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Hyperlipidema/Ischemic Heart Dz/Cardiomyopathies/Endocarditis/Pericarditis/HTN

What is the #1 Killer in the U.S.? Increased Risks? Ischemic Heart Disease Increased Risk: Cocaine, Type 1 DM, Hypercholesterolemia, FH of heart dz, males 40-70, HTN, High LDL, Low HDL, Triglyecrides, Cigarette Smoking, Obesity, Metabolic Syndrome
Atherosclerotic disease begins with lipid deposit then fibrosis, calcification, plaque formation, inflammation, angiogenesis and then stenosis of the vessels. Where does the plaque typically occur? Bifurcation of vessels. i.Occurs because of DM, smoking, INC LDL, INC BP, High Sat Fat Diet, FH ii.Endothelium does NOT function properly secondary to damage.
Ischemic Heart Disease is most commonly caused by decreased oxygen supply and an increased need sent to the heart. What’s the usual cause of blockage/inadequate perfusion? Atherosclerotic Dz
Pt presents w/stable or unstable angina/acute coronary syndrome. Pt has a squeezing heavy pressure over substernal chest that radiates to shoulder, arm, neck and jaw. Pain gets worse with exertion and emotional issues. Pain is relived with rest. Dx? Ischemic Heart Disease-Angina
Pt presents w/exertional chest pain that resolves w/rest/Nitroglycerin. Sx don’t last past 30 min. PE shows carotid bruits, abdominal aortic aneurysm and decreased pedal pulses. Fundoscopic changes are seen with HTN. See fat build ups (xanthomas). Dx? Stable Angina i. Risk Monitor: DEC smoking, BP monitoring, weight, DM testing, cholesterol panels, EKG, eye exam, creatinine
An ST-T wave change occurs during an episode of chest pain that resolves afterward. Seen with 12-lead ECG. Dx? Stable Angina
Patient presents with chest pain without exertion usually at night. EKG shows a slight S/T elevation during pain. Ischemic sx are INC in cardiac markers after long episodes. Stress testing NOT helpful. Dx? Tx? Prinzmetal’s Angina i.Nitrates and Calcium Channel Blockers
What are defining classifications of cardiovascular disease? Class 1: no limit to physical activity Class 2: slight limit to physical activity Class 3: marked limitations to physical activity Class 4: unable to carry out physical activity without discomfort. Symptoms may be present at rest.
What are ABSOLUTE contraindications for stress testing? Acute MI within 2 days Unstable Angina Pectoris Uncontrolled arrhythmiashemodynamic compromise Symptomatic severe aortic stenosis Uncontrolled heart failure Acute endocarditis,myocarditis,pericarditis Acute aortic dissection or pulm/systemic emboli
What are RELATIVE contraindications for stress testing? L main coronary stenosis Mod. stenotic valvular dz Severe HTN(sys200/dias110) Tachyarrhythmias or bradyarrhythmias including atrial fibrillation w/uncontrolled ventricular rate Hypertrophic cardiopmyopathy (and/or other forms of outflow tract obstruct
What is the purpose of exercise stress testing? How do you accomplish it? Want to reprod cardiac ischemia thru defined exertion Speed/Incline INC every 3mins(per Bruce Protocol)until HR is 85% of pt’s max HR. Look for EKG change,DEC myocardial perfusion, DEC in systolic BP(>10mmHg)
Excercise Stress Test is Unreliable for whom? Women,elderly,obese,bundle branch block,pacemaker,disabled
Pt @pre-op risk & has never had a dx ECG stress test. Suspect conduction or repolarization abnormalities & possible dx of ischemia related to wall motion devo, this has made ECG stress test hard to read. Want to perform a stress echo;to cause stress use? Dobutamine (Dobutrex)
Injecting Thallium into myocardium to see hypoperfusion. Take images @rest & under stress. Test called? Induce stress with? What can you detect? Nuclear Medicine Imaging Stress Inducers: Exercise, Adenosine (Adenoscan), Dipyridamole (Persantine), Dobutamine (Dobutrex) Detect: myocardial ischemia, location/size of injured m after MI, narrowed aa, how grafted vessels work after bypass surgery.
What is the gold standard for diagnosing coronary artery disease? a. Coronary Angiography Risk of: bleeding, arrhythmias, vessel injury, post-procedure bleeding
Patient has stable angina and is a candidiate for revascularization. Have not clearly established IHD and has survived a cardiac arrest. Possible LV dysfunction. What do you use to dx? Coronary Angiography
To treat stable angina you'd like to modify risk factors, do what? Stop smoking, treat HTN (get below 120/180), glycemic control for DM, get LDL<70mg/dl, DEC weight, cardiac rehab
To treat stable angina you'd like to use meds that DEC oxygen demand. Are? Nitrates (DEC Preload), Beta Blockers (DEC HR, BP, Contractility), Calcium Channel Blockers (DEC BP, Contractility)
To treat stable angina you'd like to increase oxygen, how? Nitrates Calcium Channel Blockers
To treat stable angina you'd like to use anti-platelet meds. Are? Aspirin, Clopidogrel, New Agents, SL Nitroglycerin, Ranolazine
To treat stable angina you'd like to revascularize. How? Percutaneous Coronary Intervention Coronary Artery Bypass Graft (CABG)
If patients don't respond well to nitrates and beta blockers during stable angina, what should you use? Calcium Channel Blockers
Patient has history of angina despite medical tx w/evidence of ischemia onn stress test. Also has single/double vessel disease. Tx? Percutaneous coronary intervention for unstable angina
Patient has left main stenosis and triple-vessel disease. What should you use to treat? Coronary Artery Bypass Grafting May use one or both internal mammary aa OR radial a OR saphenous v
Unstable angina, Non-ST segment elevation MI (NSTEMI) and Acute MI with ST-segment elevation (STEMI) are all examples of? Acute Coronary Syndromes
Pt is diabetic & old presents w/severe, long lasting chest pain @rest that’s NEW. Also has weakness, N/V, anxiety, sense of doom & denial. Pt also presents with sudden breathlessness and Levine’s sign(clenched fist held over chest to describe pain). Dx? Acute Coronary Syndrome
Erosion/Plaque rupture w/occlusion,dynamic obstruction to vasospasm(Prinzmetal’s Angina),Progressive Obstruction(restenosis following PTCA), & secondary due to INC oxygen demand/decreased supply (anemia, tachydysrhythmia) are pathophysio signs of what? Acute Coronary Syndrom
ST segment elevations with + markers are a sign of what? STEMI (ST elevation, markers increased MI)
+ markers with NO ST segment elevation is a sign of? NSTEMI (No ST elevation, markers increased MI)
NO ST segment elevations with - markers are a sign of what? Unstable Angina
To make a differential diagnosis on chest pain should look at what? Non-Ischemic Cardiovascular: Aortic Dissection Pulmonary: Pulmonary Embolus, Pneumothorax GI: Perforated Viscous
You order a 12-lead ECG, cardiac markers, imaging, Angiogram, CBC, lipids and CXR. What are you trying to dx? Acute coronary syndrome
You use TIMI, PURSUIT and GRACE to score a disease. You are trying to score the progression of what? Unstable Angina/NSTEMI
An increased TIMI risk score shows risk of death and ischemic events and an increased number of events at 14 days. How does the TIMI score relate to risk of death and ischemia? Score 0-1 Risk 4.7% Score 2 Risk 8.3% Score 3 Risk 13.2% Score 4 Risk 19.9% Score 5 Risk 26.2% Score 6-7 Risk 40.9% f.
