Cardiology Flashcards
Dilated Cardiomyopathy
Systolic dysfunction leading to dilated, weak heart.
ET: idiopathic, infections (viral, enteroviruses; coxsackievirus B), toxic (alcohol, cocaine, doxorubicin, radiation), pregnancy, autoimmune, metabolic (thyroid, vit B1 def)
SXS: systolic heart failure; left-sided - L for lung symptoms dyspnea, fatigue; right-sided - peripheral edema, JVD, hepatomegaly, GI sxs; embolic events arrythmias
PE: S3 gallop hallmark (d/t filling of dilated ventricle), mitral or tricuspid regurg
DDx: echo* (dec EF, left ventricular dilation, thin ventricular walls, ventricular hypokinesis); CXR (cardiomegaly, pulm edema, effusion); ECG (sinus tach, arrythmias)
TX: standard systolic heart failure tx; ACE-i (reduce mortality), BB (meto, carve), spironolactone, sxs control w diuretics, digoxin; AICD if EF < 35-30%
Stress (takotsubo) cardiomyopathy
Transient regional systolic dysfunction of L ventricle. No significant obstructive CAD or plaque rupture.
RFX: postmenopausal women exposed to physical/emotional stress
P: catecholamine surge, microvascular dysfunction, coronary artery spasm
SXS: substernal chest pain, dyspnea, syncope (similar to ACS)
DDX: ST elevations +/- depressions, +cardiac enzymes, coronary angio; no acute plaque rupture or obstruction, echo; apical left ventricular ballooning.
initial TX: d/t ACS mimicking; aspirin, nitroglycerin, BB, heparin, coronary angio
short-term tX: conservative/supportive care (BBs, Ace for 3-6 mos w serial imaging), anticoagulation w severe LV dysfunction o thrombus
Restrictive Cardiomyopathy
Diastolic dysfunction in non-dilated ventricle, impedes ventricular filling (dec compliance), stiff
ET: infiltrative dz (amyloidosis*, sarcoidosis, hemochromatosis, scleroderma, fibrosis, met dz), chemo, radiation
SXS: RHF; peri edema, JVD, hepatomegaly, ascites, GI sxs, LHF; lungs, dyspnea, fatigue, kussmaul’s sign (inc JVD w inspiration), +/- S3
DDX: echo* (non-dilated, normal thick ventricles, diastolic dysfxn, dilated atria) amyloidosis - bright speckled myocardium, CXR; enlarged atria, pulm congestion, ECF: low voltage QRS, arrhythmias, inc BNP, endomyocardial biopsy def dx
TX: treat underlying disorder (hemochromatosis > chelation, sarcoidosis > glucocorticoids), gentle diuresis for sxs relief, vasodilators.
Hypertrophic Cardiomyopathy
ET: Autosomal dominant genetic disorder, LV +/- RV hypertrophy with diastolic dysfunction, subaortic outflow obstruction d/t asymmetrical septal hypertrophy, worsens w increased contractility (exercise, beta agonists, digoxin) +/- dec LV volume.
SXS: dyspnea mc, angina, arrhythmias, fatigue, syncope, dizziness, sudden cardiac death (v-fib), harsh systolic crescendo-decrescendo murmur LLSB louder w dec venous return (valsalva, standing), lower w inc venous return (squatting), loud S4
DDX: echo - wall thickness, ecg - LV hypertrophy
TX: early detection –> medical mgmt –> surgical –> ICD
med; BB first line, CCB alt, for refractory surgical; myomectomy, alcohol septal ablation alt, avoid dehydration, extreme exertion, exercise, cautious use of digoxin, nitrates, diuretics
Myocarditis
ET: inflammation of heart muscle, myocellular damage leads to myocardial necrosis + dysfunction, leading to HF, mc young adults, infectious viral mc (enteroviruses, coxsackievirus B, parovirus B19, human herpes virus-6) bacterial (group A strep in rheumatic fever, lyme disease, mycoplasma), autoimmune SLE, rheumatoid arthritis, uremia, meds (clozapine, abx, methyldopa, isoniazid, indomethacin, phenytoin, sulfonamides)
SXS: asx, viral prodrome; fever, myalgias, malaise, chest pain, arrhythmia then systolic dysfuction sxs, HF; dyspnea, fatigue, s3, megacolon, pericarditis
DDX: gold; endomyocardial biopsy (severe/refractory), elevations in cardiac enzyme levels, ESR, cxr; cardiomegaly, ecg; pericarditis, echo; vent systolic dysfxn
TX: supportive, treat underlying cause and complications i.e. standard systolic HF tx (ABD)
Sinus Arrhythmia
ET: irregular rhythm starting at sinus node, beat to beat variations w breathing, inc w inspiration, dec w exp.
