Exam 1 Flashcards
1
Q
Define the difference between hypertonic, hypotonic, and isotonic IV fluids, with an example for each and what they do to the ECF/ICF
A
o Hypertonic - Solutions with solutes more concentrated than they are in the cells - initially raises the osmolality of ECF and expands it (5% Dex in H2O, 3% NaCl)
o Hypotonic - Solutions in which the solutes are less concentrated than they are in the cells - provides more water than lytes, diluting the ECF (0.45% NaCl)
o Isotonic - Fluids with the same osmolality as the cell interior - expands the ECF, no net less gain from ICF (0.9% NaCl or LR)
2
Q
What would isotonic fluid be used for?
A
Ideal for a patient with ECF volume deficit (i.e., fluid and sodium losses or hypovolemic shock)
3
Q
What would hypotonic fluids be used for? What is one caution with use of this fluid?
A
Maintenance fluids, as normal daily losses are usually hypotonic
May cause cellular swelling, need to watch for cerebral edema
4
Q
What solution is considered isotonic, but is physiologically hypotonic?
A
5% Dextrose in H2O
5
Q
What would hypertonic solution be used for? What is one caution with using it?
A
Useful for the treatment of hypovolemia and hyponatremia
Must monitor BP/lungs/and serum Na for fluid excess and intracellular dehydration
6
Q
What are the signs/symptoms of hypokalemia (5)?
A
- Ventricular dysrhythmias due to increased excitability of the cells
- Weak, thready, irregular pulse
- Muscle weakness and paralysis
- Shallow respirations
- Muscle cramping
- Hyperglycemia (poor insulin regulation)
7
Q
What will the T waves and ECG of hypokalemia look like?
A
Flattening T wave and emergence of U wave irregularity
8
Q
What may cause hypokalemia?
A
- Abnormal losses
- Elevated aldosterone and diuresis
- Diarrhea, laxative abuse, vomiting
- Metabolic alkalosis can cause K to move to ICF in exchange for H
- DKA treatment, due to urinary loss and insulin loss
9
Q
What is the treatment for hypokalemia (2)?
A
IV KCl and continuous ECG monitoring
10
Q
What are the signs/symptoms of hyperkalemia (4)?
A
- Skeletal muscle weakness and paralysis
- Leg cramping
- Disturbed cardiac conduction or arrythmias (heart block, VFib)
- Irritability, N/V/D
11
Q
What will the T waves and ECG of hyperkalemia look like?
A
Tall, peaked T waves
Cardiac depolarization decreases, leading to loss of P waves, prolonged P-R, and ST depression. QRS complex will be widened
12
Q
What is the treatment for hyperkalemia?
A
- Furosemide to expel K
- IV insulin to force K from ECF to ICF, in conjunction with glucose to avoid hypoglycemia
- IV sodium bicarbonate to correct acidosis
- IV calcium gluconate to reverse effects on depolarization
13
Q
What 4 things may cause hyperkalemia?
A
- Trauma (burns)
- Metabolic acidosis (K gets kicked out of the cell by hydrogen)
- Adrenal insufficiency or aldosterone insufficiency
- Spironolcatone and ACE inhibitors as they reduce kidneys capacity to excrete K
14
Q
What may cause hyponatremia (2)?
A
- SIADH
- Inappropriate use of sodium-free or hypotonic IV fluids
15
Q
What are the symptoms of hyponatremia?
A
Nonspecific neurological deficits, such as headache, irritability, and difficulty concentrating
Severe symptoms include confusion, vomiting, seizure, and coma
16
Q
How is hyponatremia treated?
A
Hypertonic IV saline
17
Q
What are causes of hypernatremia?
A
Deficiency in the synthesis of ADH, decrease in kidney responsiveness to ADH, which can result in profound diuresis, leading to water deficit and hypernatremia
Hyperosmolar tube feedings
Excessive sweating or increased sensible losses from high fever
Hypertonic saline or sodium bicarbonate IV
Primary aldosteronism (hypersecretion of aldosterone)
Poor LOC and no hydration
18
Q
How is hypernatremia treated?
A
- Treat the underlying cause
- Goal is to dilute sodium concentration with salt-free IV fluids, such as 5% dex in water and to promote excretion of sodium through diuretics
19
Q
What might too quick correction of hypernatremia lead to?
