OME+ Cardiac Flashcards
HTN
Path:
a vascular defect that leads to target organ damage.
What are the target organs?
brain, eyes, kidneys, and heart
Accurate BP Pearls:
How much of the cuff needs to cover the arm?
- cuff width covers 80% of arm;
What is minimum bladder circumference?
- bladder 40% of circumference;
How long sitting before taking pressure; where?
- feet on the floor after 5 min
Risk reduction from HTN control?:
Stroke, MI, HF, organ damage
In general what is the BP for ACA for everyone
< 130/80
BP goal for JNC-8 <60;
< 140/90
≥ 60;
< 150/90
≥ 65
- ≥ 65 not specified
DM/CKD
- Diabetes or CKD < 140/90
1st line Treatment by JNC-8:
1st line: lifestyle management unless BP is
2nd line: JNC-8 first-line meds: TZD, CCBs, ACEIs, ARBs,
Initiate Treatment
- Black no CKD –TZD, CCB (nondihydro verapamil; diltiazem)
- any race with CKD with or w/o DM add ACE or ARB to improve kidney outcomes
- No black & no DM or CKD: TZD, CCBs, ACEIs, ARBs
Med cautions with CCB (nondihydro)
verapamil, diltiazem inhibit P 450 3A4. Know meds that are substrates; select statins use P 450 3A4.
reduce HR and negative ionotropic. only with normal LV function and 2nd or 3rd degree AV block; good for kidney protection. NOTpost MI (either type)
Med cautions CCB dihydro (amlodipine, nife_dipine)_ NOT with CKD or diabetic nephropathy; very vasodilating. Resistant HTN
don’t use TZD -
not recommended post MI
don’t use ARB; renal function less than?
not for CAD, or CVA
Cardiac use of Aldosterone:
only post MI or HF Stage?
other indications for BB/CCB:
good for angina pectoris
Don’t use BB:
not for use in stroke; first-line med for HTN
JNC-8 pearls:
Lab values of microalbuminuria and GFR that show cardiac risk?
microalbuminuria or GFR of < 60 is a cardiac risk
postural HTN readings?
fall in BP of 20 systolic /10 diastolic within 3 mins of standing
Geriatric Considerations: Systolic increases without diastolic increased. increases with age.
Distinguish between a hypertensive urgency and a hypertensive emergency
Both are severe elevations in BP > 180/120. Emergency has evidence of TOD dysfunction. Must be transferred from primary care to ED or ICU
Murmurs
Path?
Turbulent blood flow
when do I investigate a murmur?
all murmurs grade 3+, symptomatic and all diastolic
Grade I. S1, S2 > murmur
Grade II S1, S2 = murmur
Grade III S1, S2 < murmur
Grade IV palpable thrill
Grade V
How do I Confirm Diagnosis:
with echocardiogram. (TTE or TEE)
Effect of leg raises and Valsalva on MS, AS, MR, AR:
leg raise worsens;
Valsalva improves;
all Tx with preload reduction
What is Mitral Stenosis:
obstruction of flow in diastole through the mitral valve so blood backs up into L atria and then lungs
sound?:
opening snap and diastolic decrescendo
Location:
apex
Etiology:
Rheumatic fever
S/sx:
Afib, CHF, SOB
tx:
can have a balloon valvotomy, with afib anticoagulate and cardiovert
Sports: full participation likely
Aortic Stenosis:
obstruction pumping blood out of the ventricle during systole
Etiology:
Calcification; congenital bicuspid valve. so usu elderly men; Rheumatic fever,
Pt:
old man
sound:
Crescendo-decrescendo in systole
Location:
aortic;
S/sx:
Syncope with exertion; angina with exertion; CHF (LV)
tx:
preload reduction, valve replacement, and usu will need a CABG
Mitral Regurgitation (insufficiency)
blood leaks from the Left ventricle to Left atria during systole
sound:
holosystolic radiation to axilla
Location:
cardiac apex
Etiology of acute?:
infective endocarditis or trauma;
Etiology of chronic?:
ruptured papillary muscle or chordae tendinae from cardiac ischemia, 2nd to MVP
S/sx:
Acute: Afib, CHF, pulmonary edema; FULMINANT s/sx
tx:
replace /surgery IDENTIFY ASAP
Chronic:
exertional SOB; fatigue; proceeds to dilation
Tx:
HF with normal meds but replace before CHF
Sports: an play depending on degree of ventricular enlargment.
Aortic Regurgitation (insufficiency)?
blood leaks back into the left ventricle during diastole
sound: diastolic decrescendo
Location: aorta valve
Etiology: ischemia/infection
S/sx: Acute:
cardiogenic shock
Chronic Sx:
dilated HF
tx: replace before bad stuff happens :)
HCOM and Mitral Valve prolapse leg raise and Valsalva?:
leg raise improves and Valsalva worsens;
tx by increasing preload
MVP
blood leaks into atria because
Etiology:
congenital defect of leaflets too big for annulus
pt:
pregnant women with decreased venous return
sound: holosystolic
Location: apex
S/sx: Acute:
CHF
tx: replace; expand the volume; avoid dehydration
Hypertrophic Cardio Myopathy
sound: systolic cresendo-decresendo
louder with standing
Location: apex
Etiology:
S/sx: SOB and suddent death
tx: replace
louder with standing
Still Murmur -
has a buzzing quality
hyperlipidemia
What is First line:
lifestyle changes: reduce fat; cholesterol, increased exercise, add plant sterols, increase fiber.
What reductions in lipids are usually achieved with lifestyle?
a 5-10% reduction achieved.
