Cardiology Community Health Centers LDL levels: keep < 100 in pt w/ known CHD risk equivalent (CAD, MI,

PVD, or inpatient DM). If pt has none of these problems, can keep below < 160 if 0-1 RF, < 130 if >=2 RF. Consider drug therapy only ay 30 above the threshold, unless > 2 RF. Initial DOC for newly diagnosed HTN is thiazide diuretic. Common side effect is photosensitivity, leading to a rash in sun exposed areas. Rx by stopping med, or avoid sun exposure. Thus, this is a common side efx of meds in newly diagnosed HTN. Best RF to modify to reduce risk of CAD is LDL. HTN is also good but not as good as LDL. Other stuff helps too (exercise, stop smoke, control DM), but they dont lower risk as much as LDL and HTN. Secondary HTN: Consider it in a young patient w/ high blood pressure. 90% of secondary HTN is d/t unidentified cause. Otherwise, the MCC is renovascular HTN. Look for abd or flank bruit in pt with renovascular HTN. Other causes: peho (headaches, tachy), Cushings disease (edema), advanced renal disease (edema). Retinal abnormalities is a long term effect of HTN, not seen early in disease. DM is the single most important predictor of adverse CV outcomes. Such a good predictor that DM is considered a CHD equivalent. In women, the prediction is evn more important. For people with DM, keep BP < 130/85, versus 140/90 in a healthy person. AAA: Cutoff for surgery is > 5 cm diameter. If smaller, do periodic imaging. Rapid growth can also need surgery. Big time RF is smoking. Other RF dont have as much impact as smoking cessation does. Office Amlodipine side efx: fluid retention and urticarial rash. ACEI side efx: angioedema, urticaria. Rash is usually psoriatic, not photosensitivity in nature. Note that ARB might also cause angioedema if a pt has bad experience w. ACEI. Paroxysmal a fib: present w/ EPISODIC palpitation possibly associated w/ symptoms. Same CVA risk as normal afib, so need warfarin. Either rate or rhythm control is effective if asymptomatic. If there are marked or persistent symptoms (palpitation, dizzy, dyspnea) rhythm control is better. Amiodarone is the preferred drug for rhythm control if pt also has some other structural heart disease (cardiomyopathy, CHF, CAD). Flecainide can work ONLY if pt has NO structural heart disease. It can lead to fatal arrhythmias if you give it to pt w/ structural heart disease. Ibutilide: use for acute termination of a-fib.

Fibrinogen: associated w/ increased CV risk. > 3.43 is a double risk. > 2.7 is high. Drug therapy to decrease fibrinogen hasnt been shown to be preventative. However, stopping further increase helps. Within statins, lovastatin and atorvastatin increase levels, while prava and simva dont increase. Thus, if someone is at a high level for fibrinogen, must think about which statin to use if pt also has high LDL. Nonsusstained ventricular tachy: >=3 consecutive ventricular beat w/ rate > 120, and the episode lasts < 30 sec. If you see this, pt most likely has structural heart diease. Ex. Prior MI scarring, ventricular hypertrophy, mitral valve prolapse (midsystolic click). If you pick up this rhythm on EKG, next step is to get echo and stress test to r/o ischemia. CHF: ACEI are the main therapy. Improve survival and delay progression of disease. Indicated even if pt is asymptomatic. Only contraindications are poor tolerance to drug, or renal failure or hyperkalemia. CHF: standard therapy is diuretic, ACEI, bb, digoxin, or spironolactone. ACEI is the best, and wont exacerbate confusion in a pt. digoxin could worsen confusion. If ACEI isnt well tolerated (angioedema), then hydralazine and isosorbide dinitrate is a common combination. Side efx might include drug induced lupus. Manifest as flu like symptoms (fever, malaise, myalgia, facial rash). LAD, splenomegaly can also happen. Antihistone antibody is marker of drug induced lupus. Rx is to stop drug. Hydralazine is safe in pregnancy (as are dopa, labetalol) CHF as a cause of hypoNa. The decreased CO and SBP decreases perfusion P at carotid baroreceptor, so body stimulates ADH and rennin angiotensin despite volume overload. This causes even more fluid retention, leading to hypoNa. Must correct levels gradually, not acutely. Best Rx is water restriction. CHF: syndrome which results from impaired ventricular emptying (systolid) or relaxation (diastolic). Symptoms: fatigue, weakness (d/t reduced CO), edema (d/t fluid retention). Exertion exacerbates all symptoms. Itss a syndrome, so its a clinical diagnosis based on H and P. PND, orthopnea, raised JVP, rales, S3, CXr findings (increased vascular congestion or silhouette) are major criteria. Dx is 2 major or 1 major + 2 minor. Minor criteria: bilateral LE edema, hepatomegaly, dyspnea on exertion, nocturnal cough). Digoxin toxicityL N/V, anorexia, confusion, visual disturb, cardiac abnormalities. Drugs that can cause toxicity: verapamil, quinidine, amiodarone, spironolactone. Hypercholesteremia + hypertriglyceridemia (>200): DOC is a statin. . If statin isnt good alon,e add gemfibrozil or niacin. Lone a fib: a-fib which occurs w/o any other signs of clinical heart disease (r/o CAD, TH, PE, HTN, DM, CHF). Warfarin is not necessary, just aspirin is good enough.

