (#1 is coxsackievirus B; staph, enterococci); HIV, Chagas disease (T. cruzi); Lyme carditis; Alcohol (#2 most common 2* cause); prepartum cardiomyopathy (30% mortality); drug-induced (cocain, antineoplastic agents); muscular dystrophies |
| Hypertrophic Cardiomyopathy | LV hypertrophy; histopath = disorganized myocardial cells; results in dec LV cavity/stiffness; impaired diastolic filling, inc filling pressure; outflow obstruction w/septal hypertrophy (produces systolic anterior motion of mitral valve leaflet) |
| Characteristics of Hypertrophic Cardiomyopathy (HCM) | Aka: …subaortic stenosis OR hypertrophic obstructive cardiomyopathy; affects 0.2% of pop; 50% hereditary/idiopathic; variable prognosis; sudden death <30yo, Hx of syncope, family Hx of sudden death; <15% develop DCM |
| HCM Pathophysiology | Systolic (outflow tract gradiant); Diastole (impaired diastolic filling; inc pressure); Myocardial ischemia (inc muscle mass, filling pressure, O2 demand; dec vasodil capacity, dec capillary density; abnml intramural coronary aa; systolic aa compression) |
| Asymmetric Septal Hypertrophy w/Obstruction | Blood leaks back thru mitral valve = mitral regurgitation; mitral valve presses against septum causing obstruction to blood flow thru aortic valve; systolic anterior motion of mitral valve (SAM) |
| 3 mechanisms causing intensification of dynamic pressure gradient in HCM | inc L ventricular contractiliy; dec ventricular volume (preload); dec aortic impedance and pressure (afterload) |
| Increase in gradient and loudness of murmur in HCM | Produced when contractility increases w/exercise or by reducing ventricular volume w/a valsalva, sudden standing or nitroglycerin |
| Decreased pressure gradient and loudness of murmur in HCM | Elevating arterial pressure w/squatting or sustained handgrip; increasing venous return w/passive leg raising or expanding blood volume |
| HCM Cardiac Imaging - best test | **2D echocardiogram** LVH, small left ventricular cavity, thickened septum |
| Clinical manifestation of HCM | **Hallmark - harsh systolic murmur that begins after 1st heart sound best heard at L sternal border and apex**Asymptomatic (found on echo after hearing murmur); Symptomatic (dyspnea, angina pectoris, fatigue, pre-syncope, syncope inc risk of SCD in youth; |
| Recommendations for patients <30yo if HCM is proven | Avoid competitive sport/dehydration; b-adrenergic blockers dec angina and syncope in 50%; Amiodarone dec risk of arrhythmias; maintain sinus rhythm w/pace maker; implant defribrillator?; myotomy if septum is severe; screen all 1st degree relatives for HCM |
| Recommendations for patients >30yo if HCM is proven | Low-risk pts sports ok: no V-tach on Holter, fam Hx of sudden death dt HCM, Hx of syncope/impaired consciousness, severe hemodynamic probs, exercise induced hypotension, mitral regurgitation, enlarted L atrium, paroxysmal atrial fib, abnml heart perfusion |
| Restrictive Cardiomyopathy | *hallmark: abnormal diastolic function;* rigid ventricular wall w/impaired filling (stiff heart w/o enlargement); similar to constrictive pericarditis; prognosis is poor b/c cause is progressive |
| RCM Etiology | Dt development of endomycardial fibrosis that stiffens ventricle; dt eosinophilia (Loeffler’s syndrome), amyloidosis, hemochromatosis, rxn to chemo/radiation or scleroderma, sarcoidosis, metastatic malignancy |
| RCM Pathophisiology | Cavity of LV is normal size, but stiff; short filling time; limited CO and inc filling pressure (causes dyspnea and exercise intolerance); persistently elevated venous pressure (edema, ascites, large liver); pts present w/RHF or LHF |
| RCM Cardiac Imaging | CT or MRI (identifies constrictive pericarditis); Endomyocardial biopsy (will identify myocardial fibrosis, amyloidosis, hemochromatosis, and other disorders) |
| RCM Treatment | No good therapy; drug therapy used w/caution (diuretics for high filling pressures, vasodilators may dec filling pressure, ?Ca-channel blockers to improve diastolic compliance, digitalis/inotropic NOT indicated) |
