Cardiology[2] - Archer USMLE step 3

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Archer USMLE step 3 cardiology lecture notes. These lecture notes are samples and are intended for use with Archer video lectures. For video lectures, please log in at http://www.ccsworkshop.com/Pay_Per_View.html

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Cardiology[2] - Archer USMLE step 3

  1. 1. Archer online USMLE reviews www.ccsworkshop.com All Rights reserved Archer Slides are intended for use with Archer USMLE step 3 video lectures. Hence, most slides are very brief summaries of the concepts which will be addressed in a detailed way with focus on High-yield concepts in the Video lectures. These slides are only SAMPLES
  2. 2. <ul><li>Unstable angina </li></ul><ul><li>Acute MI </li></ul><ul><li>Vaso spastic angina </li></ul><ul><li>Lab studies, cxr, ekg, CE, Cardiac cath stat and fix it if STEMI, If not STEMI  f/u with treatment  Aspirin, plavix, heparin/lmwh, beta blocker, statin, ACEI  GP IIb/IIIa inhibitors only if STEMI or progressive NSTEMI with continuous symps or progressive EKG changes </li></ul><ul><li>Differential diagnosis  costochondritis, dissection, pneumonia, panic attacks </li></ul><ul><li>MCC of epigastric pain  ACS </li></ul>
  3. 3. <ul><li>Sinus bradycardia ( HR < 60, Sinus) </li></ul><ul><li>- No symptoms, HR > 40 – observe </li></ul><ul><li>- Symptoms, HR < 60 – Atropine followed by pacemaker. First transcutaneous pacer and then transvenos pacer and if you think it’s a permanent issue, permanent pacer </li></ul><ul><li>- HR < 40 Irrespective of symptoms – Atropine and if no response , then pacemaker. </li></ul><ul><li>- Symptoms of bradycardia that needs above approach are symptoms of poor perfusion ( Shock, altered mental status, ongoing chestpain, dizziness ) or SOB (CHF) </li></ul><ul><li>Heart Blocks </li></ul><ul><li>Ventricular fibrillation / Ventricular tachycardia. </li></ul><ul><li>Papillary muscle rupture ( Acute MR )– Diagnose, stabilize first with inotropic support and IABP and then surgery ASAP </li></ul><ul><li>Ventricular septal defect – Rx similar as with papillary muscle rupture </li></ul><ul><li>Cardiogenic shock </li></ul><ul><li>Fibrinous pericarditis ( use ASA, Not NSAIDS) </li></ul><ul><li>Dresslers syndrome </li></ul>
  4. 4. <ul><li>Heart Block </li></ul><ul><ul><li>First check the EKG to make sure that the bradycardia is secondary to a heart block not just a simple sinus bradycardia. </li></ul></ul><ul><ul><li>If symptomatic bradycardia ( symptoms of poor perfusion) and if EKG shows sinus bradycardia or First degree or Mobitz type I  give atropine and proceed to Transcutaneous pacemaker ( sedate the patient before you place it) </li></ul></ul><ul><ul><li>If symptomatic bradycardia and the EKG shows Mobitz Type 2 or Third degree heart block, reach for transcutaneous pacer STAT. No role for atropine here as it does not work ( severe block) and even diminishes the ventricular rate further. ( Remember atropine acts at SA node level) </li></ul></ul><ul><ul><li>If a complete heart block  even if asymptomatic, place a transcutaneous pacer. Then Transvenos pacing and once patient is stable and if heart block is persistent, take him to OR to place a Permanent pacemaker </li></ul></ul>
  5. 5. <ul><li>Called Intra aortic balloon counterpulsation </li></ul><ul><li>Mechanism </li></ul><ul><ul><ul><li>Increases cardiac output by reducing afterload </li></ul></ul></ul><ul><ul><ul><li>Increases coronary blood flow </li></ul></ul></ul><ul><ul><ul><li>Important indications </li></ul></ul></ul><ul><ul><ul><ul><ul><li>Cardiogenic shock after anterior wall STEMI – as a bridge to coronary revascularization </li></ul></ul></ul></ul></ul><ul><ul><ul><li>Cardiogenic shock from post MI complications such as Acute MR due to papillary muscle rupture or VSD. As a bridge to surgery </li></ul></ul></ul><ul><ul><ul><li>Unstable angina </li></ul></ul></ul><ul><ul><ul><li>Post cardiothoracic surgery. </li></ul></ul></ul><ul><li>Absolute Contraindications : </li></ul><ul><ul><ul><ul><li>Aortic dissection </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Severe Aortic regurgitation </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Severe peripheral vascular disease ( ballon inflation here may cause further occlusion and limb ischemia) </li></ul></ul></ul></ul><ul><li>Some clinical questions : Remember Athero-embolism complications can occur after IABP removal </li></ul>
  6. 6. Table 1: Hemodynamic effects of IABP Therapy
  7. 7. <ul><li>Counseling – diet, life style changes – Stop smoking, cardiac diet </li></ul><ul><li>BP control under 140/90. Less than 130/80 if Diabetic. </li></ul><ul><li>LDL Cholesterol target < 100 </li></ul><ul><li>Supervised exercise program. </li></ul><ul><li>Physical activity should be slowly increased with a target to return to normal activity in 6 weeks – should perform about 30 minutes of aerobic activity daily. </li></ul><ul><li>Sub maximal stress test 7 days post MI to decide on exercise prescription. </li></ul><ul><li>Sex after MI : </li></ul><ul><ul><ul><li>Most people may return to sexual activity gradually in 4 weeks. However, people with severe anginal symptoms post MI will need further evaluation prior to returning to Sex </li></ul></ul></ul><ul><ul><ul><li>Higher levels of erectile dysfunction and decreased levels of sexual contact has been reported after MI in men. Most of it is related to anxiety ( some fear sudden death during sex). Also, remember that most post MI patients are on a beta blocker  so, evaluate if it could be the possible etiology </li></ul></ul></ul><ul><ul><ul><li>Phoshodiesterase inhibitors can be safely started post MI –however, educate the patients on its dreadful interaction with nitrates. </li></ul></ul></ul>
  8. 8. <ul><li>Diabetes Mellitus </li></ul><ul><li>Peripheral Arterial Disease </li></ul><ul><li>Abdominal Aorta Aneurysm </li></ul><ul><li>Carotid Artery Stenosis </li></ul><ul><li>TARGETS For CAD and Its Equivalents </li></ul><ul><li>LDL < 100 ( < 70 is preferred target) </li></ul><ul><li>Non HDL cholesterol < 150 ( total chol – HDL preferred<130) </li></ul><ul><li>Triglycerides < 150 </li></ul><ul><li>HDL > 40(MEN) and >50(Women) </li></ul><ul><li>B.P<130/80 ( Updated Guidelines) </li></ul><ul><li>DM nephropathy BP TARGET < 125/75 </li></ul>
  9. 9. <ul><li>A 71-year-old woman is hospitalized with an acute inferior wall myocardial infarction. On physical examination, her heart rate is 100/min, respiration rate is 18/min, and blood pressure is 171/88 mm Hg. The heart sounds are regular,with normal S1 and S2, an S4, and a grade 1/6 aortic outflow murmur at the left upper sternal border. The remainder of the physical examination is unremarkable. </li></ul><ul><li>Electrocardiography shows sinus rhythm and inferior ST-segment elevation. After the administration of aspirin, heparin, metoprolol, and nitroglycerin, cardiac catheterization shows a mid-right coronary artery occlusion, which is treated with angioplasty and stent placement. The remaining coronary arteries are normal.She does well until the second hospital day when she develops acute dyspnea. On physical examination her heart rate is 131/min, respiration rate is 40/min, and blood pressure is 88/58 mm Hg. EKG  Sinus tachycardia. There are pulmonary crackles, a hyperdynamic precordium, a summation gallop, and a short, early-systolic murmur. </li></ul><ul><li>Which of the following is the best course of emergency action for this patient? </li></ul><ul><li>( A ) Right heart catheterization </li></ul><ul><li>( B ) Bedside cardioversion </li></ul><ul><li>( C ) Bedside echocardiography </li></ul><ul><li>( D ) Coronary arteriography </li></ul>
  10. 10. <ul><li>The sudden appearance of pulmonary edema 2 to 7 days following an acute inferior infarction is characteristic of papillary muscle rupture. </li></ul><ul><li>This is a typical presentation of acute, severe mitral regurgitation due to papillary muscle rupture complicatingmyocardial infarction. </li></ul><ul><li>Ischemic papillary muscle rupture most often occurs after inferior wall myocardial infarction dueto the single vessel blood supply (posterior descending artery) of the posteromedial papillary muscle, typically 2 to 7 </li></ul><ul><li>days after acute infarction, and more often after delayed presentation. </li></ul><ul><li>Clinical presentation is that of acute pulmonaryedema, variably associated with hypotension depending on the severity of regurgitation. </li></ul><ul><li>The murmur may not be holosystolic due to a nondilated, noncompliant left atrium. </li></ul><ul><li>Transthoracic echocardiography may show the ruptured papillary muscle and mitral regurgitation, although poor image quality may necessitate transesophageal imaging. </li></ul>
  11. 11. <ul><li>A 55-year-old man is evaluated in the emergency department for chest pain of 1-hour duration. The pain is sharp,intense, and radiates to the back. There is no pleuritic component, and he denies shortness of breath. He has a 10-year history of hypertension and has smoked one pack of cigarettes daily for 35 years.On physical examination, his heart rate is 75/min and blood pressure is 168/92 mm Hg. Oxygen saturation is 98% on room air. Heart sounds are regular with an S4, a normal S1 and S2, and a grade 1/6 aortic outflow murmur. The remainder of the examination is normal. Portable chest radiography shows a normal cardiac silhouette and clear lungfields. Transthoracic echocardiography shows left ventricular hypertrophy, normal left ventricular wall motion during chest pain, and moderate aortic regurgitation. The EKG shows LVH with strain pattern. Which of the following is the best test to confirm the diagnosis? </li></ul><ul><li>( A ) Serum creatine kinase and troponin </li></ul><ul><li>( B ) Computed tomography scan of the thorax </li></ul><ul><li>( C ) Ventilation-perfusion scan </li></ul><ul><li>( D ) Coronary angiography </li></ul>
  12. 12. <ul><li>Consider aortic dissection in patients with sharp chest pain, hypertension, and aortic regurgitation. </li></ul><ul><li>Diagnostic tests for aortic dissection include computed tomography, trans esophageal echocardiography , and magnetic resonance imaging. </li></ul>
  13. 13. <ul><li>Stress test  involves stressing the heart + evaluating cardiac response to stress. </li></ul><ul><li>Indications : </li></ul><ul><ul><ul><li>Diagnose CAD ( patients with risk factors and symptoms of chestpain. Assess pre-test probability) </li></ul></ul></ul><ul><ul><ul><li>In a person with known CAD, for assessing the functional capacity i.e; safety of work/ recreation ( Sub-maximal stress test) </li></ul></ul></ul><ul><li>Contraindications : </li></ul><ul><ul><ul><li>STEMI less than 4 days </li></ul></ul></ul><ul><ul><ul><li>Acute aortic dissection </li></ul></ul></ul><ul><ul><ul><li>Myocarditis, Pericarditis </li></ul></ul></ul><ul><ul><ul><li>Third degree heartblock </li></ul></ul></ul><ul><ul><ul><li>Poorly controlled Heart failure </li></ul></ul></ul><ul><ul><ul><li>Severe AS with valve area < 1cm2 </li></ul></ul></ul><ul><li>For patients presenting with chestpain and CAD risk factors, rule out Acute MI first with serial cardiac enzymes before sending for Stress test </li></ul>
