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112 Cards in this Set
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- Back
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How would you diagnose Acute Coronary Syndrome?
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Cardiac biomarkers
EKG changes Diagnostic studies |
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What are the cardiac biomarkers, what intervals are they drawn at and what are their normal values?
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Troponin I & 2 - onset 3-12H, Peak 18-24H, duration up to 10-14 days.
Creatine Kinase total & MB - onset 3-12H, Peak 18-24H, Duration 48-72H |
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What variables give a false elevation of the troponin?
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heart failure, MI/pericarditis, sepsis, SIRS, pulmonary disease, trauma, CPR, cardioversion, ICD firings, end stage renal disease
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What are the combinations of CK? what do they signify?
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MM: skeletal muscle
BB: brain and kidney MB: cardiac Elevated CK diagnostic of MI, DK levels 2x above normal with simultaneously elevated CKMB. Elevated CKMB in presence of normal total CK suggests MI |
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What are the total cholesterol levels?
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< 200 desireable
200-239 Borderline high > or equal to 240 - high |
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what are the levels of LDL cholesterol?
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< 100mg/dL optimal
100-129 mg/dL - near optimal 130-159 borderline 160-189 - high > 190 very high |
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What are the 3 LDL goals?
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CHD and CHD risk < 100mg/dL
Multiple risk factors - < 130mg/dL 0-1 risk factors - <160mg/dL |
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Reasons for high triglycerides?
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overweight
physical inactivity cigarette smoking excess alcohol intake very high(>60%) carb diet other diseases: type 2 diabetes, CRF Drugs: corticosteroids, protease inhibitors, B-Blockers, estrogens |
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Whare are normal triglyceride levels?
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< 150mg/dL normal
Borderline-high 150-199mg/dL high - 200-499 Very high - > 500 |
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what is the VLDL?
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Surrogate for triglycerides when triglycerides > 400. Precursors of LDL.
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whats HDL?
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inversely correlated with CHD risk.
Low HDL is independent risk factor for CHD, <35 |
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Causes of low HDL?
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high triglycerides, overweight, smoking, inactivity, high carb intake, type 2 diabetes, B-Blockers, anabolic steroids, progestational agents, genetic factors. Ideal ratio of total chol. to HDL < 3. Avg. risk ratio 3-5, elevated risk - ratio >5
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what are the guidelines for checking cholesterol levels?
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fasting total, LDL, HDL, triglycerides
every 5 yrs in adults age 20 and over. if testing non-fasting only cholesterol and HDL usable. If HDL > 40mg/dL and total chol. < 200 no further testing needed. |
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whats homocysteine?
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an amino acid thats an independent risk factor for atherosclerotic vascular disease and recurrent venous thromboembolism. Normal values: 5-15 umol/L, moderate - 15-30umol/L, intermediate - 30-100umol/L, severe >100.
Just measure this in high risk pts. |
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What is C-Reactive Protein?
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Inflammatory marker, acute phase protein. may be a predictor of CHD risk. greatest usefulness in pts with intermediate risk. screening as part of global risk eval. low=1.0mg/dL, Avg=1.0-3.0, high >3.0, CRP > 8 may be an acute phase response, repeat in 2-3 wks. consistently high values represent very high risk of future CVD. Do with cholesterol evaluation.
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What does a BNP measure for?
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counterregulatory hormone released in response to high ventricular filling pressures. promotes diuresis, natriuresis nd inhibits renin-angiotensin system, endothelial secretion, systemic and renal sympathetic activity. Normal is < 100. Levels > 400 have high positive predictive value for HF as etiolog of dyspnea.
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how does CRP correlate with plaque rupture?
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THERE IS A CORRELATION BETWEEN THE LEVEL
OF C-REACTIVE PROTEIN (CRP) AND LIKELIHOOD THAT A PLAQUE WILL RUPTURE |
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what is the difference between stable plaque and unstable plaque?
