C midt Flashcards
Einthoven’s triangle) Negitive & Positive lead 1 sites:
Negitive & Positive lead 2 sites:
Negitive & Positive lead 3 sites:
=negative @ RA & positive @ LA
= negative @ RA & positive @ LL
= negative @ LA & positive @ LL
Poiseuille’s law:
Example:
= vessel w/ relative radius of 1 would transport 1mL per min at BP difference of 100mmHg. Keep pressure constant
= Less blood = vaso-press
Starling’s Law of heart:
= states that the more the myocardium is stretched, up to a certain amount, the more forceful the subsequent contraction will be
Arrhythmias) causes: 1.
2.
3.
4.
5.
6.
7.
8.
1.= Blood gas abnormalities (hypoxia & abnormal pH (haldane & Bohr)
2.= Electrolyte imbalances (Ca++, K+, Mg++)
3.= Trauma to myocardium
4.= Drug effects / toxicity
5.= Digoxin- can cause multitude of dysfunctions
6.= Myocardial ischemia, necrosis, infarction,
7.= ANS imbalance
8.= Chamber/s Distention
Atropine & Dopamine) 1. Med/ Admin/ for:
2. Atropine dosing:
3. Dopamine dosing:
(Symptomatic unstable) 4. S/S: go Cables! EX unconscious, RR<4,
5. Treatment:
Mili Amps MA (need to touch PT to feel pulse)
Pace ASAP to increase chance of pacing
1 = SBP greater than 90mmHg, “Stable to the table”
2= 1mg 3-5mins as needed (0.04mg/Kg (total 3mg)
3= “Real”2-5mcg, BC>5-10mcg/kg/min, Vaso-press> 10-20 mcg/kg/min
4= inadequate perfusion: hypoBP, AMS, etc)
5= “Straight 8 Cables!” PPM 60-80, (TCP)Transcutaneous Pacing ASAP
AV pace impulses relation w/ P waves)Atriums fire 1st then ventricles:
Atriums & Ventricles fire at same time:
Ventricles fire 1st then atriums fire 2nd:
= inverted P wave before QRS
= P wave hidden w/in QRD
= P wave after QRS (before T wave)
Blood Flow L-L) 1:
2:
3:
4:
5:
6:
7:
only vein carrying oxy/ blood:
only artery carrying deoxy: blood:
Intracardiac pressures Left>Right b/c:
= 1.Vena Cavas: recieves deoxy blood from body; SVC receives from head & upper extremities & IVC receives from areas below heart.
= 2. R-Atrium: receives deoxy blood from body via venae cavaes
= 3. R-Atrium: pumps blood through Tricuspid valve & into R-ventricle.
= 4. R-ventricle: pumps through Pulmonic valve to P/artery & on to lungs
= 5. Lungs: oxygenates blood & returns to L-atrium via pulmonary veins.
= 6. L-Atrium: sends oxygenated blood by mitral valve & into L-ventricle
= 7. L-Ventricle: pumps blood through Aortic valve>Aorta feeding oxygenated blood to the rest of the body.
= Pulmonic veins
= Pulmonary artery
= Lungs offer less resistance to blood flow than systemic circulation thus’ left myocardium is thicker than right)
Coronary) left coronary artery supplies:
Left coronary artery 2 major branches are:
= L-ventricle, Intraventricular septum, part of R-ventricle & lower conductive system
= anterior descending artery and the circumflex artery
CAD):
CVD):
= Coronary Artery disease: disease affecting coronary vessels
= Cardiovascular disease: affecting heart, peripheral blood vessels, or both
(Dysfunctions) Wandering pacemaker:
no P wave bc
No QRS:
Premature ventricular contractions:
R prime:
= > no similarities in P waves
= pathways/AV node dysfunction, block, or death
= AV node pacing and/or heart block
= Ventricle fires premature after initial ventricle contraction
= 2 R waves “dub hump” b/c pathways not in sync
Sinus Arrhythmia
= inconsistent RRs, possibly no/lil P waves, all other intervals WNL
Sinus Block) definer:
Rhythm:
P waves & PRIs:
Pacemaker site:
QRS Complexes:
= “flatline in cadence” SA node fires on time but impulse blocked
= Irregular Rhythm
= Present & normal, all followed by QRS complex, PRI: WNL
= SA Node
= Normal morphology & WNL
Sinus Bradycardia) definer:
Rhythm:
P waves & PRIs:
Pacemaker site:
QRS Complexes:
= <60BPM
= Regular Rhythm typically
= Present & normal, all followed by QRS complex, PRI: WNL
= SA Node typically
= Normal morphology & WNL
w/ Arrest) definer:
Rhythm:
P waves & PRIs:
Pacemaker site:
QRS Complexes:
= “Sinus pause on steroids”, large standstill, >1 drops
= Irregular Rhythm
= Present & normal, all followed by QRS complex, PRI: WNL
= SA Node
= Normal morphology & WNL
Sinus Tachycardia) definer:
Rhythm:
P waves & PRIs:
Pacemaker site:
QRS Complexes:
= 101 or more BPM “sharp narrow arrows”
= Regular Rhythm
= Present & normal, all followed by QRS complex, PRI: WNL
= SA Node
= Normal morphology & WNL
w/ Sinus Pause) definer:
Rate & Rhythm:
P waves & PRIs:
Pacemaker site:
QRS Complexes:
= Drop beat out of cadence & only 1 drop beat! “SA paused”
= normal or Brady & Regular Rhythm typically
= Present & normal, all followed by QRS complex, PRI: WNL
= SA Node
= Normal morphology & WNL
Horizontal Boxes) small box duration:
5 small boxes makes:
Each large box duration:
Vertical Boxes) Each small box volt & measurement:
5 small boxes makes:
Each large box voltage:
2 large boxes equivalent:
= 0.04 sec
= 1 large box
= 0.20 sec
= 0.1 mV & 1 mm
= 1 large box
= 0.5 mV
= 1 mV & 10mm
Vertical Boxes) Each small box is & what:
5 small boxes equal:
Each large box is:
2 large boxes equal
= Each small box 1 mm & 0.1mV
= 1 large box
= 0.5 mV & 5mm
= 1mV & 10mm
Einthoven’s triangle(Bipolar/limb leads) leads 2 views:
Lead 2 Negative:
Lead 2 Positive:
= Inferior wall diagonally towards left foot
= Right Arm
= Left Leg
Einthoven’s triangle(Bipolar/limb leads) leads 1 views:
Lead 1 Negative:
Lead 1 Positive:
= Left Lateral wall
= Right Arm
= Left Arm
Einthoven’s triangle(Bipolar/limb leads) leads 3 views:
Lead 3 Negative:
Lead 3 Positive:
= inferior (down & rightward) 50% MI has R ventricle Infarction
= Left Arm
= Left Leg
1 VT):
2 Definer:
3 note fusion P waves:
1= usually reentry prob
2= 100BPM or >, wide QRS
3= P waves trying to insert self in to VT
If the R is far from the P, then you have a:
FIRST DEGREE!
If some Ps don’t get through, then you have a:
= MOBITZ II!
If Ps and Qs don’t agree, then you have a:
= THIRD DEGREE!
Longer, longer, longer, drop, then you have a
= WENCKEBACH!
If the R is far from the P, then you have a:
Longer, longer, longer, drop, then you have a:
If some Ps don’t get through, then you have a:
If Ps and Qs don’t agree, then you have a:
= FIRST DEGREE!
= WENCKEBACH!
= MOBITZ II!
= THIRD DEGREE!
~⅔ heart’s mass:
Bottom of heart aka:
Top of heart aka:
Great vessels:
Aorta diameter:
= L of midline w/ remainder to right
= apex: just above diaphragm, left of midline 5th rib
= Top of heart/base: ~2nd rib.
= connect to the heart through the base.
= ~2 inch
Systole) R-side:
L-side:
= Atrium’s tricuspid valve closed & filled ventricle contracts to overcome Pulmonic-V opening it & sending de/oxy blood to lungs to oxygenate (weak & vol/ dependent (Frank Starlings)
= Atrium’s Bicuspid valve closed & filled ventricle contracts to overcome Aortic-V opening it & sending oxygenated blood to body (Strong w/ more muscle to contract)
Junctional Bradycardia)Remember:
Definer:
1= AV inherit firing rate 40-60 so <40BPM AV Brady
2= <40BPM, REG/ rhythm, AV P waves, QRS WNL (can be wide)
Junctional Bradycardia) 1. Remember:
2. Rules:
3. Etiology:
4. S/S
5. Treatment of Symptom Stable:
6. Treat of Symptom Unstable:
1= AV inherit firing rate 40-60 so <40BPM AV Brady
2= <40BPM, REG/ rhythm, AV P waves, QRS WNL but can be wide
3= +Vagal nerve tone, Patho/ slowing of SA node rate
4= Decreased HR: decreased CO, hypotension, angina, CNS S/S
5= “table” treat w/ Med admin/ of pos/ underlying cause (SBP >90)
6= (SBP<90 or AMS) “go straight 8 Cables!” PPM 60-80, Pace ASAP to increase pacing’s efficiency
KEV interpretation APPROACH) step 1:
Step 2:
Step 3:
Step 4:
Step 5:
= 1st (what is rate per min)
= 2nd Rhythm: is it regular, regularly irregular, or totally irregular
= 3rd P waves> present? All same/location, P wave in front every QRS
= 4th: PR interval> w/in norm limits, Same w/ every beat
= 5th QRS> all present, same, QRS after each P wave, w/in norm limits
Limb leads) placement:
Negative to positive makes wave:
positive to negative makes wave:
= mid forearm on M. & inside of calf (if amputee/ go less distally)
= positive wave
= negative wave
P wave) Limb leads amplitude:
Precordial “chest” leads amplitude:
= <2.5mm in limb leads Avl (2.5mV)
= <1.5mm in precordial (1.5mV)
P wave) morphology:
represents:
Limb Lead amplitude
Precordial “chest” Leads amplitude:
= + deflection in leads 1,2,&3 >Biphasic in V1
= Atrial depolarization
= <2.5
= <1.5
PVC) Bigeminy:
Trigeminy
Quadgeminy
= 2rd beat uni/PVC regularly “boom PVC” (1:1 pattern)
= 3rd beat is uni/PVC regularly “boom boom PVC)
= 4rd beat is uni/PVC regularly “boom boom boom PVC” 2-3x
PVC) Unifocal:
Multifocal:
= same fire site & shape
= dif fire spots & shape
QRS complex) morphology Q,R,S waves:
Interval duration:
Represents:
= 1st neg deflection, 1st + deflection, neg deflection following R
= 0.04 - 0.12 secs (1-3 SB)
= Ventricles depolarization
Refractory periods) Absolute:
Relative:
= end of P to apex of T wave- cells absolute Beginning of repolarization
= “some really could happen” lot of cells repolar but not all so can throw out of rhythm Commodo cordis
Sinus Bradycardia) conduction etiology:
= typically all WNL besides rate, Impulse arises from the SA node
Sinus Bradycardia) Rhythm Etiology:
Drug effects:
= Increased parasympathetic tone, Intrinsic SA node disease (old),
= digitalis, beta- blockers, calcium channel blockers
Sinus Bradycardia) Symptomology “signs”:
Treatment:
If signs of poor perfusion:
= Decreased CO & BP, angina, CNS symptoms
= Atropine if needed symptomaticly stable PT, transcutaneous pacing
= prepare for transcutaneous pacing.