SXS: normal variation of NSR
DDX: ecg - normal p waves, p-p interval variation, shorter w inspiration, longer w expiration
TX: none needed usually, if symptomatic bradycardia then atropine (pacing, epinephrine, dopamine 2nd line)
Sinus Tachycardia
ET: increased HR > 100 bpm from sinus node; physiologic - exercise, emotional stress, nl in children; pathologic - fever, hypovolemia, hypoxia, pain, infx, hemorrhage, hypoglycemia, anxiety, thyrotoxicosis, shock, sympathomimetics.
DDX: ecg - regular, rapid, normal p waves w qrs complex
TX: treat underlying cause; BB w persistent + ACS
Sinus Bradycardia
ET: decreased HR < 60 bpm from sinus node; physiologic - young athletes, vasovagal reaction, ICP, n/v; pathologic - BB, CCB, digoxin, carotid massage, gram neg sepsis, hypothyroidism, SA node ischemia.
DDX: ecg - regular, slow, normal p waves w qrs complex
TX: symptomatic/unstable - atropine, refractory - epinephrine or pacing; asymp - no tx needed if physiologic, patho - observe or cardiac consult
Cardiomyopathy
dz of heart muscle with cardiac dysfunction NOT due to other heart dz
Sick Sinus Syndrome
ET: sinus node dysfxn leading to sinus arrest w alt atrial tachyarrhythmias & bradyarrhythmias, d/t sinus node fibrosis mc, older age, corrective cardiac surgery, meds, systemic dz
SXS: intermittent sxs of bradycardia +/- tachycardia; palpitations, dizziness, lightheadedness, angina, DOE, syncope
DDX: ecg - alt brady/tachycardia
TX: hemodynamically unstable - atropine (epi, dopamine, pacing 2nd line)
long term - pacemaker, +/- AICD
First Degree AV Block
ET: AV node dysfxn leading to delayed but conducted impulses; normal variant mc; AV node dz, AMI, electrolyte disturbances, AV nodal blocking agents (BB, digoxin, CCB), myocarditis, cardiac surgery
SXS: asymp mc, sxs d/t bradycardia; fatigue, dizziness, dyspnea, CP, syncope, ams, hypotension
DDX: ecg - prolonged PR interval, all p waves w qrs complexes
TX: asymp - no tx; symp - atropine 1st, epi, pacemaker definitive if refractory
Second Degree AV Block - mobitz I (wenckebach)
ET: not all atrial impulses are conducted to ventricles (dropped QRS), commonly above bundle of HIS, normal variant, inferior wall MI, AV nodal blocking agents
DDX: ecg- progressive PRI lengthening > dropped qrs
SXS: bradycardia sxs
TX: symp - atropine 1st, epi +/- pacemaker; asymp - observe +/- cardiac consult
Second Degree AV Block - mobitz II
ET: not all atrial impulses are conducted to ventricles (dropped QRS), block commonly at bundle of HIS, rarely seen in pts w/o structural heart dz (MI, myocardial fibrosis, myocarditis, endocarditis, iatrogenic
SXS: bradycardia sxs
DDX: constant/prolonged PRI > dropped qrs
TX: atropine or temp pacing, progression to 3rd deg common so permanent pacemaker definitive
Third Degree AV Block
ET: AV dissociation = no atrial impulses reach ventricles, atria independent of ventricles; d/t MI, AV nodal blocking agents, endocarditis, myocarditis, cardiac surgery, inc vagal tone, hypothyroidism, hyperkalemia
SXS: bradycardia sxs
DDX: regular p-p intervals + regular r-r intervals but unrelated to each other
TX: acute/symp - transQ pacing, pacemaker definitive
Atrial Fibrillation
ET: multiple irritable atrial foci fire at fast rates, inc risk of atrial thrombus forming leading to cerebral or systemic embolization, most asymtomatic; d/t cardiac dz, ischemia, pulm dz, infection, cardiomyopathies, electrolyte imbalances, idiopathic, endocrine/neurologic disorder, aging, genetics, hemodynamic stress, drugs, etoh
SXS: palpitations, dizziness, fatigue, dyspnea; unstable - d/t hypoperfusion can include hypotension, ams, refractory chest pain
DDX: ecg - irregularly irregular rhythm, no p waves, atrial rate often > 250, +/- ashmans phenomenon
