Cardiovascular Flashcards
Normal total cholesterol
<200
Normal VLDL (triglycerides)
<150
Normal LDL
<100
If pt has diabetes than <70
Normal HDL
> 40
Pericarditis
Inflammation of the pericardium (outside of heart).
-Usually caused by viruses although high incidence post MI.
Signs and symptoms of pericarditis
-Precordial/retrosternal localized pleuritic chest pain.
-Pain increased with deep inspiration, coughing, swallowing or lying in recumbant position. Pain usually only lasts a few seconds.
- Pain is releived by sitting forward.
- Patient may have SOB secondary to pain with inspiration.
- Fever may be present.
Physical exam findings of pericarditis
A thorough history is paramount in making correct diagnosis.
-Pericardial friction rub (heard when patient not breathing) classically heard when patient is sitting up and leaning forward.
-Pleural friction (heard only with inspiration and expiration) rub may be present.
-Fever and dyspnea
Labs and diagnostics of pericarditis
ST segment elevation in all leads with concave ST segment elevation in multiple leads mimicking “smiling face.”
Depression of PR segment
Elevation will return to normal in a few days followed by temporary t-wave inversion.
ST segment elevation is not specific enough for differentiation between pericarditis and MI. Needs to be noted in multiple leads with smiling face.
-Elevated ESR
-Leukocytosis
-Echo to confirm pericardial fluid
-Blood cultures if bacterial cause suspected.
-BMP/CBC
Management of pericarditis
-NSAIDS are the mainstay of treatment.
-Colchicine can be used with nsaids to decreased symptoms and rate of reoccurence.
–<70kg 0.6mg PO qday
–<70kg 0.6mg PO BID
-PPIs for GI toxicity d/t NSAIDS
-Pain meds (hydrocodone)
-Corticosterioids if NSAIDS are ineffective or contraindicated (may cause viral replication)
–Dexamethasone followed by prednisone.
-Antibiotics if bacterial infection.
Monitor for tamponade, pericarditis pts more at risk than endocarditis.
Endocarditis
Infection of the endothelial layer of the heart, usually involves the cardiac valves.
A diagnosis of endocarditis must be considered in all patients who presents with a fever of unknown origin and development of a new murmur
Should also be considered in all patients who had recent heart surgery particularly valve replacement.
Causes of endocarditis
Usually caused by bacteria but can be caused by other things.
-Increased incidence associated with congenital heart disease and valvular disease.
-Predisposing factors include valve disease, recent invasive procedures such as dental surgery, GU surgery and the use of invasive catheters such as hemodialysis or burn treatments.
Signs and symptoms of endocarditis
- Fever lasting for several weeks
- Weightloss
- Nightsweats
- General sick feeling
Night sweats usually only happen in a few instances: endocarditis, TB, menopause, HIV/AIDS, hemeonc/leukemia
Physical exam finding of endocarditis
- Fever
- Murmur (may not be detectable in all patients especially in pts with right sided endocarditis).
- Skin changes:
-Osler nodes (painful) petechia, purpura, pallor, red nodes in distal phalanges.
-Splinter hemorrhage Linear subungal splinter appearing lesions or bleeds.
-Janesway lesions (painless), macules on palms and soles
-Roth spots (eyes)
-Splenomegaly.
Labs/diagnostics for endocarditis
-Blood cultures (most important test)
-WBC may be normal or elevated but will always have a shift with bands.
-ESR elevated
-May have normochronic, normocytic anemia
-Microscopic hematuria and proteinuria
-Echo to assess valvular disease involvement
-BMP
Alpha receptors
Beta Receptors
Agonist
Antagonist
-Alpha-Aid in muscle contraction and vasoconstriction
-Beta- aid in muscle relazation and vasodilation
-Agonist-is a molecule capable of binding to and functionally activating a target.
-Antagonist-is a molecule that binds to a taget and prevents other molecules from binding. They have no effect on the receptor activity.
Goal of HTN therapy
Prescribe the least number of meds possible at the lowest dose to attain acceptable BP which will ultimately decrease cardiovascular and renal morbidity and mortality.
First line agents for non-african americans with HF
- Thiazide diuretics (#1)
- ACEI
- ARBs
- CBC
Never use ACEi and ARBs together as they can cause hyperkalemia
Thiazide diuretics
- Increase excretion of sodium and water, may reduce peripheral vascular resistance.
