Cardiology Flashcards
bradycardia algorithm
UNSTABLE or symptomatic:
- hypotension
- AMS
- refractory chest pain
- acute heart failure
- -> ATROPINE 1ST LINE
- if ineffective: epinephrine infusion, dopamine infusion, transcutaneous pacing
*exception to unstable/symptomatic rule = IF 3RD DEGREE HEART BLOCK OR AV DISSOCIATION –> TRANSCUTANEOUS PACING 1ST LINE and PERMANENT PACEMAKER AS DEFINITIVE
tachycardia algorithm
UNSTABLE:
- hypotension
- AMS
- refractory chest pain
- acute heart failure
–> SYNCHRONIZED CARDIOVERSION
(if regular, narrow QRS complex, may consider adenosine)
STABLE:
-WIDE QRS (12+ sec) –> AMIODARONE (antiarrhythmic) or lidocaine, procainamide + cardicac consult
-NO WIDE QRS = vagal maneuvers, ADENOSINE (if regular and narrow QRS), BETA-BLOCKER OR CCB
- EXCEPTIONS:
- ATRIAL FLUTTER –> BETA BLOCKER OR CCB 1ST LINE
- ATRIAL FIBRILLATION –> BETA BLOCKER OR CCB 1ST LINE
- WOLFF-PARKINSON-WHITE –> PROCAINAMIDE PREFERRED (or amiodarone), avoid av nodal blockers (adenosine, bb, ccb, digoxin)
sympathetic control of heart
Sympathomimetics: EPI and NOREPI cause:
- increased excitability
- increased force of contraction
- increased SA node discharge rate (inc HR)
parasympathetic control of heart
ACETYLCHOLINE (regulated by vagus nerve) causes:
- decreased excitability
- decreased force of contraction
- decreased SA node discharge rate (dec HR)
- VAGAL STIMULATION OR VAGAL MANEUVERS = SLOW DOWN HEART RATE
- anticholinergics block the action of acetylcholine (thus increase heart rate - atropine)
atrial fibrillation
Etiologies:
cardiac dz, ischemia, pulmonary dz, infection, electrolyte imbalance, endocrine/neurologic disorders, age, genetics, hemodynamic stress, meds, drug or alcohol use
Types:
- Paroxysmal - self-terminating w/in 7 days (usually <24h)
- Persistent - fails to self-terminate, lasts >7d, requires termination (medical or electrical)
- Permanent - persistent >1y (refractory to cardioversion)
- Lone: paroxysmal, persistent or permanent w/out evidence of heart disease
-tx:
STABLE:
RATE CONTROL: preferred initial management
- BETA-BLOCKERS - metoprolol - careful w/ rx airway dz
- CCB - DILTIAZEM, verapamil (nondihydropyridines)
- DIGOXIN used in elderly - PREFERRED FOR PT W/ HYPOTN OR CHF
RHYTHM CONTROL: younger pt w/ lone a-fib
- Direct Current (synchronized) Cardioversion (if AF present for <48 hours or after 3-4 wks of antigoagulation and a TEE shows thrombi)
- Pharmacologic Control - ibutilide, flecainide, sotalol, amiodarone
- Radiofrequency Ablation - permanent pacemaker
UNSTABLE –> DIRECT CURRENT (SYNCH) CARDIOVERT
ANTICOAGULATION: all pt w/ nonvalvular a-fib should:
- ASSESSMENT OF RISK OF EMBOLI (CHA2DS2-VASc)
- DETERMINE BENEFITS V RISK OF ANTICOAGULATION
CHA2DS2 - VASc Criteria
(anti-coag risk stratification in nonvalvular a-fib)
2+ = moderate to high risk - chronic oral anti-coag rec
congestive heart failure - 1 hypertension - 1 age 75+ - 2 diabetes - 1 stroke, tia, thrombus - 2 vascular disease (prior mi, aortic plaque, pad) - 1 age 65-74 - 1 sex female - 1
anticoagulation agents
