cardiacphysiological case study on patients

Case study on cardiovascular cases

1. Cardiac Physiology
A Case-based Review
By Sohin Patel, M.D.

2. Learning Objectives
•Understand basic cardiac physiology.
•Describe the effect of common anesthetics on
the normal and diseased heart.
•Devise an anesthetic plan based on disease-
specific hemodynamic goals.

3. Teaching Objectives
•Guide the student through the slide presentation,
answering any questions that may arise.
•Allow the medical student to answer the questions
asked within the slides and, with the assistance of
the slides following the question, go over the
relevant physiology and pathophysiology.
•The cases are all independent of each other and
should each take about 5-10 minutes to review.
•If a question remains unanswered, an attending or
textbook should be consulted.

4. CASE 1
•A 23 year old medical student with no PMH
presents for a laparoscopic appendectomy. He
is currently learning about cardiac physiology
and has many questions. He turns to you and
asks, “ What drugs are you planning on using
to put me under and how will they effect my
mean arterial pressure?”

5. CASE 1
•The most common drugs used to induce
anesthesia include benzodiazepines, opioids,
induction agents, paralytics, and inhalational
anesthetics.
•MAP=COxSVR.
•SVR is primarily affected by ANS activity.
•What independent variables determine affect
CO?

6. CASE 1
•CO = SV x HR. SV = EDV –ESV and thus is affected by preload,
afterload and contractility.
ddah.org.uk

7. CASE 1
•Preload reflects the stretch of ventricular
myofilaments produced by the LVEDV.
•Afterload is the pressure against which the LV
must propel blood. This pressure is affected by
the distensibility of the aorta, resistance of
peripheral arterial vasculature, and actions of
relected waves on central aortic circulation.
•Contractility is the intrinsic force of myocardial
contraction independent of preload, afterload,
or HR.

8. CASE 1
•Anesthetic agents alter MAP by effecting one or more of the
variables just discussed.
•Benzodiazepines generally have no effect on hemodynamics.
•Opiods decrease SNS activity, decreasing SVR and HR. The
effect on CO is most obvious in patients who are volume
depleted and negligible in patients with normal volume status
and no other medications.
•Most commonly used paralytic agents do not effect
hemodynamics. Some cause histamine release, resulting in
mild hypotension. Pancuronium, however, increases HR, BP
and CO due to a possible vagolytic and sympathomimetic
effect.

9. CASE 1
•Induction agents generally
decrease SVR and preload.
Etomidate effects these
parameters the least and is
therefore used to maintain
HD stability.
•Most inhalational agents
decrease SVR and increase
HR, causing little change in
CO. Halothane, however,
decreases CO by direct
myocardial depressant
effects.
Barash, Clinical Anesthesia (6
th
ed.)

10. CASE 1
•After answering his questions, you give him 2mg of
midazolam, which promptly brings a smile to his face
and precludes him from asking any more medical
questions.
•Induction is uneventful with fentanyl, lidocaine,
propofol and rocuronium.
•You maintain anesthesia with sevoflurane, and
reverse his paralysis with neostigmine and
glycopyrrolate.
•After a few hours of vomiting in the PACU, he is
discharged home without any other complications.

11. CASE 2
•A 60 year old gentleman with a PMH of
dyslipidemia and HTN presents for an elective
shoulder arthroscopy. He is an avid tennis player,
but his play has been limited due to shoulder
pain.
•While examining him prior to surgery, you hear a
systolic murmur radiating to the carotids, best
heard at the right upper sternal border. There is
also a delay between the 1
st
heart sound and the
carotid pulse.
•An EKG shows the following….

12. http://cardiophile.org

13. CASE 2
•EKG shows LVH with strain and left atrial
enlargement.
•Investigating further, he tells you that prior to
quitting tennis because of shoulder pain, he
experienced some tightness in his chest when
playing hard, but it ceased if he rested. He also
experienced two episodes of syncope in the past
year.
•You present this information to your attending, who
asks you what you are concerned about and whether
you should go ahead with surgery?

14. CASE 2
•Given the concern for severe AS, the elective case is
cancelled and further workup is performed.
•TTE confirms your suspicion of severe AS. The AVA is
0.8cm
2
and the valve is bicuspid. There is concentric
LVH and moderate LAE. No other abnormalities are
identified and preoperative cardiac cath shows
normal coronaries.
•The pt is scheduled for aortic valve replacement. You
happen to be scheduled for this case and your
attending asks how you plan to manage his
hemodynamics pre-bypass to maintain cardiac
output and avoid myocardial ischemia?

