CardiologyI Flashcards
What are the 10 steps in the NCEP guidelines?
1: fasting lipid profile for all adults >20 q 5 yrs
2: rule out 5 causes of secondary dyslipidemia via other tests
3: Identify CHD risk equivalents
4: Determine the presence of major CHD risk factors
5: Estimate 10 yr risk with framingham pt scores
6: Determine tx goals and appropriate tx based on risk category
7: initiate TLC
8: consider drug therapy
9: identify metabolic syndrome and treat
what are the causes of secondary dyslipidemia and how do you test for them?
DM (fasting glucose), hypothyroidism (TSH), obstructive liver disease (LFT, UA), chronic renal failure (BUN, creatinine), drugs that increase LDL or decrease HDL (progestins, corticosteroids, alcohol, beta blockers, protease inhibitors, anabolic steroid, thiazide diuretics, isotretinoin)
what are the CHD risk equivalents?
DM, peripheral arterial disease, abdominal aortic aneurysm, symptomatic carotid artery disease, multiple risk factors conferring a 10 yr risk for CHD
what are the CHD major risk factors?
ADD 1 RF FOR: current smoking, HTN or on an anti-HTN med, low HDl (60 mg/dL
what is metabolic syndrome and how do you treat it?
includes 3+ of the following: abdominal obesity (waist >40 in men, >35 female), HDL150mg/dL, BP 130/85, glucose >110 mg/dL
tx: weight reduction, increase physical activity, increase unsaturated fats to lower TG and increase HDL, and add pharm measures to lower LDL like statins, niacin, or fibrate
What is the progression of TLC monitoring according to the NCEP guidelines?
1: Begin TLC (up exercise, down saturated fat and cholesterol, consider referral to dietician)
2: 6 wks evaluate LDL response, if not achieved, intensify TLC: reinforce decreasing cholesterol/saturated fats, consider adding plant stanols/sterols, increase fiber, consider referral
3: 6 wks evaluate LDL response, if not achieved consider drug therapy, instensify wt management and physical activity, initiate tx for metabolic syndrome, consider referral
4: 4-6 months monitor adherence to TLC
what is the progression of drug tx monitoring according to the NCEP guidelines?
1: initiate LDL lowering therapy: statin, nicotinic acid, bile acid resin
2: 6 wks check LDL, if not achieved up statin or add BAR or nicotinic acid
3: 6 wks check LDL, if not achieved intensify therapy or refer to lipid specialist, if achieved treat other lipid risk factors
4: 4-6 months monitor response and adherence
What are the “statin benefit groups” according to the ACC/AHA guide lines?
anyone with clinical ASCVD (atherosclerotic cardiovascular disease)
anyone with LDL >190 mg/dL
pts with LDL 70-189 at age 40-75 WITH DM (but WITHOUT ASCVD)
patients with LDL 70-189 WITHOUT DM or ASCVD but with 10 yr risk of >7.5%
If a pt doesn’t fit into one of the statin benefit groups but there is a clinical suspicious they may benefit from a statin, what are other factors that can be used to determine whether or not they should go on a statin?
LDL >160, genetic hyperlipidemia, CVD in a 1st degree male 2 mg/dL), ankle-brachial index
According to ACC/AHA when are high intensity statins used (reducing LDL by >50%)? what are 2 examples?
secondary prevention in adults 190, primary prevention in adults or adults (moderate an option for these, but not for this with DM) with DM ages 40-75 with LDL 70-189 and 10 yr risk of ASCVD 7.5%+
examples: atorvastatin 80mg daily, rosuvastatin 20-40 mg daily
According to ACC/AHA when are moderate intensity statins used (reducing LDL by 30-50%)? what are some examples?
for secondary prevention in adults
According to ACC/AHA when are low intensity statins used (reducing LDL by
for pts who cannot tolerate high or moderate dose statins. examples: fluvastatin 20-40 mg daily, lovastatin 20 mg daily
when are nonstatins recommended according to the ACC/AHA guidelines?
