Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 911 - файл
.pdf
26
https://t.me/medicina_free
broken down into two broad categories: non- ST elevation MI (NSTEMI) and ST- elevation MI (STEMI). e
NSTEMI/ unstable angina as dened by the American
BOX 5.1 REVISED CARDIAC RISK INDEX
1. History of ischemic heart disease
College of Cardiology is the clinical syndrome associated
with increased risk of cardiac death and subsequent MI10
and demonstrates ST depression or T wave inversion on the
electrocardiogram (ECG) with positive cardiac biomarkers
2. History of congestive heart failure
3. History of cerebrovascular disease (stroke or transient
ischemic attack)
(CK, CKMB, troponin I). Changes in the ECG need not be
present for diagnosis, especially if anginal equivalent is present with positive biomarkers. e NSTEMIs are most com-
4. History of diabetes requiring preoperative insulin use
5. Chronic kidney disease (creatinine > 2 mg/ dL)
monly caused by erosion of an intraluminal atheromatous
plaque with subsequent cascade of inammatory mediators
and thrombogenesis leading to decreased coronary blood
6. Undergoing suprainguinal vascular, intraperitoneal, or
intrathoracic surgery
ow to the subendocardium.1 Other less common causes of
NSTEMIs include dynamic obstruction or spasm of a coronary artery, also known as Prinzmetal’s angina; severe nar-
Risk for cardiac death, nonfatal myocardial infarction, and nonfatal cardiac arrest:
0 predictors = 0.4%, 1 predictor = 0.9%, 2 predictors = 6.6%, ≥ 3 predictors = > 11%
rowing without spasm or thrombus, such as instent stenosis
aer percutaneous coronary intervention; coronary artery
dissection; or extrinsic compression.
1
e STEMI is the syndrome of ST segment elevation
on the electrocardiogram with myocardial necrosis characterized by increased cardiac enzymes due to transmural
myocardial infarction.1 New- onset le bundle branch block
is also dened as the equivalent of a STEMI. Changes in
intraperitoneal, or intrathoracic surgeries. Depending on
the number of positive predictors (0– ≥3) the risk for peri-
operative cardiac complications is estimated at 0.4%, 0.9%,
6.6%, and >11%, respectively.14 e RCRI is a useful tool
for assessing cardiac risk in stable patients presenting for
noncardiac surgery.
ECG may be delayed and can aect diagnosis and treatment
of patients with NSTEMI and STEMI. Bundle branch and
paced rhythms can aect initial management, particularly
in the acute setting.
1,13
ASSESSMENT OF THE PATIENT: PRESENTING
SIGNS AND SYMPTOMS
RISK
Ischemic heart disease has both modiable and nonmodiable risk factors. e nonmodiable factors include increasing age, male gender, family history of ischemic heart
disease. Modiable risk factors include smoking, hyperlipidemia, hypertension, obesity, diabetes mellitus.
e type of surgery can also inuence the risk of myocardial infarction in the perioperative time period. High-
Myocardial infarction under general anesthesia can be difcult to diagnose, because the patient is unable to communicate typical symptoms such as chest pain or shortness of
breath. Hemodynamic instability may ensue following a
myocardial infarction and may be a clue to the diagnosis.
Regional wall motion abnormalities on transesophageal or
transthoracic echocardiogram are the most sensitive indicator of ischemia, followed by ECG changes and hemodynamic uctuation.
15
risk surgeries include aortic and major vascular procedures.
Intermediate- risk surgeries include carotid endarterectomy,
head and neck surgery, intraperitoneal procedures, intrathoracic procedures, orthopedic procedures, and urologic
procedures.
e Revised Cardiac Risk Index (RCRI) provides risk
stratication for perioperative cardiac adverse events based
on a multivariate analysis of comorbidities as listed on
Box 5.1. ese include coronary artery disease, congestive
heart failure, cerebrovascular disease, insulin- dependent
diabetes mellitus, renal insuciency (creatinine > 2 mg/ dL),
and high- risk surgeries including suprainguinal vascular,
TRANSESOPHAGEAL ECHOCARDIOGRAPHY
Transesophageal echocardiography allows monitoring of
ventricular volume, global myocardial function, regional
wall motion abnormalities, valve assessment, and aortic
pathology assessment. A full exam will demonstrate wall
motion as either normokinetic, hypokinetic, akinetic,
or dyskinetic while assessing for additional factors and
pathology. e transgastric midpapillary short axis view
is a preferred view for monitoring wall motion and ischemic changes, since it provides a representation of all three
26 PART II. CARDIAC CRISES
7
X Upper limit of normal lab value
Time in hours from myocardial infarction
https://t.me/medicina_free
27
coronary blood vessels and is benecial in assessment of
patients at risk for ischemia/ infarction.16 If an echocardiogram is not available, other signs may include changes in ST
segments of contiguous leads, elevation of pulmonary capillary wedge pressure, and decrease in cardiac output.
