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Fall'20 Advanced Principles II > EXAM 2 - Cardiomyopathy, Mediastinoscopy, CV Pharmacolgy > Flashcards

EXAM 2 - Cardiomyopathy, Mediastinoscopy, CV Pharmacolgy Flashcards

1
Q

All forms of cardiomyopathy can result in

A

CHF and death

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2
Q

decreased contractile state of the heart muscle that cannot be attributed to a specific external causative factor.

this refers to what pathologic cause?

A

intrinsic

intrinsic to the heart

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3
Q

factors that can cause extrinsic cardiomyopathy - ischemia, chronic inflammation, CHD, metabolic diseases (hemochromatosis) and toxins (ETOH, chemo, etc.).

this refers to what pathologic cause?

A

Extrinsic

-effect the heart

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4
Q

Name the 4 types of cardiomyopathies:

A
  1. hypertrophic
  2. dilated
  3. restrictive
  4. arrhythmogenic right ventricular CM
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5
Q

genetically transmitted cardiomyopathy

A

hypertrophic CM

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6
Q

most common cause of sudden death in pediatric and young adult populations

A

hypertrophic cardiomyopathies

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7
Q

an obstructive Hypertrophic CM is called:

A

idiopathic hypertrophic subaortic stenosis (IHSS)

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8
Q

Name the 4 major cardiac changes in HCM:

A
  1. ventricular hypertrophy
  2. decreased ventricular chamber size
  3. increased ventricular wall thickness
  4. impaired ventricular relaxation
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9
Q

the myocardial defect associated with HCM is:

A

CONTRACTILE mechanism

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10
Q

asymmetric hypertrophy of interventricular septum of LV causes a

A

left outflow tract obstruction

and hemodynamic consequences are similar to those of aortic stenosis

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11
Q

due to the presence of collagen, these are narrowed in HCM:

A

coronary artery walls

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12
Q

rapid acceleration of blood traveling through narrowed outflow tracts creates a

A

venturi effect

which pulls the anterior MV into the outflow tract. the MV leaflet further obstructs the LV outflow compromising outflow via regurg too.

* Bernoulli’s law

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13
Q

is HCM systolic or diastolic dysfunction?

A

BOTH

-Increase LVEDP in presence of low/normal EDV

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14
Q

loss of lv compliance requires a greater contribution of volume from…

A

atrial contraction

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15
Q

b/c 75% of LV preload comes from the LA in HCM, what is critical for adequate SV?

A

NSR

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16
Q

increased LVEDP decreases CPP to the Hypertrophic LV…

so in the HCM, increased myocardial O2D, thickening of CA’s decreasing perfusion all lead to:

A

ischemia

-only takes a little bit of stress to cause ischemia in these pts. (think about intubation)

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17
Q

HCM S/S:

A

DOE
angina pectoris - relieved by lying down (decrease LV outflow tract obstruction
SVT/Ventricular arrhytnmias
systolic murmur (S3 and S4? S4 gallop yes -but not sure about S3?)

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18
Q

HCM anesthetic mgmt focus on strategies that alleviate and do not increase

A

LV outflow obstruction!

  • adequate or slightly elevated LV vol
  • avoid decreased venous return or interference with Preload; and factors that decrease contractility (b/c this empties the ventricle vol more)
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19
Q

what should be treated IMMEDIATELY in HCM?

this also impacts anesthetic plans - we should not do what?

A

hypotension

-M&M says no spinal/epidural b/c they decrease preload/afterload increasing Obstruction

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20
Q

Goals for HCM:

HR:
Preload:
Afterload:
Contractility:

A

HR: NSR/ maintain
Preload: FULL - volume FIRST!
Afterload: Maintain or Increase (pure vasoconstrictor is SECOND line of defense for hyoptenstion)
Contractility: decrease (increased would lead to collapse by increasing obstruction)

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21
Q

HCM obstruction will be worsened by:

A
  • increased contractility (dig, catecholamines)
  • decreased PL (hypovolemia, vasodilators, tachy, PEEP)
  • Decreased AL (hypotension, vasodilation)

*nitrates, dig, diuretiics worsen LV obstruction

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22
Q

HCM obstruction will be decreased/improved by:

A
  • decreased contractiliy (Beta blockers, volatile anesthetics, CCB to counteract sympathetic activation if/when occurs)
  • Increased PL (Hypervolemia, bradycardia)
  • Increased AL (hypertension, alpha adrenergic stimulation)
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23
Q

First and second line of defense for hypotension in Hypertrophic CM:

A

1 - FLUID!!

