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addition to its typical workload. Conditions such as sepsis, anaphylaxis, or medication- induced vasodilation render blood vessels ineective at maintaining sucient tone
to guarantee adequate perfusion to end organs.3 Cardiac
dysfunction in sepsis is common and may manifest as
impaired uid responsiveness, decreased contractility,
and ventricular dilation. Anaphylaxis in the perioperative setting may be as high as 1 in 383 cases,4 although
the exact mortality rate is not known.5 Angiotensinconverting enzyme inhibitors may contribute to hypotension during anesthesia and have been reported as
possible contributors to cardiac arrest intraoperatively.6
All of these conditions are indicators of increased risk
when caring for a patient undergoing surgery.
In order for the heart to perfuse organs throughout
the body, adequate blood volume must be available to the
heart to pump. Several denitions for Preload exist, but
for our purposes the le ventricular end diastolic volume
(LVEDV) will serve as preload. Preload is aected by
venous pressure as well as venous return. Hypovolemia
due to blood loss, inadequate uid decit replacement,
or medication eect can dramatically decrease preload,
leading to hemodynamic instability. Estimating preload is both critical and dicult, and may be achieved
using transesophageal echocardiography (TEE), pulmonary artery occlusion pressure, central venous pressure,
pulse pressure variation, and many other measurements.
Although the reliability of some methods for assessing
preload continues to be questioned,
7– 9
the anesthesiologist should be familiar with these techniques and possess the ability to obtain measurements and interpret the
results in order to rule out a diagnosis of hypovolemia
and evaluate preload status. Most of these measurement
techniques assess response to a uid challenge rather than
an actual value for the volume of blood in the le ventricle at end diastole, and this fact should not be forgotten at the bedside when uid administration decisions
are being made.
In addition to the pipes, the other Ves sel s we discuss
are the coronary arteries, which supply blood directly to
the heart. Disruption in blood ow through the coronaries due to hypotension or hypoperfusion impedes the
myocardium from receiving adequate oxygen and thereby
produces an inability to supply enough energy for the
heart to meet demand to perfuse the body. Blockages due
to plaque buildup or rupture, lack of blood ow from
hypotension, or tachycardia increasing oxygen demand
can all cause ischemia to occur as a result of myocardial
oxygen supply/ demand mismatch. Detection of ischemic
changes with TEE and/ or electrocardiography (ECG)
may be of great importance when confronted with an
unstable patient in the perioperative period. e detection
of myocardial ischemia using leads II, V4, and V5 perioperatively has a sensitivity of 96%.10 e use of continuous
ECG in the operating room (OR) is now considered the
minimal standard of care, and it may oen demonstrate
the rst signs of ischemia intraoperatively. More recently,
there has been a suggestion that detection of troponin
leaks in patients with suspected ischemia in the perioperative period might be advantageous,11 although the usefulness of this test in the OR may be limited due to timing
of detection, which currently must be post hoc, by denition. Echocardiography is superior to ECG for detecting
ischemia and may also assist with making a diagnosis of
MI in patients with cardiac arrest.
12
e conduction of electrical activity through the heart
constitutes the Voltage component of our aide memoire
for dierential diagnosis of cardiac arrest in the OR. e
conduction system regulates the rate and also the rhythm
of the heart. e anesthesiologist must determine whether
disturbances in either the rate or rhythm are contributing to
the patient’s instability. If the patient is hemodynamically
unstable, algorithms directed at whether or not the patient
has a pulse are used rst. Pulseless dysrhythmias include
asystole, pulseless electrical activity, ventricular brillation,
and ventricular tachycardia. Pulsatile rhythms may include
symptomatic bradycardia and narrow versus wide complex
tachycardias. Identifying the correct rhythm is crucial, as
the treatment is reliant on the rhythm, but diagnosis of the
underlying cause of the dysrhythmia should not be forgotten. e potential causes are discussed in detail later in this
chapter.
Valves promote unidirectional blood ow between
the atrium to the ventricle and from the ventricle out
of the heart. In cases where a valve is diseased or injured,
blood ow may become bidirectional, obstructed, or both.
Understanding the physiologic changes with a stenotic versus regurgitant valve and the appropriate intervention are of
the utmost importance when treating an unstable patient.
