Table Of Contents
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 day 30 above the threshold, unless > 2 RF.
- Initial DOC for newly diagnosed HTN:
- is thiazide diuretic.
- A 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 don’t 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: pheno (headaches, tachy), Cushing’s 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 even 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 don’t 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 hasn’t been shown to be preventative.
- However, stopping further increase helps.
- Within statins,
- lovastatin and atorvastatin increase levels, while prava and simva don’t 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 disease. 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.
- ACEI are the main therapy.
- CHF:
- standard therapy is diuretic, ACEI, bb, digoxin, or spironolactone.
- ACEI is the best, and won’t exacerbate confusion in a pt.
- digoxin could worsen confusion.
- If ACEI isn’t 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 at carotid baroreceptor, so body stimulates ADH and renin 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 (systolic) or relaxation (diastolic).
- Symptoms:
- fatigue, weakness (d/t reduced CO), edema (d/t fluid retention).
- Exertion exacerbates all symptoms.
- Its’s a syndrome, so it’s a clinical diagnosis based on H and P.
- Dx is 2 major or 1 major + 2 minor. Minor criteria:
- PND, orthopnea, raised JVP, rales, S3, CXr findings (increased vascular congestion or silhouette) are major criteria.
- bilateral LE edema, hepatomegaly, dyspnea on exertion, nocturnal cough).
- Digoxin toxicity:
- 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 isn’t good alone 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 it’s 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 hypotension 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 hypo:
- autonomic dysfunction or intravascular volume depletion.
- Autonomic dysfunction (DM neuropathy).
- Drugs: antihypertensives, 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 first-line drug for HTN besides ACEI
- is b-blocker.
- Positive stress test:
- > 1 mm downsloping ST depression.
- NSOM is to do a 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 manifest 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 therapeutic.
- If INR > 5 but < 9, stop the 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 murmur 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.
- Murmurs 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.
Inpatient 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 doesn’t work, then must intervene w/ thrombolysis or PCA (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 a higher chance of restenosis, so angio or balloon + stent isn’t good enough.
- Multifocal atrial tachy:
- > 3 P waves of different morphologies. 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 doesn’t 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 chordae 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 hypermobility, hyperextensibility. Marfans can also cause a 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 a 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 isn’t good enough because can’t do serial evals.
- Used more in kids getting chemo, to avoid radiation exposure.
Emergency Department
- If someone presents with cardiac symptoms, but all the first-line tests come back negative,
- consider doing continuous EKG monitor for 24 h to evaluate for arrhythmias.
- Stress test with radioactive stuff:
- a 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.
- Remember that 3rd degree block is a random, no relationship at all btw A and V beating on EKG.
- Acute MI management:
- FSOM includes O2, IV access and give aspirin and nitro.
- ACEI aren’t 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.
- Don’t confuse with ST-segment depression, which is just ischemia.
- If EKG shows ST-segment elevation in 2 contiguous leads,
- 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 will 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 over L sternal border (a scratchy sound), which gets louder as pt leans forward.
- Rx is NSAIDS (or anything for pain).
- Dressler’s 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 cm, 2 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 Horner’s syndrome (miosis, ptosis, and anhidrosis) on the affected side only.
- Thus, the symptoms aren’t 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.
- BNP’s 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 Beck’s 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 also 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 aren’t 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 arteries).
- Very important to tx with 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 an urgent cardiac cath.
- Non-STEMI can be managed with serial cardiac enzymes, as can unstable angina without any EKG changes.
- TCA overdose:
- hypotension, anticholinergic effects, CNS symptoms, cardiac arrhythmia.
- Can lead to QRS prolongation and reentry 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 head EEG) are usually not valuable unless something in the H and P clearly shows that it’s a neurological etiology.