Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
CS - Y2S1B2
Cardiovascular System
| Disease | Features |
|---|---|
| Death toll of cardiovascular disease | 40% |
| Functional Classification of Heart Disease: Class I | No limitation of physical activity; ordinary physical activity doesn't cause undue fatigue, dyspnea, or anginal pain |
| Functional Classification of Heart Disease: Class II | Slight impairment of physical activity; ordinary physical activity results in symptoms |
| Functional Classification of Heart Disease: Class III | Marked limitation of physical activity; comfortable at rest, but less than ordinary activity causes symptoms |
| Functional Classification of Heart Disease: Class IV | unable to engage in any physical activity without discomfort; symptoms may be present even at rest |
| Most common symptoms of heart disease | dyspnea, chest pain, palpitations, syncope or presyncope, fatigue; none are specific (interpretation depends on entire clinical picture, and diagnostic testing) |
| Signs of heart disease | the inevitable peripheral signs: diaphoresis (sweating), cachectic appearance; cyanosis or pallor; changes in vital signs; diminished peripheral pulses or bruits; exaggerated pulses; jugular venous distention (JVD); elevated central venous pressure (CVP) |
| Dyspnea | difficulty breathing/SOB; when d/t heart disease it's precipitated or exacerbated by exertion; results from elevated left atrial and pulmonary venous pressure or hypoxia |
| Dyspnea: acute onset | or left atrial hypertension may result in pulmonary edema (accumulation of excess fluid in lung tissue); decompensated heart failure |
| Dyspnea: investigation | should be quantified by amount of activity that precipitates it; also common symptom of pulmonary disease (the etiologic distinction may be difficult); SOB may also be found in sedentary or obese individuals, anxiety states, anemia and other illnesses |
| Orthopnea | dyspnea that occurs in recumbancy (when pt lays down); results from inc in CVP; may also be in pulmonary disease or obesity |
| Paroxysmal nocturnal dyspnea (PND) | SOB that occurs abruptly 30min - 2hrs after going to bed and is relieved by sitting or standing up; more specific for cardiac disease but not diagnostic; if pt starts sleeping in a chair he's bad off |
| Chest pain or discomfort commonly result from: | pulmonary disease, pleural disease, musculoskeletal disease, esophageal disorders, cervicothoracic nerve root irritation, anxiety states, cardiovascular disease |
| Myocardial ischemia | poor circulation to myocardium for 5-20min; usu result of coronary artery disease; MOST frequent cause of cardiac pain; often a sensation of discomfort (tight/squeeze/pressure/gas) not pain; leads to potential neglect by pt and misdiagnosis by Dr |
| Explore what chest discomfort means: | jaw pain? arm pain? |
| Angina pectoris: essentials of diagnosis | Precordial chest pain; usu precip by stress or exertion; relieved rapidly by rest or nitrate drugs; electrocardiographic or scintigraphic evidence of ischemia during pain/stress testing; angiogram shows significant obstruction of major coronary arteries |
| Angina pectoris: pathology | usu d/t atherosclerosis; coronary a. spasms at lesion; unusual causes: congenital anomalies, emboli, arteritis or dissection are seen; also occurs w/absence of obstruction w/L ventricular hypertrophy, aortic stenosis, inc metabolic demands |
| Pain of Myocardial Infarction | sudden insufficiency of arterial blood to myocardium d/t occlusion of coronary a.; ischemic symptoms; anxiety/uneasiness; retrosternal/left precordial pain; jaw/shoulder/innner arms/upper abdomen/back; sternal region involved; >20min of pain; senses doom |
| Ischemic pain | often precipitated by exertion, cold temps, stress; usu relieved by rest; not all follow patterns; not related to position or respiration; usu not elicited by chest palpation; in MI, a precipitating factor is usu not present; not MI if reproducible pain |
| Ischemic pain also seen with: | hypertrophy of either ventricle or aortic disease |
| Atypical Chest Pain: not typical for angina pectoris often seen in: | myocarditis, cardiomyopathy, primary pulmonary hypertension, mitral valve prolapse |
| Palpitations | awareness of heartbeat; may be normal; may reflect cardiac output in pts w/o cardiac conditions (exercise, thyrotoxicosis, anemia, anxiety) |
| Palpitations: cardiac abnormalities | produced by inc stroke volume (regurgitant valvular disease, bradycardia); may be d/t cardiac dysrhythmias; |
| Palpitations: ventricular premature beats (PVCs) | may be sensed as extra or "skipped" beats |
| Palpitations: supraventricular/atrial (SVT) or Ventricular tachycardia (VTach or VT) | may be felt as rapid regular or irregular palpitations or "fluttering;" many pts are asymptomatic and feel faint instead; if pts get fixated they become "cardiac cripples" |
| Syncope | loss of consciousness |
| Cardiogenic syncope | most commonly results from sinus node block, atrioventricular (AV) conduction block, or ventricular tachycardia or ventricular fibrillation |
| Neurocardiogenic syncope | vasovagal syncope; inappropriate inc in vagal efferent activity often resulting from precedent inc in sympathetic cardiac stimulation; strain (valsalva) or after getting blood drawn |
| Cardiogenic syncope - continued | few prodromal symptoms; may be occasion for injury; absence of Sx helps distiguish cardiogenic syncope from vasovagal faints, postural hypertension, or seizure; also d/t aortic valve disease and hypertrophic obstructive cardiomyopathy |
| Neurocardiogenic syncope - continued | aka: vasovagal syncope; syncope may follow a brief period of diaphoresis and presyncopal symptoms; may be abrupt in onset, mimicking arrhythmia-induced syncope |
| Signs of heart disese | anxiety, resltessness as with MI; Diaphoresis - suggests hypotension or hyperadrenergic state (precardial tamponade, tachyarrhythmias or MI); cachexia in chronic low output states; cyanosis (central or peripheral) |
| Central cyanosis | due to arterial desaturation; low output states |
| Peripheral cyanosis | reflecting impaired tissue delivery of adequately saturated blood; low output state; polycythemia; peripheral vasoconstriction |
| Vital signs: HR | heart rate (50-90 is normal); High or low may be normal or may reflect noncardiac conditions (anxiety, pain, medication effect, fever, thyroid disease, pulmonary disease, anemia or hypovolemia)...HR inc 10 beats/min for every 1 degree inc in temp |
| Vital signs - if symptoms or clinical suspicion warrents: | order an ECG to diagnose arrhythmia, conduction disturbance, or other abnormality |
| Vital signs: BP | range of normal is wide: even in asymptomatic individuals, systolic below 90 or >140mmHG warrant further evaluation and follow-up; NEVER Dx a cardiac prob w/only one BP reading (it is a beat-beat window)! |
| Vital signs: respirations - Tachypnea | non-specific; respiratory rate >16/min; pulmonary disease and heart failure should be considered |
| arteriosclerotic peripheral vascular disease | most commonly causes diminished peripheral pulses; may be accompanied by bruits |