An anesthesiologist’s ability to evaluate valves using TEE is
integral for patients with diseased valves and during surgical
interventions on valves.
13
Outside of these six components, other causes of cardiac collapse must be considered. Some of these include
aortic dissection, drug overdose, toxin exposure, hypertensive crisis, disseminated intravascular coagulopathy, and
sickle cell crisis. e diagnosis and treatment for all of the
aforementioned conditions is elaborated in the remainder
16 PART II. CARDIAC CRISES
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17
Figure 4.1 Bradycardia algorithm.
inadequate for clinical situation or
Heart rate < 60 and/or rapidly falling
Note: heart rates between 40 and 60 are common in adults under general anesthesia
- Check surgical field/ anesthetic: Hypervagal vs hypovolemia?
- Check oximeter, capnometry, skin and field blood color R/O hypoxia!
- Could this be auto-PEEP?
- Check ST segment and T-wave
- Could this be gas/air embolism? thrombo/fat embolism?
- Could this be high spinal?
- Could this be local anesthetic toxicity?
- Could this be hyperkalemia?
- Monitor ECG (identify rhythm), blood pressure, oximetry, capnography
Signs or symptoms of poor perfusion caused by the bradycardia?
(e.g. acute altered mental status, ongoing chest pain, or other signs of shock)
Adequate
Observe/Monitor
- Search for contributing
causes
- Consider expert
consultation
Differential Diagnosis of
Bradycardia
Hypoxia
Hypervagal
Hypovolemia
Hyperkalemia/Hypokalemia
Hydrogen lon (acidemia)
Hypothermia
Hypoglycemia
Malignant Hyperthermia
Tamponade
Tension pneumothorax
Trauma
Thrombosis/embolus, pulmonary
Thrombosis, coronary
QT prolongation
Toxins
Pulmonary hyperTension
BRADYCARDIA
Perfusion?
Blood pressure?
Poor
If severe hypotension, persistent
poor perfusion, or low ET CO2
(<15mm Hg): start CPR
- Administer Oxygen, Assist
ventilation, Intravenous fluids wide
open, and secure the airway
AVOID hyperventilation!
- Consider atropine 0.5 mg IV while
awaiting pacer. May repeat to a total
dose of 3 mg. If ineffective, begin
transcutaneous pacing
- Consider IV bolus epinephrine 10 to
100 mcg. If response, consider
epinephrine (0.05 to 0.10 mcg/kg/min)
or dopamine (2 to 10 mcg/kg/min)
infusion while awaiting pacer or if pacing
is ineffective.
- Prepare for transcutaneous pacing:
use without delay for high-degree block
(type II second-degree block or thirddegree AV block). Esophageal pacing
appropriate with narrow QRS
- Consider CVL, arterial line
- Prepare for transvenous pacing
- Treat contributing causes
- Consider expert consultation
Y
Specific
algorithm
in addition
to below
of this chapter, but for now we consider some of the differences between the American Heart Association (AHA)
Advanced Cardiac Life Support (ACLS) and a more
anesthesia- centric ACLS approach.
Outside of the perioperative setting, ACLS is oen initiated on a person suering an unwitnessed and unmonitored cardiac arrest. As was previously mentioned, in the
OR when a patient suers cardiac arrest several monitors
relaying real- time vital signs are available both before and
during the inciting event. is can be viewed as an advantage when formulating a dierential diagnosis and making a
more directed treatment plan. An ECG provides a rhythm
for the anesthesiologist to analyze. Pulse oximetry gives the
anesthesiologist oxygen saturation throughout the arrest.
INTRODUCTION TO PERIOPERATIVE CARDIAC URGENCIES AND EMERGENCIES 17
More advanced monitoring such as TEE, arterial cannulation, and pulmonary artery catheterization can provide
clues when evaluating the patient for PE, MI, hypovolemia,
and many other causes of cardiac collapse. End- tidal carbon
dioxide may assist with diagnosis and also help to evaluate the eectiveness of chest compressions during cardiopulmonary resuscitation. In addition, access to the various
treatment options is readily available, enabling the anesthesiologist to give medications intravenously and/ or deliver
shocks in a shorter time period than in the eld. Given
these advantages, one would assume an anesthesiologist
would act quickly when presented with an unstable patient.
is is not always the case, as sometimes clinicians may fail
to recognize early signs and symptoms of imminent cardiac
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Tachycardia
- Give O2
- Monitor EKG, blood pressure, oximeter, capnometry
- Could this be:
-light anesthesia?
