Objectives:

1. Detail five classic vs. five nonclassic symptoms of CV disease

2. Describe the gender differences in male and female heart attack symptoms.

3. Describe the embryological tissues and timing for the development of human heart and blood vessels, and detail the timing of fetal heartbeat perception on echocardiograms.

4. Locate the ideal listening spots for heart valve sounds correlating to external anatomical physical exam landmarks.

5. Become familiar with the four chamber locations of the heart as projected on PA and lateral chest Xrays.

6. Detail the pericardial functions and epicardial fat functions.

7. Describe the actual motion of the myocardial muscle layers and explain why the RV and LV have different thickness.

8. Describe the differences and similarities of myocardial muscle and skeletal muscle anatomy and physiology and explain the advantage of cardiac muscle as a “functional syncytium”.

9. Describe the differences between the right and left circulations in terms of pressures, blood flow and resistances. Describe the chamber to chamber course or patterns of blood flow in the right and left sided circulations of the heart.

10. Describe the names and locations of the major coronary arteries and the names and locations of the major intracardiac electrical structures.

11. Describe the four intracardiac valve locations and their open vs. closed relationships in systole and diastole. Describe the valve problems in “stenosis” vs. “regurgitation”.

12. Describe one thing that can be seen on a coronary CT calcium scan and what disease it represents; also one thing seen on a color flow Doppler echocardiogram and what disease it represents; and one thing on a coronary or aortic arteriogram and what disease it represents.

Objectives:

1. Explain the corresponding cardiac electrical and mechanical events on the Wiggers diagram that correlate with systole:

• What happens to the AV and MV motions?
• What happens with the EKG correlating electrical waves?
• Which heart sounds correlate with each event and the direction of blood flow into and out of chambers and the rise and fall of blood pressure in the chambers?

2. Explain the corresponding cardiac electrical and mechanical events on the Wiggers diagram that correlate with diastole

• What happens to the AV and MV motions?
• What happens with the EKG correlating electrical waves?
• Which heart sounds correlate with each event and the direction of blood flow into and out of chambers and the rise and fall of blood pressure in the chambers?

3. Describe why electrical events precede mechanical events.

4. Detail why it is important to know what is happening in an inflow chamber, a pumping chamber and an outflow vessel.

5. Describe the essential and unique valve findings in “isovolumic contraction” and “isovolumic relaxation” phases and whether these phases describe flow changes or pressure changes.

6. Describe the active vs. passive nature of blood flow from LA to LV in diastole, and which portion of atrial systole is lost when atrial fibrillation occurs and how much of the cardiac output contribution is therefore lost.

7. Correlate the “a”, “c”, and “v” waves in atrial pressure wave forms and why we see these in a jugular venous pulse.

8. The average adult doesn’t change their cardiac output much in heart rates between 60-170, but does change it greatly below 60 and above 170. This means the most changeable part of the CV cycle is diastole—explain what actually happens to LV filling in heart rates of 60-170.

9. Explain the falling pressure in the last half of systole in the aorta.

10. Explain the LV ejection fraction and stroke volume by comparing the LV volume at end diastole and end systole and correlating with the heart sounds.

11. Describe the three phases of LV diastole and correlate the S3 and S4 gallop sounds with their locations in diastole.

12. Pressure volume loops clarify preload, afterload and contractility especially inside the LV. The two straight vertical lines in the pressure volume loop show great pressure changes w/o volume changes, and therefore reflect two short phases on the Wigger’s diagram. Name these. The horizontal distance between the two most vertical lines on the pressure volume loop show the different volumes between end diastole and end systole and represent which term in volume?

13. Describe the value of using the stethoscope diaphragm in S1 and S2 heart sounds vs. use of the stethoscope bell in S3 and S4 gallop sounds and where each sound correlates with EKG findings of electrical waves.

14. Describe the components of S1 in terms of mitral and tricuspid contributions (which comes first) and of S2 in terms of aortic and pulmonic contributions (which comes first).

15. Describe the four anterior chest physical exam projection locations to maximize hearing each valve sound contributions.

16. Explain normal physiological splitting of S2, and also why inspiration widens the S2 split.

Objectives:

1. Explain how the circulatory system of vessels is really two circulations in parallel with each other, instead of in series, and thus sees the entire cardiac output instead of just a percentage of cardiac output like other organs do.

2. Explain the differences in vessel resistances and pressures from the left and right sided circulations.

3. Explain how noncardiac organ systems’ blood flow can be altered to serve certain purposes like exercise, and which vessels alter their diameter the most, in order to make that happen.

4. Describe which organs decrease and which organs increase their percentages of the cardiac output in response to exercise and why that would occur.

5. In the left heart circulation, the blood pressure out of the heart is maintained at the receiving organ level but the arterial flow rate differs from organ to organ. Explain how this happens and what is one protective reason why this is beneficial to each organ?

6. The arterial pressures into an organ are greatly different than the venous pressures out of an organ, but the flow rates do not change. This is explainable through what concept, which is “additive” throughout that organ?

7. Derive MAP (mean arterial pressure) and PP (pulse pressure) from knowing the systolic and diastolic blood pressures.

8. Explain how MAP is not the same as “mean systemic pressure”.

9. Explain which one represents “mean perfusion pressure”. Explain what level of perfusion pressure prevents organ ischemia.

10. Explain how blood pressure changes with the force generated by the LV but also by the “resistance runoff” of the downstream vessels.

11. Describe the three layers of vessels and what type of tissue makes up each layer. Explain how the veins and arteries differ from each other in these layers and how capillaries differ from both, and why capillaries would differ in this way.

12. Describe how much of the body’s blood can be stored in arteries vs. capillaries vs. veins.

13. Describe the formula relating compliance, volume and pressure.

14. The reason for the arterial and venous compliance difference primarily depends on which vessel tissue layer?

15. Detail the function of valves in veins.

16. Describe one accommodation that takes vein valves into account when using large veins for CABG surgery blood flow replacement conduits.

17. Describe exactly what happens to various vessel layers with aging in arteries and what is the process called? Generally, this will naturally result in what kind of hypertension as a result of large artery changes and what kind of hypertension happens as a result of “runoff” artery changes?

18. Name the major hemodynamic factor of the LV in making systolic blood pressure and the major hemodynamic factor in making diastolic blood pressure.

19. Explain how aging causes a diastolic pressure fall and thus a widening of pulse pressure.

20. In an effort to keep perfusion pressure of organs up as diastolic pressure falls, what has to happen to cardiac output?

21. Name the major fiber difference in upstream (closer to aorta) arteries vs. downstream (closer to arterioles) arteries.

22. Name the major cell difference in arterioles’ muscle layer and also how this is most responsive to nervous system input to change resistance.

23. The largest drop in blood pressure or MAP is in which blood vessels, and results in blunting of systolic pulsations? How does this protect the next downstream vessels that follow these particular vessels? Why would this be helpful in this next set of downstream vessels?

24. Veins are a low pressure, high volume system of capacitance vessels. Describe whether they have smooth muscle cells and nervous system receptors like arteries.

25. The right heart waveforms are similar to the left heart waveforms but are all at lower pressures. Explain why this results in the RV wall thickness being only 1/3 the LV wall thickness.

Objectives:

1. Using the concepts of pressure, flow and resistance, explain why blood only goes in one direction but at varying speeds.

2. Explain why flow, cardiac output and resistance are always related and give examples of what goes up and down in normal patients, hypertensive patients, and septic shock patients.

3. Name the single most important vessel factor determining a change in resistance in the Poiseuille’s equation and how that is reflected in vasodilation and vasoconstriction or in inside-the-vessel obstructions to flow.

4. Which type of blood vessel is most likely to have tiny radius changes making huge differences in flow velocity? What are two things that distinguish why these vessels are so responsive to flow velocity changes?

5. Explain how the flow rates decrease as the total cross-sectional area of a particular kind of vessel additively increases.

6. Bernoulli’s equation deals with total energy of fluid in a tube and is conserved from one point to another. Predict what would happen to blood velocity when blood goes through tiny channels as compared to larger channels in terms of actual blood velocity in the tiny channels.

7. Give one intracardiac Doppler echocardiogram example of using Bernoulli’s equation to predict an intracardiac structure size.

8. Explain the difference between flow and perfusion.

9. Explain the difference between laminar and turbulent flow.

Review the following conditions:

• Murmur Physical Exam Findings
• Mitral Stenosis
• Aortic Stenosis
• Mitral Regurgitation
• Aortic Regurgitation
• Mitral Valve Prolapse
• Tricuspid Regurgitation
• Tricuspid Stenosis
• Pulmonic Valve Stenosis
• Pulmonic Regurgitation

Objectives for each condition:

• History taking and performing the physical examination
• Diagnostic and laboratory studies
• Formulating the most likely diagnosis
• Health maintenance, patient education, and preventive measures
• Clinical intervention
• Pharmaceutical therapeutics

Objectives:

1. Blood pressure is dependent on cardiac output (systolic) and systemic vascular resistance (diastolic). Name the other factors that go into creating each of these two major determinants.