holter monitor or telemetry can be used if a-fib not seen on ecg but suspected
TX: stable - rate control w BBs or non dihydropyridine CCBs; digoxin last resort
unstable - sync cardioversion
long term - rate control over rhythm contrpl, sync cardio or pharm cardioversion, catheter ablation or surgical MAZE procedure, anticoagulation use chad criteria
Atrial Flutter
ET: 1 irritable atrial focus firing at a fast rate, atrial rate usually ~300, inc risk of thrombosis
SXS: palpitations, dizziness, fatigue, dyspnea, CP; unstable - refractory CP, hypotension, ams
DDX: ecg - identical flutter sawtooth atrial waves, no p waves
TX: stable - vagal maneuvers, rate control w BBs or CCBs, unstable - sync cardioversion, anticoag use chad criteria, reversion to normal sinus - catheter ablation definitive, cardioversion, class IA, IC, or III antiarrhythmics
Anticoagulation candidates
Cha2ds2 - vasc score
chronic oral anticoag rec for mod - high risk (score > 2)
CHF HTN age2 > 75 7 DM S2 Stroke, TIA, thrombus Vascular dz age 65-74y Sex Female Max score: 9
anticoagulant agents
Non-vitamin K antagonist oral anticoags (NOAC) - usually preferred over warfarin d/t similar or lower rates of major bleeding, no need for INR checks, less drug interactions; dabigatran - direct thrombin inhibitor; rivaroxaban, apixaban, edoxaban - factor Xa inhibitors
warfarin - preferred for some pts - severe CKD, cost issues, bridged w heparin first, INR goal 2-3
dual antiplatelet therapy (ie aspirin + clopidogrel) - monotherapy preferred, only reserved for patient who can’t do monotherapy for w/e reason.
Paroxysmal SVT
ET: tachyarrhythmia above ventricles, umbrella term, patho - reentry circuits, AV node re-entrant tachycardia MC type (1 nl, 1 accessory pathway within AV node)
SXS: palpitations, dizziness, fatigue, dyspnea, CP; unstable - refractory CP, hypotension, ams
DDX: ecg - HR> 100, orthodromic mc; regular narrow complex tachycardia, no p waves; antidromic - regular, wide complex tachycardia mimics v tach
TX: stable (reg, narrow) - vagal maneuvers, adenosine 1st, 2nd CCBs, BBs, digoxin
stable (wide) - antiarrhythmics (amiodarone), procainamide for WPW
unstable - sync cardio
definitive- catheter ablation
Wandering Atrial Pacemaker (WAP)
ECG: HR < 100 bpm and => 3 p wave morphologies
multiple ectopic atrial foci generate impulses
multifocal atrial tachycardia
same as WAP but HR > 100 bpm, classically a/w severe COPD
Wolf Parkinson White (WPW)
ET: type of AV reciprocating tachycardia (AVRT), patho - accessory pathyway (bundle of kent) outside of AV node “preexcites” ventricles bypassing AV node, leads to delta wave (slurred upstroke, wide QRS)
SXS: palpitations, dizziness, fatigue, dyspnea, CP; unstable - refractory CP, hypotension, ams
DDX: ecg - 3 components “WPW”
Wave - delta wave
PR interval that is short
Wide qrs
TX: stable - procainamide preferred, other antiarrhyth
avoid av nodal blocking agents ABCD if wide QRS complex (exacerbates use of bundle of kent accessory pathway, worsens tachycardia)
unstable - sync cardioversion
definitive- catheter ablation
AV junctional dysrhythmias
ET: AV node/junction become dominant pacemaker, d/t sinus dz, cad, digitalis toxicity, myocarditis
DDX: ecg - regular rhythm, p waves inverted if present or not seen, narrow qrs, HR ~40-60
PVC
ET: premature beat from ventricle - wide bizzare QRS occuring earlier than expected, t-wave opposite direction of qrs, a/w compensatory pause - overall rhythm unchanged unifocal- one morphology multifocal - > 1 morph bigeminy - every other beat is PVC couplet - two PVCs in row
TX: none usually, common
Ventricular Tachycardia
ET: 3 or more consecutive PVCs, rate > 100