Ischemia causes ST segment and T wave changes. What kind? T wave Inversion: bc of delayed reploarization ST segment depression
Injury causes ST segment changes. What kind? ST elevation due to incomplete depolarization >1-2mm in 2 or more contiguous leads.
Pathologic Q waves are newly seen and enlarging; this is a sign of what? Infarction (electrically silent!)
To rule in/out disorders you use serial enzymes/EKG and monitor bed. How do you stratify risk? Stress Test Choice of Test Modifiable Factors
You provide a patient with MONA to treat Acute coronary syndrome. What does MONA stand for? Morphine Oxygen Nitroglycerine Aspirin (Antiplatelet)
You want to use thrombolytics can you treat unstable angina/NSTEMI? What about STEMI? Unstable Angina/NSTEMI: NO! STEMI: Maybe
Would you revascularize in unstable angina/NSTEMI at an early or late stage? Late
Would you revascularize in STEMI at an early or late stage? Early
How would you treat unstable angina/NSTEMI? Bedrest w/cardiac monitoring & O2 Nitrates Morphine if sx not relived by nitrates. BetaBlockers Ca Channel Blockers if not relieved by nitrates/b-blockers Anti-Thrombotic Rx: Aspirin, Clopidogrel Anti-Coagulation via Heparin Revascularization if ne
How would you treat STEMI? MONA Nitrates Morphine if sx not relived by nitrates. B-Blockers: Metoprolol Ca Channel Blockers if not relieved by nitrates/b-blockers ACE Inhibitors Anti-arrhythmics/Thrombotics Rx:Aspirin,Clopidogrel Anti-Coagulation:Heparin Statin Revascula
Patient has a history of cerebrovascular hemorrhage, stroke within the past year, poorly controlled HTN. You suspect aortic dissection and active internal bleeding. Do you prescribe Thrombolytics? NO! Those are all ABSOLUTE contraindications.
Pt uses anticoags,had a recent invasive procedureprolonged CPR,known bleeding diasthesis,pregnant &active peptic ulcer dz. Has a hemorrhagic ophthalmic condition w/a hx of severe HTN(well controlled).Used streptokinase w/in last 2yrs. Use Thrombolytics? NO! Those are all contraindications.
When you admit to the coronary care unit, when should you begin walking after bed-rest? 2-3 days
What are possible complications from acute coronary syndromes? a. Pump Failure (CHF, Cardiogenic Shock) b. Ventricle Dysrhytmia i. PVCs, VT, VF c. Pericarditis/Dressler’s Syndrom d. Cardiac Rupture/L Ventricular aneurysm e. Depression
Patient develops a fever, pericarditis, leukocytosis and pericardial and pleural effusion 2 weeks after an MI. Dx? Dressler’s Syndrome
You increase exercise tolerance, functional capacity, decrease cardiovascular mortality and emotional distress in what? Cardiac Rehabilitation
What are the 2 main lipids in blood. Both are carried in lipoproteins? a. Cholesterol: forms steroids, bile acids b. Triglycerides: transfers E from food into cells.
What are made from dietary fat, travel via portal v via thoracic duct. It’s normally completely metabolized transferring E from food into m and fat cells. Will float to the top when non-fasting serum stands. What is this? Chylomicrons
These are made in the liver from fat/carb stores and consists mostly of triglycerides. Metabolized to LDL. Is what? VLDL
The “bad” cholesterol, delivers cholest for use in PM biosynth & bile acid synth in liver. 70% taken up by liver & excreted into bile. LDL
An INC in this in arterial endothelium leads to atherosclerosis. In ppl who eat large amts of sat. FA/cholesterol or have genetic receptor defects. Issue? LDL
How do you decrease LDL? a. DEC Cholesterol Synthesis: Statins(HMG-CoA reductase inhibitors) b. INC Cholesterol Excretion: Bile acid sequestrants c. DEC Cholesterol Absorption: i. Plant stanol esters (sitostano-Benecol margarine) ii. Ezetimibe (Zetia)
This “good” cholesterol is made in the liver and consists of apoproteins & cholesterol. Participates in the reverse cholesterol transport back into liver. Decrease in this will increase risk of heart disease; is considered cardioprotective. What is this? HDL
A women with increased estrogen exercises and has 1-2 drinks/day. How does this affect her HDL? INCREASE
Pt is an obese smoker w/hypertriglyceridemia. Does not exercise and used to take anabolic steroids. How does this effect his HDL? DECREASE
How do you screen for high cholesterol? a. Fasting Lipid Panel: affects triglycerides by fasting i. Acutely ill can have falsely low levels (after acute MI for example). ii. Do NOT screen pregnant women who will show High Cholesterol.
What is the optimal level for Total cholesterol? a. <200 b. >240 is High
What is the optimal level for Triglycerides? a. <150 b. 200-499=High; >500 Very High
What is the optimal level for LDL? a. <100 b. >190 is Very High
What are levels for HDL? a. <40=Low b. >60=High
Is low cholesterol always a good thing? No! Can be a sign of AIDS, severe liver dz, Hyperthyroidism, malnutrition, chronic anemia, cerebral hemorrhage, malignancy, certain drugs.
Pt has defective LDL Receptors and therefore unregulated LDL synthesishigh cholesterol. Condition? Familial hypercholesterolemia
Patient presents with bilateral cholesterol-filled soft yellow plaques on the medial aspects of the eyelids. Dx? Xanthelasma (Bening): in 75% older pt’s
A patient has triglycerides >1000 and red-yellow papules. Dx? Eruptive Xanthomas
A patient has yellow-orange nodules (up to 2 cm in diam) on knees and elbows. Dx? Tuberous Xanthoma
On PE see cream-colored blood vessels in the fundus. Test and see tricglycerides >2000. Dx? Lipemia Retinalis
What is a MAJOR modifiable risk factor for coronary heart disease. What do you target? Hyperlipidemia. Target LDL since leads to atherosclerosis.