A
Serum sodium levels must be reduced gradually to prevent too rapid a shift of water back into the cells – overly rapid correction can result in cerebral edema
20
Q
What are the symptoms of hypernatremia?
A
Intense thirst, lethargy, agitation, seizures, and coma – this is because neurons require sodium for action potentials leading to them being easily excited
21
Q
What may cause hypocalcemia?
A
Any injury or effect on the parathyroid gland or production of PTH
Acute pancreatitis (lipolysis increases fatty acid production with Ca)
Alkalosis
22
Q
What are the symptoms of hypocalcemia?
A
Increased excitability and sustained muscle contraction (tetany)
- Laryngeal stridor, dysphagia
- Trousseau’s and Chvostek’s signs
o Trousseau – carpal spasms induced by BP cuff inflation
o Chvostek – contraction of facial muscles in response to a tap over the facial nerve in front of the ear - Numbness and tingling around the mouth or extremities
23
Q
Define Trousseau and Chvostek’s sign and what electrolyte it is associated with
A
o Trousseau – carpal spasms induced by BP cuff inflation
o Chvostek – contraction of facial muscles in response to a tap over the facial nerve in front of the ear
Hypocalcemia
24
Q
How is hypocalcemia treated?
A
- IV calcium gluconate
- Vitamin D supplementation
25
What may cause hypercalcemia?
- Most commonly caused by hyperparathyroidism or malignancy
- Vitamin D overdose
- Prolonged immobilization (bone mineral loss and increased Ca [ ])
26
What are the signs of hypercalcemia?
- Lethargy, weakness, stupor, coma
- Depressed reflexes
- Confusion and personality changes
- Bone pain, fractures
- Polyuria and dehydration
- Nephrolithiasis
27
How is hypercalcemia treated?
- Lasix with IV isotonic fluids to promote excretion of Ca
- Synthetic calcitonin
- Mobilization with weight bearing to enhance bone mineralization
28
How does the respiratory system assist in pH maintenance?
Maintain a normal pH by excreting CO2 and water, which are the byproducts of cellular metabolism
29
How does the respiratory system adjust based on acidosis and alkalosis?
The respiratory system will alter the depth of breathing to hyperventilate out CO2 or hypoventilate CO2 to retain
With increased respirations, less CO2 is in the blood, leading to alkalosis
i. The brain will inhibit the respirations as a result
ii. In metabolic alkalosis, the body will hypoventilate to retain CO2
With decreased respirations, more CO2 remains in the blood, leading to acidosis
i. The brain will increase respirations as a result
ii. In metabolic acidosis, the body will increase RR to blow off CO2 and return to alkalosis
30
How do the kidneys assist with the buffer system? What three ways does acid elimination happen in the kidneys?
Kidneys reabsorb and conserve bicarbonate or H+
i. Secretion of small amounts of free hydrogen into the renal tubule
ii. Combination of H+ with ammonia to from ammonium
iii. Excretion of weak acids
31
How does the body compensate for resp acidosis and what type of resps may cause it?
Cause - Hypoventilation
Compensation - Kidneys retain bicarbonate to increase pH
32
How does the body compensate for resp alkalosis and what type of resps may cause it?
Cause - hyperventilation
Compensation - kidneys excrete bicarbonate to lower pH
33
How does the body compensate for metabolic alkalosis?
Hypoventilation to retain CO2 and lower pH
34
How does the body compensate for metabolic acidosis?
Hyperventilation to blow off CO2 to raise pH (Kussmaul)
35
What age group has the greatest content of body water and which has the lowest?
Infants - 70 to 80% water
Older adults - 45 to 55%
36
What is an important thing to consider with KCl IV treatment?
- NEVER push direct KCl
- KCl is a vesicant and may need to be diluted
37
What may cause a thyroid storm and what type of thyroidism is it r/t?
Stressors (i.e., infection, trauma, surgery) in a patient with pre-existing hyperthyroidism
38
What are the symptoms of thyroid storm?
All hyperthyroid manifestations are intensified
Tachycardia, HF, shock, hyperthermia, restlessness, agitation, seizures, abd pain, N/V/D, delirium, and coma
39
What is the immediate therapy for thyroid storm?