sustained - >30 secs, monomorphic or polymorphic, torsades is a variant polymorphic
d/t ischemic heart dz mc, other heart stuff, prolonged QT interval, electrolyte abnl, digoxin toxicity
SXS: palpitations, dizziness, fatigue, dyspnea, CP; unstable - refractory CP, hypotension, ams
DDX: ecg- regular, wide complex tachy, no p waves
TX: stable sustained - antiarrhythmics (amiodarone, lido, procain)
unstable w pulse - sync cardiovert
VT no pulse - defibrillation + cpr
Torsades de pointes
ET: prolonged QT interval, electrolyte abnl, meds
SXS: palpitations, dizziness, fatigue, dyspnea, CP
DDX: ecg- polymorphic v tach spinning around isoelectric line
TX: IV magnesium 1st, d/c all QT prolonging drugs
V-fib
ET: type of cardiac death a/w ineffective ventricular contraction; d/t ischemic heart dz mc, other heart stuff
SXS: unresponsive, pulseless patient, syncope
DDX: erratic pattern, no p waves, coarse vs fine
TX: defib + cpr, acls
PEA
organized rhythm on monitor w/o palpable pulse
TX: cpr + epi + check for shockable rhythm every 2 min
Class 1 NA channel blockers
rhythm control
decreases Na conduction, affect phase 4 of depolarization, by blocking Na channel opening reduce SA node automaticity and cause membrane stabilization.
class IA, IB, IC; procainamide, quinidine lidocaine, flecainide
Nets play in BK for Championship
Class 2 BBs
Rate control
antagonizes beta adrenergic receptors to different degrees by decreasing slope of phase 4 (dec calcium currents - dec SA/AV node conduction).
Cardio selective B1- atenolol, metoprolol, esmolol
Nonselective B1B2 - propranolol, sotalol
Nonselective a + b1,2 - labetalol, carvedilol
Ind: rate control a-fib, a-flutter
S/E: bradycardia, AV blocks, may mask hypoglycemia sxs
CI: sinus bradycardia, 2/3rd heart blocks, CHF, shock
Caution: bronchospasm w nonselectives in asthma/copd
glucagon is antidote for BB toxicity
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Class 3 K channel blockers
rhythm control
blocks K+ efflux during phase 3 - AP prolongation/refractory period, QT interval prolongation
Ind for atrial and ventricular arrhythmias
Amiodarone (posses characteristics of other classes); sotalol
Nets play in BK for Championship
Class 4 Ca channel blockers
Rate control
Slows SA node and AV conduction (dec Ca channels - dec conduction speed, inc PR interval, prolonged refractory pd)
ind: atrial arrhythmias
SE: peripheral edema, bradycardia, Av blocks
verapamil, diltiazem
Nets play in BK for Championship
class V
Digoxin
ind: a fib, HF
inhibit ATP-ase - positive inotrope, negative chronotrope
Adenosine
I: PSVT - slows AV node conduction time and blocks Av nodal reentry pathways; pharm cardiac stress testing
AE: chest discomfort, dyspnea, flushing, bronchospasm
CI: 2/3rd heart block, WPW, wide complex tachycardias, acute MI, asthma, cOPD
Peds functional murmurs: innocent
non pathologic, caused by blood moving thru chambers, tend to be soft, position dependent, no sxs, occurs often during systole, diastolic almost always pathologic.
Still murmurs
mc innocent murmur, d/t valve leaflet vibration
2 mos - adolescence
PE: musical, vibratory, noisy, twanging, LLSB + apex
Cervical venous hum
mc continuous benign murmur, d/t turbulent blood flow from blood retuning to hear at junction btw jugular vein and SVC
2-8 yrs
PE: soft, whirling, low-pitched, RSB
dec murmur intensity: supine, jugular compression of head, rotation or flexion of head
Pulmonary ejection murmur
d/t blood flowing across pulm valve into pulm artery
older children and adolescents
mid systole in Left 2nd intercostal space, harsh
Patent foramen ovale
covered but not sealed opening btw right and left atria; not considered ASD bc it’s a fusion failure, no septal tissue missing.