- Make sure to screen for sulfa allergy before administration.
- May cause electrolyte imbalances (hypokalemia, hypomagnesium, hyperglycemia, hyponatermia, hypercalcemia) rash, and photosensitivity.
-Hydrochlorothiziade, bumetanide, aldoctone
ACE inhibitors
- Causes vasodilation and blocks sodium and water retention.
- Less effective for lowering BP and CVD events in african americans.
- Do not give if potassium >5.5
- Contraindicated in pregnancy and bilateral renal stenosis
- Do not use in combo with ARBs and renin inhibitors.
- May cause cough, rash, taste disturbances, hyperkalemia, renal impariments and angioedema.
- Make sure to monitor renal function and potassium
-prils
Most beneficial when pts has failure or large infarct, helps prevent ventricular remodeling.
ARBs
-Reserved for patients who are intolerant to ACE inhibitors.
- Same effect/warnings as ACEi
- May cause cough (substantially less than ACEi), hyperkalemia, headache, taste disturbance and renal impairment.
- artans
Calcium channel blockers
Stops calcium from entering the cells of the heart and arteries. Calcium causes the heart and arteries to squeeze more strongly. By blocking calcium, CCBs allow vessels to open and relax.
-Contraindicated in HFrEF
-May cause headache, flushing, reflex tachycardia, constipation, bradycardia and heart block.
-pines, also verapamil and diltazem.
Beta Blockers
-2nd line therapy
-Directly relaxes the heart.
-Caution use in pts with asthma and copd due to bronchospasms.
-May cause dizziness, bradycardia, 2nd or 3rd degree heart block, fatigue and decreased exercise intolerance.
Two types:
Beta 1 blockers: Cardioselective
-Atenolol, esmolol, metoprolol
Beta 2 blockers: Noncardioselective. Controls varioius aspects of metabolic activity and induce smooth muscle relaxation
-Propanolol, labetalol, carvedilol
Peripheral alpha-1 antagonists
-4th line therapy when HTN is not well controlled or when there is compelling indication (BPH)
- Causes peripheral vasodilation
- Should not be used as monotherapy for HTN
- May cause 1st dose sycope (take 1st dose at night), dry mouth, orthostasis, dizziness, headache nausea, palpitations.
- Terazosin, doxazosin
Centrally acting alpha 2 agonists
-3rd or 4th line therapy.
-Causes vasodilation and slow HR
-Methyldopa is the drug of choice in pregnancy.
-May cause withdrawal symptoms and rebound HTN if discontinued abruptly.
-Caution concurrent use with beta blockers due to bradycardia.
-May casue dry mouth, sedation, orthostasis, visual disturbances, depression, headache, bradycardia.
-methyldopa, clonidine.
Arterial vasodilators
-3rd or 4th line therapy.
-Directly relaxes the vascular smooth muscle resulting in arterial vasodilation.
-Adjust dose for renal impairment.
-Contraindicated in patients with CAD, anginal syndromes, or aortic aneurysms.
-May cause reflex tachycardia, flushing, dizziness, SLE, orthostatic hypotension, and fluid retention.
-Hydralazine, minoxidil
Direct renin inhibitors
-Does not appear to offer any advantage over other current available agents.
-Inhibits renin, which decreased plasm renin activity and inhibits the conversion of A1 to A2.
-Contraindicated in pregnancy.
-Do not use if potassium >5.5
-Do not use in combo with ACEi and ARBs
-May cause dizziness, headache, diarrhea, high potassium and renal impairment.
-Only one available: Aliskinen
Systole
Ventricular contraction
AV valves close (tricuspid and mitral valves) and semi lunar valves open (pulmonic and aortic)
Period between S1 and S2
Diastole
Semilunar valves close (pulmonic and atrial) and AV valves open (tricuspid amd mitral).
Rapid venticular filing (75%)
Atrial contraction/kick (left over 25% into ventricles)
Period between S2 and S1
Auscalatory areas of the precordium
Aortic: 2nd right ICS right of sternum
Pulmonic: 2nd left ICS left of sternum
Erbs: 3rd ICS left of sternum
Tricuspid: 5th ICS left lower sternum
Mitral: 5th ICS midclavicular at apex
S1 heart sound
S2 heart sound
S1: Signifies closure of AV valves (semilunar valves are open)
-Coincides with R wave on EKG
S2: Signifies closure of semilunar valves (AV valves open)
-Occurs at onset of diastole
Split S2 heart sound
Transient split occurs during inspiration due to late closure of pulmonic valve and early closure of aortic valve.