Unstable angina: no matter what, need a coronary angio ASAP to look at blockage and see its severity. If angio reveals pt to be high risk, consider percutaneous coronary intervention (PCI) or CABG. Remember that DM will increase rate of progression a lot. Evaluating heart ischemia in pt w/ prior CABG, poor heart function, or if there already exist baseline EKG changes: use adenosine or dipyramidole to induce ischemia and watch the technetium-99. (sestamibi). Stress echo should only be done if adenosine cant be used for some reason. Remember that arthritis can also impair exercise. Adenosine can induce bronchospasm, so if pt has COPD or asthma, adenosine is contraindicated. Use dobutamine instead. Orthostatic HypotensionL dx with fall or 20 SBP or 10 DBP. Can happen after standing up or even eating. Drop in BP must happen within 2-5 min of standing. 2 MCC ortho hytpo: autonomic dysfunction or intravascular volume depletion. Autonomic dysfunction (DM neuropathy). Drugs: antihyptrtensives, vasodilators, anti-angina drugs. Ca channel blocker: peripheral edema is common side efx. The dipines are common, but diltiazem can also cause it. Exercise stress test is FSOM in pt w/ angina symptoms.. Weight loss is the best non-drug way to decrease BP. Benefit in overall CV risk is unclear but probably helps. Other firstline drug for HTN besides ACEI is b-blocker. Positive stress test: > 1 mm downsloping ST depression. NSOM is to do cardiac cath to see where the lesions are, and to possibly to balloon stenting. Right sided endocarditis: commonly see R sided involvement or septic pulmonary emboli. Septic emboli manifests as scattered bilateral rales. Pulmonary infiltrates on both sides. IVDU is the likely cause. Otherwise, R sided disease is very uncommon. Coumadin management: If INR > 3 but < 5, just hold drug for a few days to get level to therapeuritic. If INR > 5 but < 9, stop drug and give small dose of vit K (1-2 mg). If > 9 but < 20, higher dose of vit K. If > 20, consider FFP. If at anytime pt is bleeding, give FFP. Drug interaction w/ warfarin: Amiodarone increases warfarin action. If need to have the two together, reduce warfarin by 25%. MVP: MC valve abnormality in industrialized nations. Mid to late systolic click, most easily heard over LV. Mitral regurg: holosystolic decrescendo murmur (can be 2ndary to MVP) heard in apex, radiates to axilla. Increases w/ grip, decrease w/ valsalva.

Systolic <> in LU sternal border: pulmonic stenosis. Mitral stenosis: low pitched diastolic rumble heard over the apex best when pt is lying L lat decubitis. The narrowing of the valve leads to increased P in LA, which backflows into increased P in pulmonary vasculature and R side of heart. MCC is rheumatic fever. May present as hemoptysis. LA can enlarge, leading to elevation of L mainstem bronchus, and flattening of L heart border. Mitral stenosis: opening snap with diastolic rumble. Best heard mid clavicular on L side between 5th and 6th ribs. MC congenital heart malformation: VSD. If large enough, may be symptomatic. Murmus is pansystolic murmur at LL sternal border. Should get an echo. VSD is not congenitally cyanotic, only if its big enough. Polypharmacy: Using too many diuretics, a-blocker, or nitrates can induce ortho hypo. MCC perioperative mortality: cardiac death. Highest risks: unstable angina and critical aortic stenosis. Exercise angina and MI < 6 mo ago are also decently big RF, but less than the other two. Amiodarone induced lung toxicity: MC presentation is as a chronic interstitial pneumonitis. Nonprod cough, fever, pleuritic CP, focal or diffuse interstitial opacity on CXR. Rx with d/c drug. If really bad, consider steroids. Inpt facility Metformin: higher chance of lactic acidosis (contraindicated) if renal insufficiency, hepatic dysfunction, or CHF. Thus, if pt goes to a procedure that needs contrast (ex. Cardiac cath), you must d/c metformin a bit before the procedure. Acute MI: sinus bradycardia could happen after MI. FSOM is IV atropine. If that doesnt work, then must intervene w/ thrombolysis or PTCA (angio). In the meantime, probably need to do transvenous cardiac pacing while setting up the thrombolysis . Remember that thrombolysis is contra in recent abd surgery (2 wks). If need to intervene in CAD in a pt with DM, CABG is better than angio. DM has higher chance of restenosis, so angio or balloon + stent isnt good enough. Multifocal atrial tachy: > 3 P waves of different morpho;logies. Narrow QRS, variable PR segment. MCC is hypoxia and COPD. Thus, someone showing this arrhythmia must first analyze their O2 status, since correction may eliminate the arrhythmia. Other causes are hypoK and hypoMg. Rx is always reverse the cause. If the initial therapy doesnt work, try bb or verapamil if bb is contra (COPD, asthma). Acute heart failure: MCC are papillary m. rupture, infective endocarditis, chordae tendinae rupture, and chest wall trauma . A mitral regurg makes you think of ruptured chordae tendinae. Dx DDx for chrdae tendinae rupture: IE, ischemia, MV rupture.