  14. 16. <ul><li>Exercise Stress Test (treadmill) </li></ul><ul><ul><ul><ul><ul><li>most preferred test in anyone who can exercise well as it allows to assess exercise capacity and symptoms also apart from evaluating ST segment response. </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>most sensitive if patients can reach 85% of Target Heart Rate (220-age) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>EKG component alone is sufficient if there is a Low probability of CAD. EKG component specificity is lower for patients with resting EKG changes ( LBBB, early repolarizations, LVH, WPW, pacemaker rhythms) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Combining nuclear component increases sensitivity and specificity. Nuclear imaging is preferred when patient has intermediate probability of CAD. </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>In LBBB, LVH, WPW , Paced LV rhythms, using a tachycardic stress may produce reversible defects on myocardial perfusion study in the septal area even in absence of CAD ( False Positives)  so, the solution here is to use vasodilator stress ( Stress them with out increasing the heart rate ). </li></ul></ul></ul></ul></ul>
  15. 17. <ul><li>Vasodilator Stress: Dipyrimadole (Persantine) or Adenosine Stress test </li></ul><ul><ul><li>Mechanism here is by coronary vasodilation and coronary steal phenomenon ( Diseased coronary arteries cannot dilate in response to adenosine where as healthy arteries dilate well. This leads to more coronary blood flow in healthy arteries as opposed to diseased arteries. Hence, induces ischemia which can show up as reversible defect on the Nuclear imaging) </li></ul></ul><ul><ul><li>Preferred Choice in </li></ul></ul><ul><ul><ul><ul><li>patients who cannot exercise ( osteoarthritis, joint problems, obesity, previous CVA, Peripheral arterial disease) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>patients with LBBB , those already on b-blockers ( prevents achieving target heart rate in tachycardic stress), paced rhythm, freq PVCs, poorly controlled hypertension and moderate Aortic Stenosis </li></ul></ul></ul></ul><ul><ul><li>Contraindications: </li></ul></ul><ul><ul><ul><ul><li>moderate to severe Asthma or COPD ( these agents cause bronchospasm) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>high grade heart blocks ( second or third degree </li></ul></ul></ul></ul><ul><ul><ul><ul><li>patients already on dipyridamole ( Aggrenox) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>patients with recent caffeine ingestion i.e; in last 12 to 24 hours ( caffeine blocks adenosine receptors and decreases vasodilatory properties of adenosine) </li></ul></ul></ul></ul><ul><ul><li>Adverse Effects : Chestpain, Severe headache, Hypotension – Reverse with Aminophylline </li></ul></ul><ul><ul><li>In patients who can not walk and who also have contraindications to Vasodilator stress, use Inotropic stress ( Dobutamine Stress Echo) </li></ul></ul>
  16. 18. <ul><li>Positive Inotropic Stress: Dobutamine Stress Echo </li></ul><ul><li>Mechanism : </li></ul><ul><ul><ul><li>Dobutamine increases Heart rate as well as contractility of myocardium and produces ischemia. </li></ul></ul></ul><ul><ul><ul><li>Echo is then used to evaluate wall motion abnormailities during dobutamine infusion. An ischemic myocardial wall is hypokinetic . Also, useful to evaluate VIABILITY ( when in doubt regarding myocardial stunning vs. Scar)  A scar is Akinetic and does not improve with stress. A stunned myocardium (viable) may be initially akinetic but improves with stress. </li></ul></ul></ul><ul><li>Preferred Choice in </li></ul><ul><ul><li>Patients who can not walk and who also have contra indications for Dipyridamole Stress ( Moderate to severe COPD or asthma, High grade heartblocks) </li></ul></ul><ul><ul><li>Post Ischemia patients or Ischemic Mitral regurgitation ( To assess viability) </li></ul></ul><ul><li>Not good for </li></ul><ul><ul><li>patients with LBBB, on beta blockers, paced rhythm, freq PVCs or atrial arrhythmias, or poorly controlled hypertension </li></ul></ul><ul><li>Prior to Dobutamine stress test, hold AM dose of b-blocker </li></ul>
  17. 19. <ul><li>A 52 y/o man with presents to your office with complaints of exertional chest pain for the past 4 weeks. The chest pain is usually left sided, occurs on walking about three blocks and goes away with rest. He has developed a habit of taking rest when the chest pain comes and he did not think it needed medical attention until his friend told him yesterday that it might be a symptom of heart disease. He is concerned and requests your recommendation. He denies any chest pain or shortness of breath now. He also reports no change in quality or intensity of his chest pain. His past medical history is significant for Hypertension and Smoking . His medications include lisinopril and hydrochlorthiazide. Physical examination is benign. The next best step in establishing the diagnosis in this patient is : </li></ul><ul><li>Electrocardiogram </li></ul><ul><li>2 D -Echocadiogram </li></ul><ul><li>Exercise – EKG Stress Test </li></ul><ul><li>Dobutamine Stress Echocardiogram </li></ul><ul><li>Persantin Stress Test </li></ul><ul><li>Cardiac Catheterization </li></ul>
  18. 20. <ul><li>Exercise EKG Stress test is the preferred test in evaluating patients who can walk and are presenting with symptoms typical of CAD. The patient gives a history of typical exertional chest pain that improves with rest. This highly suggestive of stable angina. </li></ul><ul><li>The patient has no chest pain now. A resting ECG is useful to show if there are any baseline changes but it will not establish the diagnosis. An ECG should be obtained during stress to establish the diagnosis of ischemic heart disease </li></ul><ul><li>In patients who can walk, Exercise stress is the preferred modality since one can also assess the symptoms, ekg changes and functional capacity. In patients who cannot walk, persantin (dipyridamole) stress is preferred </li></ul><ul><li>Dobutamine echocardiogram is reserved for patients who can not walk and have contraindications to dypridamole stress test. </li></ul>
  19. 21. <ul><li>A 65 y/o man with presents to your office with complaints of exertional chest pain for the past 4 weeks. The chest pain is usually left sided, occurs on walking about three blocks and goes away with rest. He has developed a habit of taking rest when the chest pain comes and he did not think it needed medical attention until his friend told him yesterday that it might be a symptom of heart disease. He is concerned and requests your recommendation. He denies any chest pain now. He also reports no change in quality or intensity of his chest pain. His past medical history is significant for pacemaker insertion for a symptomatic second degree heart block, Hypertension, and Smoking . His medications include lisinopril, atenolol and hydrochlorthiazide. Physical examination is benign. An EKG is obtained which reveals pacemaker rhythm with secondary ST-T changes. The next best step in establishing the diagnosis in this patient is : </li></ul><ul><li>2 D -Echocadiogram </li></ul><ul><li>Exercise Stress Test ( Treadmill Stress Test) </li></ul><ul><li>Dobutamine Stress Echocardiogram </li></ul><ul><li>Persantin Stress Test </li></ul><ul><li>Cardiac Catheterization </li></ul>
  20. 22. <ul><li>Persantin is the preferred option for stress when Exercise Stress Test is not useful or can not be done. </li></ul><ul><li>Patients with pacemaker rhythms, LBBB and severe LVH, will have baseline EKG changes that may make EKG component of the Stress test difficult. However, in these conditions, Tachycardic stress ( Exercise Stress test) may also produce false positive defects on nuclear imaging. So, the solution is to use a different type of stress such as vasodilator stress ( Persantin). Moreover, this patient was also on beta blocker which makes it difficult to achieve target heart rate during the Exercise Stress. </li></ul><ul><li>Dobutamine stress test is reserved for patients with bronchospasm or heartblocks ( in conditions where persantin is contraindicated) </li></ul><ul><li>If stress test revealed ischemia, cardiac catheterization should be performed. </li></ul>
  21. 23. <ul><li>A 65 y/o man with presents to your office with complaints of exertional chest pain for the past 4 weeks. The chest pain is usually left sided, occurs on walking about one block and goes away with rest. He denies any chest pain now. He also reports no change in quality or intensity of his chest pain He also reports having been diagnosed with peripheral arterial disease about 2 months ago for which he was advised exercise therapy. He does experience leg pain on walking about one block which also improves with rest. His past medical history is significant for moderate COPD, Hypertension and a hernia repair about 3 years ago. His medications include lisinopril, hydrochlorthiazide and tiotropium inhaler. Physical examination is benign. The next best step in establishing the diagnosis in this patient is : </li></ul><ul><li>2 D -Echocadiogram </li></ul><ul><li>Exercise Stress Test ( Treadmill Stress Test) </li></ul><ul><li>Dobutamine Stress Echocardiogram </li></ul><ul><li>Persantin Stress Test </li></ul><ul><li>Cardiac Catheterization </li></ul>
  22. 24. <ul><li>This patient presents with symptoms suggestive of ischemic heart disease. So, needs a stress test to establish diagnosis. </li></ul><ul><li>He cannot walk to his maximum secondary to peripheral arterial disease and this will limit the exercise. So, exercise stress test can not be done. </li></ul><ul><li>He has moderate COPD. Using persantin in patients with COPD/ asthma can exacerbate bronchospasm . </li></ul><ul><li>The preferred choice in this patient is, therefore, Dobutamine Stress Echo. </li></ul>
  23. 25. <ul><li>Indications </li></ul><ul><li>Types </li></ul><ul><li>Choice of stress test </li></ul><ul><li> Exercise Stress Test </li></ul><ul><li> Exercise EKG stress test </li></ul><ul><li> Exercise Stress Echocardiogram ( main advantage is in patients with long standing HTN with LVH and repolarization abnormalities on EKG and also to demonstrate myocardial viability) </li></ul><ul><li>Pharmacological Stress test ( in patients who cannot walk and in pts with LBBB, LVH, repolarization abnormalities, electronically paced ventricular rhythm, preexcitation syndromes (wpw); 1mm ST segment depressions at rest - that makes EKG less interpretable and also can have false positive nuclear results with exercise stress test)  </li></ul><ul><li> Adenosine stress test </li></ul><ul><li> Dipyridamole Stress test </li></ul><ul><li> Dobutamine Stress Echo ( demonstrates viabile myocardium) </li></ul><ul><li> Nuclear Component of stress test ( Thallium) </li></ul>
  24. 26. <ul><li>Would recommend the website : www.ecglibrary.com </li></ul><ul><li>Learn some important EKGs: </li></ul><ul><ul><ul><li>Delta wave – WPW Syndrome – treatment in case of WPW with afib </li></ul></ul></ul><ul><ul><ul><li>Acute MI </li></ul></ul></ul><ul><ul><ul><li>Acute Pericarditis </li></ul></ul></ul><ul><ul><ul><li>Electrical alternans – pericardial effusion </li></ul></ul></ul><ul><ul><ul><li>S1Q3T3 Pattern in PE </li></ul></ul></ul><ul><ul><ul><li>Differentiating tachycardias from fibrillation </li></ul></ul></ul><ul><ul><ul><li>Ventricular vs. Supraventricular ( atrial ) – wide vs. narrow-complex tachycardias ( exception – WPW with afib and LBBB with tachy are usually wide. But consider a wide complex tachycardia as a Ventricular tachycardia until proven otherwise!!) </li></ul></ul></ul>