ELECTROCARDIOGRAPHY
15
Perhaps the most commonly used monitor for myocardial
ischemia/ infarction detection used by anesthesiologists,
electrocardiography (ECG) is considered a standard ASA
monitor. Signs of ischemia can be identied by ST segment
changes including, but not limited to: T wave inversion,
QRS axis deviations, R wave changes, development of a U
wave, or the development of new bundle branch block.17
Monitoring of the ST segment in multiple leads is currently
the standard of care in detection of ischemia/ infarction,
though a ve- lead ECG is oen used intraoperatively. When
these patients. e onset of ventricular arrhythmias (premature ventricular contracts, ventricular tachycardia, etc.),
and supraventricular arrhythmias (paroxysmal supraventricular tachycardia, atrial brillation or utter) may also be
the initial presenting signs.
PULMONARY ARTERY CATHETERS
Pulmonary artery catheters may provide some evidence of
ischemic change, but are not sensitive enough to be reliable as a single monitor to detect ischemia. Acute ischemic
events may be demonstrated by sudden elevation in pulmonary artery or wedge pressure (usually > 5 mmHg of wedge
pressure elevation not related to other factors), signaling
LV dysfunction. Enhanced V waveform tracing may indicate increased le atrial pressure, possibly due to papillary
muscle dysfunction and mitral regurgitation from acute
ischemic changes.
20
monitoring the ECG, leads II and V5 have a sensitivity of
95% in identifying ischemic occurrences, though, recently
V4 was seen to be more sensitive as a single EKG precordial
lead than V5 and may be considered.18 Continuous monitoring of leads II, V4, and V5 has been shown to identify
96% of ischemic events.
19
Subendocardial ischemia results in repolarization
changes, which ultimately result in ST segment depression. Elevation of the ST segment occurs when a transmural infarction occurs due to compromised blood supply.
Classic criteria for diagnosis of ischemia is >1 mm (0.1 mV)
elevation or depression of the ST segment in two contiguous leads. e development of a new le bundle branch
block is considered evidence of MI until proven otherwise.
A prior le bundle branch, however, does not negate the
potential for myocardial ischemia, and the ECG cannot be
relied on to provide adequate information for detection in
LABORATORY
Cardiac biomarkers (CK, CK- MB, troponins) can be sent
to the laboratory for conrmation of myocardial damage. When cardiac myocytes undergo necrosis, membrane
integrity is lost, with resultant spillage of enzymes into the
systemic microvasculature. Figure 5.3 demonstrates the typical timing of important cardiac enzymes. Troponin is the
most sensitive and specic test for laboratory evaluation of
myocardial damage, with troponin I and M being the most
cardiac- specic. Troponin levels start to increase 4– 6 hours
following an insult and peak at 48 hours. Troponin elevations may persist for up to 14 days and, therefore, are not
reliable for detecting repeat myocardial injury in a patient
with recent positive biomarkers. e CK- MB isoenzyme
is sensitive for myocardial injury compared to CK alone
Myoglobin
6
5
4
3
2
1
0
MYOCARDIAL ISCHEMIA 27
20 40 60 80
Total CK
CK-MB
Troponin-I
100
120 140 160
Figure 5.3 Cardiac biomarkers are released into
systemic circulation with varying time. Troponin
increases 4– 6 hours following an insult, peaks at
48 hours, and is present for up to 14 days. CKMB is sensitive for myocardial injury compared
to total- CK alone and is utilized in the diagnostic
criteria for MI. CK- MB increases 4– 6 hours after
injury, peaks at 24 hours, and returns to baseline
in 48– 72 hours.
28
https://t.me/medicina_free
and is used in the diagnostic criteria for MI. e CK- MB
increases 4– 6 hours aer injury and peaks at 24 hours, with
is maintained if vasodilators are required for medical
management.
return to baseline in 48– 72 hours. Elevations of CK- MB
without concurrent troponin elevations should raise suspicions for false positive diagnosis of MI and enzyme release
from noncardiac tissue (skeletal muscle injury).
SUBSEQUENT TREATMENT STEPS
Aer hemodynamic stabilization of the patient and mini-
mizing myocardial oxygen demand while optimizing
MANAGEMENT OF THE PATIENT
INITIAL TREATMENT STEPS
Patients that present with myocardial ischemia in the perioperative period represent an anesthetic emergency. For
patients who become obtunded or demonstrate signicant hemodynamic collapse/ cardiogenic shock, securing a
denitive airway and providing hemodynamic stabilization
should be undertaken as the rst steps. For patients who
demonstrate suspected myocardial ischemia, but do not
have shock or mental status changes, continuous monitor-
oxygen delivery, immediate reperfusion of the myocar-
dial vasculature is the ultimate goal. Reperfusion may be
obtained through several methods: thrombolytic therapy,
percutaneous coronary intervention (mechanical throm-
bectomy, coronary stenting, etc.), and/ or coronary artery
bypass graing. Antiplatelet therapy should be adminis-
tered to reduce ongoing thrombotic formation and oen
involves the administration of aspirin and a thienopyridine
inhibitor, like clopidogrel or prasugrel. Additional antico-
agulation therapy such as heparin, bivalrudin, or enoxapa-
rin may be required as well to further reduce thrombotic
development.
ing of the patient and medical therapy is indicated without
invasive airway management.
