aneurysm of aorta and aortic valve stenosis

1. AORTIC ANEURYSM AND
STENOSIS
By: Dr. Monika Singh
Moderator: Dr Anita Pramod

3. Aneurysms and Dissection of the Aorta
 Definition
 Etiology
 Pathogenesis
 Classification
 Signs and Symptoms
 Diagnosis
 Preoperative Evaluation
 Indications for Surgery
 Management of Anesthesia
 Postoperative Management

4. Aneuryusm: An aneurysm is a dilation of all three layers of an
artery.
 The most common definition is a 50% increase in diameter
compared with normal.
Dissection: Blood surges through the intimal tear into an
extraluminal channel called the false lumen.
Blood in the false lumen can reenter the true lumen anywhere
along the course of the dissection or can rupture through the
adventitia causing massive hemorrhage.
DEFINITION

5. AORTIC
ANEURYSM
AORTIC
DISSECTION

6. Etiology
The most frequently implicated factors in the development of aortic
aneurysmal disease are:
a) Atherosclerosis
b) hypertension
c) Older age(>60)
d) Male sex
e) Family history of aneurysmal disease
f) Smoking
g) Inherited disorders eg. Marfan's syndrome, Ehlers-Danlos
syndrome, bicuspid aortic valve and nonsyndromic familial
aortic dissection.

7. Aneurysms and Dissection of the Aorta
 Definition
 Etiology
 Pathogenesis
 Classification
 Signs and Symptoms
 Diagnosis
 Preoperative Evaluation
 Indications for Surgery
 Management of Anesthesia
 Postoperative Management

8. PATHOGENESIS
Arteries are dynamically remodeling tissues that maintain their
structural and functional integrity by constantly synthesizing, degrading,
and repairing their extracellular matrix (ECM). Any alteration in the
integrity of the connective tissue can cause weakness of the aortic wall
by following mechanisms:
1. Poor intrinsic quality of vascular wall connective tissue in different
syndromes.
2. Imbalance of collagen synthesis and degradation
3. Loss of smooth muscle cells and inappropriate synthesis of
noncollagen/nonelastic ECM in the vascular wall
4. Polymorphisms of matrix metalloproteinases and/or tissue
inhibitor of metalloproteinase genes cause genetic predisposition to
aneurysm formation
5. Noninfectious causes
6. Infectious causes

9. 1. Poor intrinsic quality of vascular wall connective tissue in different
syndromes:
1. Marfans syndrome: defective synthesis of fibrillin-1 gene
2. Loeys-Dietz syndrome: mutations in TGF- receptors.
3. Ehlers-Danlos syndrome: there is defective type III collagen
synthesis.
4. Severe vitamin C deficiency:There is altered cross-linking of type III
collagen.

10. 2. Imbalance of collagen synthesis and degradation:
in atherosclerosis and vasculitis .
3. Loss of smooth muscle cells and inappropriate synthesis of
noncollagen/nonelastic ECM in the vascular wall
Ischemia(due to atherosclerois / HTN) of the aortic wall causes degenerative
changes, characterized by scarring, loss of smooth muscle cells and elastic
fibers, and abnormal deposition of GAG. Histopathologic changes described
above are termed cystic medial degeneration.

11. 4. Polymorphisms of genes cause genetic predisposition to
aneurysm formation.
 Many ascending thoracic aortic aneurysms are associated with
congenital bicuspid aortic valve.
 In Turner syndrome, there is association with bicuspid aortic
valve and aortic coarctation

12. 5. Noninfectious cause:
giant cell arteritis, Takayasu arteritis, rheumatoid arthritis,
psoriatic arthritis, ankylosing spondylitis, reactive arthritis,
Wegener granulomatosis, and Reiter syndrome.
6.Infectious cause
Eg. Syphilitic aortitis

13. Aneurysms and Dissection of the Aorta
 Definition
 Etiology
 Pathogenesis
 Classification
 Signs and Symptoms
 Diagnosis
 Preoperative Evaluation
 Indications for Surgery
 Management of Anesthesia
 Postoperative Management

14. CLASSIFICATION
Aortic aneurysms can be classified morphologically as :
1. Fusiform aneurysm: there is a uniform dilation involving the
entire circumference of the aortic wall.
2. Saccular aneurysm :is an eccentric dilation of the aorta that
communicates with the main lumen by a variably sized neck.

16. DEBAKEY CLASSIFICATION OF AORTIC DISSECTION
 Type I: The intimal tear originates in the ascending aorta and the
dissection involves the ascending aorta, arch, and variable lengths
of the descending thoracic and abdominal aorta.
 Type II: The dissection is confined to the ascending aorta.
 Type IIIa: The dissection is confined to the descending thoracic
aorta.
 Type IIIb : Extends into the abdominal aorta and iliac arteries

18. THE STANFORD CLASSIFICATION OF AORTIC
DISSECTION
Type A includes all cases in which the ascending aorta is involved by
the dissection, with or without involvement of the arch or
descending aorta. (Includes Debakey Type1 and Type 2)
Type B includes all cases in which the ascending aorta is not
involved.(includes Type 3)

19. CRAWFORD CLASSIFICATION OF THORACOABDOMINAL
AORTIC ANEURYSM
Type I : originates below the left subclavian artery and extends into the
abdominal aorta, including the celiac axis (T12)and mesenteric arteries.
Type II : involves the same areas as type I, but extends caudally to include
the infrarenal abdominal aorta.
Type III : begins in the lower descending thoracic aorta and involves the
remainder of the aorta.
Type IV : begins at the diaphragm and involves the abdominal aorta only.