| Pts at risk of STEMI (ST-Elevation Myocardial Infarct) | all pts should have risk factors identified every 3-5yrs; |
| Recommended Cholesterol levels; what drugs lower cholesterol, what are the side effects? | (blank) |
| Opportunities for Dr. intervention prior to occlusive coronary MI | (blank) |
| Patients taking nitroglycerine for angina should only take one pill; if pain doesn't improve in 5 min... | call 911 immediately; pts may receive instructions to chew aspirin (165-325mg) if not contraindicated or may receive aspirin en route to hospital |
| Physical exam for pts being evaluated for MI | ABCs, vital signs, general observation, JVD?, pulmonary auscultation (rales), cardiac auscultation (murmurs/gallops), stroke?, pulses?, systemic hypoperfusion (cool, clammy, pale, ashen?) |
| Differential Diagnosis of STEMI: life threatening | aortic dissection, pulmonary embolus, perforating ulcer, tension pneumothorax, boerhaave syndrome (esophagus rupture w/mediastinitis) |
| Differential Diagnosis for STEMI: other CV and non-ischemic problems | pericarditis, atypical angina, early repolarization, Wolff-Parkinson-White syndrome, deeply inverted Twaves (CNS lesion/apical hypertrophic cardiomyopathy), LV hypertropy, Brugada syndrome, myocarditis, hyperkalemia, BBB, vasospastic angina, HCM |
| Differential Diagnosis of STEMI: other non-cardiac problems | gastroesophageal reflux (GERD) and spasm, chest-wall pain, pleurisy, peptic ulcer disease, panic attack, cervical disc or neuropathic pain, biliary/pancreatic pain, somatization and psychogenic pain disorder |
| Aspirin is the 1st drug administered to pt suspected of MI | dose up to 325gm; containdications are: allergy, active peptic ulcer, recent Hx of GI or intracranial bleed, haemophilia, von Willebrand's disease, thrombocytopenia, severe liver disease |
| Prehospital issues related to STEMI | defibrillator capable; prehospital fibrinolysis (EMS to needle w/in 30min); EMS transport (EMS to balloon w/in 90min) |
| PCI (percutaneous coronary intervention) | the best anti-thrombosis therapy; alternative is use of lytic agents like TPA |
| Contraindications of TPA use | intracranial bleed, cerebrovascular lesion/tumors, ischemic stroke, suspected aortic dissection, active bleeding (incl menses), significant closed-head/facial trauma; others: anticoagulants, prior stroke, glucose levels, hi BP, seizure, pregnancy |
| If EKG shows inferior infarct, obtain R side leads for: | screen for R ventricular infarct, a common complication of inferior MI |
| Cardiac enzyme markers that are highly diagnostic for MI and more reliable than ECG: | Cardiac troponins and MB isozyme of CK; they can rule out MI in pts w/confusiong ECG or LBBB |
| Other drugs used emergently for STEMI | O2, nitroglycerin, morphine, b-blockers |
| PCI vs Fibrinolysis for STEMI: which has best outcome? | PCI if w/in time limits ~60min; an antithrombolytic may need to be administered if there is a delay in getting to the PCI |
| Other drugs used emergently for STEMI: | O2, Nitroglycerine (unless systolic BP <100mmHg, HR <50bpm, suspected RV infarct, use of phosphodiesterase inhibitor for erectile dysfxn in last 24hrs); Morphine (pain management); b-blockers (universally good) |
| STEMI Imaging: | CXR (rule out other pathology incl aortic dissection); TTE or TEE; contrast chest CT or MRI |
| Lytic therapy: most commonly used | TPA and Emminase |
| Use of TPA and the relationship with the ECG: | DON'T give to pt w/STdepression! Give to STEMI pts w/symptom onset w/in 12hrs &12-lead ECG a/w true post MI; Also give to pts w/STEMI symptoms for 12-24hrs w/continued ST elevation >0.1 and >2 precordial or limb leads |
| Findings a/w reperfusion assessment: | relief of symptoms, maintenance and restoration of hemodynamic and/or electrical instability; reduction of >50% of initial ST-segment elevation pattern on follow-up ECG 60-90min after initiation of therapy |
| Use of Heparin therapy | given to pts undergoing PCI or surgical revascularization; after alteplase, reteplase, tencteplace; after streptokinase, anistreplase, urokinase in pts at hi risk for systemic emboli; Vit K can REVERSE effect |
