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84 Cards in this Set
- Front
- Back
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Stroke Volume
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SV is the amount of blood ejected by the left ventricle during each systole. Variables include preload, afterload, heart rate, and contractility.
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Cardiac output
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The amount of blood pumped, in liters, from the left ventricle each minute.(CO=HRxSV)
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Preload
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Degree of myocardial fiber stretch at the end of diastole and just before contraction of the heart.
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Starlings Law
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The more the heart is filled during diastole (within limits) the more forcefully it contracts. However, excessive filling results in excessive LVED volume and pressure and a decreased cardiac output.
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Afterload
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Afterload is the pressure or resistance that the ventricles must overcome to eject blood through the semilunar valves into the peripheral blood vessels. The amount of resistance directly relates to arterial blood pressure. aortic compliance and total systemic vascular resistance affect afterload.
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Automaticity
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The ability of all cardiac cells to initiate an impulse spontaneously and repetitively
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Refractoriness
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Cardiac cells are unable to respond to a stimulus until they have recovered, or repolarized.
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Conductivity
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The transmitting of electrical impulses from cardiac cell to cardiac cell.
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Excitability
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The ability of a cell to respond to a stimulus by initiating and impulse (depolarization)
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Describe the relationship of the left ventricle to maintaining the blood pressure and adequate cardiac output.
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The left ventricle pumps oxygenated blood into the systemic arterial circulation. Proper functioning of the left ventricle ensures adequate CO, and adequate systolic and diastolic BP (Blood pressure = CO x peripheral vascular resistance)
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Three systems/mechanisms and external factors that regulate blood pressure.
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The nervous, renal, and endocrine systems. External factors that affect systolic pressure include cardiac output and arterial distention, diastolic pressure is affected by peripheral vascular resitance.
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Name three types of sensory receptors in the body that affect the autonomic nervous system in regulating the blood pressure.
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Baroreceptors, chemoreceptors, stretch receptors.
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The description of S1 and S2 refers to.....
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First and second heart sounds
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An S3 or S4 that is heard on auscultation of the heart refers to....
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Gallop
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The exchange of nutrients across the capillary membrane occurs primarily by three processes:
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Osmosis, filtration, and diffusion
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Blood pressure is?
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The force of blood exerted against the vessel walls.
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Homocysteine
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Is an amino acid that is produced when proteins breaks down.Elevated values may be an independant risk factor for the development of CVD.
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Electrolytes that affect cardiac rythem.
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Potassium, clacium, magnesium
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Electrolytes that influence fluid balance and acid base status.
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Sodium, chloride, carbon dioxide
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Purkinje cells
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Responsible for the rapid conduction of electrical impulses throughout the ventricles, leading to ventricular depolarization and ventricular muscle contration.
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P wave
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represents atrial depolarization
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PR segment
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Represents the time required for the impulse to travel through the AV node, where it is delayed, and through the bundle of His, bundle branches, and purkinje fiber network, just before ventricular depolarization.
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PR interval
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Represents the time required for atrial depolarization as well as impulse travel through the conduction system and Purkinje fiber network, inclusive of the P wave and PR segment. It is measured from the beginning of the P wave to the end of the PR segment. (measures 0.12 to 0.20)
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QRS complex
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Represents ventricular depolarization and is measured from the beginning of the Q (or R) wave to the end of the S wave.
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QRS duration
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the time required for depolarization of both ventricles. Its usually 0.04 to 0.10
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ST segment
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Represents early ventricular repolarization
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J point
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Represents the junction where the QRS complex ends and the ST segment begins
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T wave
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represents ventricular repolarization
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U wave
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represents late ventricular repolarization
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QT interval
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Represents the total time required for ventricular depolarization and repolarization and is measured from the beggining of the QRS complex to the end of the T wave
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Purkinje cells
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Responsible for the rapid conduction of electrical impulses throughout the ventricles, leading to ventricular depolarization and ventricular muscle contration.
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P wave
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represents atrial depolarization
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PR segment
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Represents the time required for the impulse to travel through the AV node, where it is delayed, and through the bundle of His, bundle branches, and purkinje fiber network, just before ventricular depolarization.
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PR interval
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Represents the time required for atrial depolarization as well as impulse travel through the conduction system and Purkinje fiber network, inclusive of the P wave and PR segment. It is measured from the beginning of the P wave to the end of the PR segment. (measures 0.12 to 0.20)
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QRS complex
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Represents ventricular depolarization and is measured from the beginning of the Q (or R) wave to the end of the S wave.
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Sinus Tachycardia
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greter than 100bpm. Usually does not exceed 160 and rarely reaches 180bpm.
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Sinus bradycardia
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Sinus node discharge is less than 60 bpm.
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Supraventricular Tachycardia
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Involves the rapid stimulation of atrial tissue at a rate of 100 to 280bpm with a mean of 170 bpm in adults and 200-300bpm in children.
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Atrial Flutter
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rapid atrial depolarization occuring at a rate of 250 to 350 times per minute.
