Exam 2 Flashcards
1
Q
Automaticity
A
Ability to initiate an impulse spontaneously and continuously
2
Q
Excitability
A
Ability to be electrically stimulated
3
Q
Conductivity
A
Ability to transmit impulse along a membrane in an orderly manner
4
Q
Contractractility
A
Ability to respond mechanically to an impulse
5
Q
Stroke volume
A
Amount of blood pumped out of left ventricle during systole
6
Q
Cardiac output
A
Liters of blood heart pumps in a minute
4-8 L/min
7
Q
Cardiac index
A
Cardiac output adjusted for body surface area
2.5-4 L/min/m2
8
Q
Preload
A
Stretch of ventricles at the end of diastole when filled with blood
9
Q
Afterload
A
Amount of resistance the heart must overcome to open aortic valve
10
Q
Electrical conduction pathway
A
SA node
AV node
Bundle of HIS
Purkinje fibers
11
Q
How many seconds is 1 small box
A
0.04
12
Q
How many seconds in one big box
A
0.20
13
Q
Most accurate way to measure HR
A
of QRS in 1 min
14
Q
How to estimate HR
A
of QRS in 6 seconds x 10
15
Q
Hard way to determine HR
A
1500/# of small boxes between R-R
300/# of large boxes between R-R
16
Q
BP formula
A
CO x SVR (systemic vascular resistance)
17
Q
SA node bpm
A
60-100
18
Q
AV node bpm
A
40-60
19
Q
HIS-purkinje fibers bpm
A
20-40
20
Q
Junctional rhythm
A
SA node fails to fire
21
Q
Common causes of PVCs
A
Caffeine
Overexertion
Digitalis toxicity
22
Q
Dysrhythmia procedural tx
A
Defibrillation
Cardioversion
Ablation
Impantable cardioverter-defibrillator
Pacemaker
23
Q
Defibrillation vs cardioversion
A
Defibrillation: Unconscious, life-threatening, unsynchronized (shock not timed with heart rhythm)
Cardioversion: Conscious with pulse, non life-threatening, synchronized
24
Q
Dysrhythmias drug tx
A
Sodium channel blockers: Lidocaine, procainamide
Beta blockers: Metoprolo
Potassium channel blockers: Amiodarine
CCB: Diltiazem
Other: Magnesium, adenosine, digoxin, epinephrine, atropine
25
Layers of heart inside to out
Endocardium
Myocardium
Epicardium
Pericardium - sac that surrounds heart
26
Troponin
Rises in 4-6 hours
Peaks 12-24 hours
Detectable for 10-14 days
27
CK-MB
Rises in 3-6 hours
Peaks in 12-24 hours
Returns to baseline in 12-48 hours
28
C-reactive protein
Inflammation marker
Risk factor for CAD
29
How long is myoglobin in blood stream
Rises and falls quickly
- Indicates muscle injury
30
Homocysteine
Increased = risk for CAD, PVD, stroke
31
Natriuretic peptide markers (types)
Atrial natriuretic peptide (ANP)
B-type natriuretic peptide (BNP)
C-type natriuretic peptide
NT pro-BNP
32
Increased BNP means
HF
33
Isoelectic line
Part of ECG with no activity between beats
34
What represents the SA node on ECG
P wave
35
What represents Bundle of HIS and Purkinje fibers on ECG
QRS complex
36
Normal PR interval length
0.12-0.20 seconds
- Start of P wave to first downward line (where Q wave starts)
37
Normal QRS interval length
Less than 0.12 seconds
38
ST-segment
Isoelectric (flat) line between QRS and T wave
Represents early ventricular repolarization
39
T wave
Represents ventricular repolarization
40
QT interval
QRS plus ST segment and T wave
- Beginning of QRS, end of T wave
Represents total time for ventricles to depolarize and repolarize
41
Voltage in 1mm (1 box vertically)
0.1mV
42
12-lead EKG
43
Sinus tachycardia treatment
Vagal maneuvers
Beta blockers
44
How do vagal maneuvers work
Stimulates vagus nerve to release acetylcholine and lower the HR
45
Sinus tachycardia symptoms
Dizziness
Dypnea
Hypotension
Angina for CAD pts
46
Paroxysmal Supraventricular Tachycardia (PSVT)
Premature atrial contractions (PAC's) trigger a run of repeated premature beats
Abrupt onset and termination
150-220 bpm
47
Paroxysmal Supraventricular Tachycardia (PSVT) tx
Adenosine
Beta blockers
CCBs
Amiodarone
Cardioversion
48
Paroxysmal Supraventricular Tachycardia (PSVT) causes
Overexertion, stress
Deep inspirations
Stimulants
Digitalis toxicity
49
Sinus bradycardia tx
Atropine - anticholinergic
Pacemaker
50
Sinus bradycardia symptoms
Hypotension
Pale, cool skin
Weakness, dizziness, syncope
Angina
Confusion
Disorientation
SOB
51
Atrial fibrillation
Irregular rhythm
No paves or measurable PR interval
