NURS 332 Flashcards
(303 cards)
1
Q
Trauma Process Steps
A
- Prep and triage
- General impression
- Primary survey
- Secondary survey
2
Q
Primary Survey
A
A: Alertness & airway
B: Breathing & ventilation
C: Circulation & control of hemorrhage
D: Disability (neuro status)
E: Exposure & environment control
F: Full set of vitals and family presence
G: Get adjuncts & give comforts
3
Q
Secondary Survey
A
H: History
H: Head-to-toe assessment
J: Just keep re-evaluating
4
Q
AVPU
A
Alert, Verbal, Pain, Unresponsive
5
Q
A: Alertness & airway - Assessment
A
AVPU, airway patency, cervical spine immobilization
6
Q
A: Alertness & airway - Interventions
A
Jaw-thrust maneuver, oro/nasopharyngeal airway (OPA/NPA), endotracheal tube (ETT)
7
Q
Ensuring ETT placement
A
1) CO2 detector (purple = good, 35-45mmHg)
2) Chest rise/fall observation
3) Auscultate epigastrium & bilateral breath sounds
8
Q
B: Breathing & Ventilation
A
Breath sounds, depth, rate and pattern, work of breathing, dyspnea, spontaneous breathing, subcut emphysema (rice krispy), tracheal deviation (LATE)
9
Q
C: Circulation and control of hemorrhage - Assessment
A
Color, temp, central pulse, control hemorrhage
10
Q
C: Circulation and control of hemorrhage - Interventions
A
Torniquet, multiple IV’s running WARM fluids
11
Q
D: Disability (neurological status)
A
GCS - eyeopening, verbal response, motor response
AVPU
Pupils
Glucose (BGM)
12
Q
E: Exposure & environment control
A
Remove clothing (injuries), warming measures (blankets, increased room temp, warm fluids)
13
Q
G: Get adjuncts & give comfort
A
L: Lab analysis
M: Monitor cardiac - 12-lead ECG
N: Naso/Orogastric tube to pump stomach
O: Oxygenation & capnography
P: Pain
14
Q
H: History
A
S: S&S
A: Allergies
M: Meds
P: Past medical hx
L: Last oral intake/LMP
E: Event leading up
15
Q
H: Head-to-toe Assessment
A
Optimize resps & cardiac function
Anterior and posterior assessment
16
Q
J: Just keep re-evaluating
A
V: VS
I: Injury & Interventions
P: Primary survey
P: Pain
17
Q
CTAS Triage
A
1) Resuscitation
2) Emergent
3) Urgent
4) Less Urgent
5) Non-Urgent
18
Q
1: Resuscitation
A
Threats to life or limb that need immediate interventions - trauma, car accident, heart stopped
19
Q
2: Emergent
A
Potential threats to life or limb/require rapid interventions (trauma, suspected MI, trouble breathing)
20
Q
3: Urgent
A
Potentially lead to a serious problem (fainting, mod trauma, head injury, asthma attack, seizures, temp > 40)
21
Q
4: Less Urgent
A
Relate to a potential deterioration (minor trauma, sore eye/ear/throat, stitches, small fracture)
22
Q
5: Non-Urgent
A
May be acute but non-urgent. Interventions can be safely delayed (minor trauma, prescription renewal, cold)
23
Q
Disaster Management
A
RPM-30-2-Can-Do
24
Q
RPM-30-2-Can do
A
R: Resps < 30
P: Perfusion - cap refill <2
M: mental status - can do commands
25
Black Triage Tag
Expectant - unlikely to survive
26
Red Triage Tag
Need immediate intervention, compromised ABC’s
27
Yellow Triage Tag
Can be delayed, potentially life threatening
28
Green Triage Tag
“Walking wounded”, unlikely to deteriorate
29
Normal pH
7.35-7.45
30
Normal PCO2 (partial pressure of CO2)
35-45mmHg
31
Normal Bicarbonate (HCO3-)
22-28mmol/L
32
Normal PaO2 (partial pressure of oxygen)
80-100mmHg
33
Low pH
Acidic
34
High pH
Alkalotic
35
Low PaCO2
Alkalotic
36
High PaCO2
Acidic
37
Low HCO3-
Acidic
38
High HCO3-
Alkalotic
39
Low PaO2
Hypoxemic
40
Respiration
Sequence of events that results in exchange of O2 & CO2 between atmosphere and body cells = WHOLE PROCESS
41
Ventilation
