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THE NEUROMUSCULAR JUNCTION
15 basic steps
1. The action potential arrives at the NEURO-MUSCULAR junction.
2. Calcium enters the presynaptic nerve terminal
3. Magnesium moves out
4. The Acetylcholine laden vesicles fuse with the presynaptic membrane
5. Acetylcholine is released then into the synaptic cleft of the neuromuscular junction through exocytosis
6. 2 Acetylcholine molecules bind to the NICOTINIC Acetylcholine receptor
7. At least 25-30% binding is needed
8. An END PLATE POTENTIAL is generated which moves across the sarcolemma and percolates the muscle cell through the T-tubule
9. The DIHYDROPYRIDINE receptor on the T-tubule then STIMULATES the RYANODINE receptor on the intracellular SARCOPLASMIC RETICULUM
10. The CALCIUM is then released from the SARCOPLASMIC RETICULUM and moves into the SARCOMERE
11. It unlocks the TROPOMYOSIN cable from ACTIN exposing the active subunit
12. The MYOSIN head is simultaneously charged into position by ATP
13. MYOSIN binds to ACTIN
14. CONTRACTION OCCURS
15. The MUSCLE SHORTENS

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PULMONARY HYPERTENSION

▪ QUESTION
What is the Definition, the Consequences & the Anesthetic Treatment Strategies for pulmonary hypertension in patients with congenital heart disease ?

▪ ANSWER
1. DEFINITION
Firstly Pulmonary Hyertension is defined as a pulmonary artery pressures greater than 25 mmHg.
2. PREVALENCE in CHD
- Pulmonary hypertension occurs in approximately 5-10% of patients with congenital heart disease
3. CONSEQUENCES
- It leads to increased morbidity and mortality in affected individuals.
- In patients with congenital heart disease, pulmonary hypertension can occur over time if the lesion is not corrected.
As the pulmonary vasculature is continually exposed to high pressures
-> VASCULAR REMODELING occurs
&
pulmonary vessels become LESS DISTENSIBLE
Over time, this leads to
-> right ventricular failure.

5. TREATMENT
Focus on
I. NON PHARMACOLOGICAL
A. Minimizing PVR and maintaining forward flow.
B. Avoiding
•Hypoxia.
•Hypercarbia.
•Acidosis.
•Hypothermia.
•Light anesthesia:
Sympathetic stimulation and pain will increase PVR.
C. Controlling ventilation
However PEEP and atelectasis will increase PVR. So it can be a catch 22 situation
D. Maintaining forward flow: Patients with pulmonary hypertension are quite preload dependent.
As such, hypovolemia should be quickly and aggressively treated.

II. PHARMACOLOGICAL Treatment consists of agents that
A. lower PVR
B. increase Inotropy .

- Inhaled nitric oxide and nitroglycerin will decrease PVR.
- Dobutamine will both decrease PVR and increase ionotropy.
- PDE III inhibitors (such as milrinone) are potent ionodilators that should be considered in acute situations.

Guidance of treatment should be based on invasive monitoring, such as PA information or TEE.

Reference
Miller's Anesthesia,
7th Edition
Page 1947