| Exaggerated pulses may indicate: | aortic regurgitation, coarctation (stricture or narrowing), patent ductus arteriosis, or other conditions that inc stroke volume |
| Carotid pulses | valuable aid to assess left ventricular function |
| Pulses - delayed upstroke | aortic stenosis |
| Pulses - Bisferiens quality | 2 palpable peaks; hypertrophic obstructive cardiomyopathy; mixed aortic regurgitation and stenosis |
| Pulses - pulsus alternans | amplitude of the pulses alternates every other beat during sinus rhythm; occurs when cardiac contractility is very depressed or w/large pericardial effusions |
| Pulses - pulsus paradoxus | decrease in systolic blood pressure during inspiration > the normal 10mmHg; valuable sign of pericardial tamponade, asthma, and COPD |
| Pulses - Jugular Venous Pulsations | provides insight into R atrial pressure; if >3cm above Angle of Louis = inc CVP; if they rise >1cm w/sustained 30sec RUQ pressure (hepatojugular reflex) = inc Central blood volume |
| Pulmonary Examination - Rales "crackles" | heard at lung bases are a sign of Congestive Heart Failure (CHF); may also be caused by localized pulmonary disease |
| Pulmonary Examination - Wheezing and Rhonchi | suggestive of obstructive pulmonary disease but may occur in left heart failure ("cardiac asthma") |
| Pulmonary Examination - Pleural Effusions | with bibasilar percussion dullness and reduced breath sounds; common in CHF |
| Edema | subcutaneous fluid collections appear 1st in lower extremities in ambulatory pts, or in sacral region of bedridden pts; in Heart Disease: edema results from elevated right atrial pressures |
| Heart Sounds: S1 | closing of mitral and tricuspid valves |
| Heart Sounds: S2 | closing of pulmonary and aotic valves; usually split w/2 components (aortic preceding) being separated more during inspiration |
| Heart Sounds: S3 | mid-diastolic sounds; occurs during rapid filling phase of ventricle after closure of aortic and pulmonary valves; may be normal in kids/YAs/pregnancy; Abnormal if ventricle is dysfunctional or mitral/tricuspid regurgitation |
| Heart Sounds: S4 | atrial gallop; triple cadence to heart sounds at rate of 100+ beats; d/t abnormal 3rd or 4th sound in addition to 1st and 2nd; usu indicative of serious disease ("stiff" or "non-compliant" ventricle) |
| Heart Sounds: clicks | high-pitched ejection sounds |
| Heart Sounds: murmurs | valvular disease; pansystolic (holosystolic) when they merge with 1st heart sound and persist thru all of systole |
| Heart Sounds: "ejection" murmurs | when they begin after the 1st heart sound and end before the second sound |
| Heart Sounds: "innocent" murmurs | often vary w/inspiration; diminish in upright position; are most often heard in thin individuals |
| Heart Sounds: "thrills" | palpable vibrations associated with murmurs |
| Unmodifiable risk factors of heart disease | age, male gender, family history of premature heart disease |
| Potentially modifiable risk factors of heart disease | smoking, high BP, blood lipid levels, physical inactivity, diabetes, obesity, psychological conditions, elevated blood homocysteine levels, markers of inflam (CRP), hyperfibrinogenemia, hormone replacement therapy (HRT) |
| Cigarette Smoking Risks: | lung cancer, emphysema, bronchitis; Vascular Disease (coronary, cerebral, peripheral); risk inc w/increasing pack-yrs |
| Effects of Quitting Smoking Cigarettes | inc risk falls rapidly over time; for coronary heart disease, approx 40% of inc risk is removed w/in 5yrs of quitting; it takes several more years of non-smoking to achieve the level associated w/non-smoker |
| High Blood Pressure Risks | cerebrovascular disease and coronary disease; CV morbidity and mortality inc as both systolic/diastolic pressures rise; hypertension is diagnosed on elevated D or S pressures; Objective of management is to achieve normalization of both S and D pressures |
| High Blood Pressure: epidemiology | 50million Americans w/ Systolic >140 or Diastolic >90mmHg; 70% aware of their diagnosis; 50% are receiving treatment; 25% are under control using a threshold of 140/90mmHg |
| High blood pressure: problems | Higher pressure results in higher disease rates; the lower the blood pressure (w/in resonable physiologic limits) the lower the level of risk; several intervention trials have clearly established the value of aggressive Tx of elevated BP |
| Lipid Fractions and Risk of Coronary Heart Disease | in fasting serum, cholesterol is carried on: VLDL, LDL and HCL (the sum = total cholesterol); most labs measure: total chol, total TGs, chol in HDL fraction; |
| Lipid fractions and disease states | some use ratio of total cholesterol:HDL cholesterol as indicator of lipid-related coronary risk; The Lower the ration the Better; this ratio may obscure important information in individual pts; Therefore, evaluate all fractions b/f beginning therapy |
| Ranges of serum lipids | no true "normal;" western pops are 10% higher than Asians; total and LDL chol rise w/age in healthy people; declines seen in acute illness w/exception of TG levels in pancreatitis; Chol levels do not remain constant over time (esp in childhood to adults) |
| Complete lipid profile in pts w/cardiovascular disease | after overnight fasting; Total cholesterol, HDL, TGs, LDL cholesterol |
| Cholesterol screening: | begin at age 20; USP-STF at 35 in M, 45 in W; unless there are other risk factors for coronary heart disease; individuals w/o CAD can be stratified by risk factors (2+ is intermed risk; <2 is low risk) |
| Screening for High Cholesterol | All pts w/CHD or CHD risk equivalents (peripheral artery disease, AAA, symptomatic carotid artery disease; pts w/IDDM); only exception is if lipid lowering in pt is not desirable for other reasons |
| Benefits of Lowering Blood Cholesterol in Men | lowers subsequent coronary heart disease morbidity and mortality and rate of progression of coronary atherosclerosis |
| Benefits of cholesterol lowering in pts w/CHD | reduces cardiovascular events, cardiovascular deaths, all-cause mortality in ment and women w/CAD; aggressive lowering causes regression of plaques in some pts; reduces progression in saphenous vein grafts; can slow/reverse carotid artery atherosclerosis |
| West of Scotland Study and AFCAPS/TexCAPS study | 31% dec in MI in mid-aged men treated w/ Pravastatin (pravachol) compared to placebo; AND, similar results w/Lovastatin (Mevacor); primary prevention studies have found less consistent effect on total mortality |
| Results of reducing cholesterol levels in healthy mid-aged men w/o CHD as primary prevention | reduces risk in proportion to the reductio of LDL cholesterol and the increase of HDL cholesterol; dec rates of MIs, new cases of angina, need for bypass procedures |
| Treatment decisions for Coronary Heart Disease are based on LDL and HDL levels | measurement of total cholesterol is only adequate screening for low-risk individuals; cholesterol >200mg/dL needs fasting LDL and HDL measurement; initial measurement is lease likely to lead to pt misinformation and misclassification |