T wave) Limb leads Amplitude:
Precordial “chest” leads amplitude:
= <5mm in LL
= <10mm in precordial
T wave) morphology:
Represents:
Duration:
Limb lead amplitude:
Precordial “chest” lead amplitude:
= + deflection, asymmetric w/ deeper downslope
= Ventricle repolarization
= QT variable calculation ()
= <5mm
= <10mm
Vaughn-Williams Antiarrhythmics) Procainamide & Lidocaine:
Aminodrone:
“lol” Labetalol:
Aminodrone:
Diltiazem:
Adenosine & Digoxin:
= Class I: Na Channel Blockers:
= Class 3: K+ Channel Blockers (“phase 3 repolar”):
= class 2 beta blockers
= class 4 Ca blockers
= miscellaneous
Accelerated idiopathic (AIVR):
2 Definer:
1= SNS anxiety releasing EPI & NORepi
2= wide QRS, 41-100BPM, Reg/ Rhythm
1 (AIVR):
2 Definer:
3 Rules:
4 Rhythm Etiology:
5 Symptomology:
6 Treatment:
1= SNS anxiety releasing EPI & NORepi
2= wide QRS, 41-100BPM, Reg/ Rhythm
3= Rules: 41-100BPM, Reg/ Rhythm,No P Waves & PRI, Pacemaker Site: Ventricles, QRS: Wide, >0.12 seconds
4= Impulses from higher pacemakers fail to reach ventricles, Discharge rate of higher pacemakers becomes < that of ventricles, Commonly found w/ AMI
5= Can sig/ decrease CO, possibly to life threatening levels.
Can be perfusing or nonperfusing: Pulseless & w/ pulse
6 poor perfusion, prepare for TCP} nonperfusing, follow (AHA) cardiac arrest protocol
Idiopathic, Ventricle Escape (IVR)
2 Definer:
1= AV slows downs so slow Bottom is faster & louder
2= QRS >3SB or 0.12secs w/ cadence & w/o P waves
1 (IVR)
2 Definer:
3 Rules:
4 Etiology:
5 Symptomology:
6 Treatment:
1= AV slows downs so slow Bottom is faster & louder
2= QRS >3SB or 0.12secs w/ cadence & w/o P waves
3= 15-40BPM, Reg rhythm, Ps & PRI N/A Pace Site: Ventricles, QRS: Wide, >0.12 secs
4= Slowing atrial pace sites, Often 1st rhythm after defib/ROSC
5= Can sig/ decrease CO possibly to life threatening Lvls,
6= If signs of poor perfusion, prepare for TCP }if slow &/or nonperfusing, “PEA/EMD” (electrical mechanical dissociation) follow (AHA) cardiac arrest protocol
1 TDP) Twisting of points
2 Definer:
3 Rules:
4 Rhythm Etiology:
5 Symptomology:
6 stable Treatment:
7 unstable Treatment:
8 Wrong treatment:
1= most common polymorphic VT “teeter toter of de & re /polarization of ventricles” (twisting ribbon)
2= Changes in shape w/ size (note w/ change of conduction)
3= 100-250BPM, usually irreg/ Rhythm, if Ps present, don’t associate w/ QRS, No PRI, QRS varies beat-beat, many ventricular pace/sites, QRS >0.12secs, morphology & size changes
4= women>men chance, certain/ mixing antiarrhythmics
5= Can cause severe hypoperfusion in perfusing rhythm,
6= (rare) MAG-SULFATE 1-0.5Gs, Overdrive pacing (ER) pacemaker faster than HR) Correct underlying electrolyte prob/s (hyperK) Ca-Cl, Na-Bicarb, LVN
7= Defib! (only time defib/ pulse) few mins before gone
8 = Amio will prolong QT & kill PT, Rx w/ antiarrhythmics usually used for treatment of VT can have disastrous consequences
Torsades De Pointes (TDP) Twisting of points
2 Definer:
1= most common polymorphic VT “teeter toter of de & re /polarization of ventricles” (twisting ribbon)
2= Changes in shape w/ size (note w/ change of conduction)
VF) ventricular Fib/quiver
2 Definer:
1= “death rattle”, never pulse,
2= Chaos, “wide QRSs”
1 VF) ventricular quiver
2 Definer:
3 Rules:
4 Rhythm Description:
5 Etiology:
6 A&P:
7 Symptomology:
8 Treatment:
1= “death rattle”, never pulse,
2= Chaos, “wide QRSs”
3= Rate, Rhythm, P-Waves, PRI, & QRS all none, Chaos firing of numerous ventricular pacing sites
4= Chaotic ventricular rhythm; presence of many reentry circuits wi/in ventricles – No ventricular depolarization or contraction, (Course <amp)(fine>amps) (Fine VF: small humps ~1sq tall, very course)
5= commonly from advanced-CAD, Commotio Cordis, Electrical shock
6= not in uniform down sarcolemma of atria draining ATP fuel tank thus going slowly to aystole
7= Pulseless & apneic
8= defib ASAP (try to avoid unhuman CPR) Follow AHA cardiac arrest algorithm, Uninterrupted quality CPR important
1 VT):
2 Definer:
3 Rules:
4 Rhythm Description:
5 Monomorphic:
6 Polymorphic:
7 Etiology:
8 Symptomology:
9 Treatment:
10 Unstable Rx:
1= usually reentry prob
2= 100BPM or >, wide QRS
3= 100-250BPM, mostly reg/ Rhythm, Ps If present don’t go w/ QRS, No PRI, Ventricles Pace Site, QRS: >0.12 secs
4= >3 ventricular complexes in succession, (rhythm overrides natural pacemaker, atria & ventricles out of sync)
5= All QRSs look alike w/ same site (most common VT)
6= QRSs have dif morphology (least common VT)
7= MI, +sympathetic tone, Acid-base disturb/, Electrolyte imbalances, Hypoxia, idiopathic causes
8= Poor SV from RVR, may severely comp/ CO & coronary artery perfusion thus may deteriorate to VF
9= (Stable} Ischemic chest pain, dyspnea =antiarrhythmic med> Ami, procain, Lido
10= HypoBP, AMS, shock S/S, acute heart failure> synchronized cardioversion (100J then 200J then 300J to max) If nonperfusing, follow AHA protocol for VFib
1 Artificial Pacemaker:
2 definers:
1= usually L upper chest adults & kids
2=Atrial line w/ P wave following, Ventricular line followed w/ QRS (wide QRS), AV sequential 1 line before the Ps & QRSs, Fail to shut down, Can fail to capture if leads displaced, Runaway pacemaker (Pacemaker running 190Bpm)
Fixed pacer:
Demand pacer:
=NONDEMAND PACER Fires continuously at preset rate, regardless of heart’s electrical activity, TC pacing nondemand
= non-fixed, Sensing device; fires only when natural HR drops
Atrial pacer:
Definers:
Treatment:
= paces only in atrium
=Atrial line w/ P wave following
= (ask PT for pacemaker card) Magnet donut, TCP, bradyC & asystole as any other PT
Ventricular pacer:
Definers:
Treatment:
= paces only in ventricle
= line before QRS complex & Wide QRS
= (ask PT for pacemaker card) Magnet donut, TCP, bradyC & asystole as any other PT
AV Sequential pacer:
Definers:
Treatment:
= paces in atrium & ventricle
= line before P wave & QRS, wide QRS
= (ask PT for pacemaker card) Magnet donut, TCP, bradyC & asystole as any other PT
Failure to capture pacer:
Definers:
Treatment:
= not shocking/pacing when supposed to
= (ask PT for pacemaker card) Magnet donut, TCP, bradyC & asystole as any other PT
1 Artificial Pacemaker:
2 definers:
3 Types of pacer locations:
4 physiology:
5 Fixed rate:
6 Demand:
7 positioning:
8 reasoning for need:
9 Problems:
10 treatment:
1= usually L upper chest adults & kids
2=Atrial line w/ P wave following, Ventricular line followed w/ QRS (wide QRS), AV sequential 1 line before the Ps & QRSs, Fail to shut down, Can fail to capture if leads displaced, Runaway pacemaker (Pacemaker running 190Bpm)
3= Types: Transesophageal, Transvessel, Internal:
4= physiology: cardiac stim/ by electrode implanted in heart
5= NONDEMAND PACER Fires continuously at preset rate, regardless of heart’s electrical activity, TC pacing nondemand
6= non-fixed, Sensing device; fires only when natural HR drops < set rate, “Only when needed”, wont fire if @ or>
7= (ALL R-SIDE) atrium, R-Ventricle, AV sequential (both),
8 PTs who have: R-atrium, Chronic high-grade heart block, Sick sinus syndrome, Episodes of severe symptomatic bradycardia
9= Battery failure (now last 5-10Yrs depending on how constant), dysfunction, failure to capture, & runaway
10= (ask PT for pacemaker card) Magnet donut, TCP, bradyC & asystole as any other PT
1 Premature Ventricular Contractions (PVC):
2 Definers:
1= >50% (Don’t + w/ HR) “Pissed off & shouting out”
2= Premature, Wide QRS, no P-wave
- 1st Degree AV Block) know:
- Definer:
1= “add to any rhythm” “gandolf slowly opening door(PRI)”
2= PRI: >than 0.20 seconds for every PRI & P-P cadence
- 2nd Degree Type I) AKA & Know:
- Definer:
1= “Morbitz 1”/“Wenckebach” rhythm & “AV turning off to fully down”
2= progressive longing PRI till drops beat then resets/starts over
- 2nd Degree Type I) AKA & Know:
- Definer:
- Rap:
- Rules:
- Symptomology:
- Treatment:
1= “Morbitz 1”/“Wenckebach” rhythm & “AV turning off to fully down”
2= progressive longing PRI till drops beat then resets/starts over
3= “Longer, longer, longer, drop, then you have a WENCKEBACH!”
4= Rate: Variable, QRS rate will be slower than atrial rate Rhythm: Irregular P Waves: Normal but some P waves don’t have a QRS PRI: longing ‘til a QRS dropped Pace-Site: SA node or atria QRS: ~normal
5= Can compromise cardiac output, Syncope, angina, Commonly MI
6= O2 as needed, 15 Lead ECG, If signs of poor perfusion, prep for transcutaneous pacing only if brady.
- 2nd Degree Type II) AKA & know:
- Definer:
1= “Mobitz 2/Intranodal” & “random extra Ps”
2= some P’s w/o QRS & same PRI/No longing before drop beat
- 2nd Degree Type II) AKA & know:
- Definer:
- Rap:
- Rules:
- Etiology:
- Symptomology:
- Treatment:
1= “Mobitz 2/Intranodal” & “random extra Ps”
2= some P’s w/o QRS & same PRI/No longing before drop beat
3= “If some Ps don’t get through, then you have a MOBITZ II!”
