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TOPICSII > Exam 2 Review > Flashcards

Exam 2 Review Flashcards

1
Q

Incidence of atherosclerosis and vascular diseases increases with

A

Advancing age.

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2
Q

Predisposing risk factors for atherosclerosis include:

A 
HTN
Insulin resistance
Dyslipidemia
Abdominal obesity
Cigarette smoking
Increasing age
Family History
Pro-inflammatory states
Pro-thrombotic state
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3
Q

Development of atherosclerosis occurs in 2 stages:

A

Endothelial injury

Inflammatory response to injury

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4
Q

Pathophysiology of Atherosclerosis: Primary injury and everything else

A

Primary injury occur as low density lipoprotein and apolipoprotein-B containing lipoproteins invade the vascular endothelium and become proinflammatory
As the inflammatory cascade starts, the subendothelial space is filled with atherogenic lipoproteins and macrophages, which form foam cells.

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5
Q

What are foam cells?

A

They form the atheromatous core of a plaque, which becomes necrotic and further enhances the inflammatory process.

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6
Q

How does plaque rupture?

A

Disruption of the fibrous cap over a lipid deposit can lead to plaque rupture and ulceration.

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7
Q

Vascular disease is not a localized phenomenon, but rather a systemic one affecting

A

multiple organs including the heart with MI and the brain with CVA

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8
Q

Leading cause of disability

A

Stroke

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9
Q

Third leading cause of death in the US

A

Stroke

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10
Q

PAD can cause

A

Claudication and Limb ischemia

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11
Q

Coronary atherosclerosis that leads to MI is the

A

Leading cause of death and disability worldwide.

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12
Q

Medical therapy for atherosclerosis

A

HTN, HLD, Diabetes,Obesity

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13
Q

How do statins help treat Atherosclerosis

A

Reduces progression and may cause regression of atherosclerotic plaques
Improve endothelial function
Reduce CV events

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14
Q

Management of atherosclerosis is basically

A

Management of contributing systemic diseases such as HTN, Hyperlipidemia, diabetes and obesity.

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15
Q

3 things that significantly slow or reverse the progression of atherosclerosis

A
  1. Chronic therapy with aspirin
  2. ACE inhibitors
  3. Smoking Cessation.
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16
Q

Therapies to be continued up to day of surgery and throughout the perioperative period?

A

Statins
ASA
B blockers

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17
Q

Aspirin side effects

A

Platelet inhibition may lead to increased bleeding.

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18
Q

Aspirin do you continue ?

A

Continue until day of surgery ESPECIALLY for carotid and PVD,

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19
Q

Clopidogrel side effects are

A

Platelet inhibition

Rare thrombotic thrombocytopenic purpura

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20
Q

Clopidogrel (Plavix) hold for

A

7 days before surgery EXCEPT CEA and Severe CAD or DES

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21
Q

Clopidogral (Plavix) and neuraxial anesthesia

A

AVOID if not held for at least 7 days.

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22
Q

Side effects of statins HMG CoA reductase inhibitors

A

Liver function test abnormalities

Rhabdomyolysis

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23
Q

Beta Blockers side effects

A 
Bronchospasm
Hypotension
Bradycardia, heart Block
Induction hypotension
Cough
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24
Q

Beta Blockers and perioperative period

A

continue throughout the periop

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25
Q

ACE inhibitors side effects

A

Induction hypotension

Cough

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26
Q

ACEI and perioperative period

A

Continue throughout the periop

Consider one half dose on day of surgery

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27
Q

Diuretics and perioperative period

A

Continue through periop

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28
Q

CCB Side effects

A

Perioperative hypotension (especially with amlodipine)

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29
Q

Consider withholding this medication day of surgery and why?

A

Amlodipine, may cause perioperative hypotension

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30
Q

Oral Hypoglycemics may cause

A

hypoglycemia intra-operatively and perio-operatively.

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31
Q

When feasible for oral hypoglycemics switch to

A

insulin preoperatively , monitor glucose

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32
Q

If a coronary stent is placed, elective surgery should be delayed, for bare metal stents

A

minimum of 6 weeks

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33
Q

If a coronary stent is placed, elective surgery should be delayed, for Drug eluting stents

A

12 months or longer.

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34
Q

Recommended indefinitely to prevent in-stent thrombosis

A

Aspirin

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35
Q

Ischemia-reperfusion injury in the vascular surgery patient: fundamental concepts

A

Reduction or interruption of blood flow stop delivery of O2, –> glucose, and other essential nutrients that are needed for AEROBIC metabolism and therefore generation of ATP is slowed. When there is no ATP cellular processes fail and cellular integrity is lost. The duration of ischemia correlates directly with the degree of cellular injury. Toxic metabolites of anaerobic metabolism accumulate in the ischemic region. Upon reperfusion, toxic metabolites are released into the circulation.

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36
Q

Prevention of Post op acute renal failure.

A

Suprarenal aortic cross-clamping 15%

Infrarenal aortic cross-clamping 5 %

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37
Q

During carotid endarterectomy What is the most common cause of stroke?

A

Emboli from the surgical site.

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38
Q

Aortic procedures can be associated with

A

Significant pulmonary complications due to LARGE FLUID SHIFTS and transfusion related acute lung injury.

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39
Q

After carotid endarterectomy , what happens

A

The carotid body on the operative side is denervated and this blunts the ventilatory response to hypoxemia.

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40
Q

The most urgent and potentially devastation complications of Carotid endarterectomy is

A

CLOT formation at the surgical site and the associated THROMBOEMBOLISM in the cerebral circulation.

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41
Q

***The most urgent and potentially devastation complications of Carotid endarterectomy is

A

CLOT formation at the surgical site and the associated THROMBOEMBOLISM in the cerebral circulation.

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42
Q

Major risk with Thoracic aortic procedures?

A

Compromise of the spinal cord vascular supply, especially the artery of ADAMKIEWICZ

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43
Q

Symptoms of Carotid artery stenosis

A

Sudden unilateral vision loss (AMAUROSIS FUGAX)

Unilateral changes in motor function, dysarthria, and aphasia

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44
Q

When is a CEA urgent?

A

If preoperative medical management with anticoagulants, and antiplatelet drugs does not control the symptoms of carotid stenosis.

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45
Q

Should be avoided with CEA?

A

Sudden reduction in BP should be avoided.

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46
Q

The Artery of Adamkiewicz usually arises at the

A

T11 - T12 level and provides the blood supply to the lower spinal cord.

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47
Q

Why do some patient are kept away during CEA?

A

Providing regional is good because awake patient can report neurological changes most reliably.