2. Explain why it is difficult to change just one factor independently in blood pressure determination without something else changing.

3. Name some disease processes that greatly impact SVR and therefore change blood pressure, and some disease processes that change the components of cardiac output (heart rate and stroke volume) so as to change blood pressure. (BP = SVR x CO).

4. Name three factors that impact stroke volume.

5. Name which arterial fibers are lost and which are gained in arteries with aging.

6. Name three organ systems that pour out chemicals/hormones to affect vascular resistance and name three chemicals that act locally on blood vessels to affect vascular resistance.

7. Describe the shorter term and longer term homeostatic blood pressure control mechanisms and which receptors (pressure, mechanical, stretch, and chemo) govern this and where they are located.

Objectives:

1. Explain the anatomic structures in a typical renal nephron and the differences in glomerular capillaries from all other body capillaries and the resulting capillary blood pressure in that location.

2. Explain the location of the PCT (proximal convoluted tubule), the Loop of Henle, and the DCT (distal convoluted tubule) and collecting ducts in a nephron and which body substances are primarily filtered in each of these sections. Particularly mention the locations of Na+ entry and exit (and therefore water entry and exit).

3. Renal blood pressure responses are more long term and slow responses to blood pressure changes for three reasons. Describe three of the reasons that slow down the response rate as compared to neurological blood pressure responses.

4. Explain which glomerular cells are baroreceptors and which glomerular cells are baroreceptors.

5. Explain the chemical changes and involved organs with the series of changes in the Renin—Angiotensin—Aldosterone system; describe which hormone is the antagonist to this system.

6. Describe the six different functions and locations of actions of Angiotensin II.

7. Correlate blood pressure drugs and drug classes with actual sites of action in the nephron.

8. Rank the power of sodium and water diuretics and drug classes with the locations of action in the nephron.

9. Explain why ACEI and ARB drugs are currently the cornerstone of blood pressure Rx in many patient types.

10. List three things at the local blood vessel level that constrict and three that vasodilate, similar to exercise as examples of local blood vessel control of blood pressure.

Review the following conditions:

• Hypertension
• Hypotension
• Shock
• Hypertensive emergency/urgency
• Orthostatic hypotension

Objectives for each condition:

• History taking and performing the physical examination
• Diagnostic and laboratory studies
• Formulating the most likely diagnosis
• Health maintenance, patient education, and preventive measures
• Clinical intervention
• Pharmaceutical therapeutics

Objectives:

1. Describe how a negative membrane potential exists at rest in cardiac myocytes and what the ion contributors to this are, across the semipermeable membrane.

2. Describe the Na+-K+ membrane exchange pump.

3. Describe what a “voltage dependent” channel is.

4. Describe the Phases 0,1,2,3, and 4 of the “action potential” in most cardiac myocytes, and exactly what happens with ion movements in each phase and therefore what happens to the numbers in membrane potentials in millivolts.

5. Correlate the above with depolarization and repolarization and exactly when contraction starts.

6. Delineate the differences in action potentials between usual cardiac myocytes and those cells with “automaticity” or pacing functions.

7. Explain how to translate from electrical signals to mechanical events per cardiac myocyte with the use of T tubules, the use of “trigger Calcium”, and the sarcoplasmic reticulum to allow actin-myosin serial overlapping “pulling hooks” to create cross bridges and effect contraction of the myocyte (essentially the systole of one cell).

8. Explain the restoration of the resting electrical and mechanical states (essentially the diastole of one cell).

9. Name some major electrical and structural differences between cardiac myocytes and skeletal myocytes that result in differences in function between these two kinds of myocytes.

Objectives:

1. Correlate and name the four phases of a Wiggers’ diagram explanation of cardiac events, with the four phases of an LV pressure volume loop diagram and explain the location on a pressure volume loop of LVEDV, LVESV and stroke volume.

2. Define preload, afterload, and contractility.

3. Name disease processes and drugs that could affect each of the above. Explain why clinical use of these factors requires both a measurement of “filling” or sarcomere length, and inotropy or calcium-related contractility, in order to understand the condition of a patient.

4. Explain how the “length tension relationship” is highly dependent on an ideal diastolic sarcomere length, which is highly dependent on preload volume, whereas inotropy or contractility is highly dependent on calcium availability and the latter can still change tension even in “ideal” sarcomere lengths.

5. Relate the length tension relationship to the amount of “overlap” or lack of overlap in the actin and myosin filaments.

6. Explain the Frank Starling relationship where (to a certain upper limit) increased preload results in increased cardiac output of LV pressures.

7. If a flow volume loop changes a single factor, explain what a loop moving right means (preload/afterload/contractility) and therefore resulting cardiac output; explain the same if the loop moved upward; explain the same if the loop moves leftward.

Objectives:

1. Define “heart failure” between the CV pump supply and the body’s metabolic needs.

2. Define “classes” of CHF and “stages” of CHF.

3. Define HFpEF, HFrEF, and HFmEF.

4. Define CHF in right vs. left, high output vs. low output and standard vs. advanced types of heart failure.

5. Explain what a MET is and correlate MET level with classes of CHF symptoms achieved.

6. Explain the advantage in treatment choices between accurately labeling patients with their CHF stages.

7. Explain the mortality advantage of certain treatments in Stage A and B patients, even before claimed CHF symptoms by class.

8. Detail the expected age and gender and racial differences in CHF populations.

9. Explain what to expect on echocardiograms in HFpEF and HfrEF.

10. Explain how a treated and compensated CHF class 2-3 (and Stage 3) pt. can be tipped over by a noncardiac event.

11. Explain lifetime risks of CHF for males and females, with and without prior MI’s, and with and without prior hypertension.

12. Explain the differences in mortality of CAD vs. CHF in the last 25-30 years.

13. Calculate the approximate one year mortality of hospitalized CHF pts. and compare this to many cancer patients.

Objectives:

1. Explain how frequently isolated PVCs occur in the general population, and whether that reliably signals structural heart disease.

2. What is the borderline PVC rate on a 24 hour HM, which in the absence of risks for CV disease, requires no further CV workup?

3. What things in the history or the appearance of PVCs signal higher CV risk?

4. Name five “correctable causes” of PVCs. If you must do further CV workup, what would you order and what are you looking for on each test?

5. There are three basic pathophysiological ways to get PVCs—name these and describe what exactly is happening and which cause is most likely associated with each one, and also which one is the most common cause of the three.

6. Name three EKG findings that would convince you a particular beat is a PVC.

7. Explain “fusion or capture beats” and “coupling intervals”.

8. Explain the danger of “R-on-T” phenomenon.

9. Name some cardiac and noncardiac conditions with PVCs of more importance.

10. Why would an EP doctor take someone with PVCs to EP testing—list four criteria?

11. Explain the difference in appearance and severity between monomorphic VT and polymorphic VT. Explain how these differ from AIVR.

12. Explain the conundrum of treating CHF and CHF drugs causing pro-arrhythmia.

13. Explain whether the complaint of syncope with ventricular arrhythmia leads to more investigation or less.

14. Explain four EKG criteria to help tell VT from SVT “with aberrancy of the QRS”. There is one criteria which is the most helpful at telling the difference and this is _________.

15. “Torsades de Pointes” is a particular VT form that more often goes with what etiology?

16. Explain the classes of ventricular antiarrhythmics and which phase of the action potential they work on.

17. Explain why we try to refrain on antiarrhythmic use in the immediate post-MI state.

18. Explain why an AICD implant would be more likely used for VT and VF or resuscitated cardiac death instead of antiarrhythmic drugs by themselves.

Objectives:

1. Discuss the CV function findings that can be seen on arterial line waveforms and also on specialized “FloTrac” lines.

2. Describe overdamping and underdamping effects on the waveforms.

3. Explain the Swan Ganz catheter and the possible waveforms, and measurements that can be obtained from the ports, the tip, and the calculations.

4. Be aware that the catheter takes advantage of a balloon tip that allows flotation with forward flow.

5. Explain why balloon inflation is designed to be only temporary and intermittent.

6. Name two purposes for a post Swan Ganz catheter insertion chest Xray.

7. Explain why it is most ideal for the tip to be in “Zone 3” of the lungs.

8.RA waves reflect CVP pressure or preload—list some clinical reasons why this might be higher than normal of 0-10 mm Hg or lower than normal.