-hypovolemia?
-hyperthermia?
-early hypoxia or hypercapnea?
-auto-PEEP?
- Perform Echo or TEE if possible
- Verity or obtain IV access
- Obtain 12 lead EKG/rhythm strip
- Measure QRS
Narrow
Narrow QRS
Is the rhythm regular?
Y
Altered mental status?
N
N
Chest pain?
Hypotension?
Wide (>0.12 sec)
Y
A: Assess Airway
B: Hypoventilation
C: Cardiac output/preload
D: Drugs (anaphylaxis/MH)
- Perform Immediate
Synchronized Cardioversion
- Verity or obtain IV access
- Consider expert consultation
- If patient becomes pulseless, see
Comprehensive algorithm
Wide QRS
Is the rhythm regular?
- Regular
- Consider vagal maneuvers
- Give adenosine 6 mg IV push
- II no response, give adenosine
12 mg IV push
Convert?
Y
- Likely re-entrant SVT
- Observe for recurrence
- Treat recurrence with
adenosine or longer acting AV
node blockers (e.g, beta
blocker or dilltiazem
- Irregular
- atrial fibrillation vs atrial flutter
vs MAT
- low ejection fraction or severe
hypotension: load Amiodarone
150 mg IV over 10 min
- normal EF and acceptable BP-
beta blocker or calcium
channel blocker
N
- If rhythm does Not convert, likely
atrial flutter, EAT, or junctional
tachycardia
- Flate control with beta blocker or
calcium channel blocker, consider
infusion
-Reevaluate and treat possible
underlying causes
Reconsider A, B, C, D
from above
Y
- Regular
- if Ventricular
tachycardia or
uncertain rhythm
give Amiodarone
150 mg IV over min
and Calcium
choloride 1 gm IV
- Amio
alternative
Lidocaine 1-1.5
mg/kg IV Q 3-5
min x3
- Prepare for
synchronized
cardioversion
- If SVT with
aberrancy, give
adenosine 6 or 12
mg IV push,
N
- Irregular
- If atrial fibrillation with
aberrancy, see irregular
narrow complex
tachycardia
- If Torsades-de-Pointes,
give Magnesium
sulfate 2 g IV over 5
minutes (esp if patient
had baseline prolonged
QT interval). Consider
repeat dose.
- If pre-excited atrial
fibrillation (AF+WPW),
consider amiodarone
150 mg IV over 10
min and expert
consultation
Figure 4.2 Tachycardia algorithm.
failure. And this may lead to failure to rescue a patient suffering from a severe adverse event.
The likely underlying causes of cardiac arrest in the
perioperative setting differ from those outside of the
OR. In addition to the H’s and T’s listed in the AHA
ACLS,15 Moitra et al.14 rightfully suggest Hypervagal,
Malignant Hyperthermia, QT prolongation, and
Pulmonary hyperTension to be included in the anesthesiologist’s differential diagnosis list. Patients are exposed
to multiple different medications and anesthetic agents
18 PART II. CARDIAC CRISES
14
cause cardiac arrest. Although anaphylaxis may also
occur outside of the OR, several medications administered to patients, particularly nondepolarizing muscle
relaxants and antibiotics, must be considered in the perioperative setting. Volatile agents and succinylcholine
may trigger malignant hyperthermia in the anesthetized
patient. Conditions such as hypovolemia or gas embolism are much less likely to occur outside of the OR, but
should be on the differential depending on the operation
perioperatively, and these compound or even ultimately
LV Shock
RV Shock
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19
Figure 4.3 LV Shock algorithm.
Hypotensive?
Perform Echo/
TEE in intubated patient
Y
Decrease
PEEP
Check CVP
and
SPV or PPV
CVP 12-22
SPV/PPV < 12%
Check SVR and
pulse pressure
N
CVP < 12 mmHg
or SPV/PPV >12%
low SvO2 or ScvO2
SPV/PPV>15%**
wide pulse pressure
narrow pulse pressure
SVR > 1600
or narrow pulse
pressure
CVP > 22
SVR < 800
or
SVR > 1000
or
Afterload Reduction
Fenoldopam
Nitroprusside
Nesiritide
Hct < 27-32?