21. Aneurysms and Dissection of the Aorta
 Definition
 Etiology
 Pathogenesis
 Classification
 Signs and Symptoms
 Diagnosis
 Preoperative Evaluation
 Indications for Surgery
 Management of Anesthesia
 Postoperative Management

22. SIGNS AND SYMPTOMS
1. Asymptomatic: Most common
2. Hoarseness: Stretching of the left recurrent laryngeal nerve.
3. Stridor: d/t compression of the trachea.
4. Dysphagia: d/t Compression of the esophagus
5. Hemoptysis :From erosion of TAAAs into bronchi or lung parenchyma
6. Dyspnea: Results from compression of the lungs.
7. Plethora and edema result from compression of the SVC.
8. Ascending aortic aneurysms can produce retrosternal pain, whereas descending ones can
cause interscapular pain
9. TAAAs can be a source of atheroembolism to peripheral tissues due to mural thrombosis
10. Otherwise, in many instances, the presenting feature is rupture or dissection, leading to
death
11. It is critical to have a high index of suspicion whenever a patient has chest pain of
unknown cause.

23. SYMPTOMS OF ABDOMINAL AORTA ANEURYSM
OR DISSECTION

24. Aneurysms and Dissection of the Aorta
 Definition
 Etiology
 Pathogenesis
 Classification
 Signs and Symptoms
 Diagnosis
 Preoperative Evaluation
 Indications for Surgery
 Management of Anesthesia
 Postoperative Management

25. DIAGONOSIS
1. CXR: Widened mediastinum
2. CT: For aneurysm size and location and for progression. CT ANGIO : GOLD
STANDARD
3. MRI: sensitive and specific for entry tear location, presence of false lumen, AR and
pericardial effusions.
4. Angiography: For severity and extent of aortic aneurysm.
5. TEE: a) Identification of mobile intimal flap is a prompt diagonosis for aortic
dissection.
b)Entry and re-entry tears can be identified.
c)AR can be identified and quantified.
d) LV function and RWMA can be identified
e) Pericardial effussion and cardiac tamponade can be diagnosed.
f)especially useful in hemodynamically unstable patients.

26. Aneurysms and Dissection of the Aorta
 Definition
 Etiology
 Pathogenesis
 Classification
 Signs and Symptoms
 Diagnosis
 Indications for Surgery
 Preoperative Evaluation
 Management of Anesthesia
 Postoperative Management

27. INDICATION OF SURGERY FOR AORTIC DISSECTION
Dissection involving ascending aorta / arch of aorta: Surgery is indicated.
Dissection in Descending aorta. Surgery indicated if:
a) Failure to control HTN
b) Continued pain
c) Enlargement on CXR, CT, angiogram
d) Development of neurological deficit
e) Evidence of renal/ GI ischemia
f) Development of aortic insufficiency

28. INDICATION OF SURGERY FOR AORTIC ANEURYSM
1. Persistent pain
2. Aortic valve involvement
3. LV strain/ coronary artery involvement
4. Diameter >5.5 cm/ rapidly expanding(>0.5cm/ year) for patients
with no comorbidities
5. The threshold for surgery is raised to 6 cm or more for patients with an
increased operative risk (e.g., the elderly or those with
comorbidities).
6. The threshold is lowered to 5 cm if a patient has a bicuspid aortic
valve as those patients are at risk for aortic rupture or dissection at a
smaller aortic diameter.
7. In patients with collagen vascular diseases such as Marfan
syndrome or Loeys-Dietz, aortic repair is recommended at 4 cm.

29. Aneurysms and Dissection of the Aorta
 Definition
 Etiology
 Pathogenesis
 Classification
 Signs and Symptoms
 Diagnosis
 Indications for Surgery
 Preoperative Evaluation
 Management of Anesthesia
 Postoperative Management

30. PREOPERATIVE EVALUATION AND RISK ASSESSMENT
 Myocardial ischemia or infarction, respiratory failure , renal
failure, and stroke are the principal causes of morbidity and
mortality.
 The goal is to diagnose comorbidities, assess the risk of adverse
outcomes, optimize medical status, and plan an anesthetic
technique that reduces the risk of complications.

31. CVS EVALUATION
Hypertension (70% to 90% of patients) and coronary artery disease
(CAD) (8O% of patients), are common. Assessment of baseline cardiac
function is mandatory .
ECG CHANGES: LVH on ECG secondary to high incidence of HTN. Ischemic
changes can be present due to coronary artery involvement
All patients should undergo pharmacologic stress/nuclear perfusion
tests to evaluate myocardial ischemic risk .
Angioplasty or CABG should be considered in patients with significant
CAD(in elective surgeries)
All antihypertensives and antianginal drugs to be continued.(except ?ACE
inhibitors and ARB)

32. BP Lowering Agents:
A.Vasodilators:
1.Nitroprusside: relaxes arterialVenous smooth muscles.
loading dose: 0.5-1 mics/kg/min
cyanide toxicity: 8-10 mics/kg/min
2. Nitroglycerine: venous>arterial
But it also improves coronary blood flow via coronary artery
vasodilatation.
infusion: 1-4 mics/kg/min