9. PA pressure waves reflect potentially normal pulmonary artery pressures or pulmonary artery hypertension. List some clinical reasons for pulmonary hypertension.

10. A “wedge” or PCWP occurs with the inflated balloon in a distal pulmonary artery and shows “back reflection” of events in the LA (similar waves to RA but at higher pressure levels). List some clinical reasons for high PCWP’s.

11. Cardiac Output is a measured value from the Swan Ganz catheter, but often by measuring a temperature drop from iced saline injected into the RA which is then “pumped” by the RV out to the thermistor tip in the pulmonary artery and measured. Name some clinical events that would impair the cardiac output calculation done in this way.

12. Cardiac output = stroke volume x heart rate… explain how and why very low or very high heart rates might affect a Fick cardiac output calculation.

13. The final calculation obtainable is resistances including SVR (systemic) and PVR (pulmonary) but are not measured and instead calculated. If SVR is calculated and is very high, name a clinical condition that this implies and if SVR is very low, name a clinical condition this implies.

14. Shunt detection can be answered by collecting blood samples in different chambers for oxygen “on the way in” with a Swan Ganz catheter placement and looking for a “step up”. Explain why this occurs. Explain what a Qp : Qs ratio is.

Objectives:

1. Describe the Killip classes for assessing CHF and mortality that existed before monitoring lines.

2. If sudden blood loss ensues, the body’s neurohumoral and renal compensatory mechanisms are designed to restore hemodynamics and blood pressure and cardiac output, but in CHF, these same mechanisms can worsen the CHF—explain.

3. Describe the “four square” chart that combines LV filling pressure on the X axis and stroke volume or cardiac output on the Y axis; label the quadrant that represents the congestive and low output patients.

4. Describe the basic Rx classes of treatments that move the patient from that quadrant into the CHF but higher output, the less CHF and higher output, and the no CHF but still low output quadrants.

5. Which is the only class where likely inotropes will be required?

6. Describe the major hemodynamic change that comes with use of diuretics, vasodilators, and inotropes.

7. Describe Forrester’s four classes of pts. with acute MI with Swan Ganz catheter measurements of PCWP and cardiac index as to who had the best PCWP and CI (dividing lines were CI of 2.2 and PCWP of 18) and who had the worst, and therefore who had the best and worst mortality.

8. Label the four Forrester classes as “cold and dry”, “cold and wet”, “warm and dry” and “warm and wet” as clinical appearances and assign those labels to the correct Forrester four square subclass.

9. Beta blockers are outside the usual acute CHF list of treatments but are used in 2 specific circumstances—describe. What is the risk in use of beta blockers?

10. There is only one oral positive inotrope which is _________ and which moves the cardiac output curve upward. The reason to avoid it in an acute MI setting is _____________.

11. There are some negative inotropes which include ________ and the risk is that the cardiac output curve shifts downward.

12. Blood volume if increased will shift the venous return (vascular function) curve to the right and raise filling pressures to the left heart. This moves the cardiac output up on the Frank Starling curve to a certain limit and improves cardiac output. Describe the starting blood pressure of a patient in whom you would use this strategy.

13. The third potential influencing factor is TPR (total peripheral resistance) but changes in TPR end up affecting both the cardiac function curves and the vascular function curves at the same time. Explain what happens to the overall cardiac output, in an example of sudden increase in TPR (in response to a hemorrhage and therefore vasoconstriction), when the cardiac function curve shifts downward because of increases in MAP, and the venous return curve rotates counterclockwise.

14. Explain what could happen to overall cardiac output, in an example of sudden decrease in TPR (like exercise), when the MAP drops and the cardiac function curve shifts upward, and the venous return increases as the venous return curve rotates counterclockwise.

15. List one IV drug that seems most like a pure vasoconstrictor and one that is a more pure vasodilator.

16. List 4 drugs that have positive inotropy and not just vasoactive actions.

17. Explain the human body locations of alpha 1 and beta 1 and beta 2 receptors. Where are the V1 receptors and the ATII receptors?

18. What is the most commonly used alpha 1 and beta 1 agonist bp Rx to aid vasoconstriction?

19. Explain the three differing actions on receptors according to the doses used of dopamine.

20. Explain the hazard of using epinephrine as a bp support medication.

21. Vasodilators like nitroglycerine and nitroprusside can be used to decrease both venous pressure and arterial pressure—which one has more arterial effects? Name one adverse side effect for each of them if treatment is prolonged.

22. Describe the advantages and disadvantages of use of dobutamine and dopamine in inotropic support.

23. Describe some longer term and shorter term mechanical (nonpharmacological) therapies to help CHF and cardiac output.

Objectives:

1. Many types of shock present with clear clues as to cause and therefore the Rx fix. Name some “volume-related” causes (volume shifts = “distributive” and volume loss = “hypovolemic”) and some “output-related” (cardiac and extracardiac = “obstructive”) causes of shock.

2. If bp = SVR X CO, then there are four shock types that primarily change SVR (name those), and two things that change the HR component of CO (name those) and two shock types that primarily affect end diastolic volume (name that one) and end systolic volume (name that one)—since EDV – ESV = SV.

3. Explain what happens to SVR if the primary and first problem is a CO decrease; explain what happens to CO if the primary and first problem is an SVR decrease.

4. The definition of shock doesn’t depend on just the bp numbers per se, but rather whether, whatever the bp is, is it ___________________ to supply the body’s metabolic needs.

5. If there is a primary SVR too low problem the primary fix will be Rx of __________.

6. If there is a primary HR problem, the primary fix will be Rx of _______if too fast or _________if too slow.

7. If there is a stroke volume problem, then a second decision is required and if low volume affecting diastolic filling the primary fix will be Rx of __________ and if the stroke volume is impairing systolic contraction then the primary fix will be Rx of __________.

8. The old classic way of labeling shock was “distributive”, “cardiogenic”, “hypovolemic” and “obstructive”—name the most common category and inside that category the most common cause.

9. Describe how a rapid but simplified ultrasound helps distinguish types of shock in ER or ICU.

10. Describe how a mixed venous O2 saturation of more than or less than 65% saturation helps sort out types of shock.

11. Describe why a serum lactate level is a marker for increased shock mortality—what kind of metabolism shift does it represent?

12. Explain the differences between “overt shock”, “occult shock” and the “shock index”.

13. List some physical exam findings that support a shock diagnosis.

14. List some things at a cellular level that support a shock diagnosis.

15. Explain how a narrow pulse pressure difference between systolic and diastolic bp may indicate a primary SVR problem with eventual systolic CO problem, whereas a widened pulse pressure difference between systolic and diastolic bp may indicated a primary CO problem having trouble keeping up with the falling SVR.

16. Septic/inflammatory shock is an SVR problem first, so the very first solution is to _____________ before proceeding to the second step of _______.

17. Explain the difference between SIRS and sepsis.

18. Explain the SOFA score and what it means for mortality. Explain the impact of the bacteria in septic shock vs. the impact of inflammatory chemicals in septic shock as to outcomes.

19. Name four actual measurements that assure that septic shock is “treated enough”—and what are those measurements generally (CVP, mixed venous O2 saturation, MAP, urine output)?

20. Describe the bedside test for CVP estimation without a central line and what to look for. Describe the rapid ultrasound test finding that confirms underfilling of the IVC from low venous return.

21. Describe the typical ultrasound findings on the rapid US in cardiogenic shock.

22. Besides acute cardiac failure from an acute MI, name some other CV causes of cardiogenic shock.

23. Name the usual first drug class of Rx used in cardiogenic types of shock and describe why to use diuretics as the third Rx in cardiogenic shock.

24. Describe why you might use dopamine for bp support if choosing to use dobutamine or milrinone for cardiogenic shock.

Objectives:

1. An example of a known chronic CHF pt. who comes in with low CO, slightly high PA pressures, low bp and high pulse is treated with low dose dobutamine to partial effect. In order to further increase dobutamine safely, we might add ________ to support the bp and avoid higher dose dobutamine’s hypotensive effects.

2. An Acute MI pt. with “warm and wet” physiology and normal bp and tachycardia is treated with IV Nitroglycerine. After that his CO rose, his stroke volume rose, and his PCWP fell and CVP fell. Where in the circulatory system did the IV nitroglycerine work to explain these better results? Where on the Frank Starling curve was he at first, and which direction did he go post Nitroglycerine to explain the better CO?

3. A 14 year old in a near coma with prior infectious symptoms and sinus tachycardia and low bp, thin build, skin tenting, and dry mucous membranes is down 6% of weight in 3 days. There is poor urine output. Do you need a CVP line? What bedside maneuver could you try to provide a sense of the CVP? Why does this work?