  25. 27. <ul><li>Atrial Fibrillation : causes ( structural, metabolic, hypoxic, hyperthyroid, sudden onset in immobilized pt  think PE )  determine whether stable or unstable </li></ul><ul><li>Stable  Rate control  drug therapy ( modify drug rxs depending on comorbidities  available Rxs are CCBs ( diltiazem), Beta blockers, Digoxin, Amiodarone </li></ul><ul><li>Unstable Afib  Emergent cardioversion </li></ul><ul><li>Rate control is enough. Synchronous cardioversion only in case by case basis  rate control is enough usually ( AFFIRM trial) {The risk of thromboembolic complication increases with a duration of atrial fibrillation exceeding 48 hours ( TEE before cardioversion to r/o thrombus if afib duration exceeded 48hrs) } </li></ul><ul><li>AFIB+ CHF  use digoxin  but it takes time and is not all that effective in rate control ( 60 mins for onset of action). So, Metoprolol should be used too here for rate control. </li></ul><ul><li>AFIB + Hypotension  digoxin, amiodarone after urgent cardioversion attempts. </li></ul><ul><li>Anticoagulation  heparin + warfarin overlap untill therapeutic INR is reached  then Cont Warfarin. Stroke risk increases with age, additional risk factors like hypertension </li></ul>
  26. 28. <ul><li>Urgent cardioversion is indicated only for “unstable” atrial fibrillation ( Remember if your patient had an afib duration > 48 hours, there is a risk that a thrombus is already present and cardioversion at this time would increase the risk of stroke. For this reason, you should do urgent cardioversion ( i.e; without prior TEE or prior anticoagulation) only when it is extremely needed – meaning in “UNSTABLE” cases </li></ul><ul><li>Recognize what is “unstable” afib : “URGENT” cardioversion is indicated here: </li></ul><ul><ul><li>A. symptomatic hypotension ( hemodynamically unstable) </li></ul></ul><ul><ul><li>B. ongoing myocardial ischemia ( Angina – high rate is not good) </li></ul></ul><ul><ul><li>C. CHF resistant to treatment ( In CHF, initially rate control with metoprolol + digoxin, give furosemide to treat CHF. If acute pulmonary edema, give Morphine also. If all these fail and patient continues in CHF/sob - cardiovert!) </li></ul></ul><ul><li>If patient does not fit above criteria, should not cardiovert with out knowing the atrial fibrillation duration. As we know “Rate control will alone suffice”, non urgent cardioversion is done only in select cases ( in patients where long-term anticoagulation is risky or unacceptable, patients where “atrial kick” will matter – advanced chf etc) </li></ul><ul><ul><li>For non-urgent cardioversion for afib, following criteria must be met: </li></ul></ul><ul><ul><ul><ul><li>Afib  < 48 hr duration </li></ul></ul></ul></ul><ul><ul><ul><ul><li>For afib > 48 hours  TEE showing no clot in left atrium </li></ul></ul></ul></ul><ul><ul><ul><ul><li>For afib > 48 hours  If TEE cannot be done or TEE showed atrial thrombus, anticoagulation for 3 weeks prior to and 4 weeks after cardioversion ( i.e; warfarin for 3 weeks, then cardiovert and then continue warfarin for another 4 weeks)   </li></ul></ul></ul></ul>
  27. 30. <ul><li>Factors that can increase the Risk of Stroke in Patients with Atrial Fibrillation </li></ul><ul><li>Increasing age </li></ul><ul><li>Rheumatic heart disease </li></ul><ul><li>Poor left ventricular function or recent congestive heart failure </li></ul><ul><li>Enlarged left atrium </li></ul><ul><li>Previous myocardial infarction </li></ul><ul><li>Hypertension </li></ul><ul><li>History of previous thrombo embolic events </li></ul>
  28. 31. <ul><li>Paroxysmal Atrial fibrillation </li></ul><ul><li>No other risk factors for stroke except atrial fibrillation. </li></ul><ul><li>Do you anticoagulate these pts with warfarin or would you just use aspirin? </li></ul><ul><li>Remember CHADS2 Score ( CHF, HTN, Age >75, DM, Previous Stroke/TIA) to predict the risk of stroke in an Atrial fibrillation patient. Each constituent in CHADS2 gives one point except “S” which gives 2 points in risk prediction. </li></ul><ul><ul><li>In a case of Atrial Fibrillation, if CHADS2 is 1 or more or if patient 60 yrs of age or more  start A/C with Warfarin </li></ul></ul><ul><ul><li>If CHADS2 zero and also, patient less than 60 yrs of age  lone Afib  ASA alone! </li></ul></ul><ul><li>Remember  Even if CHADS2 score is high, some patients are put only on ASA due to high bleeding risk ( eg: high fall risk in elderly etc.)  Weigh risk of thromboembolism with risk of hemorrhage </li></ul>
  29. 32. <ul><li>A 64-year-old woman with a history of rheumatic fever is evaluated for a 1-day history of abruptly worsening dyspnea.An echocardiogram obtained 6-months ago showed left atrial enlargement and diffuse calcification of the mitral valve and subvalvular apparatus, with a mean transmitral gradient of 9 mm Hg. On physical examination, she is sitting upright with labored breathing. Her heart rate is 144/min, respiration rate is 32/min, and blood pressure is 138/72 mm Hg. There are pulmonary crackles and the jugular venous pressure iselevated. Heart sounds are irregularly irregular with no murmurs. Electrocardiography shows atrial fibrillation with a ventricular rate of 139/min. Which of the following is the best immediate management for this patient? </li></ul><ul><li>( A ) Warfarin </li></ul><ul><li>( B ) Warfarin plus digoxin </li></ul><ul><li>( C ) Percutaneous balloon mitral valvotomy </li></ul><ul><li>( D ) Intravenous heparin and esmolol </li></ul><ul><li>( E ) Electric cardioversion </li></ul>
  30. 33. <ul><li>In acute heart failure due to atrial fibrillation, initial therapy must include heart rate control and anticoagulation. </li></ul><ul><li>Initial therapy should be aimed at heart rate control, to achieve rapid clinical improvement, and anticoagulation, to prevent left atrial thrombus formation and to lower thromboembolic risk. </li></ul><ul><li>Intravenous heparin achieves therapeutic anticoagulation rapidly, whereas oral warfarin requires several days to achieve therapeutic anticoagulation, during which time there is risk of a thromboembolic complication. </li></ul><ul><li>Although digoxin may be used to help control heart rate in atrial fibrillation, it takes time to work, and is often ineffective as a single therapeutic agent. </li></ul>
  31. 34. <ul><li>A 78-year-old woman is scheduled for a right nephrectomy for renal cell cancer. She underwent aortic and mitral valve replacement 12 years ago with St. Jude Medical bileaflet mechanical prostheses for rheumatic valvular disease. She has no other significant medical history. Her only medications are warfarin (with a target INR of 2.5 to 3.5) andantibiotic prophylaxis for endocarditis. Which of the following is the best plan for anticoagulation in the perioperative period? </li></ul><ul><li>( A ) Maintain the INR between 2.5 and 3.5 throughout the perioperative period. </li></ul><ul><li>( B ) Stop the warfarin 3 to 5 days before surgery and restart it 1 to 3 days after surgery. </li></ul><ul><li>( C ) Stop the warfarin 3 to 5 days before surgery and start heparin 3 days before surgery and again 1 day after surgery. </li></ul><ul><li>( D ) Maintain the INR between 1.5 and 2.5 throughout the perioperative period and begin the usual dose ofwarfarin 5 days after surgery. </li></ul><ul><li>( E ) Continue warfarin up to the day of surgery; administer vitamin K, 1 mg intravenously on the morning of surgery, and start heparin 1 day after surgery. </li></ul>
  32. 35. <ul><li>For patients at high risk for thrombosis, heparin should be substituted for warfarin before and immediately after surgery. </li></ul>
  33. 36. <ul><li>Polymorphic Ventricular tacycardia </li></ul><ul><li>Prolonged QT interval </li></ul><ul><li>Drugs prolonging QT interval </li></ul><ul><li>Management Principles of TCA toxicity </li></ul><ul><li> ICU admission, </li></ul><ul><li>Sodium bicarbonate infusion – Drug of choice if EKG changes are present </li></ul><ul><li>Antiarrhythmics (Lidocaine) </li></ul><ul><li>Magnesium sulfate </li></ul>
  34. 38. <ul><li>Idiopathic degeneration of the conducting system  Fibrosis, sclerosis, or calcification </li></ul><ul><li>Ischemic heart disease </li></ul><ul><li>Hypertensive heart disease </li></ul><ul><li>Valvular heart disease </li></ul><ul><li>Drugs  β-blockers, calcium-channel blockers, digitalis, amiodarone, adenosine, type IA antiarrhythmic drugs </li></ul><ul><li>Infectious diseases Lyme disease, infective endocarditis, myocarditis (various causes) </li></ul><ul><li>Heightened vagal tone  Young, healthy subjects (may be normal variant), Sleeping and Spinal/CNS injuries </li></ul><ul><li>Congenital AV block </li></ul><ul><li>Electrolyte disturbances  Hyperkalemia </li></ul><ul><li>Iatrogenic  radiofrequency ablations etc </li></ul><ul><li>Hypothyroidism </li></ul><ul><li>Infiltrative processes  Sarcoidosis, amyloidosis </li></ul><ul><li>Cardiac tumors Primary or secondary </li></ul><ul><li>Neuromuscular diseases Myotonic dystrophy,Erb's (limb-girdle) dystrophy, peroneal muscular atrophy </li></ul><ul><li>Familial </li></ul>
  35. 39. <ul><li>Start with hx  Ask about: </li></ul><ul><li>Dizziness , Weakness , Fatigue , Effort intolerance , Palpitations , Lightheadedness , Loss of consciousness (syncope)  symptomatic bradycardia </li></ul><ul><li>Chest pain ( ? MI/ Bradycardia itself) </li></ul><ul><li>Fever ( ? IE, myocarditis, Lymes disease ) </li></ul><ul><li>Rash ( also ask about tick bite, artralgias  ? Lyme carditis esply in endemic zones) </li></ul><ul><li>Arthropathy </li></ul><ul><li>Medication history ( b-blockers, nondihydropyridine CCBs, digitalis, clonidine ) </li></ul><ul><li>History or symptoms of other acute or chronic conditions that can cause heart block, such as: </li></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Previous/ recent MI (CAD) ( transient AV block common after inferior MI ) </li></ul></ul><ul><ul><li>Heart murmur </li></ul></ul><ul><ul><li>Kidney disease leading to hyperkalemia </li></ul></ul><ul><ul><li>Hypothyroidism </li></ul></ul><ul><ul><li>Previous heart surgery, catheterization procedure to close a septal defect, or electrophysiologic ablation procedure </li></ul></ul><ul><ul><li>Infective endocarditis complicated by a myocardial abscess or aortic ring involvement </li></ul></ul><ul><ul><li>Myocarditis </li></ul></ul><ul><ul><li>Tumors involving the myocardium </li></ul></ul><ul><ul><li>Muscular dystrophy ( myotonic dystrophy ) </li></ul></ul><ul><ul><li>Family history of AV block </li></ul></ul><ul><li>Athletes Heart : Athletic participation causes high vagal tone that can reduce AV nodal conduction!! </li></ul>
  36. 40. <ul><li>Physical Exam : </li></ul><ul><li>Look for: </li></ul><ul><li>Abnormalities in vital signs, such as: </li></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Bradycardia </li></ul></ul><ul><ul><li>Widened pulse pressure and bradycardia in third-degree AV block </li></ul></ul><ul><ul><li>Irregular pulse in second-degree AV block </li></ul></ul><ul><ul><li>Abnormalities in the jugular venous pulse </li></ul></ul><ul><li>Other abnormalities on cardiac exam suggesting structural disease, such as: </li></ul><ul><ul><li>Heaves </li></ul></ul><ul><ul><li>Thrills </li></ul></ul><ul><ul><li>Murmurs </li></ul></ul><ul><ul><li>Gallop sounds </li></ul></ul><ul><li>Other abnormalities on general physical exam suggesting an underlying predisposing condition, such as: </li></ul><ul><ul><li>Rash </li></ul></ul><ul><ul><li>Muscle atrophy </li></ul></ul><ul><ul><li>Fasciculations or myotonia </li></ul></ul><ul><ul><li>Chest scars from previous cardiac surgery </li></ul></ul><ul><ul><li>Peripheral signs of infective endocarditis </li></ul></ul><ul><ul><li>Signs of hypothyroidism </li></ul></ul>
  37. 41. <ul><li>Remember with regard to Heart Block after MI </li></ul><ul><li> Transient AV block is common after inferior MI. </li></ul><ul><li> AV block associated with anterior MI often indicates extensive necrosis. </li></ul><ul><li> 30-day mortality is increased among patients with MI who develop AV block compared to those who do not ( prognostic predictor) </li></ul>
  38. 42. The PR interval is 388 ms and constant. Each P wave is followed by a QRS complex.