In general, tachycardia needs to be aggressively managed, as this decreases the time for myocardial perfusion
and increases myocardial oxygen demand. Additional goals
include decreasing the ventricular end- diastolic diameter
by judicious volume management, providing adequate
pain control, supplying supplemental oxygen, and ensuring adequate oxygen- carrying capacity by red blood cell
transfusion, if signicant anemia is present. Beta blockers
are preferred over other agents for their negative chromotropic and inotropic eects. ey should be used cautiously,
however, in patients with new- onset ischemia if contraindications exist (heart failure exacerbation, bradycardia,
severe reactive airway disease, etc.). Nitroglycerin (NTG)
is a systemic venodilator and decreases myocardial demand
by decreasing preload through reduction in venous return
as well as reducing overall wall tension. Also, NTG is a
coronary arterial dilator in both patent and stenotic vessels
and increases coronary blood ow. Sodium nitroprusside
(SNP) works via conversion to nitric oxide, thus this agent
possesses arterial and venous dilatory eects. It decreases
preload by reducing venous return. is reduction in preload subsequently reduces wall tension. e ability of SNP
to reduce aerload has the additional benet of ooading
ventricular workload, thus reducing myocardial oxygen
consumption.
If hypotension develops, vasoconstrictors should be
used to ensure that adequate coronary perfusion pressure
CASE- BASED LEARNING DISCUSSION
1. You learn in your preoperative interview that the
patient sustained a myocardial infarction 3 weeks
ago. His cardiac catheterization report revealed an
80% occluded right main coronary artery. Does this
change your anesthetic plan? Would you suggest the
patient undergo coronary revascularization prior to
proceeding? What monitors would you recommend if
you do proceed to surgery?
a. ACC/ AHA guidelines recommend coronary
revascularization (CABG, PCI) before noncardiac
surgery in the following cases:
i. Signicant le main coronary artery stenosis
ii. ree vessel disease, especially if le ventricular
ejection fraction is <50%
iii. Two vessel disease with signicant LAD stenosis
and either EF <50% or ischemia demonstrated
on noninvasive testing
iv. Unstable angina or NSTEMI
v. Acute STEMI
b. ACC/ AHA task force suggests elective surgery is
associated with prohibitive risk in the rst 4– 6 weeks
aer MI due to increased risk of reinfarction.
28 PART II. CARDIAC CRISES
https://t.me/medicina_free
29
c. Electrocardiogram, specically the V5 precordial
lead and lead II can detect 96% of ischemic events.
2. Midway through the procedure, you note ST segment
depression in leads II, III, and aVF. How do you manage
the ST changes?
a. Treatment of suspected myocardial ischemia should
focus on increasing oxygen supply and decreasing
myocardial oxygen demand.
b. Increasing supply can include correcting reversible
factors such as hypoxemia, hypotension, and ensuring
oxygen carrying capacity is adequate (anemia).
c. Decreasing oxygen demand should include control
of hemodynamics including heart rate with beta
blockers (metoprolol, esmolol) and excessive
hypertension. Vasodilators (nitroglycerine,
nitroprusside, nicardipine) can be used to decrease
preload and thus wall tension.
REFERENCES
1. DeFily DV, Chilian WM. Coronary microcirculation: autoregula-
tion and metabolic control. Basic Research in Cardiology. 1995;90:
112– 8.
2. Duncker DJ, Koller A, Merkus D, Canty JM Jr. Regulation of coro-
nary blood ow in health and ischemic heart disease. Progress in
Cardiovascular Diseases. 2015;57(5):409– 22.
3. Canty JM Jr. Coronary pressure- function and steady- state pressure-
ow relations during autoregulation in the unanesthetized dog.
Circulation Research. 1988;63:821– 36.
4. Laughlin MH, Davis MJ, Secher NH, et al. Peripheral circulation.
Comprehensive Physiology. 2012;2:321– 447.
5. Furchgott RF, Zawadzki JV. e obligatory role of endothelial cells
in the relaxation of arterial smooth muscle by acetylcholine. Nature.
1980;288:373– 6.
6. Bentzon JF, Otsuka F, Virmani R, Falk E. Mechanisms of plaque
formation and rupture. Circulation Research. 2014;114:1852– 66.
7. Meier P, Gloekler S, Zbinden R, et al. Benecial eect of recruit-
able collaterals: a 10- year follow- up study in patients with stable
coronary artery disease undergoing quantitative collateral measurements. Circulation. 2007;116:975– 83.
8. Canty JM Jr., Giglia J, Kandath D. Eect of tachycardia on regional
function and transmural myocardial perfusion during graded coronary pressure reduction in conscious dogs. Circulation. 1990;82:
1815– 25.
9. Roger VL, Farkouh ME, Weston SA, et al. Sex dierences in evaluation and outcome of unstable angina. JAMA: e Journal of the
American Medical Association. 2000;283:646– 52.
10. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ ACC
Guideline for the Management of Patients with Non- ST- Elevation
Acute Coronary Syndromes: A Report of the American College of
Cardiology/ American Heart Association Task Force on Practice
Guidelines. Journal of the American College of Cardiolog y. 2014;64:
e139– 228.
11. Burke AP, Virmani R. Pathophysiology of acute myocardial infarction. Medical Clinics of North America 2007;91:553– 72; ix.