R/O tamponade
R/O tension PTX
Vasopressin
Norepinephrine
Epi ± Dobutamine
Phenylephrine
MAINTAIN SVR < 800
Dobutamine
Epinephrine
IABP
VAD
ACEi
Y
N
pRBC
Plasma
Expander
Figure 4.4 RV Shock algorithm.
Hypotensive?
Perform Echo/
TEE in intubated patient
Y
Give O2
Decrease PEEP
Hypovolemic?
Fluid Responsive?
e.g, CVP < 12-16?
N
CVP > 20
SVO2 or ScvO2 <65%**
Known or Suspected
Increased PVR?
Y
Give O2
consider Milrinone ± Vasopressin
iNO
Hct < 27-32?
Y
? Decreased
coronary perfusion?
Phenylephrine
Norepinephrine
Vasopressin
Note: these
medications may
increase PVR
Y
N
R/O tamponade?
R/O tension pneumothorax?
RV contractility?
Y
pRBC
Plasma
Expanders
Diminished
Y
Dobutamine
Milrinone
Epinephrine
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Prepare for DL
Prepare LMA
Preform DL during
CPR
ETT
Success?
N
Request 20 sec pause
ETT
Success?
N
LMA in
Ventilation
Adequate?
N
NY
Y
Done!
Y
Done!
Y
step-up in capnograph
Adequate
Mask
Ventilation?
ROSC?
+ carotid pulse
or
+ Aline/pleth
or
Y
Prepare for DL,
await next
scheduled pause
DL during pause
T = 20 sec
ETT
Success?
N
Resume CPR
Change operator,
(change tools)
mask ventilation
await scheduled
pause
Plan
Intubation
Y
Done!
Continue CPR
Alternative
Figure 4.5 Airway algorithm.
Change Tools/Operator
LMA out/DL during CPR
ETT
Success?
N
Request 20 sec pause
ETT
Success?
N
Invasive Airway
Y
Done!
Y
Done!
N
Done...
and information available from continuous intraoperative monitors.
Unlike the conventional AHA ACLS approach, the
treatments for dierent cardiac arrest scenarios in the perioperative period are not evidence based, but instead are suggested protocols derived from clinical experience. Cardiac
arrest in the OR is still a rare occurrence, with estimates of
up to only 19.7 out of 10,000 anesthetics.16 is makes it
dicult to conduct studies and provide evidence behind
Note:
Change from 30:2
preintubation
to
8-10 breaths/minute
asynchronous
postintubation
the appropriate treatment of the various causes for cardiac
arrest perioperatively. Anesthesia- centric ACLS algorithms
modify the accepted AHA ACLS algorithms (see Figures
4.1, 4.2, 4.3, 4.4, 4.5, and 4.6,).14 e remaining chapters
in this section on cardiac crises focus on some of the major
causes of severe cardiac instability and arrest in the OR and
provides details on using our monitoring systems to make
a diagnosis and treat the underlying cause of cardiac arrest
both swily and correctly in the perioperative setting.
20 PART II. CARDIAC CRISES
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21
Comprehensive Algorithm
- Check surgical field/anesthetic: Hypervagal vs hypovolemia?
- Check EKG, oximeter, capnometry, skin and field blood color, quick-check circuit
- Start CPR, call for help, defibrillator
- Hold surgery, discontinue anesthesia, ventilate with 100% O2, IVs wide open
- Check ST segment and T-wave
- Could this be gas/air embolism? thrombo/fat embolism?
- Could this be local anesthetic toxicity?
- Could this be hyperkalemia?
- Confirm EKG cardiac arrest: A-line tracing, pulse, plethysmograph, capnometer
- Start CPR Titrate to ET CO2 of > 20mm Hg, Diastolic BP > 40mm Hg
- Establish airway, Avoid Hyperventilation!
- Perform Echocardiography ASAP
Shockable Not Shockable
VF/VT
- Give 1 Shock: 200-360 J Biphasic
- Resume CPR immediately
1
- If VT: Calcium chloride 1 gram IV
Check capnometer for CO2.