| Clopidogrel (plavix) indications: | for pts receiving fibrinolytic therapy who are unable to take aspirin b/c of hypersensitivity or GI intolerance; used after stent placement, MI, and has use w/angina; it is a cardio preventive drug |
| ACE and ARBs (angiotensin receptor blockers) | inhibit renin-angiotensin-aldosterone system; given orally w/in 24hrs of STEMI to pts WITHOUT hypotension, anterior MI, previous MI, CHF/pulmonary congestion, LVEF <.4 |
| Right Ventricular Infarction: ECG findings | ST elevation in R sided leads |
| Right Ventricular Infarction: Clinical findings, hemodynamics, echo, Rx | shock w/clear lungs, elevated JVP, Kussmaul sign w/breath; Inc RA pressure; Depressed RV function; Maintain RV preload, lower RV afterload, inotropic support, reperfusion |
| VPB arrhythmia: Treatment | "electrical instability;" K+, Mg++, b-blocker |
| VT arrhythmia: Treatment | "electrical instability;" antiarrhythmics, DC shock |
| AIVR arrhythmia: Treatment | "electrical instability;" bserve unless hemodynamic compromise |
| NPJT arrhythmia: Treatment | "electrical instability;" search for cause; ex: digoxin toxicity |
| Sinus tachycardia: Treatment | "pump failure/excess sympathetic tone;" treat cause; b-blocker |
| Atrial fibrillation/flutter: Treatment | "pump failure/excess sympathetic tone;" treat cause; slow ventricular rate; DC shock |
| PSVT: Treatment | "pump failure/excess sympathetic tone;" vagal maneuvers, b-blocker, verapimil/diliazen; DC shock |
| Sinus bradycardia: Treatment | "bradyarrhythmia;" treat if hemodynamically unstable; atropine/pacing |
| Junctional arrhythmia: Treatment | "bradyarrhythmia;" treat if hemodynamically unstable; atropine/pacing |
| Smoking and STEMI | encourage pt and family to stop; provide counseling, pharm therapy, formal smoking cessation programs |
| Lowering BP and STEMI | >120/80: control wt, exercise, moderate EtOH, restrict Na, healthy diet; *if >140/90, chronic kidney dx or diabetes: add b-blockers, inhibitors of renin-angiotensin-aldosterone system and drop down to <130/80 |
| Exercise and STEMI | encourage 30-60 min of activity, at least 3-4x/wk |
| Lipid management and STEMI: TG < 200mg/dL | Goal: get LDL-C << 100mg/dL; use statins; start healthy diet w/<7% calories from sat fat and <200mg/d cholestrol; inc activity; wt managment; omega-3 FAs) |
| Lipid management and STEMI: TG > 200mg/dL | Goal: get non-HDL-C << 130mg/dL; wt managment, inc activity, stop smoking; add fibrate or niacin; consider omega-3 FAs as adjunct for high TGs |
| Weight management and STEMI | goal: BMI 18.5-24.9kg/m^2; waist circumference <35 for women, <40 for men |
| Diabetes management and STEMI | goal: HbAlc < 7% near normal fasting plasma glucose; inc activity, manage wt, manage BP and cholesterol too |
| Post-MI: ACE inhibitors | (renin-angiotensin-aldosterone system blockers); use in all pts indefinately |
| Post-MI: b-blockers | use indefinately in all pts |
| Post-MI: Aspirin | administer 75-162mg/day (or 75mg/d clopidrogel or INR 2.5-3.5 warfarin) |
| Plaque formation marker | cholesterol LDL |
| Inflammation markers (many factors, infxn?) | C-reactive protein, adhesion molecules, IL-6, TNF-a, aCD-40 ligand |
| Plaque rupture markers (MQs, MMPs) | MDA modified LDL |
| Thrombosis markers (platelet activation, thrombin) | D-dimer, complement, fibrinogen, troponin, CRP, CD40L |
| Acute coronary syndrome (ACS) clinical spectrum includes: | Non-ST-segment elevation [including: unstable angina (UA), non-Q-wave myocardial infarction (NQMI)], and ST-segment elevation MI (STEMI) |
| Coronary thrombosis results from | a rupture of an unstable plaque with resultant thrombus formation |
| Unstable plaques are characterized by: | a large lipid-rich core and only a thin, fibrous cap, which is vulnerable to rupture or erosion by inflammatory cells and activated macrophages |
| The leading cause of death worldwide: | Atherothrombosis |
| Correlation of 6-month mortality w/baseline ECG findings in pts w/ACS | risk of 6-month mortality is as great as pts w/STEMI; emphasize the improtance of aggressive in-hospital and post-discharge therapy! |