What are the 5 B’s of treatment for a thyroid storm?
Block the adverse effects of thyroid hormones and stop their over secretion
Patient will be given iodine and propranolol (beta blocker)
- Beta blocker, breathing (ventilation), body temperature (Tylenol), block synthesis/release (iodine), and block T4 to T3 conversion with a beta blocker
40
What is iodine and what is it used to treat?
Iodine rapidly inhibits the synthesis of T3 and T4 and blocks the release of these hormones into circulation within hours
Used for a thyroid storm
41
What causes myxoedema coma and what thyroidism is it r/t?
May be precipitated by infection, medications (opioids, tranquilizers, and barbiturates), cold exposure, and trauma
R/t hypothyroidism
42
What are the symptoms of myxoedema coma?
Characterized by subnormal temperature, hypotension, and hypoventilation
43
How is myxoedema coma treated?
Aggressive IV levothyroxine and high dose glucocorticoid therapy until adrenal insufficiency can be excluded
Mechanical respiratory support and telemetry
44
What condition(s) would levothyroxine be used to treat?
Myxedema coma and hypothyroidism
45
Describe the pathophysiology of Cushing's
A spectrum of clinical abnormalities characterized by endogenous hypercortisolism
46
What may cause Cushing’s?
o ACTH secreting pituitary tumor
o Iatrogenic administration
of exogenous corticosteroids (i.e., prednisone)
o Chronic or excessive production of cortisol by the adrenal cortex
47
What are the clinical manifestations of Cushing’s
Centripetal (trunk) obesity or generalized obesity
Moon face
Purplish/reddish striae on the abdomen or breasts
Hirsutism in women (excess hair around mouth and chin)
Hypertension (Mineralocorticoid excess may cause hypertension and fluid retention)
Unexplained hypokalemia
48
How does Cushing’s effect glycemic regulation in the body?
Hypoglycemia occurs because of glucose intolerance associated with cortisol-induced insulin resistance and increased gluconeogenesis by the liver
49
How is Cushing’s treated?
The underlying cause must be identified in order to treat
May require surgery or gradual tapering from corticosteroid medication
However, mitotane or ketoconazole may be used to inhibit cortisol synthesis/metabolism/production
50
What are complications post op for adrenalectomy or tumour removal for Cushing’s?
o Because the adrenal glands are highly vascular, risk of hemorrhage is increased
o Large amounts of endogenous hormone may be released by the system, leading to risk of high BP and hemorrhage
- In addition, after surgery, BP, fluid balance, and lytes tend to be unstable due to excreted hormones
51
Why would someone be given corticosteroid therapy following surgical treatment of Cushing’s?
IV corticosteroids will be given during and for days after surgery to ensure adequate response to stress of procedure
52
Define the physiology of Addison’s disease
Supply of all three classes of adrenal corticosteroids (gluco, mineral, and androgens) is reduced
53
What are causes of Addison’s crisis?
STRESS
Sudden withdrawal from corticosteroid hormone therapy, adrenal surgery, or sudden pituitary gland destruction
54
What are the manifestations of Addison’s crisis?
hypotension (particularly postural), tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, and confusion
55
How is Addison’s crisis treated?
Shock management and high dose hydrocortisone replacement
* Large volumes of 0.9% hypertonic saline and 5% dex to reverse hypotension and lyte imbalances
56
Sudden cessation of corticosteroid therapy may result in?
Addison’s crisis
57
What are four complications that may arise from corticosteroid therapy?
- Hypertension
- Reduced immunity to infection and cancers
- Reactivation of latent TB
- Inhibited antibody response to vaccines
58
What are the four broad effects of corticosteroid therapy?
1. Anti-inflammatory action
2. Immunosuppression
3. Maintenance of normal BP (potentiate norepinephrine and aldosterone - sodium and water retained, vasoconstriction)
4. Carb and protein metabolism (need to be on a high protein diet, as it may stimulate the breakdown of protein)
- Need to monitor for hyperglycaemia, as this med can induce insulin resistance
59
What is the patho of syndrome of inappropriate ADH (SIADH)?
Despite normal or low plasma osmolality, there is abnormal production or sustained secretion of ADH
60
What may cause SIADH?
