Adv. Monitoring Final Review Flashcards
(304 cards)
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)
tricuspid valve (TV) elevation during early ventricular Contraction
126
V Wave on CVP Monitor
Late systole
Systolic filling of the atrium
Venous return against a closed TV
127
X Descent on CVP
Mid systole
Atrial Relaxation
downward displacement of the TV in systole and atrial relaXation
128
Y Descent on CVP
Early diastole
Early ventricular filling
descent is due to the tricuspid valve opening during diastole; atrial emptYing
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
any increase in one component must be offset by an equal decrease in another component
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
ECF is made up of
Plasma ~20-25% (or 5% of TBW)
80% interstitial fluid
191
What PPV is associated with fluid responsiveness
PPV >14%
192
What SVV is associated with fluid responsiveness
SVV >13%
193
The point at which the pt is unresponsive to fluids indicates
other interventions such as administration of inotropes may be needed
194
demonstrating the relationship between LVEDV (preload) and stroke volume
Frank-Starling curve
195
how much blood the heart pumps out from the left ventricle each minute
Cardiac output
CO
196
accounts for the pts body size
Cardiac index
CI
197
𝑪𝑶/𝑩𝑺𝑨
CI
198
Normal Cardiac Index
2.5-4 L/min/m2
199
Normal Cardiac Output
4-8 L/min
200
preload, afterload + contractility
Stroke Volume (SV)
201
content of arterial oxygen
CaO2
202
Increasing CO will increase
the delivery of oxygen
203
mixed venous oxygen content in the pulmonary artery
cVO2
204
VO2 can be determined by
measuring the difference inspired and expired oxygen
205
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
Fick Principle
206
"VO2" /("CaO2" − "CvO2" )
Total uptake of oxygen divided by the difference in A-V oxygen concentration
CO
207
multi-factorial syndrome resulting in inadequate tissue perfusion + cellular oxygenation affecting multiple organ systems
life-threatening, generalized mal-distribution of blood flow which results in failure to deliver adequate amounts of oxygen, leading to tissue dysoxia
Shock
208
measured from the oxygen saturation of blood taken from a pulmonary artery catheter tip
MVO2
209
CaO2 - CvO2)/CaO2
O2 Extraction Ratio
210
Normal o2 Extraction Ratio
normal is ~ 0.25
211
indicates the amount of oxygen not extracted by the tissues
MvO2/SVO2
212
indicates either less oxygen is being extracted from the tissues or more oxygen is available in the blood
oxygen delivery >>> oxygen demand
High SvO2
213
indicates the tissues are extracting more oxygen or less oxygen is being delivered to the tissues
oxygen delivery <<< oxygen demand
Low sVO2
214
Vasopressor of choice for Distributive shock
Norepinephrine
215
Central line site selection
RIJ > subclavian > femoral locations
216
typically smaller in diameter
potential for injury to the thoracic duct which drains at the junction of the LIJ + L subclavian veins
Left IJ
217
most direct route to the right side of the heart
Right IJ
218
Pneumothorax
Arterial puncture / unrecognized cannulation
Infection
Arrhythmia
Trauma from wire // Retained wire
Air emboli
Chylothorax
Malposition of catheter
Complications of central line placement
219
Steep x + y descent, Tall a + v waves
CVP
Constrictive Pericarditis
220
Principal buffer in ICP
CSF
221
How do we know the PAC is in the right location?
Diastolic step-up
222
Secondary buffer in ICP
Blood
223
Brain parenchyma volume
1400 mL
224
CPP indicating poor survival
<50mmHg
225
Elevate head of bed 30 degrees
Sedation/Paralysis
Drain CSF
Osmotherapy
Barbiturate coma
Hypothermia
Decompressive craniectomy
Mild temporary hyperventilation 30-35 mmHg
Increased ICP Treatment
226
↓ amplitude + slower frequency indicates what?