Plaques are filled w/lipid core & lipid-laden mac foam cells & inflamm cells. Foam cellsTF which stimulates thrombus formation & are thin fibrous caps which separate lipid core from blood in the lumen. What are these plaques called. Old or new paradigm. a. Vulnerable plaques i. Plaques will rupture leading to thrombosis leading to MI b. NEW Paradigm!
Patient has a progressive narrowing of coronary aa leading to blockage leading to MI. What paradigm is this? OLD paradigm. Only explains 15% of MIs.
How do you treat coronary heart disease? a. Statins (lowers cholesterol) which can stabilize the plaquesDEC inflamm i. DEC coronary mortality & CVA
How low would you like LDL levels to drop to? How do you treat? a. <70 b. Diet: cholesterol lowering or mediterranean c. Exercise: 30mins moderate activity d. Meds
What are some good meds to decrease CHD via hypercholesterolemia reduction? a. HMG Co-A Reductase Inhibitors/Statins b. Fibrates c. Nicotinic Acid d. Bile Acid Sequestrants e. Cholesterol Absorption Inhibitor f. Omega3 FA
What is the first line tx for DEC LDL? Statins: HMG-CoA Reductase Inhibitors (inhibits rate-limiting step in cholesterol biosynthesis) i. Lipitor, Lescol, Mevacor, Pravachol, Crestor, Zocor
What’s a large side-effect of statin drug use? a. Myopathy i. Myalgiamyositisrhabdomyolysis ii. Check serum creatine kinase levels iii. Low risk drugs: Pravachol, Leschol, Crestor (all end in “statin”) b. Elevated LFTs (Liver Function Tests) i. Dose-Dependent, within first 3 mos.
If Pt unable to tolerate statin, should try what? a. Zetia b. Bile Acid Sequestrants c. TriCor d. Niacin
What is the only drug used for hypercholesterolemia which does NOT affect P450 system? Pravachol
Simvastatin is high regulated since high risk for myopathy. Patient has been on it for a year, should you change the rx? No, ok bc been a year.
Using low and intermediate dose Simvastatin, also on amlodipine and ranolazine. How much Simvastatin can you use? No more than 20mg.
Using low and intermediate dose Simvastatin, also on amiodraone, verapamil and diltiazem. How much Simvastatin can you use? No more than 10mg.
What should you use to decrease triglyceride levels but does cause and increased risk of myopathy when combined w/statin. It’s ideal for DM w/high cholesterol. What kind of drug? a. Fibrates (Fibric Acid Derivatives) i. DEC VLDL secretionINC FA Oxidation ii. Gemfibrozil iii. Fenofibrate iv. Fenofibric Acid (can use w/statin) v. Clofibrate
To increase HDL you can decrease VLDL production mobilizing free FA from adipocytes. They’re not as potent as statins or fibrates and can lead to skin flushing. But what is it? Nicotinic Acid (Niacin/Vitamin B3)
DEC LDL by forming a nonabsorbable complex w/bile acids in intestine, releasing Cl ions,increases the fecal loss of bile salt-bound LDL. Don't use in Pts w/hypertriglyceridemia, but can use for monotherapy in Pts who cannot handle statins. What are they? a. Bile Acid Sequestrants i. Questran ii. Colestid iii. Side Effects: constipation, farts, upset stomach
Zetia and Vytorin inhibits cholesterol absorption at the brush border of the sm intestineDEC chlolesterol to liverDEC hepatic cholesterol stoesINC blood clearance of cholesterol. Overall will decrease LDL. What kind of drug is this? Cholesterol Absorption Inhibitor
Salmon, flax seed, soybean oil, canola oil and nuts all deliver what? What does this effect? a. Omega 3 FA b. DEC triglycerides c. Omacor, Lovaza are FDA approved.
What are alternatives to decrease high cholesterol? a. Red yeast rice: DEC LDL b. Plant Sterols (Benecol): DEC Total Cholesterol c. Soluble Fiber: DEC Cholesterol
Black middle aged man presents with ventricle enlargement and systolic dysfunction that is congestive. Originally thought it was a viral URI. This is a sign of what in the heart? a. Dilation i. Usually idiopathic ii. Heart dysfunction is out of proportion to fibrosis
Pt presents with inappropriate myocardial hypertrophy in the absence of HTN or aortic stenosis. The is a sign of what? Hypertrophy
Pt has reduced filling and reduced diastolic function. There are infiltrates. This is a sign og what? Restrictive
What is the second most common direct cause to sudden death, besides coronary artery dz which is first? Cardiomyopathy
What is the leading cause of CHF? a. Dilated Cardiomyopathy i. Can be caused by Ischemic Cardiomyopathy
What is the #1 cause of sudden death in athletes? a. Hypertrophic Cardiomyopathy b. Patient presents with dyspnea (rest, exertional & nocturnal) and orthopnea leading to pulmonary congestion. This accompanies sx of hypotension, tachycardia, tachypnea, and JVD. Dx? c. Left Heart Failure
Patient presents with edema, nausea, abdominal pain and nocturia leading to systemic congestion. This accompanies sx of hypotension, tachycardia, tachypnea, and JVD. Dx? Right Heart Failure
Patient presents with low cardiac output indicative of CHF. What else might they experience? a. Fatigue & weakness b. Hypotension, tachycardia, tachypnea, JVD.
Patient drinks more than 6 drinks/day and you see supraventricular tachycardia. What is a possible dx? Stats of living? a. Alcoholic Cardiomyopathy (Dilated) i. 9% mortality if stayed clean-post 4 yrs ii. 50% mortality if continued frinking-post 4 yrs
Black mother is pregnant with twins and has cardiomyopathy in her last trimester. What is this called? Should you encourage more children? a. Peripartum Cardiomyopathy (Dilated) i. Usually recover in 6 mos ii. Discourage future pregnancies
You have asked a patient to limit activity, restrict salt (sometimes fluid if really need to decrease salt), and start taking ACE inhibitors, Diuretics, Digoxin, B-Blockers and Antiarrhythmics. What are you trying to treat? Dilated Cardiomyopathy
How do ACE Inhibitors effect cardiomyopathy? a. DEC afterload via vasodilation, DEC BP. b. Do NOT underdose. c. Captopril d. Enalapril e. Lisinopril
Hypertrophic Cardiomyopathy usually occurs without a cause for secondary hypertrophy. It’s also called asymmetric septal hypertrophy and Idiopathic hypertrophic subaortic stenosis. What does it physiologically produce? LV is hypercontractile and during systole ejects ALL its blood w/high wall stress. Have a SMALL LV cavity.
