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nrsg 212 2.3.2
O2 transport
| Question | Answer |
|---|---|
| Action potential: aka; this impulse initiates what; depolarization causes what; | electrical impulse; depolarization; cardiac contraction |
| what is a cardiac cycle | one systole + one diastole |
| what is the pacemaker of the heart | the SA node |
| conduction: the electrical impulse is initiated by what; what is location of SA node; what is beat of SA node | the SA node; SVC and RA; 60-100 |
| conduction: AV junction- what is beat; location; this will take over when what; | 40-60; atrial septum; the SA does not work; |
| conduction: Ventricles: what is the rate; what are they; this takes over when what | 30-40; bundle of his, R bundle branch, left bundle branch, purkinje fibers; AV node does not work |
| autonomic control: SNS- controls what in heart; what does it do to HR; what does it do to contractability; what does it do to nodes; does it vasocontrict or dialate; | all areas of the heart; increases it; increases; increases conduction to AV node; vasocontrict |
| autonomic control: SNS- this is aka; | fight or flight; |
| autonomic control: PSNS- what does this control in heart; what does it do to HR; what does it do to contractability; | SA, AV, and some ventricles; decreases it; decreases it; |
| what does Atropine do | it blocks the PSNS and so it increases HR |
| receptors: beta one controls what | the heart (we have one heart) |
| receptors: beta 2 controls what | the lungs (we have 3 lungs) |
| receptors: Alpha one does what | vasocontricts |
| receptors: alpha 2 controls what | tissues |
| what pt is contraindicated with beta blockers, beta blockers cause what to decrease the SNS or PSNS, when beta blockers decrease the SNS this does what | pt w/ heart block, severe hypotensioon; SNS; decreases the workload of the heart |
| Properties of heart muscle: what are they | excitabilty, automaticity, contractability, refractoriness, conductivity, |
| Properties of heart muscle: def-excitability; automaticity; contractability; | when the impulse starts to go through muscle it will start to work; impulse can be initiated any place in the Ht; Ht will contract |
| Properties of heart muscle: . def- refractoriness; conductivity | Ht has to repolarize to except a new impulse, can't receive a new impulse until the old one is finished; where ever the impulse came it can do alternate pathways to conduct impulse |
| Dysrrhythmias: Automaticity- what does a dysrrhythmia do to this; what causes these beats; | alteration on the normal rate, premature beats; ischemia, nicotine, caffeine, hyperkalemia, hypocalcemia, dig tox, atropine |
| Dysrrhythmias:conduction- what does dysrhythmias do to conduction; cause | speeds up the impulse thru the system; beta blockers, dig tox, MI, ischemia, scarring of conduction system, vagal stimulation |
| Dysrrhythmias: def of reentry | activation a second time by the same impulse |
| normal pathway of conduction is down and what | to the left |
| conduction and waveform: monitor picks up what; can the monitor tell the diff between skeletal and ht muscle | the electrical energy as it travels thru the heart on the surface of the body; no |
| list the pathway of conduction | SA node to av node to Bundle of His, the right and left bundle branches to purkinje fibers |
| where does SA node start at in ht | the atria |
| conduction and waveform: when energy travels towards the + electrode what is shown on paper; when energy travels away from the + electrode what is shown on the paper | upright deflection on paper; downward deflection on the paper |
| what is drug of choice for all slow rhythma | atropine |
| EKG Wave: what is it; def P; def Q; def R; def S; | P, QRS complex, t; atrial depolarization; 1st deflection of the QRS complex and is downward; first positive deflection occurring in the QRS; negative deflection that follows R wave |
| does everyone have a Q wave | no |
| EKG Wave: def QRS complex; def ST segment; def of T wave; def QT interval | ventricular depolarization; initial ventricular repolarization; ventricular repolarization; ventricular depo. amd repol. varies with rate, gender and age |