33. 3.Fenoldopam: D1 receptor agonist. Vasodilator action.
Increases renal blood flow, hence renal protective effect
Treats acute hypertension.
Dose: 0.05 mics/kg/min
Max dose: 0.8 mics/kg/min
4. Nicardipine: CCB
Bolus:0.5-2 mg IV
Infusion: 5-15 mg/hr

34. B. Beta- blockers:
1. Labetalol: alphabeta blocker
5-10 mg loading bolus given
If no effect reached double the dose
Can be repeated until target BP reached or total dose of 300 mg is reached.
Infusion : 1 mg/min
Small bolus dose: every 10-30 min
2. Esmolol: 1 blocker
Bolus: 500 mics/kg for 1 min
Infusion: 50 mics/kg/min
Max:300 mics/kg/min
3. Metoprolol: 2.5-5 mg bolus to max 15 -20 mg

35. Blood Product Requirements For TAAA Repair
Massive And
Rapid blood loss
is expected

36.  Five to ten units of pRBCs should be immediately available in the
operating room.
 A similar amount of fresh frozen plasmas, typically in a ratio of one per
two or three pRBCs transfused should be available .
 Platelets and Cryoprecipitate should be arranged.

37. RESPIRATORY SYSTEM
1. Postop respiratory failure is a major complication (25% to 45%
of cases) and a leading cause of mortality
2. A detailed history and thorough physical exam should be
taken(h/o smoking and COPD is common)
3. A chest radiograph can be useful at detecting underlying lung
infection. Reversible airway obstruction and pulmonary infection
should be treated with bronchodilators, antibiotics, and chest
physiotherapy
4. In the patient with severe signs and symptoms of COPD, an ABG
analysis can be done. ABG analysis can evaluate the patient's ability
to oxygenate and ventilate. Patients with severe COPD tend may be
chronically hypercarbic and hypoxic.A preoperative ABG is
particularly helpful at guiding perioperative ventilatory
management and predicting the likelihood of postoperative
mechanical ventilation in these patient
5. Preoperative pulmonary function testing
6. Incentive spirometry and preop lungs optimisation

38. RENAL SYSTEM
 Presence of preoperative CKD is the single most important predictor of
the development of acute renal failure after surgery on the thoracic aorta.
 In cases with extensive visceral compromise and aneurysmal occlusion of
more than one visceral/renal artery, a creatinine level >2.5 mg per
Dl, then it is a relative contraindication to elective surgery unless
there is evidence of potential renal function preservation or recovery with
renal artery reconstruction
 Preoperative hydration and avoidance of hypovolemia, hypotension,
low cardiac output, and nephrotoxic drugs during the perioperative
period are important to decrease the likelihood of postoperative renal
failure

39. CNS
 Duplex imaging of the carotid arteries or angiography of the
brachiocephalic and intracranial arteries may be performed
preoperatively in patients with a history of stroke or TIA.
 Patients who sustain major neurological deficit have significantly
increased risk of perioperative mortality.
 Patients with severe stenosis of one or both common or internal carotid
arteries could be considered for carotid endarterectomy before elective
surgery on the thoracic aorta.
 Thus always listen for carotid bruits and ask
TIA/CVA symptoms.

40. Preoperative Lab test
 Complete blood count
 serum electrolytes, BUN, creatinine, HbA1C
 coagulation profile
 Blood grouping and cross matching
 CXR: for s/o heart failure, pulmonary disease or pneumonia.
 PFT/ABG
 ECG:
 ECHO
 CAG
 High risk consent for surgery (with post op ICU and ventilation)

41. MANAGEMENT
OF ANESTHESIA

42. MONITORS
1. 5 lead ECG with ST segment analysis: To identify intraoperative
myocardial ischemia and arrhythmias.
2.Arterial line:
a) Right radial artery is the preferred site because if cross clamp is placed
proximal to left subclavian the flow to left UL will be occluded.
b) Rt Femoral arterial : for assesment of perfusion distal to aortic cross
clamp.
3. CVP
? PA catheter:to assess preload and afterload as well as to monitor for
perioperative left ventricular dysfunction and ischemia

43. 4.TEE: To assess global ventricular function, guide intravascular fluid therapy and
monitor for MI. visualisation of LV in end diastole allow rapid assessment of ventricular
filling .
5. Large bore IV access: into IJV and antecubital vein
6. SSEP and MEP: to monitor for spinal cord ischemia
7. Core and peripheral temperature monitoring
8. Urine output
9. Entropy, NMT, RT insertion
10. Warming devices
11. ? CPB in thoracic aneurysms
12 vasoactive agents to be kept ready in OT
13. Defib and emergency drugs

44. INDUCTION: Avoid hemodynamic changes. Opioid and etomidate can be used for
induction.
Sleeping doses of induction agents.
Muscle relaxant : hemodynamically stable muscle relaxants
High doses of methylprednisolone at induction - beneficial in reducing the
inflammatory response
Intubation: To obtund laryngoscopy and intubation response,short acting
agents such as Nitroglycerine, nicardipine, labetalol, esmolol are ideal for
hemodynamic control.
**Nitroprusside is a/w higher risk of neurological complications
Normal ETT if aneurysm involves abdominal aorta
DLT and OLV will be required for thoracoabdominal aortic aneurysm(crawford
type 1 and type 2)