If present hold CPR and check rhythm
- Continue CPR while defibrillator is charging
- Give 1 Shock: 200-360 J Biphasic
- Resume CPR immediately
- Eplnephrine 1 mg IV Repeat Q 3-5 min
- May replace 1 dose of EPi with 40 U Vaso IV
- Continue CPR while defibrillator is charging
- Give 1 shock: 200-360 J Biphasic
- Resume CPR immediately
- Consider anti-arryhthmics
- Amiodarone 300 mg IV or
- Lidocaine 1-1.5 mg/kg IV Q 3-5 min x3
- Consider Magnesium sulfate 2 grams IV
for? Torsades-de-pointes (esp in patients
with baseline prolonged QT)
Shockable rythm?
Y
Check rhythm
Shockable?
Shockable
Check rhythm
Shockable?
No
- Continue CPR
- Epinephrine 1 mg IV, repeat Q 3-5 min
May replace 1 dose of EPi with 40 Units
Vaso IV
- Consider Calcium choloride if hyperkalemia
2
No
- If Asystole, go to Box 2
- If not pulse, go to Box 2
- If pulse present, begin
post-resuscitation care
is in the differential
- If PEA:
Could this be hypovolermia?
Could this be tamponade?
Could this be tension pneumothorax?
Could this be auto-PEEP?
Could this be an embolism?
No
Asystole/PEA
Check rhythm
Shockable?
Shockable
Shockable
Go to Box 1
Figure 4.6 Comprehensive algorithm.
REFERENCES
1. Weissman PF, et al. Perioperative heart failure in noncardiac surgery.
UpToDate. 2012 March 28. Accessed March 3, 2015.
2. Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation. 2008;117(5):686– 97.
doi: 10.1161/ CIRCULATIONAHA.106.613596.
3. Zanotti- Cavazzoni SL, Hollenberg SM. Cardiac dysfunction in
severe sepsis and septic shock. Curr Opin Crit Care. 2009;15(5):
392– 7. doi: 10.1097/ MCC.0b013e3283307a4e.
INTRODUCTION TO PERIOPERATIVE CARDIAC URGENCIES AND EMERGENCIES 21
4. Savic LC, Kaura V, Yusaf M, et al.; Anaesthetic Audit and Research
Matrix Yorkshire. Incidence of suspected perioperative anaphylaxis: a
multicenter snapshot study. J Allergy Clin Immunol Pract. 2015 Feb
13. pii: S2213- 2198(15)00018- 5. doi: 10.1016/ j.jaip.2014.12.016.
[Epub ahead of print].
5. Dewachter P, Mouton- Faivre C, Emala CW. Anaphylaxis and
anesthesia: controversies and new insights. Anesthesiology. 2009;
111(5):1141– 50. doi: 10.1097/ ALN.0b013e3181bbd443.
6. Goodman SM, Krauser D, Mackenzie CR, Memtsoudis S. Cardiac
arrest during total hip arthroplasty in a patient on an angiotensin
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receptor antagonist. HSS J. 2012;8(2):175– 83. doi: 10.1007/
s11420- 011- 9225- 0. Epub 2012 May 11.
7. Mohsenin V. Assessment of preload and uid responsiveness in
intensive care unit. How good are we? J Crit Care. 2015 Jan 8. pii:
S0883- 9441(15)00006- 4. doi: 10.1016/ j.jcrc.2015.01.004. [Epub
ahead of print].
8. Sasai T, Tokioka H, Fukushima T, et al. Reliability of central venous
pressure to assess le ventricular preload for uid resuscitation in
patients with septic shock. J Intensive Care. 2014;2(1):58. doi:
10.1186/ s40560- 014- 0058- z. eCollection 2014.
9. Levitov A, Marik PE. Echocardiographic assessment of preload
responsiveness in critically ill patients. Cardiol Res Pract. 2012;
2012:819696. doi: 10.1155/ 2012/ 819696. Epub 2011 Sep 12.
10. London MJ, Hollenberg M, Wong MG, et al. Intraoperative myocardial ischemia: localization by continuous 12- lead electrocardiography. Anesthesiology. 1988;69(2):232– 41.