4= Rate P’s unaffected; QRS rate usually brady Ir/Reg/ Rhythm, P’s WNL but some w/o QRS, PRI Constant for conducted beats, Pace-Site SA node or atria, QRS WNL or wide
5= Intermittent block, Ps not conducted to ventricles via AV (Associate w/ acute MI & septal necrosis)“2-1 block” = 2 P’s before QRS
6= May comp/ CO, syncope, angina; May dev/ into complete AV-block
7= PT condition based: If signs of poor perfusion prep for trans/pacing
- 3rd Degree AV Block) AKA & know
- Definer:
1= “Complete AV-Block/dissociation” (always TCPP on) “gandalf died”
2= No relations w/ Ps & QRSs & no same PRI (top & bottom dif)
- 3rd Degree AV Block) AKA & know
- Definer:
- Rap:
- Rules:
- Etiology:
- Symptomology:
- Treatment:
1= “Complete AV-Block/dissociation” (always TCPP on) “gandalf died”
2= No relations w/ Ps & QRSs & no same PRI (top & bottom dif)
3= “If Ps and Qs don’t agree, then you have a THIRD DEGREE!”
4= P’s unaffected; QRS rate usually brady Rhythm: Ps & QRSs WNL but don’t coincide w/ other Ps: Norm w/ no relation w/ QRS Pace-Site: SA node or atria for P’s; AV node or Ventricle for QRS, QRS WNL or wide
5= NO conduction w/in atria & ventricles, Complete electrical block @/ below AV node Acute MI, Digoxin toxicity, Degen/ of conductive system
6=May severely compromise CO
7= If signs of poor perfusion, prep for immediate TCP
A-Fib) know:
Definer:
types:
= most common, (treat >150BPM), more Jules b/c more sites
= No definite P waves “Fib P waves”, Totally Irregular
= Controlled 60-150BPM & Uncontrolled <60 & >150BPM
1 A-Fib) know:
2. Definer:
3. Rules:
- Etiology:
- S/S:
- Treat:
- Types of AFib:
1= most common, only treated when >150BPM, more Js b/c more sites
2= No definite P waves, Totally Irregular
3= NEVER P waves, Pacing-sites 350-750BPM in atriums, rhythm is always totally irregular, PRI: None, QRS: Usually normal
4= AV randomly lets a impulse down after blocking shower of impulses
5= < Atrial kick CO<20-25% & preload thus <Starling then ect, AMS,
6= Ca blocker, sym unstable BPM>150 cable (120-200J) more sites to control),
7= Controlled <150 AV can control, >150 = w/ RVR, w/ 3rd degree AV block (reg rhythm(Atriums & Ventricles on own)
- Accelerated Junctional) Know by:
- Definer:
1= “Baby Tachy” faster than 60 not faster than 100
2= 61-100BPM, (from SNS & AV firing), Regular rhythm, AV P waves
- Accelerated Junctional) Know by:
- Definer:
- Symptomology:
- Treatment:
1= “Baby Tachy” faster than 60 not faster than 100
2= 61-100BPM, (from SNS & AV firing), Regular rhythm, AV P waves
3= usually does not cause a PT to have symptoms
4= Be a investigator ,History/Physical ,O2 as needed , 15 Lead ECG
- Atrial Flutter) Know:
- Definer:
- Etiology:
- Rules:
- Causes:
- S/S:
- Treat:
1= “saw tooth Ps”, count bottom of points of flutters “3 to 1 block”
2= Sawtooth Ps w/ regular rhythm
3= R-atrium impulse stuck to Ivena-cava valve triangular pathway (cabo trismis ismis) b/c jacked up autorhythmic cells & 150BPM usually when AV goes to fast
4= Atrium Rate 250-350, Reg Rhythm, Flutter P Waves, PRI Usually constant but may vary, Pace-Site Atria outside SA, QRS Usually norm
5= Occurs w/ old age, CHF, rarely from a MI
6= depends on rate,
7= Ca channel blocker, 1st line med diltiazem (or beta blocker), symp unstable & BPM>150 cables 50-100Js
Atrial Flutter) Know:
Definer:
1= “saw tooth Ps”, count bottom of points of flutters “3 to 1 block”
2= Sawtooth Ps w/ regular rhythm
- Cardiac Pharmacology)
- NA Channel Blockers:
- Beta-Blockers:
- Potassium Channel Blockers:
- Calcium Channel Blockers:
- Miscellaneous:
1= (Vaugh-Will) Classes: 1]Na, 2]Beta, 3]K, 4]Ca, Misc] Adenosine
2= (Procainamide & Lidocaine) both Widened QRS & Prolongs QT
3= (Propranolol) Prolonged PRI & Bradycardias
4= (Amiodarone) Prolonged QT
5= (Diltiazem & Verapamil) Prolonged QT & Bradycardias
6= (Adenosine & Digoxin) Prolonged QT & Bradycardias
Junctional Tachycardia) Know by:
Definer:
1= “Tachy is Tachy”
2= >100BPM, AV P waves, in cadence, QRS WNL
- Junctional Tachycardia) Know by:
- Definer:
- Etiology:
- Rules:
- Symptomatology:
- Treatment:
1= “Tachy is Tachy”
2= >100BPM, AV P waves
3= +SNS response w/ AV site & Result of AV ischemia (rarely>150)
4= >100, AV P waves & Pacing, N. QRS, ~reg/rhythm, if PRI ~<.12secs
5= usually PT doesn’t has symptoms
6= invest/, Hx, O2 PRN, 15 Lead, monitor for other arrhythmias
Junctional rhythms) aka know by:
Definer:
1= junctional escape: “pick up workload b/c something failed”
2= AV P waves & AV node rate 40-60BPM, Regular rhythm
- Junctional rhythms) aka know by:
- Definer:
- S/S:
- Rules:
- Treatment:
1= junctional escape “pick up workload b/c something failed”
2= AV P waves & AV node rate 40-60BPM, Regular rhythm
3= Slow heart rate can decrease CO; angina
4= AV: Pace site, rate, & P-waves> regular rhythm, can have >PRI
5= O2 as needed, 15 Lead ECG, underlying cause (MI commonly), If signs poor perfusion, prepare for transcutaneous pacing (TCP)
A-Fib w/ RVR) definer
type:
= AFib w/ >150BPM
Uncontrolled
1A-Fib rate problem:
2Rules:
3Types:
4conduction:
5S/S:
6Treat:
1= most common (only treated when rate problem=150BPM
2=NEVER P waves, rhythm totally irregular,
3= controlled <150 AV node can control, >150 or <60 uncontrolled
4= Different sites all shouting, atrium “quivering
5= loose / reduces atrial kick CO<20-25%, looses preload < starling
6= Ca blocker, sym unstable BPM>150 cable (120-200J) more sites to control)
A-Fib w/ SVR:
Type:
= AFib w/ <60BPM
= Uncontrolled
1Atrial Flutter:
2Rules:
3Conduction:
4Treat:
1= “3 to 1 block” R-atrium impulse stuck to I/vena-cava valve pathway
2= multiple sawtooth P waves
3= autorhythmic cells loco “saw tooth flutter waves” R-atrium impulse stuck to I/vena-cava valve triangular(cabo trismis ismis)pace site in atria
4= Ca channel blocker, 1st line med diltiazem (or beta blocker), symp unstable & BPM150> cables
1Lateral Wall high view:
2Left Lateral low view:
3Inferior wall view:
4Septal wall view:
5L-Anterior view:
1= Lead I & aVL= LA
2= Lead 1, aVL, V5 & V6: views LCX & LAD
3= 2,3,aVF: LL most common block(RCA) Lots of blockages/infarcs
4= V1 & V2: Along sternal borders blockages from LAD commonly
5= V3 & V4: left anterior wall : LAD & LMCA blocks
Lateral Wall high lead view:
Lead I & aVL= LA
Left Lateral low lead view:
Lead 1, aVL, V5 & V6: views LCX & LAD
Inferior wall leads view:
2,3,aVF: LL most common block(RCA) Lots of blockages/infarcs
Septal wall view leads:
V1 & V2: Along sternal borders blockages from LAD commonly
L-Anterior wall view leads:
= V3 & V4: LAD & LMCA blocks
1Paroxysmal Supraventricular Tachycardia (PSVT)
2Rules:
3Causes:
4 Can precipitate:
1= “ SVT sudden start & stop” not associated w/ underlying Cdisease
2= same as SVT but sudden onset, terminates abruptly
3= Stress, overexertion, smoking, ingestion of caffeine.
4=angina, hypotension, congestive heart failure.
1Paroxysmal Supraventricular Tachycardia (PSVT)
2 Definer
1= “ SVT sudden start & stop” not associated w/ underlying Cdisease
2= same as SVT but sudden onset/ends abruptly
1st line IV med in cardiac arrest
Epi
1st line med in cardiac arrest
oxygen
1Supraventricular Tachycardia (SVT)
2Rules:
3 Treat:
1= AV going NASCAR
2= No P waves, 150-250 BPM, regular rhythm
3= vagal maneuver, adenosine, unstable= cables (@50-100J) go to max)
1w/ PAC:
2Definer:
3PAC conduction:
4Causes:
5Symptoms:
6Treatmeant:
1= Premature Atrial Contractions “w/”
2= dif P wave shape w/ premature depolarization
3= Single impulse from the atria outside SA, premature depolarization
4= use of caffeine nicotine or alcohol, sympathomimetic, increased excitable “shout outs”, Ischemic heart disease, hypoxia, Digoxin,
5= PT may feel “palpitations” or “skipping” feeling in their chest
6= O2 supportive care
1w/ PAC:
2Definer:
1= Premature Atrial Contractions “w/”
2= dif P wave shape w/ premature depolarization
1Wandering Atrial Pacemaker WAP:
2Causes:
3Rules:
4Rhythm Etiology:
5 Symptomology:
6Treatment:
1= “pacing/firing comes from dif sites” May be precursor to AFib
2= atrial enlargement, L-Pump failure, getting old, metabolic disorder
3= irregular at least 3 dif P waves shapes, PRI varies, QRS WNL,
4= Transfer of pace sites from SA node to other sites in atria & AV
5= PT may c/o “palpitations” or a “skipping” feeling in their chest
6= Supportive care, Treat the underlying cause
2nd-Degree Type 2 AV block) names:
Mobitz 2 or intranodal AKA “2:1 block” rhythm
2nd-Degree Type I AV block) names
Mobitz 1 or Wenckebach
A blockage of which of the following would result in the entire left ventricle not receiving blood supply?
Left Main Coronary Artery (LMCA)
Blood cell travels from the left atrium, through what & into where?
= Mitral/Bicuspid valve & into Left Ventricle
Blood cell travels from the right atrium, through what & into where?
= Tricuspid valve & into Right ventricle
Blood cell travels from the right ventricle, through what & into where?
= Pulmonic valve & into Pulmonic arteries
A junctional bradycardia rhythm would present with a ventricular rate
less than 40 beats per minute.
A junctional tachycardia rhythm would present with a ventricular rate
greater than 100 beats per minute.
A normal P wave in Precordial leads should be:
A normal P wave Limb leads should be:
= nice & round w/ amplitude <1.5mm
= nice & round w/ amplitude <2.5mm
A normal PRI should be between
A normal QRS duration should be between:
= 0.12-0.20 seconds
= 0.04-0.12 seconds.