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STABLE PLAQUES:
– THICK FIBROUS CAP – SMALL LIPID CORE – LESS LIKELY TO RUPTURE – IT PRODCUES A NARROWING OF THE ARTERY (CORONARY) THAT LIMITS BLOOD FLOW – CAUSES SHRINKING OF THE VESSEL AT THE SITE OF THE PLAQUE WHICH IS CALLED “NEGATIVE REMODELING” UNSTABLE PLAQUES: – “VULNERABLE PLAQUE” – LARGE PLAQUE IN THE WALL OF THE ARTERY – THIN FIBROUS CAP THAT SEPARATES THE CORE OF THE PLAQUE FROM THE LUMEN – IT CAUSES THE VESSEL TO BEGIN TO EXPAND OUTWARD …CALLED “POSITIVE REMODELING” » INITIALLY THIS DOES NOT LIMIT THE SIZE OF THE ARTERY – AREA LIKELY TO RUPTURE IS THE AREA BETWEEN THE PLAQUE AND THE NORMAL ARTERIAL WALL CALLED THE “SHOULDER” » IT IS A HIGH AREA OF STRESS » ONCE IT RUPTURES IT INITATES THE CLOTTING CASCADE AND THE DEVELOPMENT OF A THROMBUS |
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Rupture of an unstable plaque causes what?
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RUPTURE AND PRODUCE A LARGE ENOUGH THROMBUS
THAT THE PATIENT BECOMES SYMPTOMATIC » UNSTABLE ANGINA » “ACUTE CORONARY SYNDROME” (Non ST segment Elevation (NSTEMI) » |
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What causes an MI?
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MI … ST segment elevation MI (STEMI)
– RUPTURE, BUT NOT PRODUCE ENOUGH OF A THROMBUS TO REDUCE BLOOD FLOW…PT IS ASYMPTOMATIC » HENCE THE PLAQUE BECOMES MORE FIBROUS – OVER TIME A VULNERABLE OR UNSTABLE PLAQUE CAN BECOME A STABLE PLAQUE AS THE CAP BECOMES MORE FIBROUS |
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What does V02 testing do?
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it differentiates cardiac vs. pulmonary limitations; used for HF pts. considering transplant.
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How do you calculate the Ankle-Brachial Index?
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lower extremity systolic pressure over brachial artery systolic pressure. The ABI is 95% sensitive and 99% specific for PAD
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How do you establish a PAD diagnosis?
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ABI
duplex US exercise test with ABI abdominal US Computed tomagraphic angiography MRA Contrast angiography |
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what is a diamond shaped murmur and where is it?
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diamond-shaped murmur
refers to the phonocardiographic tracing of a crescendo-decrescendo murmur.--see w/aortic stenosis |
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crescendo murmur
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crescendo murmur
one marked by progressively increasing loudness. crescendo-decrescendo murmur one with increasing intensity until mid- to late systole, then a decreasing intensity, giving a diamond-shaped tracing on phonocardiography. Characteristic of pulmonary stenosis. decrescendo murmur one with an intensity that gradually decreases. Heard during diastole in aortic or pulmonary valvular insufficiency. diamond-shaped murmur |
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What is the diagnostic level of the CKMB for an MI? Troponin?
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CKMB > 120 IU/L
Elevation of Troponin I (>0.35) or Troponin T(>0.2) |
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What are some of the clinical manifestations of an MI as the result of the metabolic, mechanical and electrical changes at the cellular level?
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decreased CO (decr SV)
Increased ischemia increased workload on the heart elevated wedge increased afterload (SVR) may see cardiogenic shock because of catecholemines/renin/angio starts holding water |
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Treatment of an acute MI?
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MONA
morphine, oxygen, nitro, ace inhibitor i.e. decrease preload/afterload/SVR/HR/pain/metabolic demands on the heart AND limit myocardial damage--prevent remodeling--with ACE and BB; increase systemic perfusion--give dobutamine. have them chew an aspirin. |
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What is the timing goal for administering thrombolytics?
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4-6H after the onset of s/s
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what are the contraindications for thrombolytics?
