Adv. Monitoring Final Review Flashcards
1
Q
ABG Results
A
Oxygenation
Ventilation
Acid-base status
Other: electrolytes (Ca2+, K+), hematology (Hgb, Hct), fluid status, etc.
2
Q
PO2 is measured using
A
Clark electrode
3
Q
At lower temperatures, solubility is
A
increased, leading to a reduction in partial pressure
4
Q
Alpha-Stat
A
Blood gas measurements are obtained after the analyzer warms the sample to 37° C
5
Q
Potential benefits of Alpha-Stat
A
the preservation of cerebral autoregulation + the maintenance of protein function
6
Q
pH Stat
A
Measurements are corrected to the pts temperature before they are used for acid-base and gas exchange management
Because pts are hypothermic, the PO2 + PCO2 at the pts temperature are lower and the pH higher than those measured in the analyzer at 37° C
CO2 is usually added to the oxygenator to maintain the temperature-corrected PCO2 and pH at normothermic values
7
Q
A delay in sample analysis by 20 minutes at room temperature or at 4° C can lead to
A
a decline in PaO2
The decline is attributed to the metabolic activity of leukocytes and is not observed in samples placed on ice
8
Q
The presence of an air bubble in the syringe can lead to
A
a change in the measured PaO2 toward the PO2 of the bubble and a decline in PaCO2*
PaO2 will appear increased
9
Q
3 factors that can independently affect acid-base balance
A
The partial pressure of carbon dioxide in arterial blood (PCO2)
Strong ion difference (SID)
[strong cations] – [strong anions] = [Na+ + K+ + Ca2+ + Mg2+] – [Cl- + lactate-]
Total concentration of weak acids (ATOT)
10
Q
Disturbances that ↑ the SID cause
A
Alkalosis
11
Q
disorders that ↓ the SID cause
A
Acidosis
12
Q
What acid-base abnormality would you expect from aggressive fluid resuscitation with exclusive use of Normal Saline (NS)?
A
HYPERchloremic METABOLIC acidosis
13
Q
Can you describe clinical situation resulting Cl- loss?
A
HYPOchloremic METABOLIC alkalosis caused by aggressive nasogastric suctioning
14
Q
What metabolic abnormality occurs with severe diarrhea?
A
Severe diarrhea, which is associated with loss of both K+ + Na+, reduces the SID and is associated with METABOLIC acidosis
15
Q
What metabolic abnormality occurs with aggresive use of diuretics?
A
Aggressive use of diuretics causes a net loss of free water over Na+ + Cl− and leads to contraction alkalosis
16
Q
The ventilatory control system provides respiratory compensation for
A
METABOLIC acid-base disturbances, and the response is prompt
17
Q
Carotid bodies
A
chemoreceptors located in the carotid bifurcation in the neck + brainstem; they are H+ sensitive*
18
Q
METABOLIC acidosis excites the chemoreceptors and
A
initiates a prompt increase in ventilation decreases the PCO2
19
Q
METABOLIC alkalosis silences the chemoreceptors
A
causes a prompt decrease in ventilation increases the arterial PCO2
Though patients will not decrease ventilation to apnea
20
Q
To determine if respiratory compensation is adequate, the _____ ______ calculates the expected CO2 given the measured HCO3-
A
Winter’s Formula
21
Q
PCO2 = (1.5 x [HCO3-]) + 8 ± 2
A
Winter’s formula
22
Q
How to use Winter’s formula
A
The expected CO2 is then compared to the measured CO2
If the two values are roughly equal, there is compensation
If the measured PCO2 is higher than expected, there is concurrent RESPIRATORY acidosis
If the measured PCO2 is lower than expected, there is concurrent RESPIRATORY alkalosis
23
Q
occurs when there is either an addition of acid to the blood (high anion gap) or there is loss of bicarbonate from the blood (normal anion gap)
A
Metabolic Acidosis
24
Q
The anion gap expresses
A
the difference between unmeasured cations (Ca2+, Mg2+, etc.) + anions (albumin, PO4-3, SO4-2, etc.)
