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104 Cards in this Set

  • Front
  • Back
Depolarize
to become positive from baseline
describe how the sodium channels work.
m gate opens => Na+ leaks in=> slow upstroke "slow channels"
• hit threshold potential => m/ h gates open => Na + rushes in => inc. resting potential 'fast Na channels"
• can't reach +65 b/c the higher you go=> dec. Na+ driving force, inc.K+ driving force
• m gate closes => can't start another action potential = absolute refractory period
Repolarize:
become negatitve from a positive potential
how can K+ reach its potential?
K+ can actually reach its potential of -96 (unlike Na+) b/c of K+ leak channels
Hyperpolarize
become more negative than baseline
how do you get hyperpolarization?
Net positive => Na+ /Ca2+ pump
Net negative=> Na+ /K+ pump
>>3 Na +in, 1 Ca2+ out channels reset the electrical membrane potential (1:1 in rvs direction)
>>3 Na+ out, 2 K+ in ATPase resets the concentration gradient (max activity at -96)
Automaticity
resetting the membrane potential
Charge movement:
All pumps that don't have an ATPase can be reversed ...
• Na/K pump: 3 Na + out, 2 K+ in
=> net negative charge
• Ca/Na pump: 3Na+ in + 1Ca2+ out
=> net positive charge
• Reverse Ca/Na pump: 1 Na + out, 1 Ca2+
=> net posititve charge
Current
change in membrane potential caused by movement of ions
Action potential
"all or none"=> reach threshold, then fires (any extra = "overshoot")
what ion is responsible for the resting membrane potential:
K channels are responsible for this
what ion has a higher conductance and permeability
K+: higher conductance/permeability
which ion has a greater driving force?
Na+: greater driving force
what ion is responsible to depolarize, repolarize and automaticity?
Depolarize (Na) => Repolarize (K) => Automaticity (Na)
what ion does the SA/AV node uses to depolarize?
SA/ AV nodes (use Ca2+ to depolarize)
where is the ion that is responsible for atrial depolarization and contractility?
Extracellular Ca2+ => atrial depolarization
Intracellular Ca2+ => contractility
Cardiac Action Potentials: what ions go in/out in each phase?
Phase 0:
Phase 1:
Phase 2:
Phase 3:
Phase 4:
Phase 0: Na + or Ca2+ in (depolarization)
Phase 1: K+ out (initial repolarization)
Phase 2: Ca2+ in "plateau phase" (conduction to AV node) => contractility
Phase 3: K+ out (repolarization)
Phase 4: Na +in (automaticity = hyperpolarization)- who can reset fastest => inc. slope
Absolute refractory period
all depolarization, some repolarization
Relative refractory period
rest of repolarization = >need bigger stimulus to fire
where are the following located?
SA node:
AV node:
Purkinje:
SA node: RA wall (near SVC)
AV node: interatrial septum
Purkinje: IV septum
where are the ff located?
RA/RV
LA
RA/RV- more anterior "Right behind chest"
LA - compresses esophagus
what artery supplies the SA node?
The dominant artery:
the artery that supplies the SA node
(usually the right coronary)
if a patient lose 40% coronary blood supply, what does that lead to?
lose 40% coronary blood supply=> heart failure
describe the blood supply from the aorta 85% of the blood
85% of heart:
Aorta => Left main coronary a. => L circumflex artery (LA) => marginal artery (LV)
=> LAD (ant. wall, septum, inf. wall, lower 1/3 post. wall)
15% of the blood goes through where?
15% of heart:
Aorta => Right coronary a. => (SA/AV, septum, top 2/3 post wall)=> R marginal (RV)
=> Posterior IV
increase Ca2+ =>

decrease Ca2+ =>
increase Ca2+Arrhythmia
decrease Ca2+: Heart Block
describe atrial depolarization
phases
fires/resets
Phases 0,3,4 only
Fires slow, but resets fast
why do we need to shock the heart when its arrythmic
Ex: Shock the heart to pause it so SA node (no phase 2) can take over
how does lidocaine work in arrythmias?
Lidocaine attacks ischemic tissue only=> silences ectopic site=> SA node rules
what do the ff give you: Ventricle Effects:
inc. Na+:
dec. Na +:
Ventricle Effects:
inc. Na+: Arrhvthmia
dec. Na +:Arrhythmia
(due to Na/ Ca channel)
why tetany (low Ca2+) does not affect your ventricle?
the ventricular cells has Phase 1,2:
which lengthens absolute refractory period
why do purkinjie fibers do not have control?
Fastest firing (Purkinjie fibers), resets slow=> no control
which wall of the heart holds on to contraction the longest and why?