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severe HTN (180/110)
INR > 2 or 3 cpr greater than 10 minutes recent trauma last 2-4 wks recent major surgery pregnancy gastric ulcer liver/renal disease intracranial neoplasm cva or other cardiovascular event within a year |
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WHAT DO WE USE TO PREVENT REMODELING?
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BB (neg inatropic/chronatropic)
i.e. metroprolol (selective beta 1 agonist) co-reg (alpha and beta 1 and beta 2 antagonist) |
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what are contraindications for beta blockers?
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HR < 50
BP < 95 dibetics-may mask s/s hypoglycemia--they need a cardioselective BB ppl in heart block |
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Name some risk factors for an MI.
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HTN, Hyperlipidemia, Obesity, DM
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What are some EKG changes you might see during an MI?
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ST and T wave abnormalities--if elevated its injury, if below isoelectric line it ischemia
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S/S Acute HF?
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left sided-acute
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S/S chronic HF?
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Right sided-chronic
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If have an MI what do you see?
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pulmonary edema!
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what is systolic HF?
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problem is difficulty with contraction--cant contract--will be on an inotrope, like Dig
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what is dyastolic failure?
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heart cant relax--will be on a dilator to try and help them relax.
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S/S LHF
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pulmonary s/s
L failure = lungs dyspnea, rales, wheezing, s3 |
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s/s rhf
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occur in a particular order: JVD
hepatosplenomegaly perif edema |
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best test to order to explore HF valve, wall and EF?
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echo!
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what is the HF outpatient management?
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Na restriction
water restriction rest/activity balance weight loss |
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what is the standard of care in HF?
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Ace Inhibitors often in combo with diuretic therapy. The "pril" drugs
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What is the acute mgmt in Pulm Edema?
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Lasix 40mg, if dont pee give 40 more.
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HTN definition?
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sustained elevation at least 3 times on 2 different occasions
2 categories--primary (essential) and secondary (only about 5% but are some classic presentations: estrogen use, renal dx, pregnancy, renal artery stenosis --RAS) |
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What are the TLCs for HTN?
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exercise, diet education
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what are s/s HTN?
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HA--suboccipital in back of head that gets better as day goes on.
epistaxis S4 proteinuria hematuria |
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what is normal BP?
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120/80 must be both
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what is stage I HTN?
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140/90
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stage 2 HTN?
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160/100
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what are the JNC7 guidelines for starting HTN meds?
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By stage I the patient should be on a thiazide diuretic. By stage 2, they will be on a 2 drug combo one of which is a thiazide diuretic.
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when would you not use a BB with your hypertensive pt?
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if they are diabetic or HF--need to be on an AI
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BB considerations:
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BB can cause a wheeze
some of them are alot cheaper than others, i.e. metoprolol is cheap--if they dont have insurance |
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when would you use a CaCB?
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if have a-fib, tacky, diabetic
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what are the loop diuretics?
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lasix. particularly effective in AA. also work well with elderly with isolated systolic hypertension
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what would you prescribe for your hypertensive diabetic pt?
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AI--watch for cough and if they have one switch to an ARB. There are also ARDS, but no standards of care.
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Hypertensive Urgency?
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190/110 pt is not symptomatic--use clonodine .2 up to .8
or captopril but parentarel therapy not needed |
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Hypertensive Emergency?
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220/140--nipride gtt, critical care admission and an A-line. if give nipride and get BP down, still keep them. how low do i go? as a gen rule--lower syst to betw 160-180 - grad. lowered over a period of days and d/c.
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Assesment findings in hypertensive Emergency:
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malignant HTN--
fundascopic changes with flame shaped retinal images and papiledema HTN encephalopathy intracranial hemmhorage |
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what are the 4 types of angina?
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microvascular (r/t metabolic syndrome)
classic-stable-exertional printzmetals-variant (nothing to do with atheroscl.--its coronary spasm from influx of intracellular Ca so are on a CaCB) Unstable angina-ACS, pre-infarction |
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what makes angina not an MI?
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CP--rest and pain goes away
give nitro and pain goes away |
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Physical exam for angina?