Malignancy and medications (i.e., carbamazepine, chlorpropramide, oxytocin, SSRIs)
61
What are the symptoms of SIADH?
Fluid retention, serum hypo-osmolality, dilutional hyponatremia, concentrated urine in the presence of normal or increased volume, and normal renal function
Cerebral edema, vomiting, abdominal cramps, muscle twitching, seizures
Low urine output and increased body weight/fluid excess
62
What occurs with serum and urine osmolality in SIADH?
A serum osmolality much lower than urine osmolality indicates the inappropriate excretion of concentrated urine in the presence of dilute serum
ECF volume expands, GFR increases, plasma osmolality drops, and urine gravity increases
63
What is an early sign of SIADH?
A headache due to hyponatremia
64
What are two complications of SIADH?
Cerebral edema and seizures
65
How is SIADH treated?
- IV hypertonic saline (3-5%) and diuretics
- Fluid restriction of no more than 500 mL/day
66
What is the patho of diabetes insipidus?
A deficiency of ADH production or secretion, as well as decreased renal response to ADH caused by injury
This leads to fluid and electrolyte imbalances cause by increased urine output and increased plasma osmolality
67
What are the 3 different types/causes of diabetes insipidus?
Central (neurogenic) – An interference with ADH synthesis or release (brain tumor, TBI, and CNS infections)
Nephrogenic – Inadequate renal response to ADH despite presence in adequate levels (medication therapy (especially lithium), renal damage, or hereditary renal disease)
Primary – Excessive water intake (structural lesion in the thirst centre and psychological disorder)
68
What is the osmolality and gravity of urine and serum in diabetes insipidus?
Excretion of urine with very low specific gravity in large amounts, but serum osmolality is elevated as a result of hypernatremia
69
What are the symptoms of diabetes insipidus?
- Polydipsia, nocturia, and polyuria
- If excessive fluid volume deficit – weight loss, constipation, poor turgor, hypotension tachycardia, and shock
70
What are the 7 D’s of diabetes insipidus?
o Diuresis (high urine output)
o Diluted urine
o Dry inside – hyperosmolality and hypernatremia
o Drinking a lot/excessive thirst
o Dehydrated – dry mucosa and skin
o Decreased BP
o Desmopressin and vasopressin – decrease urine output, watch for death by headache (low Na)
71
What are two complications of DI?
Hypovolemic shock and coma
72
How is DI treated?
Hypotonic saline (0.45%) to replace output and manage fluid loss
Vasopressin and desmopressin - two analogues of ADH, allowing for increased retention of water
Sodium restriction
73
What is Vasopressin?
An analogue of ADH, which allows for water retention
74
Define the patho of DKA
Acute metabolic complication of DM occurring when fats are metabolized in the absence of insulin
Caused by profound deficiency of insulin and is characterized by hyperglycemia, ketosis, metabolic acidosis, and dehydration (volume depletion)
Ketones are acidic and contribute to metabolic acidosis
75
What may cause DKA?
Illness, sepsis, stress, infection, inadequate insulin dosage, insulin omission, undiagnosed DM1, and poor self-management
76
What are the symptoms of DKA?
Polyuria and polydipsia, leading to dehydration
Tachycardia, orthostatic hypotension, lethargy, and weakness
Kussmaul’s respirations (rapid, deep breathing) are the body’s attempt to compensate for metabolic acidosis
The patient may have an acetone/sweet/fruity breath due to high levels of ketones
Hyperkalemia
77
What is the DKAA acronym for DKA signs/symptoms
Dry and high sugar (250-500 BG)
Ketones and Kussmaul resps
Abdominal pain
Acidosis metabolic less than 7.35
* Hyperkalemia
78
How is DKA treated?
Hypertonic saline (0.9%)
Once BGs reach 14 mmol/L, 5% dextrose will be added to prevent hypoglycemia
Early potassium replacement is essential because hypokalemia is a significant cause of preventable death during DKA treatment
Kill the sugar slowly with IV insulin
During IV insulin, glucose and potassium will enter the cell, resulting in rapid hypokalemia of the plasma
IV bicarbonate may also be given to reduce acidosis (only if pH is less than 7.0)
79
What are three complications of DKA treatment?