| in 12 lead EKG where is 2 Lead | the bottem strip |
| 2 Lead interprets what | rhythm |
| Rhythm interpretation: what are the steps in order; how is rate determined; how is rhythm assessed; | rate, rhythm, P waves, PR interval, QRS, ST segment, T wave, QT interval; how ever many seconds the strip is times it to make one min; from the r-r or p-p, assess all and see if regular; |
| Rhythm interpretation: how is the P wave assessed; how is PR interval assessed; how to assess the QRS interval; | is there one in front of every QRS complex and are they all the same; should be .12-.2 sec beginning from P to beg. QRS and measure all, it is <.12 sec onset of QRS to complettion of S to at width and sameness; |
| Rhythm interpretation: how is ST segment assessed; how to assess t wave; how to assess the QT interval | it is isoelectric- should be back to baseline; upright and a 1/3 of the height of QRS; < .4 second beginning of QRS to end of T wave |
| sinus Rhythms: aka; what is rate of it; what should be regular; what is PR; | normal sinus rhythm;60-100; r-r and p-p; .12 - .2 sec; < .12 seconds |
| Sinus Tachycardia: what is rate; cause; everything looks the same except what; what is done first before tx; | >100; SNS stimulation or decreased vagal nerve, increased temp, stress, decreased BP, heart failure, hypovolemia ;the rate is fast; assess |
| Any alteration of a rhythm is a what | dysrhythmia |
| Sinus Bradycardia: what is rate; what is cause; how is it treated; ex of treatment; what are s/s of symptomatic; what drugs cause this; | <60 bpm; increased vagal nerve, drugs, MI, hyperkalemia; note the cause; oxygen, atropine for symptomatic; dizziness, decreased Bp; beta blockers, calcium channel blockers, dig; |
| Atrial dysrhythmias: PAC- this stands for what; def; what is different; what is the same; | premature atrial contractions; early ectopic beat arising in the atria and interrupts the normal rhythm; Ps different; QRS the same; |
| EKG: P begins with the firing of what node; intervals between the waves reflect what; | the SA node; the length of time it takes for the impulse to travel from one area of the heart to another; |
| Atrial dysrhythmias: PAC- what do we treat; common tx | the cause; just assessment |
| Atrial dysrhythmias: PAC- when is it a PAT; | when there are 3or more consecutive PACs in a row; |
| Atrial dysrhythmias: PAT- s/s; why is BP decreased; | Pt does not feel good, SOB, chest pains, crackles in lungs; ht has no time to pump |
| Atrial dysrhythmias: PAT- how fast is heart rate; why is QRS normal; P wave is lost where; tx; | >150 bpm; bc it started in atrium; in the T wave before; carotid sinus massage, valsalva, adenosine, beta blockers, verapamil |
| Atrial dysrhythmias: Afib- def; what is irregular on EKG; what are s/s r/t; what is this pt increased risk for; | rapid caotic atrial depolarization NO atrial contraction; R-R wave,no identifiable p wave,normal QRS; heart rate; mural thrombi; |
| Atrial dysrhythmias: Afib- what contraction is not Happening; s/s; what chamber has increased risk for clot and why; what is TX; | atrial; chest pain,SOB, stasis of flow and can cause blood clot; L atrium b/c of the way it is built;coumadin |
| Atrial dysrhythmias: med Tx- name them; Adenosine is given to what dysrhythmia mostly; what does Adenosine do; what CCBs are given | oxygen, adenosine, calcium channel blockers, PATs; depresses SAand AV node activity; Cardizem,verapamil, digoxin |
| Atrial dysrhythmias: Afib- why are stroke pt admitted to telemetry; what is cause of Afib; def of mural thrombi; | b/c the stroke could of been caused by mural thrombi leading to stroke; badvalve, COPD, Coronary artery bypass, surgery, pulmonary emboli,alcoholics; clot in heart muscle |
| Heart blocks: AV blocks- def first degree; def 2nd degress; | all p wavesget thru the AV node;some p waves get through AV node,some don't |
| Heart blocks: AV blocks- 2nd degree has how many types; def of third degree; | type 1 and 2; no p waves get thru to the AV node |
| Heart blocks: AV blocks- 1st degree- what node is delayed; how long is PR interval; is QRS normal; is this a big problem | AV; > .20 sec; yes; no |