Flow of air in & out of alveoli (mechanical aspect)
42
Ventilation 3 Components
1) Mechanical movement
2) Air flows from higher-lower pressure
3) Dependent upon volume, disease, and position
43
Capnography
ETCO2 - measures “end-tidal” CO2 exhaled
44
Diffusion
Movement of gases (O2 & CO2) across permeable membrane from high-low pressure
Dependent upon pressure difference, SA, and wall thickness
45
Hemoglobin Components
Heme, protein, iron
46
Hemoglobin function
Carries oxygen in blood - has a high affinity (attraction) to O2
47
Normal Hemoglobin in Female
120-150mg/dl
48
Normal Hemoglobin in Male
135-170mg/dl
49
SpO2
% of oxygen-saturated HGB in capillary bed (>94%)
50
SaO2
% of oxygen-saturated HGB in arterial blood (>95%)
51
PaO2
Partial pressure of oxygen (amount of O2 dissolved in plasma) (80-100mmHg)
52
Hypoxemia
Low blood PaO2 level (<50mmHg)
53
Hypoxia
Inadequate cellular O2 = anaerobic metabolism
54
Oxyhemoglobin dissociation curve
Relationship between PaO2 and HGB molecule sat
When HGB is 50% saturated with oxygen, PaO2 is 27mmHg
55
LEFT shift on dissociation curve
Haldane: HGB holding oxygen TOO TIGHT - tissues are not getting enough
56
RIGHT shift on dissociation curve
Bohn: HGB not holding oxygen tight enough - tissues are getting oxygen, but SpO2 is falsely low
57
Perfusion
Arterial blood flow (peripheral or central)
58
3 P’s of Perfusion
PUMP (heart)
PIPES (vasculature)
PLASMA (blood)
59
VQ mismatch
When ventilation (V) does not match perfusion (Q) - ex. lung receives oxygen without blood flow OR lung receives blood flow but no oxygen
60
Oxygenation
The result of perfusion, ventilation, and diffusion
61
FiO2
Fraction of Inspired Oxygen
RA: 0.21 (21%)
62
Nasal Prong oxygen delivery
Adds 3% FiO2 (0.24), up to 6L/min
63
Simple mask oxygen delivery
Adds 40-60% FiO2 (0.61-0.81), up to 8-10L
64
Non-re-breather oxygen delivery
Adds 80-95% FiO2, 10-15L/min
65
High Flow & ETT ventilation oxygen delivery
Adds 21-100% FiO2
66
Respiratory Acidosis ABG Characteristics
CO2 HIGH
67
Metabolic Acidosis ABG Characteristics
HCO3- LOW
68
Respiratory Alkalosis ABG Characteristics
CO2 is LOW
69
Metabolic Alkalosis ABG Characteristics
HCO3- HIGH
70
Respiratory Acidosis
Retention of CO2 - CNS depression, neuromuscular disorder, obstructive lung disease
71
Metabolic Acidosis
Gain of Acid (H+) - DKA, lactic acidosis
Loss of base (HCO3-)
Inability to excrete acid
72
Respiratory Alkalosis
Excretion of CO2 - CNS hyperactivity (anxiety, fever, pain), hypoxemia increased ICP
73
Metabolic Alkalosis
Loss of acid (H+) - vomiting, increased aldosterone, total volume loss, admin of NaHCO3
74
Acidosis Effects on Heart
Decreased contractility = decreased CO = hypotension
Increased vasodilation = hypotension
Increase HR = vtach arrhythmia
75
Alkalosis Effects on Heart
Increased vasoconstriction
Increased HR = vtach arrhythmias, vfib, SVT
76
Acidosis Effects on Lungs
Increased RR - increased WOB = fatigue
77
Alkalosis Effects on Lungs
Decreased RR = hypoxemia
78
Acidosis Effects on Metabolic
Increased H+ move into cells - increase K+ (arrhythmias)
H+ alter ability of insulin on tissues (increase resistance, increased BGM)
79
Alkalosis Effects on Metabolic
Decreased K+ and Mg
80
Acidosis Effects on CNS
Altered mental status - COMA
81
Alkalosis Effects on CNS
Altered mental status - COMA
Seizures, tetany
82
Lung compensation for acidosis
Increased rate and depth of ventilation - attempt to rid body of CO2
83
Lung compensation for alkalosis
Decreased rate and depth of ventilation - retain CO2
84
Kidney compensation for acidosis
Kidney’s excrete H+ and conserve HCO3-