Neural depression
227
Normal SED Line Values
25-50
optimal range of anesthesia
228
Normal BIS Values
40-60*** = pt is considered to be appropriately anesthetized (i.e., unconscious)
229
100 on SED Line indicates
Pt is fully awake
230
Monitor electrical activity in the frontal + pre-frontal cortices
SED Line
231
BIS value of 0
profound state of coma or unconsciousness; isoelectric or flat EEG
232
BIS value of 100
completely awake
233
SED Line value of 0
deep anesthetic state, burst suppression
234
multiple traumas*
cardiac surgery*
obstetric procedures* (i.e. emergent C-section)
difficult intubation
PMH of awareness
Gender (3x higher in females)
Pts with acquired + inherited anesthetic resistance
Pts with reduced anesthetic requirements (i.e. cardiovascular compromise)
Age (young)
TIVA*
Use of neuromuscular blocking agents*
Risk factors for intra-op awareness
235
Slow EEG activity, delta waves predominantly present lead to burst suppression
Volatiles
236
Enhances GABA activity
EEG changes similar to barbiturates (initial excitatory spikes followed by burst suppression)
May activate seizure foci
Myoclonus can create seizure-like EEG activity
Etomidate
237
Works on GABA receptor
High doses produce burst suppression
Propofol
238
Work on GABA receptor
Initial EEG activation followed by dose-related burst suppression
i.e. methohexital + thiopental
Barbiturates
239
Dose-related decrease in EEG amplitude + frequency
Even with high doses, opioids do NOT produce an isoelectric EEG
Opioids
240
Antagonist at the NMDA receptor
allows continuation of brain electrical activity without being modulated…results in lack of proper coordination in space + time (desynchronization)
increases CMRO2
Ketamine
241
Causes fast oscillations in high beta low gamma frequency range (25-32 Hz) with slow delta oscillations
Ketamine
242
Decrease CMRO2 + CBF
Decrease EEG amplitude but do not produce burst suppression
Benzodiazepines
243
Alpha-2 agonist
EEG wave mimics slow-wave sleep/NREM sleep pattern
Dexmedetomidine
244
have excellent ability to assess dorsal column + lateral sensory tract function
SSEP
245
involves the placement of electrodes onto the arms, legs + scalp to monitor the function of the spinal cord + nerves during spine surgery
Spinal neuromonitoring
246
Because of ECG interference, evoked potentials
must be averaged to improve signal-to-noise ratio
247
Volatile agents can be used if 0.5 MAC
Paralysis is okay
Opioids + ketamine desirable
SSEP
248
exquisitely sensitive to volatile anesthetics***
TIVA is mandatory
NO paralysis
Opioids + ketamine desirable
MEP
249
occurs when CO2 elimination < CO2 production*
Respiratory Acidosis
250
= occurs when CO2 elimination > CO2 production
Respiratory Alkalosis
251
Normal Albumin
normal range is 3.5 – 5.5 g/dL)*
252
Meaning a critically ill patient may have a normal AG because of
low albumin, but still have an anion gap metabolic acidosis
253
Most non-invasive blood pressure devices are based on
oscillometry (NIBP cuffs)
254
the most unreliable oscillometric measurement
DBP
255
convert mechanical energy electrical energy through a pressure transducer; this electrical energy is then displayed as a waveform on a monitor
Arterial line
256
Re-adjusting the level of the transducer 10 cm will distort the IBP reading by
7.5 mmHg
257
is dependent on properties of the vascular wall
Dicrotic notch
258
is calculated as the area under the pressure curve
MAP
259
Compared with central aortic pressure, peripheral arterial waveforms have
higher SBP
lower DBP
260
the systolic upstroke begins ~ 60 ms later in the radial artery than
the Aorta
261
MAP in the aorta is only slightly higher than
that in the periphery
MAP remains roughly the same
262
perfusion pressure below end organs auto-regulatory range (<60-65 mm Hg) results in
impaired organ blood flow.
263
the difference between organ arterial and venous pressures. Because normal organ venous pressure is typically negligible, the organ perfusion pressure is usually equal to the organ arterial pressure, which is the MAP, thus demonstrating the direct relationship between organ blood flow and MAP
Organ perfusion pressure
264
A MAP of >65 mm Hg must be maintained to perfuse
the cerebral + coronary vasculature.
265
involves treating the underlying cause
Primary Resuscitation
266
involves ensuring adequate hemoglobin levels + intravascular volume status, and then administering other vasoactive agents to achieve the resuscitation end points.
Secondary Resuscitation
267
drugs that increase contractility (positive inotropy), and ay also cause vasoconstriction (especially in higher doses
Inotropes
268
primarily produce vasoconstriction with subsequent increase in SVR + MAP
Vasopressors
269
When are vasopressors indicated?