Differentiate between Hypertrophic Cardiomyopathy & valvular AS: which has a louder murmur if patient stands or during Valsavas? Hypertrophic Cardiomyopathy
Differentiate between Hypertrophic Cardiomyopathy & valvular AS: which has a calcified aortic valve? Valvular AS
During systole theres a dynamic outflow tract gradient. During diastole theres impaired filling & INC filling pressure. Theres myocardial ischemiaINC m mass,filling P,O2 needs. Vasodilator reserves DEC & theres systolic compression of aa.These are sx of? Hypertrophic Cardiomyopathy
Patient is asymptomatic but presents with dyspnea(shortness of breath), angina pectoris, fatigue, dizziness, palpitations, CHF. What are you concerned about? Hypertrophic Cardiomyopathy
Patient has valsalva maneuver which decreases LV cavity size leads to DEC preload/afterload. How does this effect gradient and murmur? INC gradient & murmur
Patient stands which decreases LV cavity size leading to DEC preload. How does this effect gradient and murmur? INC gradient & murmur
Patient has posextrasystolic beat which increases contractility leading to INC preload. How does this effect gradient and murmur? INC gradient & murmur
Patient squats which increases LV cavity size leading to INC preload/afterload. How does this effect gradient and murmur? DEC gradient & murmur
Patient has isometric handgrip exercise which increases afterload. How does this effect gradient and murmur? DEC gradient & murmur
Hypertrophic cardiomyopathy can lead to what 4 things? a. Sx progression b. Atrial Fibrillation c. Sudden death d. End stage w/systolic dysfunction
29 year old patient with FH of sudden death has sustained ventricular tachycardia and recurrent loss of consciousness. Has slow arrhythmia (occult conduction dz). Is at risk for what? What would you recommend? Sudden Coronary Death Avoid most compet sports >30 can participate if no contraindications.
Cannot avoid competitive sports if over 30 but have what? FH, tachycardia, loss of consciousness, impaired hemodynamics, exercise induced hypotension, moderate mitral regurg, INC L Atrium, paroxysmal atrial fibrillation, abnormal myocardial perfusion.
What are some possible managements for sudden coronary death? Beta-adrenergic blockers, diuretics for CHF sx, calcium channel blocker, amiodarone, dual chamber pacing, ventricular myotomy-myectomy, placation of anterior mitral leaflet, cardiac transplantation
Patient has abnormal diastolic fcn w/rigid ventricular wall w/impaired diastolic ventricular filling. Looks like pericarditis but CANNOT correct w/surgery. It’s the least common form of cardiomyopathy, what is it? Restrictive Cardiomyopathy Myocardial or Endomyocardial 5.Radiation, Adriamycin
Non-Infiltrate: Idiopathic, Scleroderma Infiltrate: Amyloid, Sarcoid, Gaucher dz, Hurler dz Storage dz: hemochromatosis, Fabry dz, Glycogen storage ARE all signs of what type of restrictive cardiomyopathy? Myocardial
1. Endomyocardial Fibrosis 2. Hypereosinophilic syndrome 3. Carcinoid 4. Metastatic Malignancies 5. Radiation, Adriamycin ARE all signs of what type of restrictive cardiomyopathy? Endomyocardial
Pt with prev amyloidosis & hemochromatosis presents with symptoms of R and L heart failure with a prominent jugular venous pulse. Echo-Doppler shows abnormal mitral inflow pattern (LALV) but evidence of INC LA pressure. To confirm suspected dx, test? Dx? a. Endomyocardial Biopsy b. Restrictive Myocardia
Pt with a history of TB and trauma has pericarditis and a collagen vascular disorder. What dx do you suspect? Constrictive Pericarditis
Pt has a amyloid proteins abnormally deposited and can be seen on myocardial biopsy. It is the most common cause of restrictive cardiomyopathy. Can be caused by primary dz or secondary to multiple myeloma and hypergammaglobulinemia. What is the dx? a. Amyloidosis i. >25@ have symptomatic HF
Diabetic patient is hyperpigmented and presents with cirrhosis and cardiac dysfunction. Eats a lot of iron. You are concerned about what leading to death in this patient? Tx? a. Restrictive DzDilated CardiomyopathyCongestive Heart Failure b. Tx: Phelbotomy, Chelation
Attempting to treat restrictive cardiomyopathy find that there are no real satisfactory solutions. What is NOT indicated? Digitalis and other Inotropic agents
Can heart failure occur even if a person does NOT have a cardiomyopathy? a. Yes: i. Acute MIcardiac dysfunction ii. DysrhythmiaDEC CO iii. Valvular dysfunction iv. Cardiac Tamponade from pericarditis v. Severe anemia vi. Volume Overload
Endocarditis caused by streptococci, enterococci & staphylococci along w/normal mouth organisms leads to what type of infective carditis? Native Valve Carditis
Staph Aureus is 50% of the time the cause of endocarditis in this population…What’s the pop? IV Drug Users
10-20% of Endocarditis is commonly caused by Staph, Gram – and fungi this in type of endocarditis? Prosthetic Valve Endocarditis
This Infective Endocarditis is rapidly destructive, caused by S Aureus and if untreated is fatal within 6 weeks. Acute Bacterial Endocarditis
This Infective Endocarditis is slow onset for long duration, caused by Viridans strep (a normal mouth flora). If untreated for wks-months can be fatal. Subacute Bacterial Endocarditis (SBE)
60 year-old pt w/predisposing cardiac lesion presents w/fever/murmur/chill/sweat/wt loss.Pt has small,tender/purple-red subQ nodules(Osler’s Nodes) & clubbing/splinter hemorrhages in nails.Pt has petichiae(red non-blanchmacules)thats gone in 2-3 days.Dx? Infective Endocarditis
Rare, <5% of pts, but pt has oval retinal hemorrhages w/a pale center(Roth’s spots). Has small, non-tender hemorrhagic macule nodules(Janeway Lesions). Pt has petichiae (red non-blanching macules)that disappears in 2-3 days. Dx? Infective Endocarditis
Upon running tests for infective endocarditis, what would you expect to find in common tests? a. Positive Blood Culture b. INC SED Rate c. Anemia d. Proteinuria e. +RF f. Microscopic Hematuria g. Leukocytosis h. Circ. Immune complexes
In order to dx infective endocarditis must use the Duke Criteria which was modified in 1994 to include what? a. Need echocardiograph in order to Dx. b. Includes IVDU as a predisposing heart condition.