85
Kidney compensation for alkalosis
Kidney’s retain and excrete HCO3-
86
Uncompensated ABG Characteristics
pH normal, 1 abnormal and 1 normal value (opposite system has NOT compensated)
87
Partially compensated ABG characteristics
pH abnormal, 2 abnormal values (opposite system attempting to compensate)
88
Fully compensated ABG characteristics
pH normal, 2 abnormal values (opposite system has compensated enough to normalize pH)
89
Restrictive Pulmonary Disorder
Reduced total lung capacity = loss of lung volume = compromised oxygenation
90
Extra-pulmonary causes
obesity, flail chest, muscular dystrophy
91
Internal-pulmonary causes
pneumonia, HF, pneumothorax
92
Obstructive Pulmonary Disorder
Air moves in and out at a reduced rate = air trapped = compromised oxygenation
93
Flow of Obstructive Disorders
1. air flows into lungs & gets trapped
2. difficult to exhale because alveoli can’t empty, CO2 trapped in lungs
3. Airway narrowing
4. Airway obstruction
5. Hyper-inflated lungs & decreased elastic recoil
94
Cues of Obstructive Disorders
Increased lung expansion, decreased expiratory flow, decreased FEV, normal to increased TLC, increased FRV, decreased VS, chronic abnormal ABG’s (increased PCO2, normal HCO3-, normal pH or slightly acidic, decreased PO2)
95
Asthma Control Steps
1. SABA
2. SABA, daily LTRA and SLIT
3. SABA, ICS, LTRA, or SLIT
4. SABA, medium dose ICS, LAMA, SLIT
5. SABA, further assessment, LAMA, ICS, LTRA
96
Status Asthmaticus Cues
Unable to speak, drowsy/coma, poor respiratory effort, bradycardia, paradoxical thoracoabdominal breathing, silent chest, cyanosis and O2 sats < 92%
97
Major features of status asthmaticus
Pulsus paradoxus, accessory muscle use (labored), lung hyperinflation, ABG showing hypoxemia (low PO2), sudden decrease of wheezing or decreased breath sounds
98
Acute exacerbation of COPD Symptoms
Worsened dyspnea, cough of sputum production - decreased SpO2
99
Primary causes of acute exacerbation of COPD
Infection (viral or bacterial) vs non-infective (environmental trigger)
100
Secondary causes of acute exacerbation of COPD
Pneumonia, PE, CHF, pneumothorax, rib fractures, opioid/sedative use, beta-blockers
101
Management of COPD exacerbation
Systemic corticosteroids
102
Pneumonia
Acute infection of pulmonary parenchyma that is associated with:
at least 2 symptoms (fever, chills, new cough, CP, SOB) AND crackles/bronchial lung sounds AND new opacity/consolidation on CXR
103
Treatment of Impaired gas exchange
antibiotics, support O2 needs, support cardiac status, remove exudate
104
Complications of pneumonia and impaired gas exchange
Empyema, pleural effusion, atelectasis, delayed resolution, abscess, pericarditis/endocarditis, sepsis/bacteremia
105
Empyema
Collection of puss
106
Pleural Effusion
Collection of fluid in pleural cavity
107
Atelectasis
Collapse in certain areas of the lungs
108
Complications of COVID pneumonia
Sepsis, thrombotic event, ARDS, myocardial injury, hypoxic resp failure, AKI, multisystem organ failure
109
Acute PE
Condition of impaired perfusion
large thrombi obstruct perfusion in pulmonary artery - blockage - increased pressure and resistance - increased RV workload - decreased lung perfusion
110
Diagnosis of PE
D-dimer, CT, MRI, VQ scan, CXR, TTE, ABG’s
111
D-dimer
Indicates clot but does not show where it is
112
Virchow’s Triad
1) Hypercoaguable state
2) Venous stasis
3) Vessel Injury
113
Treatment of PE
High-flow O2, mechanical ventilation, vena-cava filter (for prevention if at high risk), embolectomy, anticoagulants, thrombolytic/fibronolytic