Non-vitamin K antagonist oral anticoags (NOAC)
- usually preferred over warfarin in most cases
- DABIGATRAN (direct thrombin inhib)
- RIVAROXABAN, APIXABAN, EDOXABAN (factor Xa inhibitors)
Warfarin
- Ind: preferred for severe ckd, if c/i to NOAC (hiv pt on protease inhib tx, carbamazepine, phenytoin), cost issues
- INR GOAL 2-3
Dual antiplatelet therapy
- ASA + CLOPIDOGREL
- monotherapy > dual therapy
baroreceptors
-sense changes in arterial pressure (carotid artery stretch) and changes in aortic arch
VAGAL MANEUVERS (CAROTID MASSAGE) DEC HR -inc carotid pressure --> reflexive decrease in hr (due to inc in vagal stimulation)
autoregulation
- process by which blood flow remains constant in an organ despite changing arterial pressures (perfusion) to the organ
- IN HEART, LOCAL VASODILATORS ARE NITRIC OXIDE, OXYGEN AND ADENOSINE
CO = HR x SV
- CO on left side is different than on right side
- normal physiologic variation = DURING INSPIRATION, LEFT SIDE STROKE VOLUME DECREASES
renin-angiotensin-aldoserone system
regulates bp and water (fluid) balance
-activated w/ decrease in sbp
dec arterial BP –> kidney releases RENIN –> converts angiotensinogen to angiotensin I –> angio-converting enzyme in lungs convert ACE I to ACE II =
- inc aldosterone = inc Na retention
- inc ADH = inc H2O retention
- vasoconstriction = inc BP
- inc sympathetic tone = inc BP
- TOO MUCH RENIN = INC BP
- HYPERALDOSTERONISM ASSOCI W/ INC BP AND HYPOK (aldosterone enhances renal K excretion and Na retention)
- ACEi block effects of angiotensin II, leading to dec BP
- inhibit aldosterone, may have hyperK
- potentiate vasodilators (bradykinin) may devo cough
angiogram
GOLD STANDARD / definitive dx for:
- coronary artery dz
- peripheral arterial dz
- renal artery stenosis
- abdominal aortic aneurysms
exercise stress testing
Treadmill Test
-Bruce Protocol: + if ST depressions, exercise-induced htn or hypotn, arrhythmias, sx or hr abnormalities
Radionuclide Myocardial Perfusion Imaging (MPI)
- either SPECT or PET
- benefits: localizes regions of ischemia
pharmacologic stress test
Vasodilators w/ MPI: ADENOSINE OR DIPYRIDAMOLE
- coronary vasodilators of normal (but not dz) arteries
- ind: pt w/ baseline ECG abnormalities
- localizes region of ischemia
- C/I IN BRONCHOSPASTIC DZ (asthma and copd), 2/3rd degree heart block or sick sinus syndrome
- AVOID VASOCONSTRICTORS 24 HR BEFORE (caffeine)
stress echo
LOCALIZES REGIONS OF ISCHEMIA, depicts wall motion abnormalities, visualizes stx/fx of heart
- DOBUTAMINE - sympathomimetic, stims B-mediated inc hr/contractility (positive inotrope/chronotrope) that inc myocardial O2 demand and provokes ischemia
- ind: pt w/ c/i to vasodilators or w/ recent vasoconstrictor use
- C/I: sustained ventricular arrhythmias, severe aortic stenosis, mod-sev htn (>180), aortic dissection, pt on B-blocker
Exercise Stress Echo - another option
coronary artery disease
INADEQUATE TISSUE PERFUSION / ISCHEMIA
- due to imbalance btw dec coronary blood supply and inc demand
- ATHEROSCLEROSIS MC CAUSE, vasospasm, aoritc stenosis/aortic regurge, pulm htn, severe htn, hypertrophic cardiomyopathy