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usually normal, may have HTN transient s4, or LEVINES SIGN--90% diagnostic for angina
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ECG changes in MI
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T wave peak or inversion
ST depression is ischemia or angina ST elevation is infarction |
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what do you need for dx of MI?
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know their risk factors
know lipid panel! exercise EKG |
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Serum Lipid Levels
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TChol < 200
HDL > 40 trigly < 150 LDL < 130, 100, 70 |
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3 categories of meds used for outpt treatment of angina?
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nitrates
BB CCB |
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how do you know its not angina but an MI?
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nitro doesnt help, elephant on chest, rest doesnt help
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clinical manifestations of MI?
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impending doom, diaphoresis
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Labs/diag in MI?
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ECG changes--may show you nothing in 30% of cases. if you see, its peaked T waves, ST elevations and maybe Q waves.
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EKG pattern changes for 1 and AVL?
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lateral MI
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lead changes in 2, 3 and AVF
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inferior MI
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in a 12 lead, changes--V lead involvement, esp the pre-cordial leads, V3 and V4
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anterior, looking straight in
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Cardiac Enzymes
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100% cardioselective: ckmb and troponin i (MI)
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things to consider in management of an MI?
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give aspirin first--decr platelet aggregation
nitro 02 |
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Management guidelines for MI:
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from door to fibronolytic is 30 minutes!
door to cath lab is 90 minutes |
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Standard of care for MI
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metoprolol-or another BB if there is a contraindication
lovenox (1mg/kg) or heparin |
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Indications for pharmacologic revascularization?
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unrelieved CP of > 30 min but < 6H with ST segment elevations of greater than > .1 in 2 or more contiguous leads. Contraindications: anything that might set the pt up for bleeding, i.e. recent surgery, etc.
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how do you tell if its a superficial or deep Venous thrombosis?
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superficial? sudden onset of acute pain
deep (DVT)? pain or tenderness while walking physical exam: localized heat and erythema is superficial but big time edema distal to occlusion is DVT. get doppler |
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if superficial, whats the treatment?
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elevate extremity, warm compresses, Nsaids, d/c bc pills. DVTs--sending them home now., BR, lovenox, coumadin, walking grad reintroduced
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what is PVD?
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arteriosclerotic disease! risk factors: same as major coronary disease. age 40-70, hyperlipidemia, smoker, diabetic and comes to office w/ complaint of claudication
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physical exam for PVD?
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shiny hairless skin, dependent rubor, elevational pallor; doppler, US, ABI. management: doppler study, arteriogram, endovascular or open surgical correction, ABI.
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mgmt for PVD?
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exercise, stop smoking.
give Trental wt mgmt bypass angio manage IDDM and lipids |
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CVI
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mostly in women, genetic.
aching of LE relieved by elevation, edema after prolonged standing, night cramps of LE on physical: trophic changes w/ brown discoloration, stasis ulcerations, dermatitis, edema. no labs or diagnostics, just r/o. use elastic stockings, wt reduction, and if dermatitis--wet compresses and hydrocortisone cream. |
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Pericarditis
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on the inside. viruses are the most common cause. classic pain--localized retrosternal pruritic in nature, hurts when they take a deep breath and relieved by sitting forward. may have a friction rub and fever may or may not be present. classicly: ST elevation in all leads! esp depression of PR segment. ESR elevated. get cultures. give NSAIDS and send home. steroids are NOT given except on absolute failure of NSAIDS. monitor for tamponade!
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endocarditis
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bacteria most common cause inside heart. have to consider and exclude in any pt with a heart murmur and FUO. fever, malaise, night sweats, weight loss. they have osslers nodes-hurt, janeway lesions-not painful-on palms and soles, spliter hemmorhages. and retinal hemmorhages. WBC normal or slightly elevted. echo and Blood cultures x 3. ESR elevated. Use peniciillin G with gent; nafcillin, unipin or a pcn derivitive; if worried about mrsa think vanc.
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when are AV valves open?