for those who cannot tolerate statin dose or have no response to statins and are at high risk i.e. LDL >190, DM, or clinical ASCVD, for those with high TGs, i.e. >500
Also think about if there is another reason they aren’t responding
don’t add statins to nonstatins, nonstatins may inhibit the effects of statins
what are the TLC recommended by NCEP and ACC/AHA/
heart healthy diet: Mediterranean diet
EAT: vegetables, fruits, whole grains, low fait dairy, poultry, fish, beans, non tropical vegetable oils, nuts,
LIMIT: red meat, sweets and sugary drinks, saturated and trans fats, sodium (
what are the guidelines on monitoring statins according to ACC/AHA?
lipids at baseline, 4-12 wks after, then q 3-12 months; ALT at baseline and again if sx of hepatotoxicity occur; pre existing muscle sx, baseline CRK if risk of myopathy, CRK prn if myopathy, check adherence, consider statin reduction if two LDL measurements
what are the known causes of HTN?
known causes: sleep apnea, drug induced causes, CKD, primary aldosteronism, renovascular disease, chronic steroid therapy and cushing’s syndrome, pheochromocytoma, coarctation of the aorta, thyroid or parathyroid disease; meds that may increase it: NSAIDS, cox2, cocaine/amphetamines, sympathomimetics (decongestants, anorexiants), oral contraceptives, certain dietary supplements (ma haung, bitter oragne, guarana), corticosteroids, cyclosporine (anti rejection), erythopoietin, licorice
what are the things that HTN can cause?
major cardiovascular events 12x higher in those with HTN, MI, stroke, PE, HF, PVD, aortic dissection, afib, end stage kidney disease; target organ damage: left ventricular hypertrophy, angina or prior MI, prior coronary revascularization, HF, stroke or TIA, nephropathy, peripheral arterial disease, retinopathy
what is the equation for BP?
BP=CO X PVR
what are the natural medicines for HTN treatment?
none are considered safe or effective
What kinds of drugs are recommended for the treatment of HTN in nonblacks, blacks, and those with CKD?
TX recommended for general, nonblack, including those with DM: thiazide diuretic, CCB, ACEI, ARB; general blak , including those with DM: thiazide diuretic or CCB; age >18 with CKD: ACEI or ARB (renoprotective)
what are the three strategies for dosing antihypertensive drugs?
1) start one drug, titrate to maximum dose then add a 2nd one 2) start one drug and then add a second drug before achieving maximum dose of the initial drug 3) begin with 2 drugs at the same time, either separate or in single pill
how should HTN be monitored?
4 wks: If goal BP not reached, increase dose or add second drug (thiazide, CCB, ACEI, or ARB), continue to assess and adjust tx until goal BP reached, if cannot be reached with 2 drugs add and titrate a 3rd drug (don’t use ACEI and ARB together though) If more than 3 needed, refer to a hypertension specialist
What percentage of pts stop their anti HTN meds within 6 months
25%
What are some interventions that can improve adherence in anti HTN meds?
identify problems with drug tolerance early and switch, address increased urination with diuretics: start with low doses and advise pts to limit salt to decrease urination and don’t take the med at hs, use generics to decrease cost, educate the pt on the importance of controlling BP, spread out meds: 1 in AM, 1 in PM
what are some causes of resistant HTN?
improper BP measurement, volume overload (excess sodium intake, kidney disease and volume retention, inadequate diuretic tx), medication (non adherence, inadequate doses, drug intx), assoc conditions (obesity, excess alcohol intake, secondary HTN)
at which point is HTN considered an urgency or emergency?
when DBP >130 +TOD=emergency; when DBP>130 but no TOD=urgency
how should a HTN emergency be managed? how to manage urgency?
emergency: IV drug therapy like nitroglycerin (vasodilators) to reduce DBP to 110 within 30 minutes (gradually) then to 100 within 12-24 hours ; urgency reduce DBP to 100 within 24 hours via oral agents
what are some of the comorbidities associate with HTN?
diabetes, CAD, left ventricular hypertrophy, ischemic stroke, chronic kidney disease, peripheral artery disease
what are some of the patient related barriers to effective anti HTN tx?