15. CASE 2
Barash, Clinical Anesthesia (6
th
ed.)
Pathophysiology of Aortic Stenosis

16. CASE 2
•Based on your stated goals, what anesthetic agents would be appropriate
for this patient and why?
Barash, Clinical Anesthesia (6
th
ed.)
PreloadFull
AfterloadMaintain coronary perfusion gradient by
keeping AoDP normal to high.
ContractilityMay need inotropic support if persistent
hypotension.
Rate Avoid bradycardia (decreased CO) and
tachycardia (ischemia)
Rhythm Sinus. May need cardioversion to maintain CO.

17. CASE 2
•Anesthesia is induced with a high dose fentanyl, lidocaine and
etomidate. The patient is paralyzed with rocuronium and
anesthesia is maintained with isoflurane.
•Some time after induction, you notice the EKG tracing below
on your monitor. The BP drops precipitously. Your attending
asks you why might this be an unstable rhythm in our patient
and what you would like to do about it?
drsvenkatesan.wordpress.com

18. CASE 2
•Atrial fibrillation with rapid ventricular response can cause
decreased BP in this pt for several reasons. Ventricular
hypertrophy increases MVO
2because of increased muscle
mass ( basal demand) and increased intraventricular systolic
pressure ( demand per beat).
•Ventricular hypertrophy also decreases diastolic compliance,
increasing the atrial kick’s contribution to LVEDV from 10% to
30-40%.
•So, the current rhythm will cause decreased CO secondary to
decreased SV and tachycardia can cause myocardial ischemia
with resulting systolic dysfunction.
•You decide to cardiovert the patient. How many joules and
what mode would you use?

19. CASE 2
•After successfully cardioverting with biphasic 100J in
sync mode, the pt is initially in SB with a HR in the
40s. Because stroke volume does not increase
sufficiently with bradycardia and diastolic
dysfunction, the CO and MAP remain low, but
improved from before.
•You give a small dose of ephedrine, improving both
the HR and BP. The rest of the case proceeds
uneventfully and the pt is discharged from the
hospital 4 days later.

20. CASE 3
•A 72yo gentleman with a h/o HTN, dyslipidemia, and
50pk-yr smoking history presents to the ER with
chest pain radiating to the L shoulder.
•His BP is 190/100 and an EKG shows 2mm ST
elevations in all precordial leads and I and aVL.
•He is given supplemental O2, morphine, and
nitroglycerin. The pain subsides somewhat but does
not resolve completely and EKG is unchanged.
•Based on the EKG findings, which coronary artery is
involved and what walls of the LV does this correlate
with?

21. CASE 3
•There are three main coronary
arteries, the left anterior descending,
circumflex, and right. The LAD and
circumflex arise from the left main.
•V1 and V2 correlate with the septum;
V3-V4 with the anterior wall; V5, V6, I
and aVL with the lateral wall; and II,
III, and aVF with the inferior.
•The septum and anterior wall are
supplied by the LAD, the lateral wall
by the left circumflex, and the
inferior wall by the right coronary.
http://www.cvphysiology.com
http://radiology.rsna.org

22. CASE 3
•The pt is taken to the cath lab and
angiography shows 90% left main, 50% mid
LAD, and 60% left circumflex lesions. An IABP
in inserted and the pt is taken for urgent
CABG.
•As you are preparing for the case, your
attending asks you, “What are the principal
determinants of myocardial oxygen demand
and coronary artery blood supply?”

23. CASE 3
•Of the determinants of O2 consumption, tachycardia
generates more demand than increases in contractility and
wall stress.
•The LV is perfused during diastole. RV perfusion is continuous.
Tachycardia also decreases diastolic filling time, leading to
decreased SV, CO and coronary artery perfusion.
Barash, Clinical Anesthesia (6
th
ed.)

24. CASE 3
Pressure relationships.
1-Aortic pressure
2-LV pressure
1a-decreased pressure distal
to stenosis
2a-increased LVEDP
Barash, Clinical Anesthesia (6
th
ed.)
•Coronary vascular reserve is normally 3-5 times higher than basal flow.
Intramyocardial arterioles regulate diastolic vascular resistance. With
stenosis in epicardial vessels, intramyocardial vessels dilate to maintain
basal flow, decreasing reserve. Metabolic factors mostly determine
coronary vascular tone, not SNS or stretch receptors.
•The LV subendocardial layer is most susceptible to ischemia because of
increased systolic intraventricular pressure.

25. CASE 3
•Your pt arrives to the OR and you notice the
above blood pressure tracing. He is no longer
having chest pain.
•What does point B represent and why did the
IABP relieve our patient’s chest pain?
http://www.nurse411.com

26. CASE 3
A-Assisted systole
B-Dicrotic notch
C-Diastolic augmentation
D-Assisted aortic EDP
E-Unassisted systole
F-Unassisted aortic EDP
-Increased coronary artery perfusion
-Reduced myocardial O
2 demand
http://www.nurse411.com
•The intraaortic balloon pump is positioned between the left
subclavian artery and renal artery takeoffs. The above tracing shows
the IABP set at 2:1. The balloon inflates when the aortic valve closes,
increasing AoDP, and deflates just prior to opening of the aortic valve.
•As can be seen by the highlighted portions of the curve above, the
IABP increases coronary artery perfusion and decreases myocardial
O
2demand.

