Previous Exam 1998 Flashcards

1
Q

Mechanism of action of amiodarone and list 5 toxicities

A

Class III anti-arrhythmic agent–acts primarily on K channels but also has effect on Na and Ca channels–prolongs the action potential time and prevents repolarization

Toxicities

a. Pulmonary fibrosis
b. Hypothyroidism
c. Hepatitis/pancreatiatis
d. Increased QRS and QT intervals
e. Hypotension
f. Bradycardia
g. acute respiratory distress

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2
Q

How do you treat Afib

A

Unstable–Cardioversion, 50 to 100J, synchronised
Stable
Look for reversible cause: hypoxia/fluid overload/beta blocker with drawal/electroly

Overdrive pacing
Rate control
pharmacolocical cardioversion

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3
Q

Why does Afib occur with mitral stenosis

A

Increase in left atrial pressure causes left atrial dilation and subsequent hypertrophy. This leads to left atrial fibrosis.
The disorganization of atrial muscle fibers is associated with abnormal conduction velocity and refractory periods.
PACs due to increased automaticity or reentry can result in afib

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4
Q

Draw pressure volume loops and explain

Draw them for AS, AI, chronic vs acute

A

.

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5
Q

Indications for surgery in AS and AI

A

AS
development of symptoms
hemodynamic severity
AVA

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6
Q

Carpentier classification of mitral valve pathology

A

Type 1: normal leaflet motion
Type 2: excessive leaflet motion
Type 3a–restricted leaflet motion in diastole
3b–restricted leaflet motion in systole

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7
Q

Risk factors for coronary artery disease

A
sex (male)
age (>45 male; >55 female) 
Family history 
Diabetes
Elevated cholesterol (LDL and total HDL ratio) 
Hypertension
smoking obesity
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8
Q

Protamine reactions

A

Type 1 hypotension due to rapid administration histamine displaced from mast cells (50%)’
Type II (anaphylactoid)
a. anaphylaxis IgE mediated
b. non immune anaphylactoid heparin-protamine complexes complement mediated (brochospasm and flushing)—associated with prior protamine reaction, fish allergy, NPH
Type III: Pulmonary vasconstriction: Heparin-protamine complex stimulate thromboxane A2 from pulmonary macrophages
Treatment: stop protamine: FiO2 100%/Stop anesthetics/give heparin/back on CPB/steriods/antihistamines/
(steroids and antihistamines have no effect on type III reaction_

If re-operation needed:
pre-testing (skin or RAST ELISA) have many false positive and are not useful.
Alternatives to protamine
(allow heparin to dissipate..)
a. methylene blue (does not normalize ACT, could cause PHT)
b. lactoferrin
c. recombinant PF4–abondonded
give 1 mg of protamine over 10 minutes as a test dose.

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9
Q

What is HITT mechanism, treatment, and incidence

A

HIT type 2: occurs in 2 - 3% of patients treated with heparin (20% develop thrombosis)
HITT (HIT type 2 with thrombosis) 0.02-0.4%
Mortality 30% and amputation rate 20%

mechanism IgG antibody binds to platelet factor 4 and heparin. This complex activates platelets by their Fc receptor

Treatment: stop all heparin; anticoagulate with an alternative
1) Daparoid
2) Bivalirudin
3) Ancord
4) Hirudin
May start warfarin when platelets increase with a 5 day bridge
Warfarin for 3 months
recheck HIT titre
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10
Q

5 letter coding system for pacing

A
chamber paced 
chamber sensed 
device response to sensing
programmability/rate modulation
reserved for devices with antitachycardia function 
     pacing stimuli or countershoch
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11
Q

3 mechanisms by which LV aneurysms produce LV dysfunction

A

1) A proportion of the stroke volume is ejected into the aneurysm, this results in decreased external work; increasing preload analogous to MR (except LVEDP is also elevated). The volume overloaded LV dilates exacerbating the situation
2) Elevated LVEDP due to stiff aneurysmal segment (diastolic dysfunction and decreased subendocardial perfusion)
3) Increased wall stress on non-aneurysmal myocardium. Results in decreased perfusion of what is usually poorly supplied muscle and further dysfunction. (Laplace’s Law)

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12
Q

What is management of/options for a calcified aorta

A

One option is not to operate
CABG–off pump with no proximals, or proximals off inominate
– On pump with alternate cannulation site (transverse arch; femoral;right axillary artery)
Avoid clamp: 1) use off pump retractor (stay > 32-34 C)
2) fibrillatory arrest (25C, LV vent, electrical Vfib)
3) DHCA replace ascending aorta and do proximals

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13
Q

Management of reoperations with patent SVG to LAD bypass

A

The concern is acute post-operative hypoperfusion syndrome because the arterial graft is not able to immediately supply adequate flow

Options include:

    a. Remove vein and use IMA only
    b. replace with new vein
    c. add IMA and leave old vein
    d. replace vein and add IMA

The cleveland clinic series found option 1 was the worst. They found option 3 was the best with very incidence of significant embolization (use retrograde cardioplegia!!!)