  39. 43. Note the progressive lengthening of the PR interval until a P wave is blocked. The PR interval following the blocked P wave is shorter than the one before the blocked P wave. Progressive shortening of the R-R interval is best shown in the 5:4 cycle on the right of the strip
  40. 44. P waves are blocked intermittently. The PR interval does not change. Note the wide QRS complexes.
  41. 45. No relationship between the atrial and ventricular activity is present. The atrial rhythm is sinus at 90 beats/min. A slight sinus arrhythmia is present. The ventricular rhythm is a wide QRS escape rhythm at 26 beats/min.
  42. 46. Test Notes ECG with rhythm strip Essential to define the type and site of the block. Echocardiogram Useful to determine the presence and severity of structural heart disease  evidence of previous MI, hypertensive heart disease, valvular heart disease, and infective endocarditis. Transesophageal echocardiogram is superior to transthoracic echocardiogram in identifying aortic root abscesses and infections involving prosthetic heart valves Serum electrolytes To evaluate for hyperkalemia, especially in patients with kidney disease Cardiac enzymes (creatine kinase, cardiac troponin) Can identify ischemia/infarction or myocarditis as potential causes of AV block Lyme serology Can identify Lyme disease as a potential cause of AV block Serum digoxin level Can identify digitalis toxicity as a potential cause of AV block Thyroid function tests To evaluate for hypothyroidism Blood cultures To evaluate for evidence of bacteremia and possible infective endocarditis ( ? New onset heart block, bbb)
  43. 47. <ul><li>First step diagnose AV Block. Do not confuse with other sinus bradycardias or sinus pause, sino atrial exit blocks ( note “p” will be absent in sinus types) </li></ul><ul><li>Your next step is to look for reversible condition  medication/ infection, lymes, increased vagal tone, ischemia etc. </li></ul><ul><li>Discontinue the meds that are likely to slow AV nodal conduction. Reevaluate the patient after d/c of these meds </li></ul><ul><li>Hospitalize the pts if they are symptomatic </li></ul><ul><li>Hospitalize patients with symptomatic AV block to: </li></ul><ul><li> Confirm that syncope, presyncope, or symptoms of heart failure are due to AV block </li></ul><ul><li> Address reversible causes such as electrolyte abnormalities, hypervagotonia, myocardial ischemia, structural heart disease, and use of specific medications that can impair AV conduction </li></ul><ul><li> Determine the need for: </li></ul><ul><ul><li>Electrophysiologic studies </li></ul></ul><ul><ul><li>Temporary and/or permanent pacemaker placement </li></ul></ul>
  44. 48. <ul><li>Intravenous atropine, isoproterenol, or theophylline  to facilitate AV conduction in patients with symptomatic AV block . Do not use in those with infranodal block. </li></ul><ul><li>In patients with symptomatic bradycardia, including those with heart failure, myocardial ischemia, or hypotension, consider administering atropine to increase AV conduction </li></ul><ul><li> Remember that in patients with infranodal block ( Mobitz type 2 and Third degree heart block), atropine can increase the sinus rate without changing AV conduction  the net effect will be a diminished ventricular rate </li></ul><ul><li>In patients without ischemia  may use the β-agonist isoproterenol </li></ul><ul><li>May use methylxanthine derivative theophylline  but use cautiously in patients with myocardial ischemia. </li></ul><ul><li>Do not use isoproterenol or theophylline to treat bradyarrhythmias in patients with ischemic heart disease  coz they are potentially arrhythmogenic and may increase myocardial o2 demand. </li></ul>
  45. 49. <ul><li>Drug overdose leading to symptomatic heartblock: </li></ul><ul><li>For patients with β-blocker or calcium-channel blocker overdose  may use intravenous glucagon to improve hemodynamic parameters and AV conduction: </li></ul><ul><li>For patients with calcium-channel blocker overdose, administer  </li></ul><ul><ul><li>Intravenous calcium (calcium chloride, 10 to 20 mL of a 10% solution, or calcium gluconate, 30 to 60 mL of a 10% solution, over 5 minutes with repeated boluses every 15 minutes for a total of three to four doses or an infusion of 0.5 mEq of calcium/kg·h), which requires monitoring the serum calcium level and the ECG, or </li></ul></ul><ul><ul><li>Infusion of a high dose of insulin along with glucose </li></ul></ul><ul><li>For patients with hypotension not responding to above Rxs, start an infusion of a vasoactive (pressor) drug to maintain adequate systemic perfusion until pacing can be initiated. </li></ul>
  46. 50. <ul><li>Rule out reversible causes as discussed earlier </li></ul><ul><li>Temporary transcutaneous or transvenous pacemaker for symptomatic patients who do not respond to drug therapy </li></ul><ul><li>If AV block is not considered to be reversible , some experts recommend proceeding directly to permanent pacemaker implantation. </li></ul><ul><li>Consult a cardiologist (electrophysiologist) for implantation of a single- or dual-chamber permanent pacemaker </li></ul>
  47. 51. <ul><li>Systolic Vs Diastolic </li></ul><ul><li>Stages/ NYHA Classes </li></ul><ul><li>Management  ACEI, Beta blockers, Diuretics, Spironolactone if indicated ( stage III/ IV) </li></ul><ul><li> Cardiac Resynchronization therapy ( CRT) – Biventricular pacemaker for pts with NYHA Class III and widened QRS complex ( >0.12 sec) </li></ul><ul><li> Cardiac transplantation for pts with NYHA Class IV , Consider LVAD ( left ventricular assist device) in a pt waiting for transplantation. </li></ul><ul><li>CHF exacerbations </li></ul><ul><li> Rx acute episode – diuretics, low dose/ no b-block, treat HTN, Nitroglycerin, natrecor ( Do not use BNP to monitor response to Natrecor) </li></ul><ul><li> ? Secondary to what  accelerated HTN, MI, ACS, Atrial Fib, Medication/ diet noncompliance, Missed hemodialysis  Investigate the cause & Rx appropriately underlying cause for this exacerbation. </li></ul><ul><li> Prevent future exacerbations  Digoxin reduces morbidity but not mortality i.e; dig reduces the need for Heart failure hospitalizations. </li></ul>
  48. 52. <ul><li>Aspirin ( A must in CAD) </li></ul><ul><li>Beta Blocker ( A must! – reduces mortality by 35 to 65%) ( Contraindications for b-blocker in this setting  cardiogenic shock, 2 nd /3 rd degree heart block without pacemaker, Severe reactive airway disease </li></ul><ul><li> remember mild to moderate copd/asthma , DM, Peripheral arterial disease are not a contraindication for beta blockers) </li></ul><ul><li>ACEI/ ARBs( reduces mortality by 17-30%) esply if EF<45%, in pts with Class I – IV heart failure, asymptomatic LV dysfunction, Post MI, DM </li></ul><ul><li> remember ARBs are not a first line therapy in place of ACEI (ELITE trial) However, they have equivalent benefits as ACEIs  recommended for use in pts who are intolerant to ACEIs or as an add on therapy to ACEIs </li></ul><ul><li>Aldosterone Antagonists ( Spironolactone/ Eplerenone) reduces mortality by 15-30% in pts with class III/IV heart failure </li></ul><ul><li>Hydralazine + Nitrates ( Bidil) reduces mortality by 43% in African- Americans with Class III heart Failure when added to standard care.(The therapeutic role of these agents in HF patients other than African Americans should be further evaluated, but this represents a reasonable option for all HF patients who remain Class III or IV, irrespective of race or ethnicity) </li></ul><ul><li>Statin if Hyperlipidemia </li></ul>
  49. 53. <ul><li>Cough is a common side effect. </li></ul><ul><li>If ACEI can not be used because of cough, switch to ARB. </li></ul><ul><li>If ACEI or ARB, can not be used because of angioedema, consider using Hydralazine/ isosorbide combination. </li></ul>
  50. 54. <ul><li>In Acute CHF, Start at very low doses </li></ul><ul><li>Start at low dose with careful titration. Increase at intervals of at least 2 weeks until target dose. The ACC/AHA guidelines recommend using only those beta blockers and those doses that have been proven to reduce mortality (i.e. mortality reduction is not a class effect). </li></ul><ul><li>Initiation Titration Target </li></ul><ul><li>Carvedilol (preferred ) 3.125 mg bid. 6.25, 12.5 mg bid 25 mg bid </li></ul><ul><li>Metoprolol XL 12.5 mg daily 25, 50, 100, 150 mg daily 200 mg daily </li></ul><ul><li>Bisoprolol 1.25 mg daily 2.5, 5 mg daily 10 mg daily </li></ul><ul><li>CARVEDILOL is the preferred Beta Blocker  has better lipid profile than other beta blockers </li></ul><ul><li> COMET demonstrated that carvedilol (beta-1, beta-2, and alpha-1 blockade) provided a 17% mortality reduction compared to beta-1 selective blockade with metoprolol tartrate. </li></ul><ul><li> The COPERNICUS trial demonstrates survival benefits with carvedilol in patients with class IV heart failure and that therapy can be initiated during hospitalization. </li></ul><ul><li> IMPACT-HF demonstrates that in-hospital initiation is safe and improves treatment rates  Strongly consider initiation of carvedilol or switching from other beta blocker to carvedilol prior to heart failure hospital discharge, as this has been shown to improve patient compliance and treatment utilization. </li></ul>
  51. 55. <ul><li>LVEF < 0.35, Class II / III, all HF etiologies, ICD therapy reduces mortality by 23% (SCD-HeFT) </li></ul><ul><li>LVEF < 0.30, post MI: prophylactic ICD therapy indicated, reduces mortality by 31% (MADIT II)  Wait > 30 day after acute myocardial infarction before implanting ICD (DINAMIT) </li></ul><ul><li>QRS > 120 ms, LVEF < 0.35, NYHA III or IV: Cardiac resynchronization therapy plus ICD indicated, reduces mortality by 43% and death and hospitalization by 22%. (COMPANION) </li></ul><ul><li>Prophylactic Placement of an ICD device (with or without CRT) is recommended in conjunction with optimal medical treatment in all eligible HF patients without contraindications, as part of standard management. Education and counseling of patients prior to device placement is essential. </li></ul>
