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Chapter VI Anesthesia and the Circulatory System (II)
Section III, Microcirculation
Section IV: Cardiovascular Regulation
Section 5: The effect of anesthesia on cardiovascular function
role in the inheritance of civilization, the role of books is unprecedented
.
Section III, Microcirculation
First, the structure
Includes: arterioles, intermediate arterioles, capillaries, microcirculation, and venules
Between arterioles and venules: straight access, eucapillary and arteriovenous anastomotic branches: three blood flow pathways
.
Second, the permeability and absorption of capillaries
Colloid osmolality (mainly from albumin) is about 25 mmHg, which is an important factor
in maintaining intravascular circulating blood volume.
Third, the regulation of microcirculation
(1) Neuromodulation: peripheral vascular endings are innervated
by sympathetic and parasympathetic nerves.
(2) Body fluid regulation: the adrenal glands release catecholamines, which act on peripheral blood vessels through blood
circulation.
(3) Local regulation: divided into two types
: metabolic and myogenic.
Metabolic regulation: the concentration of K+, H+, adenosine, phosphate, magnesium salt and carbon dioxide in the blood increases, and the partial pressure of oxygen decreases, all of which cause vasodilation
.
The degree of vasodilation after severe hypoxia is in order: heart> intestine (portal vein>), kidneys> skin > skeletal muscles
Section IV: Cardiovascular Regulation
1.
Central nervous system regulation: including medulla oblongata, pons, hypothalamus and midbrain
.
Second, autonomic regulation
Innervation of the heart
1.
Cardiac sympathetic nerve: preganglionic fibers originate from the lateral angle of gray matter in the chest 1-5, which is cholinergic fibers and the transmitter is acetylcholine
.
Postganglionic fibers are adrenergic neurons and transmitters are norepinephrine
.
2.
Cardiac vagus nerve: preganglionic fibers originate from the medulla oblongata, and preganglionic and postganglionic fibers are cholinergic fibers
.
Third, cardiovascular reflex
(1) Carotid sinus and aortic arch baroreceptor reflexes
The afferent nerve fibers of the carotid sinus follow the glossopharyngeal nerve, and the afferent nerve fibers of the aortic arch enter the brainstem
with the vagus nerve, respectively.
When blood pressure drops to 50-60mmHg, baroreceptors basically lose function
.
(2) Central nervous system ischemic reflex (Cushing).
Increased intracranial pressure causes an increase in sympathetic excitability, an increase in heart rate, an increase in myocardial contractility, an increase in
blood pressure.
(3) Pulmonary vascular, coronary artery and mesenteric vascular reflexes
Elevated pulmonary artery pressure reflexibly accelerates
heart rate.
Surgery to pull the mesentery causes vagus nerve excitation, slowing the heart rate and lowering
blood pressure.
Fourth, body fluid regulation
Section 5: The effect of anesthesia on cardiovascular function
1.
Inhalation anesthetics
1.
Blood pressure and peripheral vascular resistance:
(1) All inhalation anesthetics except nitrous oxide reduce mean arterial pressure
dose-dependently.
(2) The use of nitrous oxide alone has no effect on
peripheral vascular resistance.
(3) Diflurane, sevoflurane and isoflurane have a greater effect on reducing peripheral vascular resistance than halothane
.
2.
Cardiac conduction and heart rate
(1) Inhibit the automaticity of the sinus node, excite the automaticity
of the atrioventricular node and Purkinje fibers.
(2) Halothane increases the sensitivity of the myocardium to epinephrine and easily leads to ventricular premature beats
.
3.
Coronary blood flow: most of them can dilate coronary blood vessels and increase blood flow, and isoflurane has the most obvious effect (coronary blood theft).
4.
Myocardial contractility and cardiac output:
(1) Inhibit myocardial contraction, halothane has the strongest
effect.
(2) Isoflurane and sevoflurane have little
effect on myocardial contractility.
(3) Nitrous oxide has an excitatory sympathetic effect, no myocardial inhibition in healthy people, and obvious
myocardial inhibition in cardiac insufficiency.
(4) Rapidly increasing the inhalation concentration of desflurane causes significant hypertension and accelerated
heart rate.
5.
Pulmonary blood flow: inhalation anesthetic relaxes the bronchi, dilates pulmonary blood vessels, inhibits HPV
.
Nitrous oxide significantly increases pulmonary artery pressure
.
6.
Myocardial protection and pre-adaptation: Inhalation anesthetics have a protective effect on ischemia-reperfusion injury of myocardium.
2.
Intravenous anesthetics
1.
Barbiturates: reduce arterial pressure, reflex heart rate increases
.
2.
Benzodiazepines: have little effect on blood pressure, heart rate, vascular resistance and cardiac output.
3.
Opioids: excite vagus, slow down heart rate, inhibit cardiac contractility
in large doses.
Histamine releasing effect of morphine, lowering blood pressure
.
4.
Ketamine: excitatory sympathetic nerve, suitable for anesthesia
in shock and hypovolemia patients.
However, in patients with sympathetic hyperexcitation and transmitter depletion, ketamine inhibits cardiovascular function and produces hypotension
.
5.
Propofol: inhibits sympathetic effect greater than parasympathetic, inhibits myocardial contraction
.
6.
Etomidate: no effect on sympathetic nerves, no histamine release, can not inhibit cardiovascular stress response
.
Inhibits the adrenal cortex
.
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role in the inheritance of civilization, the role of books is unprecedented
.