Previous Exam 1998 Flashcards
Mechanism of action of amiodarone and list 5 toxicities
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
How do you treat Afib
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
Why does Afib occur with mitral stenosis
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
Draw pressure volume loops and explain
Draw them for AS, AI, chronic vs acute
.
Indications for surgery in AS and AI
AS
development of symptoms
hemodynamic severity
AVA
Carpentier classification of mitral valve pathology
Type 1: normal leaflet motion
Type 2: excessive leaflet motion
Type 3a–restricted leaflet motion in diastole
3b–restricted leaflet motion in systole
Risk factors for coronary artery disease
sex (male) age (>45 male; >55 female) Family history Diabetes Elevated cholesterol (LDL and total HDL ratio) Hypertension smoking obesity
Protamine reactions
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.
What is HITT mechanism, treatment, and incidence
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
5 letter coding system for pacing
chamber paced
chamber sensed
device response to sensing
programmability/rate modulation
reserved for devices with antitachycardia function
pacing stimuli or countershoch3 mechanisms by which LV aneurysms produce LV dysfunction
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)
What is management of/options for a calcified aorta
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
Management of reoperations with patent SVG to LAD bypass
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!!!)
What nerves are related to radial artery what do they innervate
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.
Nitric oxide–List 5 effects on vascular endothelium
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.
List general uses for NO in cardiac surgery
Congenital heart disease RV dysfunction Pulmonary hypertension Cardiac transplantation ARDS Lung transplantation Acute pulmonary embolism Persistent pulmonary hypertension of the new born.
What are toxic byproducts of Nitric Oxide
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.
Picture of a mitral valve and need to identify, AV node, aortic valve, circumflex
.
Show survival curve graphs of patients with untreated AS and chronic AI
.
5 complications of senning/mustard operation
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
What is mobitz II block? how do you treat it? what type of pacemaker
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.
Describe prosthetic valve endocarditis
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.
List 3 life threatening complications of type A dissection
Aortic rupture Acute tamponade Myocardial infarction Stroke Acute aortic insufficiency
List 5 complications of bidirectional Glenn
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