25
Anion Gap (AG)=
= [Na+] - ([Cl-] + [HCO3-])*
26
Normal Anion Gap
Normal is ≤ 12 mEq/L*
27
For every 1 g/dL ↓ in [albumin], the AG
also ↓ by 2.5 mEq/L *
28
the most abundant unmeasured anion
Albumin
29
Meaning a critically ill patient may have a normal AG because of
low albumin, but still have an anion gap metabolic acidosis
30
High anion gap METABOLIC acidosis occurs when
an acid is added to the blood from an additional source
31
For high anion gap metabolic acidosis (AGMA), the ____ ____ helps to determine if a mixed acid-base disorder is present
Delta Ratio
Calculates the contribution to acidosis from the unmeasured anions
32
= (change in anion gap) / (change in bicarbonate) =∆𝐴𝐺/(∆[𝐻𝐶𝑂3−])
Delta Ratio
33
Delta Ratio of <.04
pure NAGMA
34
Delta Ratio .4-.8
mixed AGMA + NAGMA
35
Delta ratio .8-2.0
pure AGMA
36
Delta Ratio >2.0
AGMA + a pre-existing METABOLIC alkalosis
37
HCO3– is lost and Cl- levels rise to maintain electroneutrality
Normal anion gap METABOLIC acidosis occurs when
38
Steps to evaluating an ABG
1. pH acid/alkaline
2. Primary disturbance Respiratory or Metabolic
--Respiratory Opposite
--Metabolic Equal
3. Primary disturbance- Chronic or acute
4. If metabolic disturbance, is resp. compensation okay?- Winter's formula
5. If metabolic acidosis , is AG high or normal?
6. If a hAGMA, are there other metabolic disturbances?- Mixed acid-base disorder- Delta Ratio
39
pCO2 will change in which direction as the pH
Opposite
40
HCO3 will change in which direction as the ph
Equal/Same
41
Acute change in PCO2 increase by 10 leads to
HCO3 increase 1 or decrease in pH by .08
42
Chronic change in PCO2 increase by 10 leads to
HCO3 increase by 3.5 or pH decrease by .03
43
The dicrotic notch is dependent on
properties of the vascular wall
44
in Arterial waveforms, MAP is calculated as
The area under the pressure curve
45
In arterial waveforms, From the aorta to the periphery
systolic upstroke becomes steeper
systolic peak ↑
dicrotic notch appears later
diastolic wave becomes more prominent
end-diastolic pressure ↓
46
Compared with central aortic pressure, peripheral arterial waveforms have*:
higher SBP
lower DBP
wider pulse pressure
47
Damping of arterial waveform
Anything that reduces or absorbs energy in an oscillating system will ↓ the amplitude of the oscillations (damping)
Some degree of damping is required in all systems (critical damping)
48
Underdamping
artifact from catheter (catheter whip)
tachyarrhythmias
short, non-compliant tubing
↑ SBP
↓ DBP
widened pulse pressure
49
Overdamping
anything that will absorb/cause a loss of energy
bubbles + clots
kinks
vasospasm
narrow, long + compliant tubing
↓ SBP
↑ DBP
narrowed pulse pressure
slurred upstroke, absent dicrotic notch, loss of fine detail
50
Arterial waveform with Aortic stenosis
fixed obstruction reduces + slows ejection of blood from the left ventricle ↓ stroke volume
slow systolic upstroke
delayed systolic peak (pulsus tardus)
anacrotic notch
narrowed pulse pressure
waveform appears OVERdamped
51
Arterial waveform with Aortic Regurgitation
steep systolic decline
↓ diastolic pressure
widened pulse pressure
two systolic peaks (bisferens pulse)
first peak is from LV contraction, second peak is from retrograde
52
Arterial waveform with Peripheral vascular disease + HTN
non-compliant blood vessels do not stretch in response to systolic pressure steep systolic upstroke
53
Arterial waveforms during mechanical ventilation
Mechanical (positive pressure) ventilation ↓ preload observe decreases in arterial pressure baseline, SBP + MAP
54
Arterial Wavefrom during Spontaneous ventilation
during spontaneous ventilation, negative intra-thoracic pressure ↑ preload, and a variation of 10 mmHg is normal