| Braunwald Classification of High Risk Pts w/Unstable Angina | elevated TnT cardiac marker; ECG (angina at rest w/transient ST-seg changes, new BBB, sustained V-tach); PE (pulmonary edema, new/worse MR murmur, S3 or new/worse rale, hypotension, bradycardia, tachycardia, >75yo) |
| Braunwald Classification of Moderate Risk Pts w/Unstable Angina | slightly elevated TNT cardiac marker; ECG (T-wave inversion, pathological Q-waves); >70yo |
| Braunwald Classification of Low Risk Pts w/Unstable Angina | normal cardiac markers; ECG (normal/unchanged ECG during episode of chest discomfort) |
| ACS marker: Troponin | the greater the levels in pts presenting w/NSTE-ACS, the greater the risk of future mortality (actually, even small amounts are a/w risk of inc mortality) |
| ACS marker: B-type naturitic peptide (BNP) | a/w relative mortality risk |
| Management of Cardio-ischemia | bed rest, continuous ECG monitoring, supplemental O2 for SaO2 >90%; NTG, b-blockers, IV morphine, IABP for hemodynamic instability, ACEI for persistent hypertension in pts w/LV systolic dysfxn or CHF |
| Anti-platelet therapy | to prevent platelets from adhering to plaque fissure or rupture; activation/aggregation leading to thrombotic occlusion; reduces risk of MI |
| Aspirin and platelets | blocks activation of platelets by arachidonic acid |
| Thienopyridines (ticlopidine and clopidogrel) and platelets | block ADP-mediated platelet activation |
| Antithrombin therapy (heparin, low MW-heparin, direct thrombin inhibitors) and platelets | blocks thrombin-mediated platelet activation |
| Glycoprotein IIb/IIIa inhibitors and platelets | block platelet aggregation by inhibiting fibrin from binding to GPIIb/IIIa receptor |
| Contraindications of GPIIb/IIIa Therapy | active or recent bleeding; severe hypertension, any intracranial bleeds/lesions/tumors; major surgery/trauma, thrombocytopenia (<100,000); bleeding diathesis/warfarin w/elevated INR; avoid w/renal insufficiency/failure |
| Two types of Heparin: | Low MW Heparin (enoxaparin; SQ); Unfractionated Heparin (UFH; IV)...Enoxaparin is perferred unless CABG is planned w/in 24hrs |
| Heart Failure | clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill w/ or eject blood (dyspnea/SOB, fatigue, peripheral edema, JVD, BBB) |
| Congestive Heart Failure Stats | 5 million pts; 6.5 million hospital days/yr; 300,000 deaths/yr; 6-10% of people >65yo; 5.4% of health care budget ($38 billion); Incidence has doubled in last 10yrs |
| BNP (brain naturetic peptide) | direct correlation btw concentration and end diastolic pressure in left heart; can reflect heart failure |
| Echocardiogram | the single best diagnostic imaging tool for heart failure (also cost effective) |
| Suspected heart failure dt Signs/Sx: | assess presence of cardiac disease by ECG, CXR, BNP; If tests are abnormal do a ventricular fxn test by ECHO-doppler; If abnormal, pt has heart failure (systolic/diastolic); Identify etiology, evaluate severity, choose therapy |
| Stages in the evolution of heart failure | 1. HF risk w/o disease or symptoms; 2. Heart disease w/o symptoms; 3. Asymptomatic LV dysfunction; 4. Prior or current HF symptoms; 5. Refractory HF symptoms |
| Stages in the evolution of heart failure: Clinical Characteristics | 1. Hypertension, diabetes, elev cholesterol, fam Hx, cardiotoxins; 2. Heart disease (any); 3. Asymptomatic LV dysfxn; 4. Dyspnea, fatigue, dec exercise tolerance; 5. Marked symptoms at rest despite max therapy |
| Stages in the evolution of heart failure: Treatment | 1. Treat risk factors, avoid toxics, ACE-i in selected pts; 2/3. ACE-i, b-blockers in selected pts; 4. ACE-i, b-blockers, diuretics, digitalis; 5. Palliative therapy, mechanical assistive device, heart transplant |
| Major risk factors for CHF | coronary heart disease, high bp, CRP >7mg/L, ankle-arm index <0.9, inter-carotid wall thickness >1.88mm, diabetes |
| Direct causes of CHF | myocardial abnormalities (CHD), Hemodynamic overload, ventricular filling abnormalities, ventricular dyssynergy (abnml rhythm: ie LBBB where septum and lat wall contract), changes in cardiac rhythm |