114
Respiratory failure
When compensation STOPS working
1) Resp distress/insufficiency
2) Acute resp failure (2 types)
3) Respiratory arrest
115
Types of Acute resp failure
1. Oxygenation failure (PO2 < 60)
2. Ventilation failure (PCO2 > 50 and pH <7.35)
Usually a mix of BOTH types
116
Whole Process of resp distress and failure
1) disease process affects normal lung function
2) VQ mismatch and decreased PaO2
3) Body increases RR and depth
4) Increased PaO2 and decreased PaCO2
5) Compensation increases metabolic rate = increased oxygen consumption and decreased CO2 production
117
Clinical criteria of Resp failure
PaCO2 > 50 AND pH < 7.30, PaO2 < 60
118
Oxygen Failure Pulmonary Cues
Dyspnea, tachypnea, increased PVR
119
Oxygen failures CV cues
Increase BP & HR, dysrhythmias, weak thready pulse, cyanosis
120
Oxygen failure CNS cues
Altered LOC, restlessness, confusion
121
Ventilation failure pulmonary cues
Tachypnea OR bradycardia
122
Ventilation failure CV cues
Bounding pulse, increase BP & HR
123
Ventilation failure vascular cues
Headache, flushed & wet skin
124
Ventilation failure CNS cues
Lethargy, drowsiness, coma
125
Color of Pt in Resp failure
Cyanotic, grey, mottled
126
RR of Pt in resp failure
high (to compensate) and then low when tired
127
Breath sounds of pt in resp failure
None = WORST - no O2 flow
128
BP of pt in resp failure
high to compensate, then low when tired
129
HR of pt in resp failure
high to compensate, then low when tired
130
Interventions for Resp failure
maintain airway oxygenate, correct acid-base imbalances, support systems (fluids and electrolytes), treat the cause, control complications
131
Acute Respiratory Distress Syndrome (ARDS)
Lung damage causes sudden onset of resp failures
132
ARDS criteria
1. Within 1 week of insult/worsened resp symptoms
2. Bilateral opacities with no explanation
3. Resp failure NOT explained by cardiac/fluid overload
4. PEEP > 5, hypoxemia even with 100% FiO2
133
Bipap
Non-invasive positive pressure vent, 2 pressure settings
134
CPAP
continuous positive airway pressure, 1 pressure setting
135
Pericardium
Outermost layer, protects the heart. 2 layers - fibrous and serous
136
Epicardium
Visceral surface of the pericardium
137
Myocardium
Middle layer of thick muscular tissue. Does the major pumping action
138
Endocardium
Thin layer of endothelium and connective tissue - lines the valves
139
4 Chambers of the Heart
Right atrium, Right ventricles, left atrium, left ventricle
140
4 Valves
AV: tricuspid and mitral (atria to ventricle)
SL: pulmonic and aortic (ventricle to body)
141
Coronary Arteries
Supplying and draining surfaces of the heart.
142
Major Coronary Arteries
Right coronary artery (RCA)
Left main/Left coronary artery
- Left anterior descending (LAD)
- Left circumflex (LCX)
143
Hemodynamics
Study of flowing blood and of all the solid structures (such as arteries) through which it flows
144
Cardiac Output
Amount of blood the heart pumps each minute
= HR x SV
145
Components of stroke volume
Preload
Contractility
Afterload
146
Stroke Volume
Amount of blood ejected from the heart (LV) with each pump
147
Preload
Filling - pressure in the myocardial fibers at end of diastole
148
Contractility
Force/strength of the myocardial contraction
149
Afterload
Pressure/resistance which the ventricles pump to eject blood
150
Ejection Fraction
Amount of blood expelled with each contraction (50-80%)
151
Frank Starling Law
The more the heart is filled during diastole, the more forcefully it contractions
More fill = stronger contraction
152
What Systems regulate CO?