cost, limited access to health care: no one provider for them, non adherence, complicated treatments, no health insurance, knowledge deficits, lack of support, lack of provider to pt education
phases of the cardiac cycle
atrial contraction, isovolumetric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid ventricular filling, reduced ventricular filling
maximum arterial pressure experienced by aorta/aka when ventricles contract
systole
point of lowest arterial pressure aka pressure which ventricle must overcome to open aortic valve aka phase of the cardiac cycle in which the ventricles relax
diastole
when not an urgency/emergency, what is ideal to confirm that someone has HTN?
ambulatory BP monitoring (per the US Preventative Taskforce)
what are the risk factors for HTN?
poor: 56% more likely to have HTN, age: prevalence >60yrs is 65.4%, genetics: FM of premature CVD 1st degree male >55, female >65, african american ethnicity, smoking, excessive EtOH intake, inactivity, renal disease, microalbuminuria , GFR
normal sinus rhythm
60-100; must originate in SA node, activation of myocardium occurs in correct sequence with correct timing and delays
sinus arrythmia
change in sinus discharge rate, irregular. usually in children and young adults due to change in vagal tone, increases with inspiration and decreases with expiration, benign, asymptomatic
what rhythm is this: sinus rhythm >100; physiologic: infants/children, anxiety, exercise, pain; pharmacologic: epi caffeine, nicotine, cocaine, atropine; pathologic: fever, hypoxia, anemia, pulmonary embolus, hyperthyroidism
sinus tachycardia
sinus rhythm with HR
sinus bradycardia
causes of sinus bradycardia
phyiologic: athleete, sleep, vagal stimualtion; pharmacologic: beta blockers, CCBs, digoxin; pathologic: inferior MI, increased intracrnail pressure, hypothyroidism
SA node stops firing or impulse is blocked from exiting the node; latent/ectopic pacemaker can take over; often a junctional escape beat originating near AV node is seen, may have retrograde P wave, especially if PR interval is very short,this indicated that something else is firing
sinus arrest
sick sinus syndrome
abnormal sinus node functioning causing cardiac insufficiency
common in elderly, usually idiopathic, sx: dizziness, fatigue, palpitations, syncope, pre syncope, periods of atrial tachycardias alternating with sinus pauses and sinus brady cardia, tx reversible causes, pacemaker
tachy-brady syndrome
different morphology of P wave than from SA node (may be one different or many different), extra p waves may or may not produce QRS, can come at regular intervals (bigeminy, trigeminy) usually shorter PR because originating closer to AV node, interval between sinus and ectopic is shorter than between two ectopic beats
premature atrial contractions
what can cause premature atrial contractions and how do you treat them?
causes: stress, fatigue, alcohol, nicotine, caffeine, sympathomimetics, chronic lung disease, usually benign; treat underlyng cause
regular rhythm, rapid rate (140-250), p waves with uniform morphology and PR interval but different morphology than p wave from SA node, may be buried in QRS; narrow QRs (
supraventricular tachycardia
what causes supraventricular tachycardia
due to reentry of depolarization, not SA node, may originate in atria or near AV node
what causes reentrant rhythms?