| Major aggravating factors in CHF | medications (ex: Celebrex/Vioxx), new heart disease, myocardial ischemia |
| Initial/Ongoing Evaluation of CHF patients | identify heart disease, assess LVEF and fxnl capacity, assess volume status (use of diuretics: edema, rales, JVD, hepatomegaly, wt), lab assessment (electrolytes, renal fxn, repeat ECHO), assess prognosis |
| Prognosis is exponentially related to the LVEF | if LVEF is >40%, the prognosis is fairly good (90%) |
| Treatment objectives | inc survival, exercise capacity, quality of life, AND decrease morbidity, neurohormonal changes, progression of CHF, symptoms, cost |
| Treatment strategies | prevention (control risk factors), change lifestyle, treat etiologic cause/aggravating factors, drug therapy, personal care (team work) |
| Treatment strategies for selected patients | revascularization if ischemia causes HF, ICD (implantable cardiac defibrillator), ventricular resynch, ventricular assist device, transplant, artificial heart, neoangiogenesis, gene therapy |
| CHF Treatment: Pharmacologic Therapy | diuretics, ACE-i, b-blockers; (also: digitalis, spironolactone - improves survival) |
| Diuretics | essential to control symptoms secondary to fluid retention (edema, dyspnea, lung rales, JVD, hepatomegaly, pulmonary edema); prevents progression from HT to HF |
| Thiazide diuretics | inhibit the active transport of Cl-Na in the cortical diluting segment of the ascending limb of the loop of Henle |
| Loop diuretics | inhibit the transportof Cl-Na-K in the think portion of the ascending limb of the loop of Henle |
| Potassium-sparing diuretics | inhibit the reabsorption of Na in the distal convoluted and collecting tubules |
| ACE-Inhibitors | block conversion of angiotensin I to angiotensin II; blocks vasoconstriction, aldosterone, vasopressin, and sympathetics; Increase kinin levels (potent E2, F2 vasodilators) and inc release of fibrinolytic substances like tPA |
| ACE-Inhibitors: Adverse Effects | Hypotension (1st dose effect); worsening renal fxn, hypokalemia, cough, angioedema, rash, ageusia, neutropenia |
| ACE-Inhibitors: contraindications | intolerance (angioedema, anuric renal failure), bilateral renal artery stenosis |
| Beta-blockers: benefits from MOA | increase density of B1 receptors; inhibit cardiotoxicity of catecholamines, decrease neurohormonal activation, decrease HR, anti-ischemic, anti-hypertensive, anti-arrhythmic, anti-oxidant, anti-proliferative |
| Beta-blockers: Contraindications | *asthma (reactive airway disease); AV block (unless pacemaker), symptomatic hypotension/bradycardia |
| Digitalis (digoxin):MOA | inhibits Na-K ATPase pump; increases intracellular Na; activates exchange of Na and Ca; increased influx of Ca ==> increased cardiac contractility |
| Digitalis: contraintications | digoxin toxicity |
| Spironolactone | competitive antagonist/inhibitor of aldosterone receptor; decreased retention of Na and water (decreases edema), and increased excretion of K+ and Mg2+ (decreases arrhythmias), also decreases collagen deposition (dec fibrosis) |
| B-blockers: adverse effects | hypotension, fluid retention/worsening heart failure, fatigue, bradycardia/heart block (discontinue only in severe cases) |
| Inotropics | used for selected pts w/refractory HF |
| Nitrates | used in selected pts w/ischemia, angina, pulmonary congestion |
| ARB | used only in selected pts; contraindications to ACE-i |
| Antiarrhythmics | (only amiodarone) used in selected pts w/High risk arrhythmias |
| Anticoagulants | used in selected pts w/high risk of embolism |
| Ca channel blockers | only amlodipine; used in selected pts w/ischemia |
| Angiotensin II Receptor Blockers (ARB) | selective/competitive blocks against antiogensin II; prevents binding to the AT1 receptor; prevents vasoconstriction and proliferation; indicated in pts intolerant to ACE-i; ex: losartan, valsartan, irbersartan, candersartan |
| Nitrates | have hemodynamic effects: 1. venous dilation (dec preload: dec pulmonary congestion, ventricular size, ventricular wall stress, MVO2); 2. Coronary vasodilation (inc myocardial perfusion); 3. Arterial vasodilation (dec afterload, dec CO, dec BP) |