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they separate the atria from the ventricle--the tricuspid and mitral valves. the other 2 are semilunar valves--aortic and pulmonic. S1 AV closed and Semilunar (aortic and pulmonic) are open. S2 semilunar closed AV open
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S3--from what?
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assoc w/ increased fluid volume states--normal in pregnancy
kentucky kentucky kentucky |
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S4--from what?
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stiff ventricular wall from an MI or from HTN or LV hypertrophy from uncontrolled htn
tennessee tennessee |
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mitral and aortic stenosis and regurgitation
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will both be murmurring.
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murmur grading system
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1-6, i.e.6/6 can hear from doorway; 1/6 and 2/6 faint, 3/6 is audible and 4/6 has a thrill. 5/6 can hear with part of stethascope off.
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to diagnose valve problems:
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pay attn to where it is: 2nd intercostal space: aortic
5th intercostal space that is mid-chest is mitral. when do you hear it? a systolic or diastolic? MS. ARD and her buddy MR. ASS |
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what are the causes of dilated cardiomyopathies?
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The left ventricle becomes enlarged (dilated) and can't pump blood to your body with as much force as a healthy heart can.
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S/S dilated cardiomyopathy.
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Fatigue and weakness
Shortness of breath (dyspnea) when you're active or lying down Reduced ability to exercise Lightheadedness, dizziness or fainting Persistent cough or wheezing Swelling (edema) in your legs, ankles and feet Swelling of your abdomen (ascites) Sudden weight gain from fluid retention Lack of appetite and nausea Difficulty concentrating or decreased alertness Sensation of rapid, fluttering or pounding heartbeats (palpitations) |
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whats ischemic cardiomyopathy?
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reduced heart pumping (squeezing) due to coronary artery disease. These patients often have congestive heart failure.
"Ischemic" means that an organ (such as the heart) is not getting enough blood and oxygen. "Cardio" means heart and "myopathy" means muscle-related disease. Risks: •Diabetes •High blood pressure •High cholesterol •High-fat diet •Obesity •Personal or family history of heart attack, angina, unstable angina, atherosclerosis, or other coronary artery diseases •Sedentary lifestyle •Smoking |
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what is hypertrophic cardiomyopathy?
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is a disease in which the heart muscle (myocardium) becomes abnormally thick — or hypertrophied. This thickened heart muscle can make it harder for the heart to pump blood. Hypertrophic cardiomyopathy may also affect the heart's electrical system.
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what is restrictive cardiomyopathy?
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Restrictive cardiomyopathy is a serious problem that makes your heart muscle stiff. When your heart muscle is stiff, it can't stretch to allow enough blood to enter its lower chambers, the ventricles . So blood that would normally enter the heart backs up in your circulatory system.
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what would you do to treat all types of cardiomyopathy in terms of pre and after load?
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decrease them. consider transplantation.
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what are the S/S of aortic stenosis?
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Aortic valve stenosis ranges from mild to severe. Aortic valve stenosis symptoms typically develop when narrowing of the valve is severe and can include:
Chest pain (angina) or tightness Feeling faint or fainting with exertion Shortness of breath, especially with exertion Fatigue, especially during times of increased activity Heart palpitations — sensations of a rapid, fluttering heartbeat Heart murmur |
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what are the s/s aortic regurtitation?
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Fatigue and weakness, especially when you increase your activity level
Shortness of breath with exertion or when you lie flat Chest pain, discomfort or tightness, often increasing during exercise Fainting Rapid or irregular pulse Heart palpitations — sensations of a rapid, fluttering heartbeat Swollen ankles and feet |
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S/S of mitral stenosis
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Fatigue, especially during times of increased activity
Shortness of breath, especially with exertion or when you lie down Swollen feet or ankles Heart palpitations — sensations of a rapid, fluttering heartbeat Frequent respiratory infections, such as bronchitis Heavy coughing, sometimes with blood-tinged sputum Rarely, chest discomfort or chest pain |
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S/S mitral regurgitation
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Blood flowing turbulently through your heart (heart murmur)
Shortness of breath, especially with exertion or when you lie down Fatigue, especially during times of increased activity Lightheadedness Cough, especially at night or when lying down Heart palpitations — sensations of a rapid, fluttering heartbeat Swollen feet or ankles Excessive urination |
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causes of mitral regurgitation?