problems with transmission on alternate pathway or one pathway going faster than another and the impulse from the faster returns through the slower, not initiation
narrow QRS +/- buried q waves, rate 140-200 bpm, usually 1:1, usually starts by a premature beat , due to dual pathways in AV node, often occurs in structurally normal hearts
AVNRT
AVRT
accessory pathway between atria and ventricles–usually via AV node and His-purkinje system for antegrade conduction to the ventricles and accessory pathway for retrograde conduction (orthodromic), narrow QRS, may see retrograde P wave, could also be the opposite where antegrade flow through accessory tract and retrograde through His and purkinje=wide QRS=difficult to distinguish from vtach, freq with pre-excitation syndromes (wpw)
ectopic rhythm with rate >100 bpm, can be paroxysmal from atrial circuit or increased automaticity of an ectopic atrial focus, >100 bpm, may be multifocal if3 or more p wave morphologies (wandering atrial pacemaker if
atrial tachycardia
can occur in normal hearts (alcohol, caffeine, excitement), pathologic: MI, rhematic heart disease, pericarditis, mitral valve prolapse, very common, sx of palpitations, lightheadedness, dizziness, SOB, elderly or pts with HD may have syncope, pulmonary edema, myocardial ischemia, vagal maneuvers (valsalva, squat, cough) to slow conduction and increase refractory period in AV node; carotid sinus massage (only on one side), adenosine (slows last 6 hours) beta-blockers, calcium channel blockers, electrical cardioversion, ablation (long term fix) avoid triggers
supraventricular tachycardia
wolff-parkinson white syndrome
d/t accessory pathway (kent bundle) that links atria to ventricles, bypassing AV node (slurring from dual activation) activates ventricles earlier than normal (preexcitation) creating the delta wave QRS gets activated by both his-purkinje systema and accessory pathway, may also have ST abnormalities from ventircular repolarization in opposite direction of QRS, can lead to vfib/cardiac arrest, AVRT, afib, aflutter, short PR interval (
wide, bizarre QRS that looks similar to PVC but the PAC with aberrancy should have a p wave beforehand, PAC comes while ventricles not fully depolarized, usually due to refractory RBB, so signal goes through LBB and depolarizes right side from there which takes longer
aberrancy
usually d/t reentrant circuit running in tricuspid annulus, can be transitional rhythm between NSR and afib, can also be caused by underlying heart disease (ischemic heart disease, acute MI, HTN), pulmonary embolism, digoxin toxicity, sx of palpitations, fatigue, SOB, dizziness, to dx can carotid sinus massage can slow down conduction rate through AV noe and make rhythm more apparent (2:1 becomes 4:1), can tx with synchronized electrical cardioversion (DCCV), rate control with BBs, CCBs, dig, chemical conversion with anti arrythmic, ablation
atrial flutter
atrial fibrillation
irregular rhythm, slow or fast (often 120-180 if fast), no organized p waves, undulating/shimmering baseline, narrow QRS, R-R have no repetitive pattern, causes loss of atrial contraction, leading to worsening HF, if rate is fast can cause myocardial ischemia, hypotension, shock, predisposes to thrombus formatino in atria (L atrial appendage mc), multiple reentrant ciruits are occuring at once causing bombardment of AV node with impulses (>400 /min) some of which pass through at variable intervals
what are the different kids of afib?
classifications: paroxysmal: self terminatnig or intermittent, terminates without interventino within 7 days, variable recurrence, aggravated by PAC; persistent no self term in 7 days, long standing lasting >12 months, permanent: decision made to no longer pursue rhythm control
how do you tx afib?
treat reversible causes first (hypoxia, hyperthyroid), cardioversion, long term anti arrythmic, rate control via BBs or CCBs, digoxin, ablation + pacemaker, stroke reduction via anticoagulation, LARIAT (takes off left atrial appendange), watchman
what score is used to determine stroke risk in pts with nonvalvular afib?