| Heart blocks: AV blocks- 2nd degree- type one: abnormally long what; what in EKG gets longer; the PR gets so long that what happens; is QRS normal; is p-p reg; is r-r reg; cause | refractory period in the AV node; PR; the QRS is dropped; yes; yes; no; vagal tone, MI, meds |
| Heart blocks: AV blocks- 2nd degree- type two: what node has a long refractory period; is PR interval the same; is p-p reg; is r-r reg; is pr reg; cause; tx; | AV; yes; yes; no; yes; meds, ischemia from MI; pacemaker |
| Heart blocks: AV blocks- 3rd degree- what node has no conduction; what is wrong with PR interval; what is regular; cause; | the AV node; there is no PR interval; p-p, r-r, qrs; MI conduction system changes, drug toxicity,dig, cardiomyopathy, viral infections, cardiac surgery |
| what imbalance in body can cause dysrhythmias | electrolyte |
| Heart blocks: meds- atropine- what does it do; what type of blocks does it work on | it blocks parasympathetic response; 1st degree, and 2nd degree type one |
| Ventricular dysrhythmias: PVC-aka; this is the most common what; caused by what; what causes firing of ectopic pacemaker; | premature ventricular contractions; dysrhythmia; firing of ectopic pacemaker in the ventricle; MI,myocardial ischemia, hypocalcemia, acidosis,ETOH, caffeine, nicotine, drugs, |
| Ventricular dysrhythmias: PVC- what does EKG look like; the seriousness of it depends on what; | p-p reg, r-r irregular, p waves present, pr same, qrs is wide; #/minute, #/consecutive, pairs, in presence of MI |
| Ventricular dysrhythmias: Vetricular tachycardia- def; is this life threatening; what is rate; what does EKG look like; cause; tx; | 3 or more PVCs in a row; yes; 110-220/ min; no p, no pr, QRS is > .12 sec; MI, CAD, dig tox acidosis, CHF; meds, cardioversion, defibrillation; |
| Ventricular dysrhythmias: VT or SVT- where is the origin of VT; where is origin of SVT; | in the ventricle; above the ventricle; |
| Ventricular dysrhythmias: V fib- is this life threatening; def; this can cause what very quickly; assess what; tx | yes; chaotic, rapid conduction, no ventricular contraction, no cardiac output, no pulse; sudden death; leads, pulse, LOC; defibrillation, meds |
| Ventricular dysrhythmias: meds- what meds not used anymore; | lidocaine, pronestyl; |
| Ventricular dysrhythmias: meds: epinephrine- stimulates what; is there a max to give | cardiac; no |
| Ventricular dysrhythmias: meds: vasopressin: high doses cause what; | vasoconstriction; |
| Ventricular dysrhythmias: meds: amiodarone- this is first choice why; b/c of long 1/2 life what does pt need to do; when is it given; what sudden side effects can it cause; | long 1/2 life, lots of side effects though; needs to have follow up for over a month;pulseless VT, VF after CPR defib andepi vasopressin; hypotension and vasodilation |
| Ventricular dysrhythmias: meds- mag sulfate- only given when; side effects; | when there is cardiac arrest; bradycardia, flushing, sweatin, hypotension |
| Asystole: is this life threatening; def; is there a pulse; is there cardiac output; can follow what other dysrhythmias; what can cause it; what is tx; is the outcome good | yes; total absence of electrical activity; no; no; heart block or VF; hypoxia, hyper or hypo kalemia; acidosis, OD, hypothermia; correct the cause; no |
| what are some nursing dx for dysrhythmias | activity intolerance, impaired mobility, fatigue, decreased cardiac output, risk for falls, knowledge deficit, tissue perfusion- ineffective, coping; |
| defibrillation: when is it done; is pt sedated; is it synchronized; where are paddles placed; what is assessed afterward; | in an emergency in VF and pulselessVT; no; no; upper chest to right of sternum, lower chest to left of nipple; rhythm, resume CPR, vital signs; |
| cardioversion: when is it done; is it synchronized; is pt sedated; | in emergency, or elective, Afib, aflutter, SVT; yes; yes |
| pacemakers: can they be temporary; can they be permanent; these are an artificial what; | yes; yes; SA node or purkinje system or both; |
| pacemakers: external- it is trans____; when is this type done; is this preferred by pt; where do lead wires attach | cutaneous; in emergency; no bc it is uncomfortable; external monitor outside of body |