The Duke Criteria states for a definitive infective endocarditis dx you must have presence of what pathologic critera? a. Microorganisms i. From TWO SEPARATE blood cultures b. Pathologic Lesions c. Echocardiogram i. Vegetation=Postive ii. If negative, do transesophageal echo. d. MUST HAVE (a) & evidence of endocardial involvement (+Echo or new valvular regurg)
Pt presents w/prior IVDU/heart dz/fever of 100.4. Theres vascular phenom(emboli,intracranial/conjunctival hemorrhage & Janeway lesions). Also Osler’s nodes,Roth spots & single +blood culture. The echo not mtg major criteria. Part of Duke’s you're mtg? MINOR Duke’s Criteria
To treat infective endocarditis you decide to use an antimicrobial therapy. How should you administer the dose? a. With sustained bactericidal serum concen. i. MUST determine in the lab the min inhibitory conc. for EACH Pt. b. 4-6 wks of HIGH Dose therapy is common. Often use indwelling central catheter to administer.
When would you recommend surgery for infective endocarditis? a. CHF directly related to valve dysfunction b. Persistent, Uncontrolled Infection even under therapy. i. Includes evidence of perivalvular extension c. Recurrent Emboli (in presence of large vegetations)
To reduce the risk of endocarditis prior to procedures which may lead to bacterial endocarditis. Administer what? Endocarditis Prophylaxis
Pt is about to get dental work done. Has a prosthetic cardiac valve, previous endocarditis, cardiac transplant and congenital heart disease. Before dental work would you like to do anything? YES> Prescribe Endocarditis Prophylaxis If congenital heart dz:ONLY if Unrepaired cyanotic OR completely repaired congenital heart disease within 1st 6 mos after procedure. Repaired congenital heart dz w/residual defects which inhibit endotheliazation.
PPt is having a GI/GU procedure and is at high risk. Should you give endocarditis prophylaxis to prevent bacterial endocarditis? NO!
Pt with an underlying heart condition is undergoing procedure for the respiratory tract and infected skin/musculoskeletal tissue. Should you use prophylaxis? YES! Because has an underlying heart condition.
Pt is undergoing an esophageal procedure. Would like to prevent bacterial endocarditis. Rx? a. Amoxicillin 1hr prior b. If PCN allergy: i. Azithromycin, Clarithromycin or Clindamycin
Structure of the heart is a fibrous sac which holds the heart in position and separates it from surrounding structures. Prevents sudden dilation of heart w/hypervolemia and can hold 15-50 cc of pericardial fluid. What is it? Parietal Pericardium
Patient has pericarditis 6wks-6 mos. What type? Subacute Pericarditis
Patient has pericarditis <6wks. What type? Acute Pericarditis
Patient has pericarditis >6 mos. What type? Chronic Pericarditis
Patient has pericarditis that is caused by viral, pyogenic(bacterial), TB or fungal. Is this infectious or not? Infectious Pericarditis
Patient has pericarditis that is uremic, neoplastic, traumatic and secondary to acute MI. Is this infectious or not? NON-Infectious Pericarditis
Pt has pericarditis that involves rheumatic fever, collagen vascularization (SLE, RA, scleroderma) and is drug-induced (Procainamide, Hydralazine, Phenytoin, INH). What type of pericarditis? Hypersensitivity or Auto-Immune
Patient had surgery on his hear 1 wk ago and is now suffering from pericarditis. Dx? a. Postcardiac Injury i. Post-MI ii. Postpericardiotomy iii. Posttraumatic
Pt presents with slow developing chest pain that is severe, pleuritic, sharp and aggravated by breathing, coughing and position change. It’s relieved by sitting up & leaning forward. It’s aggravated by lying supine. Dx? Acute Pericarditis
In acute pericarditis hear hi/medium-pitched scratching, grating sound hear loudest thru inspiration. Comes & goes w/a 2-3 component. Sounds like pericardial friction rub. The EKG shows widespread INC ST segments. When would you expect T wave Inversion? a. T Waves would invert after several days (MI would be immed) i. See in aVR and V1
Patient presents with faint heart sounds and a chest x-ray shows a water bottle appearance. The EKG has LOW QRS Voltage. What would be the best test? Dx? Echocardiogram i. Low Voltage; QRS <.5mV b. Chest X-Ray Dx: Pericardial Effusion
When looking at a patient’s EKG you see alternating QRS sizes (Electrical Alternans). What do you suspect? Effusion w/Tamponade
What causes Pericardial Tamponade? a. When pericardial fluid accumulates in an amt large enough to cause serious obstruction to inflow of blood into ventricles (as little as 200cc). i. Neoplasia ii. Idiopathic Pericarditis iii. Uremia: renal failure
These 3 Key Features are indicative of what: INC intracardiac pressureJVD, Limitation of ventricular fillingParadoxical Pulse, DEC Cardiac OutputHypotension Tamponade
Patient presents with a greater than normal (10mmHg) DEC in systolic BP during INSPIRATION. Detected as a pulse during inspiration. What is this? a. Paradoxical Pulse i. Since both ventricles are within the confines of the DEC pericardial space, breathing in INC blood flow into R Ventricle, DEC space for L Ventricle Filling temporarily DEC LV Output.
While treating Acute Pericarditis you tell him to rest and give him Anti-Inflammatories since it’s viral/idiopathic. Should you use anticoagulants also? a. NO! b. And remember to look for signs of tamponade.
What's a multifactorial syndrome manifested by an INC of systolic, diastolic or both readings? HTN
Diagnosis of HTN usually requires increased blood P to be seen when? On at least 2 occasions unless in an urgency or emergency.
What's the most common reason for office visits & for use of Rx meds? HTN
Patients whom are normotensive at age 55 have a 90% risk of developing what? HTN
Inc age, being black, obese, excessive EtOH use, Tobacco use, Na Intake, Caffeine use and OTC meds & herbal supplements all put you at risk of what? HTN
Modifying HTN reduces your risk for what disease? Coronary Artery Disease
Pt has SBP <120 and DBP <80. Are they hypertensive or normal? Normal
Pt has SBP 120-139 and DBP 80-90. Are they hypertensive or normal? Pre-hypertension
Pt has SBP 140-159 and DBP 90-99. Are they hypertensive or normal? Hypertension, Stage 1
Pt has SBP >160 and DBP >100. Are they hypertensive or normal? Hypertension, Stage 2
Hypertension where no cause is known and there is an interaction btwn genetic & environmental factors is this type of HTN. Primary HTN (95% of pop)
Hypertension with a specific cause identified is usually seen in young pt's whose BP was well-controlled but suddenly become refractory to tx. Secondary HTN (5% of pop)
Chronic Kidney dz, Renovascular Dz and Phechromocytoma are some of the important causes of this type of hypertension. Secondary HTN (5% of pop)
34 year-old pt has severe/resistant HTN & inc Creatine after adding ACEI/ARB. Abdominal/Renal a Bruit. Dx? Renovascular disease caused by renal artery stenosis.