Does have QRS complex
52
Atrial fibrillation tx
Cardioversion
Antiocoagulants
Ablation
Amiodarone
Ibutilide
53
Signs of congestive heart failure (CHF)
MI
Electrolyte imbalance
54
Atrial flutter
Sawtooth
Loss of atrial "kick" decreases CO and leads to HF
Increases risk of stroke
55
Atrial flutter tx
- Similar to atrial fibrillation
Cardioversion
Antiocoagulants
Ablation
Amiodarone
Ibutilide
56
Premature atrial contractions (PACs)
Ectopic beats originating in the atria
57
Premature atrial contractions (PACs) tx
Observation unless symptomatic
58
Premature atrial contractions (PACs) causes
Stress
Fatigue
Caffeine
Smoking
Alcohol
Hypoxia
Electrolyte imbalance
Disease
59
Junctional dysrhythmias
SA node failed to fire so AV node become pacer
Do not suppress it - body safety mechanism
P wave abnormal
QRS normal
60
Junctional dysrhythmia tx
Atropine
61
First degree AV block
Prolonged PR interval
62
First degree AV block
Usually asymptomatic, so no treatment
63
Second degree AV block type 1
Wenckebach
P waves normal, but some not followed by QRS
P waves lengthen until a QRS is dropped
64
Second degree AV block type 2
Less common than type 1, more serious
Consistent PR intervals with dropped QRS complex
65
Second degree AV block type 2 tx
Pacemaker
66
Third degree AV block
Complete heart block
Atria and ventricles beat independently
Atrial rate greater than ventricular rate
No consistent PR interval
May lead to asystole, v tach or v fib
67
Third degree AV block tx
Pacemaker
68
Premature Ventricular Contractions (PVC's)
Ectopic beats originating in ventricles
69
Premature Ventricular Contractions assessment
Assess for apical-radial pulse deficit (difference)
70
Premature Ventricular Contractions (PVC's) tx
Correct underlying cause
Antidysrhythmic
71
Ventricular tachycardia (VT)
Three or more PCVs in a row
Absent P waves, wide QRS
May lead to ventricular fibrillation
110-250 bpm
72
Ventricular tachycardia (VT) tx
Stable VT: Medication or cardioversion
VT: CPR and defibrillation
73
Ventricular fibrillation (VF)
Chaos in ventricles
74
Ventricular fibrillation (VT) tx
CPR and defibrillation
Epinephrine and vasopressin
75
Ventricular fibrillation causes
MI
Ischemia
Diseases
Procedures
76
Ventricular fibrillation symptoms
Unresponsive
Pulseless
Apneic
77
Accelerated Idioventricular Rhythm (AIVR)
Ectopic beat originating in ventricles
SA node and AV node are less than ventricular ectopic pacemaker
40-100 bpm
78
Accelerated Idioventricular Rhythm (AIVR) tx
If symptomatic: atropine and temporary pacing
79
Asystole tx
CPR, ACLS
Epinephrine and vasopressin
80
Asystole common causes
Advanced cardiac disease
Severe conduction disturbances
End stage HF
81
Amiodarone MOA
Normalizes HR by slowing down AV node
82
Amiodarine uses
Hemodynamically stable V-tach
83
Lidocaine uses
Second line for V-tach
Less effective than amiodarone or Procainamide
Not used during code, used long term drip for v fib prophylaxis
84
Magnesium uses
V tach related to prolonged QT interval
Esp. Torsade's de Pointes
85
Magnesium MOA
Replenishes electrolytes and depresses cardiac muscles
86
Defibrillation what it is and uses
Unsynchronized shock
V fib and pulseless V tach
Most effective within 2 minutes
87
Cardioversion what it is and uses
Synchronized shock
Stable (with a pulse) V tach or supraventricular tachycardias
88
What do you do if pt becomes pulseless during cardioversion
Turn off sync button and defibrillate
89
Implantable cardioverter-defibrillator (ICD) uses
Pt with high risk for life threatening dysrhythmias
90
Implantable cardioverter-defibrillator (ICD) pt education
Incision care
Activity restrictions
Avoid magnets/MRIs
Medical alert bracelet
91
Types of hemodynamic monitoring
Arterial Pressure Monitoring
Central Venous Pressure (CVP)
Pulmonary Artery Pressure (PAP)
92
Atrial pressure monitoring considerations
Pressure bag at 300 mm Hg
Keep alarms on at all times
Use sterile non vented caps
93
How often to assess central venous pressure (CVP)
Hourly or more often to monitor trends
94
What determines stroke volume
Preload, afterload, and contractility
95
Causes of elevated systemic vascular resistance (SVR)
