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| Spontaneous electrical impulse generation. Performed by P cells |
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| Waveform having two distinct phases; partly positive and partly negative from the isoelectric line |
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| receive and conduct electrical stimulus. Performed by cardiac cells. |
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| Movement of ions across the cell membrane that causes the inside of the cell to become positive |
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| Impulse originating from a source other than the sinoatrial (SA) node |
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| Ability of the cell to respond to an outside stimulus |
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| Small bundle of nerve fibers |
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| Having a uniform size and shape |
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| The premature activation of part of the ventricle due to transmission of impulses along an accessory pathway that is not subject to the normal delay of the atrioventricular (AV) node. Travels to the ventricles via a pathway other than the AV node or bundle of HIS |
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| Condition in which an impulse returns to stimulated tissue that was previously depolarized |
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–Records the difference in voltage between the left arm (LA) and right arm (RA) electrodes (Lead I = LA minus RA) –Is horizontal. Left pole (LA) is positive and right pole (RA) is negative |
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–Records the difference in voltage between left leg (LL) and right arm (RA) electrodes (Lead II = LL minus RA) –Points diagonally downward. Its lower pole (LL) is positive and its upper pole (RA) is negative |
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–Records the difference in voltage between left leg (LL) and left arm (LA) electrodes (Lead III = LL minus LA) –Points downward. Lower pole (LL) is positive and its upper pole (LA) is negative –Einthoven’s triangle: graphic representation of standard limb leads |
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| Atrial enlargement is produced by |
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| increased atrial work or volume overload. |
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| Ventricular enlargement is caused by |
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| clinical conditions that increase the workload of the ventricle or volume overload. |
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–Notched or M shaped P wave in leads I, II, aVL (P mitrale) –Small initial upstroke of the P wave in V1 with a deep terminal negative deflection –P wave width of 0.11 seconds |
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| Right atrial enlargement (RAE) |
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–Tall peaked P waves (P pulmonale) –>2.5mm in inferior leads –Tall initial upstroke of the P wave in V1 and a terminal negative deflection –Width remains normal |
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| Right Ventricular Enlargement |
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–Right axis deviation –R wave in V1 exceeds the depth of the S wave –R wave in V1 is >7mm and >5mm in aVR –Delayed intrinsicoid deflection –RSR’ pattern in lead V1 –QRS width 0.10 seconds –Reversed R wave progression in V1-V6 |
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| Left Ventricular Enlargement |
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–Left axis deviation –R wave voltage >11mm in lead I and aVL –R wave voltage >26mm in lead V5-V6 –Height of the R wave in V5-V6 plus the depth of the S wave in V1 > 35mm –QRS is prolonged and increases in amplitude –R wave grows taller |
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| Right Bundle Branch Block (RBBB) |
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–Conduction system delay through the right bundle branch of the ventricular conduction system –QRS >0.12 seconds –RSR’ pattern with final R in V1 –QRS pattern with final wide S in V6 –Right chest lead will show T wave inversion –Complete RBBB, QRS >0.12 seconds –Incomplete RBBB, QRS 0.10 to 0.12 seconds |
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| Left Bundle Branch Block (LBBB) |
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–QS pattern > 0.12 seconds in V1 –Wide tall R wave in V6 –Septal depolarization is right to left |
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| Left Anterior Hemiblock (LAH) |
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•Branch of the LBBB •Mean QRS axis of -45 degrees or more (left axis deviation) •S wave in aVF equals or exceeds the R wave in lead I •Deep S wave in lead II •Basically: LAD + negative QRS in lead II •QRS usually <0.12 seconds |
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•Posterior branch of the LBBB •Mean QRS axis of +120 or greater (right axis deviation) •Tall R wave in lead II •Basically: RAD + tall R wave in lead II •QRS < 0.12 seconds •Rule out RVH or lateral wall MI before making this diagnosis |
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| Hyperkalemia (>9.0 mEq/L) |
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•Loss of P waves •Wide QRS (to the point of looking like a “Z”) •Sine waves •Ventricular fibrillation leading to death |
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| Hyperkalemia (>5.5 mEq/L)- |
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•Tented tall T waves •AV block •Flattened P waves and long PR interval •Slow ventricular conduction (wide QRS) |
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•U waves prominent •Ventricular ectopy •Ventricular tachycardia |
