Intermediate Cardiac Physiology Flashcards
Myocardial action potentials include phases:
0-3
What is phase 0 of the myocardial action potential?
Phase 0 is the upstroke caused by activation of fast Na+ channels.
What is phase 1 of the myocardial action potential?
Phase 1 is early rapid repolarization, characterized by fast Na+ channel inactivation and an increase in K+ permeability.
What is phase 2 of the action potential?
Phase 2, or the plateau phase is caused by Ca2+ channels opening, prolonging the action potential.
What is phase 3 of the action potential?
Phase 3, represents the closing of the Ca2+ channels and increased K+ permeability.
Ventricular myocytes have which phases compared to the SA node?
SA nodal cells have a phase 0, followed by 3, then 4 (not present in ventricular cells) characterized by a slow leak of Ca2+and Na+ into the cell that sets of a subsequent action potential.
What do volatile agents do to the SA node?
characterized by a slow leak of Ca2+and Na+ into the cell that sets of a subsequent action potential.
Intracellular calcium held in the sarcoplasmic reticulum is released into the cytoplasm following:
A. Release of troponin from the Actin/ Myosin complex
B. Calcium removal from the cell via the Na/K ATPase
C. Mitochondrial depolarization
D. Calcium inflow across the ryanodine receptor
is: D: Calcium inflow across the ryanodine receptor
Contraction of myocardial cells starts with the action potential that activates Ca2+ inflow across dihydropyridine receptors on T-tubules. The increased Ca2+ levels activate ryanodine channels on the sarcoplasmic reticulum to open and allow proportionately enormous amounts of calcium into the cell. The calcium binds to troponin C allowing actin/ myosin contraction, followed by ATPase dependent relaxation. Relaxation is characterized by uptake of Ca2+ back into the sarcoplasmic reticulum, an ATPase dependent process.
Volatile agents’ depression of myocardial contractility probably involves:
Decreased calcium release by the sarcoplasmic reticulum
Volatile agents likely depress contractility by indirectly decreasing the release of calcium from the sarcoplasmic reticulum.
Interruption of the right vagus nerve would most likely affect the:
A. Conduction velocities from SA to AV node
B. Automaticity of the SA node
C. Conduction delay at the AV node
D. Presynaptic regulation of the stellate ganglion
How are SA node and AV node innervated?
How is the heart innervated?
B: Automaticity of the SA node
Cardiac autonomic innervation tends to have the SA node supplied from the right vagus and sympathetic chain, and the AV node from the left. Parasympathetic innervation comes by way of the vagus nerve, whereas sympathetic innervation arises from T1-4 and innervates the heart by way of stellate ganglion to cardiac nerves.
Also note that this means that during SVT treatment, right carotid massage is more likely to inhibit sinus discharge and left carotid massage slows the AV node.
Does AS need more or less preload? What kind of hypertrophy does AS have?
Aortic stenosis represents a high afterload state, necessitating an increase in preload to maintain cardiac output (Starlings Law of the Heart, see above). Furthermore, concentric hypertrophy associated with aortic stenosis requires increased pressures for a given volume (less compliant, diastolic dysfunction).
Wedge pressure equals pulmonary venous pressure, which very nearly equals left atrial pressures, which very nearly equals left ventricular end diastolic pressure (LVEDP).
Yes.
In normal hearts, wedge pressure is an accurate measure of LVEDP, but not necessarily ______ .
because the pressure volume relationship is non-linear. That is to say that as volume increases, pressure may proportionately rise more (or less). Not necessarily volume. Why?
Which of the following factors account for systemic vascular resistance (SVR) being an imperfect measure for afterload:
A: It does not include elastic properties of the aorta nor viscosity of the blood
Concentric hyoertrophy is associated with:
High pressures
Which of the following are NOT consistent with left ventricular diastolic dysfunction?
A. Decreased left ventricular end diastolic pressures (LVEDP)
B. Left ventricular concentric hypertrophy
C. Elevated brain natriuretic peptide in the setting of preserved systolic ejection fraction
D. E to A ratio of < 0.8 (E is less than A)
E. Pulmonary oedema
Decreased left ventricular end diastolic pressures (LVEDP)
Diastolic dysfunction is characterized by a stiff ventricle that poorly relaxes, requiring a higher LVEDP (not lower) for filling. The higher LVEDP are transmitted back to the pulmonary system which can manifest as pulmonary oedema. Diastolic dysfunction is more likely associated with concentric hypertrophy (resulting from high pressures, rather than eccentric hypertrophy (resulting from high volumes). Doppler evaluation across the mitral valve demonstrates characteristic patterns of early diastolic flow (E) and peak atrial flow (A). Although various patterns exist, a situation with an A wave larger than an E wave is only consistent with impaired relaxation.