CHA2DS2-VASC
QRS wide, bizarre (usually >0.16 sec), not wide in every lead, no p waves but may find a retrograde P or sinus P if PVC is very late, usually followed by a long compensatory pause before next beat. Can occur in patterns: bigeminy (1 sinus beat to 1 PVC), trigeminy (two sinus beats to one PVC), ventricular beat occurs before next expected beat, benign if no HD, be concerned if frequent, 3 or more in a row, multiform, PVC falling on T wave of previous bet, could cause vtach/vfib, often occurs duing an MI, can be sx of palpitations, fatigue, SOB, especially if frequent, tx via avoid triggers, correct underlying disease, BBs, ablation, icd if underlying heart disease
premature ventricular contraction
run of 3+consecutive PVCs, due to ectopic focus or reentry in ventricles, occurs through ventricular activation (not thru normal pathway) so it doesn’t resemble bundle branch blocks, regular or slightly irregular QR,S wide, rate >100, usually 120-200, may have superimposed p waves at slower rate than QRS, monomorphic or polymorphic, (mono MC with healed infarcatinos) poly more assoc with acute MI, sustained(>30 s: medical emergency) or non sustained, can be stable initially but deteriore quickly, can be stable initially but deteriore quickly, may have sx of hypotension, shock, chest pain, sob, palpitations, dizziness, syncope, pulseless in cardiac arrest, tx if sustained: unstable/pulseless: begin cardiac arrest sequence( defib, CPR, epi, amiodarone), if stable: synchronized cardioversion, IV antiarrthmic, if no tx will go to vfib
ventricular tachycardia
causes: congenital, electrolyte imbalances, acute MI, drugs, high doses and multiple drugs that prolong QT interval (certain antiarrythmics, abx, antipsychoctics, antidepressants, antifungals, antihistamines) increase risk and also cyp450 inhibitors do too, twisting of the points/polymorphic VT, can go to vfib and sudden cardiac death, spirals around baseline, prolonged QT interval, PVC falling on lengthened t wave causes r on t and initiates tdp, tx: correct electrolyte imbalances, IV mag sulfate, overdrive pacing with IV isoproteerenol if can, temporary pacemaker placement, if unconscious: defib
torsade de pointes
ventricular fibrillation
causes: severe ischemia in hd, acute mI, hypothermia, blunt chest rrauma, severe electrolye imbalance, digitalis toxicity, irregular, undulating rhtythm, no p waves or QRS, coarse (early) fine (later), no meaningful contraction, not a vaiable rhuythm, pt is unconscious, no BP or pulse bc no cardiac output=cardiac arrest, tx: cardiac arrest sequence
what is in the ddx for narrow QRS, regular rhythm?
sinus tach, atrial flutter, supraventricular tach
what is in the ddx for narrow QRS, irregular rhythm?
afib, a flutter with variable block, multifocal atrial tach
ddx for wide QRS, regular rhythm
sinus tach with aberrancy, SVT with aberrancy, a flutter with aberrancy
ddx for wide complex, irregular
a fib with aberrancy, WPW, a flutter with variable block and aberrancy, MAT with aberrancy, polymorphic VT
conduction delay through AV node or his purkinje, or due to slowing in intra atrial conduction, causes: normal heart, structural, increased vagal tone, inferior MI, drugs that slow conduction (BB, non dihydropyridine CCBs, digoxin, usually benign as long as potential underlying causes r/o, prolonged PR interval (>0.2 s) that is fixed,each p wave has a qrs
first degree AV block
usually d/t a block in AV node, sometimes athletes (increased parasympathetic tone), acute inferior MI, myocarditis, cardiac surgery, rhematic heart disease, digitalis toxicity, generally doesn’t progress to complete heart block, pt feels a catch in their chest or a lost breath, not all p waves go through (not all have a qrs), gradual increase in PR interval until p wave fails to produce a qrs,, progressive slowing of ezch subsequent impulse in AV node until node finally fails to conduct an impulse, after dropped beat the sequence continues in any pattern (2:1, 3:2: 4:3), tx: none necessary if stable, if slow ventircular rate causes hypoperfusion may consider atropine or cardiac pacing to speed up
second degree av block type i
problem of his purkinje system, causes: acute anteroseptal MI, cardiomyopathy, higher risk of complete heart block than type I, indication for a pacemaker, some p waves not conducted to ventricules. No progressive lengthening or change of PR interval prior to or after non conducted p wave, constant PR interval, then nonconducted beat; ratio of conduced beats to nonconducted is rarely constant
second degree block type II
usually in elderly, no atrial impulses make it through, even though atria continue to depolarize, ventricles respond with escape rhythm: either junctional (40-60 bpm)below block in AV (wide QRS) or ventricular (30-45 bpm), p waves and q waves are dissociated=variable pr interval, causes: degenerative disease of conduction system, acute Mi, drugs, congenital, infectious heart disease (lyme), cardiac surgery, cardiomyopathy, rhematic haert disease, infiltrative diseases, muscular dystrophy, ventricles can’t supply enough blood! BAD, tx with atropine, pacing (transvenous or transcutaneous) permanent pacemaker
third degree av BLOCK
delay of right ventricular depol until L ventricle almost fully depolarized, causes: ischemic heart disease, rhematic heart disease, cor pulmondade, PE, myocarditis, trauma, cardiomyopathy, congenital, biventricular pacing, wide QRS >0.12 s; RSR’ in v1 and v2 due to unopposed late RV depolarization, reciprocal late broad S waves in leads I, avL, v5 and v6, ST depression and t wave inversion in v1 and v2
RBBB
blood supplied by LAD, causes: acuTE MI, ischemic heart disease, HTN, myocarditis, degernative disease of conduction system, valvular heart disease, cardiomyopathies, may have left deviation, ST-T depression and negative T wave in lateral leads, can do exercise perfusion study or echo, if new LBBB, be concerned for mI
LBBB
incomplete RBBB and ST elevation in anterior precordial leads (qrs 0.1-0.12), usually by gene mutation in young males, may have sx of syncope, cardiac arrest, tx with ICD
Brugada syndrome
what are some causes of physiologic? hypertrophy
athelete, pregnancy
what are some causes of pathologic hypertrophy?