Autonomic nervous system (ANS) and Kidneys (RAAS)
153
MAP
Mean Arterial Pressure - high BP = high map because of increased afterload
CO x SVR
154
Arterial Line indications
Need for continuous BP monitoring (hemodynamic instability, vasopressor requirement)
Frequent ABG draws
155
Arterial Line complications
Hemorrhage, hematoma, thrombosis, embolization, infection
156
Measuring Preload
Right-sided heart pressure
CVP/RAP: amount of fluid in the right side of the heart, can be measured through a CVL
NORMAL = 2-5mmHg
157
Pulmonary Artery Catheter
Measures CVP, PAP, PAWP, CO - very invasive, not used often
158
PAS
Higher pressure in systole (contracting)
normal: 20-30mmHg
159
PAD
Lower pressure in diastole (relaxing)
Normal: 10mmHg
160
Pulmonary Artery Wedge Pressure (PAWP)/Pulmonary Artery Occlusion Pressure (PAOP)
Reflects pressure in the left side of the heart (left filling)
Normal: 5-12mmHg
161
S&S of decreased CO
Delayed cap refill, tachycardia, weak pulses, hypotension, decreased urinary output, altered LOC
162
Types of Heart Failure
Left-sided (CHF)
Right sided
High-Ouptut
163
Typical causes of HF
Cardiomyopathy (HTN, diabetes, valve disease, PV disease), CAD, dysrhythmias, rheumatic fever, cardiotoxic agents, substance misuse
164
Left-Sided HF - Systolic
LV not sending much blood through, causing pooling and backup in aorta (blood “backs up” into pulmonary system)
165
Left-Sided HF diastolic
The LV loses ability to relax - STIFF (cannot fill)
166
Right-Sided HF
Result of Left HF, increases lung pressure (pulmonary HTN) or RV problems, blood flow backs up into peripheral system - right side gets tired
167
Compensatory Mechanism - SNS stimulation
Decreased CO stimulates increased HR and increase BP by vasoconstriction
168
Compensatory Mechanism - RAAS activation
NOT HELPFUL - senses decreased CO, increases preload and afterload which affects contraction - BAD because there is not enough blood to be pumped effectively
169
HF affects on heart itself
Muscle layer increases to try to compensate - hypertrophy. This is temporarily effective, BUT oxygen needs of the heart increase and needs more blood. If not getting blood, it causes cell death and the heart fails again.
170
BNP in HF
Release from ventricles when overloaded/stretched - KEY
171
Serum Electrolytes in HF
Fluid shifts, diuretics - increase Na
172
Urea and Creatinine in HF
RAAS - kidneys become damaged - urea and creatinine increase
173
HGB/HCT in HF
Effect on kidneys lead to reduced erythropoietin albuminuria - lower RBC’s and HGB
174
Albuminuria in HF
Decrease heart compliance
175
Echocardiogram in HF
Visualizes valves, pericardial effusion, chamber enlargement, thickness of walls, ejection fraction
176
CXR in HF
Cardiomegaly (enlargement of the heart, pulmonary edema)
177
ABG in HF
Hypoxemia - impaired diffusion
178
HF Acute Management - A&B
Intubation, Oxygenation (FiO2, increased pressure, and diuretics), Diuresis (removed excess fluid)
179
HF Acute Management - C
Optimize hemodynamics
Increase contractility
Vasodilation - reduce afterload/preload
Regulate HR
180
Reducing Preload in HF
Fluid management - fluid and salt restrictions , serum electrolytes, BUN, creatinine, positioning. Diuretics (loop - furosemide, thiazide - spironolactone, SGLT2i - sodium glucose cotransporter - 2 inhibitors)
181
Reducing Afterload
Improving contractility - ACE/ARB (stop RAAS from being activated), beta blockers (increase contractility and decrease HR), Nitrates (vasodilate), inotropes (increase contractility - digoxin), amiodarone (HR control and arrhythmias control), ICN (decrease HR)
182
Ventricular Assist Device - LVAD
Used as a bride to transplant - external pump/ventricle (circulates blood externally)
183
S&S of Pulmonary Edema
Pink frothy sputum, acute resp deterioration, decreases sats, SOB
183
Treatment of Pulmonary Edema
IVP furosemide - works quickly
184
S&S of RIGHT sided failure
Peripheral Edema, JVD
185
Biventricular failure S&S
JVD, 2+ edema in feet and ankles, swollen hands and fingers, distended abdomen, bibasilar crackles, productive cough with pink-tinged sputum
186
Endocarditis
Disease of the valves and chambers
187
Causes of infective endocarditis
Microbial infection - IV drug use, valve replacements, altered immunity, structural heart defects, dental procedures, hemodialysis, infections
188
Infective Endocarditis Pathophysiology
1) organism adheres to valve surface - disturbed surface of endothelium attracts platelets
2) introduction of bacteria in blood
3) bacteria settle on thrombi of heart valve
4) Forms vegetations (become like emboli)
5) Vegetations enlarge and alter valve function
189
IE - Septic vegetations on right side of heart
Lodged in pulmonary system - PE
190
IE - septic vegetations on left side of heart
Lodged all over body - brain, liver, etc.
