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