| Nitrates: clinical usage | CHF w/myocardial ischemia, orthopnea and paroxysmal nocturnal dyspnea, acute CHF/pulmonary edema, hypotension, renal insufficiency when intoerant to ACE-i |
| Positive inotropes: | Digitalis; Sympathomimetics (catecholamines, b-adrenergic agonists); Phosphodiesterase inhibitors (amrinone, milrinone, enoximone); Calcium sensitizers (levosimendan, pimobendan) |
| Positive inotropes: clinical usage for CHF | intended to inc contractility and CO to meet metabolic needs of body; *Refractory CHF a/w dec systolic fxn and cardiomegaly, depression of ejection fraction and elevated LV filling pressure; not for chronic therapy |
| Supraventricular arrhythmias | at risk for emboli; treat w/b-blocker, digitalis; second choice amiodarone; (c. Understand that when a person converts to sinus rhythm they are at risk of emboli) |
| Ventricular Arrhythmias | antiarrhythmic are ineffective; b-blockers reduce mortality and sudden death; control ischemia; control electrolyte distrubances; ICD (implantable cardiac defibrillator) is secondary prevention of sudden death, in sustained hemodynamic destabilizing VT, |
| Know how to differentiate diastolic heart failure from systolic (R vs. L sided) | Right heart failure: JVD, ascites in abdomen vs. lower leg edema; no crackles in lungs but may have significant abnormal lung fxn |
| Diastolic heart failure | wrong dx of HF or LVEF; 1* valve dx; restrict/infiltrat cardiomyopathy; pericardial constrict; episodic/reversible LV systol dysfxn; HT, ischemia; anemia/thyrotoxicosis; chronic pulm dx w/RHF; pulm HT; atrial myxoma; LVHypertrophy; diastolic dysfxn |
| Diastolic heart failure: treatment | treats as HF w/low LVEF; control hypertension, tachycardia, fluid retention, myocardial ischemia; Nitrates, diuretics |
| Heart Failure Models | Congestive (digoxin, diuretics); Hemodynamic (vasodilators); Neurohumoral (ACE inhibitors, b-blockers, spironolactone); Immunological (cytokine inhibitors) |
| Treatment strategies for CHF | Symptom relief (diuretics, vasodilators, inotropics); Prevention of dx progression (neurohormonal activation, ACE-i, b-blockers, spironolactone, ARBs?, ANP?, ET-1?); Reversal of HF (gene therapy?, anti-remodeling strategies?) |
| Recommendations for evaluation of pts: Class I | 1. H&P; 2. ability to perform activities; 3; Volume status (edema/retention); 4. Lab (blood count, electrolytes, creatine, glucose); 5. initial 12-lead ECG, CXR; 6. Initial 2D Echo or ventriculography for LV systolic fxn; 8. coronary arteriograph w/angina |
| Recommendations for pts at high risk of developing HF: Class I Stage A | 1. control systolic and diastolic HT; 2. Tx lipid disorders; 3. control other risks (smoking, EtOH, drugs); 4. ACE-i for atherosclerotic, DM, HT pts; 6. Control ventricular rate in supraventricular arrhythmias; 6. Tx thyroid; 7. eval signs/Sx of HF |
| Recommendations for pts at high risk of developing HF: Class IIa, Stage A | non-invasive evaluation of LV fxn in patients w/strong family Hx of cardiomyopathy or in those receiveing cardiotoxic interventions |
| Recommendations for pts w/asymptomatic LV systolic dysfxn: Class I, Stage B | ACE-i in pts w/previous AMI or reduced LVEF; B-blockade in pts w/recent AMI or reduced LVEF; valve repair for valvular stenosis/regurgitation; regular eval for signs/symptoms of HF; also Class I recommendations for stage A pts |
| Recommendations for Tx of Symptomatic LV Systolic Dysfxn: Class I, Stage C | diruetics for fluid retention; ACE-i in all pts; b-blockers in all stable pts; digitalis for Sx of HF; Withdrawal of drugs adversely affecting clinical status (usu antiarrhythmics, Ca-blockers, non-steroidal/anti-inflammatory drugs |
| Recommendations for Tx of Symptomatic LV systolic dyxfxn: Class IIa, Stage C | Spironolactone, exercise, angiotensin receptor blocker in pts avoiding ACE-i b/c cough or angioedema; hydralazine and a nitrate in pts who can't be given ACE-i b/c of hypotension or renal insufficiency |
