Cardiology

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Cardiology
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Acute Coronary Syndromes
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Acute Coronary Syndromes

• Unstable Angina (UA)
• Non-ST-elevation acute myocardial infarction
  (NSTEMI)
• Mostly non-Q-wave MI (NQMI)
• Few Q-wave MI (QwMI)
• ST-elevation acute myocardial infarction (STEMI)
• Mostly Q-wave MI (QwMI)
• Few non-Q-wave MI (NQMI)

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Patient History

• Identification of ACS patients
• CP, pressure, tightness, heaviness
• Radiates to neck, jaw, shoulders, back, one or
  both arms
• Indigestion, heartburn, nausea/vomiting
• Shortness of breath
• Weakness, dizziness, lightheadedness, loss of
  consciousness

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Patient History (Contd)

• Special Considerations
• Look for atypical symptoms in females, diabetics,
  and elderly
• Initial Evaluation
• Symptoms suggesting ACS require physician
  evaluation and 12-lead ECG
• Patients with known CAD should go directly to ED
  that can perform reperfusion therapy if indicated

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Early Risk Stratification

• High, Intermediate, or Low
• Figure likelihood of acute ischemia
• Base it on Hx, PE, ECG, cardiac markers
• Cardiac-specific troponin
• 12-lead ECG within 10 minutes
• If negative, repeat in 6-12h, and draw myoglobin
  or CK-MB in meantime
• Search for non-coronary causes of Sx

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Early Risk Stratification (Contd)

• Predictors of ischemia
• Traditional risk factors weakly predict risk of
  ACS (HTN, hypercholesterolemia, smoking, DM)
  although they are good predictors of poor
  outcomes, given ACS(especially peripheral or
  carotid arterial Dz)
• Family history not a useful indicator of
  diagnosis or prognosis
• Symptoms, ECG findings, cardiac markers much more
  important in risk stratification

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Early Risk Stratification (Contd)

• Smokers Paradox
• Current smoking associated with lower risk of
  death in setting of ACS
• Less severe underlying CAD
• Smokers develop thrombi on less severe plaques
  and at earlier ages

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Early Risk Stratification (Contd)

• Electrocardiogram
• gt90 patients with 1mm STE in 2 or more
  contiguous leads will have AMI
• 1-6 of patients with normal ECG will eventually
  be proved to have NSTEMI
• Serum cardiac markers
• Quantitative relationship exists between
  magnitude of elevation and adverse outcomes

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Early Risk Stratification (Contd)

• Cardiac troponins
• High specificity for cardiac muscle, virtually
  diagnostic of MI, especially with EKG changes
  (Subunits cTnT and cTnI)
• 100 of patients with MI will have elevated
  troponin within first 24 hours
• Rise within 3-6 hours of ischemic event
• Peak at approximately 24 hours
• Remain elevated for up to 7-14 days

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Early Risk Stratification (Contd)

• Cardiac troponins
• Elevated troponin with normal EKG would indicate
  unstable angina, warrant further evaluation in
  absence of EKG changes
• May benefit from GP IIb/IIIa inhibitors and LMWH

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Early Risk Stratification (Contd)

• Creatine Kinase (CK)
• Recently principal serum marker
• CK-MM (skeletal) and CK-MB (cardiac)
• Myocardial damage likely if
• CK-MB is increased 25-50, OR
• CK-MB exceeds 5 of the total CK
• Levels rise within 4-6h after ischemic event
• Levels return to normal in 36-48h

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Early Risk Stratification (Contd)

• Myoglobin
• Completely non-specific
• Elevation within 1-2 hours of cardiac event
• Brief elevation (lt24h) and non-specific
• Absence can rule out myocardial necrosis
• Useful in patient with symptoms and EKG changes
  who presents to ED before CK and troponin
  elevation is detectable

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Early Risk Stratification (Contd)

• Comparison of Cardiac Markers
• CK-MB subforms, myoglobin as most efficient for
  early diagnosis (lt6h)
• cTnT cTnI highly cardiac-specific, efficient
  for late diagnosis of MI (think both diagnosis
  prognosis)

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Early Risk Stratification (Contd)

• Integration of history with markers
• Presentation with recurrent ACS Sx one week
  following AMI
• cTnT or cTnI will be still elevated
• Screen for necrosis with myoglobin
• C-reactive protein
• With negative serum cardiac markers, elevated CRP
  leads to increased risk of adverse outcome

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Immediate Management

• Categorization using Hx, ECG, markers
• Non cardiac Dx appropriate care plan for that
  Dx
• Chronic stable angina
• Possible ACS
• Definite ACS

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Acute EKG Changes

• Decisions about fibrinolytic therapy often based
  only on Sx and ECG
• Elevation of ST-segments in 2 or more contiguous
  leads, 1mm or greater
• May or may not have T-wave inversions or Q waves