PT w/ artificial pacemaker firing at rate of 150-160BPM is:
PT w/ bradyC pulse & artificial pacemaker, You observe a rhythm that has pacemaker spikes but only a few of them actually have a QRS complex following is what:
= Runaway
= Failure to Capture
A patient presents with Atrial Fibrillation at a rate of 180-190 beats per minutes. How would you correctly describe this rhythm?
A Fib w/ RVR
Premature ectopic beat presents w/ a inverted P wave & narrow QRS:
Premature ectopic beat presents w/ an upright P wave & narrow QRS:
= Premature Junctional Contraction (PJC)
= Premature Atrial Contraction
Rhythm initiated by SA node should have a rate between:
Sinus Tachycardia has a heart rate of:
Sinus Bradycardia has a heart rate of:
= 60-100 beats per minute
= 101 & >BPM
= 59 &<BPM
A sinus rhythm presents with two PVC’s that have a completely different appearance. These PVC’s would be classified as:
Multifocal
Ventricular escape rhythm presents w/ a rate between:
Accelerated idioventricular rhythm presents w/ rate between:
Ventricular tachycardia rhythm presents w/ a rate:
= 15 & 40BPM
= 41BPM & 100BPM
= >100BPM
Absolute refractory period:
Relative refractory period:
= Apex of T wave Q-T wave apex of wave: ventricle not ready to work
= T wave top to end of T wave: (commodo cordis) cells not repolarized (torsades de pointes more dead from repolarization not in sync)
Class IV Antiarrhythmic of Vaughan-Williams Class is:
Class I Antiarrhythmic of Vaughan-Williams Class is:
Class III Antiarrhythmic of Vaughan-Williams Class is:
Class II Antiarrhythmic of Vaughan-Williams Class is:
= Calcium channel blocker
= Sodium channel blocker
= Potassium channel blocker
= Beta-Blocker
Vaughan-Williams Classification Ca-channel blocker is a:
Vaughan-Williams Classification Na-channel blocker is a:
Vaughan-Williams Classification K-channel blocker is a:
Vaughan-Williams Classification Beta-Blocker is a:
= Class IV Antiarrhythmic
= Class I Antiarrhythmic
= Class III Antiarrhythmic
= Class II Antiarrhythmic
Afterload:
= resistance against which the heart must pump against afterload become increased w/ increased ventricular workload
Amiodarone class & indication
Class 3 K channel blocker> VF/Pulseless VT unresponsive to shock, CPR & Epi, BradyCs to include AV blocks, Recurrent, hemodynamically unstable VT w/ pulse
ECG rhythm w/ following} impulse fails to leave SA node, multiple dropped beats, but cadence is right on track when it starts back up is:
= Sinus Block
ECG rhythm w/ following} SA node fails to initiate an impulse, only 1 dropped beat, Cadence is thrown off when starts back up is:
= Sinus Pause
ECG rhythm w/ following} SA node fails to initiate an impulse, multiple dropped beats, & cadence is thrown off when starts back is:
Sinus Arrest
An ECG rhythm presents with two PVC’s that are completely different in appearance and they come right after one another. These PVC’s would be classified as:
An ECG rhythm presents with two PVC’s that are exactly the same in appearance and they come right after one another. These PVC’s would be classified as:
An ECG rhythm presents with three PVC’s that are exactly the same in appearance and they come right after one another. These PVC’s would be classified as:
= Multifocal couplet
= Unifocal Couplet
= Triplets
ECG rhythm presents w/ rate 110 BPM, slightly irregular cadence, & P waves that have three or more different morphologies is classified as:
Multifocal Atrial Tachycardia
ECG rhythm presents w/ a rate of 40BPM, reg/ cadence, normal looking Ps, normal PRI for the P waves that have a QRS following, but has some P waves that don’t have a QRS after it is classified as a:
2nd Degree Type II / Mobitz 2
ECG rhythm presents w/ rate 80 BPM, reg/ cadence, norm/ shaped P wave, a prolonged but constant PRI, & norm/ QRS is classified as as:
Sinus with 1st Degree
ECG rhythm presents w/ a ventricular rate of 80 BPM, reg/ cadence, saw-tooth waves in place of P waves, & narrow QRSs is classified as:
Atrial Flutter
An ECG rhythm that presents with P waves and QRS complexes that don’t appear to coincide with each other is classified as a:
3rd Degree AV block
Normal T Wave in any chest lead should have max amplitude:
= 10 mm
Normal T Wave in any limb lead should have a max amplitude:
= 5 mm
ECG originating from SA node is producing a rhythm that has 15 small boxes in-between R-R intervals. You would recognize this ECG has a heart rate of:
Use method:
= 100 beats per minute
= small box method / 1500 by SB#
Normal T Wave in any limb lead should have a max amplitude of:
Normal T Wave in any chest lead should have a max amplitude of:
= 5 mm
= 10 mm
impulse traveling towards a positive electrode will produce a:
Impulse traveling away from a positive electrode will produce a:
= positive deflection wave ECG
= negative deflection wave ECG
ANP Atrial Natriuretic Peptide:
BNP “Brain” Natriuretic Peptide:
= released by + pressure/ atrial dilation & stress
= myocytes stretched out releases more BNP, Starlings law correlates w/ BNP “BNP + = CHF/Heart failure”
Leads V3 & V4 view
Leads V1 & V2 view
Leads 2,3, & aVF view
Leads 1, aVL, V5, V6 view
= Anterior
= Septal
= Inferior
= Lateral
RP of a cardiac autorhythmic cell is:
AP of a cardiac autorhythmic cell is:
Influx of what causes depolarization of autorhythmic cells:
Efflux of what ion causes repolarization:
= -60mVs
= -40mVs
= Calcium
= Potassium
Artsclerosis:
Atherosclerosis:
= stiffening of vessels
= build up in make up of arteries
1 Asystole:
2 Definer:
3 Rhythm Description:
4 Rhythm Etiology:
5 Symptomology:
6 Treatment:
1= no activity (most common PEDIS arrest)
2= NONE, NONE, NONE
3= Absolute no Mnt of amplitude
4= Primary event in cardiac arrest, Massive MI, ischemia, necrosis, VF, PSNS control
5= Pulseless & apneic
6= NEVER SHOCK, Prognosis for resuscitation very poor, High quality CPR, Treat underlying cause, Follow AHA algorithm
1 Asystole:
2 Definer:
1= no activity (most common PEDIS arrest)
2= NONE, NONE, NONE
Atrial appendages:
(abnormal heart birth defect) pockets that form clots on either atrium from uterine dev/,
What? Manufactured, stored, & released by Atrial M. cells in response to such things as atrial distention and sympathetic stimulation.
Atrial Natriuretic Peptide (ANP)
Atrioventricular (AV) block:
Electrical impulse is slowed or blocked as it passes through AV node
Atrioventricular valves aka & leaflets# & aka:
Atrioventricular valves Fn:
= R-Tricuspid valve beeu w/ 3 cusps & L-Bicuspid/Mitral valve w/ 2 cusps
= control blood flow between atria & ventricles via connection to specialized papillary muscles in ventricles.
AV node Heart blocks are
blocks in AV node partial or complete
“Putting a rock or pebble on a cable”
Heart blocks are
blocks in AV node partial or complete
“Putting a rock or pebble on a cable”
Heart blocks are
blocks in AV node partial or complete
“Putting a rock or pebble on a cable”
“AV node P waves” morphology:
= inverted before QRS, hidden w/in QRS, after QRS
AV pacing site defined by:
= P wave: 1 inverted before QRS, 2 hidden w/in QRS, 3 +/- after S
BBB:
Bundle Branch Block / intraventricular block: (L or R) can give P waves w/ wide QRS
Beta-Blocker:
Cardio-Selective Beta-Blockers:–
Non-selective Beta-blockers:
= blocks β adrenergic receptors
= Atenolol, Esmolol, Metoprolol
= Propranolol, Nadolol, Labetalol, Sotalol.
Blood drains from Left Coronary system via:
the 2 veins empty into:
right coronary vein empties directly into:
= anterior great cardiac vein & lateral marginal veins
= coronary sinus
= the right atrium via smaller cardiac veins.
BP form/s:
BP is related to:
= (SV x HR) x SVR or CO x SVR
= CO & peripheral resistance
Cardiac always Dos & Knows} 1.
2.
3.
4.
5.
6.
7.
8.
1.= investigator for underlying etiology
2.= 50% syncope’s cardiac related
3.= look/know underlying symptoms before ANY MED ADMIN
4.= 220-age= THR withstanding
5.= SYSTEMATIC APPROACH
6.= if don’t know call pro (cardiologist/DR)
7.= Majority of MIs inferior wall w/ RCA
8.= more time to pacing = more ineffective
Cardiac artifacts:
Causes of artifacts:
= hard to decipher iso-electrical lines w/ 0 & skewed
= M. tremors/shivering, PT mnt(moves baseline), Loose electrodes, 60-hertz interference(ungrounded electricity near you (AC current alternating in house), Machine malfunction (Dotted flat line),& electrode bad connection/ off
Cardiac depolarization:
RP of Ac:
RP of Cc:
Phases 0-4 of Cc:
= reversal charges of cell membrane inside becomes + & outside -,
= -60 slow Na & fast Ca -40
= -90 Na & -85 gap Junctions fast Na influxes
= 0 depolar, 1 early repolar, 2 plateau + for +, 3 K pumps, 4 refractory
Cardiac output formula:
= SV x HR
Cardioversion (synchronized) for:
= Tachyarrhythmias w/ pulse unstable} AFib, AF, ASVT, PSVT, SVT, VT w/ pulse
Cardioversion for:
higher start:
lower start:
= VT, SVT, ASVT, PSVT, too fast HR “convert down”
= ST>100J, 200J, 300J, 360J
= ASVT, PSVT, SVT> 50-100J (AF w/ RVR 120-200J)
Cardioversion or pharmacological intervention is only usually required for patients that present in A-Fib at what ventricular rate?
Above 150 beats per minute
Cardiovert is for:
“conVERT to normal” too fast
AV block possible causes:
MI, (inferior RCA) AV ischemia and/or necrosis, Degenerative disease of conductive system, Drug toxicity (particularly digitalis)
CHART Narrative:
Chief Complaint, History(includes SAMPLE), Assessment (head-to-toe), Rx/Treatments, Transport
Chordae Tendineae:
Heart regurgitation:
= connect valves’ leaflets to papillary-M.s to prevent valves from prolapsing into atria & allowing backflow during ventricle contraction
= papillary not working &/or valve doesn’t correctly opens so prolapse
Chromotropy goes in hand w/:
= dromotropy Speed of impulse transmission, usually goes w/ Inotropy
Chrontropy:
Inotropy:
Dromotropy:
= HR, + tropic +HR vice versa
= Contraction force
= Speed of impulse transmission, usually goes w/ Inotropy
(Electrolytes affects) Cl
Na
K
Ca
Mg
= Cl picks up Co2 (shift) to keep neutrality
= depolarizing myocardium
= depolarization & majority myocardial contractile
= influences repolarizations
= regulates contractility & rhythm
1) Common findings after getting ROSC:
2) Every min in Cardiac arrest:
3) 1st line med in cardiac arrest:
4) Compressions needed to overcome afterload:
5) Epi & reason for admin:
6) Goals during Rx of Cardiac arrest:
= ventricular rhythms,
= knocks 10% of your life
= 02
= 8-10 human compression to overcome afterload P.