What other lifestyle interventions can be added?
diet and cardio (cardio reduced insulin resistance)
What are the specific changes in lipids r/t exercise?
increase in HDL and reduction in TG and VLDL
What does high dose omegas do?
decrease TG. 1 g of EPA +DHA; from oily fish preferably
What do plant sterols do to lipid panel? (2 g/d)
decrease LDL
How can I decrease LDL-c with diet?
increase soluble or viscous fiber to 10-25 g/d
How does hypothyroidism affect lipids?
increase LDL, total cholesterol, and triglycerides
who is at > Risk from SE from statin therapy?
older, low body weight, high intensity
How much does a high-intensity statin lower LDL-C?
50%
What are the 4 categories of statin therapy and statin recommendations?
- Clinical ASCVD: high intensity for ≤ 75; mod >75
- Elevations of LDL-C 190 or greater: high intensity
- Diabetes & age 40-75 LDL-C 70-189 and NO ASCVD = moderate intensity;
- n_o ASCVD or DM but ASCVD risk is ≥ 7.5% and 40-75:_ moderate to high intensity.
HMG-CoA reductase inhibitor effect?
reduce LDL-C as much as 50%
labs and SE?/AE
- hepatic enzymes for baseline
- no grapefruit juice (Cyp450 3A4) for simvastatin, atorvastatin, lovastatin
- rhabdomyolysis and myositis
What does the NP see in lipid panel with fibrates?
Increase in HDL level and decrease TG but seldom used
What does the NP see with bile acid resins?
LDL-C reduced up to 30%; avoid drugs within 2 hours
What does the NP see with fish oil use?
TG reduced up to 30%
What does NP see with cholesterol absorption inhibitor?
reduced LDL-C 30%
How does hypothyroidism affect lipids?
increase LDL, cholesterol and triglycerides
What increases risks for SE from statin therapy?
older, low body weight, high intensity
Change in lipid panel from ezetimibe (zetia)?
a reduction in LDL-C
High-intensity statin - reduces LDL-C ≥ 50%
- Atorvastatin 40-80 mg
- rosuvastatin 20-40 mg
Mod intensity Statin: reduces LDL-C ≥ @ 30-49%
Why use?
(higher risk for adverse effects, ≥ 75; impaired renal; frailty, multiple comorbids, with a fibrate)
Dosing:
- pravastatin: 40-80 mg
- lovastatin 40 mg
- simvastatin 20-40 mg
- atorvastatin: 10-20 mg
- rosuvastatin: 5-10 mg
Low-intensity statin
LDL-C reduced < 30%
- pravastatin 10-20 mg
- lovastatin 20 mg
Statins
- What’s up with HDL and LDL. Why empiric Statins?
What is the first-line treatment for high cholesterol?
- Who needs a Statin?
- What are the vascular risk factors
- Explain the algorithm for giving a statin
- Every cell needs choleseterol.
LDL brings cholesterol to the periphery; HDL returns it to the liver
targeting a specific number did not improve outcomes. What improved outcomes (stroke, heart attack, and death) was to be on a high-intensity statin. It’s empiric.
- lifestyle; adherence
2. a. Anyone with LDL > 190
b. vascular disease: MI, CVA, PVD, CS
c. LDL 70-189 + age + diabetes;
d. LDL 70-189. + age. + calculated risk “risk factors”
3. Risk factors for vascular issues: diabetes, smoking, HTN, DLP
risk for CVD: HTN, family hx, smoking, obesity, Age > 55 women, > 45 for men
- LDL 70-189 PLUS Age 40-75 PLUS diabetes
LDL 70-189 PLUS Age 40-75 PLUS or have a 10-year calculated risk (2 or more vascular risk factors)
How are statins evaluated?
1. State labs and frequencies
- What s/sxs need investigation while on statins
- What is the correct intervention?
- Baseline values of Lipids, A1c, CK, and LFTs are required before starting a statin. You want to know what their baselines are to allow comparison if something happens.
2.
Lipids q 1 yr.
A1c DM =q3 months
CK. Muscles S/sx. What range is of concern?
LFTs. Hepatitis (RUQ tenderness/jaundice). range?
Myositis presents with soreness, weakness, or muscle pain. Hepatitis presents with right upper quadrant abdominal pain or jaundice.
- Statin-Myostitis. stop then start at lower dose when s/sx are gone
Statin-hepatitis stop . . . restart at a lower dose
2.
- What statins are prescribed for high-intensity therapy
- What exceptions are there for high-intensity statin therapy
- What are s/sxs of not tolerating statins?
- What is used when statins are not tolerated?
- Atorvastatin = lipitor. high 40, 80. moderate. 10, 20
Rosuvastatin = crestor. high. 20, 40. moderate 5, 10
- liver and renal disease, age > 75; statin intolerance.
Statin-Myositis presents with soreness, weakness, or muscle pain.
Statin-Hepatitis presents with right upper quadrant abdominal pain or jaundice.
Intervention: give moderate-intensity statin
- Fibrates. get LDL down and HDL up
Describe the therapy when pt can’t tolerate a statin?
What are the other cholesterol lower medications?
MOA?
Effects?
SE?
LDL to < 100 with medications. Of course, lifestyle modifications and adherence become paramount
Use fibrates
What labs are recommended with first diagnosis of HTN?
- FBG
- CBC
- lipid panel
- serum creatinine and eGFR
- CMP (sodium, potassium and calcium
- TSH
- urinalysis
- EKG
- optional: echo, uric acid, urine albumin: creatinine ratio
REVIEW HF
HF hx:
previous MI/ACE, angina, HTN, valvular disease, rheumatic fever, palpatations.
HF s/sx: t
tachycardia, increased JVP, displaced apical beat, S3 heart sound, murmur, pulmonary crackles, dependent edema
Diagnostic HF labs and imaging:
EDG, CXR, Echo, CBC, CMP, TSH