191
Types of Valvular disease
Stenosis, insufficiency, prolapse
192
Stenosis in Valves
tissue thickening narrows valve opening - risk of clots
193
Insufficiency in valves
allows for backflow /regurgitation - incomplete valve closure
194
Causes of Valvular disease
degeneration (weakens with age), calcific degeneration, IE, CAD, MI
195
Potential Complications of valvular disease
Arrhythmias, CMO, HF, thrombotic disorders
196
Mitral Valve Prolapse
Usually benign - can progress to regurgitation
One of the mitral leaflets is slightly curved the wrong way and allows some back flow
197
S&S Mitral Valve Prolapse
“Click murmur” - systolic murmur
Palpitations or chest pain
198
Aortic valve prolapse
Valve doesn’t close completely during diastole, so back flow into LV happens
diastolic murmur
199
Stenosis of a valve
Hardening/thickening of the valve caused by fibrosis or calcification - valve leaflets fuse (stiff and narrow)
200
Mitral Valve stenosis
Narrow valve opening obstructs BF from LA to LV (pressure increases, left atrium dilates, PAP increases, rt ventricle hypertrophy)
- rt HF, diastolic murmur
201
Aortic Valve stenosis
narrow valve opening obstructs BF from LV to aorta during systole
“wear and tear”
Left HF, systolic murmur
202
Treatment of valve stenosis
Valve repair/replacement, medication for symptoms, management of HF
203
Bicuspid aortic valve
Most common congenital cardiac malformation - 2 leaflets instead of 3
204
Complications of bicuspid aortic valve
HF, aortic aneurysm and dissection, stenosis or regurgitation
205
3 main cues of IE
Fever, NEW murmur, fatigue
206
Evidence of systemic embolization
Petechiae, janeway lesions (flat, painless reddened maculae on hands and feet) , splinter hemorrhages (nail beds), osler nodes (painful on palms of hands and soles of feet), roth spots (hemorrhagic lesions that appear as round or oval spots on retina)
207
Prosthetic (synthetic/artificial) valve replacement
Lifelong anticoagulation with warfarin
208
Bioprosthetic (tissue)
No long-term anticoagulation, not as durable (last about 7-8yrs)
209
2 types of myocardial cells
electrical (pacemaker), mechanical cell
210
Electrical (pacemaker) cells
Generation and conduction of electrical impulses
211
Mechanical cell
do actual pumping by contracting and relaxing - dependent on electrical stimulus
212
Sinoatrial (SA) node
Primary pacemaker cell - responds to needs of body and controls beat based on info it receives from nervous, circulatory, and endocrine systems
213
AV node
Receives signal from SA node (through 3 pathways) and slows the conduction from the atria to the ventricles long enough for atrial contraction (supplied by RCA)
214
Bachmans bundle
Bundle in LA
215
SA node intrinsic rate
60-100
216
AV junction intrinsic junction
40-60 (if SA fails)
217
Purkinje fibers instrinsic rate
20-40 (if AV fails)
218
Cardiac conduction
calcium, magnesium, potassium, sodium are used to develop “electricty”
219
Phase 0 of cardiac conduction
Depolarization, influx of Ca and Na
220
Phase 1 of cardiac conduction
Na channels close, hits “peak”
221
Phase 2 cardiac conduction
Influx of Ca, K slowly trickles out - prolonged depolarization
222
Phase 3 of cardiac conduction
rapid depolarization, decrease in K and Ca channels close - back to resting potential
223
Phase 4 cardiac conduction
Resting potential - leaky K channels, can not be activated again - negative
224
Phase 0-3 of cardiac conduction
Positive - in refractory period, cannot be activated
225
Depolarized
Stimulation - negative space letting positives in
226
Repolarizing
Resting - becomes more negative - when negative enough, it can be stimulated again
227
ECG paper
Small box = 0.04 seconds
Big box (5 little ones) = 0.2 seconds
Each lead = 2.5 seconds, full ECG = 10 seconds
228
Isoelectric line
Baseline of ECG
229
P wave
ATRIAL DEPOLARIZATION - atrial filling
0.08-0.11 seconds, spread of electrical impulse that depolarizes atria
230
PR Interval
0.12-0.2 seconds
231
PR segment
AV node delaying electrical impulse
232
QRS
VENTRICAL DEPOLARIZATION
<0.12 seconds
Spread of electrical impulse that depolarizes ventricles, atria repolarizes during this time
233
J point
Where S stops and ST segment begins
234
ST segment
Should be neutral (on isoelectric line)
235
T wave
VENTRICULAR REPOLARIZATION
ventricles relax
236
QT interval
total time of ventricular depolarization and repolarization - we only care if this is too long
237
6 Step ECG reading
1: rate (fast/slow?, intervals?)