12. Yeo KK, Li S, Amsterdam EA, et al. Comparison of clinical characteristics, treatments and outcomes of patients with ST- elevation
acute myocardial infarction with versus without new or presumed
new le bundle branch block (from NCDR(R)). American Journal
of Cardiology. 2012;109:497– 501.
13. ang ND, Sundstrom BW, Karlsson T, Herlitz J, Karlson BW.
ECG signs of acute myocardial ischemia in the prehospital setting of
a suspected acute coronary syndrome and its association with outcomes. American Journal of Emergency Medicine. 2014;32:601– 5.
14. Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and
prospective validation of a simple index for prediction of cardiac risk
of major noncardiac surgery. Circulation. 1999;100:1043– 9.
15. Mark JB. Multimodal detection of perioperative myocardial ischemia. Texas Heart Institute Journal. 2005;32:461– 6.
16. Shanewise JS, Cheung AT, Aronson S, et al. ASE/ SCA guidelines
for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: recommendations of the
American Society of Echocardiography Council for Intraoperative
Echocardiography and the Society of Cardiovascular Anesthesiologists
Task Force for Certication in Perioperative Transesophageal
Echocardiography. Anesthesia and Analgesia. 1999;89:870– 84.
17. Herring N, Paterson DJ. ECG diagnosis of acute ischaemia and
infarction: past, present and future. QJM: Monthly Journal of the
Association of Physicians. 2006;99:219– 30.
18. Landesberg G, Mosseri M, Wolf Y, Vesselov Y, Weissman C.
Perioperative myocardial ischemia and infarction: identication
by continuous 12- lead electrocardiogram with online ST- segment
monitoring. Anesthesiology. 2002;96:264– 70.
19. London MJ, Hollenberg M, Wong MG, et al. Intraoperative myocardial ischemia: localization by continuous 12- lead electrocardiography. Anesthesiology. 1988;69:232– 41.
20. van Daele ME, Sutherland GR, Mitchell MM, et al. Do changes
in pulmonary capillary wedge pressure adequately reect myocardial ischemia during anesthesia? A correlative preoperative
hemodynamic, electrocardiographic, and transesophageal echocardiographic study. Circulation. 1990;81:865– 71.
MYOCARDIAL ISCHEMIA 29
30
https://t.me/medicina_free
6.
AORTIC DISRUPTION
Adam J. Kingeter and Bantayehu Sileshi
CLINICAL CASE
type A or type B, with type A dissections involving the
ascending portion of the aorta with or without involveA 57- year- old man with a history of hypertension, hyperlipidemia, and a 50 pack- year smoking history presents to
the emergency department with a 1- hour history of severe
retrosternal chest pain. He describes the pain as tearing in
nature, and sudden in onset. In the emergency department,
cardiac enzymes are within normal limits and chest x- ray
and EKG are also unremarkable. His vital signs are: pulse
115, blood pressure (BP): 140/ 40, respiratory rate (RR):
16, and oxygen saturation (SpO2): 98% on room air.
ment of descending aorta, and type B being conned to
the descending aorta with no involvement of the ascend-
ing aorta. e DeBakey system classies aortic dissection
as type I, type II, or type III. Type I dissections at a mini-
mum involve the ascending aorta and aortic arch, and oen
include portions of the descending aorta. Type II dissec-
tions involve only the ascending aorta with no aortic arch or
descending aorta involvement, whereas type III dissections
involve the descending aorta and rarely the arch, but have
no involvement of the ascending aorta.
PATHOPHYSIOLOGY OF DISEASE STATE
is chapter discusses the mechanism, classication, presenting signs, and basic principles of management for aortic
dissection. Acute stabilization, diagnostic imaging, denitive management, and long- term follow up of patient management are discussed. In addition the dissection location
and its implication on principles of management and outcome are covered.
RISK
Any condition that leads to increased wall tension and
weakening of the aortic intima and media can lead to dis-
ruption. ese conditions may be grouped as: inherited,
acquired, traumatic, and iatrogenic. Inherited conditions
include connective tissue disorders such as Marfan’s syn-
drome and Ehlers- Danlos syndrome. ese genetic disor-
ders lead to abnormal collagen formation and a weakening
of the aortic wall and predisposition for dilation and rup-
MECHANISM
Aortic disruption occurs when a tear develops in the aortic
intima with passage of blood into the new space between
the intima and media. Blood continues to accumulate in
this new potential space, termed as “false lumen,” and can
spread the dissection proximally toward the aortic valve
or distally away from the heart. It is this propagation that
causes the catastrophic clinical consequences of dissection;
proximal extension can lead to involvement of the aortic
valve and coronary ostia, whereas distal extension can lead
to involvement and occlusion of the branches of the aorta.