  52. 56. <ul><li>Also called Dual chamber pacing (biventricular pacing) </li></ul><ul><li>CRT uses uses a specialized pacemaker to re-coordinate the action of the right and left ventricles in patients with heart failure. </li></ul><ul><li>In approximately 30% of patients with heart failure, an abnormality in the heart's electrical conducting system  (called an &quot;intraventricular conduction delay&quot; or bundle branch block as evidenced by widened QRS >0.12 sec) causes the two ventricles to beat in an asynchronous fashion.  This asynchrony greatly reduces the efficiency of the ventricles in patients with heart failure, whose hearts are already damaged. </li></ul><ul><li>CRT re-coordinates the beating of the two ventricles by pacing both ventricles simultaneously. This differs from typical pacemakers, which pace only the right ventricle. </li></ul>
  53. 57. <ul><li>Indications </li></ul><ul><ul><li> NYHA Functional class III/ IV heart failure despite optimal medical therapy </li></ul></ul><ul><ul><li>QRS greater than 120 msec ( suggesting intraventricular conduction delay that leads to cardiac dyssynchrony) </li></ul></ul><ul><ul><li>Systolic HF with EF<35% </li></ul></ul><ul><ul><li>Left ventricular end diastolic dimension>55mm(dilated) </li></ul></ul><ul><li>Benefits  CRT improves quality of life and reduces re-hospitalizations for worsening heart failure. </li></ul><ul><li>? Does it reduce mortality in HF  When indicated , CRT used along with ICD has been shown to reduce mortality ( COMPANION trial). The role of CRT without an ICD in reducing the mortality is still unresolved </li></ul>
  54. 58. <ul><li>A 64-year-old man is evaluated for a progressive, 3-month history of dyspnea on exertion and orthopnea. He has a 15-year history of hypertension, hyperlipidemia, chronic renal insufficiency, coronary artery disease, and ischemic cardiomyopathy.On physical examination his heart rate is 92/min and blood pressure is 144/80 mm Hg. There is elevated jugular venous pressure, pulmonary crackles, an S3, and dependent edema.The serum creatinine is 2.8 mg/dL and serum potassium is 4.9 meq/L. Echocardiography shows dilation of the left atrium, dilation and extensive scarring of the left ventricle, and an ejection fraction of 25%. In addition to digoxin and furosemide, which of the following therapies is the optimal initial management for congestive heart failure in this patient? </li></ul><ul><li>( A ) Lisinopril </li></ul><ul><li>( B ) Lisinopril and carvedilol </li></ul><ul><li>( C ) Carvedilol </li></ul><ul><li>( D ) Hydralazine and isosorbide dinitrate </li></ul><ul><li>( E ) Hydralazine, isosorbide dinitrate, and carvedilol </li></ul>
  55. 59. <ul><li>Digoxin, diuretics, afterload-reducing therapy, and ß-blockers are associated with symptomatic improvement in patients with congestive heart failure due to systolic dysfunction. </li></ul><ul><li>Afterload-reducing therapy, ß-blockers, and in patients with stage IV left heart failure, spironolactone are associated with </li></ul><ul><li>reduced mortality. </li></ul>
  56. 60. <ul><li>HOCM vs. Aortic Stenosis Murmur differentiation </li></ul><ul><li>Carotid upstroke – delayed in AS, brisk in HOCM </li></ul>
  57. 61. <ul><li>Consider placement of an ICD in patients with HCM at high risk for sudden death, regardless of whether they are symptomatic, including those with: </li></ul><ul><li>Family history of sudden death at a young age </li></ul><ul><li>Young age (<30 years) at diagnosis </li></ul><ul><li>Unexplained syncope </li></ul><ul><li>Resuscitation from cardiac arrest </li></ul><ul><li>Nonsustained or sustained VT during Holter monitoring </li></ul><ul><li>Significant LVH (wall thickness 30 mm) </li></ul><ul><li>Abnormal BP response during exercise </li></ul>
  58. 62. <ul><li>A 40-year-old man is evaluated in the office because of a 3-week history of increasing chest pressure and exertional dyspnea. Physical examination shows a pulse rate of 65/min and a blood pressure of 155/90 mm Hg. The carotid arteries have a brisk upstroke and a bifid contour. There is a grade 4/6 systolic murmur heard best at the left sternal border in the fourth left interspace. The murmur increases with the Valsalva’s maneuver and with standing. </li></ul><ul><li>Electrocardiography shows left ventricular hypertrophy. </li></ul><ul><li>Which of the following drugs will most likely improve the patient’s symptoms? </li></ul><ul><li>( A ) Digoxin </li></ul><ul><li>( B ) Furosemide </li></ul><ul><li>( C ) Lisinopril </li></ul><ul><li>( D ) Nitroglycerin </li></ul><ul><li>( E ) Metoprolol </li></ul>
  59. 63. <ul><li>Bifid carotid pulsation, double apical impulse, a murmur that increases with Valsalva's maneuver or with standing, and left ventricular hypertrophy are typical for hypertrophiccardiomyopathy(Paradoxical SAM on echo ) </li></ul><ul><li>ß-Blockers are indicated in the treatment of hypertrophiccardiomyopathy. </li></ul><ul><li>Vasodilators and other drugs that cause afterload reduction are hazardous in patients with hypertrophic cardiomyopathy. </li></ul><ul><li>“ Drugs or maneuvers that decrease left ventricular volume or afterload generally will increase the outflow tract obstruction, and those drugs that increase volume will decrease the obstruction. Thus, diuretics should not be used as initial therapy. Nitroglycerin and other vasodilators, and other drugs that cause afterload reduction, such as angiotensin-converting enzyme inhibitors, are often hazardous to use in patients with this disease because the associated preload reduction results in diminished left ventricular volume and increased outflow tract gradient. Digoxin, and other drugs that increase myocardial contractility, should be avoided because they produce an increase in outflow tract obstruction.” </li></ul>
  60. 64. <ul><li>Administer antibiotics to patients with group A streptococcal infections to prevent rheumatic fever and to patients at risk for endocarditis. ( PRIMARY PROPHYLAXIS) </li></ul><ul><li>Give patients with group A streptococcal infections prompt antibiotic therapy to reduce the risk of rheumatic fever with either  Benzathine penicillin G, 1.2 MU im once for patients >27 kg, or </li></ul><ul><ul><li>Penicillin V, 500 mg po bid-tid for 10 days for adolescents and adults </li></ul></ul><ul><li>For patients allergic to penicillin: - erythromycin/ azithromycin </li></ul><ul><li>Ensure that patients with a history of rheumatic fever, particularly rheumatic carditis, receive long-term prophylactic antibiotic therapy to prevent recurrence: ( SECONDARY PROPHYLAXIS) </li></ul><ul><ul><li>Administer benzathine penicillin G, 1.2 million units im once a month </li></ul></ul><ul><ul><ul><li>Administer every 3 weeks in high-risk patients (e.g., patients with residual carditis or who are poorly compliant or economically disadvantaged) </li></ul></ul></ul><ul><ul><li>As an alternative to benzathine penicillin G, use: </li></ul></ul><ul><ul><ul><li>Penicillin V, / Sulfadiazine or Erythromycin </li></ul></ul></ul><ul><ul><li>Continue therapy for: </li></ul></ul><ul><ul><li>Rheumatic fever prophylaxis for at least 10 years after the last episode and at least until age 40 in patients with carditis and residual cardiac valve disease </li></ul></ul><ul><ul><li>Ten years or into adulthood (whichever is longer) in patients with carditis but no valve disease </li></ul></ul><ul><ul><li>Five years or until age 21 (whichever is longer) in patients who did not have carditis </li></ul></ul>
  61. 65. <ul><li>Jones Criteria* </li></ul><ul><li>Major manifestations </li></ul><ul><li>Carditis, Polyarthritis, Chorea, Subcutaneous nodules, Erythema marginatum </li></ul><ul><li>Minor manifestations </li></ul><ul><li>Clinical findings: Arthralgia, Fever </li></ul><ul><li>Laboratory findings: Elevated acute phase reactants  Erythrocyte sedimentation rate, C-reactive protein, </li></ul><ul><li>Prolonged PR interval </li></ul><ul><li>Supporting evidence of group A streptococcal infection  Positive throat culture of rapid streptococcal antigen test, Elevated or rising streptococcal antibody titer </li></ul><ul><li>Diagnosis +  if 2 major or 1major/2minor+ preceding strep infection </li></ul>
  62. 66. <ul><li>Antibiotics  follow with primary/ secondary prophylaxis regimens as discussed earlier. </li></ul><ul><li>Antiinflammatories  a must </li></ul><ul><li>Use salicylates if polyarthritis </li></ul><ul><li>Corticosteroids if severe carditis </li></ul><ul><li>Chorea : phenobarbital, lorazepam , haloperidol, SSRIs </li></ul>
  63. 67. <ul><li>MS </li></ul><ul><li>AS </li></ul><ul><li>MR </li></ul><ul><li>AR </li></ul>
  64. 68. <ul><li>Symptoms </li></ul><ul><ul><li>Syncope during exertion </li></ul></ul><ul><ul><li>Exertional angina </li></ul></ul><ul><ul><li>Exercise intolerance </li></ul></ul><ul><ul><li>Heart failure symptoms </li></ul></ul>
  65. 69. <ul><li>Consider aortic valve replacement in patients with symptomatic AS. </li></ul><ul><li>Consider aortic valve replacement in patients with: </li></ul><ul><ul><li>Symptomatic severe AS ( ?? SEVERE AS of <1cm2 without symptoms) </li></ul></ul><ul><ul><li>Severe AS who are undergoing coronary bypass surgery </li></ul></ul><ul><ul><li>Severe AS who are undergoing surgery on the aorta or other heart valves </li></ul></ul><ul><li>Consider valve replacement in patients with moderate AS who: </li></ul><ul><ul><li>Are undergoing other cardiac or aortic surgery </li></ul></ul><ul><ul><li>Have left ventricular dysfunction </li></ul></ul><ul><ul><li>Develop hypotension on an exercise stress test </li></ul></ul><ul><li>Aortic valvuloplasty reserved for symptomatic adult patients who are not candidates for aortic valve replacement due to comorbid conditions or in patients who do not desire surgical intervention </li></ul>
  66. 70. <ul><li>Evaluate patients with AS at least annually. </li></ul><ul><li>For patients with mild AS: </li></ul><ul><ul><li>Perform a careful history and physical examination annually </li></ul></ul><ul><li>For patients with moderate to severe AS: </li></ul><ul><ul><li>Perform an interim history and physical examination every 6 months or more frequently if symptoms occur </li></ul></ul><ul><ul><li>Reinforce the need for prophylaxis against endocarditis </li></ul></ul><ul><li>Use serial echocardiograms to evaluate left ventricular hypertrophy and function in addition to the aortic valve area: </li></ul><ul><li>Annually in patients with severe AS </li></ul><ul><li>Every 2 years in patients with moderate AS </li></ul><ul><li>Every 5 years in patients with mild AS </li></ul>