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Aldosterone
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A hormone secreted by the adrenal cortex that stimulates the renal reabsorption of sodium and water and the renal excretion of potassium.The secretion of it is stimulated by either a decrease sodium level in the (ECF) or an increased sodium level in the urine.
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Antidiuretic Hormone (ADH)
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A hormone secreted from the posterior pituitary gland that increases the renal reabsorption of pure water and decreases urine output.
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Renin
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Renin acts on a plasma protein called renin substrate converting it to angiotensin I. Angiotensin I is then further converted into angiotensin II by an enzyme ACE.
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Angiotensin I
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The physiologically inactive form of angiotensin.
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Angiotensin II
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The physiologically active form of angiotensin. A protein with vasoconstrictive activity and stimulates aldosterone secretion from the adrenal cortex.
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Hypokalemia (Cardiovascular manifestations)
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variable pulse usualy rapid, thready, weak. Peripheral pulses difficult to palpate, orthostatic hypotension. ECG: ST depression, inverted T wave, Prominent U wave, Heart block.
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Hyperkalemia (Cardiovascular manifestations)
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Irregular HR usualy slow, decreased bp,ECG: Tall T waves, widened QRS complexes, prolonged PR intervals, Flat P waves. Ectopic beats. Late: dysrhythmias, ventricular fibrillation, cardiac arrest in diastole.
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Hyponatremia (Cardiovascular manifestations)
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Normovolemic: rapid pulse rate, normal bp. Hypovolemic: Rapid pulse rate, thready and weak, hypotension, central venous pressure normal or low, flat neck veins in supine position. Hypervolemic: Rapid, bounding pulse, central venous pressure normal or elevated, bp normal or elevated.
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Hypernatremia (Cardiovascular manifestations)
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Decreased myocardial contractility, diminished cardiac output, HR and BP respond to vascular volume.
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Hypocalcemia (Cardiovascular manifestations)
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Decreased hr, decreased myocardial contractility, diminished peripheral pulses, hypotension, ECG: prolonged ST interval, prolonged QT interval.
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Hypercalcemia (Cardiovascular manifestations)
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Increased hr, increased bp, bounding full peripheral pulses, ECG: Shortened ST segment, widened T wave. Potentiation of digoxin-associated toxicities, decreased clotting time. Late phase: bradycardia, cardiac arrest, sinus arrest.
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Hypophosphatemia (Cardiovascular manifestations)
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Decreased contractility, cardiomyopathy (reversible)
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Hypomagnesemia (Cardiovascular manifestations)
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ECG: Tall T waves, depressed ST segments. Dysrhythmias: ectopic beats, ventricular tachycardia, ventricular fibrillation. Hypertension.
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Common causes of Pulseless electrical activity
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hypovolemia, hypoxia, acidosis, hyperkalemia, hypokalemia, hypothermia, drug overdose, tension pneumothorax, coronary or pulmonary thrombosis, and cardiac tamponade.
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Primary pacemaker of the heart
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SA node (60-100)
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The electrical impulse of the heart moves through the ventricles from the....
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Bundle of His, right and left bundle branches, Purkinje fibers.
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Sequential order of the cardiac tissues that assume the cardiac pacemaker's role if the sinoatrial node fails to function...
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AV node, Bundle of His, Purkinje
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Class I Dysrhythmia drugs
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Class I are membrane stabilizing agents. Type IA: moderately slow conduction and prolong repolarization, Quinidine sulfate, Procainamide hydrochloride, Disopyramide phosphate, Type IB: shorten repolarization, Lidocaine, Mexiletine hydrochloride, Tocainide hydrochloride. Type IC: slow conduction and widen the QRS complex, Flecainide acetate, Propafenone hydrochloride
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Class II Dysrhythmia drugs
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Control dysrhythmias associated with excessive beta-adrenergic stimulation by competing for receptor sites and theryby decreasing heart rate and conduction velovity. Propranolo hydrochloride, Acebutolol hydrochloride, Esmolol hydrochloride, Sotalol hydrochloride.
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Class III Dysrhythmia drugs
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Lengthen the absolute refratory period and prolong repolarization and the action potential duration of ischemic cells. Amiodarone hydrochloride, Ibutilide, Dofetilide.
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Class IV Dysrhythmia drugs
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Impede the flow of calcium into the cell during depolarization, therby depressing the automaticity of the SA and AV nodes, decreasing the HR, prolonging the AV refractory period and conduction. Verapamil hydrochloride, Diltiazem hydrochloride.
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Various Dysrhythmia drugs
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Digoxin, Atropine,Adenosine, Magnesium sulfate.
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Bigeminy
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Exists when normal complexes and premature complexes occur alternately in a repetitive two beat pattern, with a pulse occuring after each premature complex so that complexes occur in pairs.
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Trigeminy
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A repetitive three-beat pattern, usually occuring as two sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating itself in triplets.
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Quadrigeminy
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Repetitive four-beat pattern, usually occuring as three sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating itself in a four-beat pattern.