-Late closure of pulmonic valve is associated with increased in venous return to the right ventricle with inspiration.
-Early closure of the aortic valve is associated with decreased venous return to the left ventricle related to an increase in pulmonary capacity during inspiration.
-Heard best in the pulmonic auscultation area
-If the patient hold his or her breath the sound dissapears
-Normal physiologic findings in children and young adults.
-May occur every 4th beat.
S3 heart sound
Referred to as ventricular gallop, “Kentucky.”
-Due to passive filling of blood into a noncomplaint left ventricle.
-Occurs with heart failure and cardiomyopathies when fluid overload is present.
-Normal sound associated with pregnancy (due to hyperdynamic states)
S4 heart sound
Reffered to atrial of presystolic gallop.
-Produced by blood entering **a non compliant left ventricle **during atrial kick.
-Associated with increased ventricular diastolic pressures.
-Heard late in diastol immediately before S1 and sounds like “Tennessee”
-Occurs in conditions such as MI, HTN, ventricular hypertrophy, and HF.
-Not heard when patient is in a-fib due to loss of atrial kick.
When S3 and S4 are heard together it’s indicative of severe myocardial failure.
Murmur grading scale
1: Barely audible
2: Audible but faint
3: Moderately loud, easily heard
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
4: Loud, associated with a thrill. “if you dont have a thrill you arent at a 4”
5: Very loud, heard with one corner of stethoscope off the chest wall
6: Loudest, no stethoscope needed
Blood flow through the heart
Superior vena cava>
Right atrium>
Tricuspid valve>
Right ventricle>
Pulmonic valve>
Pulmonary artery>
Lungs>
Pulmonary veins>
Left atrium>
Mitral valve>
Left ventricle>
Aortic valve>
Aorta>
Body
Stenosis vs regurgitation
- Stenosis- forward flow issue d/t calcification of the valve
- Regurgitation- Back up into previous chamber
Mitral stenosis
Loud S1 murmur, low pitched, mid diastolic; apical “crescendo” rumble.
Soft sound
Mitral regurgitation
Systolic murmur at 5th ICS MCL, may radiate to base or left axilla; musical blowing or high pitched; may follow S3.
Harsh sound
Associated with a holosystolic murmur
Systolic murmurs radiate
Aortic stenosis
Systolic, blowing, rough harsh murmur at 2nd right ICS usually radiating to the neck.
Soft sound.
Systolic murmurs radiate.
Aortic regurgitation
Diastolic, blowing murmur at 2nd left ICS.
Heart failure
A syndrome that results when the cardiac ouput is insufficient to meet the metabolic needs of the body.
HFrEF
Heart failure with reduced ejection fraction
-Also known as systolic failure
-Due to the inability of the heart to contract and results in decreased cardiac output.
HFpEF
Heart failure with preserved ejection fraction
Also known as diastolic failure
Inability of the heart to relax and fill, results in decreased cardiac output.
Acute heart failure
- Abrupt onset, usually follows acute MI or valve rupture.
- Blood backs up from the left ventricle to left atrium and into the lungs.
- Will have s/s of left HF:
-Dyspnea at rest
-Coarse rales over all lung fields
-Wheezing, frothy cough
-Appears generally healthy except for the acute event.
-S3 gallop (kentucky)
-Murmur of mitral regurgitation (systolic murmur loudest at apex)
Chronic heart failure
Develops as a result of inadequate compensatory mechanisms that have been employed overtime to improve cardiac output.
Right ventricle has to compensate from left ventricle not doing it’s job and leads to failure.
Will have signs of right HF:
-JVD
-Hepatomegaly, splenomegaly
-Dependent edema as a result of increase capillary hydrostatic pressure
-Paroxysmal noctural dyspnea (PND)
-Appears chronically ill
-Diffuse chest wall heave
-Displaced point of maximal impulse (PMI)
-Abdominal fullness
-Fatigue on exertion
-S3 and/or S4
Cor pulmonale
Right ventricular hypertrophy
Heart failure classifications
New York Heart Association (NYHA) Functional Classification of Heart Failure:
1- No limitations or physical activity
2- Slight limitations of physical activity. First class where pt is symptomatic.