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Preserving Myocardium

• ST-segment elevation
• ASA initially
• Cannot substitute ibuprofen, naproxen or other
  non-ASA NSAIDs
• Acceptable to substitute clopidogrel (Plavix)
  150mg STAT, then 75mg qd
• B blocker
• Fibrinolysis or percutaneous coronary
  intervention (PCI)

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Percutaneous Coronary Intervention (PCI)

• Balloon angioplasty or angioplasty with stent
  placement
• Best results when performed within 2 hours of
  symptom onset
• If this isnt possible, then fibrinolytics are
  preferred
• Advantages (over Fibrinolytics)
• Lower recurrent angina
• Less residual stenosis
• Less bleeding risk
• Higher reperfusion rates

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Fibrinolytic Therapy

• Indications for therapy
• ST-segment elevation or new left bundle-branch
  block
• Symptom onset no more than 12 hours prior to Tx
  (if Sx have resolved)
• May be given gt12 hours if Sx persist
• No upper age limit defined, but caution advised
  for the very elderly

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Fibrinolytic Therapy (Contd)

• Nonselective
• Streptokinase 1.5 MU over in 30-60 min
  Anistreplase 30mg over 5 min
• Antigenic
• Heparin coadministration not routine
• Selective
• Ateplase 100 mg over 90 min
• Reteplase 10 U x 2 over 30 min
• Non-antigenic
• Heparin coadministration - routine

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Fibrinolytic Therapy Contraindications

• Absolute
• Previous hemorrhagic stroke any time
• Other CVA lt 1 yr
• Intracranial neoplasm
• Active internal bleeding (lt2 wks)
• Suspected aortic dissection
• Relative
• BPgt 180/110
• Anticoagulants in theraputic doses INR gt2
• Recent internal bleeding (2-4 wks)
• Pregnancy
• Active PUD
• For Streptokinase/anistreplase prior exposure
  (especially 5d-2yr)

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Fibrinolytic Therapy (Contd)

• Advantages over PCI
• More universal access
• Shorter time to treatment
• Greater clinical trial data
• Lower initial cost
• Less dependent on physician experience

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Adjunctive Treatments

• Supplemental Oxygen
• No evidence of benefit in absence of hypoxemia or
  respiratory distress
• Inhaled oxygen only if SaO2 declines to less than
  90

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Adjunctive Treatments (Contd)

• Antithrombotic Therapy (not including STEMI)
• Possible ACSASA or clopidogrel, if ASA allergic
• Likely/Definite ACSASA (SQ LMWH or IV
  heparin)
• Definite ACS w/continuing ischemia or planned
  interventionASA IV heparin IV platelet GP
  IIb/IIIa antagonist

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Heparin Recommendations

• Indications
• PCI
• Reperfusion with alteplase/retaplase
• Non-ST elevation MI
• High risk for systemic emboli large or anterior
  MI, previous embolus, LV Thrombosis
• Dosage
• I.V. Heparin
• Bolus 60 Li/Kg
• Maintenance 12 U/kg/hr
• Max 1000 U/Kg if gt 70kg
• LMWH- Enoxaprin (Lovenox) 1mg/kg b.i.d
• I.V. heparin commonly used in PCI and Reperfusion
  Therapy while LMWH used in NSTEMI and high risk
  for systemic emboli

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Adjunctive Treatments (Contd)

• Sublingual nitroglycerin
• Typically give 0.4mg sublingual tablets
• Every five minutes, three doses total
• IV nitroglycerin
• Initiate for those refractory to sublingual
• Already taking IV beta-blocker
• Non-hypotensive

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Adjunctive Treatments (Contd)

• IV nitroglycerin (continued)
• Without ST-segment elevation only administer
  with angina refractory to nitro SQ and morphine
• ST-segment elevation administer for 24-48 hours
  of symptom onset
• Drug of choice for MI-associated HTN
• Keep systolic BP gt105-110mm Hg

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Adjunctive Treatments (Contd)

• Morphine Sulphate
• Analgesic of choice
• For patients who dont respond to 3 serial
  sublingual NTG tablets
• 1-5mg IV, repeat every 5-30 minutes prn
• Meperidine for those allergic to morphine

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Adjunctive Treatments (Contd)

• Beta-blockers
• Improve short long-term outcomes
• Greatest survival benefit occurs first day
• Lower mortality/re-infarction with IV compared to
  oral administration
• Start intravenously, then follow with oral
  administration in high risk patients
• Orally in intermediate and low-risk patients

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Adjunctive Treatments (Contd)

• Beta blockers
• Significant under-treatment problem
• Only 15 of MI patients get IV beta-blockers
• Only 40 get oral beta-blockers
• Contraindications
• Marked 1st degree AV block
• Any form of 2nd or 3rd degree AV block (without
  pacemaker)
• Hx asthma (Relative)
• Severe LV dysfunction with CHF