4. An elderly pt. with high bp, rales, S3 gallop and loud murmur of mitral regurgitation comes in with some high bp, borderline CO/CI, and slightly high PCWP. He is given an ACEI and the bp decreases, the CO/CI increases, and the PCWP decreases. Did the ACEI improve the CP by decrease of the bp? What is this called, and what could you use as an IV drug to accomplish the same thing? Would this decrease the severity of the mitral regurgitation?

5. A post CABG pt. is asleep on a ventilator and a Nipride drip. The pre to post bp and pulse didn’t change much, but his CO increased and PCWP decreased. Is he better, and if so why—what did the Nipride do in terms of preload, afterload or contractility?

6. A chronic CHF pt. with rales and mild hypotension got dobutamine. She didn’t change bp, pulse, PCWP or CVP much at all, but CO did go up. Dobutamine is working here on preload, afterload or contractility? What likely drug could be used next and why?

7. A middle aged male with a cardiomyopathy and a cardiac arrest and shock is on low dose dopamine and low dose dobutamine. The CO went up slightly and systolic bp went up slightly but the pulse is faster and the PCWP did not change and the poor urine output didn’t change. If we wanted to add another inotrope, what might we choose? Is his SOFA score in the 0% mortality range, the 30% mortality range or the 50% mortality range?

8. A post CABG pt. several days postop drops the bp and CVP pressures and is given IV Hetastarch. The bp rises, the pulse decreases, the CO goes up and the CVP and PCWP stay about the same. What exactly is the Hetastarch doing in the vascular space?

9. A younger female is post bone marrow transplant and has low bp and receives saline bolus and norepinephrine IV. Her bp is borderline low, her CO is very high and her SVR is very low and didn’t change much with the therapy. What type of shock is she likely showing? Where is the norepinephrine working primarily? If her mixed venous O2 saturation was 45% instead of > 70%, what does that suggest about a potential second form of shock and also what does it suggest for her prognosis?

10. A pt.’s hemodynamics have mild low bp, a sudden sinus tachycardia, improved CO and decreased SVR. There was no medication change to cause this. What is the likely age of the patient who can cause this to happen separate from medication changes?

11. A young post motorcycle accident pt. has a fractured clavicle and quiet abdomen, and dwindling urine output. The pulse has escalated, the CO has dropped and the CVP has greatly dropped. What has likely happened here? What type of shock is this?

12. A male with a cardiomyopathy had hypotension and low CO and normal CVP and PCWP. Your colleague gave IV fluids and the bp went up, pulse went down, CO went up but the CVP and PCWP also went up. Was it the right thing to do, and what to do next? Did your colleague move them in the correct direction on the Frank Starling curve?

Review the following conditions:

• Systolic Dysfunction
  
• Diastolic Dysfunction
  
• Acute Exacerbation
  
• Dilated Cardiomyopathy
  
• Hypertrophic Cardiomyopathy
  
• Restrictive Cardiomyopathy
  

Objectives for each condition:

• History taking and performing the physical examination
• Diagnostic and laboratory studies
• Formulating the most likely diagnosis
• Health maintenance, patient education, and preventive measures
• Clinical intervention
• Pharmaceutical therapeutics

Objectives:

1. Explain how the intracardiac electrical system myocytes are not grossly anatomically distinguishable from other cardiac myocytes, but instead what does distinguish them anatomically and physiologically.

2. In either Galvanometers or EKG machines, the upward EKG deflection really reflects electron flow in which direction and the downward EKG deflection reflects electron flow in which direction?

3. Explain how each of these correlates with ion flow across cell membranes and amount of depolarization and repolarization.

4. Explain why the left arm and left leg are designated as “positive”. 

5. Explain why an EKG lead located on a body part in the opposite direction to electron flow has an opposite direction of deflection.

6. Explain this phrase and how it relates to EKG findings of STT waves’ direction as compared to QRS direction (in any one lead) on things like bundle branch blocks, PVCs etc.—“when depolarization is abnormal, then repolarization will be abnormal.”

7. On myocardial cells, there are membrane potentials created by semipermeability and ion concentration differences on either side of that membrane. List where Na+, K+, Ca++, and Cl- are high vs. low on each side of the cardiac cell membrane at rest and which way things move in depolarization.

8. SA node and AV node and Purkinje fibers have a “phase 4 depolarization” which looks different than other electrical cells and is not flat but with a slow upward drift toward “less negative”. This gives them “automaticity”. Explain what this means for “backup pacing functions”.

9. Explain why the longest “pause” at the AV node is functionally advantageous for blood flow from atria to ventricles.

10. Explain two structurally different findings in AV node compared to other cardiac electrical structures that make for a longer pause.

11. Explain why P wave amplitudes are smaller than QRS amplitudes.

12. List the three bundles below the AV node and where they go and how they are reflected in the QRS (force and direction) on the EKG.

13. Explain anatomically why a right sided chest EKG lead shows more RV side electrical forces and a left sided chest EKG lead shows more LV side electrical forces and in general why most of any QRS still reflects more LV side electrical forces.

14. The normal T wave repolarization (in a normal cell) has an upward direction if the QRS wave in that lead is also upward. There are two reasons why these match direction, even though T waves are essentially opposite electrical events from QRS’s. What are these reasons for the so-called “double negative”?

15. Name normal EKG paper speed and normal width timing for smaller marker boxes and larger marker boxes on EKGs run at normal paper speeds.

16. Name normal P wave durations, normal PR intervals, normal QRS durations, and normal QT intervals (depending for that latter on heart rates—but explain what happens to QT intervals in bradycardia vs. tachycardia).

17. Normal vertical height on EKG is measured in mV with two large marker boxes reflecting 10mV. Explain height variations in P waves or QRS waves according to hypertrophy or smaller sizes—what is different about the number of cells in these chambers to produce these different appearances?

Objectives:

1. List some reasons to learn EKG interpretation instead of just relying on the computer interpretation.

2. Name the usual 11 steps in an EKG interpretation algorithm and the order for interpretation.

3. Why do we do “is it interpretable at all vs. artifacts” first? Are all artifacts uninterpretable?

4. Why do we pay attention to EKG paper speed and voltage standards as the second step?

5. If EKG paper doesn’t have printed paper speed, describe two ways to figure out paper speed.

6. Many machines have double and half buttons for both speed and voltage. If an accidental button was hit prior to EKG recording are the intervals or voltages uninterpretable?

7. Name normal PR interval and tell what it shows electrically. Name the normal QRS interval and describe what it shows in the septum electrically. Name the usual range of normal QT intervals and what it reflects electrically and also two clinical problems/changes that often are reflected in QT interval changes.

8. Describe why it is helpful to do the heart rate calculation and the rhythm assessments “simultaneously”.

9. Describe the “usual” rates for the SA node, AV node, bundle branches, and ventricle Purkinje system fibers.

10. There are three ways to calculate heart rate. What are they and name some advantages and disadvantages of each.

11. What are the 6 p-wave questions? 

12. What are the 5 questions you must ask after the p-wave questions?

13. Determine ventricular rhythm—QRS narrow or wide? His Purkinje system used or not? T wave same direction/opposite to QRS? And relationship of P to QRS—always related/sometimes related/never related to each other.

14. Are there any unusual single complexes that occur early/late/unusual shape that come on top of some underlying predominant rhythm?

15. Know if the rhythm dangerous?

16. One reason to do rate and rhythm together is that certain classic heart rates go with certain rhythms. Name three examples.

17. What is the only living human arrhythmia which is irregularly irregular?

18. Describe why it is possible or impossible to be certain about SVT with BBB vs. VT on any one EKG.

19. Name five other EKG findings that might mimic VT but are not VT.

20. Heart blocks or BBB’s mean “slow electricity” not “no electricity”. Describe the differences in conduction between first degree AVB, second degree type 1 and 2 AVB, and third degree AVB and the seriousness of each.

21. When RBBB is present or LBBB is present the QRS will widen to at least what measurement? Which part of the QRS is “delayed” in each and which EKG leads are best for seeing each one?

22. Learn to calculate the axis on any EKG.

Objectives:

1. Hypertrophy of any chamber depends on having more cells that can conduct electricity, and appear as what kind of finding on EKG on the Y or vertical axis?

2. A helpful shift of the frontal plane axis finding that confirms hypertrophy development in serial EKGs is what kind of shift?

3. Describe the classic findings of “P pulmonale” and “P mitrale” on EKG and which leads they appear in and why.

4. Explain (separate from enhanced voltage) in ventricular hypertrophies, why there are “strain” STT findings in respective EKG leads that confirm more severe ventricular hypertrophy.

5. Explain how the horizontal chest lead axis changes of the QRS (through the progression of V lead QRS height) correlate with the expected R waves vs. S waves in each lead and the “transition zone”, and what changes to expect in RV or LV hypertrophy.