45. Maintainence: low concentration of inhalation agent/ infusion of propofol with
short acting narcotic.
If SSEP and MEP are being monitored then TIVA will be optimum as inhalation
agent interfere with syanaptic conductions and will decrease amplitude of MEP
INTRAOP ANESTHETIC GOALS:
•Hypertension should be avoided
•HR(70-80) should be maintained
•Lung protective ventilation
•Urine output to be monitored closely
•Temperature maintainence
Extubation should always take place after hemodynamic and metabolic stability

46. AORTA SURGERY- TECHNIQUES
 Abdominal aortic reconstruction - Transperitoneal or
Retroperitoneal exposure.
 Retroperitoneal Approach(commonly followed) -
less fluid shift, faster return of bowel function, lower
pulmonary complications, shorter ICU stay, and lower
overall hospital cost
 more appropriate in cases of truncal obesity, serious
COPD, previous surgeries, and juxtarenal aneurysm.
 Intraoperative blood loss – 500ml to several litres

48. AORTIC CROSS CLAMPING: Blood volume
redistribution

49. Aorta cross clamping: Hemodynamic response

50. SYSTEMS AFFECTED DUE TO CROSS CLAMPING
A. CVS
B. RENAL SYSTEM
C. HUMORAL FACTORS AND COAGULATION
D. MESENTRY
E. METABOLIC DERANGEMENT
F. CSF COMPARTMENT
G. SPINAL CORD

51. Physiologic Changes with Aortic Cross-Clamping
Hemodynamic Changes
 ↑ Arterial blood pressure above the clamp
 ↓ Arterial blood pressure below the clamp
 ↑ Segmental wall motion abnormalities
 ↑ Left ventricular wall tension
 ↓ Ejection fraction
 ↓ Cardiac output
 ↓ Renal blood flow
 ↑ Pulmonary occlusion pressure
 ↑ Central venous pressure

52. THERAPEUTIC INTERVENTIONS
 Afterload reduction
 Sodium nitroprusside
 Inhaled anesthetics
 Amrinone
 Shunts and
 aorta-to-femoral bypass
 Preload reduction
 Nitroglycerin
 Controlled phlebotomy
 Atrial-to-femoral bypass

53. LOWER THE CLAMP-BETTER IT IS
 Infrarenal aortic cross-clamping has limited systemic
hemodynamic effect.
 With lower clamping, blood volume from the
infrasplanchnic vasculature may shift to the compliant
splanchnic vasculature limiting preload changes.
 Existing collateral circulation - maintain lower body
perfusion despite aortic cross-clamping.

54. A. PRELOAD AND AFTERLOAD CHANGES
 Increase in cardiac output can lead to myocardial ischemia due to
increased myocardial oxygen demand
 Due to expected sudden increase in preload, the preload at the
time of aortic clamping should be kept low.
 To decrease proximal aortic pressure(afterload) esmolol can be
used or the depth of anesthesia can be augmented.

55. SYSTEMS AFFECTED DUE TO CROSS CLAMPING
A. CVS
B. RENAL SYSTEM
C. HUMORAL FACTORS AND COAGULATION
D. MESENTRY
E. METABOLIC DERANGEMENTS
F. CSF COMPARTMENT
G. SPINAL CORD

56. B. RENAL HEMODYNAMICS
 level of aortic clamping - most important
 The incidence of acute renal failure - 5% postinfrarenal clamping, 13%
postsuprarenal clamping.
 Renal vascular resistance increases by almost 70% and do not immediately revert
after the release of cross-clamping
 Blood flow is not only reduced with aortic cross-clamping, but also redistributed,
favoring the cortical and juxtamedullary layers over the hypoxia-prone renal
medullary area

57. RENAL PROTECTION
 Fluid administration
 Drugs to augment renal perfusion
 mannitol. (12.5g/70 kg)
dopamine (2 to 3 mcg/kg per minute),
fenoldopam,
ACE inhibitors,
prostaglandins, ,
furosemide
Optimal hemodynamics and maintainence of intravascular volume.

58. SYSTEMS AFFECTED DUE TO CROSS CLAMPING
A. CVS
B. RENAL SYSTEM
C. HUMORAL FACTORS AND COAGULATION
D. MESENTRY
E. METABOLIC DERANGEMENTS
F. CSF COMPARTMENT
G. SPINAL CORD

59. C. Humoral and Coagulation Profiles
 Release of Renin, angiotensin, epinephrine, norepinephrine, PGI2, endothelin,
thromboxane A2 lactate, potassium, oxygen-free radicals, platelets activator,
cytokines, activated complement (C3 and C4), and neutrophil takes place.
 Sequestration of microaggregates and neutrophils contribute to postoperative
pulmonary dysfunction
 Mannitol administration before and after unclamping may be beneficial because of
its function as a hydroxyl free radical scavenger.