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Adjunctive Treatments (Contd)

• Angiotensin-converting enzyme inhibitors (ACEI)
• Use as afterload-reducing therapy with diminished
  LV function after MI
• Large ST-segment elevation anterior wall MIs
• EF lt normal
• Begin Rx 12-24 hours after event
• Based on HOPE trial nearly all get ACEI

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Adjunctive Treatments (Contd)

• Angiotensin-converting enzyme inhibitors (ACEI)
• ACEI slow or stop myocardial remodeling
• Shown to reduce mortality in patients with AMI,
  those with recent MI and LV dysfunction, and
  diabetics with LV dysfunction

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Adjunctive Treatments (Contd)

• Glycoprotein IIB/IIIA inhibitors
• For use with coronary stents
• For use when planning PCI
• HMG-CoA Reductase Inhibitors (statins)
• Use of statins becoming standard care for
  non-hyperlipidemic patients with acute myocardial
  infarction

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Adjunctive Treatments (Contd)

• Magnesium
• Only for correction of Mg deficits or Tx of
  torsades de pointes
• Mg deficits just as common as potassium deficits
  among those receiving diuretics
• Lidocaine and amiodarone
• No benefit from routine use during AMI
• Only when indicated as part of ACLS
• Calcium channel blockers for persistent angina
  symptoms despite B blockers and Nitrates

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Chronic Coronary Syndrome
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Chronic Coronary Syndrome (Stable Angina)

• Cardiovascular disease is the leading cause of
  death in the United States
• The morbidity and socioeconomic costs of CAD will
  increase as the geriatric population increases
• The major benefit of surgical revascularization
  is in sicker patients based on the extent of
  disease, presence of LV dysfuntion, and severity
  of angina

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Treatment Options

• Medical therapy includes cardiac medications,
  aggressive reduction of risk factors, adjuvant
  anti-platelet therapy, and anticoagulant therapy
• Percutaneous Coronary Intervention (PCI)
• Surgery - Coronary Artery Bypass Graft - CABG

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Risk Stratification

• Risk stratification variables
• Amount of jeopardized myocardium
• Frequency,severity, and stability of angina are
  predictive of subsequent cardiac event
• Number of diseased vessels
• Amount of irreversibly necrotic myocardium
  reflected by LV function - also one of the most
  significant predictors of survival
• Comorbidities

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Risk Stratification (Contd)

• Age as a predictive factor
• Older patients do not do as well with either
  surgical or medical treatment as younger
  patients, but absolute benefit is greater
• In terms of relative survival revascularization
  is better than medical therapy
• Exercise duration during stress testing is one of
  the strongest predictors of survival and outcome

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Risk Stratification (Contd)

• Low risk normal LV function, normal resting ECG,
  no CHF, and stable angina
• High risk marked decrease LV function, ECG -
  ischemic ST-T or Q, presence of CHF, unstable
  angina
• Intermediate risk dont meet all the criteria
  for either low or high risk

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High Risk - Need CABG

• NYHA Class I and II with
• L Main disease
• Severe proximal L Ant. Descending disease
• 3-vessel disease with moderate to severe LV
  dysfunction or moderate to severe ischemia
• NYHA class III or IV
• Regardless of the of vessels, stronger
  indication if LV dysfunction or significant
  ischemia

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Intermediate Risk

• Treatment choices
• PCI - doesnt prevent death or MI, can relieve
  symptoms
• Medical therapy - can prevent MI and increase
  survival
• Combination PCI and Medical

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Low Risk - Medical

• Low Risk - medical therapy indicated
• NYHA class I and II
• Single or two vessel if not L main or proximal
  LAD
• Mild ischemia
• Mild LV dysfunction
• If symptoms not relieved go to PCI, if fails then
  CABG

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Treatment Comparisons

• Mortality benefit has not been shown for PCI over
  medical, except in diabetics with 2 vessel
  disease. However, it improves exercise tolerance
  and gives more relief of angina
• Comparisons of bypass and angioplasty fail to
  show significant differences in mortality or
  infarction rates

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Treatment

• Therapeutic Life Style Changes
• Low cholesterol diet
• Smoking cessation
• Achieve and maintain ideal body weight
• 30-60 minutes of physical activity daily
• Precipitating Factors
• Strenuous activity
• Anemia
• Valvular disease
• Arrthymias

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Treatment (Contd)

• Medical Therapy
• Eliminate or control coronary risk factors
• Life style changes
• Control precipitating factors
• Appropriate anti-ischemic medications
• Risk Factors
• Hypertension
• Diabetes
• Smoking
• Hyperlipidemia
• Obesity
• Low exercise

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Medications - Nitrates

• Action
• Inhibit platelet aggregation and adhesion
• Venous arterial dilators (at higher doses)
• Indications
• Relief of angina (ischemia)
• Prophylactic to improve exercise tolerance
• Forms
• Sublingual, spray, buccal, oral, IV, topical