= Perfuse heart & coronary arteries more so RCA in arrest for A1Vasoconstrict & +afterload P. to perfuse
= Perfusion & vent: prevent arrest again w/ supporting perfusion b/c heart is weak
Failure to capture is & Rx:
Runaway pacemaker treatment:
Internal defibrillator:
= when pacemaker fails to detect & fire: TCP Rx
= cardiac magnet “donut”: (hear beep beep ) Some keep on then off or Keep off
= can give up to 500 shocks, better than external (some can shock atrials)
Anastomosis
Communication or the connecting of two or more vessels
Anastomosis
Communication or the connecting of two or more vessels
Communication or the connecting of two or more vessels is known as:
= Anastomosis
Contractilititly factors electrolyte & receptor:
= Calcium & +Beta1 effects
Contractility:
= ability of CM. cells to contract, or shorten (Actin Myosin)
Coronary arteries L&Fn:
Coronary veins & Vena Cavas pick up & drop off to:
Cornary sinus:
= Aorta, feed oxygenated blood to heart/myocardium during diastole b/c semilunar valve closed during aortic kick/
= deoxygenated blood sent to Right atrium
= vein deoxy blood back to R atrium above AA
Defib for:
amounts:
= pulseless arrhythmias VFib, Pulseless VT
= 120-200 joules for biphasic defibrillators & 300-360 joules for monophasic
Diastole:
Systole:
= 1st phase, ventricles fills w/ blood, hold 100mLs & pumps 50-70mLs
= “squeeze” 2nd phase, period of cycle myocardium is contracting
Digoxin) Typically for:
Dynamics
works bc
= CHF
= allows more Ca for better contraction
= confuses K/Na pumps
Diltiazem/Cardizem)indi/s:
Contraindications:
= 1st med for AFib/Flutter w/ RVR (>150bpm), 2nd med for SVT refractory to Adenosine
= hypoBP, CHF/cardio/shock, Wide-complex Tcardia, WPW, Hypersensitivity
Diltiazem) 1st dose:
2nd dose:
= 0.25mg/kg w/ max dose of 20mg
= 0.35 mg/kg w/ max dose of 25mg
Dobutamine) dose:
=2-20mcg/kg/min- titrate so HR doesn’t increase by >10% of baseline
Dopamine) indications:
Contraindications:
= CHF, HypoBP w/ shock signs, 2nd med for sympathetic Bcardia (after Atropine)
= hypovolemic PTs til’ vol/ replaced, pheochromocytoma, Dont mix w/ sodium bicarb
Dopamine) Effects:
Dosing:
Adult & Pedi Cardiac dose:
Adult & Pedi Vasopressor dose:
= HyperBP, Palp/s, H/A, Dizzy, Can worsen C-ischemia, necrosis W/ Extravasation
= 2–20 mcg/kg/min Titrate to response
= 5-10mcg/kg/min
= 10-20 mcg/kg/min
Dopamine) dose:
=5-20mcg/kg/min & Titrate to PT response (DONT OPEN “WIDE OPEN”)
Dotted line on ECG means
monitor not connected properly
(ECG Horizontal Boxes) small box is how long
5 small boxes:
Each large box is how long
= 0.04 sec
= 1 large box
= 0.20 sec
Ectopic
Not the normal
(Arrhythmias) Mechanism of Impulse Formation Ectopic foci:
= Enhanced automaticity; automatically depolarize, producing ectopic (abnormal) beats.
Ectopic foci:
Phases 0 & 3 of AP:
= abnormal impulse then is propagated throughout the heart
= Depolarization & Repolarization
Eintovhens triangle (bipolar) camera always at
L1 + & - leads:
L2 + & - leads:
L3 + & - leads:
= positive > Bipolar - to +
= -RA to +LA
= -LL to + LL
= -LL to + LL
Ejection Fraction (EF):
<45% usually indicates:
<30%:
= Ratio of blood pumped from the ventricle to the amount remaining @ the end of diastole/ %of blood pumped out from ventricle (60-70%)
=<45% usually indicates in or going to CHF
=<30% in CHF & chronic cardiac crip on oxy
Endocardium:
= Innermost layer, Lines heart chambers & is in contact w/ blood.
Epinephrine 1:10,000) Effects:
Admin via:
(Adult) Cardiac Arrest dose:
(Adult) Bradycardia dose:
(PEDI) Bradycardia/Cardiac Arrest dose:
(PEDI) Hypoperfusion & Severe anaphylaxis dose:
= Palpitations, Anxiety, Jitters, H/A, Dizziness, HyperBP, Tcardia, Can worsen cardiac ischemia
= IV infusion drip
= 1mg IVP/IOP every 3-5 mins
= 2-10 mcg/min IV/IO infusion
= 0.01 mg/kg or 0.1 mL/kg
= 0.1-1 mcg/kg/min infusion by Mixing 1mg of Epi 1:10 into 1L IV bag
Epinephrine 1:10,000) Indications:
Contraindications:
= Cardiac arrest, Bcardia, Normovolemic hypoBP, Anaphylaxis, Asthma
= rewards over risks so really none
Epinephrine 1:10,000): Cardiac arrest:
Bradycardia dose:
Normovolemic hypotension & severe anaphylaxis:
=1mg IVP/IOP every 3-5mins
=2-10mcg/min IV/IO infusion (0.002-
=2-10mcg per min—> mix 1mg of Epi 1:10,000 into a 1 liter bag of fluid
Equation for cardiac output:
Heart & SV volumes:
Equation for BP:
How can you make a + & - effect on it?
= CO= SV x HR
= usually squeezes 70mLs & heart holds 100-110mL
= BP=(SV X HR) X SVR
= Meds: diuretics, vaso-constructors
Fastest way to effect preload:
= IV bolus Afterload affect vaso-med
feeling a pulse is from what:
= ventricles/QRS contracting
1 fires a pacer spike before both the P wave and the QRS complex. This type of paced rhythm is known as a(n):
2 PT presents w/ artificial internal pacemaker that fires a pacer spike only before the QRS complex and there is no obvious P waves noted. This type of paced rhythm is known as a(n):
3 PT presents w/ an artificial internal pacemaker that fires a pacer spike only before the P wave & there is a wide QRS out of NL. This type of paced rhythm is known as a(n):
= AV Sequential
= Ventricular Pacer
= Atrial Pacer
Foramen Ovale:
Pulmonary stenosis:
= hole in the atrial septum that is part of the fetal blood circulation
= pulmonic valve/arteries rigid
Heart’s Endocrine hormones’:
ANP:
BNP:
= store & secretes 2 hormones released when somewhere in heart fail
= Atrial Natriuretic Peptide: made, stored, & released by atrial-M cells response to atrial distension & Sympathetic stim (counter RAAS & lessen afterload pressure)
= Brain Natriuretic peptide: secreted by ventricles response to stress to excessive stretching of myocytes & Counter RAAS
Heart’s 3 tissue layers:
= Endocardium, myocardium, & pericardium.
Hypothermia affect on heart:
= Osborn waves (J waves), <90 core usually, So irritable will/can throw to AFIB
most common causes of cardiac arrest:
= Hypoxia 1st & 2nd Hypovolemia
IF RAAS freaks out:
= BP & afterload increases
If PRI >0.20 seconds, what is occurring in electrical conduction system:
= electrical impulse is being held too long at the AV node.
In any limb lead, a normal P wave shape & maximum amplitude is:
In any chest lead, a normal P wave has maximum amplitude of:
= nice & round w/ maximum amplitude of: 0.25 mV
= maximum amplitude of: 0.15 mV
Intercalated discs:
Discs speed Vs standard cell membrane:
Syncytium:
= Special tissue bands inserted between myocardial cells that increase the rate(400x) in which AP is spread from cell-cell thus Syncytium
= 400x faster than standard cell membrane drom/Inotropy
= Group of cardiac cells physiologically function as a unit, “working together in sync” “top in syncytium to bottom”
Intranodal/Mobitz 2) Sir name
2nd-Degree Type 2 AV block
Isolated Dextrocardia:
Abdominal situs Inversus:
Situs Inversus Totalis:
= Heart on right side/flipped “Right = Left” so mirror leads, AEDs
= Spleen & Liver flipped but H normal
= “EVERYTHING WRONG” H right side
Diltiazem & Verapamil) class
Diltiazem
Verapamil
= class 4 Ca channel blocker
= 1st line med for A-Fib/Flutter w/ RVR >150 bpm, 2nd line med for SVT
refractory to adenosine
= 2nd line med for A-Fib/Flutter w/ RVR. May use as alterative after adenosine, narrow QRS complex tachycardia w/ preserved LV fn.
Junctional Arrhythmias:
(PJC) Premature Junctional Contractions
Junctional Escape Complexes and Rhythm
Junctional Bradycardia
Accelerated Junctional Rhythm
Junctional Tachycardia
Side of heart has most myocardium:
Epicardium makes what & how:
Pericardium holds what, w/ what color & Fn.:
= L side of heart (muscle)
= folds over self to make pericardium
= holds 25-50mLs straw color fluid to reduce friction, 150mL = heart can squeeze,
Labetalol) Indications:
Contraindications:
Do not administer to PTs w/ STEMI if following present:
= 2nd med/ for SVT after admin/ Adenosine, A-Fib/Flutter w/ RVR Reduce myocardial ischemia in AMI PTs w/ +HRs, Antihypertensive
= Increased risk of cardiogenic shock Hypotension Bradycardia
= signs of heart failure Low cardiac output
Labetalol) Adverse Effects:
Max dose:
Adult Dose:
= admin/ after IV Ca-channel blockers can cause severe hypotension, Bcardia, heart blocks & CHF
= 150mg
= 10 mg IV/O push 1-2 mins & May repeat every 10 mins to max dose
Labetalol):
10mg IV/IO push over 1-2mins & May repeat every 10mins to a max dose of 150mg
Leads II, III and aVF look at what part of the heart?
Inferior
Leads II, III and aVF look at what part of the heart?
Inferior wall (most common blockacke(RCA)
Leads V1 and V2 look at what part of the heart?
Septal
Leads V1 and V2 look at what part of the heart?
Septal (blockages from LAD commonly)
Leads 1, aVL, V5, V6 look at what part of heart:
L-Lateral (low view : views LCX & LAD)
Leads V3 and V4 look at what part of the heart?
L-Anteriorwall (LAD & LMCA blocks)
Leads V3 and V4 look at what part of the heart?