11. Biccard BM. Detection and management of perioperative myocardial ischemia. Curr Opin Anaesthesiol. 2014;27(3):336– 43. doi:
10.1097/ ACO.0000000000000071.
12. Memtsoudis SG, Rosenberger P, Loer M, et al. e usefulness
of transesophageal echocardiography during intraoperative cardiac arrest in noncardiac surgery. Anesth Analg. 2006;102(6):
1653– 7.
13. Lee MS, Naqvi TZ. A practical guide to the use of echocardiography in assisting structural heart disease interventions. Cardiol Clin.
2013; 31(3):441– 54. doi: 10.1016/ j.ccl.2013.04.004. Epub 2013
Jun 17.
14. Moitra VK, Gabrielli A, Maccioli GA, O’Connor MF. Anesthesia
advanced circulatory life support. Can J Anaesth. 2012;59(6):
586– 603. doi: 10.1007/ s12630- 012- 9699- 3. Epub 2012 Apr 21.
15. Field JM, Hazinski MF, Sayre MR, et al. Part 1: executive summary: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2010;122(18 Suppl 3):S640– 56. doi: 10.1161/
CIRCULATIONAHA.110.970889.
16. Ellis SJ, Newland MC, Simonson JA, et al. Anesthesia- related cardiac arrest. Anesthesiology. 2014;120(4):829– 38. doi: 10.1097/
ALN.0000000000000153.
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23
5.
MYOCARDIAL ISCHEMIA
Jeremy Bennett and Kara Siegrist
CLINICAL CASE
dominant circulation, the LCx supplies the AVN and SAN
blood supply. e LAD supplies the anterior wall of the
A 57- year- old male with a past medical history of hypertension, hyperlipidemia, diabetes mellitus, and coronary artery
disease presents for right carotid endarterectomy for 75%–
99% occlusion of the vessel. Anesthetic plan is for general
endotracheal anesthesia with arterial line placement and
peripheral intravenous access.
heart and anterior two- thirds of the interventricular septum
via septal perforators and diagonal branches. Venous blood
returns to the right atrium via the coronary sinus, which
empties the le ventricle and signicant portions of the right
ventricle. Additional venous drainage is performed via the
anterior cardiac veins, which drain directly into the right
atrium, with a small portion of blood being returned directly
PATHOPHYSIOLOGY OF DISEASE STATE
ANATOMY
e myocardium is supplied by the right coronary artery
(RCA) and le main coronary artery (LMCA) arising from
the right and le sinus of Valsalva respectively, as demonstrated in Figure 5.1. e LMCA is a relatively short vessel
that divides into the le anterior descending (LAD) branch
and the le circumex (LCx) branch. Occasionally a third
vessel arises from the LMCA known as the ramus intermedius, which supplies the high lateral wall of the le ventricle.
into the le heart via the thebesian veins.
MECHANISM
Myocardial ischemia occurs when the myocardial oxygen
supply is not adequate to meet oxygen demand. Myocardial
oxygen demand is determined by three factors: wall tension,
heart rate, and contractility. Heart rate both aects myocar-
dial oxygen consumption and decreases diastolic perfusion
time, thus tachycardia can have multiple negative eects on
myocardial oxygen balance. Wall tension is determined by
the Law of Laplace:
Coronary dominance is determined by arterial contribution of
the posterior descending artery (PDA), with the RCA demon-
T = PR/ 2h
strating dominance in 85%– 90% of people. In the other 15%
of patients the LCx supplies the PDA, with a small portion of
patients having codominance due to contributions from both
the RCA and LCx to the inferior septal perforator branches.
Where T = wall tension, P = intraventricular pressure,
R = ventricular radius, and h = ventricular wall thickness.
Wall tension is aected by preload and aerload, with
increases in both resulting in increased wall tension.
VENTRICULAR BLOOD SUPPLY
e RCA supplies the inferior (posterior) wall of the le ventricle, the anterior and posterior walls of the right ventricle,
and the posterior third of the interventricular septum via the
PDA. Additionally, the atrioventricular node (AVN) is supplied in 90% of patients via the conus branch, and the sinoatrial node (SAN) in 60% of patients. e LCx runs through
the atrioventricular groove and supplies the lateral wall of the
le ventricle via obtuse marginal arteries. In patients with le
Myocardial Oxygen Supply
Myocardial oxygen supply is determined by coronary blood
ow autoregulation, coronary ow reserve, and arterial oxy-
gen content.