exaggerated in pts with cardiac tamponade or restrictive pericarditis
55
Pulmonary Artery catheter can measure
CO
SBP, DBP
PAOP/PCWP
Phtn- MPAP
MVO2 Sat
SVR and PVR
Temp
56
CO=
SV x HR
57
MAP-CVP=
CO x SVR
58
Cardiogenic shock
Poor cardiac function - ischemia
* Low CO & MAP, high SVR ~ sympathetic response
59
Hypovolemic Shock
EBL, GI, 3rd space
* Low CO & MAP, high SVR ~ sympathetic response
60
Distributive Shock
sepsis, anaphylaxis, neurogenic, adrenal
* Low/normal CO, low SVR & MAP ~ warm, bounding pulses
61
Obstructive Shock
tamponade, tension pneumothorax, massive PE
* High CVP / low MAP, equalization pressures R & L cardiac pressures, pulsus
paradoxus
62
Tx cardiogenic shock
* Inotropes = Dobutamine
* Vasopressor for coronary perfusion = Vasopressin or Phenylephrine
* Mechanical = intra-aortic balloon pump or ECMO
63
Hypovolemic shock Tx
Fluids crystalloids/colloids, careful with NaCl due to chloride
64
Distributive shock Tx
* Fluids
* Inotropes & Vasopressors
* Steroids
65
Obstructive Shock Tx
* Tamponade - Cardio paracentesis
* Tension Pneumothorax - Chest tube
* Embolus – Thrombolysis / Pulmonary Embolectomy
66
Electroencephalography (EEG)
= continuous monitoring of electrical activity in the superficial layer of cells in the cerebral cortex
small, metal discs are attached to the scalp
67
Beta brain waves
>12 Hz
usually generalized in distribution
68
Alpha Brain Waves
8-12 Hz
found during wakefulness with eyes closed
69
Theta Brain waves
4-8 Hz
frequent in children + young adults
common when drowsy
70
Delta Brain waves
1-4 Hz
normal during sleep
abnormal while awake (adult)
71
Light anesthesia brain waves
high frequency beta waves > 12 Hz
disorganized topography with lots of variability
occipital/posterior predominance
72
Transition/Asleep brain waves
mid frequency alpha/theta waves
organized topography with less variability
frontal region
73
Deep brain waves
low frequency delta waves
burst suppression
flat EEG
74
Normal BIS number
40-60
75
SED Line normal number
25-50
76
Anesthesia Awareness
both consciousness + recall of surgical events
occurs in ~1 or 2 : 1,000 surgical cases
77
Which anesthetic drugs produce burst suppression on an EEG
Barbiturates
Propofol
Etomidate
Volatile Anesthetics
78
TBW- Total Body Water
60% body weight in males
50-55% in women
ICF+ ECF
Inversely proportional to amount of adipose tissue in the body
79
ICF is what percent of TBW
2/3 TBW
80
ECF is what percent of TBW
1/3 TBW
Interstitial fluid ~ 75-80%
Plasma ~20-25% (or 5% of TBW)
81
EBV Preterm neonate
100 mL/kg
82
Full-term neonate EBV
90 mL/kg
83
Infant EBV
80 mL/kg
84
Child EBV
75 mL/kg
85
Adult male EBV
75mL/kg
86
Adult female EBV
65 mL/kg
87
using hemodynamic parameters and the assessment of fluid bolus responsiveness have been suggested to guide fluid delivery, as opposed to empiric administration
Goal-Directed fluid therapy
88
4-2-1 Rule
From 0 to 10 kg: 4 mL/kg/hr
From 10 to 20 kg: 40 mL + 2 mL/kg/hr above 10 kg
For greater than 20 kg: 60 mL + 1 mL/kg/hr above 20 kg
Or simply, if the pt is >20 kg, add 40 to their weight to get the hourly maintenance rate in mLs
89
Urine output should be kept between
0.5-2 mL/kg per hour, with 0.5 mL/kg per hour being the minimum.***
90
_______ ______ is widely used to guide initial fluid resuscitation needs in the burn patient
Parkland Formula
91
Parkland formula
4 mL x weight (kg) x %TBSA burn*
½ of calculated fluid is given in the first 8 hrs post-burn*
½ is given in the next 16 hrs
92
Rule of Nines
for an adult burn pt assessment, this is the most expeditious method to estimate TBSA
The head is 9% TBSA
Each arm is 9% TBSA
Each leg is 18% TBSA
The anterior + posterior trunk each represent 18% TBSA
93
a measurement of ions in the blood and is normally 280 mOsm.
