3. A 72-year-old female, with a history
of diabetes mellitus, with no allergy.
Coronary angiography revealed:
• LAD: tight lesion at the bifurcation
with D1& D2 has tight ostial lesion.
• LCX: Diffusely disease.
• OM: Diffusely disease.

4. • LV: Normal size and wall thickness
Moderately impaired LV systolic
function.
Moderate global hypokinesia.
EF= 40%.
• Other chambers and valves were
normal.

5. • Premedication: Pt was pre medicatated
by P.O. valium 5 mg at midnight and 6 Am,
plus 10 mg morphine on calling to OR.
• Arterial cannulation was done before
induction of GA, while venous CVP and
large bore cannula were inserted
after smooth un eventual induction of

6. • Maintenance of anesthesia was
carried by Propofol, nimbex infusion,
and supplemental titrated doses of
midazolam, Fentanyl, and Morphine
guided by BSI, and the operative steps.
• Heparin achieved satisfactory ACT
result.

8. • Ventilator was kept on with
- A low tidal volume 150 ML
- FI02 50%
- Frequency 12/min.
• Maintenance of Anesthesia by
Propofol, Nimbex infusion, and
supplemental of midazolam, Fentanyl,

9. • Preparing adequate equivalent
Protamine dose ready for infusion
• Preparing blood and its product.
• Adrenaline 50 n g started during the
second proximal anastomosis.
• Reassume normal mechanical
ventilation.
• Achieving HR. 108 and BP 130/ 80
• CVP reading had a mean of 10. It was
temporally elevated with the filling

11. • Insulin infusion together with K
correction was the second natural
inotropic to be administrated.
• Drop by drop Protamine started very
slowly while Bp was 156/90.
• According to protocol; Platelets
infusion started, and were to be
followed by blood and FFP according
to CVP reading guide and surgeon
advice.

12. • Blood pressure was gradually
dropping and accordingly inotropic
adrenaline does was increased to
maximum 200 ng ,
• Noradrenalin was administrated and
also reached maximum 200 ng in order
to keep the systolic Bp in the range of

13. • When ½ Protamine had been given,
Anesthetist requested to discontinue
protamine infusion, Surgeon insisted
to finish Protamine before removing
the aortic cannula.
• Maximum doses of nor and adrenaline
infusion were able to maintain a

15. • Increasing insulin infusion to 6U/H
• Running maximum K infusion 40 MEq/hr
• Protamine was finished
• Considering NaHC03 for correction of
acidosis.
• Discussing nitroglycerin infusion with
the surgeon to lower the CVP reading,

17. • Despite Maximum inotrope and
vasopressors
• Systolic BP started rapid dropping
120- 100- 80- till 67 mmHg
• RV Distension
• 40 mmHg reading of CVP
• Sluggish myocardial contractility
• Ventricular arrhythmia
• Bradycardia

18. • Hyperventilation
• Inotropic and vasopressors kept
maximum
• Bolus Adrenaline 1 mg
• Surgeon regretted, & incriminated
nitroglycerine to be the cause of the
catastrophe, and requested to
administrate bolus 1 g Calcium
chloride.
• Internal cardiac massage for less
than ½ min was effective to over come

19. • Bp restored to 240/130
• Development of ventricular
arrhythmia necessitate bolus
lidocaine followed by 2 mg /kg / hr
infusion
• Marked acidosis necessitated
administration of a total dose of 200

21. • Pt was weaned form IABP and
Pacemaker and extubated
successfully within 24 hr.
• Elevated Renal function tests were
returned to normal with in 5 days.

23. • Protamine remains the mainstay drug
for heparin
neutralization during cardiac
surgery. Frequently, protamine
causes transient hypotension from
histamine release, which is more
apparent if rapidly injected

24. • The systemic hypotension typically
occurs secondary to poor LV filling
associated with the severe RV
dysfunction.
• In our case maximum inotropes and
vasopressors were able to maintain
BP and coronary perfusion till the

25. • Protamine systemic hypotension
mediated by:
1- Histamine release
2- Endothelium derived relaxing
factor, i.e., NO
• This vasodilating effect is not
observed in the presence of a heparin-
protamine complex.
• Protamine-induced severe pulmonary

26. During CPB, complement activation
takes place.
• The production of prostacyclin, a
potent vasodilating prostaglandin,
increases during the early stages of
CPB, but decreases progressively
during re warming and reperfusion of
the lungs.
• The production vasoconstricting
thromboxane A2 and B2 follows an
opposite pattern, reaching the

27. • Thromboxane are at their highest
levels at the time of Protamine
administration
• Acid-base interaction between
protamine and heparin “polyanionic
polycationic interaction” further more
activate complement and potentiate
the pulmonary vasoconstricting effect
of thromboxane possibly aggravated
by concomitant platelets
administration.

28. • Inotropic support of the failing
myocardium may combine calcium with
adrenaline in an attempt to augment
the haemodynamic actions of each
drug.
• Calcium blunts adrenaline induced
increases in blood pressure and
cardiac output in animals and human.
• Ca blunts epinephrine's beta-
adrenergic actions in postoperative
cardiac surgery patients.

29. During myocardial ischemia there
is a Membrane
depolarization
• Fall in ATP and loss of
• Rise in lactate excitability
• Decrease in intracellular pH
• Increase in the intracellular
Ca which further consumes ATP.
• Membrane ionic pumps and Ventricular
channels are disrupted fibrillation

30. The main causes of reperfusion
injury following prolonged ischemia
• Cytosolic Ca2+ loading Exacerbate
• Generation of mitochondrial
reactive oxygen species dysfunction

31. • Ventricular fibrillation
• Myocardial stunning
• Loss of intracellular proteins
Further
• Promoting an compromise
inflammatory response the cardiac
function
• Cytokine release
• Complement activation

32. 1- Stop Protamine administration if it
was not finished.
2- Re heparinization to decrease
heparin-protamine complexes and
stopping thromboxane release from
macrophages
3- Hyper ventilation with 100% FI02
4- Maximum inotropic and vasopressors
given through a left atrial
catheter………… Why?

33. 1- Inhaled: prostacyclin, nitric oxide.
2- Nitroglycerin, but it increases
pulmonary shunt
3- Cyclic AMP-specific
phosphodiesterase inhibitors
e.g. milrinone amrinone, enoximone,
but they
result in systemic hypotension
4- Ketanserin

34. • Nitroglycerine exerts a direct effect
on the pulmonary circulation in doses
that do not affect systemic
resistance vessels or the myocardium
and do not activate neurohumoral
reflexes
• Uniquely it reduces pulmonary artery
pressures in addition to pulmonary
vascular resistance due to its ability
to dilate venous capacitance vessels.

35. • Ketanserin is a quinazoline
derivative that selectively blocks
S2-serotonergic receptors. it has α1
receptor blocking and H1
histaminergic antagonistic
properties.
• Unlike Nitroglycerine the use of I.V
ketanserin 1.0 to 2.0 mg, over a period
of 10 minutes, does not change, shunt
fraction, does not block hypoxic

36. • The fear of postoperative bleeding,
the urge to transfuse blood products
for haemostatic purposes, the over
looking of the developing clinical
status; were the reasons beyond all
of these catastrophes happened in
this case.
• Settled appropriate protocols for
management of possible complications
and sticking to it is much more prudent