CASE STUDY: Buster Hart has a myocardial infarct (heart attack) and his blood

pressure drops. Explain why his blood pressure drops and describe the neural
mechanisms that would attempt to compensate for the decreased blood pressure. In
Buster’s case, his blood pressure was abnormally low following the myocardial infarct.
Gradually (within a few days), however, it returned to normal. Explain how the long term
mechanisms would compensate for this. Hint – think about hormonal effects.

ANSWER: The myocardial infarct damages the heart and reduces its ability to pump
blood and thus will have a drop in blood pressure. With a decrease in cardiac output
there is a decrease in blood pressure and blood oxygen and an increase in carbon
dioxide levels. Neural mechanisms: The baroreceptor reflexes and the chemoreceptor
reflexes compensate by increasing heart rate, stroke volume, and vasoconstriction
(peripheral resistance), all of which increase blood pressure. Hormonal effects: In the
days following the myocardial infarct, long term mechanisms compensate for the still
low blood pressure. The renin-angiotensin-aldosterone mechanism increases
vasoconstriction and reduces fluid loss in the kidneys. With an increase in blood
volume, blood pressure increases.

Explain why blood pressure drops:

Describe the neural mechanism: Heart compensation is the mechanism that the body uses to
maintain stable blood pressure levels. The blood pressure of Mr. Hart went back to normal
because of this mechanism.

Since Mr. Hart’s blood pressure drops, the heart rate will increase to return the heart rate back
to normal. This activity was received by the baroreceptors and sent via vagus nerve and
glossopharyngeal nerve to the NTS in the brainstem.

Due to Myocardial Infarction, there is a decrease in blood pressure.

This results in the sudden stimulation of the baroreceptor. The baroreceptor stimulation leads to
a release of hormones such as ADH to compensate for the decreased blood pressure. This
leads to the stimulation of the NTS or the nucleus of the solitary tract located in the medulla
oblongata. This then stimulates the Autonomic nervous system of the body. Specifically
triggering sympathetic & parasympathetic responses. The sympathetic nervous system starts to
release epinephrine. This causes the heart to increase contraction and constrict blood vessels,
which then results in an increase in blood pressure. As for the parasympathetic, it will halt its
function for its function is to balance the action of the sympathetic response.

On the other hand, if there is an increase in blood pressure, the NTS will deliver a different
response to the ANS which will allow the parasympathetic system to balance the action of the
sympathetic system, releasing epinephrine. Leading to decrease in blood pressure.
Baroreceptors monitor blood pressure
Chemoreceptors monitor chemical composition

The baroreceptors are major short-term mechanisms for regulating the mean arterial blood
pressure.
Changes in blood pressure increase or decrease the stretch in carotid sinus wall and stimulate
baroreceptors. Impulses are sent over sensory fibers in the glossopharyngeal nerves to the
cardio vascular center in the medulla oblongata.
The aortic reflex which maintain the general systolic blood pressure works in a similar manner.
If the mabp drops, there is less stretch and fewer signal are sent to the brain stem

If there’s a decrease in blood pressure, the baroreceptors sense it as a decrease in tension.

Baroreceptors fire at a lower than normal rate and the information is again transmitted to the
NTS that is located in the medulla oblongata the NTS reacts by refraining parasympathetic and
activating sympathetic activities. The sympathetic system releases norepinephrine which acts
on the SA nodes to increase heart rate; on cardiac myocytes to increase stroke volume and on
smooth muscles cells of blood vessels to cause vassoconstriction.

Together, these events rapidly bring UP blood pressure levels back to normal.

The chemoreceptors in the medulla oblongata monitor the bloods carbon dioxide and pH. The
decrease of blood oxygen, increase of carbon dioxide, and decrease of pH decrease the
parasympathetic and increase the sympathetic stimulation of the heart. The decrease of
parasympathetic stimulation of the heart result to the increase of heart rate, while the increase
of the sympathetic stimulation of the heart result to the increase of heart rate and stroke volume.
Also, the increase of sympathetic stimulation of blood vessels, increases the vesseles
constriction. The vessels narrow down because of the sympathetic stimulation.
ANSWER: The myocardial infarct damages the heart and reduces its ability to pump
blood and thus will have a drop in blood pressure. With a decrease in cardiac output
there is a decrease in blood pressure and blood oxygen and an increase in carbon
dioxide levels. Neural mechanisms: The baroreceptor reflexes and the chemoreceptor
reflexes compensate by increasing heart rate, stroke volume, and vasoconstriction
(peripheral resistance), all of which increase blood pressure.
If there’s a decrease in blood pressure, the baroreceptors sense it as a decrease in tension.
Baroreceptors fire at a lower than normal rate and the information is again transmitted to the
NTS that is located in the medulla oblongata the NTS reacts by decreasing the parasympathetic
and increasing sympathetic stimulation of the heart, resulting in an increased heart rate and
force of contraction. . The sympathetic system releases norepinephrine which acts on the SA
nodes to increase heart rate; on cardiac myocytes to increase stroke volume and on smooth
muscles cells of blood vessels to cause vassoconstriction.

The chemoreceptors in the medulla oblongata monitor the bloods carbon dioxide and pH. The
decrease of blood oxygen, increase of carbon dioxide, and decrease of pH decrease the
parasympathetic and increase the sympathetic stimulation of the heart. The decrease of
parasympathetic stimulation of the heart result to the increase of heart rate, while the increase
of the sympathetic stimulation of the heart result to the increase of heart rate and stroke volume.
Also, the increase of sympathetic stimulation of blood vessels, increases the vesseles
constriction. The vessels narrow down because of the sympathetic stimulation.
SCRIPT

Nakaranas po ang anak niyo ng myocardial infarct oh heart attack, nagkaron ng damage sa
kanyang heart kaya naman nahirapan ito mag pump ng blood, at doon po bumaba ang
kaniyang blood pressure.

So meron po tayong mechanism sa katawan natin na nag aattempt mag compensate sa change
ng blood pressure. Eto po ang Neural mechanism. Andito po yung Baroreceptor reflex at
chemoreceptor reflex. Ang baroreceptors minomonitor nila ang blood pressure, sa
chemoreceptors naman ay yung chemical composition. Ngayon sa case po ni Mr. Hart, nag
decrease yung kaniyang blood pressure. Pag nag ddecrease ang blood pressure, nassense ito
ng baroreceptors , at bumababa yung pag send ng signal neto at yung information ay ittransmit
ulit sa NTS, yung nts oh yung nucleus tractus solitarius ay located sa brain specifically sa
medulla oblongata natin yung asa lower part ng brain. Yung NTS magrreact siya by decreasing
parasympathetic and increasing the sympathetic stimulation of the heart, which results in an
increased heart rate and force of contraction.

Yung chemoreceptor reflex naman since sa case nga ni Mr. Hart nagkakaroon ng decrease in
Oxygen at level ng pH at tumataas naman ang level ng Carbon dioxide. Same lang ang process
nila na dinidicrease ang parasympathetic stimulation at iniincrease yung sympathetic stimulation
ng heart na nag rresult din sa pag increase ng heart rate at stroke volume.

Sa madaling salita po ay iniincrease ang heart rate, stroke volume, at nagkakaron ng

vasoconstriction or yung pag tighten ng muscles sa blood vessels natin para maging maliit yung
space. Lahat ito ay para magincrease ang heart rate. Yung mga binaggit ko ay yung attempt ng
neural machanism para mabalik ang blood pressure ni Mr. Hart to normal.