Plasma osmolality
94
Administration of excessive normal saline can cause
HYPERchloremic metabolic acidosis from the excess Cl- concentrations administered and dilution of serum bicarbonate levels*
95
What type of metabolic derangement is Hyperchloremia?
HYPERchloremic acidosis is a NON-anion gap acidosis as the body is able to compensate and raise serum chloride concentrations to maintain electrical neutrality in these examples.
96
LR Contains
130 Na+, 109 Cl-, 4 K+, 3 Ca2+, 28 lactate* (originally designed to be used as a buffer as lactate is converted into bicarbonate in the liver)
97
Plasmalyte contains
140 Na+, 98 Cl-, 5 K+, 3 Mg2+, 27 Acetate, 23 Gluconate
98
Each liter of albumin contains
145 Na+, 145 Cl-, <2 K+
Also contains 50 g/L albumin
99
How does esophageal doppler measure intravascular volume?
uses a flexible transesophageal Doppler ultrasound probe to measure blood flow velocity in the descending thoracic aorta estimates SV
ECHO can quickly estimate LV size + volume status
100
Fluid responsiveness
= “the ability of the heart to respond to alterations in filling volume by modifying stroke volume.”
101
Pulse Pressure Variation (PPV) =
(𝑃𝑃𝑚𝑎𝑥−𝑃𝑃𝑚𝑖𝑛)/𝑃𝑃𝑚𝑒𝑎𝑛 × 100
PPV >14% associated with fluid responsiveness
102
Stroke Volume Variation (SVV) =
(𝑆𝑉𝑚𝑎𝑥−𝑆𝑉𝑚𝑖𝑛)/𝑆𝑉𝑚𝑒𝑎𝑛 × 100
SVV >13% associated with fluid responsiveness
103
The ultimate target of goal-directed fluid therapy
optimization of pt-specific Frank-Starling Curve
104
The FloTrac system was specifically designed to
provide continuous access to clinically validated parameters and flow-based parameters.”
Cardiac Output (CO)
Stroke Volume (SV)
Stroke Volume Variation (SVV)
105
𝐶𝑂/𝐵𝑆𝐴
Normal 2.5-4.0 L/min/m2
Relationship between cardiac output and body surface area (BSA)
Cardiac Index
106
= (𝑆𝑉𝑚𝑎𝑥−𝑆𝑉𝑚𝑖𝑛)/𝑆𝑉𝑚𝑒𝑎𝑛 × 100
SVV
107
Normal SVV
10-15%, >15% may indicate HYPOvolemia
108
During mechanical ventilation, SVV is
the difference in SV or arterial pressure observed during a respiratory cycle; SVV is caused by the shunting of blood secondary to positive pressure associated with mechanical ventilation
Changes in afterload and venous return (preload) cause SVV
109
Central Venous Oxygen Saturation (SCVO2
Normal >70%
Balance between the delivery and consumption of oxygen (DO2 - VO2); low values indicate increased oxygen extraction or decreased oxygen delivery. Higher levels are seen with impaired oxygen utilization and extraction
110
Brainstem auditory evoked potentials (BAEPs)
Measures the auditory pathway from the cochlear hair cell to the primary auditory cortex
An auditory stimulus (a device that generates loud, repetitive ticks) is placed over the auditory canal. The response is then measured from electrodes located on the external ear or scalp. Both ipsilateral and contralateral signals are recorded
111
Visual evoked potentials (VEPs)
Measures the optic pathway from the retina to the visual cortex of the occipital lobe
112
Somatosensory Evoked Potentials (SSEPs)
monitor the dorsal column–medial lemniscus pathway which mediates tactile discrimination, vibration, + proprioception
stimulation of sensory receptors in the skin initiates peripheral sensory nerves
113
Motor Evoked Potentials
monitor motor pathways via the pyramidal tract and ventral horn
transcranial electrical stimulation elicits excitation of corticospinal projections at multiple levels
the electrical potential is recorded at the spinal cord or muscle groups
114
LAtency
the time between the stimulus + the detected response (signal
115
Amplitude
Strength of the signals
116
What can indicate potential injury of the spinal cord?