| pacemakers: epicardial- where do lead wires attach; | to ht muscle after cardiac surgery and attached to an external generator; |
| pacemakers: endocardial: where do lead wires attach | in the ventricleand to a generator |
| pacemakers: why do ppl get them; | b/c they haveimproper rhythm; |
| pacemakers: endocardial- temporary- when is it done; how is it placed; | in emergency or elective; large vein into the inferior vena cava or into apex of right ventricle; |
| pacemakers: endocardial- permanent- where is it placed | superior vena cava int atria of r ventricle or apex of right ventricle |
| pacemakers: pacemakers work on demand meaning what; | it works when the heart is not working |
| pacemakers: permanent pacemaker classifications: what does o stand for; A for; V fr; D for; T for; I for; | none; atria, ventricle, dual, triggered, inhibited; |
| pacemakers: post op care for permanent- why is there an overnight stay; when is it reprogrammed; why is left arm slinged; how is pacemakers function checks | to monitor function; b4 discharge; b/c there should be no vigorious activity to arm for 6 wks; via phone |
| pacemakers: ICD- aka; what does it do; | implanted cardio-defibrillator; it paces and defibrillates and cardioverts |
| life vest: who wears it; this allows clinician what; when is not worn; | pt who is at sudden risk for cardiac arrest; time to assess the patient's needs for an ICD; while showering; |
| pottassiums effect on heart rhythm: hyperkalemia- what does t wave look like; what happens to QSR: what happens to P waves; pt may have what dysrhythmia; what happens to ST; | wide tall tented T wave; QRS is wide; small or absent; afib or VF; small or absent ST; |
| potasiums effect on heart rhythm: hypokalemia- what does T wave look like; what does U look like; what dysrhythmias can this cause; what does ST look like; | small or absent; U is big; 1st or 2nd degree block; it is depressed; |
| dig effects on heart rhythm: what happens to QT, what happens to ST; what dysrhythmias can it cause; | it is shortened; down sloping ST,; PAT, atrial tach with block, VT and VF |
| CPR adult: what is chest compressions to breaths ratio; what is compression rate; how long should breath be; should be very little pause for ventilation, why? | 30:2; 100/min; over one second, enough to make the chest rise; emphasis is on return to compression |
| AED/ Defibrillation: what is course of action; first shock eliminates what | defib one time and then CPR with rhytm checks every 2 min; VF 85% of the time |
| def of cardiac arrest | the absence of a pulse in the large arteries of an unconscious victim who is not breathing |
| EKG: the intervals between the waves (PR, QRS, and QT) reflect what; these intervals are measured and deviations from the norm reflects what | the length of time it takes for the impulse to travel from one area of the heart to another; pathology |
| def of systole | contraction of the myocardium |
| systole results of the ejection of blood from what | the ventricles |
| def of diastole | relaxation of the myocardim |
| diastole allows for what | filling of the ventricles |
| HR is primarily regulated by what | ANS |
| heart: def preload | the volume of blood in the ventricles at the end of diastole before the next contraction |
| heart: def of afterload; what is afterload effected by | the peripheral resistance against which the left ventricle must pump; size of ventricle, wall tension, and arterial blood pressure |
| is arterial blood pressure is elevated the ventricles do what | will meet increased resistance when ejecting the blood, increasing the work demand |
| increased work demand of the heart results in what | ventricular hypertrophy - enlargement of the heart |
| what is the only artery that carries de-oxygenated blood | pulmonary artery away from right ventricle |
| what is the only vein that carries oxygenated blood | the pulmonary vein to left atrium |
| the autonomic nervous system consists ofwhat | the SNS and PNS |
| ANS: simulation of PNS or SNS increases the hr, speed of impulse conduction through the AV node, and force of atrial and ventricular contractions | SNS |
| adrenergic receptors: where are they located; stimulation of these causes what | in vascular smooth muscle; vasocontriction |