| Goals for LDL Cholesterol: CHD, PVD or DM | LDL <100 |
| Goals for LDL Cholesterol: Multiple (2+) risk factors | LDL <130 |
| Goals for LDL Cholesterol: 0-1 risk factor | LDL <160 |
| Physical inactivity | association btw less active life and inc risk of coronary heart disease; |
| Exercise | dec likelihood of CHD; favorable effect on HDL w/yrs of exercise; synergistic w/wt loss in lowering LDL/HDL in mod obese men; TGs lowered after single bout of exercise or chronic vigorous exercise |
| Obesity - Framingham Heart Study | weight reduction should lower risk of CHD whether thru lowered BP and/or cholesterol level as a lowered risk factor in itself |
| Diabetes | powerful independent risk factor of CVD; which is a major cause of death in diabetics; aim to normalize glucose levels and monitor other coexistant risk factors |
| Markers of inflammation: another strong risk factor for CAD | CRP (C-reactive ptn) - is the BEST characherized inflam marker; Serum fibrinogen; ESR; Homocysteine |
| High sensitivity CRP | levels >10ug/mL often found in systemic inflam; <1 = low risk for furture CV events; 1-3 = intermediate risk; >3 = high risk for future CV event |
| Coronary Heart Disease | aka: atherosclerotic coronary heart disease; the most common CV disability and death in US; M8x > F, but equal risk after age 70; Peak manifestations: 50-60yo; |
| Risk Factors for CHD | fam hx of onset b/f 50; age; male; blood lipid abnorm; diabetes; insulin resistance/metabolic syndrome; HTN; smoking; elevated homocysteine; CRP; hyperfibrinogenemia; hypoestrogenemia in women |
| CHD: Pathophysiology | abnml lipid metab/excess intake of chol/unsat fats (+ genetics) initiates atherosclerotic proces of fatty streaks (oxid of LDL, macrophage migration, foam cells, smooth muscle migration, fibrous cap, calcification of lesion and narrowing of artery) |
| The Fate of Athrogenic plaques: | remain stable or progress OR rupture/extrusion of lipids/intravascular thrombosis...outcome depends on occlusion or thrombolysis; Tx or spontaneous stabilization; Occlusions result in symptoms of angina or MI |
| Athrogenic Plaque Vulnerability | higher lipid content; higher [macrophage]; very thin fibrous cap; usu in young individuals w/sudden death as the first manifestation of coronary disease |
| Atherosclerosis progression | d/t inflam response in vessel wall; initiated or worsened by infectious agents; high CRP may play role in process (can activate endothelial cell adhesion expression and chomotaxis and inhibits NO synthase to promote lipid deposition/plaque instability) |
| Atherosclerosis; Treatment of lipid abnormalities | delays progression and can produce regression; fewer new lesions develop; endothelial fxn may be restored; coronary event rates are reduced |
| Effects of HMG-CoA reductase inhibitors | "statins" lower LDL cholesterol in clinical trials; prevents death, coronary events and strokes; even in pts who experienced previous coronary events (secondary prevention) |
| Aggressive lipid lowering therapy should be instituted in all pts with: | dyslipidemia and CAD, cerebrovascular or peripheral vascular disease; red of LDL is a primary prevention in pts w/o atherosclerosis (<135mg/dL) |
| Metabolic Syndrome | Insulin resistance and hyperinsulinemia have a role in the pathogenesis of atherosclerosis; inc risk of disease (diabetes is diagnosed if fasting glucose >125) |
| Metabolic Syndrome: Therapeutic Goals | correct hyperglycemia, manage high BP, address dyslipidemias, be cautious of therapies which actually elevate lipids (b-blockers for HTN) or inc insulin resistance w/aggravation of diabetes (niacin) |
| Metabolic Syndrome: features | central obesity, high BP, high TGs low HDL (<40), insulin resistance; LDL should be below 160...100 is best |
| Myocardial oxygen demand | determined by HR, contractility, ventricular wall tension (fxn of ventricular vol and intraventricular pressure); inc in one or more determinants (exercise, stress, adrenergic activity) triggers inc in myocardial O2 demand; ischemia results w/o O2 rise |
| Myocardial Oxygen Supply | governed by coronary blood flow/ability of myocardium to extract O2; heart always takes O2 w/near max efficiency from blood, even under situations of minimal demand so there is little potential for enhanced O2 extraction to counter inc O2 demands |
| Coronary blood flow | can inc several fold in normals d/t vasodilation at arteriolar level; myocardial ischemia results when autoregulatory vasodilation is prevented by stenosis or endothelial dysfxn; coronary blood cannot inc proportional to rising O2 demands |
| Myocardial ischemia | may occur when O2 demands are constant but there is a primary dec in coronary blood flow mediated by: 1. coronary a. spasm, 2. rapid evolution of plaque disruption, 3. intermittent microvascular plugging by platelet aggregates |
| Myocardial ischemia | some episodes are symptomatic causing angina pectoris; others are silent and brought on by emotional/mental stress; |
| Myocardial hibernation and shunting | areas of myocardium that are persistantly underperfused but still viable may develop sustained contractile dysfxn ==> an adaptive response to L ventricular failure; reversible w/coronary revascularization |
| Myocardial hibernation can be identified by: | radionucleotide testing, PET, contrast-enhanced MRI, or its retained response to inotropic stimulation w/dobutamine |
| Myocardial Stunning | occurrence of persistant contractile dysfxn following prolonged or repetitive episodes of myocardial ischemia |
| Acute Coronary Syndromes | ischemic heart dx ranges from angina to actue MI and sudden cardiac death; "Acute Coronary Syndrome" is spontaneous ischemia (unstable angina, non-ST-segment elevation MI and ST-segment elevation MI; single continuum of plaque rupture/thrombus formation |
| Cardiac Diagnostic Testing Modalities | CXR, echocardiogram, electrocardiogram (ECG), transesophageal echocardiography, MRI, Cardiac catheterization and angiography (R and L heart catherization) |
| Other specialized non-invasive cardiac testing procedures | Frequently overused; limited utility for asymptomatic dx; not a substitute for clinical eval; stress testing, ambulatory electrocardiography (Halter monitor), cardiac nuclear medicine tests, cardiac CT |
| Chest x-ray | provides info about normal size of heart, pulmonary circulation, pirmary pulmonary dx and aortic abnormalities; AP, LAT, portable...calcifications in older pts will allow you to visualize aorta more in xrays |
| Electrocardiogram (ECG) | cardiac rhythm, conduction abnormalities, evidence of ventricular hypertrophy/MI/myocardial ischemia; Non-specific ST segment and T wave changes may reflect the above, but are also noted with: E-lyte imbalance/drugs/other conditions |
| Echocardiogram | provides more reliable info about: chamber size, hypertrophy, pericardial effusions, valvular abnormalities, congenital abnormalities; has largely replaced x-ray eval of cardiac dx (non-invasive/widely available/color enhanced) |