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Sinus Tachycardia treatment
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Treat underlying cause. If pt has angina give O2, rest, administer nitroglycerin or morphine as ordered. Beta-adrenergic blocking agents may also be prescribed for client with inappropriate sympathetic nervous system stimulation.
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Sinus Bradycardia treatment
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Treatment is necessary only if the client is symptomatic (has hypotension, diaphoresis, chest discomfort or pain, pulmonary congestion, or altered LOC): Atropine, ocygen, pacemaker, avoid parasympathetic stimulation.
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PAC treatment
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Correct underlying problem: anxiety, stress, caffine. Medication: propranolol, sedatives.
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Supraventricular rhythms treatment
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Correct underlying problem: CHF, COPD, asthma, stress, drugs. Medication: diltiazem, adenosine, digitalis, propranolol, esmolol, amiodarone. Vagal stim with carotid massage, valsalva maneuvers, overdrive atrial pacing, synchronized cardioversion.
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PVC and ventricular tachycardia (not sustained) treatment
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Correction of underlying problem: infection, electrolye, drugs, MI, hypoxia, CHF, stress, fatigue, or nicotine. Meds: Lidocaine bolus and infusion, procainamide bolus and infusion, magnesium sulfate infusion, class I and II antidysrhytmics, Amiodarone.
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Atrial Flutter treatment
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Medication:Oxygen, Diltiazem, Amiodarone, propranolol, esmolol, ibutilide, digitalis. Atrial overdive pacing, cardioversion, catheter or surgical ablation.
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Atrial Fibrillation treatment
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Medication: Amiodarone, diltiazem, ibutilide, verapamil. Anticoagulation, atrial overdrive pacing, cardioversion, surgery
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Sustained Ventricular Tachycardia treatment
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Medication: lidocaine bolus and infusion, procainamide bolus and infusion, amiodarone, magnesium sulfate infusion. If unstable: synchronized cardioversion. If pulseless: d-fib, CPR
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Ventricular Fibrilation treatment
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D-fib, CPR, Medication: vasopressin, epinephrine, amiodarone, magnesium sulfate.
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Ventricular asystole treatment
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CPR, medication: epinephrine, atropine, pacemaker.
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Medications used for cardiac arrest?
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Epinephrine, Amiodarone hydrochloride, Dopamine hydrochloride, Dobutamine hydrochloride, Norepinephrine, Sodium bicarbonate, Isoproterenol, Calcium chloride, Vasopressin.
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Drug of choice for symptomatic bradycardia
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Atropine
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High-Output Failure
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Occurs when cardiac output remains normal or above normal. High-output failure is caused by increased metabolic needs or hyperkinetic conditions, such as septicemia (fever), anemia, and hyperthyroidism.
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Key features of Left sided heart failure
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Decreased cardiac output: fatigue, weakness, oliguria during the day,angina, confusion, restlessness, dizziness, tachycardia, palpatations, pallor, weak peripheral pulses, cool extremities. Pulmonary congestion: hacking cough worse at night, dyspnea/breathlessness, crackles or wheezes in lungs, frothy pink tinged sputum, tachypnea, S3/S4 summation gallop.
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Key features of Right sided heart failure
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Systemic congestion: JVD, enlarged liver and spleen, anorexia and nausea, dependant edema (legs and sacrum), distended abdomen, swollen hands and fingers, polyuria at night, weight gain, increased blood pressure (from excess volume) or decreased blood pressure (from failure)
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Compensatory mechanism for increased cardiac output: SNS-adrenergic receptors
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Action: increased HR (beta adrenergic) and blood pressure from vasoconstriction (alpha-adrenergic). There is also increased venous return to the heart, which stretches the myocardial fibers. This increased stretch is a preload that makes a more forceful contraction, increasing stroke volume and CO. Long term effects: Increased oxygen demand; increased afterload, which is the resistance against which the heart must pump: too much myocardial stretch (preload)
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Compensatory mechanism for increased cardiac output: Cardiac hypertrophy
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Action: The walls of the heart become thick, increasing muscle mass and increasing the force of contraction. Long-term effect: The heart cannot meet the increased oxygen demand that hypertrophied condition requires.
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Compensatory mechanism for increased cardiac output:Hormonal response
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Action: Activates the renin-angiotensin system, which raises the blood pressure by increasing fluid retention and vasoconstriction. Long term effect: This eventually increases the stretch (preload) and the resistance (afterload). Ventricular remodeling may develop.
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Left Heart failure Systolic ventricular dysfunction
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Definition: Left ventricle is unable to contract forcefully. LV is unable to eject blood adequately into the circulation. Effect on System: Cardiac output decreaes. Symptoms of inadequate tissue perfusion, pulmonary and systemic congestion occur.
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Left Heart failure Diastolic ventricular dysfunction
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Definition: Left ventricle is unable to relax during diastole; this prevents the ventricle from filling. Effect on system: Diminished tissue perfusion and decreased cardiac output. Symptoms similar to those of systolic dysfunction.
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