| Baroreceptors: where are they located; they are sensitive to what; stimulation of these causes what | aortic arch, and carotid sinus; stretch or pressure in the arterial system; enhances the parasympathetic influence |
| chemoreceptors: located where; they can cause what; when these are stimulated it can cause what | in the aortic arch and carotid body; changes in BP and HR; increase in cardiac activity |
| def of BP, def of systolic BP; def of diastolic BP | a measure of the pressure exterted by blood against the walls of arterial systems; is the peak pressure exerted against the arteries when the heart contracts; residual pressure of the arterial system during ventricular relaxation |
| what is the invasive way to measure BP | a catheter is inserted into an artery and pressure is measured directly |
| def of pulse pressure | diff between the SBP and DBP |
| aging heart: cardiac valves become thicker and stiffer from what; these changes show in what s.s; turbulent blood across the effected valve results in what | lipid accumulation, degeneration of collagen and fibrosis; regurgitation of blood when the valveshould be closed; murmer |
| how is pitting edema assessed | from +1 mild to +4 very deep pitting |
| how are pulses graded | O- absent to 4+ bounding |
| what is the term for a palpated vibrating pulse | thrill |
| cap refill: with normal peripheral blood flow the cap refill will be how long | < 3 seconds |
| def of heaves | sustained lifts of the chest wall in the precordial area that can be seen or palpated, usually no pulse is felt here |
| stimulation of the vagus nerve causes what | a decreased rate of firing of the SA node, slowed impulse conduction of the AV node and decreased force of cardiac muscle contraction |
| def of ecletrocardiogram | the graphic tracing of the electrical impulses produced in the heart |
| EKG: how is wave form on the EKG produced | by the movement of charged ions across the membrane of the myocardial cells |
| cardiac cell: the membrane has what type of permeability; what is the concentration of potassium in cell; what is the concentration of sodium in cell; what is concentration of potassium outside cell; what is concentration of sodium outside of cell | semipermeability; high; low; low; high |
| cardiac cell: the inside of the cell at rest is said to be what; it is negative compared to what; when a cell is stimulated it allows what to move into it; when sodium moves into the cell the cell becomes what; this positive is called what; | polarized; the outside; sodium; positive; depolarization; |
| when is MCL chest lead used | it is a modified lead and is only used when there are 3 leads are available for monitoring |
| ECG: monitoring leads should be based on what | pt clinical situation |
| ECG: one small square represents what; one large square equals what; | .04 sec or .1 millivolt; .2 sec |
| ECG: on paper the upward and downward deflections measure what | voltage |
| ECG: what is artifact ; why is artifact a problem | a distortion of the Baseline and waveform sen on the ECG; b/c accurate interpretation of cardiac rhythm is difficult when an artifact is present |
| telemetry monitoring: def; | is the observation of a patient's HR and rhythm to rapidly diagnose dysrhythmias, ischemia, or infarctionl |
| def of normal sinus rhythm: | a rhythm that originates at the SA node and follows the normal conduction pattern of the cardiac ccycle |
| passage of an electrical impulse through the atria is aka; what contracts with this | depolarization of the atria; the atria |
| PR interval: represents what; | the time period for the impulse to spread through the atria, AV node, bundle of HIS and purkingie fibers; |
| QRS complex: represents what; it also represents the time of what | depolarization of the ventricles; ventricular depolarization |
| ST segment: this is the time between __ and __; this segment should be isotonic, what is isotonic; | time between ventricular depolarization and ventricular repolarization; flat with no electrical impulse |
| T wave: def | repolarization of the ventricles; |
| QT interval: represents the total time for what | depolarization and repolarization of the ventricles |