Too rapid of administration of IV fluid and lowering of BG may lead to cerebral edema
Death by hypokalemia
Severe hypoglycemia from lower BGs too quickly
80
Define the patho of HHS
A life-threatening syndrome that can occur in the patient with DM who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion
Due to HHS producing fewer symptoms in the earlier stages, BGs can climb quite high before it is recognized
81
What can cause HHS?
Illness, infection, old age, impaired thirst sensation, functional inability to replace fluids, polyuria, or increasing mental depression
82
What are the symptoms of HHS?
Severe neurological symptoms - somnolence, coma, seizures, hemiparesis, and aphasia
Extreme dehydration, very high BGs
83
Define the HHNS acronym for HHS
Highest sugar (>600)
Higher fluid loss and extreme dehydration
Head change (LOC, confusion, neurological manifestations)
No ketones, no acid, no fruity breath
Slower onset and stable potassium
84
What is the biggest complication of HHS?
Hypovolemia
85
What is the treatment for HHS?
- Immediate IV of 0.9% or 0.45% NS
- Regular insulin IV bolus, followed by an infusion
- IV dex once BGs reach 14 mmol/L
86
What is the major complication of treating a hypertensive crisis too quickly?
Cerebral edema (decreased cerebral perfusion) and stroke
87
Describe the patho for hypertensive crisis
A severe and abrupt elevation in BP, arbitrarily defined as a DBP above 120 mmHg
Rising BP triggers endothelial damage and the release of vasoconstrictors – a vicious rising cycle of BP occurs, leading to life-threatening damage to organs
Classified by degree of organ damage and the rapidity with which the BP must be lowered
88
What causes HPN crisis?
Most commonly occurs in patients who have a history of HPN and have failed to adhere to medication regime or have been undermedicated.
May also be r/t cocaine/drug use
89
What are the complications of hypertensive crisis?
BP is severely elevated and there is evidence of acute organ damage, specifically to CNS
Include hypertensive encephalopathy, hemorrhage, acute LVF with pulmonary edema, MI, renal failure, and aortic aneurysm
90
What are the symptoms of hypertensive crisis?
Headache, nausea, vomiting, seizures, confusion, stupor. unstable angina, infarction, pulmonary edema, dyspnea
91
What medications are used to treat hypertensive crisis? What is the best med to treat it?
Sodium nitroprusside is the most effective treatment (vasodilator)
- May use other dilators like nitroglycerin and hydralazine
Beta blockers - labetalol (reduces CO and SNS vasoconstriction, leading to reduced contractility and renin secretion decrease)
ACE inhibitor - enalapril (prevent vasoconstriction)
92
Where would a mitral valve stenosis murmur be heard?
At the apex of the heart
93
What is the difference between stenosis and regurgitation?
Stenosis is the stiffening of a valve, leading to obstructed blood flow and pressure differences
Regurgitation is backward blood flow
94
What complications can regurgitation and stenosis lead to?
Hypertrophy and dilation of the ventricles
Mitral stenosis may lead to emboli from blood stasis
Regurgitation may lead to pulmonary edema, pulmonary HPN, and ventricular failure
95
How is stenosis and regurgitation treated?
Medications - Anti-coagulation to reduce thrombus risk, digoxin for arrhythmias and beta blockers to slow ventricular response
Surgical - mechanical or biological valve replacements
96
Is a valve replacement surgery a palliative or curative approach?
All valve surgeries are palliative and not curative
97
Define the patho of acute decompensating HF
Pulmonary venous pressure increases as a result of decreased efficiency of the left ventricle, resulting in engorgement of the pulmonary vascular system
The lungs become less compliant and there is increased resistance in the small airways
98
What is the most common complication of acute decomposating HF?
Pulmonary edema, most commonly caused by acute left ventricular failure secondary to acute MI
99
What are the signs and symptoms of acute decompensating HF?
Anxious, fatigue, tachycardia
Severe dyspnea, use of accessory muscles, resp >30, orthopnea, wheezing, coughing, frothy/blood-tinged sputum, crackles, wheezes, and rhonchi
Pale, cyanotic, cold, clammy
100
What are the six interventions for acute decompensating HF?