| Echocardiography | measure LV size, function, thickness; LV regional wall motion assessed; size of all 4 chambers; morphology of heart valves; allows Dx of: hypertrophic cardiomyopathy, pericardial effusion, mitral valve prolapse, vavlular vegitations, cardiac tumors |
| Doppler Ultrasound | qualitative or quantitative estimation of transvalvular gradients, pulmonary artery pressure, valvular regurgitation, intraventricular shunts |
| Color doppler ultrasound | visually demonstrates patterns and directionality of flow; useful in evaluating congenital heart disease |
| Doppler Echocardiography | ultrasound reflects off RBCs to measure velocity of flow across valves, w/in cardiac chambers, thru great vessels; color flow doppler displays blood velocity in real time superimposd on 2D image; blue toward/red away from transducer; green=turbulance |
| Transesophageal Echocardiography (TEE) | improved quality of echos; info about posterior structures (esp atria, AV valves and prosthetic valves; monitors pts in surgery; sensitive to detecting aortic dissection |
| TEE: detection | severe atherosclerosis of asc. aorta (d/t embolic stroke/CVA/or TIA); detects Latrial thrombi, valvular vegetations, & eccentric mitral regurgitant jets (esp w/prosthetic valves); absense of atrial thrombi identifies pts in atrial fib low risk ebolization |
| Exercise Electrocardiography | aka: stress testing w/bike or treadmill; most useful non-invasive for angina pts; ischemia absent at rest is detected by precipitation chest pain or ST segment depression; combined w/imaging (nuclear/echo/MRI); |
| Bruce protocol for stress testing | increases treadmill speed and elevation every 3 min until limited by symptoms |
| Exercise Elecctrocardiography: Precautions and Risks | one infarction or death/1000 tests; pts who have pain at rest or minimal activity shouldn't be tested; aortic stenosis is contraindicated; stop test when hypotension/ventricular or supraventricular arrhythmias occur >3-4mm ST depression) |
| Exercise Electrocardiography: Indications employed to | confirm Dx of angina; determine severity of limitation of activity d/t angina; assess prognosis in pts w/known coronary disease (incl recovering MIs) by detecting grps at high or low risk; evaluate responses to therapy; screen silent coronary disease |
| Scintigraphic Assessment of Ischemia: Myocardial perfusion scintigraphy | radionucleotide images of blood flow; zone of hypoperfusion (ischemia or scar); if myocardium is viable, defects "fill in" or reverse as blood flow equalizes = reversible ischemia |
| Mycoardial scintigraphy indications | difficult to read rest/exercise ECG (L bundle branch block, baseline ST-T change, low voltage); confirm +exercise ECG in asymptomatic pt; localize ischemia; ischemia vs. infarct; completeness of bypass/angioplasty; prognisis in known coronary disease |
| Cardiolite Scan Result: Normal | <1% risk of cardiac death/MI; Risk factgor modification in addition to current regimen |
| Cardiolite Scan Result: Mildly abnormal | low risk of cardiac death, intermediate risk of MI; aggressive risk factor modification/medical treatment |
| Cardiolite Scan Result: Moderately to severly abnormal | intermediate-to-high risk of BOTH cardiac death and MI; catheterization (possible revascularization)/risk factor modification |
| SPECT (Single photon emission computed tomography) | similar to CT or MRI; visualizes fxnl info about specific organ/system; radioisotope tracer injected, ingested, or inhaled; as isotop decays, gamma rays collected and a CT picture is made |
| Radionucleotide angiography | images L ventricle/measures ejection fraction and wall motion; resting abnormalities in coronary disease = infarction; abnormalities only w/exercise = stress-induced ischemia (may dec fraction..inc in norml pts); less specific older pts w/other heart prob |
| Stress echocardiography | enhances ECGs/alternative to nuc med procedures; echo done during/after exercise; transient depression of segmental wall motion = ischemia; dobutamine (inotropic - contractility) or dipyridamole (persantine) infusion is effective if pt cannot do exercise |
| Cardiac MRI | becoming preferred method of evaluating many cardiac conditions, incl pericardial and congenital abnormalities; used w/gadolinium contrast agents to assess myocardial perfusion and viability |
| Positon emission tomography (PET) | positron agents demonstrate perfusion or metabolism of myocardium; distinguishes "stunned"-transiently dysfxnl myocardium from scar with persistant glycolytic metabolism tracer FDG in regions of dec flow; cyclotrons disturb positron agents |
| Cardiac Catheterization and Angiography | the GOLD STANDARD test for assessment of many hemodynamic and anatomic heart abnormalities; invasive ==> uses intravascular and intracardiac catheters; costly, dangerous, but still necessary |
| Right heart catheterization | convenient to perform bedside/OR/lab; measures R atrial/R ventricular/pulmonary artery/pulmonary capillary wedge pressure, oxygen saturation and cardiac output; provides hemodynamic monitoring for pt |
| Wedge pressure | indicator of left atrial pressure |
| Hemodynamic monitoring | helpful in management/treatment of shock, heart failure, complicated MI, respiratory failure and postoperative hemodynamic instability; |
| Right heart catheterization: Risks | pneumothorax, bleeding, arrhythmias, pulmonary artery rupture, pulmonary emboli, infections |
| Left heart catheterization | via femoral a; evaluates cardiac valves and left ventricular function; mitral stenosis and aortic stenosis quantified by pressure gradients across valves; ejection fraction/regional wall motion; Confirms need for valve surgery/obtain coronary angiograms |
| Cardiac Electrophysiology | electrical impluse starts in SA node (posterior RA), travels across/contracts atria to AV node Bundle of His down R/L bundle branches, depolarizing/contracting ventricles |
| ECG definitions - depolarization | spread of electrical stimulation thru heart |
| ECG definitions - repolarization | return of stimulated heart cells to resting state |
| ECG defined | measure of electrical stimulation of heart; the synchronized pattern of repolarization and depolarization are represented as waves on ECG |
| ECG Complexes - P wave | atrial depolarization; stimulation |
| ECG Complexes - QRS complex | ventricular depolarization; stimulation |
| ECG Complexes - ST segment, T wave, U wave | ventricular repolarization; recovery |
| P wave is at max when: | half the atria depolarizes |
| The electrical charge is 0 when: | all the atria depolarizes |
| The QRS up stroke is when: | half the ventricles depolarize |
| The QRS down stroke is when: | the ventricles are fully depolarized |
| The T-wave is when: | the ventricles are repolarized |
| ECG: PR interval | the time from initial stimulation of atria to initial stimulation of ventricles |
| ECG: ST segment, T wave and U wave (if present) | produced by ventricular repolarization |
| Parts of QRS Complex: first downward deflection | Q wave |
| Parts of QRS Complex: First upward deflection | R wave |