6. True or false in chest lead interpretation—“what happens in an S wave in a right sided lead is reflecting the same things as what is happening in an R wave in a left sided lead (and vice versa).” Explain why that helps in interpretation of bundle branch blocks or ventricular hypertrophies that “don’t quite meet” standard criteria.

7. RV hypertrophy has many fewer criteria than LV hypertrophy and can have a particular confounding interpretation in what type of MI?

8. Voltage figures prominently in LVH determination criteria—describe two different common criteria using voltage measurements in certain leads to help determine LVH.

9. How do you know if down-sloping STT’s in left sided chest leads are really from LVH or from ischemia on any one EKG?

10. Explain whether LVH by EKG criteria has proven reliable as a measure of severity of hypertension effects.

11. Explain the difference in STT changes in “pressure hypertrophy” and “volume hypertrophy”.

12. Explain the coronary blood supply for the major “heart blocks- associated” conduction system anatomical structures (SA node, AV node, right and left bundles).

13. Which BBB is more consequential in reflecting more myocardial damage?

14. Explain why ventricular hypertrophies that develop over time can result in a BBB.

15. Explain why LBBB obscures anterior STT changes of ischemia and obscures anterior Q waves of MI.

16. Name three diseases that more likely have RBBB and three diseases that more likely have LBBB.

17. Explain “rate-dependent BBB” and which (RBBB vs LBBB) is more serious.

18. Explain what “Ashmann’s phenomenon” is and how it differs from PVC’s.

19. Explain Brugada syndrome EKG findings and its severity and consequence. Explain which fascicular block (hemiblock) is more common and why.

20. Explain what “bifascicular block” is and its severity and consequence and “trifascicular block” and its severity and consequence.

Objectives:

1. Describe some EKG differences from a “normal septal activation” Q wave from a myocardial infarction Q wave and why this is important.

2. Explain which leads may have an exception to the rule, “once the EKG shows a pathological Q wave, it will always remain thereafter”.

3. Explain why a “true posterior MI” has a new tall R wave instead of a new Q wave.

4. Explain the depth of myocardial wall MI involvement if a pathological Q wave is seen vs. just ST segment or T wave changes.

5. The easiest, least expensive, most available test to do to convince yourself of ischemia after an equivocal EKG is ___________. The reason for this is that the only real disease process of the heart which can change an EKG within minutes is not hypertrophy, LVH, BBB or WPW or cardiomyopathy but rather ____________.

6. Describe which five groups of leads reflect which coronary involvement.

7. Explain the variability of the RCA (right coronary artery) involvement in inferior lead changes.

8. Explain how “upstream” the coronary lesion is in the LAD if more vs. less chest leads are involved with changes, and the effect of this on severity.

9. Explain what an “RV infarct” is from, and which coronary is most likely involved, and what kind of special EKG leads are used to see this.

10. Timing of ischemic changes occur serially on EKGs. Describe which changes (T waves, ST segments, Q waves) occur first, and in which order as to coming and going, and why Q waves are the most persistent of them all, and which changes represent the most damage and the most recoverability.

11. Describe which EKG changes go with the phrases “ischemia”, “injury” and “infarction”.

12. Explain “reciprocal changes” on an EKG and why if present, they are helpful in confirming true infarct in progress.

13. Explain why, in the era of thrombolytics and acute stent interventions, that the classic “timing of MI EKG changes” may not hold as true in ischemia? What is happening to change the timing?

14. List some non-ischemic reasons for T wave changes.

15. Describe ST segment elevation shapes of “coved upwards” (“smile”) vs. “coved downwards” (“frown”) and the significance of these in distinguishing MI from pericarditis.

16. Explain the ST description in “normal early repolarization” and who this is typically seen in, on EKGs.

17. List five classic pericarditis EKG changes and out of all the criteria, the presence or absence of which one is most useful at distinguishing true MI from pericarditis.

18. Explain why Holter or Treadmill ST segment changes that come and go may not represent coronary occlusion in progress but instead represent which kind of coronary pathological process.

19. Describe whether or not “symmetrical” vs. “asymmetrical” STT changes can reliably distinguish ischemia from hypertrophy.

Objectives:

1. Describe electrolyte EKG effects as follows

• High K+ including the series of changes on EKG, in order of worsening hyperkalemia; and why does the first step in ischemia look the same as the first step in higher K+. What is happening at the myocardial cell level?
• Low K+: explain the three EKG changes that can be seen and whether or not these correlate with actual K+ level.
• Hypocalcemia changes and which interval changes on EKG and what is the dangerous rhythm which might be produced from that.
• Hypercalcemia and which interval changes with that.

2. List three changes on EKG that happen with hypothermia.

3. Describe what a “J wave” or “Osborn wave” looks like.

4. What is the potential advantage of slowed CV metabolism (as seen in certain EKG findings) in near drowning in cold water?

5. Explain the difference between digitalis effect and digitalis toxicity.

6. Describe the “classic arrhythmia” that comes frequently with digitalis toxicity and the two components of “increased automaticity” and “increased AV block at AV node” and which of these components goes with which of the two parts of the “classic arrhythmia”.

7. Describe whether the digitalis level must be high in order to see this classic arrhythmia of digitalis toxicity.

8. Understand normal vs. abnormal QT intervals (and association with expected QT intervals for heart rate).

9. Explain the potential for harm from prolonged QT intervals for heart rate.

10. Describe three drug classes that could prolong the QT interval. Explain the formula for QTc interval calculation and an approximation of that.

11. Explain what timing interval in cardiac function shortens as heart rate speeds up which is why the QT changes with heart rates.

12. Athlete’s hearts EKGs can have findings that have findings that can be confused with pathological findings. Name five EKG findings on the “Seattle Criteria” that are actually normal in athletes, vs. five EKG criteria that are more likely representing abnormal EKG findings in athletes.

13. Explain the components of a pacemaker and the components of a defibrillator.

14. Explain which types of EKG pathologies have an indication for a pacemaker and which types of EKG pathologies have an indication for a defibrillator.

15. Explain the location of the leads in a one wire, two wire, and three wire devices.

16. Explain the EKG appearance difference between “unipolar” and “bipolar” leads and how the conduction between metal pieces determines how they look on the EKG.

17. Why does a ventricularly paced beat look different on the QRS and STT’s than a normally conducted beat in the same patient? Which direction is conduction going, in each case? Does every beat in a dual chamber pacemaker produce the same spike and P and QRS appearance?

18. Explain the “pacing lingo” for the pacemaker code for chamber paced/chamber sensed/and triggered or inhibited/rate responsiveness.

19. Explain the difference between pacemakers and defibrillators in terms of generators and leads. Why does every defibrillator also have pacing capability?

20. If you only see spikes and no P and no QRS waves, this is called “loss of capture”—what is actually happening with the device and what is actually happening with the myocardium?

Objectives:

1. Correlate the Wiggers’ diagram EKG events (QRS and T wave) with the mechanical events (AV valve closures and semilunar valve openings and then AV valve openings and semilunar valve closures) specifically with regard to timing of S1, and S2 and actual ventricular systole and diastole.

2. Describe isovolumic contraction and isovolumic relaxation and correlate these with S1 and S2.

3. Normal valve leaflets make sounds when they close or open?

4. Describe which valves are closing first with S1 and then with S2 and which AV valves and which semilunar valves occur in which order (in a normal heart).

5. Describe which heart sound of S1 and S2 is lower pitched and longer and which is higher pitched and shorter. Correlate this with the square area of the respective valves. These sounds should be listened to with what part of the stethoscope to aid distinguishing pitch?

6. The S1 component will be heard at the same time the _________upstroke is felt.

7. Describe the anterior chest locations of the four areas to listen for heart sounds.

8. Any disease that maintains MV leaflets more separated for longer will result in a louder MV component of S1. Name three diseases that likely result in loud S1 and three that result in softer S1.

9. Name three diseases that “get in the way” of hearing the loudness of S1.

10. Name some diseases that vary the loudness of S1 from beat to beat.

11. Describe the two anterior chest areas of where to listen closely for the components of S2.

12. Describe “normal S2 splitting” and exactly what happens in the heart and lungs to make it occur.

13. There are also abnormal S2 splitting patterns like “wide but mobile”—name some diseases that go with that.

14. The pattern of “wide and fixed splitting of S2” is classic for what disease?

15. Name some disease that have a pattern of “reversed and paradoxical”.

16. S3 and S4 are gallop sounds that both occur in diastole. Which is early diastole and what does it represent mechanically, and which is late diastole and what does it represent mechanically?