2: rhythm (regular? wide/narrow WRS? p-wave?)
3: p=waves (upright? uniform? prior to WRS?)
4: PR interval (0.12-0.20 seconds, prolonged = blockage)
5: QRS (< 0.12 seconcds, wide ventricles = bad)
6: interpret
238
R-R interval
Ventricular BPM
239
Sequence Method
Select R wave on dark pink line - next dark line as shows 300, 150, 100, 75, 60 and 50 (where next r wave finds, that is the HR)
240
Bundle Branch Block
Functional or pathological block in one of the major branches of intraventricular conduction system - ventricles NOT depolarized simultaneously (using detour because main highway is blocked)
241
Hypokalaemia on ECG
T-wave inversion, ST depression, prominent U wave
242
Hyperkalemia on ECG
Peaked T waves, P wave flattening, PR prolongation, wide QRS
243
S&S of Dysrrhythmias
Vitals: fluctuating HR, increased RR, low SpO2
Lungs: crackles if fluids backed up
Heart sounds: may hear S3 and S4
PV: slow CO (> cap refill, weak pulses)
Pulse deficit: difference in apical and radial pulse
244
SINUS
Originates from SA node
245
Normal Sinus Rhythm
Rate: atrial and ventricular rates 60-100
Rhythm: atrial and ventricle rhythms regular
P waves: present, upright, consistent configuration, 1 p-wave before each QRS
PR interval: 0.12-0.2 seconds, constant
QRS duration: 0.06-0.12 seconds, constant
246
Sinus Bradycardia
Everything normal on ECG EXCEPT HR is < 60 BPM
247
Sinus Tachycardia
Everything normal on ECG EXCEPT HR >100BPM
248
Premature Atrial Contraction (PAC)
Atrial tissue fires an impulse before the next sinus impulse is due - triggers ventricles responding sooner than expected (QRS fires too fast on ECG)
249
Causes of PAC
Stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol, drugs.
250
Atrial Flutter
Too many P waves - saw-toothed /flutter waves - atrium continuously contracting, ventricles always getting a stimulus but only contract (QRS) when they are repolarizedT
251
Treatment of atrial flutter
Beta-blockers, ca channel blockers, cardiovert, ablations
252
Biggest Complication of atrial flutter
risk of clot due to stasis.