HTN
Vasopressors
Aortic stenosis
Hypothermia
96
Causes of decreased systemic vascular resistance (SVR)
Septic shock
Anaphylactic shock
Neurogenic shock
Vasodilators
Medication side effects
97
Causes of elevated pulmonary vascular resistance (PVR)
Pulmonary HTN
Hypoxia
Pulmonary embolism
Pulmonary stenosis
98
Causes of decreased pulmonary vascular resistance (PVR)
Vasodilators
Medication side effects
99
Causes of elevated contractility
Hypercalcemia
Positive inotropic meds
Sympathetic stimulation
100
Causes of decreased contractility
Hyperkalemia
Hypocalcemia
Myocardial ischemia
Negative inotropic meds
Hypercapnea
Hypoxia
Acidosis
101
T1DM patho
Islets of Langerhans is damaged
Pancreatic beta cells don't produce insulin
102
Carbohydrates are broken down into
Glucose
Galactose
Fructose
103
Where are excess carbohydrates stored
Liver and muscle
If stored glucose is not used, it is stored as fat
104
Glycogenesis
Conversion of excess glucose to glycogen
105
Glycogenolysis
Conversion of glycogen to glucose
106
Gluconeogenesis
Proteins are broken down into amino acids and converted to glucose in the liver
107
Ketogenic diet
Low carb
High fat
Uses insulin
108
Diabetic diet
High carbs
No insulin
109
How does stress/acute illness affect blood glucose
Catecholamines (epinephrine, norepinephrine, dopamine) stimulate liver to produce more glucose (gluconeogenesis) and to breakdown glycogen to release more glucose
Reduces effectiveness of insulin, leading to insulin resistance
- Results in hyperglycemia
110
Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS)
T2DM
BG over 600
Severe dehydration
Mild ketosis
Visual disturbances
Weight loss
Insufficient insulin
111
DKA
T1DM, no insulin
Metabolic acidosis - Kussmaul respirations, GI symptoms, fruity breath, positive urine ketones
112
Precipitating factors of DKA
Illness
Infections
Inadequate insulin
Undiagnosed T1DM
Poor management, neglect
113
Precipitating factors of HHNS
UTI's, pneumonia, sepsis
Acute illness
Newly dx T2DM
Impaired thirst, inability to replace fluids
114
What type of insulin is used for infusions
Regular insulin
115
DKA/HHNS complications
Hypokalemia
Hypoglycemia
Fluid volume overload
HF
Cerebral edema
Thrombosis
Metabolic acidosis
Adult respiratory distress syndrome
116
Type 1 Respiratory failure
Hypoxemic
Gas exchange problem
Problem with oxygen transport *outside* the lungs
117
Type 2 Respiratory failure
Hypoxemic and Hypercapneic
Ineffective breathing pattern
Problems *within* the lungs
ex. COPD, asthma, muscular dystrophy
118
Acute Respiratory Failure (ARF)
Inadequate gas exchange leading to hypoxemia and/or hypercapnia
Condition not disease
ARDS is a type of ARF
119
Hypoxemic ARF
Oxygenation failure
PaO2 or O2 concentration under 60
120
Hypercapnic ARF
Ventilatory failure
PaCO2 over 48
pH under 7.35
121
Ventilation-Perfusion (V/Q) mismatch
Imbalance between airflow and blood flow in lungs
122
Complications of ARF
Metabolic acidosis
Decreased cardiac output
Impaired renal function
123
Acute Respiratory Distress Syndrome (ARDS)
Sudden, progressive form of ARF
Injury to alveolar-capillary membranes
Increases permeability, fluid leakage into alveoli, hypoxemia ("white-lungs")
Inflammation worsens
124
Phases of Acute Respiratory Distress Syndrome (ARDS)
Exudative/injury phase
Proliferative/Reparative phase
Fibrotic/Chronic phase
125
Exudative/injury phase (ARDS)
1-7 days
Neutrophils infiltrate
Capillary damage
Increased permeability
Fluid accumulates in alveoli
Intrapulmonary shunt
126
Proliferative/Reparative phase (ARDS)
1-2 weeks
Fibroblast proliferation
Lungs fibrous
Lung compliance decreases
Worsening hypoxemia
127
Fibrotic/Chronic phase (ARDS)
2-3 weeks
Extensive fibrosis (permanent)
Severely decreased lung compliance
Persistent hypoxemia
128
Complications of Acute Respiratory Distress Syndrome (ARDS)
Ventilator-associated pneumonia (VAP)
Barotrauma
Volutrauma
Stress ulcers
Renal failure
129
Causes of Acute Respiratory Distress Syndrome (ARDS)
Direct: Pneumonia, chest trauma
Indirect: **Sepsis**, burns
130
Non-Invasive Ventilation (NIV)
CPAP
BiPAP
131