| Recommendations for pts w/Refractory End-stage HF: Class I, Stage D | meticulous identification/control of fluid retention; referral for cardiac transplantation in eligible; referral to HF program; other class I recommendations for Staget A, B and C! |
| Cardiac Myxoma | most common primary cardiac tumor; benign; obstructive cardiac symptoms (pulmonary edema, progressive cardiac failure, embolic symptoms); Constitutional symptoms (dt associated endocrine problems, ex: Carney Complex - acromegaly); presents in 40-50yo |
| Most common complication with cardiac myxoma | mitral valve obstruction...no blood into Left ventricle prevents cardiac output |
| Cushings disease and myxomas | although related, myxomas are so rare that you may never find a cushing's pt w/one |
| Metastatic Cardiac Tumor | most common heart tumors seen; NOT PRIMARY; usu from breast, lung; cardiac tamponade from compression on ventricle and dec cardiac output; pt can die |
| Angiosarcoma | malignant tumor; non-specific, possible chest pain, SOB, malaise, fever |
| Familial cardiac myxomas | occurs w/other abnormalities as "Carney Complex." Musculoskeletal manifestations; perinatal myosin heavy chain is underlying cause of Carney complex variant (**mutation of contractile proteins relevant to cardiac tumorigenesis) |
| Why is heart disease bad? | it's worse than cancer b/c 50% of diagnosed will be dead in 2years if you can't fix the problem; most are valvular abnormalities |
| Congenital Valvular Disease | bicuspid aortic valve is most commonly seen in adult cardiology |
| Acquired valvular disease | Degenerative, rheumatic, inflammation, infectious (endocarditis), functional (mitral/tricuspid valves) |
| Prosthetic valvular disease | Any prosthesis put into a heart is considered abnormal…make sure it is better than what is being replaced |
| Trends of valvular disease | Aortic and mitral disease are common; Pulmonic is not found in adults, but is commonly related to congenital heart disease in children; Tricuspid disease is very unusual in general |
| Class I | Benefit >>> Risk, procedure/treatment SHOULD be performed/administered |
| Class II | Benefit >> Risk, additional studies w/focused objectives needed; it is REASONABLE to perform procedure/administer treatment |
| Class III | Benefit > Risk, additional studies w/broad objectives needed, additional registry data would help; procedure/treatment may be CONSIDERED |
| Class IV | Benefit < Risk, no additional studies needed; procedure/treatment should NOT be performed/administered since it is NOT HELPFUL and may be HARMFUL |
| Right Heart Failure | trouble breathing (SOB) when lying down, leg edema, crackles in lungs due to congestion, systolic hrt murmur more common, hrt will appear either dilated or hypertrophied on X-ray. L axis deviation |
| Left Heart Failure | hard to diagnose at first. R axis deviation due to hypertrophied R ventricle, lungs are usually clear unless L hrt failure is also present, abdominal ascites due to hepatic portal congestion, jugular venous distension (JVD) |
| Acute valvular disease | 2 categories: Prosthetic valvular regurgitation (shock/heart failure) AND Infection (staph endocarditis = leaky valves) |
| Subacute valvular disease | Subacute bacterial endocarditis (tired, SOB, fever, pains) OR Rheumatic heart disease (uncommon) |
| Chronic valvular disease | Valvular heart disease can be compensated (what we want) or uncompensated |
| Latent/indolent valvular disease | Mitral stenosis dt rheumatic heart disease from strep pyogenes as child (ask Jones Criteria; can develop pulmonary edema w/labor) |
| Clinical manifestations | Abnml exam (murmurs; learn timing); dyspnea & fatigue (main Sx of heart failure); angina (typically aortic stenosis dt poor flow to heart muscle); syncope (pt can’t exercise/pass out); sudden cardiac death |
| CXR | sees heart shadow, lung congestion, pericardium, aortic notch |
| Angiogram | sees blood flow thru coronary aa, etc |
| Echocardiogram | shows dynamic heart motion, valves, regurgitation, cardiac output |
| Heart Catheter (Swan-Ganz) | shows pressures in different areas of venous blood flow and pulmonary capillary wedge pressure |
