Classes of drug used to treat pulmonary hypertension?
1. CCB (not verapamil - too much negative inotropy)
2. Prostacyclin analogs (epoprostenol - IV, iloprost - aerosol)
3. PDE-inhibitors (sildenafil)
4. Endothelin receptor antagonists (bosentan - oral)
How does hypoxia affect pulmonary vascular resistance? Hypercarbia? Acidosis? Hypothermia?
They all increase PVR and RV afterload
How does nitrous oxide affect the pulmonary vasculature?
Vasoconstricts the pulmonary vasculature
What pressors should you avoid in patients with pulmonary hypertension?
Alpha agonists (increases PVR)
What prolongs the plateau phase of the myocardial action potential?
Calcium channel opening (Ca++ in, K+ out)
How does the SA node depolarize itself?
Slow leak of Ca++ into the cell that triggers an action potential
How do volatile anesthetics affect the SA and AV node?
Depresses both nodes (SA node more so than AV node)
How do opioids affect the SA and AV nodes?
Increases AV nodal conduction time but less effect on SA node
What nerves (SNS and PSNS) innervates the SA node?
The right vagus and sympathetic chain (T1-T4)
What nerve innervates the AV node?
Left vagus nerve
What is the difference between SVR and afterload?
Afterload: arterial impedance to ejection (vaso-elastic properties of the aorta, arteriolar tone, density/viscosity of blood) SVR: only measure arteriolar tone
What is LVEDP (increased or decreased) for a patient with diastolic dysfunction?
Increased (needed for filling)
What supplies the posterior mitral papillary muscle?
Posterior descending artery
What supplies the anterior mitral papillary muscle?
Left circumflex and LAD
When does the right ventricle get perfused? The left?
Right: Diastole and systole Left: Only during diastole
Major risk factors for cardiovascular risk?
Acute/recent MI (within 6 months), unstable angina, high grade AV block symptomatic ventricular arrhythmias, SVTs with uncontrolled ventricular rate, severe valvular disease
Intermediate risk factors for cardiovascular risk?
DM, MI >6 months ago, compensated CHF, renal insufficiency, mild angina
What is the most sensitive and specific monitor for intraop MI?
TEE (wall motion abnormalities)
What are the BP and HR goals for a patient with severe mitral regurgitation?
Decreased afterload (forward flow) and moderately high HR (80-100)
What are the findings for Tetralogy of Fallot?
PROV P: Pulmonary stenosis R: RV hypertrophy O: Overriding aorta V: VSD
Describes the cardiopulmonary bypass circuit.
RA -> venous reservoir -> oxygenator and heat exchanger -> adds/removes CO2 -> main pump -> arterial filter -> aorta
What is pH-stat?
pH is kept static (if patient is cold, the temperature corrected ABG should have a pH of 7.4); hypothermia increases CO2 solubility (decreased pCO2), so CO2 has to be added to the patient's blood to keep the pH static. When the blood is warmed in the analyzer to 37C, the added CO2 causes a respiratory acidosis picture.
What is alpha-stat?
No CO2 is added to the circuit and at 37C, the pH is 7.4. When the patient is cooled and CO2 solubility increases (decreased pCO2), there is an apparent respiratory alkalosis.
Neurologic outcomes are worse with alpha stat or pH stat?
What is a common complication with TAA repairs?
Lower extremity paralysis (10%) due to the anterior spinal artery (Artery of Adamkiewicz) which can be cut off feeding the lower thoracic and upper lumbar spinal cord; anterior spinal cord = motor, pain/temp, light touch (proprioception, deep touch, and vibratory senses often spared - dorsal/posterior spinal cord)
Pulsus paradoxus + muffled heart sounds + electrical alternans and JVD?
Patient with hypertension and aortic dissection needs what initial treatment?
Beta-blocker drip (reduce shear forces by decreasing HR and contractility)
When do you hear an S3 heart sound and why?
Early diastole just after S2 As atrial blood reverberates against poorly functioning ventricular walls that relax slowly, you get a knocking sound
What happens to preload (RV and LV), afterload, blood pressure during spontaneous inspiration?
Intrathoracic and pleural pressures are negative -> increased RV preload
Increased pulmonary venous capacitance -> decreased LV preload
Slightly increased afterload -> slight decrease in BP (from decreased preload and increased afterload)
Why does your heart rate increase slightly with inspiration?
Inhibition of vagal tone (respiratory sinus arrhythmia)
What is responsible for the S1 heart sound? S2? S3? S4?
S1: beginning of systole when mitral and tricuspid valves close (just after QRS complex) S2: end of systole when aortic valve and pulmonic valves close (just after T wave) S3: dilated cardiomyopathy, just after S2 S4: hypertrophic cardiomyopathy, before S1
What would cause a pathologic split S2?
1. ASD (L to R shunt)
2. Pulmonary stenosis
3. Inspiration (since RV preload increases and LV preload decreases from increased pulmonary capacitance)
What is the formula for LV perfusion pressure?
Aortic diastolic pressure - LV end diastolic pressure (LVEDP)
What can happen if you give nitroglycerin to a patient who is having an MI?
Coronary steal: you can shift blood away from stenotic coronary distributions that require high perfusion pressures
Explain how a muscle contraction takes place.
1. Ca released by the SR from an AP
2. Ca binds troponin which is then displaced from the actin-myosin binding site
3. Myosin that was bound to actin is released by binding to ATP
4. ATP is hydrolyzed to ADP and phosphate (which is released so Myosin can bind to actin)
5. ADP is released -> power stroke
6. Myosin-Actin requires binding to another ATP to release
What is the mechanism of action for amiodarone?