Anterior wall holds on to contraction longest=> longest phase 2
EKG wave: P wave: atrium and phase
P wave = Atrial depolarization (Phase 0)
EKG wave: PR interval: heart mechanics and phase
PR = Conduction from SA to AV node (Phase 2)
EKG Waves:Q wave
Q wave= Ventricle septum depolarization
EKG Waves: R wave
R wave =Ventricle anterior wall depolarization
EKG Waves: S wave
S wave = Ventricle posterior wall depolarization
EKG Waves: QRS
phase
QRS =Total ventricular depolarization (Phase 0)
EKG Waves: QT
what happens if its too long?
QT = Ventricular depolarization/ repolarization
(if too long, ectopic sites take over)
EKG Waves: ST segment
define
phase
ST segment= Ventricle "plateau phase" (Phase 2)
EKG Waves: T wave
phase
define
T wave =Ventricle repolarization (Phase 3)
EKG Waves: U wave
define
phase
U wave = Ventricle automaticity (Phase 4)
what does the height of the EKG mean? tall? short?
Height= voltage:
Tall => enlarged ventricle
Short => small or compressed ventricle (or inflammation)
what does the width of the EKG mean? narrow and wide?
Width = duration:
Narrow = > hypertrophy
Wide => dilated
where are these leads located?
V1-2:
V3-4:
V5-6:
I/ AVL:
II/III/ AVF:
V1-2: Septal
V3-4: Anterior
V5-6: Low lateral
I/AVL: High lateral
II/III/ AVF: Inferior
how does depolariation happend?
SA node => AV node and LA => pause => IV septum => to RV
=> around apex to post side of heart
what fibers are responsible to make the atrium beat together?
bachman fibers
how does repolarization occur?
starts on the posterior side of heart, opposite of depolarization
where are the following bipolar leads located and what part of the heart does it sees?
Lead 1:
Lead 2:
Lead 3:
AVR:
A VL:
A VF:
Lead 1: right arm to left arm, looking at heart from + electrode on L arm (sees left side)
Lead 2: right arm to left leg (sees RV)
Lead 3: left arm to left foot (sees LV)
AVR: on right arm (sees RA)
A VL: on left arm (sees LA)
A VF: left foot (sees apex)
what are the precordial leads for?
Precordial leads: use V 1 and V 2 to see IV septum
Where does each precordial lead located and what part of the heart it sees?
V1
V2
V3
V4
V5
V6
V1 - right upper sternal border (sees RA)
V2 -left upper sternal border (sees LA)
V3 - no anatomical site, half-way between V2and V4 (sees anterior wall)
V4 - left lower sternal border (sees apex)
V 5 - mid-clavicular line (sees LV)
V6 - mid-axillary line (sees LV)
what does a positive deflection mean on an EKG and negative deflection?
Electrodes only detect positive charges: see a wave coming toward it = > + reflection
coming away from it=> - reflection
what would you see on an EKG when you see the ff.
⇧K:
⇩K:
⇧Ca:
⇩Ca:
⇧K: peaked T waves
⇩K: U wave
⇧Ca: short QT
⇩Ca: prolonged QT
how to calculate the max heart rate
max heart rate = 220 - age
Atrial arrhythmias Tx
use Ca+ to depolarize=> use Ca channel blocker, then Warfarin
Ventricular arrhythmias Tx
use Na+ to depolarize => use Na channel blocker
1st Degree heart block: define, pathogenesis and Tx.
PR >5 small squares ~> bad SA node (Tx: exercise)
what are the 2 types of 2nd degree heart block?
Mobitz 1
Mobitz II
what is mobitz type 1, what node is defective and Tx
Mobitz 1: PR lengthens "winks" until drops QRS
~> bad AV node
(Tx: Pacemaker if sx)
what is mobitz II and tx?
PR fixed, but some QRS are gone ~> bad His-P (Tx: Pacemaker)
3rd Degree heart block and Tx?
Regular P-P and R-R, but don't correspond ~> destroyed AV (rx: Pacemaker)
what is an overdrive Pacemakers:
use guidewire to get control away from ectopic site
what are On-demand Pacemakers? what does each letter mean?
1 st letter
2nd letter
3rd letter
On-demand Pacemakers:
1st letter = chamber location
2nd letter = chamber you are sensing
3rd letter = what you want pacemaker to do (I=inhibit)
PSVT Tx:
1) Monitored carotid massage
2) Adenosine
Premature Ventricular Complexes (PVCs): Premature Beat:
QRS has a pause after it
(PVCs): Bigeminy:
PVC every other beat
(PVCs): Trigeminy:
PVC every third beat
(PVCs): Ventricular Flutter: describe and tx
ribbon-like, "Torsade de Pointes"
• Tx: Mg, β -blocker
(PVCs): Ventricular Tachycardia: describe and tx
>>3+ consecutive beats with HR> 150, looks like mountains
>>Tx: Amiodarone if BP normal, otherwise tx like V Fib
(PCV): Ventricular Fibrillation: describe and tx?