SXS: most asymp, strokes from paradoxical embolism, decompression sickness, migraine, acute limb ischemia
DDX: echo
TX: percutaneous device closure, surgical PFO closure
(stroke - antiplatelet or anticoag)
ASD
Abnl opening in atrial septum btw right and left atrium
P: allows for left to right shunt (noncyanotic); ostium secundum mc type
SXS: most asymp in childhood, often start in 3rd decade or later
children; recurrent resp infection, failure to thrive, exertional dyspnea
adolescents/adults; exertional dyspnea, easy fatigability, palpitations, atrial arrhythmias, syncope, HF, paradoxical emboli
PE: systolic ejection cres-dec flow murmur at pulmonic area (LUSB), wide fixed split s2 doesn’t vary w respirations
DDX: echo best
TX: small asd < 5mm may be observed (most close spontaneously in 1st yr of life); surgical correction if > 1 cm or symptomatic, percutaneous transcatheter closure vs surgical.
PDA
persistent communication btw descending thoracic aorta and main pulmonary artery after birth, noncyanotic, rfx - prematurity, female, fetal hypoxia
patho: continued prostaglandin E1 production & low arterial oxygen content
SXS: most asymp, poor feeding, wt loss, frequent lower rest tract infxns, pulm congestion, infective endocarditis; eisenmenger syndrome
PE: continuous machine like murmur loudest at pulmonic area/LUSB, wide pulse pressure
DDX: echo
TX: nsaids 1st line (IV indomethacin) bc inhibit prostaglandin synthesis, surgical correction (best done before 1-3 yrs)
Coarctation of Aorta
ET: congenital narrowing of aortic lumen often a/w bicuspid aortic valve, results in HTN in UE & hypotension in LE often, types; post ductal - narrowing distal to ductus arteriosum, pre-ductal narrowing proximal to DA
SXS: range from asymp to HF, shock; bilat claudication, DOE, syncope, babies; failure to thrive, poor feeding; diminished or delayed LE pulses, systolic murmur radiating to back, scapula or chest
DDX: echo best, cxr - posterior rib notching, 3 sign, angio gold standard
TX: corrective surgery or transcatheter based intervention, prostanglandin E1 preoperatively to stabilize, maintains PDA
Cardioversion
direct current or pharm
most successful when done within 7 days after onset
echo needed prior to procedure (ensure no atrial clots)
AF > 48 hrs - anticoag for at least 3 weeks prior
AF < 48 hrs - anticoag recommended
anticoag MUST be continued for 4 wks after procedure
HFrEF aka systolic heart failure
definition
classified by NYHA or AHA staging
Results in decreased heart pump function
LV EF < 40% –> insufficient amounts of oxygenated blood being delivered to meet demands of tissues/organs.
may develop asymptomatic structural and/or functional left ventricular changes, a precursor stage important to identify since prompt initiation of management may lower heart failure-related mortality
Common causes of HFrEF
DDX
Etiology: CAD, dilated cardiomyopathy (genetics, viral infxn, alcohol, chemotherapy), valvular heart dz (related to both pressure and volume overload), systemic hypertension, infiltrative disorders, infectious (IE, HIV), myocarditis, arrhythmias, high output cardiac failure (severe anemia, hyperthyroidism, sepsis, paget dz), metabolic, hormonal, or nutritional abnormalities,
DDX: other causes of dyspnea; asthma, COPD, sleep apnea, PE, non cardiogenic pulmonary edema, arrhythmia, infection, ILD, anemia
peripheral edema; renal dz, hepatic dz, hypoproteinemia, venous insufficiency, drugs
HFrEF clinical presentation
DOE or at rest, fatigue, abdominal distention, LE swelling, orthopnea, PND, evidence of vol overload; elevated JVP, peripheral edema, rales, or diminished perfusion (cold extremities)
HFrEF diagnostics
12 lead EKG, CXR, labs; CBC, CMP, UA, fasting lipid profile, TSH, BNP, TTE
HFrEF management
ACE/ARB, BBs, symptomatic/vol overload add loop diuretics, consider SGLT2 inhibitor, black patients with sx add hydralazine + isosorbide dinitrate, refractory sx HF + EF < 35% + serum cr < 2.5 in men or < 2.0 in women + K < 5 add aldosterone antagonist, digoxin for persistent or severe sx