Aortic disruption is classied by the segment or segments of the aorta aected. e two commonly used classication systems are the Stanford system and the DeBakey
system. e Stanford system classies dissections as either
ture. Acquired conditions such as hypertension, smoking,
and dyslipidemia lead to intimal thickening, brosis, and
calcication, which predispose the aorta to intimal disruption. Traumatic aortic dissection is the result of a rapid
deceleration event such as a high- speed motor vehicle collision or a fall from height. is rapid deceleration leads to
development of excessive shear forces along the aortic wall
between the pendulum of the heart and the anchoring retroperitoneal portion of the aorta. ese shear forces lead
to tearing of the intima. Lastly, iatrogenic dissection of the
aorta can occur during invasive catheter interventions or
during manipulation of the aorta during valve surgery or
coronary bypass procedures.
e incidence of aortic dissection increases with age,
with an average age of onset for type A dissection of 61
years, and an average age of onset for type B dissection of 66
30
https://t.me/medicina_free
31
1– 4
years.
a genetic etiology underlying their dissection; the mean
age of dissection in patients with Marfan’s syndrome is 35.5
Gender is also a risk factor for aortic dissection, with men
having an age- adjusted incidence of thoracic dissection
more than double that of women (5.2 per 100,000 per year
compared to 2.2 per 100,000 per year for women).
increase the risk of thoracic aorta dissection, and may in fact
be precursors to the dissection itself. One of the most well
established risk factors for dissection is aortic aneurysm.
e International Registry of Acute Aortic Dissections
(IRAD) shows that approximately 16% of patients with
a dissection have a known aortic aneurysm.6 However, it
should be noted that in the IRAD database, 59% of dissections occurred at ascending aortic diameters less than 5.5
cm and 40% occurred at diameters less than 5 cm.7 e risk
of dissection increases with diameter of the aneurysm, and
the yearly rate has been shown to be approximately 1.5%
for aortic diameters greater than 4 cm, 2.5% for diameters
greater than 5 cm, and 3.7% for diameters greater than 6
cm.8 In the same paper, threshold diameters were identied above which the risk of complications increased by
approximately 10- fold. In the thoracic region that diameter
An important caveat to this trend is patients with
1
Certain clinical conditions are known to signicantly
with a type A dissection.6 Half of all patients in one longitudinal study experienced a “painless” interval following
initial onset of pain that lasted hours to days before the pain
returned. In the same study, less than half of patients experiencing an acute dissection presented with hypertension,
and only 36% were in shock at the time of presentation.
3
Patients experiencing an acute type B dissection also
typically present with acute onset of chest, back, and/ or
abdominal pain. e incidence of stroke is lower in comparison to type A dissection, however type B dissections may
present with other ischemic complications such as spinal
cord ischemia and lower extremity paralysis secondary to
involvement of the anterior spinal artery feeding branches,
or pulseless lower extremities due to occlusion of the iliac
3,6
vessels.
Up to 30% of patients presenting with aortic dissection are initially thought to have another pathologic process occurring such as myocardial ischemia or pulmonary
embolus.6 e picture may be further clouded by the fact
that serum biomarkers such as troponin and D- dimer are
oen elevated in the setting of acute aortic dissection.9 A
high clinical index of suspicion for dissection should be
maintained for patients presenting with acute onset of chest
pain, as mortality increases if treatment is delayed.
was 6 cm, and in the descending aorta that diameter was
7 cm.8 e correlation between aneurysmal diameter and
dissection rate is not surprising, as wall tension increases
proportionally with diameter, in accordance with the Law
of Laplace.
Mortality varies by location and extent of the dissection, as well as modality of treatment. Early diagnosis and
treatment is key, as early mortality rate in acute dissec-
MANAGEMENT OF THE PATIENT
Patients with suspected acute aortic dissection should be
quickly evaluated with diagnostic imaging and be admitted to an intensive care unit for aggressive hemodynamic
management.
tion is as high as 1% per hour, with prehospital mortality
being as high as 20% in one longitudinal study.4 According
to most recent estimates, overall in- hospital mortality for
acute Stanford type A dissections is 30%, and 13% for acute
Stanford type B dissections.
1– 3
INITIAL DIAGNOSTIC AND TREATMENT STEPS
e initial diagnostic test in most cases of aortic dissec-
tion is chest x- ray. e classical ndings of a widened
mediastinum or abnormal aortic contour are present in
ASSESSMENT OF THE PATIENT: PRESENTING
SIGNS AND SYMPTOMS
approximately 80% of patients with acute aortic dissection.
Nevertheless, up to 15% patients who are later found to
have an acute dissection have a normal chest x- ray on pre-
sentation.6 Irrespective of chest x- ray ndings, additional
Type A dissections typically present with sudden onset of
severe chest and/ or back pain, with abdominal pain, syncope, and stroke also being common at presentation. If the
dissection propagates proximally to involve the aortic valve,
acute aortic valve regurgitation may lead to acute congestive
heart failure on presentation. A diastolic murmur consistent
with aortic regurgitation is seen in 40%– 50% of patients
imaging must be obtained to determine the precise location
and extent of the dissection. Currently the three most com-
mon modalities are computed tomography (CT), echo-
cardiography, and magnetic resonance imaging (MRI). In
the IRAD patient population the initial diagnostic test was
CT in 61% of patients, transesophageal echocardiography
(TEE) or transthoracic echocardiography (TTE) in 33% of
AORTIC DISRUPTION 31
32
Arterial pressur
https://t.me/medicina_free
patients, and MRI in 2%. Oen multiple imaging modalities are used to determine the location and extent of the dissection, with an average of 1.8 imaging modalities used for
diagnosis.
