PATHOPHYSIOLOGY

NAUSEA AND
VOMITTING
BY: RAJHMUNIRAN KANDASAMY

NAUSEA VS VOMITING ???

Nausea - uneasiness of thestomachthat often comes
before vomiting.
Vomiting- forcible voluntary or involuntary emptying
("throwing up") of stomach contents through themouth.
NAUSEA 1ST THEN VOMIT

WHY NAUSEA IN THIS PATIENT ?

Vomiting and sinus bradycardia this may occur as a result
of excessive vagal stimulation, which is most common
in inferior MI
Nausea and vomiting may also be aggravated by opiates
given for pain relief
Basically Nausea and Vomiting is A Typical Syptom of A
Serius Underlying Condition of A Patient Which Needs
Immediate Attention

MECHANISMS BEHIND IT !
"The vagus nerve is part of the parasympathetic nervous system .
The sympathetic nervous system is the ""fight or flight"" part of the autonomic
nervous system, whereas the parasympathetic is the rest and digest" part.
The sympathetic side acts to speed things up; increase heart rate, blood pressure,
respiratory rate, dilate pupils, shunt blood away from the GI tract, etc.
The parasympathetic acts to slow things down; lower heart rate, decrease blood
pressure, increase salivation, increase blood flow to the GI tract, etc. The two systems
are always balancing each other.
The confusing part is that when you INCREASE the activity of the parasympathetic
nervous system you DECREASE the activity of the heart; so increased vagal tone
slows heart rate, decreases contractility, and lowers blood pressure.
When the heart is excitable and has certain types of arrythmia, increasing vagal
stimulation can slow the heart down enough to allow the normal pacemaker
functions to take over again (called ""converting"" an arrythmia).

PATHOPHYSIOLOGY

Muscle ischaemia
Acute infarction
Vagal stimulation

Altered autonomic activity (parasympathetic act)

Stimulate chemoreceptor trigger zone- vomiting centre
Nausea

EXTRA : COMPENSATORY
MECHANISM DUE TO VAGAL
STIMULATION

Stimulation of the right vagus nerve.

After transmission excitation through parasympathetic
ganglia ACh is released in the SA node of the heart.
Slowing or stoppage of the heart ensues. The
response is mediated by muscarinic receptors that
activate potassium channels in the supraventricular
cells of the heart.
In the SA node, activation of potassium efflux
causes hyperpolarization .This decreases the rate
of diastolic depolarization. Thus, heart rate is
slowed.