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MV prolapse
rheumatic fever endocarditis prior MI untreated HTN congenital heart failure |
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causes of mitral stenosis?
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rheumatic fever (most common cause--we dont see rheum fever much anymore and its decreased the mitral stenosis too), congenital heart defect, blood clots, tumors, calcium deposits
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how do you treat mitral stenosis? mitral regurgitation?
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mitral stenosis: Diuretics. These drugs can reduce fluid accumulation in your lungs or elsewhere.
Blood thinners (anticoagulants). These medications help to prevent blood clots from forming. Antibiotics. Your doctor may recommend antibiotics before certain dental or medical procedures to reduce the risk of bacteria entering your bloodstream and causing an infection in your heart (endocarditis). Mitral regurgitation: surgery. Medication can't correct a deformity of a mitral valve. But medications such as diuretics are available to relieve fluid accumulation in your lungs or legs, which can accompany mitral valve regurgitation. High blood pressure makes mitral valve regurgitation worse, so if you have high blood pressure, your doctor may prescribe medication to help lower it. Following a low-salt diet helps prevent fluid buildup and helps control blood pressure. |
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how do you treat aortic stenosis? aortic regurg?
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aortic stenosis: can have surgery. No medications can reverse aortic valve stenosis. However, your doctor may prescribe certain medications to help your heart, such as ones to control heart rhythm disturbances associated with aortic valve stenosis. Research suggests that lowering cholesterol, especially with statin medications, may prevent or slow the development of aortic stenosis
aortic regurg: Medication can't eliminate aortic valve regurgitation. However, your doctor may prescribe certain medications to reduce the severity of aortic valve regurgitation, control blood pressure and try to prevent fluid buildup. If you have aortic valve regurgitation, your doctor may recommend that you take antibiotics before certain dental or medical procedures to prevent the heart infection endocarditis. |
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what is aortic stenosis caused from?
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congenital heart defect, rheumatic fever, calcium build up on the valve.
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what is nipride and how do you titrate it?
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potent vasodilator--works directly on vessels without autonomic interference. Nitroprusside administered i.v. to hypertensive and normotensive patients produced a marked lowering of the arterial blood pressure, a slight increase in heart rate, a mild decrease in cardiac output, and a moderate diminution in calculated total peripheral vascular resistance. The usual dose rate is 0.5 to 8 µg/kg/min, but infusion at the upper dose rate should never last more than 10 minutes. If blood pressure has not been adequately controlled after 10 minutes of infusion at 8 µg/kg/min, administration of nitroprusside should be terminated immediately. Infusion rates greater than 8 µg/kg/min are virtually never required.
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after an MI, your patient is on what?
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an ace inhibitor and BB to prevent remodeling. may add spironolactone if there is an increase in aldosterone
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What would you expect to hear with rupture of the papillary muscle?
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mitral regurgitation. loud systolic crescendo-decresendo murmur heard at apex; shift in PMI, pulm. edema, hemoptysis, angina and syncope, CP. diagnose pap muscle dysfunc 1-7 days post MI, most common w/ inferior MI, dramatic onset of HF w/ pulm. edema. dx w/ sudden presence of murmur, increase in wedge pressures
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what kinds of EKG changes will occur after an MI?
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0-12H you'll see PVCs-disparity between healthy and ischemic cells and their rate of depolarizations
at 12-48H post, increase in automaticity, increase in catacholamines, increase in excitability. can have 2nd degree HB (wenckebach and mobitz II), complete heart block. In Mobitz II, you will see a constant PR interval you must have a wide QRS in V-1 to call it a BBB. If V1 is QRS wider, that normally is the beginning of a BBB. Do BP and get pacer. |
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how are compensatory mechanisms post MI not good for you?
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you retain fluid from renin/angiotensin/sympath NS and myocard stretched too far (Frank Starling) and
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