253
ECG characteristics of atrial fibrillation
rate - hard to calculate
rhythm - irregular
ration - multiple p waves
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What is the most common sustained arrhythmias
Atrial fibrillation
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Atrial fibrillation ECG
Indiscernible P waves (no PR interval, normal QRS, ventricles are irregular rhythm)
256
Atrial fibrillation Complications
decreased SV by 25%, potential for clots and HF
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Treatment for atrial fibrillation
Anticoagulants, beta-blockers, ca channel blockers, antiarrhythmics (digoxin)
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Supraventricular Tachycardia (SVT)
Originated in AV node, NO P waves (can’t see them) - AV getting stimulated too fast, normal QRS, rate 150-250
259
Treatment for SVT
Modified valsava maneuver, beta blockers, ca channel blockers, antiarrhythmics, IV adenosine
260
IV Adenosine
Stop electrical impulses in the heart to allow SA to start firing again
261
Premature Ventricular Contraction (PVC)
Result of increased irritability of ventricular cells - signal coming from ventricles instead of atria
NO p waves before QRS
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R-on-T phenomenon
BAD - v-tach from improperly timed electrical impulses on later part of the T wave (ventricular repolarization)
263
PVC bigeminy
Every second (normal, PVC)
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PVC trigeminy
Every third (normal, normal, PVC)
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Unifocal PVC
Single irritable focus - all look the same
266
Multifocal PVC
Multiple irritable foci - all look different
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Ventricular Tachycardia
3 or more consecutive PVCs occurring rapidly, 100-200bpm, no P waves
268
Torsades de points
Polymorphic - smaller and bigger pattern (not consistent) - give IV magnesium
269
Sustained V tach
If for > 30 seconds
270
Non-sustained v tach
anything less than 30 seconds
271
Treatment for v tach
CPR and defibrillation if pulse is lost, antiarrhythmics
272
Ventricle Fibrillation
Electrical chaos in ventricles
273
Course v fib
Bumpy on ECG
274
Fine v fib
smoother on ECG
275
Asystole
Cardiac standstill, complete stop of electrical impulses (no rate or rhythm or CO or pulse)
276
Pulseless Electrical Activity (PEA)
Any organized rhythm without a central pulse (pt always unresponsive)
277
S&S of decreased CO due to arrhythmias
Weak, lightheaded, chest pain, delayed cap refill, palpitations, change in LOC, resp distress or apnea
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Algorithm for symptomatic bradycardia
HR <60 AND S&S
1) ABC - O2, IV
2) 12 lead ECG
3) treat the cause
4) decide if pt has adequate CO
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Algorithm for Tachycardia
1) ABCs - O2, IV, pulse
2) 12-lead ECG
3) unstable - cardiovert (defibrillate)
280
H’s of Lethal arrhythmias
Hypoxia, Hypothermia, Hyper/hypokalemia, Hypovolemia, Hydrogen ion (acidosis)
281
T’s of Lethal arrhythmias
Toxins, Tamponade, Trauma, Thrombosis, Tension pneumothorax
282
Defibrillation
Delivery of an electrical current across the heart muscles over a very brief period to terminate an abnormal heart rhythm
283
Cardiac Arrest Algorithm
1) Check central pulse - if nothing call code blue
2) call for help/code, get AED and defibrillator
3) Start CRP
4) Start IV, get O2 on (BVM)
5) Treat H’s and T’s or cause if known
284
Algorithm if VF/PVT
Assess rhythm - shockable - defibrillation, clear patient for 360J/AED shock (<10 seconds)
285
Algorithm for PEA/Asystole
Assess rhythm - not shockable
CPR
Drugs
286
Types of Acute Coronary Syndrome
1. Stable Angina
2. Unstable Angina
3. NSTEMI
4. STEMI
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Stable Angina
Angina pain develops when there is increased demand in the setting of stable atherosclerotic plaque - vessel unable to dilate enough to allow adequate blood flow to meet myocardial demand - normal ECG
288
Unstable Angina
Plaque ruptures and a thrombus forms around the ruptured plaque, causing partial occlusion of the vessel. Angina pain occurs at rest or progressed rapidly over a short period of time. ECG - normal OR inverted T waves OR ST depression
289
NSTEMI
The plaque ruptures and thrombus formation causes partial occlusion to the vessel that results in injury and infarct to the subendocardial myocardium. ECG - normal OR inverted T waves OR ST depression
290
STEMI
Complete occlusion of the blood vessel lumen resulting in transmural injury and infarct to the myocardium, troponin changes. ECG - hyperacute T waves OR ST elevation
291
S&S of ACS
Pain/discomfort/pressure, PSNS (N/V), diaphoresis, SOB/dyspnea, anxiety, fatigue, signs of impaired CO
292
Hyperacute Phase
Tall T wave
293
Early Acute phase
Tall T wave, elevated ST-segment
294
Later acute phase
Inverted T wave, elevated ST segment
295
Fully evolved phase
Inverted T wave, elevated ST segment
296
Management of ACS
Heparin IV infusion, DAPT (ASA, clopidogrel or ticagrelor)
297
Troponin function
Protein in muscles - decrease shows a problem with the heart
298
CK-MB Function
Increased when there is heart damage
299
Myoglobin Function
protein in the muscles that supply oxygen - means low red blood cells
300
CRP function
protein synthesized by the liver, marker for inflammation or infection
301
Lipid profile (cholesterol, LDL, triglycerides, HDL) Functions
Plaque in vessels
302
INR/PT/aPTT Function
Ability of blood to clot