  67. 71. <ul><li>A 71-year-old woman is evaluated for fatigue and a gradual decrease in stamina during the past 3 years. Her physical examination shows a grade 2/6 crescendo-decrescendo systolic murmur heard loudest at the right upper sternal border. Which of the following features suggest that the murmur is caused by hemodynamically significant </li></ul><ul><li>aortic stenosis? </li></ul><ul><li>( A ) The murmur encompasses S1 </li></ul><ul><li>( B ) The first component of S2 is accentuated </li></ul><ul><li>( C ) The murmur peaks in the latter half of systole </li></ul><ul><li>( D ) There is an associated diastolic murmur </li></ul><ul><li>( E ) The murmur is associated with a widened pulse pressure </li></ul>
  68. 72. <ul><li>Remember murmur only occurs when there is flow across this narrow valve. Murmur cant occur early if there is severe stenosis ‘coz no flow occurs until left ventricle contracts enough to build a gradient in pressures. </li></ul><ul><li>Clinical features that are associated with the murmur of hemodynamically significant aortic stenosis include a late-peaking murmur that encompasses S2, a diminished aortic component, and a diminished and delayed carotid pulse. </li></ul><ul><li>These also suggest Aortic stenosis rather than just a sclerosis </li></ul>
  69. 73. <ul><li>A 41-year-old man with a history of a bicuspid aortic valve comes to the office for a routine follow-up examination. He runs 20 miles per week and swims 1000 yards twice weekly. He denies exertional dyspnea or declining exercise tolerance. His only medication is antibiotic prophylaxis for endocarditis. On physical examination, his heart rate is 68/min and blood pressure is 142/56 mm Hg. The cardiac apex is enlarged. The heart sounds are regular with a normal S1 and S2 and a grade 2/4 decrescendo diastolic murmur heard best at the right upper sternal border. Echocardiography shows mild left ventricular dilation; the left ventricular ejection </li></ul><ul><li>fraction is 70%. Which of the following is the best management for this patient? </li></ul><ul><li>( A ) An angiotensin-converting enzyme inhibitor </li></ul><ul><li>( B ) Rest and exercise radionuclide vetriculography </li></ul><ul><li>( C ) Exercise thallium scintigraphy </li></ul><ul><li>( D ) Heart catheterization with left ventriculography </li></ul><ul><li>( E ) Aortic valve replacement </li></ul>
  70. 74. <ul><li>Use vasodilators in patients with aortic regurgitation and </li></ul><ul><li>hypertension, left ventricular dilation, or in symptomatic </li></ul><ul><li>patients. </li></ul><ul><li>This is an asymptomatic man with severe aortic regurgitation, mild left ventricular dilation, and normal left ventricular systolic function. </li></ul><ul><li>“ Vasodilator therapy is indicated in patients with any degree of aortic regurgitation and systolic hypertension, in asymptomatic patients with severe regurgitation and left ventricular dilation (as with this patient), or in patients with severe regurgitation and symptoms of left ventricular systolic dysfunction but a contraindication for surgery. Data show that angiotensin-converting enzyme inhibitors increase exercise capacity and that nifedipine may delay the needfor surgery. In the absence of direct comparisons between the two, present recommendations suggest that either agent is acceptable” </li></ul><ul><li>Aortic valve replacement is indicated for severe aortic regurgitation plus symptoms, left ventricular systolic dysfunction, or substantial left ventricular dilation (>70 to 75mm in diastole or >50 to 55 mm in systole). </li></ul><ul><li>Assessment of left ventricular systolic function using radionuclide ventriculography or invasive left ventriculography is indicated only if the information is not available using echocardiography. </li></ul>
  71. 76. <ul><li>I n case of Infective Endocarditis, most often questions are on Prophylaxis – where to give it? How do you decide? What advise will you give patient etc!! </li></ul><ul><li>In case of IE prophylaxis  First determine if the patient has a cardiac condition that puts him at HIGH risk for IE or not and then determine whether the planned procedure presents a significant risk of bacteremia with organisms known to cause IE. </li></ul><ul><li>As per AHA (2007) guidelines, IE prophylaxis is recommended only in HIGH RISK cardiac conditions prior to high risk dental procedures alone. No prophylaxis is recommended for Moderate risk cardiac conditions (i.e; Rheumatic Heart Disease, MS, MR, MVP with MR, VSD, AS are no longer an indication for IE prophylaxis prior to ANY procedure!) </li></ul><ul><li>As per AHA-2007 guidelines, No prophylaxis is recommended in ANY cardiac condition prior to GI/ GU procedures </li></ul><ul><li>If USMLE Step3 has not updated their questions so as to meet the above guidelines, you will most likely receive a credit for such a question. </li></ul>
  72. 77. <ul><li>Cardiac Conditions Associated with Endocarditis </li></ul><ul><li>Endocarditis prophylaxis recommended </li></ul><ul><li>High-risk category </li></ul><ul><li>Prosthetic cardiac valves,bioprosthetic and homograft valves </li></ul><ul><li>Previous bacterial endocarditis </li></ul><ul><li>Complex cyanotic congenital heart disease (e.g., single ventricle states, transposition of the great arteries, tetralogy of Fallot) </li></ul><ul><li>Surgically constructed systemic pulmonary shunts or conduits </li></ul><ul><li>Endocarditis prophylaxis not recommended </li></ul><ul><li>Moderate-risk category </li></ul><ul><li>Most other congenital cardiac malformations (other than above and below) </li></ul><ul><li>Acquired valvar dysfunction (e.g., rheumatic heart disease) </li></ul><ul><li>Hypertrophic cardiomyopathy </li></ul><ul><li>Mitral valve prolapse with valvar regurgitation and/or thickened leaflets </li></ul><ul><li>Negligible-risk category (no greater risk than the general population) </li></ul><ul><li>Isolated secundum atrial septal defect </li></ul><ul><li>Surgical repair of atrial septal defect </li></ul><ul><li>ventricular septal defect, or patent ductus arteriosus (without residua beyond 6 months) </li></ul><ul><li>Previous coronary artery bypass graft surgery </li></ul><ul><li>Mitral valve prolapse without valvar regurgitation </li></ul><ul><li>Physiologic, functional, or innocent heart murmurs </li></ul><ul><li>Previous Kawasaki disease without valvar dysfunction </li></ul><ul><li>Previous rheumatic fever without valvar dysfunction </li></ul><ul><li>Cardiac pacemakers (intravascular and epicardial) and implanted defibrillators </li></ul>
  73. 78. <ul><li>IE prophylaxis recommended only for patients at highest risk for IE - prosthetic heart valves, previous IE, cyanotic congenital heart malformations, and surgically constructed systemic pulmonary shunts and injection drug users. </li></ul><ul><li>Patients at moderate risk for IE ( those with non cyanotic congenital heart disease, HOCM, MVP with regurgitation and acquired valvular dysfunction i.e; rheumatic valvular disease) are no longer a candidates for prophylaxis prior to any procedure. </li></ul><ul><li>Although IE occurs rarely, it’s high mortality ( 20 – 40% mortality rate) prompts experts to recommend antibiotic prophylaxis among high-risk patients for IE . </li></ul>
  74. 79. <ul><li>Procedures associated with high rates of bacteremia </li></ul><ul><li> most dental procedures; </li></ul><ul><li> some upper respiratory tract procedures </li></ul>
  75. 80. <ul><li>Dental procedures associated with high rates of bacteremia (>10%) with organisms known to cause IE  </li></ul><ul><li>Tooth extraction, </li></ul><ul><li>Routine cleaning and scaling </li></ul><ul><li>Any procedure involving gingival manipulation. </li></ul><ul><li>Low risk for bacteremia (No prophylaxis)  Fluoride treatment, Placement of removable orthodontic or prosthodontic appliances, Placement of rubber dam and Postoperative suture removal </li></ul>
  76. 81. <ul><li>Gastrointestinal procedures </li></ul><ul><li>Tonsillectomy, </li></ul><ul><li>Esophageal stricture dilation </li></ul><ul><li>Endoscopic retrograde cholangiography </li></ul><ul><li>variceal sclerotherapy. </li></ul><ul><li>Routine gastrointestinal procedures, including upper endoscopy or colonoscopy (with or without biopsy) </li></ul>
  77. 82. <ul><li>Transrectal biopsy of the prostate, </li></ul><ul><li>Cystoscopy </li></ul><ul><li>Urethral dilation. </li></ul><ul><li>Insertion of a Foley catheter into an infected bladder. </li></ul><ul><li>Uncomplicated Vaginal delivery </li></ul><ul><li>Caesarian section </li></ul><ul><li>Uterine D&C </li></ul><ul><li>Insertion/ removal of IUDs. </li></ul>
  78. 83. <ul><li>Rigid bronchoscopy is associated with high rates of bacteremia, whereas flexible bronchoscopy is not. </li></ul><ul><li>Give prophylaxis prior to rigid bronchoscopy </li></ul>
  79. 84. Class Procedures – High Risk Antibiotic regimens Dental Routine cleaning Tooth extraction Periodontal procedures Dental implant placement Reimplantation of avulsed teeth Endodontic instrumentation (root canal) <ul><li>Preferred oral regimen: Amoxicillin, 2 gm po </li></ul><ul><li>Oral alternative regimens: </li></ul><ul><li>Clindamycin 600 mg po, Cephalexin, 2 gm po,Cefadroxil, 2 gm po,Azithromycin, 500 mg po, Clarithromycin, 500 mg po </li></ul><ul><li>Preferred intravenous regimen: Ampicillin, 2 gm iv </li></ul><ul><li>Intravenous alternative regimen: Cefazolin, 1 gm iv, Clindamycin, 600 mg iv </li></ul>Pulmonary Rigid bronchoscopy, Surgical operations that involve respiratory mucosa Same as for dental procedures
  80. 85. <ul><li>Oral medications should be taken 60 minutes before the procedure; intravenous medications should be administered 30 minutes before the procedure. Only a single dose is recommended. </li></ul><ul><li>Azithromycin has been recommended as an alternative to clindamycin in children. </li></ul>
  81. 86. An IV drug abuser who recently survived an infective endocarditis episode come to you and says that she cannot give up IVDA but requests you for prophylaxis because she is a high risk for IE as she continues to inject herself putting herself at a risk for bacteremia  what would you do??