1. Use of diuretics to reduce venous return and alleviate pulmonary vascular pressure
2. High Fowler’s position to improve venous return, IV nitro to decreased preload
3. Decrease after load - if CO improves, pulmonary congestion decreases
4. Improve gas exchange through IV morphine to reduce preload and after load, therein decreasing O2 demand of myocardium
5. Improve cardiac function through inotropic therapy
6. Reduce anxiety - sedative action of morphine
101
Define unstable angina
Chest pain that is new in onset, occurs at rest, or has a worsening pattern
May be from chronic stable angina or the first clinical manifestation of CAD
Unpredictable and emergent
102
What are the signs and symptoms of a STEMI/NSTEMI?
PAIN
Dyspnea
Cool, ashen skin
Tachycardia and hypertension, which will eventually become hypotension due to decreased CO
Nausea
Fever
Decrease urine output
103
Why is the skin pale, cool, and ashen with MI?
During initial stage of MI, catecholamines (epinephrine and norepi) are released from ischemic myocardial cells, leading to release of glycogen, diaphoresis, and vasoconstriction of peripheral blood vessels
104
Why do people present with nausea with MI?
Reflex stimulation of vomiting centre by severe pain or from vasovagal reflexes initiated in the area of infarcted myocardium
105
Why would MI patients have a fever?
Systemic manifestation of the inflammatory process caused by myocardial cell death
106
What is the healing trajectory of an MI?
6 weeks after MI, scar tissue replaces necrotic tissue, and the injured area is said to be healed (may manifest as uncoordinated wall motion, ventricular dysfunction, or pump failure due to poor malleability of the scar tissue)
107
What are the 7 complications of an MI?
1. Dysrhythmias - typically heart block or VFib
2. HF
3. Cardiogenic shock - Inadequate oxygen and nutrients are supplied to the tissues because of severe left ventricular failure; requires PCI to open the narrowed coronary arteries
4. Papillary muscle dysfunction/mitral valve regurgitation – Occurs if infarcted areas include or are adjacent to papillary muscle that attaches to the mitral valve
5. Ventricular aneurysm - Infarcted myocardial wall becomes thinned and bulges during contraction
6. Pericarditis
7. Dressler’s syndrome - Pericarditis with effusion and fever that develops 4-6 weeks after MI
108
What complication usually appears within 4-6 weeks of an MI and has a fever?
Dressler’s syndrome
109
What three lab values would be necessary with an MI patient? What is their peak time?
CK-MB (3-12hrs), troponin (3-12hours), and myoglobin (<5hrs, one of the first markers)
110
How is NSTEMI/STEMI treated (6)?
1. Initiate IV
2. SL or chewable ASA and heparin
3. Nitroglycerin
4. O2 administration
5. Telemetry/ongoing ECG
6. Emergent PCI or fibrinolytic
111
What is a common complication of fibrinolytic therapy, other than bleeding? And what intervention reduces this risk?
Reocclusion of the artery – the site of the thrombus is unstable, and another clot may form, or spasm of the artery may occur
IV heparin therapy is initiated in conjunction with antiplatelets
112
What test would indicate the resolution of an MI?
The return of the ST segment to baseline on ECG
Other markers include resolution of chest pain and rapid rise of CK-MB
113
What are the two best diagnostics for MI?
Troponin and ECG
114
How do beta blockers work? What are the side effects?
Reduces BP by antagonizing beta 1 adrenergic effects – decreases CO and reduces sympathetic vasoconstrictor tone and decreases renin secretion
May cause bronchospasm, heart blocks, impaired circulation, rebound hypertension
115
How do calcium channel blockers work? Side effects?
Block movement of extracellular calcium into cells, causing vasodilation and decreased SVR
May cause nausea, headache, dizziness, peripheral edema, reflex tachycardia or bradycardia
116
How do ARBs work? Side effects?
Prevent action of angiotensin II and produce vasodilation, and increased salt and water excretion
May cause hyperkalemia and decreased kidney function
117
How long will it take to see an effect of ARBs on BP?
Effect on BP may not be seen for up to 3-6 weeks
118
What is resonium used for?
Used to treat high levels of potassium/hyperkalemia
119
What is the ERAS tool and what does it stand for?