60. SYSTEMS AFFECTED DUE TO CROSS CLAMPING
A. CVS
B. RENAL SYSTEM
C. HUMORAL FACTORS AND COAGULATION
D. MESENTRY
E. METABOLIC DERANGEMENTS
F. CSF COMPARTMENT
G. SPINAL CORD

61. D. MESENTRIC ISCHEMIA
 Mesenteric organs.: Visceral ischemia occurs with supraceliac
aortic cross-clamping.
 Bowel ischemia can also lead to an increase in intestinal
permeability with subsequent bacterial translocation,
endotoxemia, and sepsis.
 Endovascular repair - less intestinal ischemic events
 High doses of methylprednisolone at induction - beneficial in
reducing the inflammatory response

62. SYSTEMS AFFECTED DUE TO CROSS CLAMPING
A. CVS
B. RENAL SYSTEM
C. HUMORAL FACTORS AND COAGULATION
D. MESENTRY
E. METABOLIC DERANGEMENTS
F. CSF COMPARTMENT
G. SPINAL CORD

63. E. Metabolic Changes
 ↓ Total-body oxygen consumption
 ↓ Total-body carbon dioxide production
 ↑ Mixed venous oxygen saturation
 ↓ Total-body oxygen extraction
 ↑ Epinephrine and norepinephrine
 Respiratory alkalosis
 Metabolic acidosis
INTERVENTION: analysis of arterial blood gases and electrolytes levels
should be performed carefully.sodabicarb should be given to treat
metabolic acidosis. Hyperkalemia should be treated aggressively
with calcium chloride and soda bicarb.

64. SYSTEMS AFFECTED DUE TO CROSS CLAMPING
A. CVS
B. RENAL SYSTEM
C. HUMORAL FACTORS AND COAGULATION
D. MESENTRY
E. METABOLIC DERANGEMENTS
F. CSF COMPARTMENT
G. SPINAL CORD

65. CSF:
Intracranial hypertension due to systemic hypertension above the
clamp produces redistribution of blood volume and engorgement of
the intracranial compartment(intracranial hypervolemia). The CSF
will get redistributed to spinal space.
.

66. SYSTEMS AFFECTED DUE TO CROSS CLAMPING
A. CVS
B. RENAL SYSTEM
C. HUMORAL FACTORS AND COAGULATION
D. MESENTRY
E. METABOLIC DERANGEMENTS
F. CSF COMPARTMENT
G. SPINAL CORD

67. F. SPINAL CORD ISCHEMIA AND PROTECTION
The spinal cord is supplied by three longitudinal arteries:
a) single anterior spinal artery: supplies the anterior two-thirds of
the spinal cord(75%)
b) paired posterior spinal arteries: supply the posterior one-third
of the spinal cord(25%)

68.  The posterior spinal artery which supplies the sensory tracts in the
spinal cord receive flow from posterior and inferior cerebellar arteries ,
vertebral arteries and posterior radicular arteries.
 Anterior spinal artery:
a) the cervical portion of anterior spinal artery receives flow from vertebral
arteries.
b) The thoracic portion is supplied by anterior radicular arteries.
c) The largest of radicular arteries is called the GREAT RADICULAR
ARTERIES/ARTERY OF ADAMKIEWICZ which is the major blood supply to
lower two thirds of spinal cord
d) The segmental supplier of GRA is variable but is located between T9-T12
in 75% of cases. This variation in origin of GRA explains why even
infrarenal cross clamping is a/w 0.25% incidence of paraplegia

70. Spinal cord perfusion pressure

71.  spinal cord injury is linearly proportional to aortic cross-clamp
time. spinal cord injury is minimal if the aortic cross-clamp time is
less than 15 minutes.
 Thus, spinal cord ischemia may be induced by
1. injury to the anterior spinal artery,
2. distal aortic hypotension during aortic cross-clamping,
3. perioperative hypotension
4. significant increases of CSF pressure
5. perioperative hypoxemia(autoregulation of spinal blood flow is
lost)

72. Spinal Cord Protection Technique:
1. Partial circulatory assistance (left atrium–to–femoral artery
bypass)
2. Cerebrospinal fluid drainage
3. Reduction of spinal cord metabolism by moderate hypothermia
(30° to 32° C) including spinal cooling.
4. Reimplantation of critical intercostal arteries when possible
5. Avoidance of hyperglycemia, and the use of mannitol,
corticosteroids, and/or calcium channel blockers
6. Maintenance of proximal hypertension during cross-clamping,

74. UNCLAMPING OF AORTA

76. MECHANISM BEHIND CHANGES AFTER UNCLAMPING
1. Hypotension:
a) Due to central hypovolumia caused by blood volume
redistribution and pooling into reperfused tissue.
b) Hypoxia mediated vasodilatation
c) Release of vasoactive and myocardial depressant
metabolites from ischemic tissue such as lactic acid.
2 Hypoxemia: due to returning of large volume of desaturated
blood which returns to heart from hypoperfused tissue below
cross clamp, thus causing temporary systemic hypoxemia.

77. 3. Metabolic:
a) Hyperglycemia due to surgical stress
b) Hyperkalemia, hypocalcemia due to massive blood transfusion
4. Acidosis: Acute metabolic acidosis can cause ventricular
irritability, decreased myocardial contractility and profound
vasodilatation

78. Therapeutic Interventions
 ↓ Inhaled anesthetics
 ↓ Vasodilators
 ↑ Fluid administration (TEE can be helpful in determining adequacy of
volume replacement)
 ↑ Vasoconstrictor drugs
 Reapply cross-clamp for severe hypotension
 Consider mannitol
 Consider sodium bicarbonate
 Hypotension >few minutes after removing the cross-clamp then consider
unrecognized bleeding.