3- Marked limitations of physical activity
4- Severe inability to carry out any physical activity. Symptomatic all the time.
Management of HF
- Non-pharmacological:
-Sodium restriction
-Rest/activity balance
-Weight reduction - Phamacological:
-ACE inhibitor or ARB (for pts unable to take ACE due to renal insufficiency, couch, angioedema.
-Beta blocker
-Diuretics
Cardiomyopathies
Any disorder that affects the heart muscle.
An idiopathic disorder causing cardiac muscle dysfunction that may result in systolic or diastolic heart failure not due to atherosclerosis, HTN or valve disease.
S/S are just like heart failure
Management of cardiomyopathies
Management is just like heart failure
For symptomatic relief:
ACEi or ARBS
Diuretics
Beta blockers
Dilated cardiomyopathy
- Dilation of the heart muscles, the most common type.
- Abnormal systolic pump function also known as HFrEF.
- Systolic heart failure.
Hypertrophic cardiomyopathy
Hypertrophy of the left ventricle and occasionally the right ventricle.
Diastolic heart failure also known as HFpEF.
Stiff left ventricle during diastole that restricts ventricular filling.
Restrictive cardiomyopathy
Scarring/stiffening of the heart muscle, the least common type.
Inadequate diastolic filling.
Primary/essential vs secondary HTN
Primary/essential: Most common 95%
Secondary: 55, secondary to other known causes such as estrogen use, renal disease, pregnancy, endocrine disorders, renal artery stenosis (#1 cause).
HTN S/S
- Often none, known as silent killer.
- Elevated BP
- Suboccipital pulsating headache occuring early in the morning and resolving throughout the day, with severe HTN.
- Epistaxis
- Dizziness/lightheadedness
- S4 related to left ventricular hypertrophy
- AV nicking
- Tearing chest pain may indicate aortic dissection.
Lab/diagnostics of HTN
Order tests to rule out other causes of -HTN such as:
-Renovascular disease studies
-CXR
-Aldosterone levels to rule out aldosteronism
-Cortisol levels to rule out cushings
-UA, CBC, BMP, etc.
If all is normal, then it’s primary/essential HTN
BP categories
2-3 BP measurements on 2-3 seperate occasions
Normal: <120 AND <80
Elevated: 120-129 AND <80
Stage 1: 130-139 OR 80-89
Stage 2: >140 OR >90
Management of HTN (non pharmacological)
- Restrict dietary sodium (where Na+ goes water goes, making the heart work harder)
- Weight loss if overweight
- DASH diet (dietary approaches to stop HTN)
- -Rich in fruits, veggies, low fat products.
- Exercise
- Stress management
- Reduction or eliminate alcohol
- Smoking cessation
- Maintenance of adequate potassium, mag, calcium
When to start therapy based off BP and ADCVD risk
- Normal BP: <120 AND <80
-Promote optimal lifestyle habits and reassess in 1 year - Elevated: 120-129 AND <80
-Nonpharmalogical therapy and reasses in 3-6 months. - Stage 1: 130-139 OR 80-89
-W/O ASCVD risk- Nonpharmacological therapy and reasses in 3-6 months.
-With ASCVD risk- Nonpharmacological therapy plus BP lowering med, reassess in 1 month. - Stage 2: >140 OR >90
-Nonpharmacological therapy plus 2 BP meds from 2 different classes.
First line agents for african americans with HF
Thiazide diuretic
CCB
First line agents for diabetic pts with HF
ACEi or ARB
First line agents for CKD with HF
ACEi
HTN urgency
> 180/110
* Situations associated with severe BP elevation in otherwise stable pts without acute or impending change in target end organ damage or dysfunction.
* May be due to noncompliance with HTN meds
* May or may not be associated with severe headaches, SOB, epistaxis or severe anxiety.
* Treatment: restarting or revamping HTN therapy or captopril, clonodine, labetalol.
Hypertensive emergency
> 180/120
* Associated with evidence of new or worsening target organ damage.
* Requires immediate (w/in 1 hour) BP reduction to prevent or limit target organ damage.