Which of the following are compensatory mechanisms to maintain blood pressure when changing from a supine position to standing:
A. Autotransfusion from lower extremities
B. Renin-angiotensin-aldosterone system
C. Increased vasoconstriction
D. Sodium retention
C: Increased vasoconstriction
Immediate, short term mechanisms controlling blood pressure are a function of the autonomic nervous system. Controlling vasomotor tone (resistance), heart rate & contractility (cardiac output). Recall that blood pressure is essentially cardiac output multiplied by resistance (V= I X R, Ohm’s Law). Baroreceptors at carotid sinus (bulb) and aortic arch decrease discharge in response to dropping blood pressure, which lessens the inhibition of the sympathetic system, and increases inhibition of vagal tone. The carotid sinus communicates with the brainstem via Herings nerve (part of glosopharyngeal). The opposite is true when the BP is high: the receptors discharge increases, which increases its inhibition of the sympathetic nervous system. The pathways within the brainstem are complex and we do not think you’ll be expected to know them. Renin-angiotensin-aldosterone system and sodium retention are intermediate and long-term mechanism of blood pressure control and take minutes to days for full effect. A full description is found in the renal section and is discussed in the Basic Cardiac Physiology section as well. Autotransfusion from lower extremities may occur when changing from standing to supine, or in trendelenberg position.
How would Acute mitral regurgitation (MR) due to anterior papillary muscle ischaemia present?
The posterior mitral papillary muscle is typically solely supplied by the PDA; whereas the anterior papillary muscle has dual supply from left circumflex and LAD. This would present with flash pulmonary oedema, low cardiac output, and large bizarre V waves on wedged PA catheter tracing.
In times of hypoxia, NO is released (among other factors) which vasodilate coronaries further (unless there is stenosis!).
True
Who is more likely to suffer ischemia-endocardium or epicardium?
The endocardium is more likely to suffer ischemia, presenting with ST depressions than the epicardium. Typically when the epicardium is ischaemic, both the epi- and endo-cardium is ischaemic, presenting with ST elevations.
NSTEMI is a what?
To be clear, most NSTEMIs are the result of supply and demand with coronary disease below the threshold requiring intervention.
Match the best treatment with the clinical presentation:
1 Defibrilation with biphasic 200 J 2 Cardioversion with biphasic 120 J 3 6 mg Adenosine IV push 4 Diltiazem drip 5 Trans-cutaneous pacing CHOICES
A) Pt with sudden onset AV nodal re-entry, HR 160, BP 110/ 50
B) Pt with atrial fibrillation (A-Fib) with HR 170, BP 55/ 38
C) Pt with widened QRS, HR 39, BP 63 / 44
D) Pt with A-fib, HR 147, BP 153/ 78
E) Pt with ventricular fibrillation, no pulse or BP
- E. Pts with ventricular fibrillation should receive chest compressions, defibrillation at 360 J monophasic or 200 J biphasic, and epinephrine per ACLS protocols 2. B. The patient has unstable A-fib and will require emergent cardioversion to escape the grips of death 3. A. SVTs can often be broke by 6 mg of adenosine. 12 mg should be tried next twice over before cardioversion is attempted in a patient with a stable BP 4. D. A-fib with rapid ventricular rates (RVR) and stable BP can be effectively treated with B-blockers, Ca-channel blockers, and adenosine. A patient with a stable BP does not require emergent cardioversion, although it remains a viable option if the A-Fib has persisted less than 48 hours. 5. C. This patient likely has a 3rd degree heart block and an unstable BP. Immediate percutaneous pacing should be employed while a more permanent solution is sought.
What are the major cardiac risk factors?
These are: unstable or severe angina, myocardial infarction (MI) within a month, heart blocks (mobitz II or type III), major ventricular arrhythmias, supraventricular arrhythmias (such as a-fib/ flutter) with rapid ventricular rate (RVR), active or severe heart failure, or severe valvular stenotic disease. If any of these are present they need to be addressed prior to surgery.
If a patient can’t do METs due to physical impediments, but it’s not a major surgery-then what?
Now we have to further stratify him by “clinical risk factors,” formally called “intermediate risk factors,” back when the guidelines were more straight forward. Clinical risk factors are: ischaemic heart disease, compensated heart failure, diabetes (especially insulin dependent), renal insufficiency (especially CKD with creatinine greater than 2.0), and CVA. If the patient has none of these risk factors, he is deemed good to go without further cardiac evaluation (may need pulmonary evaluation still, but that’s a different story). A patient with 1-2 of these clinical risk factors qualify for a stress test, should the patient and cardiologist feel it will change management (versus continuing medical management with heart rate control).