| Parts of QRS Complex: If there is a second upward deflection | R' (R-prime) |
| Parts of QRS Complex: The first downward deflection following an upward deflection | S wave (not a Q wave) |
| Parts of QRS Complex: if there's only one downward deflection | QS wave |
| Electrical, Pressure and Heart Sound Correlation | Peak of P wave begins atrial contraction (1st pressure spike); Peak of QRS begins ventricular contraction (2nd pressure spike); Rise & fall of pressure curve = first and second heart sounds |
| Lead Placements: Chest (6) | The precordial leads define a horizontal or transverse plane and view electrical forces moving anteriorly and posteriorly; R side of sternum, L side of sternum, midclavicular, midaxial, then btw |
| Lead Placements: Limbs (4) | axis measured in 360 degree coronal plane; designated 0 at left; +90 inferiorly; +180 to left; -90 superiorly |
| Lead Placements: Limb lead I | makes L arm positive and R arm negative; angle of orientation is 0 degrees |
| Lead Placements: Limb lead II | makes legs positive and R arm negative; angle of orientation is 60 degrees |
| Lead Placements: Limb lead III | makes legs positive and L arm negative; angle of orientation is 120 degrees |
| Lead Placements: Limb lead AVL | makes L arm positive and other limbs negative; angle of orientation is -30 degrees |
| Lead Placements: Limb lead AVR | makes R arm positive and other limbs negative; angle of orientation is: -150 degrees |
| Lead Placements: Limb lead AVF | makes legs positive and other limbs negative; angle of orientation: +90 degrees |
| Predicting Positive or Negative Deflections: Positive deflection | an atrial or ventricular depolarization that is traveling towards a given lead at less than a 90degree angle |
| Predicting Positive or Negative Deflections: Isoelectric (+ = - deflection) | an atrial or ventricular depolarization that is traveling at a 90degree angle to a give lead |
| Predicting Positive or Negative Deflections: Negative deflection | an atrial or ventricular depolarization that is traveling away from a given lead at an angle greater than 90 degrees |
| Precordial Chest Leads | REMEMBER: the R ventricle lies anteriorly (leads V1 and V2) and medially and L ventrical lies posteriorly and laterally (leads V5 and V6) |
| ECG Leads: V1, V2, V3, V4 | anterior group |
| ECG Leads: I, AVL, V5, V6 | left lateral group |
| ECG Leads: II, III, AVF | Inferior |
| Septal Depolarization | the vector is directed RIGHTWARD and ANTERIORLY; resulting in a positive deflection (R wave) in V1 and a negative deflection (Q wave) in left ventricular epicardial leads (V5) |
| Ventricular Axis: Major activation of L and R ventricles | force is oriented to the Left, inferiorly and posteriorly: In a normal heart: V1 = Negative and V6 = Positive |
| T wave axis: Repolarization | the mean vector is oriented Leftward, inferiorly and anteriorly |
| Cardiac Pacemaker Rate and Rhythm | normally set by SA node in posterior wall of R atrium; if SA node doesn't function properly, there are potential (ectopic) pacemakers in all parts of the heart, including atria, AV node or ventricles |
| Ectopic Atrial Pacemakers | can occur anywhere in heart or atria if SA node is diseased; they are programmed to fire ~75bpm |
| Idionodal rhythms | if atria malfunction, an ectopic AV nodal rhythm is produced ~60bpm |
| Idioventricular rhythms | if atria and AV nodes malfunction, node rhythm is ~40bpm |
| Determining Regular Rhythms | you don't necessarily know that the rhythm is coming from SA node; Estabilishing a regular rhythm allows us to assess accurate rate; Count P waves for each QRS complex and determine that all R wave peaks are equidistant from each other |
| Determining Rate (Quick Method) | count number of large boxes (0.2ms) btw R wave peaks as 300, 150, 100, 75, 60, 50 |
| Rate/Irregular Rhythm | if rhythm is irregular, the quick method of rate determination is not accurate; Use the marks at top of ECG strip; Take the # of R waves in 6 seconds (2 hash marks) and multiply it by 10. |
| R-R intervals are different; No P waves | atrial fibrillation |
| Types of Irregular Rhythms | regular rhythm with extra beat/skips; Regular Irregular Rhythms; Irregularly irregular rhythms; Heart Blocks; Tachycardia (>100bpm) or Bradycardia (<60bpm) |
| Determining Axis | QRS represents depolarization to L ventricle and subsequent contraction; Depolarization occurs from summation of vectors from AV node thru ventricles as "mean QRS vector/axis" |
| Normal QRS Axis | between 0 and +90 degrees |
| Left QRS Axis Deviation | Any axis btw 0 and -90 degrees |
| Right QRS Axis Deviation | Any axis btw +90 and -90 degrees |
| Rapid Determination of Axis: Normal | Leads I and AVF are POSITIVE deflections |
| Rapid Determination of Axis: Right Axis Deviation | If Lead I is DOWN and AVF is UP |
| Rapid Determination of Axis: Left Axis Deviation | If lead I is UP and AVF is DOWN |
| Causes of Right Axis Deviation | large left ventricular infarction; Severe pulmonary hypertension with resultant right ventricular hypertrophy; |
| Causes of Left Axis Deviation | Extreme left ventricular hypertrophy; Extreme obesity (abdominal) pushing up diaphragm; Mild LVH with right ventricular infarct |
| QRS Axis can be determined in AP plane as well: Normal | Lead V2 is directly in front of AV node; If V2 is NEGATIVE, the axis is poterior |
| Atrial and T wave Axis | harbingers of pathology; determine approx axis based on height of positive deflections on 12 lead ECG |
| Block Rhythms: SA blocks | miss a complete cycle d/t lack of impulse from SA node |
| Block Rhythms: AV Node Block (1st Degree) | creates longer delay b/f ventricles are stimulated from P wave; Prolonged PR interval (>0.2s; larger than 5 little boxes) |
| Block Rhythms: AV Node Block (2nd Degree) | occurs when it takes 2 or more atrial impulses to stimulate a QRS; named by the number of blocked P waves; Once the AV node fires, QRS morphology remains normal (indicating the block is in AV node only) |
| Second Degree AV Block: Wenckebach Phenomenon | occurs when PR interval becomes progressively longer until the AV node is not stimulated (no QRS); Mobitz I block; considered a STABLE rhythm, no major concern, but could be a harbinger...1st degree block never drops a beat |
| Second Degree AV Block: Mobitz II | occurs without prolongation of PR interval, but QRS is dropped; an inherently UNSTABLE rhythm |
| Third Degree Hear Block: Complete Heart Block | no atrial stimulation of AV node (no association btw atria and ventricles); Ventricles must be paced independently; COMPLETELY UNSTABLE; P wave is buried in QRS - they have no correlation; dissociation; ventricular escape; Pt needs a pace maker!!! |
| Complete Heart Block | the pacemaker must be the AV node or the ventricles; location is distinguished by ventricular rate and QRS morphology |
| Bundle Branch Block | occurs in either Right or Left side; a delay in conduction creates delay in ventricular firing; REMEMBER: both ventricles fire simultaneously normally |
| Bundle Branch Block: split ventricular firing | results in an R and R' wave; QRS interval is >0.12sec or 3 small boxes |