Coronary Blood Flow
Coronary blood ow (CBF) is composed of coronary
perfusion pressure (CPP) and coronary vascular resistance
23
24
Pulmonary
sinus node
ANTERIOR VIEW
Right atrial
appendage
Phasic coronary blood flow
Aortic pressure
Time (sec)
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veins
Circumflex
branch of left
coronary artery
Great
cardiac
vein
Coronary
sinus
POSTERIOR VIEW
Superior
vena cava
Aorta
Right
coronary
artery
Anterior
coronary
veins
Figure 5.1 Anatomy of coronary ar terial and venous circulation.
Reprinted with permission from Koeppen & Statton: Berne and Levy
Physiology, 6th ed.
Left atrium
Superior
vena cava
Area of
Inferior
vena cava
Right
coronary
artery
Posterior descending
branch of night
coronary artery
Left coronary
artery
Circumflex
branch
Descending
branch
Great
cardiac
vein
Pulmonary
artery
to ow. Normal coronary blood ow is approximately 5%
of total cardiac output, or roughly 250 cc/ min. Coronary
perfusion pressure equals aortic diastolic pressure minus
le ventricular end diastolic pressure (CPP = AoDBP
– LVEDP). Resistance to ow is dependent on coronary
vascular tone and patency of the vessels. During systole, particularly in the le ventricle, subendocardial pressures reach
systemic pressure, resulting in transmitted pressure across
the blood vessel. is results in near absence of eective forward ow in the le ventricle with dependence on diastole
for forward blood ow, whereas the right ventricle receives
arterial ow in both systole and diastole (Figure 5.2).
Coronary blood ow is maintained relatively constant over a range of pressures, with maximal vasodilation occurring at lowest pressures. is is accomplished
by adjustments in vascular diameter related to myogenic
and metabolic demands, known as autoregulation.1 e
120
100
(mm Hg)
80
100
80
60
40
20
0
(mL/min)
15
10
5
0
0.2 0.4 0.6
Figure 5.2 Pressure tracings of left and right ventricular blood ows as
compared to aortic systolic and diastolic pressures. The left ventricle
primarily receives blood ow during diastole due to reduced systolic
coronary blood during ventricular contraction. In contrast, the right
ventricle receives coronary blood ow during both systole and diastole.
SOURCE: Reprinted with permission from Koeppen & Statton: Berne and Levy Physiology,
6th ed.
Left
coronary
artery
Right
coronary artery
0.8 1
endocardium of the heart is most susceptible to autoregulatory failure and reduction in blood ow because of
transmural variations in autoregulation. Subendocardial
autoregulation has been demonstrated to be stable in
normal animals at mean arterial pressures (MAPs) of 40
mmHg.
2,3
Pressures below this result in autoregulatory
failure and subendocardial ischemia. Due to alterations in
autoregulation with coronary artery disease (CAD), failure to maintain vascular patency and CBF begins to occur
at higher MAP.
Coronary Vascular Reserve
e dierence between autoregulated ow and maximal
coronary artery blood ow is the coronary vascular reserve.
Reduction in cross- sectional area of a blood vessel results
in vasodilation to maintain metabolic needs. Reduction
in pressure across a stenotic lesion occurs and can result
in signicant changes to CBF, as ow is proportional to
radius to the fourth power (Poiseuille’s law). While the
blood supply is maintained, however, the vascular reserve is
decreased. As the eective coronary intraluminal opening is
reduced, autoregulation may be maximal and coronary vascular reserve is negated. Increases in heart rate may result in
autoregulatory failure at higher MAP, resulting in increased
24 PART II. CARDIAC CRISES
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25
susceptibility to subendocardial or transmural ischemia in
patients with CAD.