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–Prolonged PR interval –Shortened QT interval and ST segment –Ventricular arrhythmias may occur if severe imbalance –Increased risk for digitalis toxicity |
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–QT prolongation with increased risk for arrhythmias (torsades de pointes) –Prolonged ST segment, normal T wave morphology |
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| Hypermagnesemia (>2.5 mEq/L) |
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•Prolonged PR interval •Widened QRS complex •Tall T waves •Atrioventricular block •Cardiac arrest |
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| Hypomagnesemia (<1.5 mEq/L) |
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•Prolonged QT and PR interval •ST segment depression •Premature ventricular complexes (warning signs!!) •Torsades de pointes |
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| Radiographic visualization of blood vessels after injection of a radiopaque substance |
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| Volume of blood ejected from the left ventricle in one minute |
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| Decreased blood flow to the myocardium due to obstruction of the inflow of arterial blood |
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| Maximum heart rate (target heart rate) |
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| Age-related, estimated value representing the number of beats per minute when the heart is working at its maximum capacity |
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| Stress test in which the heart is exercised (stressed) pharmacologically, or via cardiovascular exercise, and an injected radionuclide tracer is used to image the heart |
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| Delivery of nutritive arterial blood flow to the capillary bed of an organ or organs |
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| Diagnostic electrocardiographic test which indirectly reflects arterial blood flow to the heart before, during, and after a controlled period of increasingly strenuous exercise |
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| Technetium-99m sestamibi (Cardiolite) |
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| Preferred radionuclide preparation for nuclear stress testing |
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| Radionuclide used in nuclear stress testing |
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| Three mechanisms to control muscle blood flow |
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•Local regulation •Nervous system regulation •Humoral regulation |
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of blood flow in each individual tissue is controlled mainly in proportion to that tissue’s need for perfusion •Cells release vasodilator substances in response to low oxygen supplies i.e. potassium ions, hydrogen ions, CO2, lactic acid, and adenosine |
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| Nervous System Regulation |
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of blood flow which affects large segments of the systemic circulation shifts blood from nonmuscular vascular beds to the muscles during exercise •Vasomotor center sends increased sympathetic impulses to veins that serve as blood reservoirs (abdominal organs such as liver, spleen, and also skin) resulting in vasoconstriction which permits the distribution of blood to the skeletal muscles. |
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of blood flow is due to various substances such as hormones, ions, and chemicals which are produced by various parts of the body in response to various effects such as sympathetic stimulation and changes in blood pressure . •These effects cause vasoconstriction/vasodilation of the vascular system. •Vasoconstrictor agents include Epinephrine, Norepinephrine, Angiotensin, Anti Diuretic Hormone (ADH) , and increased Calcium ion concentration. •Vasodilation agents include Kinin, Serokinin, Histamine, increased CO2, K+, Na+, Mg and decreased H. |
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| Resting musculature receives how much of the cardiac output |
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| Vasoconstricted areas (blood reservoirs) can make available an additional _________of blood to the muscle and greatly increases local blood flow. (in the active muscles) |
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| What is the primary purpose for cardiac stress test? |
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| Increase the oxygen requirements of the heart in order to unmask the presence of CAD. |
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| Absolute Contraindications for stress testing |
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•Acute febrile illness. •Acute ECG changes of myocardial ischemia. •Uncontrolled heart failure. •Pulmonary edema. •Unstable angina. •Acute myocarditis, pericarditis. •Uncontrolled hypertension –Above 250 mmHg systolic – 120 mmHg diastolic •Uncontrolled asthma. |
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| Relative Contraindications for stress testing |
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•Recent MI (less than 4 weeks). •Aortic valve disease. •Resting Tachycardia (above 120 BPM). •Severe electrolyte imbalance. •Thromboembolic disorders. •Resting ECG abnormalities. •Poorly controlled diabetes. •Epilepsy. •CVA. •Respiratory failure. |
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•A maximal, variable work load test where both the speed and angle on inclination (also called % grade) of the treadmill increase in discrete stages. •The patient walks or runs on the treadmill through stages which are progressive work loads. •The stages progress every 3 minutes until the patient reaches maximum exercise capacity (target heart rate) or an indication to stop the test develops. •(220 BPM - age) x 90% = HR |