* Blood pressure may be lower with any of the following:
-HTN encephalopathy
-Malignant hyperthermia
-ICH
-Unstable angina
-Acute MI
-Acute HF
-Dissecting aortic aneurysm
-Eclampsia
Treatment:
-ICU admission
-Nicardipine, nitroprusside
-Do not decrease too quickly unless there is a compelling condition (above).
–<140 over 1st hour and <120 if aortic dissection.
-For no compelling condition, no more than 25% reduction in BP w/in 1st hour then if stable <160 within next 2-6 hours then normal next 24-48 hours.
Angina
“Squeezing and choking of the chest” related to ischemia.
Types:
* Stable (classic or chronic)
* Prinzmetal’s angina
* Unstable
* Microvascular
Stable (classic or chronic)
- Intermittent chest pain or discomfort with a predictable pattern: the same onset, intensity and duration.
- Most often induced by exercise, but also can be induced by emotional distress.
- May last 1-2 min to 10-20 min, and looks like a heart attack.
- EKG demonstrates ST depression
- Can result from rupture of athersclerotic plaques that develop over time or a coronary spasm.
- Nitro may relieve pain by vasodilation and rest by decreasing oxygen consumption.
- Controlled with lifestyle changes and medications.
Prinzmetal’s Angina
- Precipitating event is coronary artery spasm and may occur in the absence of atherosclerosis.
- Can occur anytime including rest.
EKG should ST elevation - Due to sudden influx of intracellular calcium, so CCB is prescribed as treatment.
Unstable Angina
- Chest pain that lasts longer than 20-30 min.
- Pattern of attacks usually progresses with increased frequency, duration and intensity.
- EKG shows ST depression with T wave inversion.
- Sublingual nitro helps relieve pain.
- Increased incidence of MI within 6 months after onset of angina.
Microvascular angina
A metabolic syndrome
Chest pain that mimics angina
No evidence of abnormal angiogram, CT or coronary spasms.
Evidence o coronary microvascular function impairment.
Inferior MI
Leads 2, 3, avf
Sites:
Right Coronary Artey
Inferiorlateral MI
Leads 2, 3, AVF, V5, V6
Right coronary artery
Left circumflex artery
Anterior MI
Leads V3, V4
Left anterior descending artery
Anterolateral MI and lateral MI
Leads 1, AVL, V3, V4
Left anterior descending
Left circumflex
Anteroseptal
Leads V1, V2, V3, V4
Left anterioir descending artery
Cardiac enzymes
Troponin is cardiac specific, troponin I rises slightly faster than troponin T.
-normal 0-0.04
CK-MB
Myoglobin
Statin therapy
Goal is to get LDL to goal by maximal dose of statin, not by a specific LDL number.
- High Intensity Statin Therapy:
-Daily dose lowers LDL by <50%
-Atorvastatin 40-80mg
-Rosuvastatin 20-40mg - Moderate Intensity Statin Therapy
-Daily dose lowers LDL by 30-50%
-Atorvastatin 10-20mg
-Rosuvastatin 5-10mg - Low Intensity Statin Therapy
-Daily dose lowers LDL by <30%
-10mg statins
Other lipid lowering agents
- Bile acid sequestrants
-Lowers LDL, may increase triglycerides
-Cholestyramine
-Colesevelam
-Colestipol - Fibrates
-Decrease triglycerides, lowers LDL and increased HDL
-Gemfibrozil
-Fenofibrate
-Fenofibric - Cholesterol absorption inhibitors
-Used in combo with a statin to lower LDL
-Esetimibe - Niacin
-Decreases LDL and triglycerides and increases HDL
-Immediate release and extended release preparations
-High doses of niacin may cause flushing sensation
Myocardial infarction
Leading cause of death in U.S.
Necorsis of myocardial tissue
- Most common causes: CAD and cardiomyopathies
- S/S: Most have history of anginal pain
-Most infarcts occur at rest
-Nitro has little effect
-Cold swear, weakness, impending doom, apprehension, light headedness, syncope, dyspnea, cough, N/V.
Physical exam findings:
-Dysrhythmia common
-S4 very common
-Wheezing
-Pulmonary crackles
-Low grade fever
-Tachycardia
Lab/diagnostics of MI
First degree AV block
PR interval >0.20 seconds
Second degree type 1 AV block
Wenckebach or mobitz type 1
Longer longer longer drop then you have a wenckebach
PR interval gradually gets longer until a QRS complex is dropped
Second degree type 2 AV block
Mobitz type 2
Atrial rhythm is regular, the PR interval is constant, but the ventricular rhythm is irregular and dropped QRS complexes occur.