79. ENDOVASCULAR ABDOMINAL
AORTA REPAIR

80.  Gaining access to the lumen of the abdominal aorta,
usually via small incisions over the femoral
vessels/iliac vessels
 Arterial sheaths between 16F and 27F are then
advanced into the iliac/femoral arteries and up into the
AAA sac.
 Associated with less hemodynamic stress, endocrine
stress, cytokine release, decline in respiratory function,
compared with open repair

81.  General or regional anesthesia is acceptable for this procedure.
 Local/sedation techniques have been be used successfully for endoAAAR
and endoTAAR.
 Monitoring consists of at least intravascular blood pressure and urine
output monitoring.
 The potential for conversion to an open aneurysm repair must be
considered.

82. Major complications –
a) aneurysm rupture during the time of graft implantation
b) renal insufficiency secondary to contrast use
c) migration of the graft with changes in configuration of the aortic
aneurysm sac
d) endoleak

84. EMERGENCY
AORTIC SURGERY

85.  Overall mortality for a ruptured aortic aneurysm is greater than 50%.
 The worst prognosis occurs in
a) patients older than 80 years
b) systolic blood pressure of less than 80 mm Hg on admission.
c) a prior history of hypertension, angina, or previous MI
d) an operating time of greater than 4 hours.
e) a systolic blood pressure less than 100 mm Hg at the end of surgery
f) blood loss greater than 11,000 mL.
g) Retroperitoneal rupture is more likely to be associated with a
higher rate of survival

86.  Symptoms - pain, faintness or frank collapse, and
vomiting. Rupture frequently accompanied by shock.
 Pulsatile abdominal mass indicates dissection or
rupture
 rapid-sequence tracheal intubation after small doses
of etomidate (0.1 mg/kg) and a steroid to be done.
 Rapid control of the proximal portion of the aorta is
done -balloon may be passed from the femoral artery
under fluoroscopic control to occlude the aorta above
the site of rupture

87. • Now, the patient is resuscitated - with crystalloid,
colloid, packed red blood cells, and even type-specific
cross-matched blood, O-negative washed red blood cells
 large-bore peripheral or central venous catheters are
secured.
 Once the aorta is controlled, additional venous access
and a radial, brachial, or axillary arterial line are
secured.
 CVP or pulmonary artery catheter can now be put
 Echocardiographic probe can be inserted now - rapid
assessment of left ventricular volume and contractility.

88. Dopamine, epinephrine, or norepinephrine and
Vasopressin – to be started.
 acidosis- give sodium bicarbonate and increase
ventilation to help eliminate CO2
 Paralyze and administer propofol, midazolam, and/or
opioids to these patients if they are hemodynamically
stable

89. AORTIC STENOSIS

90. A. ETIOLOGY
B. PATHOPHYSIOLOGY
C. CHANGE IN PV LOOP DUE TO AORTIC STENOSIS
D. DIAGNOSIS
E. MANGEMENT OF ANESTHESIA
F. AS AND SURGERIES.

91. ETIOLOGY
1. Degeneration and calcification: is a process of aging.
2. Presence of a bicuspid aortic valve
3. Rheumatic heart disease
4. Infective endocarditis.
5. Associated with systemic hypertension and
hypercholesterolemia.
6. Atherosclerotic aortic stenosis

92.  Aortic stenosis represents a chronic systolic pressure load on the left
ventricle.
 This elevation increases wall tension in accordance with
 Laplace's law: Wall tension  (Pressure X Radius) /(2 X Wall thickness)
 The ventricle undergoes parallel duplication of muscle fibers in an
attempt to compensate for the increase in tension.
 This results in increased wall thickness or concentric (common center)
hypertrophy and some decrease in radius, thereby normalizing wall stress

94. AS PRESSURE VOLUME LOOP

95. DIAGONOSIS
The classic clinical symptoms of critical aortic stenosis are
1. Angina pectoris
2. Syncope
3. Dyspnea on exertion.
The onset of these symptoms has been shown to
correlate with an average time to death of 5, 3, and 2 years, respectively.
About 75% of symptomatic patients will die within 3 years if they do not
have a valve replacement

96.  SIGNS
1. Slow rising , small volume apex
2. Heaving apex beat
3. S4 may be heard
4. Ejection click(indicates valvular AS and excludes supra and
subvalvular AS:disappears on calcification of aortic valve)
5. Carotid thrill
6. Murmur: A rough, ejection systolic murmur loudest in the aortic
area radiating to carotids and apex
7. AS murmur: low pitched, rough, rasping in character

97. Severity
1. According to S2:
a) Mild stenosis: A2 followed by P2
b) Moderate stenosis: A2 is delayed giving rise to single S2
c) Severe stenosis: reverse splitting of S2(P2-A2)
2. According to valve area:
Normal: 3-4 cm2
Severe: <0.75 cm2/m2 body surface area
Critical: <0.5 cm2/ m2 body surface area

98. 3. Long murmur and late peaking of murmur.
4. According to gradient across aortic valve:
Normal gradient : 0 m Hg
Mild AS : < 25 mm Hg
Moderate AS : 25-40 mm Hg
Severe AS : > 40 mm Hg
5. Silent AS: When severe AS with CCF, here AS murmur is not heard, but
murmur reappears on treating failure.
When MS is associated with AS, usually MS masks the signs of AS

99. INVESTIGATIONS
ECG: LVH with strain pattern
Chest X ray: Post stenotic dilatation of ascending aorta
ECHO: calcified valve, 2D images demonstrating limited aortic valve opening and
motion and left ventricular concentric hypertrophy
Doppler: turbulent, high-velocity jet across the aortic valve,
Cardiac catheterisation
Coronary angiography
Exercise stress testing: to evaluate asymptomatic patients with moderate to
severe aortic stenosis and to identify those with poor exercise tolerance and/or
an abnormal blood pressure response to exercise. Patients with exercise-
induced symptoms might benefit from aortic valve replacement.