- RF: DIABETES (WORST), CIGARETTE SMOKING, HYPERLIPIDEMIA, HTN, MALES, AGE (>45 MEN, >55 W), FAMILY HX
Pathophysio:
- FATTY STREAK FORMATION - LIPID DEPOSITION IN WBC –> smooth muscle proliferation
- formation of early plaque: LDL enters endothemlium in fatty streak and oxidized, attracts macrophages to ingest LDL and become foam cells, attract more macrophages, fibroblasts, inflam cells
- formation of fibrous (mature) plaque: proliferating smooth muscle cells and connective tissue becomes incorporated into plaque, FIBROUS CAP results in narrowing of lumen +/-calcification to stabilize
-MYCARDIAL ISCHEMIA: narrowing of lumen reduces blood flow in conditions of increased demand = ischemia
>70% reduction when pt are symptomatic
angina pectoris
SUBSTERNAL CHEST PAIN BROUGHT ON BY EXERTION
Class 1: only w/ unusually strenuous activity
Class 2: w/ prolonged or rigorous activity, slight limitation
Class 3: w/ usual daily activity, marked limitation
Class 4: angina at rest
-sx:
HISTORY IMPORTANT
-CHEST PAIN: substernal, poorly localized, exertional
-radiation: ARM (esp ulnar surfaces of forearm and hand), TEETH, LOWER JAW, back, epigastrium or shoulders
-SHORT DURATION <30 MIN (often 1-5 min)
-LEVINE’S SIGN - clenched fist over chest
-pain relieved w/ rest or nitroglycerin (predictable)
diagnosis of ischemic heart disease
Workup: ECG initial, STRESS TEST, ANGIOGRAPHY IS GOLD STANDARD
ECG
-ST DEPRESSION = CLASSIC (horizontal or downslope)
-RESTING ECG NORMAL IN 50%
+/- T wave inversion/nonspp ST changes
-presence of left ventricular hypertrophy assoc w/ inc adverse outcome
STRESS TEST - most useful non-invasive screen tool
Treadmill Test
-Bruce Protocol: + if ST depressions, exercise-induced htn or hypotn, arrhythmias, sx or hr abnormalities
Radionuclide Myocardial Perfusion Imaging (MPI)
- Ind: PT W/ BASELINE ECG ABNORMAL –> LOCALIZE
- ADENOSINE OR DIPYRIDAMOLE (dilate normal arteries, not diseased ones) - used if pt can’t tolerate exercise
- C/I: ASTHMATICS
Stress Echo
LOCALIZES REGIONS OF ISCHEMIA, depicts wall motion abnormalities, visualizes stx/fx of heart
CORONARY ANGIOGRAPHY
- DEFINITIVE DX / GOLD STANDARD
- defines location and extent of CAD
- Ind:
- confirm/exclude CAD in pt w/ symptoms
- confirm/exclude CAD in pt w/ negative noninvasive tests
- pt who may need revascularization (PTCA or CABG)
percutaneous transluminal coronary angioplasty PTCA
Indications:
- 1 or 2 VESSEL DISEASE NOT INVOLVING LEFT MAIN CORONARY ARTERY AND WHEN VENTRICULAR FX IS NORMAL/NEAR NORMAL
- restenosis occurs in 30% w/in 3 months after PTCA so restenosis can be reduced w/ stents
Stents:
- provide safety net and reduces restenosis rates
- some stents have drug-eluting properties
- ASA + CLOPIDOGREL effective in preventing stent thrombosis
coronary artery bypass graft CABG
Indications:
-LEFT MAIN CORONARY ARTERY DISEASE, SYMPTOMATIC OR CRITICAL STENOTIC (>70%)
3-VESSEL DISEASE or decreased left ventricular EJECTION FRACTION <40%
medical management of angina
NITROGLYCERIN (NITRATES)