Third degreen AV block
Complete heart block
Atrial and ventricular rhythms are regular but there is not relationship between the P wave and QRS complex.
Atrial fibrillation
If unstable, cardiovert
If stable, do a TEE before cardiovert to rule out left atrial appendage thrombus, if no thrombus proceed to cardiovert.
Anticoagulation for 4 weeks after cardiovery due to atrial stunning and not contracting normally.
If pt has been on uninterrupted anticoagulants for 3 weeks a TEE is not warranted before cardiovert.
After conversion to NSR, antiarrhythmics may be nessesary to sustain rhythm.
CHA2DS2-VASc
Used to assess the risk of strokes in Afib pts.
1-Congestive heart failure
1-Hypertension
2-Age >75 (doubled)
1-Diabetes
2-Stroke (doubled)
1-Vascular disease
1-Age 65-74
1-Sex category (female)
Score of 0=no anticoagulation
Score of 1= oral anticoagulation or antiplatelet
Score of >2= oral anticoagulation
HAS-BLED
Helps assess bleeding risk in afib pts.
Hypertension
Abnormal liver and renal function
Stroke
Bleeding tendency/predisposition
Labile INR for pts taking warfarin
Elderly
Drugs/alcohol
A score of 1= low risk of bleeding
A score of 2= moderate risk and anticoagulation should be considered
A score of 3 or more= high risk for major bleeding and the pt should be routinely assessed for risk vs benefits of anticoagulation.
Peripheral vascular disease
Arteriosclerotic narrowing of the lumen of arteries resulting in decreased blood supply to extremities.
Usually caused by atherosclerosis, hyperlipidemia, smoking, DM.
S/S:
-Complaints of calf pain (claudication)
-Cold/numbness in extremities
-Progresses to pain at rest
Physical findings:
-Shiny/hairless skin
-Dependent rubor
-Pallor upon elevation
-Cyanosis
-Ulcerations
Reduced pulses
Lab/diagnostics:
-Ankle brachial index (1 is normal, <1 is abnormal)
-Arteriography is most definitive test
Management:
-Stop smoking and all tobacco use.
-Exercise, walk 1 hour a day to increase collateral circulation
-Cilostazol- antiplatelet drug and vasodilator
-Weight reduction
-Manage diabetes and hyperlipidemia
-Angioplasty
-Bypass surgery
-Amputation
Chronic venous insufficiency
Impaired venous return due to either destruction of valves, changes due to deep thrombophlebitis, leg trauma, or sustained elevation of venous pressure (HF)
More common in women than men
S/S:
-Aching of lower extremities relieved by elevation
-Edema after prolonged standing
-Night cramps of the lower extremities
Physical findings:
-Trophic changes with brownish discoloration
-Stasis leg ulcers
-Edema of lower extremities
-Dermatitis may be common
-Cool to touch
Lab/diagnostics:
-Nonspecific diagnostics
-R/O edema due to heart failure and other causes such as May Thurner syndrome which is compression of left common iliac vein by overlying right common iliac artery=LLE DVT
Management:
-Bedrest with legs elevated to diminish chronic edema
-Use of heavy duty elastic support stockings
-Weight reduction
-Treat dermatitis or ulcers as indicated
-Acute weeping dermatitis:
–Tap water compresses
–Hydrocolloid dressing
–For less acute use hydrocortisone cream.
Cardiac tamponade
Accumulation of blood and/or fluid in the pericardial space, resulting in a life threatening decrease in cardiac output.
Physical exam findings:
-Becks triad:
–JVD
–Narrow pulse pressure
–distantheart tones
-Tachycardia
-Pulsus paradoxus
-change in LOC
Lab/diagnostics:
-ECHO is gold standard
-CXR may show widened mediastinum
Management:
-pericardiocentesis
-treat shock
Management of endocarditis
For subacute endocarditis, empiric therapy is usually not started until blood cultures identify pathogen.
For acute endocarditis, usually due to staphylococcus aureus, streptococci and enterococci. So empiric therapy is started with vancomysin until culture results are avilable.