| MRI | static image can show coronary arteries, pericardial fluid, aortic aneurysm |
| Oxymetry | peripheral measurement at finger for O2 sat |
| special angiograph techniques | transthoracic echocardiogram; transesophageal echo (can see vegetations of endocarditis) |
| Congenital valvular diseases - “Collagen” | Ehlers-Danlos, Marfans, Pseudoxanthoma elasticum |
| Rheumatic valvular diseases | Acute/latent/chronic; prophylasis for dental procedures; mitral valve usu involved (stenosis/insufficiency), aortic stenosis/insuff, or aortic stenosis; pulmonic is almost never involved |
| Infectious valvular disease: acute | Staph aureus, sever illness, rapid destruction, surgery often needed, OPERATE immediately |
| Infectious valvular disease: subacute | Strep viridans; vague/nonspecific illness; slowly progressive (months); antibiotics are main treatment |
| Degenerative valvular disease: calcification | Cardiac fibroskeleton, aortic valve, mitral annulus |
| Degenerative valvular disease: myxomatous change | Mitral vavle (single mitral valve replacement); aortic valve |
| Mitral apparatus | Mitral valve leaflets, chordae tendineae, papillary muscles, left ventricle, mitral annulus, left atrium |
| Murmur evaluation | Timing (systolic v. diastolic); Clicks (mitral - mid-diastolic); Snaps (mitral - diastolic; classic mitral stenosis inc intensity of S1); Character (ejection; crescendo/decrescendo; holosystolic; rumble; blowing (aortic regurgitation)) |
| Senile aortic stenosis | Presents in 70s-80s; fibrous encroachment; rigid; can’t open/close valve; normally very calcified |
| Bicupsid aortic stenosis | Congenital anomaly; presents in 40s-60s |
| Aortic stenosis | Valvular, Supravalvular (ring/web above; coarctation if close to subclavian); Subvalvular (membrane forms in L ventricular outflow track); Hypertrophic (muscular, cardiomyopathic illness) |
| Aortic stenosis symptoms | None, dyspnea, angina, effort syncope, congestive heart failure |
| Aortic stenosis signs | EKG (LVH, LBBB, LAE, LAD); Echo (LVH, LV size/fxn; AV/VLOT velocities, continuity equation - for a given valvular area measure velocity & that at stenotic location, modified Bernoulli equation, associated abnormalities) |
| Aortic Insufficiency | Aorto-annular ectasia, bicuspid AV, calcific, rheumatic, infectious, HTN, dissection, marfans, trauma, seronegative spondylarthropathies, RA, arteritis, autoimmune; regurgitation is historically dt syphilis |
| AI Symptoms | Well tolerated when young, dyspnea, nocturnal angina, palpitations |
| AI Signs | Head bob, water hammer, nail bed pulsations, double pulse, fem booming pulses, systolic/diastolic bruits, pop BP > arm +60, uvula |
| Mitral Stenosis | ECHO is best test!! Source of Arrhythmias; Require SBE prophylaxis (subacute bacterial endocarditis); Rheumatic, carcinoid, infiltrative, vegetations, neoplasm, mid-diastolic murmur |
| Know all the diagnostic signs and that it can cause R hrt failure as well | Mitral facies, palpable S1, inc S1 loudness, inc P2, diastolic rumble w/presystolic accentuation, pulmonary HTN/RV failure, asymptomatic, dyspnea, adverse tachycardia, atrial arrhythmias, hemoptysis |
| Mitral Valve Prolapse | Echocardiographic phenomenon; usu causes nothing; common in Marfans, Ehlers-Danlos; anxiety/fatigue/palpitations/orthostasis; neurocirculatory asthenia (chest pain that isn’t angina) |
| Signs of MVP | Click-murmur; dynamic ausculatation, EKG, echo |
| Mitral Regurgitation | 80% are healthy; MR detected on Doppler; many etiologies; no Sx, but causes HF; may be dt disease of valve leaflets (ex: MVP or rheumatic mitral-valve disease), alterations fxn/structure of left ventricle dt ischemia or dilated cardiomyopathy |
| Tricuspid Valve Disease | Regurgitation, stenosis (rare, exclusively rheumatic) |
| 28) Tricuspid Valve Disease: Signs and Sx | Right heart failure (ascities, hepato/splenomegaly, peripheral edema, systemic venous HT, Caravello’s sign (murmur is louder on inspiration = R heart prob); clear lungs |
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bscaryp