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| •Usually used for post MI patients using Bruce protocol but starts at a slower pace. |
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•Not used very often. •Depends mainly on increases in angle of inclination at a constant speed with 2 minute stages. |
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| General signs and symptoms leading to termination of a stress test |
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•Severe chest pain suggestive of angina. •Severe dyspnea. •Dizziness or faintness. •Sudden onset of pallor and sweating. •Onset of cyanosis. |
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| ECG Signs to stop a stress test |
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•Frequent PVC’s (R-on-T, Short runs of VT) •Atrial Fibrillation when absent at rest. •2nd or 3rd degree block. •Ischemic changes –Marked ST depression, T wave inversion, Q wave appear. •Appearance of BBB pattern |
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| Blood pressure signs to stop a stress test |
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•Fall of systolic pressure below resting value. •Fall of more than 20 mmHg in systolic pressure after the normal exercise rise. •Systolic blood pressure in excess of 300 mmHg or diastolic pressure in excess of 140 mmHg. |
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| Indication for Nuclear stress testing |
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•To increase diagnostic detail for CAD in patients with high false positive results in cardiac stress testing. •Some believe that cardiac stress test results accuracy increases from 50% accuracy to 90% accuracy. |
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| Commonly used intravenous radionuclides for nuclear stress testing |
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•Thallium – 201 •Cardiolite •Sestamibi (generic for cardiolite, also methoxy isobutyl isonitrile or MIBI) •Technetium-99m (Tc99m) |
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| Thallium-201 Myocardial Perfusion Imaging |
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| assessment of relative differences in blood flow among cardiac segments using resting and exercise Thallium scanning. |
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| Major ST depression at low workloads indicates what? |
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| severe anterior wall ischemia |
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| ST elevation in II, III, and aVF |
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| severe inferior wall ischemia |
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| Exercised-induced increase in amplitude of the T wave in V2 is predictive of what? |
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| anterior wall ischemia (“Peaked T Waves”) |
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| Exercise-induced T wave inversion indicates what? |
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| ST segment elevation with an upward concavity is usually ________, especially when seen in healthy, asymptomatic individuals |
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| ST segment elevation with a downward convexity is usually indicative of what? |
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| Although ST elevation with an upward concavity and J point notching often reflects a normal variant, this is only true if the patient is asymptomatic. The same ST pattern in a patient with chest pain must be assumed abnormal and due to _____________ until proven otherwise |
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False Positive ST/T Changes |
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•Digitalis •Hypokalemia •Computer averaging •Increased sympathetic tone •Hyperventilation and orthostatic changes •Convex ST segment depression •ST segment variability (False Negative Test Results cannot be relied upon) |
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| may induce ST depression in patients with no CAD |
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| a common cause of false-positive ST depression |
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| If the ST depression is seen only in the inferior leads (II, III, and aVF) there is a good possibility of what? |
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| Atrial infarction is indicated by reciprocal elevation in opposite leads; inferior MI is usually evident |
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| Atrial infarction is indicated by reciprocal depression in opposite leads |
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| Prominent R wave in lead V1 |
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| Posterior wall MI is indicated |
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| Cardiac Disease Effect Major Prognostic Findings |
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•Significant ST segment depression beginning at low exercise intensity. •Angina pectoris during exercise, typical, convincing. •BP drop early •Short exercise time ( < 66% predicted). |
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| Cardiac Disease Effect Minor Prognostic Findings |
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•Minor ST segment depression. •Ventricular arrhythmia provoked by exercise. •Negative U wave appearing post exercise. |
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| abnormal Q waves in leads V4-V6 |
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| abnormal Q waves in at least two consecutive leads in V2-V4 |
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| abnormal Q waves in leads V1-V3(and sometimes V4) |
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| abnormal Q waves in leads I and aVL |
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| abnormal Q waves in at least two of leads II, III, and aVF |
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