17. Which is called the “ventricular gallop” and which is called the “atrial gallop”?

18. Which part of a stethoscope should be used to hear S3 and S4 best, and why?

19. What is the rhythm mnemonic that you can say to train your ear to hear the diastolic patterns of S3 and of S4?

20. What is a summation gallop and what is its significance? Name some normal circumstances where S3 might be normal instead of pathological, and some disease processes where S3 is pathological.

21. Can one hear an S4 in atrial fibrillation? Why or why not?

22. Name one instance where S4 could be normal and one disease process where S4 is pathological.

Objectives:

1. It is critical in murmurs to distinguish systole from diastole reliably. A systolic murmur basically happens if systolic flow is exiting in a normal direction through an exit door which is ____________ or exiting in a backwards direction to a chamber which is _______________.

2. A diastolic murmur is heard if blood goes ___________ into a chamber whose valve should be __________ but is not, or goes in a forward direction into a chamber whose exit door is ______________. (use words like hampered in opening, normally closed off, backward flow, closed but is not, hampered in opening).

3. Name the six factors that go into identifying murmurs.

4. What is the reason to identify all these factors? Which timing (systolic or diastolic) could represent an innocent murmur and which is always pathological?

5. What is a palpable thrill and how does it divide murmur intensity grades?

6. Who is most likely to have an innocent or functional murmur?

7. Name five characteristics that are more convincing that a particular systolic murmur is an innocent or functional murmur.

8. Name three of the five possible causes of innocent murmurs of childhood.

9. What percent of pediatric murmurs in a general screening primary care clinic turn out to be pathological?

10. Of the common adult valvular murmurs which three are the most common systolic?

11. Describe their classic six ways of descriptions of these three murmurs.

12. Describe what happens to sound loudness of S2 and the murmur loudness in progressive aortic stenosis. Describe why this doesn’t work to quantitate severity in mitral regurgitation.

13. How does the MV prolapse murmur sound different from other forms of mitral regurgitation?

14. Of the common adult valvular murmurs which two are the most common diastolic? Of the two of these, which is far more common now, and why? Which one is best heard with the bell in one particular patient position?

15. Describe the classic six ways of description of these two diastolic murmurs.

16. Name a classic pediatric “continuous” murmur.

17. How is a “venous hum” of childhood different from this pediatric continuous murmur? Describe the sound differences between the continuous murmur just described and the adult combination AS/AI murmur.

18. Some murmurs are still tough to distinguish so using “the company they keep” give clues that are convincing for accurate murmur diagnosis. For AS, describe some characteristic EKG and CxR and echo supportive findings.

19. For MR, describe some characteristic EKG and CxR and echo supportive findings.

20. For AI, describe one physical exam characteristic on blood pressure that signifies worsened severity. Which one of these diseases can result on the largest CxR LV size?

21. For MS, describe the likely LV size on EKG or echo or CxR.

22. Describe the characteristic age ranges of children with these various forms of innocent murmurs like peripheral PS, venous hum and Still’s murmur, and pulmonary flow murmurs?

Objectives:

1. Describe the “click” and “snap” as opening sounds of what valves and where they occur in timing of systole and diastole. Can they be normal? Can they be multiple? Which one changes with patient position?

2. What is the pitch of clicks and snaps as compared to gallops, and therefore it is best heard with what part of the stethoscope?

3. Describe the sound of pericardial and pleural friction rubs. Compare how closely a pericardial rub sounds to your ear canal as compared to murmurs.

4. There is one easy patient maneuver to tell the difference between pleural rubs and pericardial rubs—what is this?

5. What is the disease significance of a pericardial knock?

6. What is a “tumor plop” from? Which one of these sounds is associated with “upright syncope”?

7. Feeling a pulse can help in diagnosis. Feeling a “collapsing pulse” or “Corrigan’s water hammer pulse” goes with which disease process?

8. Where would you look for Quincke’s pulsations and deMusset’s sign or Lighthouse sign on a patient physical exam?

9. Explain pulsus paradoxus. Can you find this in normal patients?

10. Explain how to use a bp cuff to demonstrate this if the difference is more than 10 mm Hg difference.

11. List the three disease processes that might produce pulsus paradoxus of more than 10 mm hg difference.

12. Name the jugular venous waves and descents and describe what each represents in terms of intracardiac events.

13. What maneuver could the examiner do to differentiate carotid pulsation events from jugular venous pulsation events?

14. Explain how to estimate CVP pressure by looking at the level of the top of the JVP waves compared to the vertical level drawn from the sternomanubrial angle on the patient at 30 degrees elevation (and added to 5 cm).

15. What is the cm of water pressure number beyond which this patient is “hypervolemic”?

16. “Cannon a waves” occur with atrial contraction against a closed TV. Name three rhythm diagnoses where “cannon a waves” might be seen in the jugular venous waves.

17. Describe hepatojugular reflux.

18. Describe Kussmaul’s sign.

19. Peripheral edema is made worse by gravity and distance of the body part from the heart and is made better by having adequate large molecule proteins intravascularly to hang onto water inside small vessels.

20. Explain why a barely compensated CHF patient during the day might have pitting dependent edema and then instead during the night would have less edema and more CHF exacerbations of PND (paroxysmal nocturnal dyspnea).

21. Pitting only works if and when the fluid is _____________ in location which explains why _____________ location of fluid is nonpitting.

22. Name three medications that can themselves cause pitting edema.

Objectives:

1. Aortic Stenosis comes in differing types and has a trimodal age distribution. Explain which types appear in which age groups.

2. Explain why a bicuspid AV doesn’t promote laminar flow like a tricuspid AV would.

3. Explain how a congenital bicuspid AV stenosis patient can worsen their AS over time. And also involve their aortic root.

4. Explain the difference between AV sclerosis and senile AV stenosis.

5. Explain why we operate with AV replacement on senile AS sooner than we used to.

6. Describe which symptom (Angina, dizzy/syncope, or dyspnea) goes with 2 years to live, 3 years to live or 5 years to live in AS patients. Which is the most common presentation?

7. What happened to AS longevity comparing the “after 1980’s” to “before 1980’s”?

8. What percent of AS patients have additional CAD?

9. Can you tell the angina of pure AS from the angina of AS plus CAD?

10. The murmur of AS is typically “diamond-shaped” crescendo- decrescendo in systole with a softer S2 with progressive disease. Explain why the murmur severity doesn’t reliably show AS valve obstructive severity and why the S2 softens with worsening AV gradient.

11. What are classic echo findings on AV for AS and the LV wall thickness/chamber size for AS?

12. In the cath lab, there is a classic variation on the Wigger’s diagram in AS which shows what difference between the LV pressure waveform and the aortic waveform?

13. Name the four solutions to critical AS. Name the pros and cons to each.

14. Only some patients with AV sclerosis proceed to valvular AV stenosis. What could be done to prevent this?

15. Do you need to generally give SBE antibiotic prophylaxis to AS patients? How about anticoagulation for embolic protection?

16. Contrast the “bounce back ability” of the LV function in AS vs. AI once the valve is fixed or replaced.

17. Explain the difference found on the Wigger’s diagram in AI in what happens to diastolic pressure in the aorta and in the LV? Therefore, the LV will enlarge in ________ before the walls ____________.

18. Explain a couple of causes of acute AI.

19. Causes of AI in the developing world are usually due to __________ but in the U.S. and industrialized world are usually due to __________.

20. What is the classic murmur of AI?

21. A shorter duration of AI in diastole (more blood backwards sliding quickly) means what in AI severity?

22. A high volume diastolic jet of AI tends to “superfill” the coronaries and makes it ____________ to get simultaneous AI and CAD.

23. Name three other physical exam findings you might see with at least moderate AI.

24. A marker of AI worsening on bp on exam or in the cath lab is a drop of ____________.

25. The size of the heart on CxR in a chronic AI patient is remarkably _________.

26. Is echo is a good tool at assessing severity of chronic AI by looking at the LV size, even if the patient is asymptomatic?

27. There may be reasons to operate an AI pt. earlier than just what the valve would suggest—name some reasons.

28. What could you do medically for Rx that is nonsurgical while following a chronic AI patient, before they qualify for surgery?

29. Do you generally need to give SBE antibiotic prophylaxis to AI patients? How about anticoagulation for embolic protection?

30. Explain what measures are taken to assess athletes with AI and sports participation.

Objectives:

1. Name some differences anatomically of the MV from the AV and PV and the TV.

2. Why can we not easily use a patient’s TV as a substitute for their MV surgically?

3. Name some diseases or disease groups that impair the MV and which portion of the MV do these diseases affect?

4. Explain how after an acute MI, mitral regurgitation could occur either early or late.

5. Compare the size of the LV chamber and LV walls in chronic AS to the size of the LV chamber and LV walls in chronic MR. Explain the impact of this on postop MR recovery vs. postop AS recovery.