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14
Q

What nerves are related to radial artery what do they innervate

A

Superficial branch of radial nerve: anterior to pronator teres, posterior to brachioradialis, supplies sensation to the dorsum of hand (middle finger to thumb)

lateral antebrachial cutaneous nerve (proximal) and medial antebrachial cutaneous nerve (distal) that supply sensation to the lateral aspects of the forearm (branches of the musculocutaneous nerve).

Median nerve: may be injured proximal or distal. Supplies sensation to palmar surface of hand and on the dorsal surface sensation to tips of digits.

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15
Q

Nitric oxide–List 5 effects on vascular endothelium

A

Nitric oxide stimulates endothelial enzyme guanylate cyclase, increasing cGMP, leading to vascular smooth muscle relaxation and decreased cyctosolic calcium. NO or its absence contributes to reperfusion injury and coronary vasospasm. NO also inhibits platelet aggregation. Dosing 2 to 20 ppm.

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16
Q

List general uses for NO in cardiac surgery

A
Congenital heart disease
RV dysfunction
Pulmonary hypertension 
Cardiac transplantation
ARDS
Lung transplantation
Acute pulmonary embolism
Persistent pulmonary hypertension of the new born.
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17
Q

What are toxic byproducts of Nitric Oxide

A

Toxicity of NO is due to tis own direct action and to its chemical by products
High concentrations of NO cause pulmonary edema and can lead to death. Inhalation of lower concentrations can cause cellular death and impaired surfactant production.

Most toxic byproduct is Nitrogen Dioxide, produced whenever NO is in contact with oygen, > 10ppm is toxic, cell damage, hemorrhage, pulmonary edema and death.

Less toxic byproducts include methemoblobin and peroxynitrite (rare causes of txicity in a clinical setting). After diffusing through capillaries, free NO blinds Hb to form nitrosyl-Hb which is oxidized to me-Hb which is eventually reduced back to Hb.

18
Q

Picture of a mitral valve and need to identify, AV node, aortic valve, circumflex

A

.

19
Q

Show survival curve graphs of patients with untreated AS and chronic AI

A

.

20
Q

5 complications of senning/mustard operation

A

1) Baffle leaks: 28% incidence rate. most are small
2) SVC obstruction
3) IVC obstruction
4) Pulmonary venous obstruction
5) Stenosis of left pulmonary venous channel
6) Dysrhythmias
7) RV dysfunction

21
Q

What is mobitz II block? how do you treat it? what type of pacemaker

A

Mobitz II is a type 2 degree AV block usually associated with infranodal block. It is characterized by intermittent dropped beats preceded by a constant PR interval. It frequently progresses to complete AV block and risk of sudden death is high. Therefore pacemaker is needed. The pacemaker must be one that does not depend on AV conduction. So ventricular sequential pacing is appropriate.

22
Q

Describe prosthetic valve endocarditis

A

Complication of valve replacement (0.6to0.9/year. Early < 60 days or late > 60 days. Diagnosis is made essentially the same way (Duke criteria). Echo (TEE) is the best and usually underestimates severity.

Complications are essentially the same as NVE. Local, systemic, and embolic. Local complications include abscess, perforation, fistulization, paravacular leaks.

23
Q

List 3 life threatening complications of type A dissection

A
Aortic rupture
Acute tamponade
Myocardial infarction 
Stroke 
Acute aortic insufficiency
24
Q

List 5 complications of bidirectional Glenn

A

1) SVC syndrome–systemic arterial hypertension secondary to cerebral venous hypertension
2) Worsening cyanosis due to decompression into the asygous vein
3) chylothorax
4) pleuro-pericardial effusions
5) supraventricular arrythmias
6) pulmonary AV connections
7) patient growth relatively less CO supply upper body

25
Q

How does carcinoid syndrome present

A

Hot flashes with tachycardia associated with violacious skin changes in the torso. Vasodilatory phenomena related to serotonin and bradykinin release

50% of patients develop valve disease with most have a small intestinal primary. In most cases it is on right side.

Pathophysiology is related to deposition of plaques on the endcardium of the valves and the atria to serotonin and bradykininn. TR is most common.