2. Pure vasoconstrictor (Neo)

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24
Q

Dilated cardiomyopathy (DCM) is the most common form and most often occurs in:

A

adults

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25
Q

DCM may develop in what type of pts:

A
  • genetic predisposition (duchenne muscular dystrophy)
  • viral inflammation from metabolic abnormalities
  • autoimmune mechanisms
  • toxins
  • Men > Women
  • women during pregnancy
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26
Q

DCM is eccentric or concentric?

A

eccentric

  • overall size and vol are enlarged d/t volume overload
  • sarcomeres lengthen or increase in number (rather than thicken in concentric)
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27
Q

eccentric hypertrophy results in compliance problems leading to diastolic dysfunction - hypertrophy affects which ventricles?

A

BOTH Left and Right ventricles

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28
Q

LV chambers increase in size w/o associated increase in diameter of the V-walls or interventricular septum. This decreased SV due to decreased contractility leads to diastolic dysfunction.

What law is this an example of?

A

law of laplace

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29
Q

DCM results in LV HF with pulm congestion or biventricular failure leads to severe CHF. these pts are at increased risk of:

A

thromboembolism as a result of stasis (inadequate ventricular emptying)

—-> patients are on anti-coagulant tx

30
Q

S/S of DCM:

A
  • angina
  • JVD
  • weakness
  • rales
  • tachy
  • Atrial and ventricular dysrhythmias (a.fib)
  • A/V regurg.
31
Q

Anesthetic Goals for DCM:

HR:
Preload:
Afterload:
Contractility:

A

Goals for DCM:

HR: Maintain (or slow down/control if A.fib)
Preload: maintain
Afterload: Reduce
Contractility: Increase?

32
Q

Anesthetic management for DCM includes:

A
  • Diuretics
  • ACE I
  • Digoxin
  • Dual chamber pacing, LVAD
  • Opioids good – no direct effect on myocardial contractility
  • Careful titration of INH anesthetics (myocardial depression)
33
Q

what induction agent would you use for DCM pt?

A

Etomidate

34
Q

Restrictive Cardiomyopathy (RCM) represents conditions in which the myocardium or endomyocardium muscle layer is affected.

Causes of RCM include:

A
  • genetic predisposition
  • infiltrative disease (SARCOIDOSIS)
  • storage disease (Hemachromotosis)
  • endomyocardial dystunction (endomyocardial fibrosis)
35
Q

Does RCM occur in children?

A

rarely

36
Q

Mortality rate with RCM….

A

is high once symptoms begin

37
Q

Sarcoidosis is what kind of CM?

A

Restrictive

38
Q

Hemachromotosis is what kind of CM?

A

restrictive CM

39
Q

Stiff and noncompliant ventricles restrict ventricular filling decreasing ventricular EDV (reduced PL) despite near normal systolic function (SV is decreased).

Systolic ejection remains relatively normal due to atria compensation to atrial vol overload (atria dilates)

RA pressures elevate significantly ===

A

15-20mmHg and

Pulm artery systolic pressure increases as high as 50 mmhg

40
Q

Anesthetic management of Restrictive CM includes:

A
  • similar to DCM

- use diuretics, Na and fluid restriction, anticoagulation, and tx dyshrhythmias

41
Q

Anesthetic Goals for RCM:

HR:
Preload:
Afterload:
Contractility:

A

HR: NSR
Preload: Maintain
Afterload: Increase
Contractility: maintain

42
Q

in RCM pts - what is preferred:

a. Higher doses of narcotics as opposed to increased volatile anesthetics
b. Higher doses of narcotics and no volatile anesthetics
c. No narcotics and only volatile anesthetics

A

a. Higher doses of narcotics as opposed to increased volatile anesthetics

  • volatiles okay
  • opioids okay
  • Titrate opioids carefully to MINIMIZE myocardial depression. Volatiles depress heart rapidly.
43
Q

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) - unique feature of this CM is that the diagnosis is made:

A

post mortum
(sudden cardiac death is common)

* Rarely have a pt with past hx of this!*

44
Q

is ARVC genetically inherited?