  82. 87. <ul><li>For injection drug users, there is no preventive strategy that could be effective other than discontinuing injection drug use. </li></ul>
  83. 88. <ul><li>Look for fever, new murmur, look for heart blocks on EKG, Blood cultures, TEE. </li></ul><ul><li>TEE shows vegetations and if pt has other criteria for IE but negative blood cx  think about previous partial Rx vs. HACEK organisms. </li></ul><ul><li>If TEE shows vegetations, cultures –ve, no other suspicion of atypical bugs or partial Rx  reconsider ur diagnosis ( most likely not IE ) </li></ul><ul><li>Antibiotics  nafcillin + gentamicin. In IVDA  Vancomycin + gentamycin ( S.viridans, Enterococci are most common bugs that cause SBE. In IVDA, S.aureus should be strongly suspected. Gentamicin is added for synergism) </li></ul><ul><li>Recognizing and managing complications  aortic valve abscess, acute AR, Acute renal failure, Septic Embolism ( a new LBBB on EKG can indicate an abscess) </li></ul><ul><li>You should not anticoagulate IE patients! </li></ul>
  84. 89. <ul><li>A 58-year-old man is evaluated for acute dyspnea and hypotension of 1-hour’s duration. He was hospitalized for fevers, chills, and weight loss after a routine dental cleaning 2 weeks ago. Blood cultures were positive for gram-positive cocci. Echocardiography showed a mobile, soft-tissue density mass on the aortic valve. Therapy with intravenous vancomycin and gentamicin was begun, and the patient was doing well until this morning.On physical examination, his heart rate is 108/min, respiration rate is 52/min, and blood pressure is 84/54 mm Hg.The cardiac apex is not displaced, murmurs are not heard, but diffuse crackles are present. After initiation of mechanical ventilation, portable chest radiography shows a normal cardiac silhouette and interstitial edema. Repeat electrocardiography shows sinus tachycardia and T-wave inversion in the inferior and lateral leads. Echocardiography shows severe aortic regurgitation. Which of the following is the best immediate therapy for this patient? </li></ul><ul><li>( A ) Intravenous heparin and a ventilation-perfusion scan </li></ul><ul><li>( B ) Intravenous ß-blockers and an angiotensin-converting enzyme inhibitor </li></ul><ul><li>( C ) Intravenous isoproterenol and nitroprusside </li></ul><ul><li>( D ) Intravenous furosemide and an aortic balloon pump </li></ul><ul><li>( E ) Left heart catheterization </li></ul>
  85. 90. <ul><li>Treat acute severe aortic regurgitation with nitroprusside, isoproterenol, and chronotropic agents (or temporary pacing). </li></ul><ul><li>An intra-aortic balloon pump is contraindicated in the setting of severe aortic regurgitation. </li></ul><ul><li>ß-Blockers should be avoided in acute aortic regurgitation.  Slowing the heart rate increases the diastolic interval and exacebates AR </li></ul><ul><li>“ The patient presents with aortic valve endocarditis, but quickly develops acute, severe aortic regurgitation with hemodynamic collapse. The physical findings of aortic regurgitation are often subtle or absent when aortic regurgitation occurs abruptly. Without time for compensatory left ventricular dilation, increased stroke volume and widened pulse pressure are absent, and the diastolic murmur may be brief or absent due to rapid equilibration of aortic and left ventricular pressures. Echocardiography confirms the clinical suspicion of acute, severe aortic regurgitation, and immediate therapy should be aimed at hemodynamic stabilization before surgery.” </li></ul><ul><li>The medical management of acute, severe aortic regurgitation is aimed at  afterload reduction to decrease the severity of regurgitation, inotropic agents to support blood pressure, and chronotropic agents (or temporary pacing) to increase heart rate and thereby decrease the diastolic interval and the severity of regurgitation. Nitroprusside and isoproterenol are appropriate first-line therapeutic interventions. </li></ul>
  86. 91. <ul><li>Symptoms – differentiate the pain from neuropathy, pseudocluadication ( lumbar canal stenosis) and Thromboangitis Obliterans (Bergers disease) </li></ul><ul><li>Differentiate Pseudoclaudication ( claudication pain does not occur with standing. But pseudoclaudication appears with standing) </li></ul><ul><li>Relief time : 5 mins of rest ( conversely, relief in pseudoclaudication occurs 30 mins after sitting or changing position) </li></ul><ul><li>Investigations  ABI, Arterial doppler, MRA (only if surgery is planned) </li></ul><ul><li>Management : 2 goals  Deal with PAD symps and then also deal with increased CAD/CVD/Mortality risk </li></ul><ul><li> Exercise therapy, supervised  best to improve walking distance </li></ul><ul><li> Cilostozol ( phosphodiesterase inhibitor) causes 40 -50% improvement in walking distance over 6 month period. ( contraindicated in Heart failure) </li></ul><ul><li> clopidogrel to deal with CAD/ mortality risk. Preferred antiplatelet therapy over aspirin in PAD pts ( CAPRIE study) </li></ul><ul><li>Surgery in select cases ( not responsive to medical Rx; Severe symps causing occupational/ life disability; risk vs.benefit ratio) </li></ul><ul><li>Cardiovascular stress test </li></ul>
  87. 93. <ul><li>Primary/ essential  follow ups, stages of HTN ( JNC VII criteria ), Lifestyle modifications, Drug Rx, choice of antihypertensive, Caution with ACEI in pregnant/ reproductive age group females </li></ul><ul><li>Secondary  whom to suspect and whom to screen ( not obese, < 30yr age group, no family hx, metabolic abnormalities on labs, ? episodic) coarctation of aorta ( Rx – Sx), hyperaldosteronism, hyperthroidism, hypercalcemia, Renal artery stenosis, Phaeochromocytoma, liddles syndrome, licorice abuse, medication induced (OCPills, NSAIDs) </li></ul>
  88. 94. Lifestyle Modification Approximate SBP Reduction Weight Reduction 5 to 10 mm Hg for every 10kg weight reduction DASH Diet 8 to 14 mm Hg Dietary Sodium Restriction 2 to 8 mm Hg Physical activity 4 to 9 mm hg Moderation of alcohol use 2 to 4 mm hg
  89. 95. <ul><li>BP Classification SBP DBP </li></ul><ul><li>Normal <120 and <80 </li></ul><ul><li>Prehypertension 120-139 or 80-89 </li></ul><ul><li>Stage 1 hypertension 140-159 or 90-99 </li></ul><ul><li>Stage 2 hypertension =/>160 or =/>100 </li></ul><ul><li> In adults (>18 years), note that classification is based on an average of 2 or more readings obtained at 2 or more separate visits . </li></ul><ul><li> When white coat HTN is suspected or if the diagnosis of sustained HTN is not certain, consider ambulatory BP monitoring or self-recorded (home) BP measurements. </li></ul>
  90. 96. <ul><li>SBP is more important Cardiovascular risk factor. </li></ul><ul><li>Cardiovascular disease risk doubles with each 20/10mmHg increment over 115/75. </li></ul><ul><li>Targets </li></ul><ul><ul><li>140/90 </li></ul></ul><ul><ul><li>130/80 if diabetic or CKD </li></ul></ul><ul><ul><li>125/75 if Diabetic Nephropathy ( microalbuminuria) </li></ul></ul><ul><li>Consider 2 agents if BP >20/10 above goal. One agent should usually be Thiazide diuretic. Second agent can be ACEI, ARB, Beta blocker or Calcium channel blockers. </li></ul><ul><li>Two or more agents usually required for effective control of blood pressure </li></ul><ul><li>Thiazides are first choice and first line agents in most cases. ( ALLHAT Trial) </li></ul>
  91. 97. <ul><li>The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial. </li></ul><ul><li>ALLHAT reiterated the importance of Diuretic as an initial therapy in Hypertension </li></ul><ul><ul><ul><li>Diuretics are more effective than ACEIs and CCBs in reducing the complications of HTN such as heart failure and angina in all races. </li></ul></ul></ul><ul><ul><ul><li>Diuretics reduced the incidence of stroke in african american population more than ACEI. </li></ul></ul></ul><ul><ul><ul><li>Diuretics are inexpensive agents. </li></ul></ul></ul><ul><ul><ul><li>For these reasons, Thiazide-type diuretics should be preferred for first-step antihypertensive drug therapy. </li></ul></ul></ul><ul><ul><ul><li>In diabetics with HTN, Thiazides should be considered as a first-line therapy, despite the fact that they may adversely affect insulin resistance and potassium balance in some individuals because the advantage is that they reduced cardiovascular events better than ACEIs or CCBs ( unless there is a compelling indication for ACEI such as microalbuminuria or Chronic Kidney Disease) </li></ul></ul></ul>
  92. 100. <ul><li>ACEI must be used in Diabetic patients with evidence of nephropathy ( microalbuminuria) unless there are contraindications. </li></ul><ul><li>Beta blockers reduce mortality in post MI patients and must be used Post MI </li></ul><ul><li>ACEI must be used in post MI patients if the EF is less than 45% </li></ul><ul><li>CKD is a compelling indication for ACEI </li></ul><ul><li>In patients with history of TIA/ CVA – ACEI and Diuretics have been shown to reduce the risk of recurrent stroke ( PROGRESS trial). </li></ul><ul><li>In CHF, use antihypertensives depending on the class of heart failure ( as discussed in previous slides). Betablockers and ACEIs are must in all classes of CHF unless contraindicated. Spironolactone must be added in Class III/ IV heart failure. Hydralazine/ Isosorbide combination is useful in african americans with Class III heart failure </li></ul>
  93. 101. <ul><li>Resistant or Refractory hypertension is defined as failure of concomitant use of three or more different antihypertensive agents ( one of which is a diuretic) to lower blood pressure to less than 140/90 mmHg in all age groups. </li></ul><ul><li>Uncontrolled blood pressure increases the risk of stroke, CHF, Aortic dissection, MI and Renal failure. </li></ul>
  94. 102. <ul><li>If response to maximal therapy is inadequate, consider the following possibilities. </li></ul><ul><li>White coat HTN </li></ul><ul><li>Suboptimal adherence to therapy </li></ul><ul><li>Volume overload </li></ul><ul><li>Concomitant drug-related causes, such as use of NSAIDs , Oral contraceptives , black licorice, Erythropoetin and Psychotropic drugs. </li></ul><ul><li>Alcohol use. </li></ul><ul><li>Recreational drugs </li></ul><ul><li>Associated conditions, such as smoking or Sleep apnea ( early morning headaches and excessive day time sleepiness, Obesity are some clues to OSA) </li></ul><ul><li>Secondary HTN </li></ul>