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48
Q

Other CEA cases done under GA relies on what monitors

A

EEG
SSEPs
Transcranial Doppler
Cerebral Oximetry.

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49
Q

Anesthesia for CEA

A

Both General and regional safe

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50
Q

For both types of anesthesia patient should be

A

awake and cooperative at the end of the procedure for ongoing neurological assessment.

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51
Q

CEA pts have a high incidence of

A

CAD and hypertensive heart disease

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52
Q

Use in combination to offset the ETT stimulation

A

Etomidate

Esmolol

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53
Q

The majority of CVAs are caused by

A

Emboli from the surgical site.

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54
Q

Regional anesthesia for CEA

A

Deep and superficial Cervical Plexus blocks
Cervical anesthesia
Local infiltration

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55
Q

Recommended CEA monitors

A

ASA monitors

Intra-arterial BP Because BP control is vital during CEA

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56
Q

Carotid Angioplasty with stenting, vs CEA

A

Carotid stenting is associated with a higher risk of periprocedural stroke and death.

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57
Q

What should prompt immediate Ultrasound after CEA?

A

New onset neurologic change after surgery should prompt immediate US and possible reoperation.

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58
Q

Other possible adverse effects after CEA

A

Hypotension
hypertension
MI
Recurrent nerve injuries

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59
Q

Associated with increased mortality and increase cardiac and neurologic complications?

A

Uncontrolled severe hypertension with CEA.

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60
Q

CEREBRAL HYPERPERFUSION SYNDROME symptoms

A

Headaches
Seizures
Focal neurological signs.

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61
Q

Can obstruct the airways?

A

Expanding wound hematoma.May need emergent evacuation of the hematoma before an adequate airway can be re-established.

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62
Q

One of the greater anesthetic management challenge

A

Rupture of an Aortic aneurysm

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63
Q

True surgical emergency

A

Rupture of an Aortic aneurysm

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64
Q

Risk factors for AAA (MASHHLL)

A 
Male sex
Advanced age
Smoking
Hypertension
High Fibrinogen
Low serum high density lipoprotein (low HDL)
Low platelet
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65
Q

Aneurysm that should be consider for surgical endovascular repair

A

> 5 cm

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66
Q

Task force screening for Aortic Aneurysm

A

Screening for AAA is recommended for men> 65 years with a SMOKING HISTORY

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67
Q

Medical management of aortic aneurysm includes

A

Smoking cessation

Control of HTN, dyslipidemia, DM and diet

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68
Q

Smaller AAA such as size_________require what?

A

4 - 5.4 requires frequent ultrasound monitoring for progression.

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69
Q

Dominant treatment modality for AAA is

A

Endovascular aneurysm repair (EVAR)

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70
Q

First line/Dominant treatment modality for AAA is

A

Endovascular aneurysm repair (EVAR)

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71
Q

In EVAR what artery is used to introduce the stent grafts inside the aneurysm?

A

Femoral artery

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72
Q

Stent grafts inserted to prevent

A

further enlargement and rupture.

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73
Q

Complications of EVAR

A

Graft leak
intraoperative conversion to open repair
Vascular injury
Inability to seal the graft against the wall of the aorta.

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74
Q

When compared EVAR to open surgical repair

A

EVAR is associated with shorter recovery times

lower 30-day mortality rates

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75
Q

For the open surgical repair two approaches?

A

Anterior Transperitoneal laparotomy

Anterolateral retroperitoneal approach

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76
Q

Retroperitoneal appraoach for open aortic aneurysm repair- Advantages

A

Less fluid shifts
Faster return of bowel function
Lower pulmonary complications
Shorter ICU stays

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77
Q

The higher the level of clamping

A

The greater the stress will be on the LV and the HIGHER the incidence of ischemic injury to the gut, kidney, and spinal cord.

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78
Q

Must be used during open repair of aortic aneurysm

A

Systemic anticoagulation

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79
Q

Can be employed to enhance spinal perfusion pressure

A

Spinal fluid drainage during thoracic aneurysm

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80
Q

One of the greatest anesthetic management challenges

A

Thoracoabdominal aortic aneurysm surgery because it involves the descending thoracic and abdominal aorta requiring expansive incision extending into these cavities, one lung ventilation, and the use of CPB.

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81
Q

During thoracic procedures, spinal cord ischemia may be detected through the use of

A

SSEPs

MEPs

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82
Q

Done to improve spinal cord perfusion?

A

Lumbar subarachnoid drain used to remove CSF

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83
Q

Most common reason for emergency Aortic surgery?

A

Rupture or leaking of an aortic aneurysm

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84
Q

Aortic aneurysm rupture has a mortality rate of

A

85%

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85
Q

Aortic aneurysm rupture has a mortality rate of 85% unless surgery is done immediately, rate is then

A

50%

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86
Q

If patient survives aortic aneurysm surgeries they are at risk for

A

MI, pulmonary injury

SCI

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87
Q

Rupture most common occur into the

A

Retroperitoneum

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88
Q

Needed for emergency aneurysm surgeries

A

Massive blood loss
Preparations for blood replacement
Rapid infusion devices.

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89
Q

Lower Extremity revascularization surgery : 3 indications

A

Claudication
Ischemic rest pain or ulceration
Gangrene

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90
Q

High risk LE revascularization procedures

A

ileofemoral bypass
Femoral-femoral bypass
Aortafemoral bypass

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91
Q

LE revascularization procedures done to

A

Reestablish blood flow to an ischemic extremity and relieve debilitating symptoms of claudication.

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92
Q

LE revascularization what is painful and can lead to tachycardia?

A

Tunneling the graft

Deployment of the stent.

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93
Q

What is given prior to the deployment of a graft?

A

Heparin

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94
Q

Use to keep graft patency after the procedure

A

Heparin.

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95
Q

Atherosclerosis occurs in 2 stages, the first is _______

A

Endothelial injury

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96
Q

Atherosclerosis occurs in 2 stages, the first is endothelial injury, the second is

A

An inflammatory response

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97
Q

What % of men over the age of 65 have carotid stenosis?

A

Over 40%

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98
Q

How long should elective surgery be delayed after the placement of a DES?

A

12 months

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99
Q

The risk of cardiac related death or nonfatal MI after CEA is

A

less than 5%

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100
Q

S/S of cerebral hyperperfusion syndrome after CEA include

A

Headaches, seizures and focal neurological deficits

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101
Q

At what diameter should an aortic aneurysm be considered fro surgical repair?