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Medications Beta Blockers

• Action changes pathophysiology to decrease
  symptomatic silent ischemia, and frequency of
  cardiac events
• Indications decrease symptoms decrease
  mortality
• Examples cardioselective acebutolol, atenolol,
  and metoprolol

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Medications Beta-Blockers (Contd)

• For patients with asthma selective B1
  (myocardial) are better, but at higher doses the
  selectivity is lost
• Beta-blocker use does improve survival post MI

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Medications Calcium Channel Blockers

• Action block calcium entry into the myocardial
  smooth muscle ? muscle relaxation vasodilation
• Indications decrease silent and overt ischemia
• Examples amlodipine and felodipine are both safe
  in CHF. Avoid short acting dihydropyridines

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Medical Therapy

• Start with monotherapy - a beta blocker (strong
  data)
• Combination therapy if response not adequate
• Beta-blocker nitrate
• Beta-blocker calcium channel blocker
• Beta blocker calcium channel blocker nitrate

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Medications - Aspirin

• Decreases vasoconstriction and platelet
  activation by inhibiting production of
  thromboxane A2
• Decreases
• Short long term mortality
• Rate of cardiac events
• Stroke
• Acute myocardial syndromes

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Medications Lipid Lowering

• Decreasing LDL lowers risk of fatal non-fatal
  cardiac events
• Decreasing cholesterol with statins slows
  progression of plaque may decrease plaque
• Goal LDL with CAD lt 100

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Medications - Antioxidants

• Vitamin A - no proven benefit
• Vitamin E recent trials (HOPE), no benefit

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Heart Failure
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Heart Failure

• Definition Insufficient cardiac function to
  meet the bodys needs
• Clinically a combination of rales and an S-3
  gallop are highly suggestive of heart failure
• Right-sided heart failure can present as pitting
  edema, JVD, and hepatojugular reflux (HJR)

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Symptoms of Heart Failure

• SOB
• Fatigue
• Lack of Energy
• Lightheadedness
• Confusion
• Dyspnea
• Orthopnea

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Physical Findings

• Rales
• Pedal Edema
• JVD
• HJR
• Sinus Tachycardia
• S-3 Gallop (Best heard with the bell and with the
  patient in the left lateral decubitus position)

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Systolic Dysfunction

• The walls of the ventricles are thin with reduced
  contractility
• With end-stage disease the patient has dilation
  of at least three cardiac chambers

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Diastolic Dysfunction

• With diastolic dysfunction we see concentric
  hypertrophy of the ventricles with impaired
  diastolic filling which results in decreased
  stroke volume and decrease cardiac output
• Thickened ventricular chamber walls with
  preserved or increased contractility
• Normal or increased ejection fraction
• Incidence 40 of heart failure in those gt65 yr

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Diastolic Dysfunction (Contd)

• Systolic and Diastolic Dysfunction often overlap
• Typically patients with HTN develop concentric
  hypertrophy first
• If HTN remains untreated the systolic dysfunction
  may result

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Classification Systems

• ACC/AHA
• Stage A Risk factors only
• Stage B Decreased EF without symptoms
• Stage C Symptoms
• Stage D Symptoms at rest

• NYHA
• Class I No limitation of activity
• Class II Ordinary activity causes symptoms
• Class III Minimal activity causes symptoms
• Class IV Symptoms at rest

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Diagnosis

• Clinical As indicated above the diagnosis of
  CHF is primarily a clinical one. See Symptoms and
  Physical Findings above
• Diagnostics An echocardiogram should be
  obtained to evaluate ventricular size and to
  measure EF, but remember the EF may be normal or
  increased in diastolic dysfunction
• Brain Natriuretic Peptide (BNP) is a serum test
  which can be suggestive of CHF however, the
  diagnosis can usually be made clinically

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Treatment

• Treatment of the patient with CHF is aimed
  primarily at reducing symptoms, improving
  functional ability, and reducing the risk of
  progression of heart failure
• Reducing risk factors of CHF such as HTN,
  hypercholesterolemia, DM, sedentary lifestyle,
  obesity, and smoking can be of benefit

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Treatment (Contd)

• Diastolic Dysfunction Remember the problem is
  the inability of the myocardium to relax
  secondary to hypertrophy and subsequent decreased
  compliance
• Therefore positive inotropic agents should not be
  used
• Negative inotropic agents such as B-blockers or
  calcium channel blockers are useful

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Treatment (Contd)

• Treatment similar to Chronic Coronary Syndrome
• Diuretics may provide symptomatic relief but
  excess use can reduce filling pressure and lower
  cardiac output