due to reduced diastolic lling time as well as increases
in myocardial oxygen demand. Because of this, the le
ventricular subendocardium does not receive blood ow
Arterial Oxygen Delivery
Arterial oxygen delivery is determined by oxygen content
and CBF. Arterial oxygen content is determined by the
equation:
during systole, and therefore is more vulnerable than
other endocardial layers to ischemia.8 e right ventricle
is not able to generate as high pressures as the le ventricle, thus is perfused both during systole and diastole
and depends mostly on mean arterial pressure for its per-
CaO2 = 1.34 × Hg × oxygen saturation × (0.0031 × PaO2)
ere are four primary determinants of coronary blood
ow: perfusion pressure, myocardial compression, metabolism, and neurohumoral control. At rest, coronary extraction of oxygen is at near maximal capacity, around 80%,
giving the heart the highest arterial- venous O2 dierence of
any organ. us, in times of increased demand, the heart
compensates by increasing ow via coronary vasodilation
mediated by autoregulatory mechanisms. Vasodilation
occurs by chemical and neural mediators including hypoxia,
hypercarbia, acidosis, adenosine, nitric oxide prostaglandins, and vagally mediated dilation.
4,5
Myocardial infarctions (MIs) are dened by myocardial cell death secondary to prolonged ischemia and can be
caused by factors that increase myocardial oxygen demand
or decrease oxygen supply. Myocardial oxygen supply is
decreased by coronary occlusion (platelet aggregation and
thrombus formation at the site of plaque rupture, vasospasm, etc.), hypotension, tachycardia (less diastolic coronary perfusion time for le ventricle), and hypoxemia.
ere is a signicant debate over the exact mechanism
of perioperative MI. For most MIs that lead to a patient
requiring cardiac revascularization, most ischemia results
from atherosclerotic plaque rupture and thrombus formation, causing a transient or prolonged obstruction to ow
through coronary arteries.6 Plaques that accumulate slowly
over time can generally be compensated for by vessel dilation and creation of collateral blood vessels. However, most
perioperative ischemia is believed to result from stable atherosclerotic plaque that, in the setting of increased myocardial oxygen demand, result in a supply- demand mismatch
(type 2 MI). s In patients with sucient collateralization,
complete total occlusion of a coronary artery may result in
little to no impairment of blood supply.7 However, acute
problems can arise if plaque rupture occurs with thrombus
formation and acute occlusion occurs before eective collateralization has occurred.
Acute coronary syndromes result due to sudden
decreases in CBF. e le ventricle is perfused mostly
during diastole due to compression of the coronary arteries during systole. Tachycardia reduces eective CBF
fusion gradient.
ANGINA PECTORIS AND
MYOCARDIAL INFARCTION
Angina pectoris is most oen described as precordial chest
pain, oen precipitated by physical exertion and stress, and
is oen relieved by rest or nitrates. Angina can be classied as chronic stable angina or acute unstable angina.
Regardless of type, it is oen due to atherosclerotic heart
disease with reduction in CBF to areas of the heart. Angina
can also occur in patients without CAD, such as in aortic
stenosis, severe le ventricular hypertrophy, vasospasm,
marked anemia, markedly elevated metabolic requirement,
or paroxysmal tachycardias. Patients oen report a sense
of chest tightness, squeezing, burning, or choking rather
than sharp pain. e location is traditionally described as
behind or to the le of the sternum and may radiate down
the le arm, though presentation is markedly variable,
with women expressing “typical symptoms” only about
63%–70% of the time.
9
Angina pectoris can be classied as chronic stable or
unstable angina. Chronic stable angina is chest pain that
is stable in presentation, meaning the degree of exertion
and stress that precipitate angina remains relatively stable
over time. ese patients likely have CAD, but of a degree
that collateralization may have occurred or the degree of
stenosis does not represent a signicant reduction in blood
ow. Patients with unstable angina are considered to have
ischemia that is acute in nature or present with a sudden
change and/ or worsening of chronic stable angina pain.
Unstable angina is considered part of the acute coronary
syndrome.
Acute coronary syndrome comprises unstable angina,
non ST- elevation MI (NSTEMI), and ST- elevation MI
(STEMI). Acute coronary syndrome can be diagnosed by
three presentations: (1) rest angina that last for 20 minutes or more, (2) new- onset angina that limits activity, or
(3) an increase in angina beyond normal “chronic” presentation. Unstable angina and NSTEMI dier based on
whether the degree of myocardial ischemia results in tissue
damage and enzyme leak. Myocardial infarctions can be
MYOCARDIAL ISCHEMIA 25
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