| Right Bundle Branch Block | anterior chest leads look at R ventricle (V1 and V2); the Left ventricle fires first |
| Left Bundle Branch Block | the R-S-R' is evident in lateral chest leads on left ventrical (V5 and V6); Right ventricle fires first |
| General Principles of Bundle Branch Blocks: Rate dependent | BBB only manifests on ECG over a certain rate |
| General Principles of Bundle Branch Blocks: Incomplete BBB | R-S-R' exists with a normal QRS interval |
| General Principles of Bundle Branch Blocks: Myocardial Infarction | may not be diagnosed w/ coexisting LBBB |
| General Principles of All Blocks: STABLE Rhythms | First and Second Degree AV Blocks (variable rate and Wenckebach) and Chronic BBB |
| General Principles of All Blocks: UNSTABLE Rhythms | Mobitz II second degree AV block, Newly-formed BBB, and Third Degree AV blocks |
| Step by Step Approach to ECG Reading | 1. Quickly assess normal rhythm; 2. Determine Rate; 3. Determine Axis; 4. Measure PR-interval; 5. Measure QRS-interval; 6. Evaluate for Blocks; 7. Assess for Pathology |
| Atrial Abnormality and Hypertrophy: Lead II | evaluates atria as the most positive vector of depolarization |
| Atrial Abnormality and Hypertrophy: Lead V1 | evaluates atria d/t its position on the chest |
| Atrial Abnormality: Left Atrium | Broad, humped P waves in lead II; Biphasic, widened P wave in V2 w/significant negative deflection |
| Atrial Abnormality: Right Atrium/Pulmonale | Peaked P wave in Leads II and V1 |
| Left Ventricular Hypertrophy | deepens the S wave in V1 and heightens the R wave in V6 |
| Right Ventricular Hypertrophy | causes RAD with tall R wave in V1 and Biphasic complex in V6 |
| Left Ventricular Hypertrophy | sum of S wave in V1 and R wave in V5 or V6 >35mm; R wave >11mm in lead aVL; Associated with "strain pattern" repolarization abnormality; Horizontal (0) axis and widened QRS or frank BBB; Secondary LAE |
| Fascicular Blocks (hemiblocks) | while the RBB is one wire, the Left divides into anterior and posterior fascicles; Either of these fascicles may be blocked, but do not widen QRS, only change the axis |
| Left Anterior Fascicular Block (LAFB) | left axis deviation w/o widened QRS, hypertrophy, or strain pattern; a fairly common block |
| Left Posterior Fascicular Block (LPFB) | difficult Dx to make, as other causes of RAD occur w/o concommitant abnormalities; RAD w/o QRS widening of LVH; Isolated case is rare; can also have bifascicular and trifascicular blocks |
| Ischemia | lack of blood supply to muscle; Represented by: symmetrically inverted T waves and ST segment depression w/normal a T wave |
| Injury | ongoing (acute) injury resulting in prolonged ischemia; ST elevation may be 1mm or more; T waves may be normal, inverted, or hyperacute (peaked) |
| Infarction | irreversible injury resulting from prolonged injury; myocardial cell death may be subendocardial or transmural; localized by the leads that they are seen in |
| Transmural Infarction | full thickness myocardial injury; production of significant Q waves signify a completed infarction (insignificant Q waves occur normally) |
| Evolving Infarction | ST elevation and peaked T waves...24hrs later: ST elevation with Q waves and loss of R waves |
| Reversible Ischemia | ST depression signifying ischemia of subendocardial injury REVERSED following nitroglycerin administration |
| Miscellaneous ECG Effects: Moderate Hyper K+ | Wide, flat P wave; Wide QRS; Peaked T wave |
| Miscellaneous ECG Effects: Extreme Hyper K+ | No P wave; Wide QRS |
| Miscellaneous ECG Effects: Moderate Hypo K+ | Flat T wave; U wave |
| Miscellaneous ECG Effects: Extreme Hypo K+ | Prominent U wave |
| Miscellaneous ECG Effects: Hypercalcemia | shortens repolarization; short Q-T interval |
| Miscellaneous ECG Effects: Hypocalcemia | prolongs repolarization; prolonged Q-T interval |
| Pericarditis | diffuse flate ST elevations across precordium w/reciprocal ST depression in aVR; Low amplitude R waves w/all leads affected |
| Sinus Arrhythmia | may be normal if regularly irregular and corresponds to breathing; IF irregular, irregular it is due to sick sinus rhythm secondary to CAD (varying rhythm w/ identical P waves) |
| Multifocal Atrial Rhythms | characterized by changing P wave morphology, indicating multiple atrial ectopic foci; If P wave is negative atrial pacemaker is in Left atrium; QRS conducts normally, although irregular, irregular rhythm |
| Atrial Fibrillation | atrial "bag of worms" w/multiple atrial foci creating artificial baseline w/o P waves; Rhythm is always irregular since only random impulses reach the AV node; Rhythm may be tachycardic or bradycardic |
| Premature Rhythms | premature atrial contractions, premature AV nodal contractions, Premature Ventricular contractions |
| Atrial Premature Beats (PACs) | premature ectopic atrial focus that produces different morphology P wave that originates early; AV node picks up and transmits impulse normally |
| AV Nodal Premature Beats | Premature ectopic foci originates from AV node; Complex will have no P wave, but the QRS will be conducted thru the normal bundle branch system |
| Premature Ventricular Contraction (PVCs) | ectopic focus originates from ventricle (thus, no P wave); generally a wide complex d/t myocardial conduction instead of BB conduction; there is a compensatory pause afterwards |
| PVC Properties | may be multifocal or unifocal; they may be coupled w/normal beats; if RIR - may name based on occurrence; may be isolated or occur in runs (mulit/unifocal) |
| A PVC Run of 4 or more: | Ventricular Tachycardia (v-tach) |
| When do we worry about PVCs? | when there's more than 6/min; Multifocal PVCs; long runs of PVCs (esp if they don't perfuse); PVCs that fall on T waves |
| Escape Beats | Atrial Escape Beats, AV Nodal Escape Beats, Ventricular Escape Beats, Sinus Arrest |
| Atrial Escape Beats | occur after a pause; P wave morphology is different d/t ectopic foci; Atria become "impatient" with lack of sinus beat |
| AV Nodal Escape Beats | after pause, NO atrial ectopic focus fires, so AV fires; QRS appears normal d/t normal AV node - bundle branch conduction |
| Ventricular Escape Beats | ventricles fire if atria or AV node do not fire after sinus pause; essentially identical to PVCs (only w/o being premature) |
| Sinus Arrest | during sinus pause, no new ectopic pacemaker fires; the sinus node may send out an escape beat after 2 cycles have been missed |
| Tachyarrhythmias | supraventricular tachycardia, ventricular tachycardia, atrial flutter, ventricular flutter, ventricular fibrillation |
| Supraventricular Tachycardia | may originate in AV node or atria; Generally RIR; rate usu >150; |
| Supraventricular Tachycardia: Paroxysmal Atrial Tachycardia (PAT) | if P waves are discernable |
| Supraventricular Tachycardia: Paroxysmal Nodal Tachycardia (PNT) | if no P waves are discernable |
| Atrial Flutter | atrial ectopic pacemaker is firing at 250-350bpm! P waves identical to unifocal atrial pacemaker; Only occasional atrial stimuli will fire the ventricle; Named for the block (2:1, 3:1, etc) |