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Treatment ACE Inhibitors

• Treatment of choice for patients with diastolic
  dysfunction because they may reduce ventricular
  hypertrophy
• Also treatment of choice for patients with
  systolic dysfunction
• Use cautiously to avoid excessive BP lowering
  which could impair ventricular filling

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Valvular Disease

• Aortic Stenosis
• Mitral Stenosis
• Aortic Regurgitation
• Mitral Regurgitation
• Mitral Valve Prolapse
• All require SBE prophylaxis

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Aortic Stenosis

• Usually idiopathic
• Calcification degeneration of aortic leaflets
• Symptoms - angina, exertional syncope, dyspnea
• Average survival after symptom onset is 2-3 years
• Critical stenosis valve area lt 0.8cm2, or
  gradient of gt 50 mm Hg

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Aortic Stenosis (Contd)

• Systolic ejection murmur radiates to the neck,
  peak of murmur moves later into systole as
  stenosis increases, increased stenosis leads to
  softer murmur
• Monitor by echocardiography
• Mild every 5 years
• Moderate every 2 years
• Severe annually
• No medical treatment

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Aortic Stenosis Treatment

• Surgical valve replacement indicated if moderate
  to severe aortic stenosis and symptoms or signs
  of left ventricular dysfunction
• Prognosis with surgery is excellent
• Should not do stress testing, especially if
  symptomatic

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Mitral Stenosis

• Commonly a sequela of rheumatic fever
• Womengtmen, progressive -slowly early in the
  course, then accelerates with time
• Usual onset of sxs. with A-fib or pregnancy
  causing L heart failure, can be R sided, can
  have hemoptysis
• Apical rumbling, diastolic murmur may have
  opening snap, loudest early diastole, loud 1st
  heart sound is common

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Mitral Stenosis (Contd)

• Echocardiography -- use for diagnosis
  determining treatment options
• Asymptomatic - Follow up
• Mild symptoms - diuresis
• Moderate/severe - Surgical options balloon
  valvotomy, open commissurotomy, mitral valve
  replacement

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Aortic Regurgitation

• Common Causes rheumatic fever, endocarditis,
  collagen vascular disease, aortic dissection,
  syphilis bicuspid valve
• Increased stroke volume leads to systolic HTN and
  high pulse pressure and increased afterload
  causes LV systolic dysfunction
• May be asymptomatic until severe LV dysfunction,
  early on is reversible - later not
• Diastolic blowing murmur, L sternal border may
  have diastolic rumble apex

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Aortic Regurgitation (Contd)

• Asymptomatic with severe regurg
• Annual Echo
• Consider long-acting nifedipine, ACE, or
  hydralazine
• Asymptomatic with milder regurg
• Echo if any change in symptoms
• Symptomatic more than mild Class
• Should have replacement or reconstruction of
  valve to avoid LV damage
• Do before LVEF lt55, end syst. dimensiongt 55mm,
  or end dias. dimension gt75mm

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Mitral Regurgitation

• Causes
• Infective endocarditis
• Degenerative valvular disease
• Rheumatic Fever
• Mechanics
• Vol. overload causes LVH and LA enlargement
  leading to impaired LV function, and pulmonary
  hypertension
• PE
• Holosystolic murmur, may radiate to axilla, upper
  sternal border, or subscapular
• May have displacement of LV impulse, soft S1, S2
  widely split, S3 indicates severe disease not
  necessarily failure

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Mitral Regurgitation (Contd)

• Evaluation
• Echo for etiology, morphology semi-quantitative
  estimate of severity
• Damage can occur before symptoms are present
• Surgery (repair better than replacement)
  indicated if
• LV dysfunction
• Moderate to severe symptoms
• Ejection fractionlt60
• End-systolic dimension close to 45mm

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Mitral Valve Prolapse

• Definition
• Billowing of one or both mitral valve leaflets
  into the L atrium during systole
• May be accompanied by mitral regurgitation
• Prevalence
• Previously felt to be about 15
• Now 2-6 in the general population
• Symptoms attributed to MVP
• Palpitations
• Anxiety
• Chest pain
• Hyperventilation
• Dyspnea

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Mitral Valve Prolapse (Contd)

• PE findings
• Mid-systolic click often with late systolic
  murmur
• Standing--decreased end diastolic volume -- click
  and murmur shortly after S1
• Squatting --increased end diastolic volume --
  click and murmur more toward S2
• More common in patients with thoracic skeletal
  abnormalities
• Echo for diagnosis, repeat only if mitral
  regurgitation

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Mitral Valve Prolapse (Contd)

• Management
• Asymptomatic - reassurance
• Symptomatic - Beta blockers, cessation of
  tobacco, alcohol, and caffeine may help
• SBE prophylaxis if mitral regurgitation, audible
  click and murmur, or regurgitation on Echo
• Hx of focal neuro events give ASA, stop smoking
  and oral contraceptives

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Mitral Valve Prolapse Monitoring