A

yes

45
Q

S/S that can occur with ARVC:

A
  • occur during childhood
  • often during adolescence (sports related exercise)
  • RV CO is decreased – dilation and outflow tract obstruction of RV
  • Ventricular dysrhythmias are common (PVCs, VT, Vfib)
  • catecholamine sensitive! (natural catecholamines)
46
Q

Anesthetic Management of ARVC:

A
  • ID and tx fatal dysrhythmias
  • avoid excessive catecholamine release (hypoxia, hypotension, hypercarbia, surgical stimulation)

**Amiodorone works well for Ventricular dysrhythmias

47
Q

standard method for evaluation and staging of medastinal lymph nodes is done via

A

mediastinoscopy

48
Q

The most common mediastinal diagnostic procedure is a :

A

cervical mediastinoscopy

  • small transverse incision is made in the midline of the lower neck in the suprasternal notch
  • the mediastinoscope is inserted TOWARD the CARINA via BLUNT dissection
49
Q

What arteries do we have to be extremely mindful of during mediastinoscopy?

A
  1. Innominate artery

2. pulmonary artery

50
Q

what does the innominate artery supply?

A

the right arm and the right common carotid

*pts who do not have good cerebral collateral circulation are at risk for cerebrovascular ischemia with innominate compression.

51
Q

During your pre-op assessment for a mediastinoscopy, what is the focus?

why?

A
  • identifying the presence of a significant mediastinal mass

- potential for catastrophic airway obstruction or CV collapse on induction of anesthesia

52
Q

How do you assess the pt in preop before a mediastinoscopy?

A
  • ability to lie supine
  • presence of a cough or dyspnea

**any of this may indicate an increased difficulty in ability to protect airway; cv collapse

53
Q

what is the obstruction of the SVC?

s/s?

A

SVC syndrome

s/s: SOB, lightheadness, neck and chest vein distension, edema to face and UE’s

54
Q

what are the important considerations for SVC syndrome?

what goes where?

A
  • NIBP to Left Arm
  • Radial ALine and SpO2 on the RIGHT
  • to monitor for innominate artery compression
55
Q

Patients with lung CA may have Eaton-lambert syndrome (ca-ch antibodies) with sensitivity to what anesthetic agents?

A

Depolarizing and Non-depolarizing NMB

56
Q

the most severe complication of mediastinoscopy is

A

major hemorrhage.

be prepared for emergent thoracotomy!!

57
Q

an a-line is not necessary for all cases. however, it is mandatory to monitor the PULSE in which arm?

A

Right

58
Q

what can be used to provide lung isolation in the event of an emergency during mediastinoscopy?

A

a bronchial blocker

59
Q

during mediastinoscopy, if the hemorrhage originates from a tear in the SVC, where must your volume replacement and drug tx be administered from?

A

femoral line

-to get below the tear

60
Q

an increase in peak inspiratory pressure during mediastinoscopy may be attributed to ….

A

pneumothorax

61
Q

If injury to the RLN is suspected, the vocal cords should be ____ while the patient is ______.

A

the vocal cords should be visualized

while the pt is spontaneously breathing

62
Q

An absolute contraindication to mediastinoscopy is:

A

PRIOR mediastinoscopy

63
Q

during mediastinoscopy, the tip of the medistinoscope is intrathoracic and therefore it is directly exposed to

A

pleural pressure

64
Q

possible stimulation/result? from compression or stretching of the trachea, vagus nerve, or great vessels.

A

autonomic reflexes

65
Q

Relative contraindications for mediastinoscopy include:

A

SVC obstruction
Tracheal deviation
Thoracic aortic aneurysm
Cerebrovascular dx

66
Q

anesthetic consideration for managing mediastinoscopy PRE-OP:

A

a-line

minimal premedication

67
Q

anesthetic consideration for managing mediastinoscopy INDUCTION

A
  • -awake FOI if sympotomatic in supine position
  • or mask induction w/Sevo/O2 to maintain spontaneous respirations
  • Re-inforced ETT
  • **SURGEON ON STANDBY incase of airway collapse
68
Q

anesthetic consideration for managing mediastinoscopy MAINTENANCE:

A
  • short acting NMBD’s

- Positive Pressure Ventilation (to reduce air embolism)

69
Q

anesthetic consideration for managing mediastinoscopy EMERGENCE:

A

visualize cords

70
Q

anesthetic consideration for managing mediastinoscopy POST-OP:

A

CXR

Laryngeal Nerve damage may require re-intubation

Fall'20 Advanced Principles II (7 decks)

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