- inc O2 and dilation (blood flow), reduces coronary vasospasm, decreased preload by venodilation
- sublingual most effective
- if no relief w/ 1st dose, give 2nd/3rd q5 minutes - no relief suspect ACS
- can be used prophylactically (5 min before activity)
- deteriorates w/ moisture, light, air
- SE: ha, flush, tolerance, hypotn, peripheral edema, TACHYPHYLAXIS (nitrate-free period for 8r)
- C/I: SBP <90, RV INFARCT, SILDENAFIL (OTHER PDE-5)
BETA-BLOCKERS
-inc O2 by prolonging coronary artery filling time (diastole), reduces O2 requirements during stress (negative chrono/inotrope)
IND: 1ST LINE MANAGEMENT FOR CHORONIC
CA CHANNEL BLOCKERS
-prevents/terminates ischemia induced by vasospasm (dilates), decreased contractility, heart rate, afterload
IND: pt who can’t use BB, PRINZMETAL ANGINA
ASPIRIN
- prevents platelet activation/aggregation
- doesn’t address supply/demand, but prevents progression, reduces risk of thrombosis
classic outpatient chronic (stable) angina regimen
daily ASA
sublingual nitroglycerin prn
daily BB and STATIN
acute coronary syndrome (ACS)
SX OF ACUTE MYOCARDIAL ISCHEMIA 2RY TO ACUTE PLAQUE RUPTURE AND VARYING DEGREES OF CORONARY ARTERY THROMBOSIS (OCCLUSION)
-Includes: UNSTABLE ANGINA, NSTEMI AND STEMI
Unstable Angina
- angina that is new, crescendo, or at rest >30 min (90% occlusion can cause sx at rest)
- thrombosis: subtotal occlusion
- ECG: ST DEPRESSION and/or T-wave inversions
- cardiac enzymes: NEG
NSTEMI
- angina that is new, crescendo, or at rest >30 min (90% occlusion can cause sx at rest)
- thrombosis: subtotal occlusion
- ECG: ST DEPRESSION and/or T-wave inversions
- cardiac enzymes: POS (cell death)
STEMI
- angina that is new, crescendo, or at rest >30 min (90% occlusion can cause sx at rest)
- thrombosis: TOTAL occlusion
- ECG: ST ELEVATIONS
- cardiac enzymes: POS
etiologies:
- ATHEROSCLEROSIS (MC CAUSE) –> PLAQUE RUPTURE
- CORONARY ARTERY VASOSPASM: cocaine, variant (prinzmetal angina)
symptoms:
- angina pain (>30 min), not relieved w/ rest or nitro
- SYMPATHETIC STIMULATION - tachy/palp, n/v, dizzy
- silent MI - about 25%, esp women, elderly, dm, obese
- PE usually normal +/- S4
diagnostic:
-ECG
-CARDIAC MARKERS - STD 3 SETS q8
-troponin most sensitive and specific
CK/CK-MB: appears 4-6 h, peaks 12-24 h, returns 3-4 d
TROP I + T: appears 4-8 h, peaks 12-24 h, returns 7-10 d
*trop may be falsely elevated in pt w/ renal failure, advanced HF, acute PE, CVA
management of unstable angina or NSTEMI
2 Parts:
- ANTITHROMBOTIC TX
- ASA (antiplatelet)
- CLOPDOGREL (antiplatelet)
- UNFRACTIONATED HEPARIN (anticoag)
- LOW MOLECULAR WEIGHT HEPARIN (ENOXAPRAIN / LOVENOX) (anticoag)
- fondaparinux (anticoag) - ADJUNCTIVE THERAPY
- B-BLOCKERS - metoprolol
- Nitrates - dec sx, doesn’t dec mortality
- Morphine - pain and venodilation, dec preload
- CCB - DOC in VASOSPASTIC DISORDER (cocaine, prinzmental/variant angina)
management of STEMI
3 Parts:
- REPERFUSION TX (MOST IMPORTANT)
- done w/in 12 hours of sx onset
PERCUTANEOUS CORONARY INTERVENTION (PCI)
- best w/in 3H OF SX (esp w/in 90 min)
- better than thrombolytics