100. MONITORS
ECG
Arterial line: before induction
Central venous catheter
PA catheter: NOT PREFERRED AS IT MAY CAUSE ARRYTHMIA
TEE
 Pulmonary artery occlusion pressure may overestimate left
ventricular EDV because of the decreased compliance of the
hypertrophied left ventricle

101. HEMODYNAMIC GOALS
 PRELOAD: FULL
 AFTERLOAD: MAITAIN CORONARY PERFUSION GRADIENT
 CONTRACTILITY IS NOT A PROBLEM: may require inotropic
support if hypotension persist.
 RATE: AVOID BRADY AND TACHY
 RHYTHM: Always sinus. May need cardioversion in nonsinus or
fast rhythms.
 MVO2: avoid tachyand hypotension
 CPB: contractility augmentation may be required secondary to
myocardial stunning.

102. MANAGEMENT OF ANESTHESIA
PREMEDICATION:Incremental doses of midazolam 0.5 mg intravenously
would be administered. Remember that there may be significant delay
in the onset of effect of intravenous medications secondary to pooling
in the pulmonary and left atrial systems
Induction:
An opioid induction agent may be useful if left ventricular function is
compromised.
BDZ and etomidate can be used. Ketamine may induce tachycardia and
should be avoided.
Hemodynamically neutral relaxants(rocuronium, cisatracurium,
vecuronimum) should be used

103. MANAGEMENT OF ANESTHESIA
1. Normal sinus rhythm must be maintained: Left ventricle is dependent on a
properly timed atrial contraction to produce an optimal left ventricular EDV.
Loss of atrial contraction, as during junctional rhythm or atrial fibrillation, may
produce a dramatic decrease in stroke volume and blood pressure.
2. Heart rate: is important because it determines the time available for
ventricular filling, for ejection of the stroke volume, and for coronary perfusion
Tachycardia: decreases the time for left ventricular filling and ejection and
reduces cardiac output.
Bradycardia: overdistention of the left ventricle
1 The onset of junctional rhythm or bradycardia requires prompt treatment
with glycopyrrolate, atropine, or ephedrine
2 Tachycardia: beta blockers/ esmolol
3 SVT: cardioversion to be done

104. 3. Optimize intravascular fluid volume to maintain left
ventricular filling and venous return.
4. Plasma potassium concentrations should be monitored and
maintained within the normal range.
5. Potential surgical causes of haemodynamic instability should
be considered and modified wherever possible, e.g. using a hip
prosthesis that does not require cement.
6. As for all valve lesions, appropriate antibiotic prophylaxis
should be given and strict aseptic precautions adhered to.

105. 7.HYPOTENSION
• No Hypotension:
• Hypotension reduces coronary blood low and results in myocardial
ischemia and further deterioration in left ventricular function and
cardiac output.
• Aggressive treatment of hypotension is mandatory to prevent
cardiogenic shock and/or cardiac arrest. (norepinephrine,
phenylephrine or mephentermine must be at hand)
• CPR is not effective in patients with aortic stenosis because it is
difficult to create an adequate stroke volume across a stenotic
aortic valve with cardiac compression.
 Anaesthetic techniques that reduce systemic vascular resistance
(e.g. regional neuroaxial techniques) must be used with
extreme caution although successful cases of carefully titrated
epidural and spinal blocks using catheters have been reported

106. PATIENT WITH AORTIC STENOSIS
1. Patients are prone for sudden death so valve replacement is normally
needed
2. Surgical Valve replacement when systolic gradient across the valve is >40
mm Hg and when there is progression of LV dysfunction
3. If patient is unfit for surgery, percutaneous transluminal aortic valvuloplasty
can be tried. It is also useful in children and young adults with congenital AS,
and also as a bridge to surgery in patients with severe LV dysfunction
4. Simple commisural incision under direct vision is also done
5. Transcatheter aortic valve replacement can be done.

107. AORTIC STENOSIS AND CPB for AVR
 These patients are dependent on their atrial kick for adequate ventricular
filling volume and can rapidly become hypotensive and ischemic following
the onset of supraventricular tachycardia or atrial fibrillation (which are
not uncommon during atrial cannulation)
Therefore, it is of particular importance that every preparation for
the initiation of CPB be made before atrial manipulation.
 Increased muscle mass of ventricular hypertrophy can be more difficult to
adequately protect with cardioplegia. Careful attention to surface cooling,
myocardial temperature measurement, and the use of retrograde
cardioplegia can be helpful.

108.  Following aortic valve replacement, hypertension from left
ventricular output now unopposed by any valvular lesion can
result in stress on suture lines and excessive bleeding.
 It is important to remember that the compliance of the left
ventricle is unchanged by surgery and still critically dependent on
adequate preload and sinus rhythm.