HTN, valvular disease
right atrial enlargement signs and causes
amplitude of first p wave increases to >2.5 mm in inferior leads (II, III, avF) or >0.5 in v1, duration remains same, may have right devation, causes: severe lung disease, tricuspid stenosis, pulm HTN
left atrial enlargement causes: what it can lead to, and how to identify it
causes: mitral valve disease, HTN, aortic stenosis, hypertrophic cardiomyopahy
can lead to afib
2nd part of p wave increaes in amplitude and druation, may be m shaped; terminal portion drops 1 mm below isoelectric line in v1 (could be biphasic) and increase in terminal p wave duratoin (>0.04 sec) , usually no axis deviation seen
right ventricular hypertrophy causes, signs
causes: pulmonary HTN, pulmonic stenosis, mitral stenosis/insufficiency, severe lung disease, posterior MI
signs: right axis dev from increased muscle mass, R wave progression through precordial leads reverses due to increased anterior forces: v1: r wave>s; v6 s wave>r, ST depression and t wave inversion in r precordial leads, RAD, st depression and t wave inversion in precordials
left ventricular hypertrophy causes, signs
causes: HTN, acute MI, aortic stenosis, insufficiency, hypertrophic cardiomyopathy, R wave in v5 or v6+s wave in v1 or v2 >35 mm or R wave in v5>26 or R wave in V6>18 mm, R wave amplitude in v6 is greater than v5, precordia lleads more sensitive than the limb leads for LVH, ST depression and t wave inversion in v5-v6, I, avL, LAD
r axis deviation, voltage for LVH, prominent r wave in v1-v2, prominent s wave in v5-v6, tall biphasic RS complexes
biventricular hypertrophy
what are the indications for a pacemaker?
2nd degree type II or 3rd degree heart block, symptomatic bradycardia, uncontrolled atrial fibrillation
how do implantable cardioverter debrillators work?
first tries to take over fast paces and over drive it, if fails it will shock you
what are some different ways to test for arrhythmias?
holter monitor (24-48 hrs), event monitor (30 days), stress EKG, loop recorder (injected in chest, 3 YRS)
what is the #1 killer in women?
CHD
soft, waxy fat like substance found in the nervous system, skin, muscle, liver, intestines, and heart
cholesterol
what percentage of cholesterol is produced by the liver?
about 80%- for cell membranes, hormones, bile acid, vit D
a lipoprotein that carries cholesterol to different parts of the body but in excess can leave deposits on arterial walls
LDL
lipoprotein that removes excess cholesterol from tissues and carries it to liver for disposal
HDL
what is req’d for the absorption of dietary fat?
chylomicrons
how long does it take circulating chylomicrons to disappear as they circulate in the blood?