26
Q

What is pacemaker syndrome

A

associated with single chamber ventricular pacing
related to AV dissociationor to the periodic development of retrograde AV nodal conduction
symptoms result from elevated atrial and venous pressures
malaise,fatigability, light, syncope
dyspnea, orthopnea, neck
due to lower blood pressure and cardiac output that often exist during VVIpacing
symptoms are worse with retrograde AV nodal conduction
management is insertion of AV sequential pacing

27
Q

What is management of HOCM

A
Pharmacologic 
	beta blockers
	Verapamil
Alcohol induced septal ablation 
Traditional cardiac surgery
	septal myectomy
28
Q

Type of DORV

A

subaortic
subpulmonary
double committed
noncomitted

29
Q

How is DORV classified–relation of what to what>

A

Classified by the anatomy of the VSD

30
Q

55 year old male with ASD
How do you calcaulate Qp:Qs and PVR

What are the contraindications to operating

A

Qp:Qs < 1.5
PVR >6 -8 Wood untis
Irreversible R–L shunting
Eisenmenger’s synrome

31
Q

What are difference between LITA and radial artery

A

.

32
Q

List general uses of nitric oxide in cardiac surgery

A
Transplant
Pulmonary hypertension post valve surgery 
	associated RV failure 
Pediatric cardiac surgery 
ARDS
Lung transplantation 
Acute PE
33
Q

List 5 complications of Senning/Mustard

A
Baffle leak
	28% incidence
Obstructed SVC 
Obstructed IVC
Atrial arrhythmias
pulmonary vein obtruction 
stenosis of left pulmonary venous channel
RV dysfunction and TR
34
Q

Post transplant lymphoproliferative disorder

A

primary mechanism appears to be attenuation of t-lympohcyte control over EBV stimulated B-lymphocyte proliferation

Diagnosis 
	most patients present with at 1 tumor
		2/3 extranodal 
	skin lesions can be biopsied 
	GI bleeding indicated GI lesions 
	H/A can indicate CNS lesions 
	recurrent URTI may indicated lung lesinos 
	CXR--lymoadenopathy 
	Biopsy is the definitive diganostic test
35
Q

What is treatment of PTLPD

A

Reduction in immunosuppresion
High dose acyclovir to attentuate EBV replication
Cytokine therapy
radriotherapy and chemotherapy

36
Q

What are predisposing factor for PTLPD

A

monoclonal and polyclonal antibody therapy

Chronic immunosuppression

37
Q

Pre-op factors which predict increased likelihood of low cardiac output syndrome

A

.

38
Q

Describe aortic root enlargement procedures–list and describe incisions

A

Nicks: incision through non coronary sinus and annulus, up to attachment of anterior mitral leaflet

Manougian: incision between the left coroanary and non coronary sinus, through the intravlvular trigone and the central fibrous origin of the anterior mitral leaflet

Konno: longitudinal incision in the anterior wall extended to the left of the right coronary artery across the annulus and into both the IV septum and the RV anterior wall
dacron patch sewn to the LV side of the IV septum to close the VSD, prostehtic valve inserted, rest of dacron used to close aortotomy.
pericardial patch to close the RVOT

39
Q

Describe the steps for air in the arterial line while on CPB

A

Stop CPB
Clamp arterial line
Notify anesthiologist

40
Q

List 8 ways to protect brain on DHCA

A
Hypothermia 
Antegrade cerebral perfusion 
Retrograde cerebral perfusion 
Packing the head in ice
avoiding hyperglycemia
mannitol 
pH stat
steroids 
barbiturates
41
Q

What are indications for LVAD as bridge to transplant

A
Patient must be suitable for cardiac transplant
CI < 2
SBP < 80mmHg
PCWP > 20 
U/O < 20 cc/hr
SVR> 2100
42
Q

What is SAM? Predisposing factors? What is it due to? How do you fix it? Non surgical measures to decrease SAM

A

SAM–Systolic Anterior Motion–abnormal motion of the anterior leaflet of MV causing LVOTO
a. occurs in 4.5 to 10% patients
b. only occurs in pts with degenerative MV disease
Predisposing factors
a. redundant posterior leaflet (height >1.5cm)
b. small hyperkinetic ventricles
c. narrow aorto-mitral angle
d. Undersized ring
e. hypovolemia with catecholamines
It is due to
a. anterior displacement of line of leaflet coaptation pushing into the LVOT
Surgical repair
a. Mitral Valve replacement with resection of anterior leaflet
b. Sliding annuloplasty of posterior leaflet
c. Alfeiri stick
Non-surgical repair
a. Stop inotropes
b. volume load
c. increase afterload (alpha 1 agents)