109. POST OPERATIVE
 Monitor patients with invasive monitoring
 Adequate pain control avoids catecholamine induced tachycardia and
hypertension
 Maintain appropriate intavascular filling, BP and sinus rhythm.
 NSAID not to be used as these patients are in incresed risk of renal failure

110. PERIPHERAL ARTERY BYPASS

111.  Peripheral arterial disease results in compromised blood low to the
extremities.
 Chronic impairment - atherosclerosis,
acute arterial occlussion- arterial embolism
 Peripheral arterial insuiciency is an ankle-brachial index of less than 0.9.
 The ankle-brachial index is calculated as the ratio of the systolic blood
pressure at the ankle to the systolic blood pressure in the brachial artery.

112. RISK FACTORS
1. older age
2. h/o smoking
3. family history
4. Smoking
5. diabetes mellitus
6. Hypertension
7. obesity,
8. dyslipidemia.

113. SYMPTOMS
1. Intermittent claudication: the metabolic requirements of
exercising skeletal muscles exceed oxygen delivery.
2. Rest Pain: when the arterial blood supply does not meet even the
minimal nutritional requirements of the affected extremity.

114. SIGNS
 Decreased or absent arterial pulses are the most reliable physical
findings associated with peripheral arterial disease.
 Signs of chronic leg ischemia include subcutaneous atrophy, hair
loss, coolness, pallor, cyanosis, and dependent redness.
 Patients may report relief with hanging the affected extremity over
the edge of the bed, a move that increases hydrostatic pressure in
the arterioles of the affected limb.

115. DIAGONOSIS
1. Doppler ultrasonography
 In the presence of severe ischemia, the arterial waveform may be
entirely absent.
2. The ankle-brachial index is a quantitative means of assessing the
presence and severity of peripheral arterial stenosis. A ratio of less
than 0.9 is associated with claudication, a ratio of less than 0.4 with
rest pain, and a ratio of less than 0.25 with ischemic ulceration or
impending gangrene.

116. 3. Duplex ultrasonography can identify areas of plaque formation
and calcification as well as blood flow abnormalities caused by
arterial stenoses.
4.. Transcutaneous oximetry can be used to assess the severity of
skin ischemia in patients with peripheral arterial disease. The
normal transcutaneous oxygen tension of a resting foot is
approximately 60 mm Hg. It may be less than 40 mm Hg in patients
with skin ischemia.
4.MRI and contrast angiography are used to guide endovascular
intervention or surgical bypass.

117. TREATMENT
Medical therapy:
1. Supervised exercise training programs :can improve the walking capacity of
patients with peripheral arterial disease even though no change in ankle-
brachial index can be demonstrated.
2. Stop smoking: Patients who stop smoking have a more favorable prognosis
than those who continue to smoke.
3.Aggressive lipid-lowering therapy: It slows the progression of
peripheral atherosclerosis.
4.Treatment of diabetes mellitus : It can slow microvascular disease
progression.

118. Surgical management:
Revascularization: indicated in patients with disabling claudication ,
ischemic rest pain or impending limb loss.
can be achieved by endovascular interventions or surgical
reconstruction
 Endovascular interventions : Percutaneous transluminal
angioplasty of arteries can be done
 Has a high success rate in iliac arteries. Low success in femoral and
popliteal arteries.
 After percutaneous transluminal angioplasty and stenting of
peripheral vessels, restenosis remains a signiicant problem,
particularly in long lesions, small-diameter vessels, and recurrently
stenotic lesions

119.  Surgical reconstruction
 Aortobifemoral bypass is a surgical procedure used to treat
aortoiliac disease.
 Femorofemoral bypass can be performed in patients with
unilateral iliac artery obstruction.
 Infrainguinal bypass procedures using saphenous vein grafts or
synthetic grafts include femoropopliteal and tibioperoneal
reconstruction.
 Amputation is frequently necessary for patients with advanced
limb ischemia in whom revascularization is not possible or has
failed.
 Lumbar sympathectomy is occasionally used to treat critical limb
ischemia in cases of persistent vasospasm.

120. MANAGEMENT OF ANESTHESIA
 The principal risk during reconstructive peripheral vascular surgery is
myocardial ischemia, due to the high prevalence of CAD in this patient
population.
 Because patients with claudication are usually unable to perform an
exercise stress test, pharmacologic stress testing with or without
echocardiography or nuclear imaging is helpful.
 Depending on the severity of coronary artery disease treatment of the
ischemic heart disease by percutaneous coronary intervention or
coronary artery bypass grating may be considered before
revascularization surgery is performed.
 (ACC/AHA) guidelines, unstable angina is considered an active cardiac
condition requiring treatment or optimization before nonemergent
surgery.
 However, in patients with anatomically significant but stable coronary
artery disease vascular surgery can proceed,

121.  Epidural or spinal anesthesia offers the advantages of:
a) increased graft blood low,
b) postoperative analgesia
c) less activation of the coagulation system, few
d) postoperative respiratory complications.
 Intraoperative heparinization is not, in itself, a contraindication to
epidural anesthesia, but risk of bleeding may increase when the patient is
also taking other anticoagulants or antiplatelet agents.
 If epidural catheter placement is attempted,it should occur at least 1
hour before intraoperative heparinization.
 In addition, before placement of the catheter is attempted,the surgical team
should be consulted regarding the possible need to delay the procedure in
the event of a bloody tap.