6
Initial treatment steps are geared toward hemodynamic
stabilization with close attention to blood pressure and
heart rate. e goal during this phase of treatment is prevention of dissection propagation by reducing aortic wall
tension and shear stress. Intravenous beta blockers are the
initial drugs of choice, as they reduce the force of ventricular contraction and heart rate. In cases of refractory hypertension, intravenous vasodilatory agents such as sodium
nitroprusside or nicardipine may be used with caution so as
to prevent reexive tachycardia. Pain control is also important during this phase and can help with hemodynamic stabilization. Intravenous opioids such as morphine, fentanyl,
and hydromorphone are excellent choices, due to their
rapid onset and predictable pharmacokinetics.
Complicating lesions such as cardiac tamponade and
acute aortic insuciency that may be present in patients
with type A dissections need to be recognized prior to
induction of anesthesia for denitive correction of the dissection. Cardiac tamponade develops when the dissection
extends proximally toward the aortic valve and allows for the
accumulation of blood in the pericardium. Cardiac tamponade is the leading cause of mortality in patients with acute
type A dissection and is present in 8%– 31% of patients presenting with acute type A aortic dissection.10 Physical exam
and laboratory ndings consistent with tamponade include
Beck’s triad (hypotension, elevated JVD, and mued heart
sounds), electrical alternans on EKG, and pulsus paradoxus
(Figure 6.1). Patients are usually diaphoretic and tachycardic
due to increased sympathetic tone in an attempt to maintain cardiac output. Acute tamponade leads to equalization
of pressure in all cardiac chambers thus preventing forward
ow and cardiac output. Patients in tamponade are dependent on preload to maintain cardiac output, and anything
that leads to increased venous capacitance or decreased
contractility can lead to complete cardiovascular collapse.
Unlike tamponade associated with other causes, rapid pericardiocentesis risks worsening the dissection and can lead to
increased mortality if not performed in a controlled man-
11,12
ner.
When available, clinicians should perform a limited
transthoracic echo in patients presenting emergently to the
operating theater with aortic dissection, to evaluate presence
or absence of tamponade. If patient has tamponade, then
patients should be draped and prepped for surgery prior to
induction, and should have arterial and central venous access
as well. Induction should be rapid, and agents that depress
cardiac contractility or increase venous capacitance, such as
propofol, should be avoided in favor of agents such as ketamine or etomidate. Positive pressure ventilation leads to
increased intrathoracic pressure and reduced venous return;
therefore ventilator pressures should be kept as low as possible until the tamponade is released.
Acute aortic insuciency (AI) leads to congestive heart
failure, as a signicant amount of ejected stroke volume
rushes back across the incompetent aortic valve during
diastole leading to ventricular dilation and elevated end
diastolic volume (LV- EDV) and pressure (LV- EDP). e
elevated LV- EDP leads to decreased ow across the mitral
valve and can cause pulmonary edema and right heart failure. As previously stated, approximately one- half to onethird of all patients with aortic dissection present with
aortic insuciency (AI).6 Patients with acute AI usually
demonstrate ndings consistent with cardiogenic shock,
such as hypotension, pallor, tachycardia, and cool extremities. Physical exam ndings suggestive of AI include a widened pulse pressure (Corrigan’s, or water- hammer pulse),
and a diastolic decrescendo murmur following an early
Figure 6.1 Panel A shows screenshot of a patient’s vitals, demonstrating pulsus paradoxus (panel C) with no electrical alterans. Panel B shows electrical
alterans.
32 PART II. CARDIAC CRISES
BA
C
e
100
90
80
70
60
50
40
(mmHg)
30
20
10
0
Inspiration Inspiration
https://t.me/medicina_free
33
Signs and Symptoms
Cardiac Tamponade
• Muffled heart sounds
• Jugular venous distention
• Narrow pulse pressure
• Tachycardia
• Pulsus paradoxus
• Electrical alternans
All Patients with Aortic
Dissection
• Tight heart rate control;
Figure 6.2 Summary of signs and symptoms of
aortic dissection patients with cardiac tamponade
and aortic insufciency. Also summarized is the
anesthetic goal for patients presenting with these
clinical ndings.
avoid tachycardia
• Tight blood pressure
control; avoid
hypertension
S1 (mitral valve closure). e mnemonic “Fast, Forward,
and Full” describes the basic approach to management of
patients with AI. A faster heart rate leaves less time for back
ow across the valve, a low aerload promotes forward ow
of blood with less regurgitation, and volume keeps lling
pressures elevated to maintain forward ow. Keeping aerload low and maintaining venous tone should be prioritized
during induction of anesthesia in these patients. Liberal use
of narcotics limits use of venodilating agents such as propofol and inhalational anesthetics (Figure 6.2).
• Tachycardia
• Widened pulse pressure
• Diastolic decrescendo murmer
• Shortness of breath
Anesthetic Goals
Patients with Tamponade
• Maintain spontaneous
respirations until surgical
relief of tamponade
• Avoid bradycardia
• Avoid sympathectomy
• Maintain preload
le common carotid artery is required, hypothermic circulatory arrest may be necessary. Hypothermic arrest involves
cooling the patient to <24 degrees Celsius with cessation of
blood circulation. It is used in cases when cerebral perfusion
via the bypass circuit cannot be maintained, and relies on
the decreased cellular metabolism during hypothermia to
prevent hypoxic damage.