6. A classic cath lab finding for chronic MR is “tall V waves” on the atrial pressure tracing. What does this represent?

7. MV prolapse is a special case of MR with “floppy” leaflets and chordae and variable valve regurgitation. What should you expect with frequency and with prognosis compared to other sources of MR?

8. Explain what creates the click and what creates the murmur.

9. Explain the correlation of symptoms in MV prolapse patients vs. symptoms in patients with other causes of MR.

10. Contrast murmur severity in MR vs. murmur severity in AS and what this means for worsening disease processes.

11. Discuss the pros and cons of MV repair vs. MV replacement and discuss which is more technically difficult to do.

12. Discuss the SBE endocarditis prophylaxis recommendations in MR.

Objectives:

1. Describe the actual pathology of the MV in mitral stenosis and its most common cause.

2. Describe the risk if repeated rheumatic fever attacks.

3. Name the four most common symptoms of significant MS. Why do fever and other causes of fast heart rates “bring out” symptoms from occult MS?

4. Name some physical exam findings in MS separate from and including the classic murmur.

5. Explain why early MS has an easily heard S1 and later MS has a more inaudible S1.

6. Explain some expected EKG findings in MS.

7. Describe some classic CxR findings in MS.

8. Name some classic echo findings in MS. Describe the usefulness of 3D echo vs. the usual 2D echo in MS surgeries.

9. How many years usually pass between a first rheumatic fever episode to severe MS?

10. What is the type of treatment significance for MS of a “mitral valve echo score”?

11. MS happens more in females. Explain why this might impact treatment choices at certain ages.

12. Explain why MS patients often are on Coumadin/Warfarin.

13. Why do we use diuretics, beta blockers or calcium blockers and digoxin in MS patients who await surgery?

14. Atrial fibrillation can be “all by itself” or caused from many other CV diseases. Define “paroxysmal”, “persistent”, “long-standing persistent”, and permanent and how that impacts treatment choices.

15. Explain why “valvular atrial fibrillation” and “nonvalvular atrial fibrillation” impacts anticoagulant choices.

16. Explain whether or not patients are accurate at identifying their atrial fibrillation.

17. There are two decisions in Afib Rx—one is about anticoagulation but the other is deciding between two Rx strategies of ___________ or ___________.

18. Explain the CHAD2DS2-VASc score and what it implies in anticoagulant choices of Rx.

19. Name the drugs that “rate control” atrial fibrillation and why you would choose this strategy.

20. Name some true antiarrhythmic drugs that control atrial fibrillation and why you would choose this strategy.

21. Which antiarrhythmic has the lowest rate of recurrent atrial fibrillation?

22. Explain when DC cardioversion is most successful and long-lasting as a conversion strategy.

23. Explain when atrial fibrillation ablation procedures would be unlikely to give long term success. Does the mere presence of atrial fibrillation affect mortality?

Objectives:

1. Explain how frequently isolated PVCs occur in the general population, and whether that reliably signals structural heart disease.

2. What is the borderline PVC rate on a 24 hour HM, which in the absence of risks for CV disease, requires no further CV workup?

3. What things in the history or the appearance of PVCs signal higher CV risk?

4. Name five “correctable causes” of PVCs.

5. If you must do further CV workup, what would you order and what are you looking for on each test?

6. There are three basic pathophysiological ways to get PVCs—name these and describe what exactly is happening and which cause is most likely associated with each one, and also which one is the most common cause of the three.

7. Name three EKG findings that would convince you a particular beat is a PVC.

8. Explain “fusion or capture beats” and “coupling intervals”.

9. Explain the danger of “R-on-T” phenomenon.

10. Name some cardiac and noncardiac conditions with PVCs of more importance.

11. Why would an EP doctor take someone with PVCs to EP testing—list four criteria?

12. Explain the difference in appearance and severity between monomorphic VT and polymorphic VT. Explain how these differ from AIVR.

13. Explain the conundrum of treating CHF and CHF drugs causing pro-arrhythmia.

14. Explain whether the complaint of syncope with ventricular arrhythmia leads to more investigation or less.

15. Explain four EKG criteria to help tell VT from SVT “with aberrancy of the QRS”.

16. There is one criteria which is the most helpful at telling the difference and this is _________.

17. “Torsades de Pointes” is a particular VT form that more often goes with what etiology?

18. Explain the classes of ventricular antiarrhythmics and which phase of the action potential they work on.

19. Explain why we try to refrain on antiarrhythmic use in the immediate post-MI state.

20. Explain why an AICD implant would be more likely used for VT and VF or resuscitated cardiac death instead of antiarrhythmic drugs by themselves.

Objectives:

1. What generates the PR interval on EKG and what happens to that in first degree AVB? What is the difference of finding this in a young patient vs. an older patient?

2. What else besides diseases can cause first degree AVB?

3. What does it mean for prognosis if first degree AVB is combined with a BBB?

4. What should be used to treat first degree AVB, if anything?

5. Describe the two types of second degree AVB and differences between their EKG appearances, and prognosis, and where in the conduction system is the most likely site of abnormality.

6. Which location of an MI most often can lead to Mobitz I second degree AVB and why?

7. What physical exam maneuver could you do to tell the difference in the two types of second degree AVB (in resuscitation-equipped settings), and why does that work to differentiate?

8. What Rx can you use to temporarily, and also to more permanently, fix second degree AVB?

9. Explain the advantages and disadvantages of external pacing.

10. What does the term “pacemaker-dependent” mean?

11. Permanent pacing is often used for third degree (“complete”) AVB. Describe exactly what happens to the atrial and ventricular conduction on EKGs in 3 rd degree AVB.

12. Describe how much conduction goes through the AV node.

13. Describe the usual QRS width in 3 rd degree AVB and why that occurs.

14. Name a few diseases that can produce 3 rd degree AVB.

15. How many wires are typically used, at a minimum, in pacing to correct third degree AVB?

16. Permanent pacing is often used in which two types of heart block and much less likely used in which two types of heart block?

17. Explain from an electrical conduction point of view why a paced beat results in a wider QRS on EKG whereas a nonpaced individual QRS might be more narrow on EKG?

18. Why is an implanted lead tip conduction surface so small on an implanted pacemaker whereas an external lead patch is so large in surface area?

Review the following conditions:

• Atrial Fibrillation and Atrial Flutter
  
• Heart Block
  
• Supraventricular Tachycardia
  
• Wolff-Parkinson-White Syndrome
  
• Premature Beats
  
• Ventricular Arrhythmias
  

Objectives for each condition:

• History taking and performing the physical examination
• Diagnostic and laboratory studies
• Formulating the most likely diagnosis
• Health maintenance, patient education, and preventive measures
• Clinical intervention
• Pharmaceutical therapeutics

Objectives:

1. Explain the rapid drop since 1975 in first CVD event and stroke and mortality, and which risk factor managements changed/improved to make that happen in the last 40-50 years.

2. Which risk factors are “going in the wrong direction”?

3. Explain why it is easier to convince patients to “have a procedure to fix CAD” than to avert risk factors to avert CAD formation?

4. Explain in terms of the timeframe for atheroma formation vs. experience of symptoms.

5. Which risk factor that is modifiable has the most impact in improving mortality?

6. Take an example of a 45 year old male with ideal risk factors managed vs. a 45 year old male with 2 CV risks not ideally managed—what is the number of years of survival advantage of the former, generally?

7. Do antioxidant vitamin ingestions prevent mortality in CAD?

8. Explain the impact on CAD from aspirin, Fish Oil, use of statins to decrease LDL.

9. From a vascular point of view, smoking cessation results in “normalization” of CAD mortality risk in what period of time?

10. What percent of the U.S. population actually meets the recommended level of aerobic physical activity?

11. Explain obesity trends in adults and youth over the last 20 years.

12. Explain how “metabolic syndrome” has a ten year risk of CAD event which is as high as patients with a prior MI or CVA.

13. What percent of Type 2 DM patients end up with some vascular disease in their lifetime?

14. Explain the “J curve” in alcohol intake and CAD events.

15. Explain the age range where atheroma starts.

16. What is the difference in histology of plaques in teens to 30’s vs. adults in the 40-60 age range?

17. Describe the five general stages of plaque formation.

18. What is the difference in symptoms and anatomy/histology between “stable plaque” and “unstable plaque”?

19. There is one drug class which “thickens the fibrous cap on plaque” –describe which class and what happens to number of CAD events and mortality if this class is used.

20. A ruptured plaque results in blood flow changes as a result of what kind of pathophysiology in the vessel at the endothelium?

21. Compare invasive tools like intracoronary angiograms and intravascular ultrasounds and perception of plaque severity vs. noninvasive tools like coronary artery calcium scores and coronary CTAs.

