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.

• LV: Normal size and wall thickness

Moderately impaired LV systolic

function.

Moderate global hypokinesia.

EF= 40%.

• Other chambers and valves were

normal.

• 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

GA, using Etomidate, Fentanyl,

• 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.

• Except of elevation of BS and its

• 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,

and Morphine given on bypass machine

• 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 of the heart.

• 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.

• By the time Half dose of Protamine

• 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

• 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

systolic BP above 120.

• 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,

He agreed and it was started. Shortly

• 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

• Bolus Adrenaline was ineffective to

• 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 PH hence inotropes, & vasopressors was able to work effectively on the LV.

• 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

• 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.

• 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

• APH is a clinical diagnosis

• 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

development of critical PH, with the

• 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 vasoconstriction and circulatory

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 highest plasma levels after re

• 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.

• Serotonin and other vasoactive

• 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.

• It opposes the stimulant effect of

During myocardial ischemia there is a

• Fall in ATP

• Rise in lactate

• Decrease in intracellular pH

• Increase in the intracellular

Ca which further consumes ATP.

• Membrane ionic pumps and

channels are disrupted

Membrane depolarization

and loss of excitability

Ventricular fibrillation

The main causes of reperfusion injury following prolonged ischemia

• Cytosolic Ca2+ loading

• Generation of

reactive oxygen species

Exacerbate mitochondrial

dysfunction

• Ventricular fibrillation

• Myocardial stunning

• Loss of intracellular proteins

• Promoting an

inflammatory response

• Cytokine release

• Complement activation

Further compromise the cardiac

function

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?

5- Consider Phosphodiesterase

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

• 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.

• 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 pulmonary vasoconstriction

• 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 rather than to regret, blame, or