12 hours
____ eventually becomes LDL after depositing cholesterol in tissues (intermediate step)
VLDL
calories ingested in a meal but not initially used are covered to what for storage in fat cells?
triglycerides
what is the pathophysiology behind atherogenesis?
first elevated plasma LDL allows infiltration of native LDL particles through endothelium into intimal layer of arterial wall. They are then oxidized and macrophages ingest them=foam cells (but they can’t digest them). these foam cells eventually form a fatty streak lesion which can cause immunologic and inflammatory changes leading to progressive damage of vessel wall. collagen migrates to this streak which forms a fibrous plaque which can rupture. this causes platelet aggregation->thrombin->fibrin-> thrombus and occlusion
what are the RFs for atherosclerosis?
smoking, HTN, low HDL 45 women >55) obesity, inactivity, atherogenic diet, proinflammatory factors (CRP), impaired fasting glucose
what are some signs/sx of dyslipidemia?
many asymptomatic until severe. May have chest pain, palipitations, sweating, anxiety, SOB, LO, abdominal pain, sudden death; signs: pancreatitis, HTN, abomdinal pain, BMI >30, eruptive xanthomas (deposits of lipids in skin); xanthelasma (cholesterol deposits on eyelids); arcus senilis (choles deposit or white ring around iris), peripheral polyneuropathy, waist >40 in men or >35 in women
what is the calculation for LDL?
TC- (TG/5 +HDL); (tg/5 +hdl is VLDL) may get erroneous values if TG >400
what are some risk factors of dyslipidemia?
CVD: angina, mI; cerebrovascular disease: TIA, stroke, PVD: claudication, mesenteric ischemia, renal artery stenosis
what protein when elevated indicates risk for rupture of plaques?
CRP
what are some disorders that predispose people to elevated lipids?
PREDISPOSING DISORDERS: ELEVATEd LDL: familial hypercholesterolemia (heterozygote :xanthomas in adulthood and vasclar disease 30-50 yr, homozygote: xanthomas in adulthood and vascular disease in childhood) familial defective apo b-100, polygenic hypercholesterolemia, ELEVATED VLDL AND CHYLOMICRONS: familial hypertriglyceridemia, familial LPL deficiency, familial Apo C-II deficiency; ELEVATED LDL AND VLDL: combined hyperlipidemia, dysbetalipoproteinemia
list fats in order of how much you should have them in your diet from highest to lowest
monounsatured fats>polyunsaturated fats>saturated fats
how much fiber should you get per day?
20-30 g
what % of calories should be protein, carbs, and fats?
protein 15%, fats 25-35%, carbs 50-60%
how much fluid should be between the pericardial sac/
50 mL of ultra filtrate of plasma
what’s the mc cause of pericarditis? what are some other causes?
85% idiopathic (assumed viral or autoimmune); infectious (prodrome of flu like ilness, viral>bacterial>mycoplasma>fungal>parasitic) radiation, neoplasm, trauma, metabolic (hypothyroidism, uremia–worsening kidney disease can’t clear BUN), cardiac: dressler’s syndrome (post cardiac injury syndrome), myocarditis, dissecting aortic aneurysm; autoimmune: rhematic disease, SLE, RA, MCTD, scleroderma, wegener’s, srcoid, IBD, GCA, rhematic fever, drugs–procainamide, INH, hydralazine (BP pill), doxorubicin (chemo)
what are some of the sx experienced by someone with pericarditis?
sudden, sharp, stabbing, pleuritic, chest pain (>95%)from contact of chest wall with inflamed pericardium, improved by sittng up and leaning forward. Pericardial friction rub: scratchy/squeaking sound heard with diaphragm over LSB when pt holding breath and leaning forward. EKG changes–widespread STE or PR depression; pericardial effusion: inflammatory cells and serum accumulate in pericardial space
what are some of the EKG findings you would find on someone with a pericarditis?
if cause of pericarditis doesn’t cause inflammation of epicardium, you won’t see EKG changes. EKG changes: stage 1: (within hours to days) PR deviation upward in aVR and downward in most other leads, stage 2: normalization of ST and PR segments (within first week), stage 3: diffuse TWI, not seen in some pts (after 2 weeks), stage 4: (after 2 weeks) normalization of EKG or indefinite persistence of TWI; diffuse EKG findins (not localized) unlikely to see reciprocal changes, likely PR segment changes, may see alternating q wave height because heart is wobbling in sac
what labs would you run for pericarditis?