22. Which pair can “see” plaque earlier in any particular patient?

23. Which kind of plaque (“soft” and lipid-filled vs. “hard” and calcium-filled) is the more unstable type and leads to acute events?

24. Most “genetics” of early age CAD appear more polygenic. One exception to this is the “statin resistant high LDL patients” who appear to have a single gene variation. Name the recent non-statin Rx which is successfully used in those patients to decrease LDL receptors?

Objectives:

1. Describe classic angina and some “anginal equivalents” and which patient groups have each.

2. Could non-classic chest pain have no angina/CAD but still have a serious cause?

3. Does angina always mean CAD?

4. Name four things determining myocardial O2 demand and four things determining myocardial O2 supply?

5. Name drugs which address each category for angina Rx.

6. Describe why chest pain which is in the skin is easy to pinpoint whereas internal chest pain from a thoracic organ is difficult for the patient to pinpoint.

7. Name some diseases of supply and demand that are not from CAD typical atheroma but can cause angina.

8. Name three physical exam signs, which if present during angina and disappear with resolution, are pretty convincing for CAD as the cause.

9. What is the difference between angina and acute coronary syndrome (NSTEMI/STEMI) in the coronary itself?

10. Describe the difference between “type 1 MI’s” and “type 2 MI’s” as far as causes; also describe what happens to troponin levels in each of these and the time course of the troponins in each.

11. Explain why the course of action in type 1 MI may differ from the course of action in type 2 MI.

12. What are some reasons that a patient with unstable angina or acute coronary syndrome would go to the cath lab and have normal appearing coronaries?

13. Describe “cardiac syndrome X” or “microvascular angina”.

14. What is the difference between vasospasm of Prinzmetal’s angina and “microvascular angina” on coronary arteriogram appearances?

Objectives:

1. Explain how the “pretest probability of disease” greatly influences the value of likely CAD in treadmill tests.

2. Explain how a treadmill with classic ST segment changes greatly improves the probability of CAD as a cause in the “middle ranges of risk” rather than in very high or very low risk populations.

3. Explain the “Duke score” on a treadmill test and what it tells you.

4. Explain sensitivity and specificity for statistics of test results.

5. If someone cannot achieve 85% maximum predicted heart rate for age with exercise, what happens to the sensitivity and specificity of treadmill test results?

9. If the patient’s resting EKG is already abnormal on the ST segments, what happens if you exercise them, and get more ST segment abnormalities in terms of CAD likelihood and accuracy of results?

10. What are five resting EKG abnormalities which obscure ST interpretation and might lead you to order an imaging stress test instead of a plain treadmill?

11. What is the “female problem” with ordering plain treadmill test results?

12. What could be added to a plain treadmill to improve test results accuracy for CAD diagnosis?

13. What is the change that is looked for on stress echoes to indicate ischemia vs. the change looked for on stress nuclear tests to indicate ischemia?

14. Name the four general coronary artery calcification score divisions.

15. Explain how a CAC score would add to the ASCVD 10 year risk calculators to advise more aggressive risk management.

16. Compare how the coronary artery calcium score performs in risk calculation compared to hs-CRP or hs-troponin or homocysteine or BNP.

17. Explain which two CAC score groups where adding a statin makes a mortality and event risk difference over the next ten years.

18. Is a coronary CTA with iodine dye equal in accuracy of CAD severity to a coronary angiogram done in the cath lab?

19. Comparing a coronary CTA to a coronary catheterization, which is less invasive?

Objectives:

1. CAD is often progressive despite Rx in either noninvasive angina medication treatment, or invasive interventional treatment. Therefore, it is incumbent on the clinician to provide risk factor management, and reassessment along a long timeline. This involves judgments about _______ and _________. This may involve function (as tested by __________) and mortality impact (as measured by _________) and severity or CAD burden.

2. Name 4 medication groups that have actually been proven to prevent progression or improve outcomes.

3. Which angina drug is usually used first but should not be used in vasospasm (and why not)?

4. How do calcium blockers work in the supply- demand ratio?

5. What’s the biggest problem with use of nitrates?

6. Why is Ranexa used last in angina?

7. How does EECP (enhanced external counter pulsation) work to treat angina?

8. When would invasive treatment of angioplasty/stents or CABG surgery be used instead of just medical management?

9. Do invasive treatments of CAD prevent future events? If so, when?

10. What is the coronary pathophysiology that led to “coated stents” being invented? What are the advantages and disadvantages between vein grafts being used for bypass graft surgery vs. arterial grafts?

11. Why are vein grafts turned upside down before attaching to the distal coronary in CABG surgery?

12. Name some in-the-cath-lab risks of doing PTCA/stents. Name how intracoronary ultrasound is used.

13. Lay out the differences in choosing to do CABG or PTCA/stents in terms of vessel number, acute MI or chronic CAD, left main (unprotected) CAD, and diabetes.

14. Fill in these blanks comparing PTCA/stents and CABG:

• The risk of procedure-related CVA is higher at 30 days with _______.
• The risk of death is higher at five years with _______.
• The risk of all cause death at ten years is _____________.

15. What is the SYNTAX score? Why is it used?

16. If you follow patients post CABG over time, there are only a few things that make a statistically significant difference in long term outcomes of mortality—name three.

17. Why do post CABG patients often develop atrial fibrillation postop and how long does it last?

Review the following conditions:

• Hyperlipidemia
  
• Hypertriglyceridemia
  
• Stable Angina
  
• Prinzmetal Angina
  
• Peripheral Arterial Disease
  
• Acute Coronary Syndrome
  

Objectives for each condition:

• History taking and performing the physical examination
• Diagnostic and laboratory studies
• Formulating the most likely diagnosis
• Health maintenance, patient education, and preventive measures
• Clinical intervention
• Pharmaceutical therapeutics

Review the following conditions:

• Cyanotic vs. Acyanotic Heart Disease
  
• Atrial Septal Defect
  
• Ventricular Septal Defect
  
• Patent Ductus Arteriosus
• Coarctation of the Aorta
• Tetralogy of Fallot
• Transportation of the Great Vessels

Objectives for each condition:

• History taking and performing the physical examination
• Diagnostic and laboratory studies
• Formulating the most likely diagnosis
• Health maintenance, patient education, and preventive measures
• Clinical intervention
• Pharmaceutical therapeutics

Review the following conditions:

• Bacterial Endocarditis
  
• Acute Pericarditis
  
• Pericardial Effusion and Cardiac Tamponade
  

Objectives for each condition:

• History taking and performing the physical examination
• Diagnostic and laboratory studies
• Formulating the most likely diagnosis
• Health maintenance, patient education, and preventive measures
• Clinical intervention
• Pharmaceutical therapeutics

Review the following conditions:

• Abdominal Aortic Aneurysm
• Aortic Dissection
• Arterial Embolism
• Vascular Insufficiency

Objectives for each condition:

• History taking and performing the physical examination
• Diagnostic and laboratory studies
• Formulating the most likely diagnosis
• Health maintenance, patient education, and preventive measures
• Clinical intervention
• Pharmaceutical therapeutics

Review the following medications:

• Heart Rate and Contractility
  • Introduction to physiology
  • Digoxin
  • Dopamine
  • Dobutamine
  • Norepinephrine
  • Epinephrine
• Antiarrhythmics
  • Action Potential
  • Class IA Antiarrhythmics
  • Class IB Antiarrhythmics
  • Class IC Antiarrhythmics
  • Class II Antiarrhythmics
  • Class III Antiarrhythmics
  • Class IV Antiarrhythmics
  • Adenosine
• Antihypertensives
  • Calcium Channel Blockers
  • Alpha-2 Agonists
  • Alpha-1 Antagonists
• Congestive Heart Failure
  • Beta Blockers
  • ACE Inhibitors
  • ARBs
  • Aldosterone Antagonist
  • Ivabradine
  • Sacubitril/Valsartan
  • Thiazide Diuretics
  • Loop diuretics
• Coronary Artery Disease
  • Nitroglycerin
  • Aspirin
  • P2Y12 Receptor Antagonists
  • Glycoprotein IIb/IIIa Inhibitors
  • Thrombolytics
  • Cilostazol
• Anticoagulation
  • Factor Xa Inhibitor
  • Dabigatran
  • Heparin
  • Warfarin
• Hyperlipidemia
  • HMG-CoA Reductase Inhibitors (Statins)
  • Niacin
  • Fibric Acid Derivatives (Fibrates)

Objectives for each medication:

• Under stand relevant human physiology
• Know the mechanism of action
• Contraindications
• Adverse reactions (high-yield)
• Toxicity (if relevant)
• Information as to when the drug is used
• When the medication is first line, second line, and third line
• Clinical considerations (pearls for practice)