| Rate of conduction system: rate of SA node; rate of AV node; rate of Bundle of his or purkingi fibers | 60-110 sec; 40-60; 20 -40 sec |
| def automaticity | the heart has specialized cells in the nodes that can discharge spontaneously |
| def of excitability; the level of excitability is determined by what | the property of the myocardial tissure that allows it to be depolarized by a stimulus; the length of time after depolarization that the tissues can be restimulated |
| common causes of heart dysrhythmias: what are some cardiac conditions; other conditions | accessory pathways, cardiomyopathy, conduction defects, heart failure, myocardial cell degeneration, myocardial infarction, valve disease; acid base imbalance, alcohol, caffeine, connective tissue disorders, drug effects,electric shock, electrolyte,shock |
| hear blocks: what happens to the unblocked areas; | they are activated earlier than the unblocked areas; |
| Assessing cardiac rhythm: note p wave- there should be one for every what; | QRS complex; |
| emergency management of dysrhythmias: Clinical manis of dysrhythmias; | ireg. rate/rhythm, decreased BP/increased BP, decreased o2 sats, chest pain, dizziness, dyspnea, restlessness, confusion, decreased LOC, numbness, weakness, cold clammy skin, diaphoresis, pallor, palpitations, N/V |
| emergency management of dysrhythmias: interventions- initial/immediate ones; ongoing monitoring | ensure airway, admin. o2 via NC, v/s, 12 lead ecg, identify rhythm, establish iv access, identify dysrhythmia; vs, LOC, o2 sats, cardiac rhythm, admin antidysrhythmic drugs, intubation in res. distress, initiate cardiac life support |
| Holter monitor: def; device important how; | device that records the ECG while the patient is ambulatory, records heart rhythm for 24-48 hours; helps dx dysrhythmias and evaling drug effectiveness |
| sinus bardycardia: the rhythm is same as sinus rhythm but what fire less; s/s; tx | SA node fires less then 60 bpm; pale, cool skin, hypotension, weakness, angina, dizziness syncope, confusion, SOB; atropine or pacemaker |
| sinu...................s tachycardia: tx is based on what; ex oftx: is tachycardia is caused by pain, it should resolve with what; meds to treat it; | underlying cause, pain meds; adenosine or beta blockerks |
| adenosine: brief periods of what in ECG may be observed; | Asystole; |
| premature atrial contractions: aka; why is P wave distorted; once signal hits v node is it conducted normally | PAC; b/c an eptopic beat travels across the atria within an abnormal pathway; yes |
| premature atrial contractions: causes; is rhythm regular; what is different; tx | caffeine tobacco, hypoxia, electrolyte imbalance, hyperthyroidism, COPD, CAD, valvular disease, no; pwave, pr interval; beta blockers |
| atrial fibrillation: there is a total disorgination of what; this diorgination causes loss of what; is it chronic; is it intermittent; most common what; prevalence increases with what | atrial electrical activity; effective atrial contraction; yes; yes; dysrhythmia in usa; age |
| afib: causes; is atrial rate elevated or slow; what is diff on ecg; what is same; | underlying heart disease; extremely elevated 300-600 bpm; p wave, pr interval; qrs |
| afib: there is a loss of atrial kick and this causes decreased what; what is biggest risk factor with this; how is ventricular rate controlled; | CO; risk of stroke- mural thrombi; with CC blockers, beta blockers, dig; |
| afib: how does cardioversion help; why is anticoagulant therapy important; anticoagulant drug of choice; what is therapeutic level of Coumadin; | converts afib to normal sinus rhythm; prevents clots; coumadin; 2-3 INR |
| PVC: aka; def; what is ecg is premature and wide; ventricular tachycardia occurs when there are how many PVCs in a row; there is great risk for what; | premature ventricular contractions; contraction originating in an ectopic focus in the ventricles; the QRS; 3; PVC to initiate Vfib |
| PVC: causes; is rhythm regular; why is is rhythm not regular; what happens to p wave; | stimulants, stress, Hr, CAD, MI, fever,hypoxia; no; b/c of premature beats; it is barely visable; |