THROMBOLYTIC (FIBRINOLYTIC) THERAPY
- use if PCI not option
- ALEPLASE (rTPA) - dissolves clot, RISK REBLEED
- STREPTOKINASE - least chance of intracranial bleed
- ANTITHROMBOTICS
- ASA
- HEPARIN
- Glycoprotein - ADJUNCTIVE THERAPY
- B-BLOCKERS - dec wall tension
- ACE INHIBITORS - slows progress of CHF, dec ventricular remodeling
- Nitrates
- Morphine
- Additional: K + Mg replete, STATINS, monitor BP, glucose
thrombolytic/fibrinolysis contraindications in ACS
Absolute:
- PREVIOUS INTRACRANIAL HEMORRHAGE
- NON-HEMORRHAGIC STROKE W/IN 6 MONTHS OR CLOSED HEAD/FACIAL TRAUMA W/IN 3 MONTHS
- intracranial neoplasm, aneurysm, AVM
- active internal bleeding
- suspected aortic dissection
Relative:
- SBP > 180 on presentation
- INR >2 or known bleeding diathesis
- trauma/major surgery in last 2 weeks
- recent internal bleed w/in 2 weeks
- prior streptokinase exposure, pregnancy
heart failure
MC CAUSE IS CORONARY ARTERY DISEASE
LEFT: MC CAUSE CAD + HTN, valvular dz, cardiomyopathies
RIGHT: MC CAUSE IS L-SIDED HF, PULMONARY DZ (copd, pulm htn), mitral stenosis
SYSTOLIC: -DEC EJECTION FRACTION \+/- S3 GALLOP -THIN VENTRICLE WALLS -DILATED LV CHAMBER -MC FORM OF HF -etiologies: post-MI, dilated cardiomyopathy, myocarditis (can be acute)
DIASTOLIC: -NORMAL EJECTION FRACTION \+/- S4 GALLOP -THICK VENTRICLE WALLS, SMALL LV CHAMBER -assoc w/ normal heart size -etiologies: HTN, left ventricular hypertrophy, elderly, vlave disease, cardiomyopathies, constrictive pericarditis
heart failure cont…
Initial insult leads to INC AFTERLOAD, INC PRELOAD OR DEC CONTRACTILITY –> compensations over time lead to deterioration:
- sympathetic nervous system activation
- myocyte hypertrophy/remodeling
- RAAS activation (fluid overload, ventricular remodeling/hypertrophy)
-sx:
LEFT:
- INC PULMONARY VENOUS PRESSURE FROM FLUID BACKING UP INTO LUNGS
- DYSPNEA MC
- PULMONARY CONGESTION/EDEMA: rales, rhonchi, nonproductive cough, pink frothy sputum, wheezing (CHF MC CAUSE OF TRANSUDATIVE PLEURAL EFFUSIONS)
- HYPERTENSION, CHEYNE-STOKES BREATHING, cyanosis
- Increased adrenergic activation - pale skin, sweat, tachy, poor perfusion
RIGHT:
- INC SYSTEMIC VENOUS PRESSURE –> SIGNS OF SYSTEMIC FLUID RETENTION
- PERIPHERAL EDEMA
- JUGULAR VENOUS DISTENTION
- GI/HEPATIC CONGESTION: n/v, hepatosplenomegaly, ruq tenderness, anorexia
-dx:
ECHO MOST USEFUL TEST (EF IMPORTANT FOR PROGNOSIS)
-normal EF = 55-60%
-EF <35% = inc mortality –> defibrilator placement
CXR - especially for congestive heart failure
-KERLEY B LINES, CARDIOMEGALY, PLEURAL EFFUSIONS, PULM EDEMA
BNP - MAY ID CHF AS CAUSE OF DYSPNEA IN ER
- indicates severity and prognosis
- ventricles release BNP during volume overload (congestive hf)
- BNP >100 = CHF likely
heart failure treatment
Initial: ACEI (+ DIURETIC for symptoms)
-ACEI > BB - best 2 drugs for decreased mortality
Meds that decrease mortality:
ACEI, ARB, BB, NITRATES + HYDRALAZINE, SPIRONOLACTONE
Outpatient Regimen:
ACE + DIURETIC –> ADD B-BLOCKER
+/- hydralazine + nitrates, digoxin
IMPLANTABLE CARDIOVERTER DEFIBRILLATOR IN PT W/ EF <35%