CBC, inflammtory markers (CRP, sedimentation rate), troponin (takes about 3 hrs for them to show from onset of pain, if elevated they are usually minimally indicated myopericarditis and indicate myocardial inflammation) (these may change over time, need repeats, CXR, (cardiomegaly doesn’t develop until >200 mL of fluid in space) echocardiography (often normal but evaluates for effusion and tamponade), IF INDICATED: tuberculin skin test, ANA (rheumat.), HIV serology, CT (ex. TB, lung cancer), DO NOT ROUTINELY OBTAIN VIRAL STUDIES (yield is low and management doesn’t change)
what are the 3 D’s of cardiac tamponade?
3 Ds” decreased BP, distended neck veins, distant or muffled heart sounds
what is the normal sequence of events during inspiration and what happens in cardiac tamponade?
usually normal inspiration leads to negative intrathoracic pressure, bringing venous blood back to R side of heart, which causes small bulge in L heart and a slight decrease in systolic BP by no more than 10 mmHg; if tamponade: septal bulge is too much for L heart and it will cause a severe drop in SV and greater than 10 mmHg drop in sbp
what usually causes myocarditis? what are som other causes?
usually viral, esp in developed countries: parvo B19; HHV 6, cocksackie, adeno, CMV, EBV, HCV (same as URI stuff) bacterial: staph, strep if undeveloped countries: usually rhematic fever chagas disease, HIV; non infectious: cardiotoxins like ETOH, CO, cocaine, heavy metals, hypersensitivity rxns like to abx, diuetics, lithium, systemic disorders like celiac, CVD, wegener’s SLE, HE, kawasaki, radiation
what is the gold standard for evaluating myocarditis? what are some other good tests?
endomyocardial bx is gold std, but this is invasive,most can be dx’d based on clinical presentation; do EMB if results will change how managed, esp in pts with HF for
how do you treat myocarditis?
underlyng causes first like CMV, lyme, etc. NO NSAIDS. Restrict activity, treat for HF if cardiomyopathy developed. Complete recovery of LV in 6 months
what are some of the sx experienced by someone with myocarditis?
may have viral prodrome or rash, inflammation may be focal or diffuse, can involve any or all of heart chambers, can result in dilated cardiomyopathy (10%), chest pain, HF, cardiogenic shock, arrythmias, new onset heart blocks, sudden death
what can this cause?: vegetation: mass of platelets, fibrin, microorganisms, inflammatory cells, BACTERIAL: strep viridans(65%), staph aureus (20%) enterococus (10%) other gram negative bacteria 5% (HACEK) (gram neg less likely to adhere to valves), can also be from >60 yo: more likely to have degenerated valves and undergo valve replacement; male, IV drug use, poor dentition, structural heart disease: valvular disease, RHD, MVP, AV, congential hear disease: AV,bicuspid, AV, pulm stenosis , VSD, PDS, coard and TOF, prosthetic heart valve up to 4% of pts within first year after valve, hx of endocarditis (recur 9%), intravascular device: picc, central line, shunts, hospital stays (inserting things a lot), chronic demodialysis, HIV infection
endocarditis
what EKG findings and other findings would you expect in someone with endocarditis?
fever/ SIRS (systemic inflammatory response syndrome), new murmur, new HF, less specific skin findings: petechiae on extremities, palate, conjuctive, splinter hemorrhages: non blanching, linear reddish brown under nail bed; more specific skin findings: janeway lesions: macular non tender lesions on palmsand soles, osler’s nodes: painful pads of fingers and toes; roth spots: exudative, hemorrhageic lesions of retina, all these from septic microemboli
all pts with staph aureus need to be evaluated for what?
infective endocarditis
What test should you perform right away for anyone with suspicious of endocarditis?
Echo because it can allow detection and characterization of vegetation, evaluate valve fcn, hemodynamics, and detect abscesses
when is it reasonable to go straight to TEE instead of TTE first?
prosthetic valve, prior valvular abnormality, limited TTE windows, poor view