Ehlers Danlos syndrome: mitral valve degeneration can happen, leading to chordae rupture. Pes planus and scoliosis are common findings. Joint hypoermobility, hyperextensibility. Marfans can also cause rupture. Anticoagulation for mechanical valves: mechanical mitral and aortic valves need INR between 2.5-3.5. Torsades de pointes: look for an EKG showing a QT interval prolongation, followed by some sort of clear arrhythmia. Frequent variation in QRS morphology is more likely torsades. Rx for torsades with hemodynamic compromise is immediate defibrillation. Once pt is stable, then give MgSO4. Remember that the lab value for Mg is unreliable, so just give it regardless of levels. If Mg therapy fails, then do temporary transvenous pacemaker. Synchronized cardioversion: for v-tach, a fib. s/p MI, best to hold sexual activity for 6 weeks after the event. If there were complications because of the MI, need to further evaluate. A-fib: First line for rate control is Ca channel blocker. Diltiazem is good. Propranolol is good alternative if diltiazem is contra (significant CHF, cardiac conduction system disease). Cancer drugs w/ CV side efx: -rubicin and mitoxantrone. These are cardiotoxic, so should get baseline radionuclide ventriculography (RVG) can detect early toxicity. This can do noninvasive serial monitoring of cardiac function. Multiple gated blood pool (MUGA) is also good. Echo isnt good enough because cant do serial evals. Used more in kids getting chemo, to avoid radiation exposure. ED If someone presents with cardiac symptoms, but all the first line tests come back negative, consider doing continuous EKLG monitor for 24 h to evaluate for arrhythmias. Stress test with radioactive stuff: perfusion defect is a place where blood flow is not the same as elsewhere. Lateral wall of LV is supplied by L circumflex, so defect there is likely this vessel. In a pt with acute MI, Ca channel blockers may actually be harmful. Think about this b/c often they might be on the drug to control HTN. In contrast, bb, ACEI, and statins can help prevent CAD. 2nd degree AV block: Rx with permanent cardiac pacemaker insertion. (aka transvenous pacemaker). This helps prevent progression to Type III block. Remmebr that 3rd degree block is a random, no relationship at all btw A and V beating on EKG. Acute MI management: FSOM include O2, IV access and give aspirin and nitro. ACEI arent used acutely but reduces mortality if taken for the weeks after an MI. bb helps w/ decrease myocardial demand and controls HR. Can give after aspirin, nitro, and morphine.

Acute MI: If EKG shows ST segment elevation in 2 contiguous leads, then thrombolytics are indicated, and if pt presents within 12-24 h of symptoms. Must give NO before getting the EKG. Contra for thrombolytics are active bleed, any intracranial event (bleed, ischemia, neoplasm), SBP > 180, or trauma. Dont confuse with ST segment depression, which is just ischemia. Flash pulmonary edema: Presents w/ acute onset of SOB. No previous history necessary. Hypertensive crisis can cause it, so look for a very high BP. CXR looks like lots of edema, and there willl be diffuse crackles. FSOM in any flash pul edema is give O2 (O2 sat will be low), morphine, and IV furosemide (loop diuretics). If the cause is HTN crisis, the preferred drug to give is IV NO or nitroprusside. Other causes of flash pul edema: mitral stenosis or acute aortic/mitral regurg. Thus, after someone has an episode of this, get an echo. Bb are CONTRAINDICATED in acute heart failure, can slow heart too much and lead to death. Cardiogenic pulmonary edema: Initial Rx is similar: O2, morphine (reduces work of breathing), and a loop diuretic. Cardiogenic shock complicated by hypotension: dopamine is a good choice. Acute pericarditis: can be infarct associated, and happen after an MI (esp. transmural). The associated CP depends on position, and worsens w/ deep inspiration. EKG has diffuse ST elevation w/ PR depression. Rub is heard voer L sternal border (a scratchy sound), which gets louder as pt leans forward. Rx is NSAIDS (or anything for pain). Dresslers syndrome: happens in MI pt and after cardiac surgery. Usually develops weeks/months after MI not days. Presents w/ fever, leukocytosis, pleuritic chest pain, and pericardial rub. Thus, very similar to pericarditis, but look at the time course. Q waves are indicative of old infarct (days old sometimes) Aortic stenosis: Area of aortic valve < 1 cm2 is considered severe stenosis. Onset of symptoms has a big effect on prognosis, so prompt intervention is important in symptomatic aortic stenosis (syncope, angina, dyspnea). Rx w/ aortic valve replacement will reduce mortality. Balloon valvulotomy has only transient efficacy, and high procedural morbidity. Carotid artery dissection: presents w/ unilateral headache + associated Horners syndrome (miosis, ptosis, and anhidrosis) on the affected side only. Thus, symptoms arent bilateral. Some causes are trauma, CT disease, smoking, seatbelts in MVA. Dx is MRA. If MRA fails, then catheter angio is definitive test. Rx is with anticoagulation w/ heparin or platelet agents. Pt with this dissection is at high risk of developing cerebral infarction. MCC of CHF is ischemic heart disease. Thus, if you diagnose a new case of CHF, and are still trying to look for etiology, first r/o coronary lesions with a cardiac stress test. Other causes of CHF are HTN, and valve or renovascular disease. BNP is not useful in this case. BNPs main