| PVC: what is wrong with T wave; they often don't produce a peripheral pulse why; tx; | it is long and disorted; b/c they do not generate a sufficient ventricular contraction; cause is treated |
| V tach: aka; this is at run of 3 or more ___; what ends up taking control as the pacemaker; what is sustained Vtach; | ventricular tachycardia; PVc; the ventricles; lasting more than 30 secs; |
| Vtach: why is it considered life threatening; | b/c decreased CO and the possibility of deterioration to ventricular fib which is lethal; |
| v tach: what is ventricular rate; P wave is what; QRS complex is different how; | 150-250 beats; buried in the QRS and not measureable; it is disorted and long; |
| v tach: what is considered stable and unstable; clinical manis; cardioversion is used when; | stable if pt has pulse, unstable with out pulse; hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest, the drug therapy is ineffective; |
| v fib: mechanically what is happening; causes; ECG characteristics; pt will die why; tx | the ventricle is quivering and there is no effective contraction, so no CO occurs; mi, chronic CAD, hypoxemia, hyperkalemia, acidosis, drug toxicity; HR not measurable, rhythm irregular, pulseless, apneitc state; immediate initiation of CPR defibrill |
| Asystole: def; prognosis is what | total absence of ventricular electrical activity; very poor |
| sudden cardiac death: results from what; | usually v fib v tach; |
| def prodysrhythmias | antidysrhythmic drugs may cause life threatening dysrhythmias |
| defibrillation: most effective method of what; | terminating ventricular fibrillation and pulseless VT; |
| what type of heart needs a pacemaker | AV block, bundle branch block, cardiomyopathy, HF, SA node dysfunction, tachy dysrhythmias |
| pacemaker: why is arm and shoulder movement limited | to prevent dislodgement of the newly implanted pacing leads |
| what is goal of pacemaker implantatation | should be to enhance physiologic functioning and the quality of life |
| pacemakers: why should pulse be monitored | it is monitored to know if it drops below the pre determined rate |
| what is a complete heart block | third degree av block |
| first degree av block: every impulse is conducted to the ventricles, but what is different about AV conduction; cause; | the av conduction is prolonged; mi,cad, hyperthyroidism, drugs; |
| first degree av block: is HR and Rhythm normal; what is the only thing diff; what is tx | yes; pr interval is prolonged; none usually- just monitoring |
| second degree av block type 1: what rate is normal atrial or ventricular; what rate is slower; why is ventricular rate slower; what is skipped from time to time; | atrial; ventricular; due to nonconducted or blocked QRS complex; QRS complex b/c pr interval lengthens so much |
| second degree av block type 1: cause; tx if symptomatic; | MI; atropine is used to increased hr, temporary pacemaker, observe rhythm, ; |
| second degree av block type 2: what happens; why is this serious; | p wave is not conducted with block in bundle branches; certain number of impulses from SA node is not transderred to the ventricles(2 p waves to one QRS complex); |
| second degree av block type 2: cause; is atrial rate normal; is ventricular rate normal; what is different; why is it serious | mi, dig toxicity, CAD; yes; no; QRS complex is long , can progress into a 3rd degree heart block; |
| second degree av block type 2: tx | pacemaker asap |
| third degree heart block: def; is atrial rate and rhythm normal; what is ventricular rate; is there any time relation between the pr interval and the QRs; tx | no impulse comes from the atria and atria contracts independently from the ventricles; yes; super slow 20-60; no; pacemaker asap |
| acute coronary syndrome: ischemia- what ecg changes are seen with ischemia; why is there T wave inversion; | ST segment depression or t wave inversion; occurs in response to electrical disturbance in the myocardial cells due to an inadequate supply of oxygen; |
| when will T wave inversion resolve | when treated aka blood and o2 is restored |
| syncope: def; what are the 2 types; | brief lapse in consciousness; cardiovascular and non cardiovascular |
Created by:
jmkettel
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