Class III anti-arrhythmic agent (also class Ia, II, and IV) Potassium-blocking agent (delay phase 3 repolarization) AV nodal blocker
What are the major side effects of amiodarone?
1. Pulmonary fibrosis
2. Hypothyroidism/Hyperthyroidism (less common)
3. Transaminitis -> cirrhosis
4. Peripheral neuropathies
What is LaPlace's law?
Tension = Pressure * radium / (2 * wall thickness)
What is Poiseuille's law?
Laminar flow rate = Q = (pi * P * r^4) / (8 * n * l) P = Pressure r = radius n = viscosity l = length of tubing
Which is the primary contributor to SVR: aorta, Windkessel vessels, arterioles, capillaries
What are some unknown effects of beta blockers?
1. Beta-2 antagonism can cause bronchospasms
2. Anti-nociceptive properties
3. Decrease glycogenolysis and glucagon secretion
4. Decreases aqueous humor secretion
5. Decrease production of renin/ang II/aldosterone
6. Decreases peripheral conversion of T4 to T3
In a healthy adult, at what HR will you have the maximal increase in cardiac index?
In a healthy adult, what HR will have the greatest stroke volume?
Name the organs that receive the greatest cardiac output under normal resting conditions.
1. Liver (19%) 2. Muscle (19%) 3. Heart & lungs (19%) 4. Kidneys (16%) 5. Brain (10%)
What is the reflex in a patient who is hypovolemic suddenly goes from supine to standing and gets bradycardic and hypotensive?
von Bezold-Jarisch reflex If low pressures are sensed in LV, mechano- and chemo-receptors fire -> vagal afferents -> bradycardia and hypotension + coronary vasodilation
What is the Bainbridge reflex?
Paradoxical tachycardia in response to fluid bolus Decreased vagal tone -> increased HR
What sensors are located in the carotid sinus and how does it work?
Baroreceptors Increased BP -> increased firing via Hering nerve (glossopharyngeal) -> inhibition of SNS -> decreased HR
What sensors are located in the carotid and aortic bodies and how does this work?
Chemoreceptors In carotid body -> low O2/acidemia -> Herring nerve (glossopharyngeal) -> increase ventilation In aortic body -> low O2/acidemia -> vagus nerve -> increase ventilation
What cellular downstream effects happen when an alpha-1 receptor is activated?
Gq receptor -> PLC -> IP3 formation -> Ca release from SR -> increased contraction
What are the cellular downstream effects when beta-2 receptor is activated?
Gs receptor -> PKA -> cAMP -> Ca back into the SR -> relaxation
What are the cellular downstream effects when nitric oxide acts on the vessels?
NO diffuses -> guanylate cyclase -> cGMP -> relaxation
How soon after a bare metal stent is placed can an elective case happen? After drug-eluting stent? After balloon angioplasty?
BMS: 1 month after DES: 6 months if surgery is urgent, 12 months if elective PCI: 14 days after
What would increase the Frank-Starling curve up and to the left?
1. Increased contractility 2. Decreased afterload
What would increase the isovolumetric relaxation time?
Diastolic dysfunction; since relaxation is an active process requiring energy, poorly complaint ventricles will relax slower
What is the Starling Equation?
Starling forces help describe net movement of fluid in and out of capillaries Q = kA * [(Pc-Pi) + o * (pi * i - pi * c)] Q: net fluid filtration k: capillary filtration coefficient A: area of the membrane Pc: capillary hydrostatic pressure Pi: interstitial hydrostatic pressure pi*i: interstitial osmotic pressure pi*c: capillary osmotic pressure
Name the different phases of a myocardial action potential
Phase 0: Upstroke caused by activation of fast Na+ channels
Phase 1: Early rapid repolarization (fast Na+ channel inactivation and increase in K+ permeability)
Phase 2: Plateau phase (Ca++ channels)
Phase 3: Closing of Ca++ channels and increased K+ permeability
Phase 4: Resting potential (Na/K+ pump)
How do volatile anesthetics affect myocardial contractility and why?
Depresses contractility, likely from decreasing the release of Ca+ from the sarcoplasmic reticulum
How is compliance affected if there is LV hypertrophy? Chronic tamponade?
Both decreased compliance (volume held per pressure)
What is the normal valve area for the mitral valve? What about severe mitral stenosis? What is the normal trans-valvular gradient of the mitral valve? What about in severe MS?
Area: normal = 5 cm2, severe = 1 cm2
Gradient: normal = <2 mmHg, severe = >12 mmHg
What is important about cardiac compensation in a patient with aortic stenosis who suddenly goes into atrial fibrilation?
AS patients have an elevated LVEDP and rely on an atrial kick for ventricular filling; A. fib will get rid of the atrial kick -> decreased cardiac output
What would happen to a patient with hypertrophic cardiomyopathy if he were given a beta blocker?
Decreased outflow obstruction (secondary to decreased contractility and decreased HR)
Should you give a patient with cardiac tamponade a beta blocker? IV fluids?
Beta-blocker: No because external pressure on the ventricles make the CO dependent on HR
IV fluids: Yes because you need ot paintain preload
What is the formula for oxygen carrying capacity?
CaO2 = 1.34 * Hgb * SaO2 - 0.003 * PaO2
What is the formula for oxygen delivery?
DO2 = CaO2 * CO
What is dysoxia?
When oxygen consumption starts to decrease secondary to limited oxygen delivery