Lecture 1 Flashcards
DEF: Analgesia
The diminution or elimination of pain
DEF: Conscious Sedation
Minimally depressed state of consciousness that:
- Retains ability to independently maintain airway and
- Respond appropriately to stimuli/commands
DEF: Minimal Sedation
Minimally depressed state that:
- Retains ability to independently maintain airway
- Respond normally to tactile/verbal stimulation
- Cardio unaffected
DEF: Moderate Sedation
Pt responds PURPOSEFULLY to verbal commands
- Retains ability to maintain airway
- Cardio usually maintained
DEF: Deep Sedation
Pt cannot be easily aroused
BUT responds purposefully to REPEATED or PAINFUL stimuli
- May not be able to maintain airway- may need assistance
- Cardio usually maintained
DEF: General Anesthesia
Pt not arousable, even w/ painful stimuli
- Independent airway often impaired- require assistance via positive pressure ventilation
- Cardio function may be impaired
Enteral Administration Types
Oral, Sublingual, Rectal
Parenteral Administration Types
IM, IV, IN, Inhalation, submucosal, subcutaneous, intraosseous
- Bypass GI tract
Heart orientation in chest
- Rotated 30 deg to the left lateral side
- R. Ventricle is most anterior
Tricuspid Valve
Between R. atrium and R. ventricle
Mitral Valve
Between L atrium and L ventricle
Normal heart’s “pacemaker”
Sinoatrial Node
Normal Cardiac Conduction Pathway
SA Node–> AV Node –> Bundle of HIS–> splits left and right here–> Purkinje Fibers –> to cardiac muscle cells
Intrinsic Rate of SA Node
60-100 bpm
Intrinsic Rate of AV Node
40-60 bpm
Intrinsic Rate of Bundle of His
40-60 bpm
Intrinsic Rate of Purkinje Fibers
20-40 bpm
If SA Node fails to initiate an impulse, what happens?
AV Junction (Consists of AV Node and Bundle of His) takes over as the pain pacemaker and heart rate will have a rate of 40-60 bpm
Characteristics of AV Junction as the Pacemaker
- Rate of 40-60 bpm
- Rhythms have a missing or inverted P-Wave!
What if both SA Node and then AV Junction fail??
The ventricles will fire impulses themselves at a rate of 20-40 bpm
What is the effect on the QRS complex of the heart relying on the ventricles for the pulse rather than the SA node or AV Junction?
QRS complex will be wide - >120ms
Normal is 80-120ms
AKA “fast response AP’s”
Non-Pacemaker AP’s
Have rapid depolarization
AKA “slow response AP’s”
Pacemaker AP’s
Have slow depolarization
Found in SA and AV nodes
Opening of what channels start depolarization in Non-Pacemaker cardiac cells
Na Channels
Opening of what channels start depolarization in Pacemaker Cells
Ca Channels
Which cardiac cells have a true resting membrane potential and what is it?
Non-pacemaker cells
-90 mV
Explain the Non-pacemaker cell AP graph
Phase 4 - resting potential at -90mV due to K leaving cell–>
Cell gets rapidly depolarized to -70mV–>
Phase 0 - Rapid depolarization - Fast Na channels open and K channels close –> membrane potential gets more positive
Phase 1 - Initial repolarization due to opening of transient K channels
Phase 2 - Plateau phase- due to L-type Ca channels still open – prolongs AP
Phase 3 - K channels open and Ca channels close allowing full repolarization back to Phase 4
Non pacemaker cell Phase 1
Initial repolarization due to opening of transient K channels which cause short-lived hyperpolarization
Non pacemaker cell Phase 0
Depolarization caused by opening of Fast Na channels at -70
L Ca channels also open at -40
and K channels close
Non pacemaker Phase 2
Plateau phase - due to L Ca channels still open–> causes plateau
Non pacemaker Phase 3
Opening of K channels and closing of L Ca channels–> Repolzarization
Non pacemaker Phase 4
-90 mV - most negative - due to K channels open and K leaving cell
AP in Non-pacemaker cells primarily determined by what channels
Fast Na channels, L type Ca channels, and K conductance
Depolarizing current in SA node AP’s carried by what ion?