A

Greater than 5.0cm

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102
Q

AAA Incidence and age

A

3-10% Over 50 years old (Nagelhout)

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103
Q

AAA more common in

A

Men

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104
Q

AAA #1 Risk factors

A

Smoking

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105
Q

Surgery intervention is recommended for AAA

A

AAA > 5.5 cm or GREATER

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106
Q

AAA other Risk factors

A 
Male 
Older Age (>50) 
CAD
HTN
Low HDL
High Fibrinogen
High Cholesterol
Family History
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107
Q

Ruptured AAA Incidence

A

35-94%

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108
Q

ABove the clamp you get _____below to the clamp you get ______

A

HTN ; HoTN

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109
Q

The higher the level of the cross clamping the

A

greater the stress to the LV

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110
Q

Most common site is of clamping and why?

A

MOST COMMON site is INFRARENAL because most aneurysm are below the levels of the renal artery.

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111
Q

Preclamp you can give this medication

A

Mannitol 0.25 - 0.5 g/kg IV to maintain UO and preserve renal function

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112
Q

Five minutes before cross clamp give

A

heparin

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113
Q

Obtain baseline _______ ,_____Mns after administration, and then every _______ while the clamp is in place

A

5 minutes, 3 minutes, every 30 minutes.

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114
Q

Cross clamping derangements

IADPI

A 
Sudden increase afterload
decrease preload
Increased filling pressure
Decreased renal perfusion
Decrease perfusion of viscera below clamp
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115
Q

The placement of the clamp determines the

A

Degress of derangement.

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116
Q

Infrarenal clamp avoids

A

Ischemia to most major organ

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117
Q

LEAST Hemodynamics effects : CLAMP

A

InFRARENAL

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118
Q

MOST Hemodynamics effects : CLAMP

A

SUPRACELIAC

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119
Q

Most dramatic changes occur during

A

Cross clamping

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120
Q

AORTIC CLAMPING leads to an

A

Increase in SNS stimulation catecholamines, aldosterone, cortisol
increase in Afterload

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121
Q

2 concerns during aortic clamping

A

CHF and LV dysfunction is a concern.

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122
Q

Metabolites from ANAEROBIC metabolism →

A

LACTATE

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123
Q

Effects of release :

A

Vasodilation, decrease SVR, decrease venous return which is called DECLAMPING SHOCK SYNDROME (DSS)

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124
Q

Declamping shock syndrome is characterized

A

Vasodilation, decrease SVR, decrease venous return

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125
Q

Declamping associated with: BP

A

HYPOTENSION

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126
Q

2 main mechanism with hypotension after declamping

A

Relative Hypovolemia

Myocardial depression

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127
Q

Partally responsible for declamping hemodynamic instability:

A

Venous endothelin “ET1” is partially responsible

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128
Q

ET1 effect on Heart

A

ET1, Positive inotrope on heart, Vasoconstricting effect on blood vessels

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129
Q

Ischemic REPERFUSION INJURY →

A

occurs during cross clamping and unclamping (cross clamping -ischemia; unclamping - reperfusion)

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130
Q

Declamping Release substances include

A

reactive oxygen species, increased intracellular calcium which inhibits mitochondrial activity and ATP.

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131
Q

NO REFLOW PHENOMENON occurs when the

A

microvasculature is occluded by platelets, neutrophils and thrombi causing inadequate perfusion and further increase in cellular necrosis.

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132
Q

Other manifestations with ischemic reperfusion include

A

tissue injury, ARDS, compartment syndrome, MODS.

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133
Q

LIST the physiologic changes associated with aortic cross-clamping

A 
Increase arterial BP above the clamp
Decrease BP below the clamp
Increase wall motion abnormalities 
Decreased EF and CO 
Decrease Renal blood flow 
Increase pulmonary occlusion pressure (PAOP)
Increase in CVP
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134
Q

Increase arterial BP above the clamp → leads to what metabolic changes?

A

decrease total body O2 consumption

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135
Q

Intra-operative interventions of increase arterial BP above the clamp

A

TX: DECREASE AFTERLOAD with sodium nitroprusside, volatile anesthetics, milrinone and shunts

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136
Q

Decrease BP below the clamp what metabolic changes?

A

Decrease in the CO2 production

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137
Q

Decrease BP below the clamp : intraoperative interventions?

A

REDUCE PRELOAD with nitroglycerine, atria-femoral bypass

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138
Q

Increase wall motion abnormalities leads to what metabolic changes?

A

Increase mixed venous O2 saturation

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139
Q

Increase wall motion abnormalities intraoperative interventions:

A

RENAL PROTECTION with fluid and diuretics : mannitol, furosemide, dopamine, N-Acetylcysteine

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140
Q

Decreased EF and CO leads to what metabolic changes?

A

Decrease Total body oxygen extraction

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141
Q

Decreased EF and CO Intraoperative interventions

A

Miscellaneous : hypothermia, decrease minute ventilation, and sodium bicarbonate

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142
Q

Decrease Renal blood flow leads to what metabolic change

A

INCREASED CATECHOLAMINE RELEASE

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143
Q

Increase pulmonary occlusion pressure (PAOP) metabolic changes

A

respiratory alkalosis

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144
Q

Increase in CVP leads to what metabolic changes

A

leads to METABOLIC ACIDOSIS

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145
Q

ACUTE KIDNEY INJURY (AKI)

Tissue distal to the aortic clamp are

A

underperfused

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146
Q

RBF can be decreased by as much as

A

80%

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147
Q

Suprarenal Cross clamp Time longer than_____increase risk of what?

A

30 minutes increases risk of renal failure.

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148
Q

Most IMPORTANT INTERVENTION to protect from AKI are :

A

Minimize aortic clamp time, aggressive hemodynamics stabilization

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149
Q

4 Medications that can help prevent AKI are:

A

Dopamine, bicarbonate, furosemide, mannitol

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150
Q

SPINAL CORD ISCHEMIA can Causes

A

PARAPLEGIA

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151
Q

Incidence of spinal cord ischemia

A

1-13% of the time

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152
Q

Spinal arteries supplying the spinal cord are

A

2 posterior arteries (20%) , 1 anterior artery (80%), supplies the cord

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153
Q

ARTERY OF ADAMKIEWICZ provides

A

transverse levels

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154
Q

Level of ARTERY of ADAMKIEWICZ is

A

T8 - T12

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155
Q

Interruption of blood flow to the artery of adamkiewicz in absence of collateral blood flow can cause

A

PARAPLEGIA

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156
Q

Interruption of blood flow to which artery can cause PARAPLEGIA →

A

ARTERY OF ADAMKIEWICZ

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157
Q

SPINAL CORD PROTECTION Strategy :

A

Mild hypothermia, CSF drainage, Distal aortic perfusion with SBP > 120mmHg

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158
Q

Ischemic colon injury from

A

INFERIOR MESENTERIC ARTERY

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159
Q

2nd most common vascular surgery in US

A

CEA

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160
Q

The risk of cardiac - related death or nonfatal MI after CEA is

A

less than 5%

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161
Q

1st most common VASCULAR surgery is

A

CORONARY REVASCULARIZATION

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162
Q

Framingham Study: Stroke Risk _____after a TIA and ___% ____years after a TIA

A

30% 2 years after a TIA, and 55% 12 years after TIA

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163
Q

Leading cause of death after vascular surgery?.