do not use nondihydropyridine CCB with neg inotropy
ICD for patients in stage C
HFrEF patho
something causes myocardial injury –> maladaptive changes in surviving myocytes aka pathologic “remodelling” of ventricle leading to dilation and impaired contractility. Untreated this systolic dysfunction progresses to continued myocyte death + systemic responses aka neurohumoral activation of SNS + RAAS due decr systolic fxn. Upregulation of factors to counterbalance this activation; NPs, bradykinin, prostaglandins, cytokines, endothelin. Incr end diastolic vol and pressure result in dyspnea/congestion
a-fib definition
multiple foci fire continuously in the atria causing it to quiver and a chaotic pattern with totally irregular, rapid ventricular rate. Atrial rate > 400 bmp (most impulses blocked so ventricular rate btw 75-175. Increases risk of thromboembolism and hemodynamic compromise
a-fib causes
heart disease; CAD, MI, HTN, MV disease pericarditis and pericardial trauma (surgery) pulmonary disease; PE thyroid disease systemic illness; sepsis, malignancy, DM stress excessive alcohol intake sick sinus syndrome pheochromocytoma
a-fib clinical features
fatigue, exertional dyspnea
palpitations, dizziness, angina, syncope
irregularly irregular pulse
blood stasis, intramural thrombi
a-fib diagnostics
ecg - irregularly irregular rhythm
a-fib treatment
A) HDUnstable; immediate electrical cardioversion to sinus rhythm
HDS; rate control, determine pulse if too rapid just treat. Target rate = 60-100 bpm
BETA BLOCKERS, CCBs alternative.
digoxin or amiodarone for ventricular systolic dysfunction
B) cardioversion after rate control for: HDU, worsening sxs, first a-fib ever. Pharm cardioversion if electrical fails (ibutilide, procainamide, flecainide, sotalol, amiodarone)
C) anticoagulation for CVA prevention; if afib onset > 48 hrs or unknown anticoag for 3 weeks before and 4 weeks after OR TEE before cardioversion
D) chronic afib- rate control with BB or CCB, chronic anticoagulation
Hypertensive Emergency Gen info
> 220/120 + end organ damage
immediate tx indicated
severe elevated BP + no end organ damage = hypertensive urgency; rarely require emergency therapy, can be lowered over 24 hrs
Assess systems; eyes (papilledema), CNS (ams, intracranial hemorrhage, hypertensive encephalopathy; when BP is markedly elevated + neuro findings like confusion), kidneys (renal failure, hematuria) heart (USA< MI, CHF + pulmonary edema, aortic dissection), lungs (pulmonary edema)
May lead to posterior reversible encephalopathy syndrome (PRES)
Hypertensive Emergency causes
aldosterone associated - hyperaldosternism
renin associated - renal artery stenosis, cirrhosis, polycystic kidney disease, CHF,
non-renin, non-aldo associated - cushings, stimulants, pheochromocytoma
Hypertensive Emergency clinical features
severe HA, visual disturbances, AMS
Hypertensive Emergency treatment
reduce MAP < 25% in 1-2 hours aka get patient out of danger zone, then reduce gradually
if severe (dia > 130) or hypertensive encephalopathy IV agents, nitroglycerin, nitroprusside, nicardipine, hydralazine, esmolol, labetalol
Oral agents for urgency; captopril, clonidine, labetalol, nifedipine, diazoxide lowered over 24 hrs
Pericarditis definition
inflammation of the pericardial sac - isolated finding or part of underlying dz
Pericarditis causes
idiopathic, postviral, infectious viral ( coxsackievirus, echovirus, adenovirus, EBV, influenza, HIV, hepatitis A orB), bacterial (TB), fungal, toxoplasmosis
acute MI
Uremia
Collagen vascular dz (SLE, scleroderma, rheumatoid-arthritis, sarcoidosis)
Neoplasm (hodgkin lymphoma, breast, lung cancers), Dressler syndrome
Amyloidosis
Radiation
Trauma
Pericarditis clinical features
Majority recover in 1-3 weeks
complications: pericardial effusion, cardiac tamponade
pleuritic chest pain, pain is positional, aggrevated by lying supine, coughing, swallowing, and deep inspiration. Pain relieved by sitting up and leaning forward.