No recognizable QRS, looks like quivers
• Tx: Alternate Shock/Drugs (200~> 300~> 360]):
In ACLS what does Epinephrine do?
lowers threshold for cardioversion
In ACLS what does Vasopressin "ADH" do?
holds H20 to ⇧BP
In ACLS what does Amiodarone do?
blocks K, stops all cells
In ACLS what does Lidocaine do?
blocks Na, stops ventricle, only acts on ischemic tissue
In ACLS what does Procainamide do?
blocks Na, stops ventricle
In ACLS what does Mg do?
makes cells less likely to depolarize'
when do you synchronize or unsynchronize when you shock?
(+) Pulse: synchronize when you shock
No Pulse/V Fib: unsynchronized
what are the 3 type of atrial arrythmias?
Premature Atrial Contraction:
Atrial Flutter:
Atrial Fibrillation:
what is Premature Atrial Contraction?
has a pause after it
what is Atrial Flutter
sawtooth pattern
what is Atrial Fibrillation
describe pulse and p waves
irregularly irregular, no p waves
Atrial Arrhythmias complete tx
1) Slow rythym: Diltiazem/Metoprolol (for HR > 120)
2) Increase contraction: Digoxin
3) Chemical Cardioversion: Amiodraone
4) Anticoagulate (for A Fib >48hr): Warfarin, Heparin
>>>Start 3 wk before cardioversion; stop 3wk after sinus rhythm
Electrolyte Imbalance (K+, Ca2+, Mg2+) Tx:
• Hyperkalemia means there is more K+ in the bloodstream (not the cell)
• Ca2+ and Mg2+ get to the door first in the race with Na +
• Dilute with NS first ... If all else fails, do hemodialysis
Low Mg: pathogenesis and mngmt
more likely to depolarize ~> monitor DTR, outs, EKG, vitals q10min
• Give Mg sulfate
how to calculate corrected calcium
Corrected Ca:
0.8 (4-Albumin) + Ca2+
what factors can causes increase Ca:
• ⇧PTH
• ⇧VitD
• Cancer
High Mg management
less likely to depolarize
1) Ca Gluconate (move Mg out of the way)
2) Furosemide (pee Mg out)
Low Ca: physiology of the cell and management
more likely to depolarize
• Ca Gluconate
Chovstek's sign:
tap facial nerve => muscle spasm
Trousseau's sign
BP check causes carpal spasm
High Ca: mngmtn (5 steps)
less likely to depolarize (except atrium)
1) NS
2) Furosemide - pee Ca/Mg out
3) Calcitonin - intranasal
4) Pamidronate (bisphosphonate)- if Ca >16, takes 3 days to work
5) Mithramycin
Low K:
depolariation
EKG and why?
mangement and how much?
less likely to depolarize, narrow T waves/u waves (K+ leaves => negative cell)
• Give K+ (< 10mEq/hr)
High K: management
more likely to depolarize, peaked T waves
"Can I Beat K?"
1) Ca gluconate- save the SA node (unless pt is on digoxin)
2) Insulin/Glucose (or Albuterol IV) - pushes K and glucose into cells (Na/glucose ~> Na/K pumps)
3) Bicarb - make kidney pee K+ out
4) Kayexalate- cation exchange resin to poop K out
Low Na: mngmnt
more likely to depolarize (Na goes out of cell -> Ca flows in -> + cell)
• 0.9% NS (<0.5 mEq/hr to avoid central pontine myelonisis)
very low Na (Na <120): mngmnt
Seizures: 3% NaCl
High Na: mngmnt
more (early) then less (late) likely to depolarize
(Na in -> + cell ->Na leaves via Na/ K pump)
Tx: 1/2 NS
Low PO4: mngmnt
Give phosphate
High PO4: mngmnt
Refeeding Syndrome in anorexics
1) Ca Carbonate (binds P04 in gut)
2) Insulin/Glucose (rapid P04 exchange)
what is milk Alkali Syndrome and tx?
EKG
• Eat lots of Ca, short QT
• Tx: IVF ~> Lasix (get rid of Ca)
what is a colloid solution?
Colloid: Albumin
what is a crystalloid solution?
Crystalloid: Na
what drug increases potassium?
ACE-I
what beta agonist drug decreases potassium?
Albuterol