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nrsg 212 2.3.2

O2 transport

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