Excess renin release due to DEC in renal blood flow & perfusion pressure leads to renal artery stenosis which leads to what? HTN
What would you use to dx a renovascular disease? Angiography
Treatment for Renovascular Disease? Angioplasty Stenting Bypass Medical Management
On angiography you see "string of beads" appearance (Fibromuscular hyperplasia) and renal a stenosis. Dx?? Renovascular disease which could lead to HTN
Catecholamine-secreting tumors that come from chromaffin cells of the adrenal medulla & sympathetic ganglia is the physiology of this rare disease. Pheochromocytoma
Pt experiences "spells" of episodic headaches, sweating & tachycardia. You obtain urine/plasma fractioned metanephrine & catecholamines. What do you suspect? Pheochromocytoma
This disease is usually asymptomatic, possible headache. Can have more specific sx depending on secondary causes/complications. HTN
When examining the eye you see copper/silver wire appearance, AV nicking, exudates, arteriolosclerosis, hemorrhages, cotton wool spots & papilledema. Possible dx? HTN
On physical exam you see a L ventricle heave and renal masses or bruits over aorta or renal a. Dx? HTN
CBC, BMP (Electrolytes, renal fcn & glucose), Urinalysis, Fasting Lipid Panels and uric acid tests can all test for what? HTN
An increase in this lab could be a sign of relative contraindication to diuretics. Uric Acid
An inc in LV myocardial fibers in response to chronic pressure load from HTN is called what? Left Ventricle Hypertrophy
Heart failure, LVDD, ventricular arrhythmias, MI and sudden death can all be caused by this. Left Ventricle Hypertrophy
To evaluate pt's with sx and/or signs of cardiac disease should use what lab? Echocardiogram
What's the overall goal of treatment for BP<140/90 or <130/80 in patients with DM or CKD? Decrease cardiovascular disease & renal morbidity & mortality.
To treat BP<140/90 or <130/80 in patients with DM or CKD can use what? Pharmacologic agents OR Nonpharmacologic lifestyle modifications.
Lifestyle modifications to decrease cardiovascular disease includes what? DASH diet Na reduction Wt reduction Physical activity Moderate EtOH consumption Stop tobacco use Decrease Stress
Before giving a patient with renovascular disease angiograph, what should you try first. Though angiograph IS the gold standard. Ultrasound or CT scan
Diuretic, b-blockers, ACE-I, Angiotensin II R blockers (ARB), Renin-I, CaChannel Blocker(CCB), a-blockers and drugs w/central sympatholytic action are all used for what? HTN
ALDO ANT stands for what? Aldosterone Antagonist
When giving a pt diuretics you may see an increase in these lab values. Glucose, Uric Acid, possibly lipids
Diuretics which impair Na at the distal tubule & connecting segment (perhaps even the early cortical collecting tubule) is what type of diuretic? Thiazide-Type Diuretic
Diuretics which impair Na at the thick ascending limb of the loop of Henle is this type of diuretic. Loop Diuretic
Diuretics which impair Na at the aldosterone-sensitive principal cells in the cortical collecting tubule is what type of diuretic? Potassium Sparing Diuretic
Diuretics which impair Na in part of the proximal tubule is what type of diuretic? Acetazolamide & Mannitol Diuretic
This type of diuretic dec plasma Vol, CO. Long-term it dec peripheral vascular resistance. You'll need to watch for DEC K+ or Na+. Thiazide Diuretics: Hydrochlorathiozide, Metolazone, Indapimide, Chlorthalidone
Hydrochlorothiazide (Hydo-Diuril) is this type of diuretic. Thiazide Diuretic
When giving this diuretic you need to watch for electrolyte abnormalities (specifically DEC K+) & dehydration. Loop Diuretics Lasix, Bumex, Demedex, Edecrin
Furosemide (Lasix) is this type of diuretic. Loop Diuretic
Also known as aldosterone receptor blockers, it's often used in w/other anti-HTN. You must watch for INC K+ and this diuretic can cause breast pain/gynecomastia. Potassium-Sparing Diuretic Spironolactone, Amiloride, Eplerenone
Spironolactone (Aldactone) is this type of diuretic. Potassium-Sparing Diuretic
Dyazide, Maxzide & Aldactazide are all difft types of what? Combination Diuretic medications.
These drugs dec HR, CO & Renin release and are useful in pt's with Angina, CAD, stable HF, Migraines, Anxiety Tremor. b-Adrenergic Blocking Agents
Cardiac b-1 receptors target where? Cardioselectivity (heart)
b-2 receptors target where? Bronchi & Vasculature
Patient has lung disease and now a bronchospasm. See sinus node dysfcn/AV conduction depression leading to bradycardia/AV block. Possible side-effects from what drug? b-adrenergic Blocking Agents
b-adrenergic Blocking Agents can mask symptoms of this disease. Hypoglycemia
Drugs that end in "lol" are all examples of what type of drugs? b-adrenergic Blocking Agents
Atenolol & Metoprolol both target this beta receptor. beta-1 adrenergics
Trandate & Coreg are examples of what type of b-adrenergic blockers? Combined a- and b- blockers.