fever, leukocytosis
-+ preceding viral illness
pericardial friction rub
Pericarditis diagnosis
ECG - diffuse ST elevation and PR depression
Pericarditis treatment
Self-limiting, resolve 2-6 weeks treat underlying cause if known nsaids mainstay, colchicine glucocorticoids if refractory uncomplicated cases - outpatient fever, leukocytosis, pericardial effusion, other worrisome sx - inpatient
USA general info and def
oxygen demand unchanged, supply is decreased 2ry to reduced resting coronary flow. Stable angina is d/t increased demand.
USA significant bc indicates stenosis that has enlarged via thrombosis
- Chronic angina now with increased frequency, duration, or intensity
- New onset angina that is severe and worsening
- Angina at rest
USA diagnosis
exclude MI
stabilize with medical mgmt before stress testing or should undergo cardiac cath
USA treatment
hospital admission on the floor with continuous cardiac monitoring
IV access
Supplemental O2
pain control with nitrates and morphine
treat as MI except no fibrinolysis; aspirin + clopidogrel (CURE trial) 9-12 months, BBs, LMWH 2 days aka enoxaparin (essence trial), nitrates, O2, if undergoing PTCA or stenting glycoprotein inhibitors as adjunts, morphine controversial, replace deficient electrolytes
? cardiac cath/revascularization; if responsive to medical therapy then perform stress ECG to assess need for cath
If medical therapy fails or ECG showing ischemia persisting 48 hrs then cath
other indications for PCI; hemodynamic instability, ventricular arrhythmias, new MR, new septal defect
After acute tx; continue aspirin, BB, nitrates, reduce rfx; smoking cessation, weight loss, tx diabetes, HTN, HLD (statin! care trial)
MI gen info
necrosis of myocardium as a result of interruption of blood supply (after thrombotic occlusion of coronary artery previously narrowed by atherosclerosis)
30% mortality rate; half of deaths prehospital
Most have hx of angina, CAD rfx, hx of arrythmias
MI clinical features
chest pain - intense substernal pressure sensation; crushing, elephant standing on my chest, radiation to neck, jaw, arms, back, left side, does not respond to nitro, can be asx dyspnea diaphoresis weakness, fatigue N/V sense of impending doom syncope sudden cardiac death d/t v-fib
MI diagnosis
ECG - peaked T waves, ST segment elevation (transmural injury and can be diagnostic of acute infarct), Q waves, T wave inversion, ST segment depression (subendocardial injury)
ST segment elevation infarct: transmural, tends to be larger
Non-ST segment elevation infarct: subendocardial (inner 1/3-1/5 of the wall), tends to be smaller, presents similar to USA
gold standard - trops; trop I and T (incr 3-5 hrs, peaks 24-48 hrs, nl 5-14 days), greater sensitivity and specificity than CK-MB, 3 serial, on admission and q 8 hrs for 24 hrs, can be falsely elevated in patients with renal failure
CKMB less commonly used; rises 4-8 hrs, peaks 24 hrs, nl 2-3 days, better in detecting recurrent infarction
MI treatment
admit patient to cardiac monitored floor (CCU), IV access, give O2 and analgesics
aspirin - reduce mortality
BBs - reduce mortality
ACEi - reduce mortality
statins - reduce risk of further coronary events (PROVE IT TIMI 22 Trial Atorvas 80 mg)
O2
nitrates - venodilation, decr demand, incr supply, pain
morphine- venodilation, decr demand, incr supply, pain
heparin - LMWH enoxaparin reduces risk of another MI
revascularization - benefit highest when done early (90 min door to balloon); options include thrombolysis > PCI (unless delayed presentation), CABG
Clopidogrel for those who get a stent in PCI (30 days for bare metal stent, 12 months for drug-eluting stent)
Cardiac Rehab - reduce sx and prolong survival
MI complications
pump failure - CHF arrhythmias sinus tachycardia sinus bradycardia asystole AV block recurrent infarction mechanical complications; free wall rupture, rupture of IV septum, papillary muscle rupture, ventricular pseudoaneurysm, ventricular aneursym acute pericarditis dressler syndrome