• Asymptomatic with no or mild mitral
  regurgitation
• Evaluate clinically each 3 - 5 years
• Repeat Echo if CV symptoms develop, a change in
  physical findings suggests progression of mitral
  regurg, or high risk characteristics on initial
  Echo
• High-risk patients
• Annual exam

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Arrhythmias

• Palpitations
• Supraventricular Tachycardia
• Atrial Fibrillation
• Wide-complex Tachycardia

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Palpitations

• Common non-specific symptom of cardiac
  arrhythmias
• History
• When did they start?
• What sets it off?
• How long does it last?
• Other symptoms with it?
• Drug, diet, past medical, psych history

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Palpitations (Contd)

• BASIC WORK UP
• Physical exam
• ECG
• Electrolytes
• CBC
• Chem panel

• OTHER TESTS
• Stress test
• Holter monitor
• Event monitor
• Echo
• EP stimulation studies
• Cardiac cath

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Supraventricular Tachycardia

• Narrow QRS (? ½ large box)
• Keys to management
• Determine if regular or irregular
• Determine if patient hemodynamically stable
• If not stable then cardiovert immediately
• Determine etiology

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Supraventricular Tachycardia (Contd)
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Supraventricular Tachycardia Treatment

• Hemodynamically Unstable
• Cardiovert with 100 - 200 joules
• Hemodynamically Stable
• In ED
• Vagal maneuver
• Adenosine or I.V. AV nodal blocking drug
• Treat underlying condition
• Hypoxia, heart failure, acid/base disturbance

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Atrial Fibrillation Interpretation

• Irregularly irregular
• No evidence of sinus p-wave activity
• If QRS wide - not V-tach because irregularly
  irregular
• If no P-waves - look at lead II on ECG
• If ventricular response to new onset a-fib (lt150)
  consider drug effect, acute MI or sick sinus
  syndrome

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Atrial Fibrillation Management

• Hemodynamically UNstable
• SYNCHRONIZED CARDIOVERSION
• Hemodynamically Stable
• Find cause
• Fix cause if possible
• Slow ventricular response
• Convert rhythm
• Prevent thromboembolism

93
Atrial Fibrillation Causes

• Most common causes
• Heart Failure
• Ischemic Heart Disease
• Hypertensive Heart Disease
• Studies to help find and fix causes
• ECG, Echo
• Labs - Thyroid, Chem profile, CBC, Drug screen
  (consider cocaine)
• CXR

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Treatment of AfibRate Control or Conversion

• No differences in morbidity or mortality between
  options
• Rate control
• AV nodal blocking B blockers, Diltiazem/Verapamil
  , Digoxin
• Amiodarone
• Conversion
• Electrical conversion with or without drug
  therapy
• Drug conversion
• Flecainide not in structural heart disease
• Procainamide/quinidine used less 2 to side
  effects and proarrhythmic effects
• Sotalol/Amiodarone more commonly used

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Atrial FibrillationPrevent Thromboembolism

• New onset A-fib
• No heparin if converted within 48 hrs
• Takes 2 - 3 days for clot to form
• Afib gt 48 hours
• Anticoagulate for 3 weeks before attempting
  cardioversion
• TEE (no clot) LMWH/heparin immediate
  cardioversion
• Paroxysmal A-fib treated the same
• Anticoagulate for 3-4 weeks past conversion

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Wide Complex Tachycardia (WCT)

• Fast, regular, wide QRS, no atrial activity
  identified
• VT accounts for 80 of regular WCT
• Other causes
• SVT with pre-existing BBB
• SVT with aberrant conduction

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Wide Complex TachycardiaManagement

• NO pulse
• Unsynchronized defibrillation
• Pulse hemodynamically unstable
• Synchronized cardioversion
• Pulse hemodynamically stable
• Presume VT - lidocaine or amiodarone
• Refine diagnosis by looking at ECG
• Cardiovert if
• Patient decompensates
• Medical treatment unsuccessful

98
Abdominal Aortic Aneurysms (AAA)

• 10th leading cause of death
• Localized dilation gt 4cm
• 90 infrarenal
• Most asymptomatic
• Pulsatile abdominal mass
• Incidental finding on U/S, CT
• Rupture risk related to size
• 4-5cm low risk
• gt7cm 75 rupture/5 years
• Major risk factors male, age, smoking

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Abdominal Aortic Aneurysms (AAA) (Contd)

• U/S best for diagnosis/surveillance
• Surgical repair if
• gt 5cm in low surgical risk patient
• gt 6cm high risk (MI, CHF, angina)
• Expansion gt 0.5cm/6 months
• Surgical excision graft vs. endovascular stent
• 3x gt risk of death from aneurysm than elective
  repair

100
Aortic Dissection

• Stanford classification
• Type A ascending aorta and arch
• Type B descending aorta
• Mostly age 60-89 males (31)
• Marfans age 30-49
• Sudden onset of severe, persistent, tearing chest
  pain