Enhanced recovery after surgery
A guideline that indicates specific steps that should be completed at pre, intra, and post op - enhance recovery and reduce hospital time
120
What is the role of the pre-op nurse?
Prepares room with team
Sterile and unsterile
Client advocate throughout surgical experience
Assess
Support and comfort
Inform
121
What is the role of the circulating nurse?
Remains in unsterile field
Oversees process
Documents
Assessment, clinical Problems,
Diagnoses and Interventions
Surgical count pre and post
Monitoring
122
What is the role of the scrub nurse?
Follows designated scrub procedure
Gowned and gloved in sterile attire
Remains in sterile field
Monitors:
Ongoing Asepsis
Surgical Count
Handling of equipment
Specimens
123
What is the role of the registered first assistant nurse?
Registered perioperative nurse with formal surgical education
Under the direct supervision of the surgeon:
Manipulate tissue
Handle instruments
Provide exposure to surgical site
Assist with homeostasis
Perform suturing
124
What 6 things occur in the time out?
1. All team members introduce themselves by name and role
2. Surgeon, anesthesiologist, and nurse have verbally confirmed patient, procedure, and site
3. Review of anticipated events by surgeon, anesthesiologist, and nurse
- Surgeon: critical or unexpected steps, procedure duration, risk of >500mL blood loss
- Anesthesia: patient-specific concerns and adequate IV access & fluid planned
- Nurse: sterility or equipment issues
4. Applicable medication concerns
- Thromboprophylaxis ordered
- Prophylactic antibiotics given within last 60 mins
5. Essential imaging displayed
6. Any other questions or concerns before proceeding?
125
List and define the four types of anesthesia?
1. General - reversible state of unconsciousness with loss of sensation of the entire body
2. Sedation - decreased LOC or relaxed state, but not fully conscious
3. Regional - blocks sensation in a large region or portion of the body
4. Local - blocks sensation in a specific area of the body
126
What are the 5 adjuncts to general anesthesia?
Induction agents IV, opioids, benzodiazepines, neuromuscular blocking agents, and anti-emetics
127
What two induction agents will be given with anesthesia?
Propofol and ketamine
128
Why would opioids be given during surgery?
Sedation, analgesia, and respiratory depression
129
Why would benzodizapines be given as an adjunct for general anesthesia? What is one example?
Midazolam
Premedication for amnesia, induction of anesthesia
130
What three medications would be given as anti-emetics for surgery?
Metoclopramide, ondansetron, and dimenhydrinate
131
Why would neuromuscular blocking agents be given as an adjunct for anesthesia? Give an example of one
Intubation, relaxation and paralysis, interruption of nerve impulses, long duration
Succinylcholine - an indirect anticholinergic
132
What are three types of local anesthesia and give brief descriptions of each
1. Peripheral - injecting local anaesthetic into or around a specific nerve or group of nerves, typically for chronic pain
2. Spinal - Injection of agent into CSF of subarachnoid space,
Autonomic, sensory, and motor blockade
Usually below L2
3. Epidural - Injection of agent into epidural space
Does not enter CSF
Binds to nerve roots as they enter and exit the spinal cord
Sensory pathways blocked, but motor fibres intact
133
Describe the difference between spinal and epidural local anesthetic
Spinal - provides TOTAL block of autonomic/sensory/motor and goes into the CSF
Epidural - does NOT go into the CSF and only causes sensory blockade
134
What are three common symptoms of autonomic nervous system blockade?
Bradycardia, hypotension, N/V
135
What is malignant hyperthermia?
Hyperthermia with rigidity of skeletal muscles
Often occurs with exposure to succinylcholine, especially in conjunction with inhalation agents
Usually occurs under general anaesthesia but may also occur in recovery
HEREDITARY
136
What does the ASA score help us identify pre op?
Helps us identify potential risks
137
What is a LATE sign of malignant hyperthermia? And what are other symptoms?
Rise in temperature
Tachycardia
Tachypnea
Hypercarbia
Ventricular dysrhythmias
138
What is a major complication intra and post op?
Blood loss/hemorrhage
139
What is succinylcholine and what would it be used for? What might it cause in individuals with a specific predisposition?
An indirect anticholinergic that is used as a neuromuscular blocker to cause rapid paralysis in surgery
May cause malignant hyperthermia