A decrease of 50% in amplitude or an increase of 10% in latency
117
EMG
monitors somatic efferent nerve activity + evaluates the functional integrity of individual nerves on certain muscle groups
118
NIM- Neural Integrity Monitor
EMG endotracheal tube (Medtronic) = special flexometallic ETT with conductive silver ink contact electrodes + audiovisual alarms
119
Cerebral oximeters
estimate regional tissue oxygenation by transcutaneous measurement of the frontal cortex, an area that is vulnerable area to changes in oxygen supply/demand
120
Normal Cerebral Oximetry values
60-80%
121
Adequate cerebral oxygenation depends on a balance between
Oxygen delivery and Oxygen consumption
122
Zeroing
the use of atmospheric pressure as a reference standard against which all other pressures are measured
123
Test used for determining if collateral flow is present for arterial line placement
Allen Test
124
A wave on CVP Monitor
End Diastole
Atrial Contraction
125
C wave on CVP MOnitor
Early systole
Tricuspid bulging (IVC)
126
V Wave on CVP Monitor
Late systole
Systolic filling of the atrium
127
X Descent on CVP
Mid systole
Atrial Relaxation
128
Y Descent on CVP
Early diastole
Early ventricular filling
129
ECF Is made up of
80% interstitial fluid
20% plasma
130
Delivery of oxygen (DO2)
DO2 = CO x CaO2
CaO2 = content of arterial oxygen
Critical illness and surgical stress lead to a systemic inflammatory response + increased oxygen demand
Increasing CO will increase the delivery of oxygen
131
Consumption of Oxygen (Vo2)
VO2 = (CO x CaO2)−(CO x CvO2)
CvO2 = mixed venous oxygen content in the pulmonary artery
VO2 can be determined by measuring the difference inspired and expired oxygen
132
Fick Principle
the uptake of a substance (oxygen) by an organ is related to the amount of blood flow to that organ and the arterio-venous (A-V) concentration difference of the substance
133
CO = "VO2" /("CaO2" − "CvO2" )
Total uptake of oxygen divided by the difference in A-V oxygen concentration
Fick Principle
134
Oxygen Extraction Ratio
(CaO2 - CvO2)/CaO2
normal is ~ 0.25
135
A-fib CVP waveform
Loss of A wave
136
Tricuspid regurgitation CVP Waveform
fusion of c + v waves
137
Canon A wave on CVP
AV-dissociation, Complete heart block, Pulmonary HTN
138
Pulmonary HTN, Tricuspid stenosis
on CVP Waveform
Attenuated y wave, Tall a wave
139
Cardiac tamponade CVP Waveform
Dominant x descent, Absent y descent
140
Monro-Kellie Hypothesis =
the cranial compartment incompressible and volume inside the skull is constant
141
Cerebral perfusion pressure (CPP) =
Arterial pressure-ICP
CPP = MAP - ICP or CVP (whichever is higher)*
142
Normal CPP
Normal range 70-90 mmHg
143
the largest + most important buffer system in the body*
Carbonic Acid system
144
AICDs consist of
Consists of pacing/sensing/defibrillation electrode and a generator
145
Indications for AICDs
Primary prevention
Secondary prevention: Aims to prevent sudden cardiac death in patients with prior episode of sustained VT, VF
146
Permanent Pacemakers
Device implanted in the subcutaneous left chest wall
Consists of a generator/battery unit and 1 to 3 wires depending on indication and intended use (1 RA/1 RV) or RA/RV/ Coronary sinus and ventricular wall
Wires are tunneled subcutaneously into the subclavian vein and eventually into the right side of the heart
147
Leadless pacemakers
Self contained generator and electrode system implanted directly into the right ventricle (Both a generator and electrode) Access R Femoral, Right side of the heart, tag the bottom/apex of heart in RV and implant pacemaker. Hard to retrieve once implanted, embedded in cardiac tissue. Cannot detect atrial current in RA