A

STROKE

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164
Q

Stroke often related to a

A

decrease Cerebral blood flow

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165
Q

What is AMAUROSIS FUGAX →

A

Unilateral (monocular) blindness, 25% of people with high grade carotid artery stenosis

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166
Q

AMAUROSIS FUGAX -> caused by

A

microthrombi in the internal carotid artery leading to a decreased blood flow to the OPTIC NERVE

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167
Q

Nerve affected by amaurosis Fugax

A

OPTIC NERVE

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168
Q

The most URGENT and devastation complication of CEA is

A

CLOT FORMATION at THE SURGICAL SITE and the associated thromboembolism to the cerebral circulation

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169
Q

BEST Measure of adequate CBF is

A

an AWAKE PATIENT

170
Q

What is the Gold standard for identifying neurological deficits related to coronary artery cross clamping

A

EEG monitoring

171
Q

EEG assesses for

A

CORTICAL electrical function and a

LOSS OF BETA WAVE ACTIVITY, LOWER AMPLITUDE, and emergence of SLOW WAVE ACTIVITY

172
Q

STUMP PRESSURE assess what

A

To assess COLLATERAL FLOW

173
Q

Stump pressure is a Gross measurement of the pressure within

A

the circle of WIllis

174
Q

A stump pressure of less than______Means what?

A

40-50 mmHg means NEUROLOGIC HYPOPERFUSION and is an INDICATION FOR A SHUNT

175
Q

SOMATOSENSORY EVOKED POTENTIALS reflect what

A

Reflect sensory integrity of the spinal cord in the brain

176
Q

List 5 ways of neuromonitoring during CEA

A 
EEG
Stump pressure
SSEPs
TCD
NIRS
177
Q

TRANSCRANIAL DOPPLER : Assess

A

velocity of blood flow in the MIDDLE CEREBRAL ARTERY

178
Q

Transcranial Doppler assesses which artery

A

Middle cerebral artery

179
Q

NEAR INFRARED SPECTROSCOPY : Assess

A

CEREBRAL REGIONAL OXYGEN SATURATION.

180
Q

NIRS indication of cerebral ischemia?

A

> 20%reduction is indicative of CEREBRAL ISCHEMIA

181
Q

Which technique best assess regional cerebral oxygen saturation ->

A

Near infrared spectroscopy.

182
Q

3 ways to protect the brain and prevent ischemia (IDA)

A
  1. INCREASE collateral flow with a SHUNT
  2. DECREASE CMRO2 with volatile anesthetics
  3. AVOID hyperglycemia
183
Q

CO2 during neurosurgery

A

Maintain normocarbia

184
Q

Anesthetics to avoid

A

AVOID ETOMIDATE, and NITROUS

185
Q

Which gas provide the BEST PROTECTION AGAINST CEREBRAL ISCHEMIA?

A

ISOFLURANE

186
Q

Signs and symptoms of cerebral hyperperfusion syndrome after CEA include

A

headaches, seizures and FOCAL NEUROLOGICAL DEFICITS

187
Q

Most common complication of CEA is

A

STROKE by microemboli

188
Q

Other Complications of CEA

A

MI, Bradycardia , HoTN
Stent thrombosis, HORNER’s SYNDROME
Hemorrhage
Carotid Artery rupture

189
Q

Leads to anterior spinal cord syndrome?

A

Damage to artery of adamkiewitcz

190
Q

Regional for surgery of Lower extremities

A

EPIDURAL BEST option with MANY ADVANTAGES

191
Q

If they have combined general and epidural is associated with

A

30% reduction in death

192
Q

Lower incidence of (3) with epidural anesthesia

A

MI, stroke and respiratory failure

193
Q

A positive consideration for administering INHALATIONAL and IV Anesthetics is that they

A

DECREASE the rate of OXYGEN DEMAND

194
Q

RISK that neuraxial can lead to

A

EPIDURAL Hematoma formation

195
Q

STUMP PRESSURE To assess

A

COLLATERAL FLOW

196
Q

Provide the blood flow to the CIRCLE of willis during the CEA

A

NON-OPERATIVE carotid artery and the BASILAR artery

197
Q

Stump pressure Gross measurement of the

A

pressure within the circle of WIllis

198
Q

EVAR is good because it associated with

A

LOWER MORTALITY , Shorter recovery time, decrease procedure time.

199
Q

More common with EVAR

A

Re-interventions or having 2 surgeries

200
Q

EVAR is associated with no

A

cross clamping , no prolonged period of extreme hypotension

201
Q

During EVAR what is done?

A

FEMORAL ARTERY used to introduce stent graft to aneurysm

202
Q

Endovascular Aortic repair (EVAR) →

A

because of the ENDO leak or GRAFT LEAK

203
Q

Most significant advantages EVAR

A

NO CROSS CLAMPING, NO LARGE INCISION (chest to pelvis.

204
Q

Open approaches: 2 approaches

A

anterior transperitoneal OR anterolateral retroperitoneal approaches

205
Q

Questions: All are indications for FFPs except
Question 2:
Question 3;

A

Hypovolemia with a normal Hgb (FFP is not used for volume status, only for blood)

206
Q

For surgeries with significant blood loss, the best alternative to RBC transfusion is

A

Blood Salvage with cell Saver.

207
Q

For craniotomy indication for platelet is when platelet is

A

100,000,

208
Q

(No spontaneous bleed until platelets

A

less than 10,000,

209
Q

Recommended indications for platelet infusion include all EXCEPT

A

Platelet count 25,000 in asymptomatic patients.

210
Q

Major surgeries indications for platelets

A

50000

211
Q

It is the component of choice to improve oxygen carrying capacity.
1 unit increases Hgb by 1 g/dl and Hematocrit by 3 %

A

PRBCS

212
Q

One unit of PRBCs is good for

A

40 days,

213
Q

One unit of PRBC contains _____ml of RBCs

A

250 ml of RBCs,

214
Q

PRBCs hematocrit is

A

65%.