This class of drug inhibits the renin-angiotensin-aldosterone system. This inhibits bradykinin degradation & stimulates synthesis of vasodilating PGEs. Angiotensin-Converting Enzyme Inhibitors (ACE-I)
This class of drugs for HTN is the DOC for pt's with DM since it delays the progression of CKD. You will need to check for proteinuria or microalbuminuria. Angiotensin-Converting Enzyme Inhibitors (ACE-I)
Dry cough, Angioedema, Rash, Hyperkalemia, Acute Renal Failure and Hypotension in pt's with B/L renal a stenosis are side effects of this type of drug. You should therefore check BMP after starting. Angiotensin-Converting Enzyme Inhibitors (ACE-I)
This class of drug always ends in "pril" Angiotensin-Converting Enzyme Inhibitors (ACE-I)
Patients with DM or HF can use this to tx HTN but side-effects are hyperkalemia, acute renal failure, angioedema(less common than with ACE-I) and hypotension in pt's w/ B/L renal a stenosis. Angiotensin II Receptor Blockers
This class of drug always ends in "sartan" and come in combo w/Hydo-Diuril(HCTZ) Angiotensin II Receptor Blockers
This class of drug works by inactivating the renin cleavage of angiotensin (which is the rate-limiting step in renin-angiotensin cascade) Renin Inhibitors
This is the top choice for using a diuretic. Hydo-Diuril(HCTZ)
Angioedema, Hyperkalemia & Hypotension are all side effects for this class of drugs. Renin Inhibitors
Aliskerin (Tekturna) is the basis for this class of drugs. All other drugs different still use this as part of its composition. Renin Inhibitor
This class of drugs causes peripheral vasodilation and need to be used cautiously in pt's w/HF. Can be used for ppl w/angina & arrhythmias. Ca-Channel Blocker
This drug is rarely used alone. Usually used when there are associated conditions. Beta-Blockers
HA, Peripheral Edema, Flushing, Palpitations, Bradycardia & constipation are all side effects of this class of drugs. Ca-Channel Blocker
This class of drug ends in "pine" Ca-Channel Blocker
This class of drug blocks post-synaptic alpha receptors to relax smooth m and decrease PVR. Not generally used as a 1st Line tx for HTN but is helpful if pt has BPH Alpha-Adrenoreceptor Antagonists
This class of drug ends in "zosin" Alpha-Adrenoreceptor Antagonists
Syncope/hypotension after 1st dose, postural hypotension, dizziness, palpitations and HA are all side effects for this class of drugs? Alpha-Adrenoreceptor Antagonists
This class of drugs stimulates a-adrenergic receptors in CNS and is used as a 2nd/3rd line agent for HTN. Side-effects include sedation, dry mouth & fatigue. Drugs w/Central Sympatholytic Action
Patient has been on a drug w/central sympatholytic action and has rebound HTN. Drug? Clonidine (Catapres)
Pregnant patient has HTN. Drug used? Methyldopa (Aldomet)
If pt is pre-hypertension(S120-139/D80-89) without compelling indication. Drugs? No anti HTN drug indicated
If pt is pre-hypertension(S120-139/D80-89) with compelling indication. Drugs? Drug(s) for compelling indications
If pt is Stage 1 hypertension(S140-159/D90-99) without compelling indication. Drugs? Thiazide-Type Diuretics -Maybe ACEI, ARB, B-Block, CCB or combos
If pt is Stage 1 hypertension(S140-159/D90-99) with compelling indication. Drugs? Drug(s) for compelling indications and diuretics, ACEI, ARB, B-blocker, CCB as needed.
If pt is Stage 2 hypertension(S>160/D>100) without compelling indication. Drugs? 2-Drug Combo Thiazide-Type Diuretic + CEI/ARB/b-blocke or CCB
If pt is Stage 2 hypertension(S>160/D>100) with compelling indication. Drugs? Drug(s) for compelling indications Other antiHTN drugs(diuretics, ACEI, ARB, B-Block, CCB)
Beta-Blockers is the initial therapy for these compelling indications: Heart Failure, Post-Myocardial Infarction, High CVD disk, DM
THIAZ is the initial therapy for these compelling indications: Heart Failure, High CVD risj, DM, recurrent stroke prevention
ACE-I is the initial therapy for these compelling indications: Heart Failure, Post-MI, High CVD risk, DM, Chronic kidney dz, recurrent stroke prevention
Ca-Channel Blockers are the initial therapy for these compelling indications: High CVD risk, DM
ARB is the initial therapy for these compelling indications: Heart Failure, DM, Chronic Kidney Sz
ALDO is the initial therapy for these compelling indications: Heart Failure, Post-MI Infarcton
ANT are the initial therapy for these compelling indications: Heart Failure, Post-MI
These patients are at an increased risk for cardiovascular events & need more agressive tx to drop BP <130/80. Diabetics or CKD patients
Diabetics should be given these drugs to dec BP <130/80. Want to decrease diabetic nephropathy. ACE-I or ARB or Renin Inhibitors
Patients w/CKD should be given these drugs to dec BP <130/80. ACE-I or ARB
To protect kidney function in non-DM kidney disease what should you inhibit? Renin-Angiotensin System -Use ACE-I or ARB
In patients with CKD you often treat with this for volume control as kidney disease progresses. Diuretics (Loop)
Blacks are more likely to have HTN & more susceptible to CV complications of HTN. They respond differently to antihypertensives. What should you treat with? Diuretics or a diuretic/CCB combo
Should you use ACE-I or ARB on black patients? No. Less effective & can have increased risk of angioedema.
Patient presents with specific BP paramaters unspecified by JNC7 WITHOUT acute target organ damage. HTN Urgency or Emergency? HTN Urgency
Patient presents w/(S>180/D>120) WITH acute target organ damage. HTN Urgency or Emergency? HTN Emergency
If patient presents w/a HTN Urgency/Emergency you don't want to do what too quickly because of risk of coronary/cerebral/renal hypoperfusion which can lead to ischemia. Decrease BP too quickly
Angina, CAD, Hypertensive HD, Cardiovascular Accidents, Transient Ischemic Attack, Chronic Kindey Dz due to nephrosclerosis, peripheral vascular dz (Aortic dissection) & retinopathy all what? Complications of HTN
Targeting Organ Damage is what? Complication of HTN
L Ventricle Hypertrophy on ECG and Echo can lead to HF/LVDD, ventricular arrhythmias, myocardial ischemia & sudden death in this disease. Hypertensive Heart Disease (Complication from HTN)
Stroke incidence, MI and heart failure all do what when you lower BP. Reduce risk.