purpose is to distinguish between cardiogenic pulmonary edema from primary pulmonary conditions. Acute aortic dissection: Usually presents in older male with long history of HTN and atherosclerosis. In younger pt, think CT disease (Marfan, Ehler Danlos), inflammatory vasculitis, aortic valve problem, or cocaine. Presents w/ sudden onset of sharp tearing chest or back pain. If tear happens in ascending aorta, pt may develop acute aortic insufficiency, causing acute heart failure. Dissection could also extend into coronary vessels, leading to cardiac tamponade or hemothorax. PE shows difference in BP between 2 arms. CXR can show mediastinal widening. TEE is Dx of choice. FSOM is to give bb to lower SBP and LV contractility to < 100-120 mmHg and < 60 bpm. If bb is not enough to lower BP, give sodium nitroprusside. After this is achieved, go to surgery right away. Syncope w/o any apparent cause is most likely neurocardiogenic. Prodrome of nausea, lightheadedness, pallor, and diaphoresis. Precipitating events include prolonged standing, exertion, venipunture, or painful stimulus. Ventricular tachy vs. sus supraventricular tachy: supra has regular, narrow QRS complexes. Ventricular tachy has wide QRS complexes. A flutter is in a sawtooth pattern. WPW syndrome: delta wave is a upstroke of QRS that is slurred. It may present as SVT. If verapamil or bb are given to WPW pt, v fib may occur d/t increased accessory pathway conduction. Pericardial effusion: can happen in response to pericarditis or any malignancy. If too much fluid gets out, and tamponade develops, presents as Becks triad: hypotension, muffled heart sounds, and elevated JVP. SOB is present. Dx is echo emergently and Rx is surgery. Equal diastolic P on all chambers on cardiac cath is aldo present. Pericardiocentesis is life saving. Chest pain relieved by NO is probably cardiogenic. Get cardiac enzymes. A-fib which is hemodynamically unstable: Must do synchronized cardioversion. (in sync w/ the R wave). If pt is stable, then you can convert to normal w/ drug (amiodarone, sotalol). These agents arent for long term rate control. Long term rate control is with diltiazem or metoprolol. Asynchronized cardioversion is TOC for ventricular fibrillation Acute arterial occlusion: MCC are recent MI and afib. Presents as sudden symptoms usually in LE (numbness, coldness, delayed capillary refill, pulse deficit in distal adrteries). Very important to immediate IV heparin followed by continuous heparin infusion. Cocaine induced myocardial ischemia: Initial Rx is nitrates, benzos, or Ca channel blocker. If no improvement with these (d/t possibility of coronary artery thrombosis), then do immediate coronary angiography. A distinct feature of cocaine induced vasospasm is that it might lead to coronary artery thrombosis.

Acute coronary syndrome: STEMI on EKG requires urgent cardiac cath. Non-STEMI can be managed with serial cardiac enzymes, as can unstable angina without any EKG changes. TCA overdose: hypotension, anticholingergic effects, CNS symptoms, cardiac arrhythmia. Can lead to QRS prolongation and reentrey arrhythmia (v-tach, vfib, torsades). Best agent for TCA induced cardiotoxicity is sodium bicarbonate. Lidocaine is the best anti-arrhythmic for TCA induced arrhythmias. Syncope can be diagnosed by EKG + H/P in 70% of cases. FSOM in a new syncopal episode is EKG. Neurological testing (CT hea,d EEG) are usually not valuable unless something in the H and P clearly shows that its a neurological etiology.