101
Aortic Dissection (Contd)

• Risk factors
• Hypertension
• Pregnancy
• Chest trauma
• Cocaine use
• Cardiovascular surgery
• Marfans syndrome
• Ehlers-Danlos syndrome

102
Aortic Dissection (Contd)

• Suggestive CXR findings
• Wide superior mediastinum
• Abnormal aortic contour
• Left pleural effusion
• Double density of descending aorta
• Diagnosis
• TEE (best if patient unstable)
• MRA (best if stable - good vascular anatomy)
• Also by CT or Spiral CT
• Angiogram

103
Aortic Dissection (Contd)

• Treatment requires emergent aggressive reduction
  of
• Blood Pressure - systolic lt 110
• Pulsatile flow (avoid tachycardia)
• Recommend IV propranolol or sodium nitroprusside
• Type A - emergent surgical repair
• Type B - aggressive drug therapy

104
Peripheral Arterial Occlusive Disease

• Claudication of lower extremities
• Ankle-brachial index (ABI) lt1.0
• Roughly correlates with severity
• Rest pain with ABI lt 0.3
• Pain-free distance walked indicates severity
• 2 blocks mild
• 1 block moderate
• 1/2 block severe
• Rest pain at night implies severe insufficiency
  and impending limb loss

105
Peripheral Arterial Occlusive Disease (Contd)

• Therapy
• Smoking cessation
• Blood pressure control
• Lipid control
• Daily walking (stop for claudication)
• Thromboendarterectomy
• Percutaneous transluminal angioplasty (PTA)
• Surgical graft

106
Peripheral Arterial Occlusive Disease (Contd)

• Drug Treatment
• Low dose aspirin (80-325mg daily)
• Cilostazol (Pletal) - increase pain-free walking
• ASA/Clopidogrel (Plavix) - reduce vascular
  complication
• Sildenafil (Viagra) for associated impotence
  (caution with nitrate use)

107
Hypertension

• Reduce BP to prevent
• Stroke
• Cardiac disease
• Renal failure

108
Determine Blood Pressure Stage

• Optimal lt120 / lt80
• Normal lt130 / lt85
• High-Normal 130 - 139 / 85 - 89
• Stage 1 HTN 140 159 / 90 - 99
• Stage 2 HTN 160 - 179 / 100 - 109
• Stage 3 HTN ? 180 / ? 110

109
Major Risk Factors

• Smoking
• Dyslipidemia
• Diabetes Mellitus
• Age gt 60 years
• Gender
• Men Postmenopausal Women
• Family History of Cardiovascular Disease
• Women lt age 65 Men lt age 55

110
Risk Group Determinants

• Target Organ Damage (TOD)
• Stroke or TIA
• Nephropathy
• Peripheral Arterial Disease
• Hypertensive Retinopathy

• Clinical Cardiovascular Disease (CCD)
• Left Ventricular Hypertrophy
• Angina / Prior MI
• Prior CABG
• Heart Failure

111
Treatment Recommendations

• Risk Group A No major risk factors No TOD/CCD
• High-normal (130-139/85-89)
• Lifestyle modification
• Stage 1 (140-159/90-99)
• Lifestyle modification (up to 12 months)
• Stages 2 and 3 (?160/?100)
• Drug therapy Lifestyle modification

112
Treatment Recommendations (Contd)

• Risk Group B at least one major risk factor, not
  including diabetes, no TOD/CCD
• High-normal (130-139/85-89)
• Lifestyle modification
• Stage 1(140-159/90-99)
• Lifestyle modification (up to 6 months)
• For patients with multiple risk factors,
  clinicians should consider drugs as initial
  therapy
• Stages 2 and 3 (?160/?100)
• Drug therapy Lifestyle modification

113
Treatment Recommendations (Contd)

• Risk Group CTOD/CCD and/or diabetes, with or
  without other risk factors
• High-normal (130-139/85-89)
• Lifestyle modification
• Drug Therapy for those with heart failure, renal
  insufficiency or diabetes Lifestyle modification
• Stage 1(140-159/90-99)
• Drug therapy Lifestyle modification
• Stages 2 and 3 (?160/?100)
• Drug therapy Lifestyle modification

114
Treatment of HTN

• Start with a diuretic or beta-blocker
• Unless compelling indications for other drugs
• If no response, try a drug from another class or
  add a second agent from a different class
• Use a diuretic if not already used

115
HTN Drug Treatment

• Diuretics
• Decrease mortality in hypertensive patients
• Reduce stroke risk in elderly with isolated
  systolic hypertension
• /- beta blocker or long-acting dihydropyridine
  calcium channel blocker