Type B dissections are usually treated medically, as surgical repair has not been shown to be superior. Surgical
therapy is reserved for patients with life- threatening com-
Aortic Insufficiency
Patients with Acute Aortic
Insufficiency
• Avoid bradycardia
• Avoid excess afterload
• Maintain preload
plications such as impending aortic rupture or occlusion of
SUBSEQUENT TREATMENT STEPS
Denitive treatment of the dissection varies by location
and extent of the dissection. Type A dissections typically
require surgical intervention, as mortality rates for those
treated medically are more than double those who undergo
surgical repair.6 e goal of surgical repair is prevention
of aortic rupture or continued dissection. e procedure
itself classically involves excising the portion of the aorta
containing the intimal tear, obliterating entry into the false
a major aortic branch. Medical treatment of type B dissections involves regulation of heart rate and blood pressure,
with serial imaging to document progression of the dissection. As with acute management, beta blockade is the gold
standard for heart rate and blood pressure control with a
goal heart rate less than 60 and goal systolic blood pressure less than 120.14 Interventional procedures for type B
dissections are becoming more common, with many studies demonstrating high rates of survival and low rates of
complicates.
13
dissection lumen both proximally and distally, and lastly
placing an interposition gra into the excised portion of
the aorta.12 Depending on the proximal extent of the dissection, the aortic valve may need to be replaced or repaired
and resuspended. Distal extension of the dissection with
occlusion of aortic side branches may be treated with reimplantation of the branches, or via an endovascular approach
with balloon dilation or stent placement.13 Repairs of the
aortic arch and ascending aorta require cardiopulmonary
bypass, and if reimplantation of the innominate artery or
LONG- TERM FOLLOW UP
With the exception of traumatic and iatrogenic dissections, a patient who develops an acute aortic dissection has
a systemic process that does not end with the repair of the
vessel. Long- term follow up is necessary for serial imaging and aggressive medical therapy to treat, when able, the
contributing medical conditions such as hypertension and
hyperlipidemia. It has been estimated that up to a third of
AORTIC DISRUPTION 33
34
https://t.me/medicina_free
patients who survive the initial episode and treatment of
REFERENCES
acute aortic dissection will experience a complication such
as extension of dissection, aneurysmal dilation, or aortic
rupture.
6,13,15
As with acute treatment of dissection, longterm management of this group of patients requires close
attention to blood pressure control and a high index of suspicion for life- threatening complications.
CASE- BASED LEARNING DISCUSSION
1. Given our patient’s vital signs and presentation, what
diagnostic test(s) would you order? Would your choice
of diagnostic test(s) change if his vital signs were: HR:
120 BP: 80/ 45 RR: 22 SpO2: 93% on 2L NC?
2. Given our patient’s vital signs, what complication of
dissections do you suspect? How will this impact your
hemodynamic management of the patient?
3. Our patient is diagnosed with a Stanford Type A
dissection extending from the aortic root to just distal
of the le subclavian artery. e decision is made to
proceed to the operating room for emergency repair.
What vascular access and monitoring would you like
for the case? Any laboratory values or tests you would
like before proceeding? What is your plan for induction
and airway management?
4. e surgeon decides to go on complete circulatory
arrest for repair of the aneurysm. What preparations
need to be made prior to instituting circulatory arrest?
How long can circulatory arrest be safely tolerated?
5. e patient undergoes a complete aortic root
reconstruction for his type A aortic dissection with a
total of 17 minutes of circulatory arrest. Postoperatively
he is transported to the cardiovascular ICU intubated
and sedated. What are your hemodynamic goals
postoperatively? Given this type of operation, what sort
of complications could be expected for this patient?
6. Aer 5 days in the CVICU, the patient is discharged
home. What follow up is necessary for this patient?
What medications should be continued on his discharge?
1. LeMaire SA, Russell L. Epidemiology of thoracic aortic dissection.
National Review of Cardiology. 2011;8(2):103– 13.
2. Clouse WD, et al. Acute aortic dissection: population- based incidence compared with degenerative aortic aneurysm rupture. Mayo
Clin Proceedings. 2004;79(2): p. 176– 80.
3. Mészáros I, et al. Epidemiology and clinicopathology of aortic dissection. Chest. 2000;117(5):1271– 8.
4. Olsson C, et al. oracic aortic aneurysm and dissection: increasing prevalence and improved outcomes reported in a nationwide
population- based study of more than 14,000 cases from 1987 to
2002. Circulation. 2006;114(24):2611– 8.
5. Januzzi JL, et al. Comparison of aortic dissection in patients with
and without Marfan’s syndrome (results from the International
Registry of Aortic Dissection). Am J Cardiol. 2004;94(3):400– 2.
6. Hagan PG, et al. e International Registry of Acute Aortic
Dissection (IRAD): new insights into an old disease. JAMA. 2000;
283(7):897– 903.
7. Pape LA, et al. Aortic diameter >or = 5.5 cm is not a good predictor of type A aortic dissection: observations from the International
Registry of Acute Aortic Dissection (IRAD). Circulation. 2007;
116(10):1120– 7.