Invasive Mechanical Ventilation
Endotracheal or nasotracheal
Gradually wean
Daily extubation screening
132
Meds for Acute Respiratory Distress Syndrome (ARDS)
Corticosteroids - inflammation
Vasodilators, Bronchodilators -ventilation
Anxiety meds
133
Prerenal AKI causes
60% of cases
Factors outside the kidneys
Ex. severe dehydration, HF, decreased CO, vasoconstriction
134
Intrinsic renal AKI causes
30-40% of cases
Direct damage to kidneys, specifically renal tubules and basement membranes
Ex. prolonged ischemia, nephrotoxins (arsenic, mercury, iron), hemoglobin release from hemolyzed RBC's, or myoglobin release from necrotic muscle cells
Acute tubular necrosis (ATN) is common
135
Postrenal AKI causes
5-10% of cases
Obstruction after kidneys
Ex. BPH, hyperplasia, prostate CA, calculi, tubular obstruction (uric acid crystals), trauma, extrarenal tumors
136
Difference between Prerenal and Intrinsic AKI urine osmolality
Prerenal: Over 500
- Conserving water and concentrating urine
Intrinsic: Under 350
- Damaged kidneys cannot concentrate urine
137
Difference between Prerenal and Intrinsic AKI urine sodium
Prerenal: under 20
- Conserving sodium (water) reduced sodium in urine
Intrinsic: Over 40
- Damaged kidneys cannot conserve sodium
138
Difference between Prerenal and Intrinsic AKI casts and/or sediment
Prerenal: None
- Kidneys still work
Intrinsic: Present d/t damaged kidneys
139
Difference between Prerenal and Intrinsic AKI urine specific gravity
Prerenal: Over 1.018
- Kidneys concentrate urine to conserve water
Intrinsic: Under 1.012
- Damaged kidneys cannot concentrate urine
140
Difference between Prerenal and Intrinsic AKI BUN/Creatinine
Prerenal: Over 20/40
- Able to concentrate creatinine in urine
Intrinsic: Under 15/20
- Damaged kidneys retain BUN/creat in body, so there's less in urine
141
Ways to restore renal perfusion in prerenal AKI
Improve CO
- Isotonic IV fluids
- Monitor for fluid volume overload
- Maintain MAP at 70 or greater
- Monitor CVP
Relieve obstruction
- Renal doppler, angiography, or stent placement
142
Other ways to prevent further renal injury in AKI
Avoid nephrotoxic drugs/drugs excreted by kidneys
Prophylactic acetylcysteine if contrast dye is used (prevents contrast-induced nephropathy)
Aseptic technique to prevent infections
143
Tx for hyperkalemia
Limit intake
Kayexalate
IV calcium (chloride or gluconate) to shift potassium into cells
Insulin, sodium bicarbonate
Dialysis
144
Tx for hyperphosphatemia
Hydration
Dietary restriction
Calcium supplementation
Phosphate binders (ex. calcium carbonate, Renagel)
145
Renal Replacement Therapy (RRT) uses
Fluid volume overload
Hyperkalemia
Metabolic acidosis
High BUN
MS changes
Pericarditis
Cardiac tamponade
146
What does Renal Replacement Therapy (RRT) include
Hemodialysis (HD)
Peritoneal dialysis (PD)
Continuous renal replacement therapy (CRRT)
147
Why is peritoneal dialysis limited in use for AKI
Slow treatment
Kidney dysfunction progresses quickly in AKI
Ineffective at removing urea efficiently
Fluid in peritoneum can impair respiratory function
Poorer pt outcomes compared to other RRT
Peritonitis: fatal appendix rupture
148
Advantages of hemodialysis
Rapid electrolyte correction
Restores fluid balance
Restores acid-base balance
149
Disadvantages of hemodialysis
Obtaining vascular access is challenging
Risk of hypotension
Muscle cramps
Blood loss
150
Advantages of Renal Replacement Therapy (RRT)
Continuous instead of intermittent
Uses convection instead of dialysate
Less hemodynamic instability
Less need for constant monitoring
Simple equipment
151
Disadvantages of Renal Replacement Therapy (RRT)
Requires a central venous catheter
Slower to remove waste products than hemodialysis
152
RIFLE
Risk
Injury
Failure
Loss
End-stage kidney disease
153
Casts
Masses of RBC and WBC that form after cellular damage
Form in renal tubules
Composed of cells, proteins, or other substances
154
Sediment
Cells, crystals, and debris in urine
155
Kidney ultrasonography use
Often first test done because it doesn't use nephrotoxic contrast agents
156
Renal biopsy use
Best method for confirming intrarenal causes of AKI