215
Q

PRBCs give

A

Given 1 ml for each 2 ml of blood loss

216
Q

1 unit of PRBCs increases Hgb by ____and Hct by ___

A

1 g/dl; 3%

217
Q

FFPs Contains all the

A

coagulation factors

218
Q

FFP : It is stored for

A

1 year at -10 C

219
Q

FFP Thawed, kept in the fridge

A

for 5 days

220
Q

FFP Volume

A

Volume 200-250 ml

221
Q

Indications for FFP administration:

A

Reversal of effect of warfarin
Vitamin K deficiency
Correction of coagulopathy

222
Q

FFP and PT/PTT

A

Used to treat elevated PT/PTT that is greater than 1.5 x normal

223
Q

FFP Dose for reversal of warfarin

A

is 5-8 ml/kg

224
Q

FFP Dose for ALL Other purpose of administration except for reversal of heparin

A

Dose is 10-20 ml/kg

225
Q

FFP discouraged if

A

INR < 2

226
Q

FFP and coagulation levels

A

increase coagulation levels by 20-30 %

227
Q

1 unit of whole blood is about

A

6 units of platelet concentrate

228
Q

Platelets shelf life and implications

A

SHORT Shelf life - 5 days because PRONE TO BACTERIAL GROWTH

229
Q

Dose of platelet

A

1 platelet concentrate per 10 kg of body weight

230
Q

1 unit raise platelet count by

A

30,000 - 60,000

231
Q

Indication for platelet Less than

A

50,000

232
Q

CRYOPRECIPITATE and factor VII

A

Contains 100 units of factor VIII

233
Q

Cryoprecipiate Contains

A

fibrinogen, fibronectin, and von willebrand Factor

234
Q
  • Recommended for von willebrand disease, and for deficit of fibrinogen < 100
A

Cryoprecipitate

235
Q

How is Cryo administered

A

Must be administered RAPIDLY through a FILTER

236
Q

Cryo and fibrinogen

A

10 units of cryoprecipitate contains 2 g of fibrinogen

237
Q

Colloids administration should be AVOIDED with

A

SUSPECTED or known TBI

238
Q

Colloids expands what volume?

A

plasma volume rather than interstitial fluid volume

239
Q

Colloids have less

A

fluid requirement, LESS PERIPHERAL AND PULMONARY EDEMA

240
Q

No mortality difference of colloids administration in

A

septic patients

241
Q

Worst OUTCOMES AND HIGHER MORTALITY.(not in US)

A

Hydroxethyl starch (HES)

242
Q

Crystalloids are

A

inexpensive, non allergenic, and do not inhibit coagulation

243
Q

Colloids are (disadvantages)

A

expensive, allergenic, and linked to RENAL FAILURE AND COAGULATION

244
Q

Colloids advantages: infusion volume , edema and length of time in plasma volume?

A

Smaller infused volume
Less peripheral edema
Prolonged increase in plasma volume

245
Q

Colloids Disadvantages:

A 
Greater cost
Coagulopathy
Pulmonary EDEMA
Decreased GFR
Osmotic diuresis
Greater duration of excessive volume expansion
246
Q

Crystalloids advantages

A

Lower cost
Greater urinary flow
Interstitial fluid replacement

247
Q

Crystalloids disadvantages

A

Transient increase in Intravascular volume

Transient hemodynamic improvement

248
Q

Crystalloids edema diagnosis

A 
Peripheral edema (protein dilution)
Pulmonary edema (protein dilution + high PAOP)
249
Q

All of the following IV solution are ISOTONIC , Except:

A

25% Albumin

250
Q

ISOTONIC SOLUTIONS are :

A

LR, plasmalyte, NS

251
Q

NS composition

Na, CL, ph, OsmoLality

A

154 Na+
154 Cl-
pH 5.6
OsmoLAlity 310

252
Q

LR composition

A

Sodium, Chloride, Potassium, Calcium, Lactate

253
Q

LR ph and osmolality

A

pH 6.2

OsmoLAlity 275

254
Q

LR composition numbers

A 
Na+ 130
Cl- 110
K+ 4.0
Ca 3.0
Lactate 28
pH 6.2
OsmoLAlity 275
255
Q

Plasmalyte composition

A

Sodium, Potassium, chloride, Magnesium, Glucose

256
Q

Plasmalyte composition

Na, K, Cl, Mag, glucose ph and osmoloLality

A 
Na 140
K+ 5
Cl- 98
Mag 3.0
Glucose 23
pH 7.4
OsmoLALITY is 295
257
Q

Plasma Composition

A

Sodium, Potassium, Chloride, Magnesium, Calcium,

258
Q

Plasma composition numbers :

Na+, K+, Cl-, Mag Ca2+, ph, osmolality.

A 
Na 142
K+ 4
Cl 103
Mag 2.0
Ca2+ 5
pH 7.4
OsmoLAlity is 291
259
Q

Preferable for resuscitation of dehydration conditions such as fasting , active GI losses, polyuria, and

A

Crystalloids

260
Q

Administration of isotonic affects the entire ECV

A

Crystalloids

261
Q

MOST COMMONLY ADMINISTERED IV FLUIDS, however is the LEAST PHYSIOLOGICAL

A

NSS crystalloid

262
Q

Large volume of NS lead to

A

increase SALT and WATER retention

263
Q

3% Saline is given to

A

trauma and head injury patients, and for VOLUME EXPANSION

264
Q

Can lead to HYPERCHLOREMIC METABOLIC ACIDOSIS

A

NSS crystalloids

265
Q

Hyperchloremia does what?

A

impairs renal handling of bicarbonate and DECREASES GFR

266
Q

HYPERMETABOLIC conditions fluid

A

NSS crystalloids

267
Q

Beneficial for restoration of circulating intravascular volume, decrease in hormone mediated vasoconstriction

A

NSS crystalloids

268
Q

Preservation of microcirculatory flow

LAck of allergic potential

A

NSS crystalloids

269
Q

NSS and crystalloids metabolism

A

Easily metabolized and renally cleared

Ability to expand plasma volume transient

270
Q

Can lead to mild METABOLIC ALKALOSIS

A

LR

271
Q

LR and Blood Products

A

Contraindicated with BLOOD PRODUCTS because of risk of coagulation

272
Q

Compatible with blood products

A

PLASMA LYTE and NSS

273
Q

T/F Crystalloids are more ALLOGENIC than colloids?