27. CASE 3
•After attaching all monitors to the patient,
obtaining adequate IV access and pre-
oxygenating, you are ready to induce
anesthesia.
•What agents would you use and what are your
hemodynamic goals in terms of preload,
afterload, contractility, rate and rhythm?

28. CASE 3
Barash, Clinical Anesthesia (6
th
ed.)
PreloadKeep heart small. Decrease wall tension and
LVEDP. Increase perfusion pressure gradient
AfterloadHTN better than hypotension
ContractilityDepression (if LV function is normal)
Rate Slow
Rhythm Sinus

29. CASE 3
•To maintain HD stability on induction, high dose opioids are important due
to their lack of myocardial depression, reduction in HR, and blunting of
sympathetic response from laryngoscopy.
•Lidocaine also blunts the response to laryngoscopy, although doses of
2mg/kg must be used for this effect.
•Of the induction agents, etomidate maintains the most stable BP. Propofol,
however, can also be used with concurrently administered phenylephrine
to prevent the drop in SVR and MAP.
•Of the volatile anesthetics, isoflurane dilates coronary arteries the most,
although the clinical significance at <1 MAC is negligible. Volatile
anesthetics have the added benefit of protecting the myocardium from
ischemia and reperfusion injury and decreasing MI size.

30. CASE 4
•You are evaluating a patient for scheduled
MVR tomorrow. The pt is 45 yrs old with a h/o
bacterial endocarditis and remote IVDA.
•According to old records, he initially presented
to the ER 6 yrs ago with pulmonary edema.
TTE showed 1-2+ MR with valvular vegetations
and EF of 60% with no other abnl.
•TTE 2 weeks ago showed 3+ MR, left atrial
enlargement, LVESD of 45mm, and EF 55%.
EKG showed…

31. CASE 4
Ispub.com

32. CASE 4
•You call your attending, who has a reputation for
“pimping,” to discuss the case. As expected, he
has a list of questions he wants you to answer.
1. What is the difference between LVH in AS vs.
MR?
2. What classes of agents would you use to treat
acute MR?
3. Why has this patient’s MR worsened over time
even though his infective endocarditis was
treated appropriately?

33. CASE 4
•In chronic mitral regurgitation, eccentric hypertrophy of the LV develops,
as opposed to the concentric hypertrophy of AS.
http://www.cvphysiology.com
http://scielo.br

34. CASE 4
•Acute MR, as may present with bacterial endocarditis, MV
prolapse, or ruptured chordaeleads to increased volume in
the LV and LA.
•A certain percentage of the stroke volume, the regurgitant
fraction, is directed from the LV to the LA.
•The increased LAP from the increased volume is
transmitted to the pulmonary vasculature, causing
pulmonary HTN and edema.
http://www.h4heart.com

35. CASE 4
•To medically treat acute MR, the goals would be to increase forward
flow and decrease LA and LV volume, and hence LV and LA
pressures.
•If BP tolerates, afterload reducers such as SNP, diuretics such as
lasix, and inotropes such as dobutamine or milrinone would all be
helpful.
•A mildly tachycardic and hypotensive patient would be ideal.
•If the acute MR is able to be treated medically, pt’s may live for
years without any symptoms.
•The MR, however, worsens over time. At first, during the
compensated phase, ever-increasing LV volume dilates the LV.
Progressive dilatation eventually leads to LV dysfunction and
worsening MR.
•The MR worsens because progressive dilation of the LV and LA
increases the MV annulus, causing the leaflets to no longer coapt.

36. CASE 4
•Ideally, as in our patient, MVR should take place in
the transitional phase of MR, prior to development
of permanent LV dysfunction.
http://heartnet.bjmu.edu.cn

37. CASE 4
•The next day, you induce the pt successfully,
being careful to keep him slightly tachycardic
and mildly hypotensive.
•The valve is replaced successfully, however,
when attempting to come off bypass, the pt is
hypotensive. You give phenylephrine, which
does not improve the BP.
•Your attending is not surprised and asks you
why you think it is difficult to separate this pt
from bypass despite successful MVR.

38. CASE 4
•You realize that with the MV now fixed, the LV
no longer has a low-pressure vent (into the
LA) during systole.
•The increased afterload uncovers the existing
LV dysfunction. You start the pt on an inotrope
and are now able to separate from bypass
without much difficulty.
•The rest of the case is uneventful and your
pt’s LV function improves over the next few
days.