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