Anterior
Lidocaine) Class:
Dynamics:
= Ib Antiarrhythmic
= Blocks Na channels in cardiac cells thus depolarization slows & decreases automaticity in ventricles
Lidocaine) Max dose:
Cardiac Arrest from VF/pVT dose:
Refractory VF dose:
Perfusing Arrhythmia dose:
Maintenance Infusion dose:
= 3 mg/kg
= 1-1.5 mg/kg IV/IO
= may give additional 0.5-0.75 mg/kg IV/IO in 5-10 mins
= may give additional 0.5-0.75 mg/kg IV/IO in 5-10 mins
= 1-4mg/min (30-50 mcg/kg/min)
Lidocaine): Cardiac arrest from VF/pVT:
Perfusing Arrhythmia:
Maintenance Infusion:
=1-1.5mg/kg IV/IO
For refractory VF, may give additional 0.5-0.75mg/kg IV/IO in 5-10mins→ max dose is 3mg/kg
=1-1.5mg/kg IV/IO
For refractory VF, may give additional 0.5-0.75mg/kg IV/IO in 5-10mins→ max dose is 3mg/kg
=1-4mg/min (30-50mcg/kg/min)
Lown Grading system:
benign or malignant for PVCs Grade 0-5 worst-dead
Lown-Ganong
Bundle of James connects posterior internodal pathway to bundle of his (short PRI)
Lown-Ganong) definer:
Pathway name & path:
= has short PRI interval
= Bundle of James connects posterior internodal pathway to bundle of his
Mahaim
Accessory connects to Below bundle of his (wide QRS) looks like VTach
Major vessels of the body:
3 main Major Vessels) 1:
2:
3:
= all branch off of the aorta
= Ascending: comes directly from the heart.
= Thoracic: curves inferiorly & goes through the chest (or thorax).
= Abdominal: goes through diaphragm & enters the ABDMN
Match the Labels
H= Aorta
I= Pulmonary Artery
J= Left Pulmonary Veins
K= Left Atrium
L= Bicuspid Valve
M= Aortic Valve
N= Left Ventricle
O= Papillary Muscle
Match the Labels
A= SA Node
B= AV Node
C= Interventricular Septum
D= Right Bundle Branch
E= Purkinje System
F= Purkinje Fibers
G= Left Bundle Branch
H= Bundle of His
I= AV Junction
J= Internodal Pathways
K= Bachmann’s Bundle
Match the labels
A= Superior Vena Cava
B= Pulmonary Valve
C= Right Pulmonary Veins
D= Right Atrium
E= Tricuspid Valve
F= Chordae Tendineae
G= Right Ventricle
H= Inferior Vena Cava
Med causing a direct increase in PSNS:
Med/ directly blocking the PSNS is:
Parts of heart innervated by PSNS:
Difference in agonist & antagonist:
= Parasympathomimetic
= Parasympatholytic
= AV & SA node
= Ag: stims & Ant: inhibits
Medical PT) Unstable:
Stable:
= AMS, Rapid assess, Basline V/S, Hx of present illness & SAMPLE
= SBP >90, Hx of present illness (HPI), Perform Focused, Assessment, Hx of present illness & SAMPLE
MONA):
M:
O:
N:
A:
= Morphine, Oxygen 94-98%, Nitro, Aspirin
= Morphine: never
= Oxy: maybe
= Nitro maybe: 2nd w/ MI if not contra (decrease afterload)
= Aspirin: maybe (most important) should always 1st line
Morphine) indications:
Contraindications:
= Ischemic chest pain not relieved by Nitro
= Known hypersensitivity to drug Uncorrected hypoBP (SBP<90)
Morphine): STEMI:
NSTEMI-ACS:
= 2-4mg IV/IO (slow); may give + doses of 2-8mg IV at 5-15min intervals
=0.1mg/kg IV/IO (slow) or IM up to 10mg
1st & 2nd most common heart defect:
ASD Atrial Septum Defect:
VSD Ventricle Septum Defect:
= ASD atrial septum defect then VSD ventricle septum defect
= hole in atriums’ septum; when breaths & closes, CAUSES L-R SHUNT, overloads right side decreases BP
= hole in ventricle’s septum L→R shunt, R-side balloons > hypertrophic
Most common dysrhythmia
= Atrial Fibulation
Multifocal Atrial Tachycardia (MAT):
Rules:
1= multiple firing/pacemaker sites (is a rhythm) “WAP w/ RVR”
2= >100BPM, irregular, at least 3 dif/ P wave shapes
PVC) Couplet:
Triplets:
Run on VT:
= 2PVCs back to back “couple coming” (Can be multi/unifocal)
= 3PVCs in row “poligemist” (Can be multi/unifocal)
= >3PVCs in a consecutive row
Myocardium:
= Thick middle layer, Resembles skeletal muscle but has electrical properties like smooth muscle, Conducts electrical impulses for heart contraction.
Natural pacemaker of the heart is:
If SA Node failed to initiate a impulse, what is 1st back-up firing site?
If both SA & AV fails what is last firing site:
= SA node
= AV node
= Purjunkie
Nitroglycerin) indications:
Contraindications
= Symptoms suggestive of Myocardial ischemia CHF
= HypoBP (SBP<90 or >30 below baseline BP) Severe Bcardia<50bpm, Tcardia>100bpm, Use of phosphodiesterase inhibitors (Boner pills) in last 48 hours, Increased ICP
Nitroglycerin) effects:
dose:
=H/A, Dizziness, Weakness, Tcardia, HypoBP (tablets lose effectiveness after exposed to sun/air)
= 0.4mg SL (pill or spray) → repeat 3x (Q5 mins) for total dose of 1.2mg
DONT SHAKE SPRAY B/C AFFECTS DOSE
NORepi) Indi:
Contra:
Effects:
= Normovolemic hypotension, Septic shock, Cardiogenic shock
= hypovolemia PTs til’ Vol/replacement occurred
= Hypertension, Organ ischemia, Cardiac arrhythmia, Tissue necrosis w/ extravasation, Palpitations, Anxiety, N/V
NORepi) Adult Dose:
Pediatric Dose:
= 0.1–0.5 mcg/kg/min IV/IO infusion
= 0.1–2 mcg/kg/min IV/IO infusion
Norm/ ventricle ejects ~2/3s blood it contains @ after systole, known as
Ejection Fraction
Normal Sinus
All WNL
A normal QRS has a duration between:
A normal PRI has a duration between:
= 0.04-0.12 secs / 1-3SB
= 0.12 - 0.20 secs/ 3-5SB
Normal ECG paper speed is
On ECG paper, 1 Small horizontal box represents:
On ECG paper, 1 Large horizontal box represents
= 25mm/sec
= 0.04 secs
= 0.20 secs
On ECG paper, one small vertical box represents:
On ECG paper, one large vertical box represents:
= 0.1mV/ 1mm
= 0.5mV/ 5mm
only condition A-Fib has cadence:
Afib w/ 3rd degree In rhythm “Gandalf dead so Atriums & Ventricles doing own thing
Orthodromic Re-entry loop:
Antidromic Re-entry loop
= Clockwise rentry conduction loop >narrow QRS
= counterclockwise reentry conduction loop > wide QRS
Oxy freeradicals affect what most:
Definition:
= Neurons & cardio myocytes the most killing them
= apopcytosis cell suicide
Which part of the heart has the most muscle:
Oxygenated blood returns to left atrium via:
Blood cell travels from L-ventricle, through what valve & into What:
Deoxy/ blood travels from R-ventricle to lungs through what:
= Left Ventricle
= Pulmonic Vein
= Aortic valve & aorta
= Pulmonic artery
P Wave Asystole:
P waves ventricles dont pick up b/c 3rd degree HB (type of PEA)
Pacemaker sites of ventricles:
(pacemaker detector put on ECG)
Internal pace ECG mode:
External pace ECG mode:
= usually L-ventricle, R-ventricle, in-between
= internal/external
= has line pointing outline
= has filled in line
Pacing is for:
“picking up the pace” too slow
R-atrial enlargement:
Upside down P wave cause:
= changes P wave “P Pulmonele” b/c ventricle backing up or vasodialation, L-Pump failure P mitria “P wave double humps”,
= impulse comes from AV or below atrias
Fossa Ovalis:
Patent Foramen Ovale (PFO):
Forman Ovale A&P:
= depression in R-Atrium remnant of Foramen Ovale
= ASD; hole in atriums septum that didnt close after out of uterus in fetus
= b/c fetus fluid in lung/heart & closes w/ 1st breath b/c lungs neg/ pressure
Pectinate ”comb” muscles L. & Fn:
Chordae Tendineae L. & Fn:
= @ Atriums’ to contract for Mitral & Tricuspid valves
= heart tendons connect to Papillary-M.s, down to open atria valves
Pericardium:
Visceral pericardium (epicardium):
Parietal pericardium:
= Protective sac around the heart w/ 2 layers:
= Inner layer, in contact w/ heart muscle
= Outer, fibrous layer
Phases 0, 1, 2, 3, 4 of CC: Phase0:
Phase1:
Phase2:
Phase3:
Phase4:
= depolarization Cell gap Junction rapid Na influx by an impulse gen/ed elsewhere in heart. Na then stops entering cell once inside +
= K slowly leaves cell slowly returning cell to normal negative charge
= “plateau” M contraction: Ca+ interrupts w/ influxing into cell. (M.s ussing Ca for contraction). This plateau phase slows repolarization
= Repolarization: cessation Ca influx & rapid K efflux
= Refractory & moving ions back to original seats for RP
Preexcitation Disorders of Conduction)Most Common:
2nd:
3rd
= – 1st Wolff Parkinson White (WPW) syndrome
= 2nd Lown-Ganong Levine Syndrome
= 3rd Mahaim Fiber Tachycardia
- (Preexcitation Syndromes SVT (AVRT)) Know:
Most common PS & Etiology:
1= needs accessory pathway & “Ventricles’ back-door w/o passing AV”
2= WPW most common Wolff-Parkinson bundle of Kent (allows SA fired impulse use accessory path to pass AV to prefire) usually R-side dif/ wave morph ) delta wave “2nd P wave slides/slurs to QRS” to pre excite
Preexcitation Syndromes SVT (AVRT)) Know:
2nd Accessory Pathway:
1= needs accessory pathway & “Ventricles’ back-door w/o passing AV”
3= 2nd lown ganong Levine
- (Preexcitation Syndromes SVT (AVRT)) Know:
- Most common PS & Etiology:
- 2nd Accessory Pathway:
- 3rd APS:
- Orthodromic Re-entry loop:
- Antidromic Re-entry loop
- Treat:
1= needs accessory pathway & “Ventricles’ back-door w/o passing AV”
2= WPW most common Wolff-Parkinson bundle of Kent (allows SA fired impulse use accessory path to pass AV to prefire) usually R-side dif/ wave morph ) delta wave “2nd P wave slides/slurs to QRS” to pre excite
3= 2nd lown ganong Levine
4= 3rd Mahaim Fiber Tcardia
5= Clockwise rentry narrow complex
6= counterclockwise- QRS wide
7 =procainamide 1a Na blocker, (if no procain) sedate & cardiovert) cardioversion 50-100J
Preload:
= pressure (volume) w/in the ventricles at the end of diastole & Also commonly called the end diastolic volume (frank starlings law)
1 Premature Ventricular Contractions (PVC):
2 Definers:
3 types:
4 Symptomology:
5 Treatment:
6 Meds:
1= >50% (Don’t + w/ HR) “Pissed off & shouting out”
2= Premature, Wide QRS, no P-wave
3= Benign or Malignant (“>6 PVCs per min)
4= PT may c/o “palpitations” or “skipping” feeling in chest
5= Isolated PVCs in PTs w/ no underlying heart disease usually have no sig/ & usually require no treatment! (majority dont need treat) heart disease w/ ACS, PVCs maybe treated w/
antiarrhythmic med
6= Lidocaine, Amiodarone, Procainamide (best)
PRI measured by:
PRI “PR/PRI” interval rep/s:
A normal PRI interval range:
prolonged PRI indicates:
= distance from beginning of P wave to beginning of QRS complex.