Eliminates risk of pocket infections, lead dislodgment, and lead fracture
Provide only single-chamber ventricular pacing and lack defibrillation capacity
Pacemaker is inserted via the femoral vein and is tethered or screwed into the myocardium
Hard to retrieve because they get embedded into cardiac tissue; may need to be abandoned
148
Universal 5 position code
Position 1 - chambers paced
Position 2 - chambers sensed
Position 3 - how the pacemaker responds to a sensed event
Position 4 - rate modulation
Position 5 - specifies the location or absence of multisite pacing- subcategory of cardiac resynchronization mode
Pacemaker Nomenclature
149
Position 1 of pacemaker
Indicates which chambers are being paced
A = Right Atrium
V = Right Ventricle
D = Both the right atrium and the ventricle
150
Position 2 of Pacemaker
Where in the heart is the pacemaker sensing electrical activity
A = Right atrium
V = Ventricle
D = Both the right atrium and the ventricle
O = Nothing (pacemaker set at a specific rate, does not matter what the heart is doing)- Not detecting
151
Position 3 of Pacemaker
How the pacemaker responds to sensed electrical activity
I = Pacemaker activity is inhibited (it does not pace when electrical signal is sensed)
T = Triggered (electrical activity triggers pacemaker)
D = Can be both inhibited and triggered
For use in dual chamber pacemaker (leads in RA and RV)
If atrial activity is sensed, the ventricle is paced after a slight delay
If ventricular activity is sensed during the delay, the pacemaker is inhibited
O = No response to sensed electrical activity
152
When the pacemaker senses atrial firing,
delay, fires ventricular lead for ventricle to contract in coordination- dual (inhibited AND Triggered)
153
Position 4 of Pacemaker
Rate modulation- Pacemaker senses physical activity- vibration and increases rate of pacing to meet the cardiac demands
R = There is rate modulation
O = there is no rate modulation
Rate modulation means there are sensors in the device that can sense physical activity (minute ventilation, vibration) and increase the rate of pacing
154
Position 5 Pacemaker
Location of multisite pacing- Subcategory of cardiac resynchrconization. Map out where the pm should fire, optimizing cardiac output
Usually used in setting of heart failure for biventricular pacing (CRT)
Can lead to better synchrony and improved outcomes
A = multisite pacing in the artium
V = multisite pacing in the ventricle(s)
D = multisite pacing in atrium and ventricle(s)
O = no multisite pacing
155
Magnets for ICD
stops anti-tachy-arrhythmia therapy
156
Magnet on ICD/Pacemaker
will continue its pacemaker activity.
157
If an ICD is turned off,
put on defib pads because the ICD is off and external source will be required
158
Pacers w magnet
go to standard setting ex. VOO @80 or VOO@90 based on manufacturer settings
159
Asynchronous pacing
Pacemaker programmed to pace at a fixed rate, without attempting to sense or react to native cardiac activity
Sensing capability is turned off
Often used during surgical procedures or during an MRI
Prevents electrocautery from inhibiting the pacemaker and causing asystole in patient in pacemaker dependent
160
Concern with asynchronous pacing
May lead to competition between native and paced rhythms
Concern for R on T phenomenon. Magnet set at high rate, helps prevent R on T phenomenon
161
R on T Phenomenon
is a PVC that occurs towards the end of a T wave of the preceding heart beat. It can lead to ventricular tachycardia
It is often associated with Long QT Syndrome (Anti-emetics,etc.)