The initial drug therapy for most is what? Thiazide-Type Diuretics
In this condition women are dx later & survive longer? Heart Failure
Abnormal cardiac fcn is responsible for inability of heart to pump blood at needed rate that can result from any structural/fcnal cardiac disorder. Heart Failure
You can control sx of heart failure by doing what? DEC Cardiac workload Control salt/water retention Enhance myocardial contractility
Infection, Anemia, Arrhythmia, Fluid overload, HTN, MI, PW and Endo/myocarditis all cause what? Heart Failure
What effects contractility? Metabolic condition of cells ANS/Hormones
What effects Afterload? Peripheral Vascular Resistance Arterial Pressure Preload Arterial Wall Compliance Blood Viscosity
ANS Influences what in heart? Heart Rate & Contractility
Venous Return effects what performance influencer? Preload
Preload is effected by what? EDV Filling Time Compliance Filling Pressure Atrial Systole Pericardium
Systolic and Diastolic Dysfunction are a sign of what? Left Sided Heart Failure
Abnormalities that effect the R venticle result in this. Most commonly caused by L-sided heart failure. Edema, Venous Distension & Ascites -->R Heart Sided Failure
Increased pressure L Atrium and pulmo vv & capillaries=pulm edema from this condition Left Heart Failure
Increased afterolad on R Ventricle can cause this Right Heart Failure
An ejection fraction lower than 40% is a sign of what? Systolic Dysfunction
A normal ejection fraction caused by angina, fibrosis or infiltrations can lead to this dysfunction. Diastolic Dysfunction
Acute Ischemia called Angina
Example of infiltrate Sarcoid
Patient who is at high risk for developing heart failure, but has no structural abnormalities Stage A
Pt w/a structural disorder of heart but no sx of heart failure Stage B
Pt w/past or current sx associated w/underlying structural dz Stage C
End-Stage Disease Stage D
Edema, Rales at the Bases, JVD and S3/4 are signs of what? Heart Failure
Patient presents w/dyspnea, fatigue, cough. Signs of what? Heart Failure
Dyspnea that progressively worsens from DOE to Orthopnea to PND to Dyspnea at rest sign of what Heart Failure
Dependent Edema secondary to volume overload sign of what Heart Failure
Fatigue secondary to low perfusion sign of? Heart Failure
Cough (Nocturnal, non-productive), early satiety secondary to hepatic congestion, and nocturia secondary to increased renal perfusion when pt lying down all signs of? Heart Failure
PND, JVD, Rales, Cardiomegaly, Pulm Edema, S3 Gallop, INC Venous Pressure & Hepatojugular reflex all sign of what? Major Criteria for Heart Failure
LE Edema, Nocturnal cough, DOE, Hepatomegaly, Pleural Effusion, DEC vital capacity & tachycardia all what? Minor Criteria for Heart Failure
More than 4.5kg weight loss over 5 days sign of what (Major or Minor)? Heart Failure
Dyspnea, Diaphoresis, Tachypnea, Tachycardia, Rales S3-S4 all signs of? L Heart Failure
Peripheral edema, RUQ pain/discomfort, JVD & Ascites all signs of? R Heart Failure
What's the most common cause of right heart failure? L Heart Failure
Hx of valvular dz, DM, CAD, S3 or S4, Mitral Regurg, Rales, Cardiomegaly & JVD all signs of what? Systolic Dysfunction
Hx of HTN, S4, Rales & LVH all sign of? Diastolic Dysfunction
Ejection fraction is >45%. Dx? Normal
Signs/Sx of heart failure+ejection fraction <40% sign of what dysfunction? Systolic Dysfunction
Signs/Sx of heart failure+ejection fraction normal sign of what dysfunction? Diastolic Dysfunction
What can exacerbate a pre-existing HF that would show up on CBC? Anemia
What can present as heart failure/exacerbate it? Hypothyroidism (see on Thyroid Panel)
Use CMP in Heart Failure to ck what? If pt is DM-->HF
Test liver function in heart failure, why? Hepatic congestions
Electrolye, Fe studies, UA & Lipid Panel all used to see what? Heart Failure
This marker for heart failure is released in response to stretching of ventricular wall. INC levels(<100pg/ml) show failure. Brain-Type Natriuretic Peptide (BNP)
The higher the level of this, the poorer the prognosis. Brain-Type Natriuretic Peptide (BNP)
What do you use to differentiate btwn pulmonary & cardiac dz in pt w/dyspnea/inconclusive PE. Brain-Type Natriuretic Peptide (BNP)
If you reduce this, will lower congestive sx. Preload
If you reduce this, will improve cardiac fcn Afterload
Pt has Stage A/Class I, II, III. Tx? ACE Inhibitor
Pt has Stage B/Class I, IIb, III. Tx? ACE Inhibitor B-Blockers Diuretics
Pt has Stage C, Tx? ACE Inhibitor B-Blockers Diuretics
Recommended tx for ALL patients with heart failure ACE Inhibitor Digoxin Diuretics
More common in older females w/HTN, DM. Diastolic Dysfunction
This drug reduces mortality in symptomatic & non-symptomatic pts. Reducing severity, sx, hospitilizations. ACE Inhibitors
What should NOT be considered contraindications in heart failure when treating with ACE Inhibitors. Renal Dysfunction & Cough
If ACE Inhibitors are NOT tolerated you should use these (esp if pt is symptomatic). Ck BP, renal fcn & electrolytes Angiotensin-Receptor Blockers (ARBs)
Should only use this drug in heart failure if pt is stable, ACE Inhibitors were started to stabilize. Be careful because CAN exacerbate sx. Do NOT give if pt decompensating. Beta Blockers
In Heart Failure this type of Diuretic is preferred normally. Loop Diuretics
In Heart Failure you can use this drug for pts with HTN & Fluid overload. Thiazide Diuretics
This aldosterone antagonist(w/K sparing effects) used for pts w/at rest dyspnea within past 6mos. Post MI w/systolic dysfunction). Spironolactone
This aldosterone antagonist may result in hyperkalemia. Spironolactone
Pt's with concomitant atrial fibrillation use this drug. Enhances exercise tolerance. Start low dose. Digoxin
Na Restriciton, Daily Wt Measure, Influenza vaccine, pneumovax, physical activity & close F/U all good for tx of? Heart Failure
NSAIDs, Glucophage, Viagra, Cialis, Levitra, TCAs, Sporanox & Tegretol all worsen this dz? Heart Failure
This complication of heart failure comes from INC in venous P. Pt will present w/dyspnea,productive cough & diaphoresis. Pulmonary Edema(from HF)
Pt has rales, wheezes & rhonchi. Dx? Pulmonary Edema(from HF)
CXR shows Kerley B lines, edema & cardiomegaly. Pulm capillary wedge P> 25mmHf. Dx? Pulmonary Edema(from HF)
Management of Pulm Edema includes MOND? Morphine(DEC anxiety & work of breathing) Oxygen Nitrates(DEC preload & capillary wedge P) Diuretics(DEC fluid & congestion)
This occurs as a complication of Heart Failure when sx progress beyond the tx plan. Most commonly caused by inadequate plan. Also by cardiac conditions,URI & new meds. Decompensation
To test for decompensation you would focus your cardiac exam to include what? Body wt, HVD, Hepatomegaly, Chest/Lungs, Cardiac Exam
If you think pt has decompensation may see changes in this lab? Potassium
If there's no improvement with suspected decompensation should do what? Refer to Inpatient
To treat for Decompensation(complication of heart failure use what)? MONgD Morphine, Oxygen, Nitroglycerin, Diuretcs
What are the most common deaths in heart failure? Progressive Pump Failure (Decompensation) & Arrhythmias.
Progressive Pump Failure Decompensation
What is recommended for the secondary prevention of CVD. May have impact on overall survival. Statins
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