116
Drug Treatment

• Beta-blockers - various kinds
• Cardioselective (?1gt ?2 receptor effects) at low
  doses
• Intrinsic Sympathomimetic Activity (ISA)
• Less bradycardia, less HDL lowering/TG raising
• Clinical utility - undefined

117
HTN Drug Treatment (Contd)

• ACE Inhibitors
• Reduce mortality in CAD (HOPE trial)
• Prolong survival in CHF or LV dysfunction after
  MI
• Preserve renal function in diabetes
• Angiotensin II Receptor Blockers
• Avoids cough
• Studies support some benefits of ACEIs but data
  not as vigorous

118
HTN Drug Treatment (Contd)

• Calcium-Channel Blockers
• Work via vasodilation
• Risk of CAD CHF may be greater vs. ACEI,
  beta-blockers, diuretics
• Others
• Direct vasodilators (hydralazine, minoxidil)
• ?-blockers (prazosin, terazosin, doxazosin)
• Central ?-agonists (clonidine, methyldopa,)
• Adrenergic antagonists (reserpine, guanadrel)

119
Hyperlipidemia

• Adult Treatment Panel III (ATP III)
• Adjust intensity of lipid reduction to patients
  CHD risk
• Reduce risk most in those at highest risk
• Intensive lipid lowering in CHD patients
• New focus on primary prevention in patients with
  multiple risk factors
• LDL is a major cause of CHD
• LDL-lowering is initial focus of therapy

120
Screening Recommendations

• ATP III
• Fasting Lipid Profile every 5 years after age 20
• Non-fasting Total Cholesterol HDL as second
  choice
• ACP USPSTF
• All men gt 35 years, women gt 45 years old
• Young adults (gt20) with other risk factors

121
Classification (From ATP III)

• LDL Cholesterol - Primary Target of Therapy
• lt 100 Optimal
• 100-129 Near Optimal
• 130-159 Borderline High
• 160-189 High
• gt190 Very high

• Total Cholesterol
• lt200 Desirable
• 200-239 Borderline High
• gt240 High
• HDL Cholesterol
• lt40 Low
• gt60 High

122
Determine Risk Factors

• CHD or equivalent
• Clinical CHD or diabetes
• Symptomatic carotid artery disease
• Peripheral arterial disease
• Abdominal Aortic Aneurysm

• Major Risk Factors
• Cigarette smoking
• Hypertension
• Low HDL (lt 40)
• Family history of premature CHD
• Father/brother lt 55yrs
• Mother/sisterlt 65 yrs
• Age
• Men gt 45 yrs
• Women gt 55 yrs

123
LDL Goals

• CHD or equivalent (10 year risk gt20)
• LDL Goal lt100
• 2 Risk Factors (10 year risk lt20)
• LDL Goal lt130
• 0-1 Risk Factors
• LDL Goal lt160
• Start Therapuetic Lifestyle Change when LDL gt goal

124
LDL Drug Management

• CHD or equivalent (10 year risk gt20)
• Consider drug therapy LDL gt 130
• 2 Risk Factors(10 year risk lt20)
• If 10 year risk 10 20
• Consider drug therapy LDL gt 130
• If 10 year risk lt10
• Consider drug therapy LDL gt 160
• 0-1 Risk Factors
• Consider drug therapy LDL gt 190

125
Dietary Management

• Therapeutic Lifestyle Change (TLC)
• ATP III term for diet weight management
  physical activity
• Diet (similar to old Step 2 diet)
• Reduce Fat (25 - 30 of calories)
• Limit saturated fat (lt7 calories) and
  cholesterol (lt 200 mg)

126
Medications

• Statins (HMG CoA reductase inhibitors)
• Lower LDL 18-55
• Raise HDL 5-15
• Lower Triglycerides (Tg) 7-30
• Bile acid sequestrants
• Lower LDL 15-30
• Raise HDL 3-5
• Tg no change or increased

• Nicotinic acid (Niacin)
• Lower LDL 5-25
• Raise HDL 15-35
• Lower Tg 20-50
• Fibric acids
• Lower LDL 5-20
• Raise HDL 10-20
• Lower Tg 20-50

127
HMG CoA Reductase Inhibitors (Statins)

• Usually drug of choice
• Inhibit formation of cholesterol
• Reduce MI and total mortality (with or without
  CHD)
• Reduce risk of stroke
• Require liver enzyme monitoring
• Baseline, 12 wks after initiation/dose increase,
  then periodically
• Side effects
• Myositis (lt0.7), hepatitis (lt0.3)

128
Other Medications

• Niacin
• Causes prostaglandin-mediated flushing
• Overcome by aspirin pre-treatment
• Adverse effect of hepatitis
• Bile-acid sequestrants (Cholestyramine)
• Liver converts cholesterol to bile acids
• Cause constipation and gas
• Fibric Acids (Gemfibrozil, Fenofibrate)
• Possible cholelithiasis, hepatitis, myositis