8. Eleeriades JA. Natural history of thoracic aortic aneurysms: indications for surgery, and surgical versus nonsurgical risks. Ann orac
Surg. 2002;74(5):S1877– 80; discussion S1892– 8.
9. Weber T, et al. D- dimer in acute aortic dissection. Chest. 2003;
123(5):1375– 8.
10. Rampoldi V, et al. Simple risk models to predict surgical mortality
in acute type A aortic dissection: the International Registry of Acute
Aortic Dissection score. Ann orac Surg. 2007;83(1):55– 61.
11. Isselbacher EM, Cigarroa JE, Eagle KA. Cardiac tamponade complicating proximal aortic dissection: is pericardiocentesis harmful?
Circulation. 1994;90(5):2375– 8.
12. Hayashi T, et al. Impact of controlled pericardial drainage on critical
cardiac tamponade with acute type A aortic dissection. Circulation.
2012;126(11 Suppl 1):S97– S101.
13. White RA, et al. Report on the results of thoracic endovascular
aortic repair for acute, complicated, type B aortic dissection at
30 days and 1 year from a multidisciplinary subcommittee of the
Society for Vascular Surgery Outcomes Committee. J Vasc Surg.
2011;53(4):1082– 90.
14. Hiratzka LF, et al. 2010 ACCF/ AHA/ AATS/ ACR/ ASA/
SCA/ SCAI/ SIR/ STS/ SVM guidelines for the diagnosis and
management of patients with oracic Aortic Disease: a report
of the American College of Cardiology Foundation/ American
Heart Association Task Force on Practice Guidelines, American
Association for oracic Surgery, American College of Radiology,
American Stroke Association, Society of Cardiovascular
Anesthesiologists, Society for Cardiovascular Angiography and
Interventions, Society of Interventional Radiology, Society of
oracic Surgeons, and Society for Vascular Medicine. Circulation.
2010;121(13):e266– 369.
15. Driever R, et al. Long- term eectiveness of operative procedures for Stanford type a aortic dissections. J Card Surg. 2004;
19(3):240– 5.
34 PART II. CARDIAC CRISES
https://t.me/medicina_free
35
7.
CARDIAC DYSRHYTHMIAS
Mark Henry and Robert J. Deegan
CLINICAL CASE
arrhythmias are liable to recur. In addition, perioperative
arrhythmias may be harbingers of events that, in the absence
A 55- year- old male with hypertension, coronary artery dis-
of timely intervention, will lead to cardiovascular collapse.
ease, heart failure (EF 40%), COPD and diabetes is admitted with right upper quadrant abdominal pain and found to
A…. B…. C….
have cholecystitis. He is scheduled for a laparoscopic cholecystectomy. e procedure is being performed using general endotracheal anesthesia. At the start of the procedure,
the surgeon makes a skin incision and begins insuation of
CO2 for pneumoperitoneum. As you watch the monitor,
the patient’s heart rate goes from 72 bpm to 48 bpm.
INTRODUCTION AND GENERAL APPROACH
Perioperative arrhythmias are a very common issue, aecting 70% of patients. While the majority of these are benign,
signicant hemodynamic instability occurs in 2.2% of
cases, and this can be a precursor to cardiac arrest.1 While
the incidence of intraoperative cardiac arrest is relatively
low at 6.7 per 10,000 cases,2 looking at the broader perioperative period reveals a much higher rate of 50 per 10,000
patients within 30 days of surgery.3 As approximately 70%
of patients with perioperative arrest do not survive to discharge,3 prevention is of extreme importance.
Prevention of cardiac arrest involves increased vigilance
in the presence of known risk factors (higher American
Society of Anesthesiologists physical status, higher transfusion rates, emergency surgery, and poor functional status
prior to surgery).2 In addition, early detection and appropriate therapy are oen necessary to prevent deterioration
of a perfusing arrhythmia into an unstable rhythm.
Since ventilation- and airway- related cardiac events are
relatively common in the perioperative period, attention to
the airway is a reasonable rst approach for the potentially
unstable patient presenting with a pulsatile arrhythmia.
Useful initial measures include4:
• Increase inspired O2 to 100%
• Conrm airway patency and position (verify presence of
end- tidal CO2)
• Perform airway toilet, treat bronchospasm
• Ensure adequacy of IV access
• Support blood pressure
• Call for help
• Acquire a debrillator and a pacemaker (including
transcutaneous pacing capability)
If necessary, suspend surgery and anesthetic administration.
THREE QUESTIONS
Stable or unstable?
Wide or narrow complex?
Regular or irregular?
Paramount in the approach to perioperative arrhythmias should be identication and correction of the inciting stimulus while simultaneously pursuing eorts to
restore disordered circulation. Perioperative arrhythmias,
and in particular intraoperative arrhythmias, are commonly attributable to specic stimuli (e.g., pain, hypoxia,
or hypotension). Without cessation of the culprit stimulus,
STABLE VERSUS UNSTABLE
One of the rst assessments of the patient with perioperative
arrhythmia ought to be the identication of the presence or
absence of clinical stability. Clinical instability is identied
35
Соседние файлы в папке @xirurgi_2025