  95. 103. <ul><li>Medication non compliance is a major barrier in adequately controlling the blood pressure </li></ul><ul><li>Side effects and cost can reduce the adherence. </li></ul><ul><li>Some Important Side Effects: </li></ul><ul><ul><li>Beta blockers : Erectile Dysfunction, Fatigue, Depression </li></ul></ul><ul><ul><li>CCBs: Ankle Edema </li></ul></ul><ul><ul><li>ACEIs : Cough, angioedema ( rare) </li></ul></ul><ul><ul><li>Thiazides : hypokalemia, gout (hyperuricemia), hypercalcemia ( low dose thiazide is not contraindicated in gout) </li></ul></ul><ul><ul><li>Direct vasodilators ( Hydralazine, minoxidil ) – fluid retention, headache. </li></ul></ul><ul><ul><li>Spironolactone – gynecomastia, impotence </li></ul></ul><ul><ul><li>Hydralazine – drug induced lupus 9 anti histone +ve, anti dsdna negative) </li></ul></ul>
  96. 104. <ul><li>Before searching for causes of secondary hypertension which involves expensive testing, more common issues like appropriateness of the regimen, possible drug interactions, associated conditions like alcohol or drug use, poor adherence to treatment, white coat/office hypertension, volume overload, obesity and sleep apnea should be carefully evaluated and investigated! </li></ul><ul><li>After eliminating and reversal of these reversible contributing factors , if the BP is still not controlled, consider and rule out secondary HTN. </li></ul><ul><li>However, if there are any clues that point to secondary HTN ( hypokalemia on labs, episodic HTN and headaches, Abdominal bruit, rib notching on chest x-ray, Radio-femoral delay on physical exam ), that particular entity should be promptly investigated and treated. </li></ul>
  97. 105. <ul><li>NSAIDS reduce vasodilatory prostaglandins and cause afferent renal vasoconstriction and reduced renal blood flow. </li></ul><ul><li>What NSAIDS can do to your patients? </li></ul><ul><ul><ul><li>Worsen Renal insufficiency ( vasomotor component or allergic interstitial nephritis) </li></ul></ul></ul><ul><ul><ul><li>Cause Refractory Hypertension </li></ul></ul></ul><ul><ul><ul><li>Cause CHF exacerbation by causing fluid retention ( activates Renin-angiotensin axis) </li></ul></ul></ul><ul><ul><ul><li>Increase the risk of cardiovascular events. </li></ul></ul></ul><ul><ul><ul><li>Can lead to NSAID induced gastritis or Peptic ulcer </li></ul></ul></ul><ul><li>Avoid NSAIDS in </li></ul><ul><ul><ul><li>Renal Insufficiency </li></ul></ul></ul><ul><ul><ul><li>Very Elderly due to risk of renal insufficiency </li></ul></ul></ul><ul><ul><ul><li>Acute Coronary Syndrome scenarios </li></ul></ul></ul><ul><ul><ul><li>Difficult to control Hypertension </li></ul></ul></ul><ul><ul><ul><li>Congestive Heart Failure </li></ul></ul></ul>
  98. 106. <ul><li>NSAIDs are common over the counter drugs. </li></ul><ul><li>People often self medicate with NSAIDs for pain eg: osteoarthritis , low backache etc </li></ul><ul><li>Whenever a patient was previously stabilized on a given antihypertensive regimen becomes resistant to the therapy, first question to be asked is if the patient started using NSAIDs. </li></ul><ul><li>NSAIDs interfere with actions of beta blockers, thiazide diuretics, loop diuretics and ACEI. Patients taking these drugs should be warned against the use of NSAIDs. </li></ul>
  99. 107. <ul><li>Oral contraceptive pills can lead to worsening of pre-existent Hypertension in some women. </li></ul><ul><li>OCPs can also cause new onset overt HTN in women who were previously normotensive. </li></ul><ul><li>Malignant HTN can also occur in rare cases after starting OCPills </li></ul><ul><li>Management : </li></ul><ul><ul><ul><li>Discontinue OC pills in the above scenarios. </li></ul></ul></ul><ul><ul><ul><li>Return to baseline blood pressure may take 2 to 12 months after cessation of therapy. </li></ul></ul></ul><ul><ul><ul><li>Do not start OC Pills in women greater than 35 years and who also smoke since it can cause additive cardiovascular risk. </li></ul></ul></ul>
  100. 108. <ul><li>Consider it as a cause of refractory hypertension if there are clues such as obesity, neck circumference > 17 cm, snoring at night and excessive day time sleepiness. </li></ul><ul><li>Get a Sleep study ( Polysomnogram) </li></ul><ul><li>Weight reduction strategies and address secondary causes of obesity ( hypothyroidism) </li></ul><ul><li>If diagnosis confirmed, treat with CPAP at nights ( CPAP has improved BP in some studies in patients with OSA) </li></ul>
  101. 109. <ul><li>When to evaluate? </li></ul><ul><li>Causes </li></ul><ul><li>Work up </li></ul><ul><li>Treatment </li></ul>
  102. 110. <ul><li>Under age 16 or new onset diastolic Hypertension (>100 mm hg) above age 55 . </li></ul><ul><li>Under age 30 - if resistant to two or more drugs or if does not have any risk factors like morbod obesity or family history of essential HTN. </li></ul><ul><li>Any time when there is a clue on the physical exam ( cushingoid facies, central obesity, delayed femoral pulses, low blood pressure in lower extremities ) or lab values ( unexplained hypokalemia) that may suggest secondary cause. </li></ul><ul><li>Refractory hypertension after the contributory causes have been ruled out or treated. </li></ul><ul><li>Hospitalization for Hypertensive Crises ( although most common cause for crises is medication non compliance) </li></ul>
  103. 111. <ul><li>Delayed femoral pulses or low BP in lower extremities or hypertension in upper extremities  Coarctation of aorta </li></ul><ul><li>Abdominal bruit  Renal artery stenosis </li></ul><ul><li>Cushingoid facies, central obesity, ecchymoses, striae  cushing syndrome </li></ul><ul><li>Triad of pounding headache, palpitations and sweating associated with elevated BP or paroxysmal elevations of BP in a patient with otherwise stable HTN  Pheochromocytoma </li></ul><ul><li>Neck circumference > 17cm, smoring at nights, excessive day time sleepiness  Obstructive sleep apnea </li></ul>
  104. 112. <ul><li>PAC/ PRA ratio – r/o primary hyperaldosteronism ( ratio > 20 is suggestive, greater than 60 more specific). Confirm with 24 hr urinary aldosterone </li></ul><ul><li>Plasma metanephrines or 24 hr urinary metanephrines – r/o pheochromocytoma ( 24 hr urinary is more specific as well as very sensitive) </li></ul><ul><li>Dexamethasone suppression test ( Start with low dose Dexa - give 1mg Dexa and check early morning cortisol – should be less than 2.5 mcg%) r/o cushings syndrome. </li></ul><ul><li>Renal Artery MRA ( r/o renal artery stenosis) </li></ul><ul><li>Coarctation of aorta : CXR and then, MRA/ Echo </li></ul><ul><li>TSH r/o hyperthyroidism </li></ul><ul><li>Calcium r/o hypercalcemia ( hyperparathyroidism) </li></ul>
  105. 113. <ul><li>Clinical clues for diagnosing Renovascular HTN: </li></ul><ul><ul><ul><li>History and clinical findings ( abdominal bruit) </li></ul></ul></ul><ul><ul><ul><li>Sudden onset of HTN above age 55 </li></ul></ul></ul><ul><ul><ul><li>Sudden resistant HTN in previously well controlled BP. </li></ul></ul></ul><ul><ul><ul><li>Worsening renal function after starting ACEI or ARB </li></ul></ul></ul><ul><ul><ul><li>( define ACEI induced ARF) </li></ul></ul></ul><ul><ul><ul><li>Malignant HTN ( Hypertensive emergency – i.e. with target organ dysfunction) </li></ul></ul></ul><ul><ul><ul><li>Recurrent “flash” pulmonary edema </li></ul></ul></ul><ul><ul><ul><li>Low K on lab values ( remember renovascular HTN leads to secondary Hyperaldosteronism) </li></ul></ul></ul><ul><li>Causes: Atherosclerosis of Renal artery in the elderly, fibromuscular hyperplasia in the Young </li></ul><ul><li>Diagnosis : Renal MRA ( MRA is the preferred screening test now for patients with atherosclerotic renovascular disease. Renal Doppler ultrasound was the first screening test earlier but where available, MRA is better since Doppler requires techinical expertise and requires longer time to perform ) </li></ul><ul><li>Therapy : Medical ( use diuretic, add spironolactone, consider alpha blockers, consider minoxidil or hydralazine), Rx  Percutaneous transluminal angioplasty with or with out stent </li></ul>
  106. 114. <ul><li>Vasculopathy involving medium and large arteries. </li></ul><ul><li>Renal arteries are most commonly involved and the second most affected arteries are the carotids. </li></ul><ul><li>Seen commonly in Young and middle aged women. </li></ul><ul><li>Most often it is asymptomatic but can lead to Refractory hypertension. </li></ul><ul><li>Diagnostic tests involve ultrasound, MRA and angiography. Ultrasound may have a low sensitivity in asymptomatic patients. MRA is the preferred test of choice. Angiogram is the gold standard and should be used when treatment is considered. </li></ul><ul><li>Therapy : </li></ul><ul><ul><li>Asymptomatic patients – Observe </li></ul></ul><ul><ul><li>Refractory Hypertension – Angiogram and Percutaneous transluminal angioplasty of the renal artery. Stenting may be needed in complicated cases. </li></ul></ul>
  107. 115. <ul><li>Other causes and work up for secondary Hypertension – please refer Endocrinology section </li></ul>
  108. 116. <ul><li>Resistant Hypertension : after addressing the issues discussed in previous slides, add following agents in refractory HTN for better control : </li></ul><ul><ul><ul><li>Nifedepine ( Procardia XL) </li></ul></ul></ul><ul><ul><ul><li>Minoxidil </li></ul></ul></ul><ul><ul><ul><li>Hydralazine </li></ul></ul></ul><ul><ul><ul><li>Add Spironolactone </li></ul></ul></ul><ul><li>Hypertensive Urgencies </li></ul><ul><ul><ul><li>Captopril is preferred choice ( short acting and can be titrated ) </li></ul></ul></ul><ul><ul><ul><li>Labetalol </li></ul></ul></ul><ul><ul><ul><li>Fenoldapam ( preferred in patients with severe asthma/ copd where beta blocker is contraindicated) </li></ul></ul></ul><ul><li>Hypertensive Emergencies ( associated with target organ dysfunction – CHF, Flash pulmonary edema, Papilledema, Blindness, Encephalopathy, Acute Renal Failure) </li></ul><ul><ul><ul><li>Put an Arterial line for monitoring MAP adequately </li></ul></ul></ul><ul><ul><ul><li>Sodium Nitroprusside </li></ul></ul></ul><ul><ul><ul><li>Labetalol drip </li></ul></ul></ul><ul><ul><ul><li>Nitroglycerin drip if patient has concomitant CHF ( reduces preload ) . </li></ul></ul></ul>
  109. 117. <ul><li>NSAID related </li></ul><ul><li>OSA related/ identifying and treating </li></ul><ul><li>OCP related/ worsening HTN after starting OCP </li></ul><ul><li>Choosing initial therapy in HTN </li></ul><ul><li>Treating HTN urgency and Emergency </li></ul><ul><li>Fenoldapam use </li></ul>
  110. 118. END!

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