Slow Ca currents
Explain the Pacemaker cell AP graph
Phase 4 - spontaneous depolarization up from -60 to -40 due to funny currents of slow inward Na, then T Ca channels open, then L Ca channels open–> until action potential reached around -40 (K channels close too)
Phase 0 - Depolarization! Primarily via L Ca channels
Phase 3 - Repolarization - via K channels openning and L Ca channels closing
Pacemaker cell Phase 0
Depolarization! Via L Ca channels!
Pacemaker cell Phase 4
K channels closing, Funny currents from slow Na inward, then T Ca channels open, and the L Ca channels open further depolarizing until reached AP threshold
Pacemaker cell Phase 3
Repolarization due to K channels opening and L Ca Channels closing
AP in Pacemaker cells primarily determined by changes in which Ion conductance
Ca and K
Hyperkalemia effect on cardiac rate
Bradycardia!!
DEF: Preload
The end diastolic volume in the left and right ventricles
The stretching of the muscle cells to their extend after passive filling and then atrial contraction and right before ventricular contraction
DEF: Afterload
The pressure in the left venticle during ejection- essentially the load against which the heart ejects blood
The greater the aortic pressure, the greater the afterload
DEF: Normal Sinus Rhythm
60-100 bpm
Each QRS preceded by normal, upright P wave
QRS complexes
Draw out normal sinus rhythm
__–__v^v__^___
Causes of longer duration QRS
Hyperkalemia
Bundle Branch Block
DEF: P Wave
Depolarization of the atria
DEF: PR Interval
Time it takes for electrical impulse to get from SA node thru the AV node
Normal: .12-.20 sec
DEF: QRS Complex
Rapid depolarization of the ventricles
Normal: 0.08-.12 sec
DEF: T Wave
Repolarization of the ventricles
DEF: QT Interval
Depolarization and Repolarization of the ventricles
Normal:
Effect of Myocardial Ischemia on EKG
Depression of ST segment or
Flattening or inverting of T wave
Effect of STEMI on EKG
ST segment elevation
DEF: METs
Metabolic Equivalents of Tasks
1 MET is 3.5mL of O2 per kg of body weight
Must be able to meet 4 METs to climb a flight of stairs or walk two blocks
BASICALLY a measure of ability to complete daily tasks
METs
Can’t climb flight of stairs
At greater risk of cardiovascular problem
Someone with METs
Administer less Epi?
Make sure don’t have quick or large changes in pulse or BP
DEF: Ejection Fraction
% of blood leaving heart each time it contracts
Normal Ejection Fraction
55-70%
Evidence of Systolic Heart Failure
Ejection Fraction
DEF: Baroreceptor Reflex
Homeostatic mech to maintain BP
How does Baroreceptor Reflex work?
Provides a negative feedback loop–> if senses elevated BP, it sends signal to heart to decrease rate so as to dec BP
A dec in BP causes dec baroreceptor activation and thus causes heart rate to inc due to lack of signals from baroreceptor
Baroreceptor slows down HR by activation or Parasymps and Inactivation or Symps
Baroreceptor locations
Aortic arch and carotid sinus
Drug eluting vs. Bare metal stent
Drug eluting stents release drug to reduce restenosis
Use of anti-platelet therapy with Drug eluting vs bare metal stents
Okay to treat bare metal stent pt 1 mo after placement if only on aspirin. Have to wait 6 mo to a year for drug eluting to take only aspirin
What provides innervation to the heart?
Vagus N.
Parasympathetic predominance on heart leads to
Slowing the HR
Parsympathetics on the Heart
Release Ach–> goes to Muscarinic receptors–> opens K channels–> slows heart depolarization
Sympathetic predominance on the heart leads to
Increasing the HR
Sympathetics on the Heart
Release NE and E –> goes to B1 receptors–> opens Na and Ca channels–> inc rate of depolarization –> Inc HR
Parasympathetics use which receptors on heart?
Muscarinic
Sympathetics use with receptors on heart?
B1