A

FALSE

274
Q

Used to estimate fasting deficit and surgical and insensible losses

A

4-2-1

275
Q

Used to replace fluid deficit

A

4-2-1

276
Q

Prophylactic volume administration is outdated,

A

and can lead to fluid overload

277
Q

Fluid management techniques that account for

A

3rd spacing, results in poor clinical outcomes

278
Q

Urine output as an indicator of volume status is

A

NOT ACCURATE

279
Q

Positive fluid balance in a trial resulted in an

A

increase rate of Acute Renal Failure in those with sepsis

280
Q

ERAS and clear fluid

A

Allows clear fluid 2 HOURS prior to surgery so the patient is in a euvolemic state

281
Q

Bowel Prep And ERAS

A

It avoids the routine use of a BOWEL PREP

282
Q

Carbohydrate drinks and ERAS

A

2 hours before (carb loading, NO fasting)

283
Q

ERAS and glucose

A

Maintain adequate insulin and glucose level

284
Q

ERAS and dehydration

A

Decrease state of dehydration prior to surgery

285
Q

ERAS and NG tube

A

NO NG tube, early PO, early foley removal
Early MOBILIZATION
NO drains

286
Q

Less likely to develop hypotension from hypovolemia

A

Early discontinuation of IV fluids

Start PO intake soon

287
Q

Hyponatremia Symptoms

A 
Cerebral edema
Impaired thermoregulatory control
Lethargy, coma, seizures
Nausa
Reflex impairments
288
Q

Hypernatremia Symptoms

A

Weakness
Lethargy, coma, seizures
DEMYELINATING LESIONS
Intracerebral or Subarachonid hemorrhage

289
Q

Hypokalemia

A 
Muscle weakness
Respiratory failure
Rhabdomyolosis
Ileus
Cardiac arrhythmias
290
Q

ECG changes

A

(blunted T waves and the presence of U waves)

291
Q

Hypokalemia Symptoms

A 
Muscle weakness
Respiratory failure
Rhabdomyolosis
Ileus
Cardiac arrhythmias
Nephrogenic DI
292
Q

ECG changes

A

blunted T waves and the presence of U waves

293
Q

HYPERKALEMIA Symptoms

A 
Severe muscle weakness
Ascending paralysis
Cardiac conduction abnormalities
ECG changes
Cardiac arrhythmias
294
Q

Mild Hyperkalemia 5.5 - 6.5 →

A

Peaked T waves,Prolonged PR segment

295
Q

Moderate Hyperkalemia 6.5 -8 →

A

Loss of P wave, Prolonged QRS, ST segment elevation, Ectopic beats and escape rhythms

296
Q

Severe Hyperkalemia > 8 ->

A

Sinus wave, Progressive widening of QRS complex, Vfib, asystole, axis deviations, BB blocks, Fascicular blocks.

297
Q

Hypertonic fluids :

A

Mannitol and Hypertonic Saline

298
Q

Hypertonic Saline is MOST commonly used for

A

sympatomatic hyponatremia

299
Q

Mannitol is used to

A

reduce ICP

300
Q

Hypertonic fluids draw

A

interstitial fluid into the intravascular space

301
Q

Mannitol and Mechanism

A

inhibitsREABSORPTION of free WATER and Sodium in the kidney resulting in a Large diuresis.

302
Q

Mannitol,For the Treatment of

A

elevated ICP, HYPERTONIC SALINE is SUPERIOR

303
Q

Clinical indicators of tissue hypoxia

A 
Base deficit > 2 mEq/L
Lactate > 2.5 mmol/L
Cap refill > 2 sec
Cold mottled skin
Mixed venous oxygen saturation < 65%
Central Venous oxygen saturation < 70%
304
Q

Most common cause of Transfusion related death

A

TRALI

305
Q

National heart and lung diagnostic criteria:

A

Acute, NONCARDIOGENIC pulmonary edema with Bilateral infiltrates and a P/F < 300

306
Q

Pathology of TRALI

A

Breakdown of capillary alveolar membrane
Interstitial pulmonary edema
Microscopic alveolar hemorrhage

307
Q

Occurs as a result of Alloantibodies

A

TRALI

308
Q

TRALI definition

A

Defined as ACUTE LUNG INJURY within 6 hours of Blood transfusion

309
Q

Presenting symptoms of TRALI:

Cause

A

Increase O2 requirements to ARDS

310
Q

TRALI treatment

A

Treatment is supportive

DOES NOT RESPOND to diuretics.

311
Q

Theories for the cause of TRALI

A

Theory 1. Antibodies in the donor plasma activate neutrophils leading to pulmonary capillary leakage. Theory 2. Stressor like sepsis, leads to neutrophils in the lungs.

312
Q

Most IMPORTANT complication of heparin therapy

A

Heparin Induced Thrombocytopenia

313
Q

HIT is Characterized by

A

microvascular thrombosis secondary to platelet activating IgG antibodies to the heparin and platelet factor IV complex

314
Q

HIT and lovenox

A

Less likely to occur with lovenox

315
Q

When is HIT suspected?

A

Should be suspected in anyone with decrease >50% decrease in platelet count from baseline OR total platelet count of < 100 while on heparin with normal baseline levels.

316
Q

1 out 5 % of patients TYPICALLY after

A

5-10 DAYS

317
Q

Classical PRESENTATION of HIT:

A

Thrombocytopenia, RESISTANCE TO HEPARIN, THROMBOSIS, Positive assay

318
Q

Worst type of HIT

A

Type II HIT i

319
Q

HIT: Type I onset

A

1-4 days

320
Q

HIT: Type II onset

A

5 days - 15 days

321
Q

Recombinant activated factor seven (VII) used for

WIll reverse prolonged INR

A

For hemophilia A and B

Inhibitor disorders of factor, VII, VIII, IX

322
Q

UNIVERSAL HEMOSTATIC AGENT

A

Recombinant activated factor seven (VII)

323
Q

Mechanism of action of Recombinant activated factor seven (VII)

A

ACCELERATED thrombin formation at the site of endothelial injury.

324
Q

Dose of factor VII

A

Dose 20-100 mcg/kg

325
Q

Dose of factor VII for Hemophillia

A

90-120 mcg/kg

326
Q

Factor VII is good for

A

GOOD for patients suffering from critical bleeding

327
Q

Reverse prolonged INR

A

Activated factor Seven

328
Q

Factor VII does not work with

A

Does NOT WORK IN ACIDOSIS or HYPOTHERMIA

329
Q

Prothrombin complex concentrates (PCC)

Usually

A

Factor II, IX, X and sometimes VII

330
Q

Indicated for Hemophillia patients

A

PCC

Factor VII

331
Q

Most commonly used for REVERSAL AGENT FOR WARFARIN and oral anticoagulants

A

PCC

332
Q

Risk. with PCC

A

RISK: Arterial and thromboembolism

333
Q

CONTRAINDICATIONS of PCC:

A

DIC

334
Q

Anesthetic medications that promote cerebral protection

A

Propofol
Dexdemetomidine
Inhalation anesthetics

335
Q

Propofol and cerebral protection

A

It decreases CMRO2 by 40%

336
Q

Dexdemetomidine and cerebral protection→

A

decrease CMRO2

337
Q

Inhlation anesthetics and cerebral protection→

A

decrease CMRO2 in a dose dependent

338
Q

How soon must fresh frozen plasma be transfused

once thawed?