= time impulse takes from atria-ventricles “Gatekeeper Gandolf”
= 0.12-0.20 sec / 3-5 SB
= a delay in the AV node & possible HB
Procainamide & Lidocaine) class
= class 1A&B Na Channel Blockers
= Alterative to Amiodarone in cardiac arrest V-Fib/pVT, Stable monomorphic Ventricular TachyC w/ presserved LVF
= V-Tach with a pulse, pre-excitation rhythms (WPW) >50% QRS width
Procainamide) max dose:
Recurrent VF/VT:
Urgent situations:
Maintenance Infusion:
= (max total dose: 17mg/kg)
= 20mg/min (max total dose: 17mg/kg)
= up to 50mg/min may admin/ to total dose (max 17mg/kg)
= 1-4mg/min
Procainamide)effect:
4 ending points:
= Drowsy, Slurred speech, Confusion, Seizures, HypoBP
= 1. Termination of rhythm, 2. HypoBP, 3. Widening QRS>50%, 4. Meet the max total 17mg/kg/min dose
Procainamide): Recurrent VF/VT:
Maintenance Infusion:
Urgent situationships:
= 20mg/min (max total dose: 17mg/kg)
= 1-4mg/min
= up to 50mg/min may be admin/ to total dose of 17mg/kg
Propranolol, Labetalol, Metoprolol) class
Labetalol
Metoprolol
= class 2 Beta Blockers
= 2nd line med for SVT after Adenosine, A-fib/flutter w/RVR, Reduce myocardical ischemia in AMI PT’s w/elevated HR, Antihypertensive
= Hypertension, 2nd line med for A-Fib/A-Flutter w/ RVR, & SVT
Pulseless & apneic in non-perfusing rhythm: CPR rpid defib
Treatment of bradyarrhythmias, asystole,VF dif/s:
Defibrillation:
= CPR rapid defib
= same treatment as with any patient.
= Don’t discharge paddles directly over battery pack & at<1in
QRS interval measured:
QRS interval represents
QRS interval range:
QRS interval Q,R,&S:
= distance from 1st deflection of complex to last deflection
= time needed for ventricle depolarization (bundle of his > ventricles)
= 0.04-0.12secs / 1-3SB
= 1st -deflection not >1SB, 1st +deflection, -deflection after R
QRS sharp edge “knife” bc:
coming from a side of heart
QT interval:
RR interval:
= any action in ventricles
= measuring HR
Rapid influx of ion causes a autorhythmic cell to depolarize:
Rapid influx of ion causes a contractile cell to depolarize:
Efflux of what ion causes both cardiac cells to repolarize:
= Calcium
= Sodium
= Potassium
Re-entry loops
= stuck in nascar loop in a chambers pathway causing SVT / no P waves
Cardiac cell communication w/ ions
Phase 0 of the cardiac contractile cell:
Phase 1 of the cardiac contractile cell:
Phase 2 of the cardiac contractile cell:
Phase 3 of the cardiac contractile cell:
Phase 4 of the cardiac contractile cell:
= gab junction & intercalated disc 400x faster
= P0) Depolarization
= P1) slow K efflux
= P2) Plateau> Slow Ca in & K out “- for +”
= P3) Repolarization> rapid K efflux
= P4) Refractory Na/K pumps & Ca pumps out
RP of the cardiac contractile cell occurs at:
AP of the cardiac contractile cell occurs at:
ion causes contractile cell to depolarize?
ion contractile cell to repolarize?
= -90mV
= -85mv
= Sodium
= Potassium
Rs 6sec strip method:
big box method:
Small box method:
Triplicate method:
= # of Rs x 10
= 1R to R BB#s then 300/BB#
= 1R-R SB#s then 1500/ SB#
= descend W/ SB 300, 150, 100, 75, 50, 43, 38
RVR:
SVR:
= Rapid ventricular response
= Slow ventricular response
SA node rate:
AV node rate:
Purjunkie rate:
=100-60BPM
=60-40BPM
=40-15BPM
SA Pacemaker P wave shapes
Upright P waves & QRS both WNL
Semilunar valves:
Semilunar valves FN:
Left Semilunar valve:
Right Semilunar valve:
= Aortic & Pulmonic
= reg/ blood flow between ventricles & arteries into which empty. They permit 1-way m-nt of blood & prevent backflow
= Aortic valve connects L-ventricle to aorta.
= Pulmonic valve connects R-ventricle to pulmonary artery
Semilunar valves:
Semilunar valves Fn:
= L-Aortic valve: connects L-Ventricle to Aorta to body & R-Pulmonic valve: R-Ventricle to pulmonic artery to lungs
= reg/ blood flow between ventricles & arteries into which empty. They permit 1-way m-nt of blood & prevent backflow
Sick Sinus Syndrome
Not arrhythmia per se; combination of arrhythmias; sinus node diseased or ischemic. Wild swings in HR, Ischemia of SA node,
Sick Sinus Syndrome:
Rhythm Etiology:
Causes:
S/S:
Treatment:
= “ICU death bed multiorgan fail/dysfunction”: organs dying b/c lacking perfusion, Very rare, Pre cursor to death, No P / beat
= Not arrhythmia per se; combo of arrhythmias; Wild swings in HR,
= SA node diseased or ischemic, Digoxin toxicity, getting old
= Frequent or prolonged episodes may comp/ CO resulting in syncope.
= If signs of poor perfusion, prepare for transcutaneous pacing.
Sinus Arrest) Conduction:
Causes:
= Fails to discharge for period, thus a of cardiac standstill.
= Ischemia of SA node, Digitalis toxicity, Excessive vagal tone, Degenerative fibrotic disease (getting old)
Sinus Arrest)
more than 1 dropped beat & out of cadence
Sinus arrhythmia
All WNL but is not in cadence
Sinus Block)
“Block be in cadence” 1 or more dropped beats IN CADENCE “Gandolf Blocks a beat/s”
Sinus Block) Conduction:
Causes:
= SA node firing blocked for period, thus a brief cardiac “Hold”
= Ischemia of SA node, Digitalis toxicity, Excessive vagal tone, Degenerative fibrotic disease (getting old)
Sinus Brady
All WNL but HR <60
Sinus Pause
“Gandolf messes up flow by pausing it” 1 dropped beat OUT OF CADENCE, SA node, regular rhythms
Sinus Pause) Conduction:
Causes:
= SA node fails to discharge for brief period, thus missing 1 PT seg/
= Ischemia of SA node, Digitalis toxicity, Excessive vagal tone, Degenerative fibrotic disease (getting old)
Sinus Tachycardia
All WNL but HR >100
ST segment:
QT segment:
U wave:
P-T segment:
RR segment:
= Ventricle contraction
= Any action in ventricles
= “late bloomer”
= 1 cardiac cycle
= provides Rate & Rhythm
Starling’s Law of heart:
= states that the more the myocardium is stretched, up to a certain amount, the more forceful the subsequent contraction will be
Stroke volume:
3 factors that affect stroke volume:
= amount of blood ejected by heart in 1 contraction, varies 60-100mLs w/ average 70mL
= preload, afterload, & contractility
Sync Cardioversion:
TCP:
Cardioversion
= “defib in sync”
= “Pick up the pace”
= “Convert/ to slower & normal”
Systematic approach
- rate, 2. rhythm, 3. P waves, 4. PRI, 5. QRS
Systemic vascular resistance:
Nitro dynamics:
= how dilated arteries are
= decreases afterload pressure > decreases workload & O2 demand
T wave represents:
T wave amplitude:
= Repolarization of ventricles
= <5mm in LL <10mm in precordial
TCP dose & check:
= 60-80Ma (80 1st) Mechanical beat w/ every electrical beat & increase by 2Mili-Amps
The SA Node is found where in the heart?
The AV Node is found where in the heart?
Purjunkie System found where in the heart?
= Upper right of atrium
= In the lower right of atrium
= Septum to bottom of ventricles
The coronary vessels A&P
coronary vessels receive blood during diastole when the heart relaxes b/c aortic valve leaflets cover the coronary artery openings (ostia) during systole.