This can occur with pacemakers when set in an asynchronous mode
The Pacemaker can stimulate the ventricles during a native T wave, leading the ventricular arrhythmia
162
Heart conduction system
SA Node (right atrium) - atrial contraction
Bachmann’s Bundle carries electrical signal to the left atrium
AV Node (interatrial septum) - delay allowing ventricles to fill
Left and right bundles of His
Purkinje fibers
Ventricular myocytes
163
Primary Pacemaker
SA node located near the RA/SVC junction
HR of 100 bpm influenced by sympathetic and parasympathetic inputs
164
Secondary Pacemakers
AV node, 40-60 bpm
Left and right bundle branches, 30-40 bpm
Purkinje fibers, 30-40 bpm
165
If the SA Node fails to generate an AP,
other pacemakers can generate a action potential. Muscarinic receptors
166
Pacemaker AP
Phase 4- HCN Funny current, T-Type Ca2+ Channels
Phase 0- L-type Ca2+ channels
Phase 3- Voltage-gated K+ Channels
167
Phase 4: Diastolic depolarization
If “funny channels” are activated by cell repolarization, allow inward sodium current
Rate of depolarization sets heart rate
168
L-type voltage-gated Ca2+ channels allow calcium influx rapidly depolarizing the cell
Phase 0: Rapid depolarization/upstroke
169
Phase 3- repolarization
Voltage gated potassium channels open, allowing potassium efflux
170
Ventricular AP
Phase 4: Resting potential
Phase 0: Rapid depolarization
Voltage gated sodium channel-depends on
Phase 1: Rapid repolarization
Potassium efflux
Phase 2: Plateau
Calcium influx
Potassium efflux
Phase 3: repolarization
Potassium efflux
171
1st Degree AV Block
PR interval greater than 200 ms in length (normal 120-200 ms)
Causes include AV nodal disease, enhanced vagal tone, myocarditis, acute myocardial infarction, electrolyte abnormalities, and medication
No pacemaker needed
172
2nd Degree AV Block
Mobitz type I and II
173
Mobitz I (Wenckebach)
Progressive prolongation of the PR interval on consecutive beats followed by a blocked P wave (dropped QRS complex)
Atrial rhythm is regular
No pacemaker required unless symptomatic
174
Mobitz II
Intermittently non-conducted P waves
Often progresses to complete heart block
Treated with implanted pacemaker
175
3rd Degree AV Block
Electrical signal from SA node does not reach the ventricles
Escape rhythm generated by accessory pacemaker in the lower chambers will activate the ventricles
Regular P-P intervals faster than normal
Regular R-R intervals
Wide QRS
Common causes are ischemia, congenital heart block, iatrogenic (magnesium overload)
Treated with transcutaneous/transvenous or implanted pacemaker
176
Sick Sinus Syndrome/ Sinus Node Dysfunction
Tachycardia - bradycardia
Atrial fibrillation
Atrial flutter
Paroxysmal SVT
Sinus bradycardia
Sinus arrest
w/wo junctional escape
177
Symptomatic chronotropic incompetence
Type of sinus node dysfunction
Impaired heart rate response to exercise, generally defined as failure to achieve 85 percent of the age-predicted maximum heart rate
Fatigue or light headedness with activity
Usually diagnosed on stress test
Should rule out other causes such as coronary artery disease prior to pacemaker implantation (L Heart Cath before implanting PPM)
178
Temporary Cardiac Pacing
Used in the setting of acute bradycardia that leads to hemodynamic instability
Methods:
Transvenous
Transcutaneous
Epicardial (we do after cardiac surgery)
Transesophageal
179
Cardiac Resynchronization Therapy (CRT
Leads placed in right ventricle and left ventricle (via coronary sinus to a coronary vein)-
RA-> Coronary Sinus -> LV
Indications:
HF symptoms, LBBB with QRS ≥150 ms, EF ≤35 percent
Asymptomatic LV systolic dysfunction
EF < 50% and another indication for a CIED
Synchronizes electrical activity and function of the ventricles
Improves EF and survival
180
Twiddler’s syndrome
- generator twists around in the pocket
Leads to changes in threshold at which device paces or defibrillates
181
Decrease in LVEF due to pacing of the RV
LVEF of <50%, absolute decline of LVEF by ≥10% and/or new-onset heart failure (HF) symptoms or atrial fibrillation (AF) after pacemaker implantation
Pacemaker-induced cardiomyopathy
182
MR-Safe
The device or implant is non-magnetic, non-electrically conductive, and is safe for use in an MRI machine
183
MR-Conditional
A device or implant that may contain magnetic, electrically conductive, or RF-reactive components that is safe for operations in proximity to the MRI, provided that certain settings are used in the MRI scan
184
MR-Unsafe
Objects that are significantly magnetic and pose a threat to person undergoing MRI- Older pacemakers from the 90s
185
LVOT Area x LVOT VTI
SV
186
(LVOT Area x LVOT VTI) x HR
CO
187
SV (mL/cycle) x HR (bpm)
CO mL/min
188
TEB- Thoracic electrical bioimpedance
a form of plethysmography; fluid within the thorax causes impedance (resistance to electrical current)
189
THoracic Bioreactance
more closely relates to the aortic
blood flow; the phase shift in voltage across the aorta depends on pulsatile flow
190