A

Within 24 hours

339
Q

Six hours after a patient received a transfusion with 2 units of fresh frozen plasma and 1 unit of platelets, she presents with hypoxia, ever, and noncardiogenic pulmonary edema. What complication do you suspect?

A

Transfusion-related acute lung injury

340
Q

A 44-year-old 50-kg male received 750 mL of fresh frozen plasma. What percent of normal would you expect his clotting actor concentration to achieve post transfusion?

A

(D) 30%

341
Q

Which is NOT an indication of cryoprecipitate administration?

A

Antithrombin deficiency

342
Q

Indication of cryoprecipitate administration?

A

Fibrinogen levels < 80-100 mg/dL
Factor XIII deficiency
Preoperative prophylaxis or patient with von
Willebrand disease

343
Q

What is the approximate half-life of serum albumin?

A

21 days

344
Q

A patient receives large volumes of 0.9% normal saline during a case. What is the risk associated with this?

A

Hyperchloremic Metabolic acidosis

345
Q

An adult patient’s platelet count is 25,000/μL. After transfusing the patient with 2 units of apheresis platelets, what would you expect the platelet count to be?

A

85,000-145,000/μL

346
Q

Which statement about fresh frozen plasma (FFP) administration is correct?

A

(A) Each unit of FFP will increase the level of each

clotting factor by 2-3% in adults.

347
Q

Each unit of FFP will increase the level of each

clotting factor by

A

2-3% in adults.

348
Q

The initial therapeutic dose of FFP is

A

10-15 mL/kg.

349
Q

What is the treatment of choice or hyponatremic patients with decreased total body sodium content?

A

0.9% NS

350
Q

Heparin Induced Thrombocytopenia is a

A

TYPE-II CYTOTOXIC Hypersensitivity REACTION

351
Q

At what value do serious complications of hyponatremia

manifest?

A

120 mEq/L

352
Q

Which sodium disturbance increases Minimum Alveolar Concentration (MAC)?

A

HYPERNATREMIA

353
Q

A patient’s serum potassium level is 7.2 mEq/L. In
which sequential order will cardiac manifestations of
hyperkalemia progress?

A

Peaked T waves
Widened QRS complex
loss of P wave
Sine wave

354
Q

The goal of FFP administration is to achieve

A

30% of the normal coagulation factor concentration.

355
Q

A unit of FFP will increase the level of each clotting actor by

A

2-3% in adults

356
Q

A patient is undergoing an elective abdominal aortic aneurysm (AAA) repair. What drug are you most likely to administer after aortic clamping?

A

NITROGLYCERIN

357
Q

A patient undergoing repair of a descending thoracic
aortic aneurysm is found postoperatively to exhibit
loss of lower extremity motor function bilaterally.
What is the most likely cause?

A

Blood flow to the anterior spinal cord was

damaged during the surgery.

358
Q

Which type of surgical procedure will result in the
greatest increase in afterload accompanied by acute
hypertension during aortic cross-clamping?

A

Stanford type A dissection of the Ascending Aorta

359
Q

The more proximal the clamp is applied

A

the more marked the effects.

360
Q

Since the ascending aorta is most proximal, it

will experience the

A

greatest increase in afterload if it is cross-clamped with the heart beating.

361
Q

The most serious acute complication associated with carotid artery stenting (CAS) is

A

stroke

362
Q

The most serious acute complication associated with carotid artery stenting (CAS) is stroke, which can occur due to

A

thromboembolism, hypoperfusion, hyperperfusion syndrome, or hemorrhage.

363
Q

Regional anesthesia for carotid endarterectomy

A

Superficial/deep cervical plexus blocks

364
Q

What type of plasma donor has the highest risk of causing TRALI in recipient?

A

Multiparous female donors.

365
Q

Recipient antibodies to HLA on donor leukocytes ->

A

influx of neutrophils

366
Q

Which complications are most concerning following

carotid endarterectomy?

A

HTN and hypoxemia

367
Q

One unit of whole blood or packed red cells will raise the

hematocrit by_____and the hemoglobin by_____

A

3% ; 1 g/dL.

368
Q

In adults, a pool of six platelet concentrates, or a single

apheresis unit should increase the platelet count by

A

20 000- 60 000/μL.

369
Q

Commonly, the platelet count is raised to at least

A

50 000/μL,

370
Q

A pool of _____platelet concentrates make one unit

A

six platelets.

371
Q

Recombinant activated factors VII (rFVII)—This product
is known to enhance thrombin generation and has
been approved specifically for patients with

A

Factor VII deficiency (hemophilia).

372
Q

Prothrombin Complex Concentrate (PCC) (trade name Octaplex or Ocplex[1]) is a combination of blood clotting

A

factors II, VII, IX and X, as well as protein C and S.[1] It

373
Q

This product Reverses the effect of warfarin (a coumarin anti-coagulant) and is used in cases of significant bleeding in patients with a coagulopathy (INR > 8.0, prolonged prothrombin time, raised d-dimer).

A

Prothrombin Complex Concentrate (PCC)

374
Q

What is the PRINCIPAL RISK FACTOR for TRALI?

A

The presence of HLA antibodies in DONOR PLASMA

375
Q

In TRALI, 1st theory:

A

HLA-Antibodies activates the complement cascade, resulting in neutrophils recruitment to the pulmonary vasculature, and subsequent activation. Neutrophil activation leads to endothelial damage and capillary leak, the basis for pulmonary edema.

376
Q

In TRALI ,2nd theory : Two-hit model

A

The first hit involves neutrophil sequestration in the lungs due to a trigger (surgery, massive transfusion, infection). Upon receiving a transfusion with donor antibodies against HLA or HNA subtypes, the antibodies activate the sequestered neutrophils causing neutrophil-mediated lung injury.

377
Q

A TRALI reaction meets the following criteria:

A
  • An acute onset of hypoxemia within 6 hours of transfusion.
  • Bilateral pulmonary infiltrates on chest X-ray.
  • No cardiogenic cause of the pulmonary edema (pulmonary capillary wedge pressures <18 mm Hg).
  • No preexisting lung injury.
378
Q

Can have a detrimental effect on TRALI –>

A

Diuretics

379
Q

TRALI-> It is most closely associated with

A

fresh frozen plasma (FFP) transfusion, but also occurs with packed red blood cells (PRBCs).