| Ventricular Tachycardia | ventricular ectopic pacemaker; rate >150; run of 4+ PVCs; highly UNSTABLE rhythm |
| Ventricular Flutter | produced by single ectopic ventricular focus; rate bts 200-300bpm; highly UNSTABLE rhythm |
| Ventricular Fibrillation | multiple ventricular foci causing chaotic twitching of ventricles; ventricular "bag of worms;" there is no effective pumping or cardiac output! |
| Asystole | complete lack of electrical activity and pumping of heart; along w/V-fib it is considered Cardiac Arrest; not always a perfectly flat line |
| 4 Major Behavioral Risks that can be modified | Smoking (cigar, cigarette, marijuana, pipe, etc); Diet (trans-fat consumption, inc produce, low CHO/switch to whole grains); Exercise (CV fitness); Weight control (BMI <30, ideally <25) |
| Tobacco dependence | a chronic disease that deserves treatment for users willing to quit, unwilling to quit and former users; the most effective intervention tool to reduce illness, prevent death, and increase quality of life |
| Patients willing to quit using tobacco: treat with the "5 As" | Ask, advise, assess, assist, arrange |
| Patients unwilling to quit tobacco at this time should be treated with the "5 Rs" motivational intervention | relevance, risks, rewards, roadblocks, repetition |
| Patients who recently quit tobacco should be provided with | relapse prevention treatment |
| Counseling/behavioral therapies found effective for tobacco cessation | practical counseling (problemsolving/skills training); social support (intra-treatment); secure social support outside treatment (extra-Tx social support) |
| Smoking | the single most damaging acquired behavior, 75% of alll lung cancers can be prevented |
| Surgeon General Report on Diseases Associated with Smoking | SOB, exacerbationo of asthma, harm to pregnancy, impotence, infertility, inc serum CO; MI, stroke, cancers (lung, oral, larynx, pharynx, esophagus, pancreas, bladder, cervix); COPD; lung cancer/heart disease in family (low birth weight, SIDS, OM, URI/LRI) |
| Why is smoking a difficult habit to break? | psychological, chemical, social dependence |
| Prevention/Cessation Strategies | counseling, nicotine replacement therapy (NRT), *Combo of both is BEST;* 80% will need to "quit" more than once |
| Counseling: Prevention | usu targeted at schools (peers, advertising); more of a public health issue w/questionable success rate |
| Counseling: Cessation | assessment with 5As and 5Rs |
| 5As: Ask | identify and document tobacco use status for every pt at every visit |
| 5As: Advise | in a clear, strong, personalized manner, urge every tobacco user to quit |
| 5As: Assess | is the tobacco user willing to make the quit attempt at this time? |
| 5As: Assisst | for the pt willing to make a quit attempt, use counseling and pharmacotherapy to help him/her quit |
| 5As: Arrange | schedule follow-up contact, in person or by telephone, preferably w/in the first week after the quit date |
| Smoking Cessation Counseling | ID the problem (how many cigarettes are too many? 1); Compute pack years (2packs/day for 10yrs = 20pack years...document) |
| Smoking Cessation Counseling: Cold turkey | is pt really capable? this is the toughest way; if it fails they will lose their will power; try to convince them not to do it cold turkey |
| Smoking Cessation Counseling: Establis | a gradual decrease in consumption followed by an exact quit date; make a contract; be prepared to repeat |
| Smoking Cessation Plan | remove all cigs from house and ration them out per day; tell people you are quiting for moral support; replace oral stimulation w/sugarless gum; find a support person/group; call Dr if you break contract (usu 4 wks, w/ a decrease in consumption each week) |
| Nicotine Replacement Therapy | done w/patches, inhaler, nasal spray or gum with stages of nicotine concentration (21mg, 14mg, 7mg); Begin replacement after quit date to avoid incorrect usage |
| Other Smoking Cessation Pharmacotherapy | First-line Bupropion (wellbutrin); 2nd line - Clonidine, Nortriptyline; these are categorized as anti-depressants that have been shown to decrease cravings/desires |
| Dieting | think of diets as either losing weight or maintaining neutral wieght; exercise is not a substitute for dieting |
| Body Mass Index | current standard for determining obesity; weight in kg/height in meters^2 |
| Weight loss plans | you can lose weight w/o exercise, but it helps on many levels |
| Low fat diet: | label reading and difficult eating regimen |
| Low CHO diet: | label reading, some degree of regimented eating |
| Low caloric intake diet: | simple plans, easy to follow, but poorly sustainable |
| Approach to weight loss | same as w/smoking cessation; ID eating habits (actual food consumed); discuss options w/pt (rapid loss, gradual, strict regimen, less intense, etc); establish a plan with a contract |
| Role of insulin | most powerful stimulator of CHO metab/fat storage default; most powerful antagonist of catabolic processes (glycolysis, gluconeogenesis); you cannot lose weight when insulin is ciruculating in blood stream (tough for diabetics/cortisol pts) |
| Low fat diet | eliminate as many fats as possible (esp trans and saturated); ZONE and South Beach programs; distractors: it's very hard to find food w/o fats (must prepare at home); poor efficacy, slow; intense label reading |
| Low caloric intake | starvation concept; <2000cal/day usu achieves wt loss (1250cal/day = 1kg dec in 2wks); Slim Fast, Optifast, Weight Watchers; Benefits - quick wt loss, support grps; Distractors: had to maintain; Weight Watchers provides very gradual results |
| Low Carbohydrate | Atkins or Atkins-like; does not raise cholesterol levels; Benefits - produces moderate rate of wt loss; large variety of flavorful foods (best for diabetics dt minimal effect on insulin); Distractors - requires complex learning curve/label; not vegetarian |
| Pharmacotherapy for Weight Loss: Phenteramine | metabolic stimulant; can use up to 60 days |
| Pharmacotherapy for Weight Loss: Sibutramine | anti-depressant; reuptake inhibitor of seratonin and NE; found to have independent wt loss properties |
| Pharmacotherapy for Weight Loss: Orlistat | inhibits lipase in intestine (sits in intestines to force fats thru GI; Diarrhea side effect cause many pts to quit |
| Guidelines for Activity Prescription | meet safety, effectiveness, education/motivation criteria; appropriat warm-ups and cool-downs should be emphasized; appropriate "prescriptions" should pay attention to conditions that may worsen during certain activities |
| FITT Principle: Frequency | 3-5 days/wk; be careful to establish a regular habit before recommending levels that may not be sustainable in long term |
| FITT Principle: Intensity | to avoid musculoskeletal injury and promote compliance; start low-moderate intensity and gradually progress over wks/months to more vigorous efforts; increase duration rather than intensity to optimize caloric expenditure |
| FITT Principle: Time | 30-60min using gradual progression (ex: multiple short bursts are as good as single long bout) |