Normal QRS duration:
Normal PRI duration:
= 0.04 - 0.12 seconds
= 0.12 - 0.20 secs
1st negative deflection following the R wave is the:
What wave on ECG represents repolarization of the ventricles:
The first negative deflection following the P wave is the:
What wave on ECG represents depolarization of ventricles:
1st positive deflection following the P wave is:
What wave on an ECG represents depolarization of the atriums:
= S wave
= T wave
= Q wave
= QRS wave
= R wave
= P wave
1st step when deciphering an ECG rhythm is:
2nd step when deciphering an ECG rhythm is:
3rd step when deciphering an ECG rhythm is:
4th step when deciphering an ECG rhythm is:
5th step when deciphering an ECG rhythm is:
= To calculate the heart rate
= Determine if the rhythm has a normal or abnormal cadence
= Evaluate the P Waves
= Measure the PR Interval
= Evaluate the QRS complexes
The period of an ECG that is most vulnerable to an ectopic beat causing the patient to go into a lethal rhythm is known as the:
= Relative Refractory Period (& its segmentation)
Purkinje System has an inherent firing rate of:
AV Node has an inherent firing rate of:
SA Node has an inherent firing rate of:
= 15-40BPM
= 40-60BPM
= 60-100BPM
The RP of a myocardial contractile cell is how many mV’s:
The AP of a myocardial contractile cell is how many mV’s:
What channels in cardiac contractile cells bring about depolarization:
When cardiac contractile cell starts to repolarize – what ion is leaving:
= -90mV
= -85mV
= Voltage gated Na channels
= Potassium
(Coronary) Right coronary artery supplies:
Right Coronary arteries’ 2 major branches:
= portion of R-atrium & ventricle, upper portion of conduction system
= posterior descending artery & marginal artery
The upward slurring of the isoelectric line after the P wave up into the QRS complex that is associated with Wolff Parkinson White Syndrome (WPW) is known as the:
The accessory pathway associated with Wolff Parkinson White Syndrome (WPW) is known as the:
= Delta wave
= Bundle of Kent
Triplicate method:
6 sec method:
R to R small box method:
R to R big box method:
= for HR> Big box RR descends 300,150,100,75,50,50,43,38
= Count # of complexes in a 6-sec strip X 10
= Count small boxes between R waves then /1500 EX: 1500 / 22 = 68
= (only regular rhythm) Count big boxes between R waves then divide 300 by this number EX 300 / 4 = 75
Triplicate method:
= for HR> Big box RR descends 300,150,100,75,50,50,43,38
6 sec method:
= Count # of complexes in a 6-sec strip X 10
R to R small box method:
Count small boxes between R waves then /1500 EX: 1500 / 22 = 68
R to R big box method:
= (only regular rhythm) Count big boxes between R waves then divide 300 by this number EX 300 / 4 = 75
Tunica intima:
Tunica media:
Tunica adventitia/externa:
Lumen:
= inside layer/ tissue of heart
= middle layer/muscle of heart
= external layer of heart
= where blood flows throughs
U wave:
= “late bloomers” repolarization (hypothermic PTs)
Unipolar leads:
Unipolar lead camera:
= 1 polarity(need 4 LL) aVR, aVL, aVF(Wilson’s central terminal)
= Starts at middle point of lines look to center terminal
Unipolar Limb Leads:
aVR:
aVL:
aVF:
= Augmented by the cardiac monitor
= Right Arm positive (inferior)
= Left Arm positive (lateral )
= Left Leg positive (inferior)
V1 & V2
V1 V2 leads view:
Septum
V3 & V4
V3 V4 leads look at
Left lateral wall
V5 & V6
V5 V6 leads look at
Inferior
Vaughn Williams Classification System:
Class I meds:
Class II meds:
Down regulation:
Never mix what w/ what b/c:
Class III meds:
Class IV meds:
Miscellaneous meds:
= Antiarrhythmic med classes by pharmacodynamics
= Sodium channel blockers
= Beta-Blockers
= takes away/blocks CA cells channels:
= Never mix Ca blocker w/ Beta blockers→ stops heart
= Potassium channel blockers “phase 3 K”
= Calcium channel blockers
= Miscellaneous EX Adenosine→ dif/ & adenosine receptors
Ventricle rhythms:
= IVR, AIVR, Agonal, PVC, VT, TdP, VF, asystole, Pacemaker
Ventricles have more muscles so P wave
“eat P wave” if AV fires same as ventricles
Ventricular Arrhythmias:
= from Disorders/sturbances of Conduction, Maybe found in PTa w/ HX of an MI, CHF, CAD
Can go into later from MI
Post ROSC & last breath
Ventricular rhythms definer:
QRS >0.12secs or 3 small boxes w/ no P waves
Verapamil) indications:
Contraindications:
= 2nd med for A-Fib/Flutter w/ RVR, May use as alterative med (after adenosine), narrow QRS complex Tcardia w/ preserved LV function
= HypoBP (SBP<90), CHF/cardio/ shock, Wide-complex Tcardia, WPW
Hypersensitivity to med
Verapamil): 1st:
2nd:
Max dose:
=2.5-5mg IV/IO bolus over 2-3mins
= 5-10mg over 2-3 mins
=20mg
w/ (PJC) Premature Junctional Contraction) 1Rules:
2CANNOT HAVE B/C:
3Compensatory pause
4Non-compensatory pause
1= rate by rhythm, usually slightly irregular, P waves are either inverted before, +after, or hidden w/in QRS
2=have upright P wave (up P= PAC)
3= keeps cadence
4= doesn’t keep cadence
- 1st Degree AV Block) know:
- Definer:
- Rap:
- Rules:
- Etiology:
- Cause:
- Symptoms:
- Treat:
1= “add to any rhythm” “gandolf slowly opening door(PRI)”
2= PRI: >than 0.20 seconds for every PRI & P-P cadence
3= “If the R is far from the P, then you have a FIRST DEGREE!”
4= BPM & rhythm is underlying rhythm, P Waves: Norm/ shape, PRI >0.20secs Pace-Site: SA or atria, QRS: Usually normal
5= Delay in AV node rather than actual block (increases PRI), Not a rhythm but a condition w/in another rhythm
6= Ischemia @ AV junction, MI/@AV, getting old, arteriosclerosis
7= PT usually don’t have symptoms
8= investigate, History/Physical, O2 as needed, 15 Lead ECG
w/ A/V Sequential regain:
atrial kick
WCT monomorphic VT stable:
WCT monomorphic VT Unstable:
= Procainamide 20-50mg/min until 4 ending points, Amiodarone: Max dose 2.2grams in 24Hrs, Sotalol: 100mg (1.5mg/kg), Lidocaine: 1-1.5mg/kg repeat at ½ dose every 5-10mins max of 3mg/kg
= cardioversion: 100J, 200J, 300J, 360J
Wenckebach) Sir name
2nd-Degree Type I AV block
What does the P wave represent on an ECG:
What does the T wave represent on an ECG:
What does the QRS wave represent on an ECG:
= Arterial depolarization
= Ventricular depolarization
= electrical activity in ventricles
What channels in the autorhythmic cells depolarization:
Ap of autorhythmic cell occurs at:
RPof autorhythmic cell occurs at:
ion causes autorhythmic cell to depolarize:
ion causes autorhythmic cell to repolarize:
= Ca channels
= -40mV
= -60mV
= Calcium
= Potassium
What is considered the normal max amplitude of a P wave in lead II?
What is considered the normal max amplitude of a P wave in lead V1?
= 2.5mm
= 1.5mm
What is considered the normal max amplitude of a T wave in lead I?
What is considered the normal max amplitude of a T wave in lead V1?
= 5mm
= 10mm
What is the intrinsic firing rate of SA,AV node, & Purkinje System:
= SA: 60-100BPM, AV: 40-60BPM, Purkinje System: 15-40BPM
What is the most prevalent extracellular ion?
What is the most prevalent intracellular ion? Potassium
= Sodium
= Potassium
1st step when deciphering an ECG rhythm?
2nd step when deciphering an ECG rhythm?
3rd step when deciphering an ECG rhythm?
4th step when deciphering an ECG rhythm?
5th step when deciphering an ECG rhythm?
= Calculate HR
= Determine if rhythm has normal cadence
= P waves
= Measure PRI
= Evaluate the QRS complexes
What med is preferred antiarrhythmic for treatment of (TdP):
Most common type of polymorphic V-Tach is:
= Mag-Sulfate
= (TdP) Torsades de Pointes
When obtaining a 12 lead ECG, where do you place V2?
When obtaining a 12 lead ECG, where do you place V5?
When obtaining a 12 lead ECG, where do you place V6?
When obtaining a 12 lead ECG, where do you place V3?
When obtaining a 12 lead ECG, where do you place V1?
When obtaining a 12 lead ECG, where do you place V4?
When obtaining a 15 lead ECG, where do you place V4R?
= 4th ICS just left of Sternum
= Left 5th ICS anterior of auxiliary
= 5th ICS midaxillary
= ½ in between V2 & V4
= Right of Sternum 4th ICS
= 5th ICS left Midclavicular
= Right ICS midclavicular
When obtaining a 12 lead ECG, where do you place V1?
When obtaining a 12 lead ECG, where do you place V2?
= Right of Sternum 4th ICS
= 4th ICS just left of Sternum
When obtaining a 12 lead ECG, where do you place V3?
When obtaining a 12 lead ECG, where do you place V4?
= ½ in between V2 & V4
= 5th ICS left Midclavicular
When obtaining a 12 lead ECG, where do you place V5?
When obtaining a 12 lead ECG, where do you place V6?
When obtaining a 15 lead ECG, where do you place V4R?
= Left 5th ICS anterior of auxiliary
= 5th ICS midaxillary
= Right ICS midclavicular
When in diastole, which of the valves are open?
Mitral & tricuspid
in Systole & pumping blood from ventricles, which valves are open:
Pulmonic & Aortic
Lead III+ placed:
Lead II+ placed
Lead I+ placed:
Lead III– placed:
Lead II– placed:
Lead I– placed:
= Left leg
= left leg
= left arm
= left arm
= right arm
= right arm
Which coronary artery feeds the anterior wall of the left ventricle?
Left Anterior Descending (LAD)
Which coronary artery feeds the inferior wall of the heart?
Right Coronary Artery (RCA)
Which coronary artery feeds the left lateral wall of the heart?
Left Circumflex (LCX)
Which ECG component represents atrial depolarization?
Which ECG component represents ventricular depolarization?
Which ECG component represents ventricular repolarization?
= P wave
= QRS Complex
= T Wave
Which ion has the greatest influence on muscular contraction:
= Calcium
WPW definer:
Name of assessory pathway:
= has delta wave “wave leaning into R wave”
= Bundle of Kent
WPW) Antidromic loop:
Treatmeats:
= Counterclockwise reentry w/ wide QRS
= procainamide 1a Na blocker, (if no procain) sedate & cardiovert) cardioversion
WPW) Orthodromic loop;
Treatmeats:
= Clockwise reentry w/ narrow complex
= procainamide 1a Na blocker, (if no procain) sedate & cardiovert) cardioversion
WPW) Orthodromic loop;
Antidromic loop:
Treatmeats:
= Clockwise reentry w/ narrow complex
= Counterclockwise reentry w/ wide QRS
= procainamide 1a Na blocker, (if no procain) sedate & cardiovert) cardioversion
You are treating a patient that is in cardiac arrest and you attach them to the cardiac monitor. The ECG presents with P waves that have a regular cadence, but there are absolutely no QRS complexes. This rhythm would be classified as:
P Wave Asystole
You respond for an unconscious patient. Upon arrival you find a 54-year-old male lying supine on the ground with his family performing CPR. You attach your cardiac monitor and find a chaotic rhythm with no identifiable P waves, QRS complexes, or T waves. Based on this information, you would identify this rhythm as:
Ventricular fibrillation
What? secreted by the ventricles of the heart in response to excessive stretching of the ventricle myocytes.
Brain Natriuretic Peptide (BNP)
Med for the treatment of Torsades de Pointes (TdP)
Mag-Sulfate
Mag-Sulfate)Cardiac arrest due to suspected hypomagnesemia/ Tdp:
Tdp w/ pulse:
Maintenance infusion:
= 1-2grams diluted in 10mL
= 1-2grams mixed in 50-100mL admin/ over 5-60mins
=0.5-1gram per hour
TDP med & dose
= Mag-Sulfate} 1-2Gs mixed in 50-100mL/5-60mins & maintaince 0.5-1G/Hr
Bradycardia med
= Atropine 1mg/3mins,
AF w/ RVR & AF med
= Diltiazem/Cardizem} 0.25mg/kg max 20mg, 0.35 max 25mg
WPW / VT w/ pulse med
= Procainamide
Atrial Kick
the contraction “kick” @ end of systole to give more blood to ventricles accounts for 20-30%
VSD=
Right side balloon out & hypertrophic
Isolated Dextrocardia=
(Hearts on right side) Heart is flipped “Right is Left”, so have to mirror leads, AEDs,
Abdominal situs Inversus=
Spleen & Liver flipped but H normal
Situs Inversus Totali
s= “EVERYTHING WRONG” H right side
ASD:
Left to right shunt→ overloads right side decreases BP
Heart’s ENdocrine organ horomones:
stores & secretes 2 hormones, when released failings heart} BNP & ANP
ANP Atrial natriuretic peptide:
made, stored, & released by atrial M> cells in response to atrial distension & Sympathetic stim & counters RAAS system, Decreases afterload pressure
BNP Brain Natriuretic peptide:
secreted by ventricles in response to stress to excessive stretching of myocytes & Counter RAAS