380
Q

The Biggest concern with heparin therapy is

A

Heparin Induced Thrombocytopenia

381
Q

Unfractionated heparin interacts with

A

PLATELET FACTOR 4 (PF4) → trigger igG mediated antibody specific to the heparin-platelet 4 complex

382
Q

2 types of HIT

Type 1 mild →

A

causes mild Thrombocytopenia and recovers within a few days even in the presence of heparin.

383
Q

PCC coagulation factors - how much FFP is one dose of PCC equivalent to

A

II, VII, IX, X 8-16 units of FFP

384
Q

Which factor is FFP deficient in

A

VIII

385
Q

Prevention of AKI after AAA aortic cross clamping

A

A. mannitol - inc. RBF, vasodilator, inc. renal prostaglandin, dec. renal renin furosemide
B. vasodilator maintain adequate vascular volume

386
Q

Factors effecting hemodynamic changes after aortic cross clamping

A
  1. level of cross clamp (most important) volume status pre-existing cardiac disease (coronary disease, aortic regurg, CHF
387
Q

Treatment of hypertension after cross clamp placement

A

preload reduction - nitroglycerin

afterload reduction - nitroprusside

388
Q

Risk of PPC open and EVAR

A

endovascular 3% vs open 16% AAA repair risk of PPC -

389
Q

PPC : Spinal vs general

A

spinal/epidural anesthetics less PPC than general anesthesia

390
Q

Which blood product has the highest incidence of transfusion related sepsis?

A

platelets because stored at room temperature

391
Q

Incidence of HIT is

A

2.5%

392
Q

What fluid should be used as carrier for blood?

A

plasmalyte normal saline ^do not contain any calcium*

393
Q

TRALI antibodies

A

antibodies in donor plasma activating recipient leukocytes -> recipient neutrophil activation

394
Q

Fresh frozen plasma contains what clotting

factors?

A

contains all coagulation factors except platelets.

395
Q

Which factors are most abundant in FFP?

A

Factors V and VIll are most labile and are the most abundant factors in FFP

396
Q

Factor with the shortest half life?

A

Factor VII has the shortest half-life, which is 4-6 hours.

397
Q

Transfusions of fresh frozen plasma (FFP) are indicated for:

A

( l) isolated coagulation factor deficiencies;

(2) reversal of warfarin therapy;
(3) correctionof coagulopathies associated with liver disease
(4) after massive transfusions with continued bleeding even after platelet transfusions.

398
Q

What is the dosing for fresh frozen plasma (FFP)?

A

General dosing of fresh frozen plasma (FFP) is 10-15 ml/kg, which is expected to bring clotting factor levels to at least 30% of normal.

399
Q

What is the dosing of FFP for reversal of warfarin?

A

Dosing of FFP for reversal of warfarin therapy is 5-8 ml/kg.

400
Q

What coagulation factors are found in cryoprecipitate?

A

Cryoprecipitate contains factor VIII:C, VIII:vWF, XIII and fibrinogen (factor I).

401
Q

Cryoprecipitate is a concentrated source ofl. Remember:

A

fibrinogen (I), Factor VIII, Factor XIII, and vWF.

402
Q

One unit of cryoprecipitate has enough

A

fibrinogento increase fibrinogen levels 5-7 mg/dL

403
Q

How do you obtain cryoprecipitate?

A

is recovered from fresh frozen plasma thawed at 4 degrees C.

404
Q

What may be given to treat the patient with a fibrinogen {factor I) deficiency?

A

Cryoprecipitate

405
Q

Transfusion-related acute lung injury (TRALI) is characterized by

A

dyspnea and arterial hypoxemia secondary to noncardiogenic pulmonary edema.

406
Q

The diagnosis ofTRALI is confirmed when pulmonary edema occurs in the

A

absence of left atrial hypertension and the pulmonary edema fluid has high protein content.

407
Q

The edema in TRALI has a

A

High protein content

408
Q

Why should hypotension be avoided in the patient undergoing carotid endarterectomy surgery?

A

There is a loss of autoregulation in ischemic areas of the brain. Because perfusion in these areas is pressure dependent, hypotension should be avoided.

409
Q

Postoperative hypertension may be due to

A

surgical denervation of the ipsilateral carotid baroreceptor, chemical denervation of the baroreceptor OR carotid sinus dysfunction from surgical trauma.

410
Q

When the clamp is removed after repair of an abdominal aortic aneurysm, would you increase or decrease minute
ventilation? Does this change in minute ventilation promote “steal” or “inverse steal” (Robin Hood effect)?

A 
A temporary increase in minute ventilation may be useful for the control of acidosis. The hypocarbia associated with increased ventilation would tend to constrict vessels and decrease perfusion to tissues located proximal to
the clamp, thereby diverting blood to ischemic tissues (those tissues distal to the clamp). This is inverse steal, 
 Hood effect (robbing from the rich and giving to the poor).
411
Q

Symptomatic hyperkalemia is often not present until serum levels are >6.5 mEq/L, and its treatment should initially include

A

administration of parenteral calcium as a cardiac membrane stabilizer.

412
Q

Abnormalities of serum sodium are most often due to some form of

A

abnormal renal water regulation.

413
Q

Hypernatremia should not be corrected more quickly than

A

∼0.7 mEq/hr, t

414
Q

Hypokalemia Early electrocardiogram (ECG) findings include

A

blunted T waves and the presence of U waves.

415
Q

After carotid endarterectomy, the carotid body on the operative side is

A

denervated and this blunts the ventilatory response to hypoxemia and virtually eliminates this response after bilateral carotid endarterectomy.

416
Q

When compared with open surgical repair, EVAR is associated with

A

shorter recover times and lower 30-day mortality rates (1.4% vs. 4.2%) but no difference in mortality rates at intermediate and long-term follow-up.

417
Q

The annual risk of aneurysmal rupture is directly related to its diameter:

A

1% for aneurysms measuring <4.0 cm, 2% for aneurysms 4.0 to 4.9 cm, and 20% for aneurysms >5.0 cm. All aneurysms >5.0 cm should be considered for surgical or endovascular repair.

418
Q

Aortic aneurysm rupture has a mortality rate of

A

85% unless surgery is performed immediately, and even then the mortality rate is 50%.

419
Q

Nevertheless, EVAR is not without complications, including

A

graft leak and intraoperative conversion to open repair because of aneurysm rupture, vascular injury, or inability to seal the graft against the wall of the aorta

420
Q

Risk of cardiac related death or nonfatal MI after carotid endarterectomy is

A

5%

421
Q

What coagulation factor is responsible for conversion of fibrinogen to fibrin?

A

Thrombin

TOPICSII (4 decks)

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