| FITT Principle: Type | low-impact activites that are convenient, accessible, and perceived as enjoyable by the participant (walking, cycling, aerobics, water exercise) |
| FITT: improve cardiorespiratory fitness in healthy, overweight, or obese adults - moderate intensity | estimated using 55-70% of age-predicted maximal heart rate |
| Strength/Resistance Training | recommended as adjunct to aerobic conditioning bc is assists in maintaining BMR and imp strength and performance of activities of daily living; 3-5x/wk with 1 set of 8-15 repetitions with 8-10 different exercises for all major muscle groups |
| Daily Lifestyle Activities | should be emphasized to inc overall physical activity levels and energy expenditure (climbing stairs, walking greater distances, gardening, house cleaning) |
| The most common cyanotic heart disease occurs from a single event | Tetralogy of Fallot; dt undivided chambers/outlet from bulbus cordis (normally v-septum is composed of 2 segments from top and bottom/fusion in middle; failure of outlet septum causes VSD, pulmonary stenosis, overriding aorta, R ventricular hypertrophy) |
| Angiogram of Tetralogy of Fallot | right cath; R --> L shunt thru VSD; pulmonary stenosis visualized; deox blood passes into aorta (the problem is that too much deox blood is being circulated to body and not to lungs) |
| Most common cyanotic newborn disease | Transposition of the Great Arteries; aorta from R ventricle, pulmonary artery from L ventricle; sets up 2 completely independent circuits and baby's O2 saturation is practically 0 (exception: patent foramen ovale); |
| Transposition repair | aorta and pulmonary aa are switched; opening in atrial septum is closed; patent ductus arteriosus is divided and closed off; coronary arteries are re-implanted |
| Truncus arteriosus | pulmonary aa arise from aorta; truncal valve (occasionally quadracuspid, stenotic or insufficient) overrides the VSD; VSD is extremely large and lungs get flooded w/blood |
| Tricuspid Atresia | cyanotic; atretic (missing) tricuspid valve; hypoplastic R ventricle; atrial septal defect; pulmonary stenosis; *there is only one pumping chamber; surgery bypasses R ventricle and vena cava is connected to R pulmonary artery; L ventricle dilates |
| Total anomalous pulmonary venous return | pulmonary veins drain below the diaphragm and are obstructed; atrial septal defect |
| Acute Rheumatic Fever | systemic (heart/joints/skin/CNS/SQ tissues) infam dx; delayed/dt pharyngeal GAS infxn; its greatest significance relates to the heart (acute and chronically) |
| Worldwide impact of ARF | declining in developed world except in lower socioeconomic groups and developing nations |
| How is diagosis of ARF established?? | Jones Criteria; 2 major or 1 major + 2 minor; mimetic flares |
| Major Jones Criteria Manifestations | carditis, polyarthritis, chorea, E. marginatum, SQ nodules |
| Supporting evidence of antecedent GAS infection | + throat culture or rapid strep antigen test; elevated or **rising antibody titer** |
| Minor Jones Criteria Manifestations | Clinical findings (arthralgia, fever); Lab findings (inc ARP, ESR, CRP), prolonged PR-interval (1st degree AV block) |
| The easier way to remember Jones Criteria for ARF: J-O-N-E-S | joints, carditis (o looks like heart), nodules, erythema marginatum, sydenham's chorea |
| The role of GAS infxn is supported by the following observations: | ARF outbreaks follow epidemics of strep throat/scarlet fever (both GAS); Tx of strep throat dec incidence of ARF; antimicrobial prophylaxis prevents recurrence in known ARF pts; most pts have elevated antistrep Abs (ASO, hyaluronidase, streptokinase) |
| How does GAS cause ARF? | infxn damages immune response by host; involves microbial antigens cross-reacting w/target organs (molecular mimicry); M-protein is good for detecting Ab production against cardiac myosin/sarcolemmal membrane and acute rheumatic heart disease |
| ARF relationship w/clinical and lab criteria | latent period of 18days; 25% have pos throat culture; rapid GAS antigen test is specific but not sensitive; only a rising/peaking titer distinguishes infxn from carrier state; 1/3 of pts don't recall prior illness |
| Specific antibodies to confirm ARF | ASO (80% of pts); anti-DNAse B; anti-streptokinase, antihyaluronidase, anti-DNAse; normal range depends on pts age, geographical location, epidemiological state, time of year; If >2 Abs are present the likelihood of disease inc |
| ARF clinical findings | Arthritis (most common; migratory/asymmetric; responds to ASA/NSAIDs); erythema marginatum (flat enlarging macule rings); Subcutaneous nodules (usu over boney prominences in kids); Sydenhams' Chorea (face, arm movements; girls); Carditis (young pts) |
| ARF Carditis suspected by: | pericarditis, cardiomegally, CHF - R or L; mitral/aortic regurgitation murmurs (mitral stenosis, cor pulmonale); Carey-Coombs Murmur |
| Carey-Coombs Mumur | dt mitral valve disease |
| Austin-flint murmur | when aortic valve has murmur too |
| ARF Carditis Specific Abnormalities | EKG has elevated P or T wave; Increased quality of heart sounds; Sinus tachycardia; Arrhythmia or ectopic beats; 1st degree AV block dt prolonged PR interval |
| Rheumatic heart disease | pay attention to mitral valve and L atrium; complication of atrial fibrillation is thrombus formation and emboli; mitral regurgitation |
| Myocardial aschoff body | elongated irregular multinucleated cells surrounded by palisading cells dt chronic inflammation; no microbe present; Pathognomonic for ARF |
| Differential for ARF | RA, osteomyelitis (fever/bone/joint pain); endocarditis, chronic meningococcemia dt sydenham's chorea; SLE; Lyme disease (erythema chronica migrans); sicke cell anemia |
| Complications of ARF | CHF in severe cases; Rheumatic heart disease; arrhythmia, pericarditis w/effusion; rheumatic pneumonitis |
| Treatment of ARF | ASA, PCN, CS; Prevention/prophylaxis of recurrent ARF - PCN, Sulfonamides/erythromycin |
| Prognosis of ARF | initial episodes (months in kids, wks in adults); 1-2% immediate mortality; Persistant RHD (poor prognosis; 30% kids die in 10yrs, 60% have abnml valves, <10% have sx heart disease) |
| Secondary prevention of RHD | continuous prophylaxis (controversial as to how long); PCN G for life; erythromycin; prophylactic antibiotics prior to invasive procedures incl dental surgery |
| RHD | results from single or repeated attacks of ARF; rigidity/deformity of valve cusps, fusion of commissures, shortend/fused chrodae dt valvular inflam; stenosis/insufficiency mostly mitral valve > aortic > tricuspid >>> pulmonary (very rare) |
| RHD details | Hx of ARF in 60%; 1st clue is murmur; echo; mitral valve; begin antigoag |
| Prophylactic antibiotics in moderate risk of significant bacteremia | dental procedures, GU procedures; lower bowel endoscopy |
| Prevention of Recurrent ARF | PCN (parenteral or oral); Sulfonamides/Erythromycin (if PCN allergic); Ampicillin, Clindamycin, Cephalosporin, Azithromycin or Clarithromycin |
Created by:
bscaryp