There is a decrease of >30 mmHg from baseline SBP pressure or MAP <60 mmHg
Condition results in end-organ dysfunction secondary to hypoperfusion
270
the force + velocity of cardiac muscle contraction
Inotropy
271
refers to a drug that produces positive inotropy (increased contractility
Inotrope
272
agents that produce inotropy + vasodilation
Isoproterenol, milrinone, dobutamine
Inodilators
273
agents that produce inotropy + vasoconstriction
Inoconstrictors
274
Venodilation associated with its use ↓ venous return (preload), resulting in a minimal increase in CO and a drop in MAP
Isuprel
275
Because a transplanted heart is denervated, ________ is commonly used following cardiac transplantation to maintain an elevated HR + CO
Isuprel/Isoproterenol
276
Limited to situations in which hypotension + shock result from bradycardia or heart block
Isoproterenol
277
that ↑ intracellular concentrations of cyclic adenosine monophosphate (cAMP) in myocytes + vascular smooth muscle cells resulting in ↑ myocardial contractility and smooth muscle relaxation in the pulmonary + systemic circulation
Milrinone
278
Improves diastolic relaxation (lusitropy)
Milrinone
279
Stimulates primarily β1-receptors + β2-receptors, resulting in ↑ chronotropy, inotropy, + systemic and pulmonary vasodilation ultimately ↑ HR + CO while decreasing SVR with or without a small reduction in MAP
Dobutamine
280
the most common mechanical device, it consists of a thin catheter with a long balloon attached at the tip and a computer console at the other end, which then inflates or deflates the balloon with Helium gas in correlation to cardiac contraction
The balloon sits in the aorta 2–3 cm distal to the origin of the left subclavian artery, resulting in maximal augmentation of coronary arteries while reducing the risk of embolization to the cerebral vessels + occlusion of the LSCA
The balloon has a pressure transducer, which produces a waveform
IABP
281
Balloon inflation is triggered at the beginning of diastole, then deflates at the beginning of systole. The deflation of the balloon assists the LV by ↓ aortic end-diastolic pressure and aortic fluid volume
Theoretically ↑ coronary perfusion
Counter pulsation technique
282
Indications for IABP
Cardiogenic shock
Refractory ischemia
Failure to wean from CPB
283
Contraindications for IABP
Aortic insufficiency
Arrhythmias
Aortic dissection
Aortic aneurysm
Severe peripheral vascular disease
284
Blood is pumped from the LV into the ascending aorta, while helping to maintain a systemic circulation at an upper rate between 2.5-5.0 L/min
Results in almost immediate + sustained off-loading of the LV, while ↑ overall systemic CO
Impella
285
Using retrograde femoral artery access, the _____ device is placed in the left ventricle across the aortic valve
Impella
286
(most common) in the treatment of acute myocardial infarction complicated by cardiogenic shock, and to facilitate high-risk coronary angioplasty
In the treatment of cardiomyopathy with acute decompensation, postcardiotomy shock, + off-pump coronary bypass surgery
Indications for Impella
287
percutaneously placed and diverts blood from the left atrial to the iliac artery, bypassing the left ventricle
transseptal cannula position
Tandem Heart
288
It is powered by an external centrifugal pump that provides up to 3.5-5 L/min of forward flow by standard implantation technique
TandemHeart
289
Placement requires BOTH arterial + venous access at the femoral vessels
TandemHeart
290
assumes the pump function of a failing left ventricle by utilizing a mechanical pump
Inlet cannula is placed in the apex of the left ventricle (LV) and blood is diverted to the ascending (most common) or descending aorta
LVAD
291
Can be used a bridge to transplant (BTT) or destination therapy (DT)
LVAD
292
flow include preload + afterload (pressure gradient across the pump), RV function, and the speed of the pump (revolutions per minute (RPM))
Factors that affect LVAD
293
common complication of LVAD
obstruction of inflow or outflow cannula
294
occur when the LV is under filled due to RV failure or hypovolemia. If suspected, it should be treated aggressively with a fluid challenge. The VAD personnel may also ↓ the pump speed temporarily to allow for improved LV filling
Suction event
295
defined as five or fewer contractions in 10 minutes, averaged over a 30-minute window
Normal contractions
296
defined as greater than 5 contractions in 10 minutes, averaged over a 30-minute window
Tachysystole
297
Internal monitoring may be necessary via an electrode on the fetal scalp for continuous and most accurate FHR monitoring
A peak or threshold voltage of the fetal R wave from the electrode is used
Can only been placed is cervix is dilated and membranes ruptured
Rupturing membranes can cause fetal injury or amnionitis
Fetal scalp monitoring
298
110-160beats/min
Increased with premature fetus, maternal fever, amnionitis, hyperthyroid, maternal medications (beta agonist, anticholinergic)
Baseline FHM
299
Increases of at least 15beats/min for more than 15 seconds but less than 2 minutes
Accelerations
300
Decreased HR at or following peak contraction
As few as 5bpm
Relates to a decrease of arterial oxygen on chemoreceptors
With normal variability- can be due to maternal hypoxia or hypotension and is usually reversible
Late Decels
301
FHR:4 accels in 40minutes
Fetal breathing: 30 seconds
Fetal movements: Truncal
Flexion/Extension: arm/leg activity
Amniotic fluid
BPP
Biophysical profile
302
8-10 No concern
6 Ambiguous
2-4 Concerns for hypoxia, acidosis, immediate delivery
0 immediate delivery
BPP Scores
303
Prior 24 weeks gestation-
Pre and post monitoring
304
After 24 weeks gestation
Make clear plan with OB
Availability of trained staff for emergent C/S
Availability of trained pediatric team for neonatal resuscitation
High risk surgeries: abdominal, thoracic, neuro
