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blood pressure lateral pressure exerted by the flowing blood on aortic vessel wall
Pressure
Definition
Physio. significance
Systolic
Diastolic
peripheral resistance
Pulse
systolic diastolic
stroke Volume
perfusion pressure
pressure
Mean blood
pressure
b)
Factors affecting BP
Physical
BP= CO X PR or BP = SV X HR X PR
Physiological
Factors increasing BP- obesity, salt intake, exercise, anxiety, meals, cold, old
age
Factors decreasing BP- child, female, sleep, standing,
Pathological
(Clinical)
secondary(Renal)
Factors decreasing BP (cause of hypotension )- shock
Vasomotor centre (VMC)
Structure of VMC
1) Vasoconstrictor area or area C-l. - located bilaterally in the anterolateral portions of
upper medulla.
2) Vasodilator area or area A-l- located bilaterally in anterolateral portions of lower half of
medulla.
3) Sensory area or A-2- located bilaterally in the tractus solitarius, in the poster lateral
portions of the medulla and lower pons.
Inputs of VMC
1) inhibitory inputs- from baroreceptors (carotid and aortic sinus thro 9 and 10 cranial
nerves to NTS), lungs, parts of cerebral cortex and limbic system including hypothalamus.
1) excitatory inputs- from chemoreceptors (carotid and aortic body thro 9 and 10 cranial
nerves to NTS), pain receptors from skin and joints, parts of cerebral cortex and limbic
system including hypothalamus. Hypoxia and hypercapnia in brain (due to cerebral
ischemia) is strong direct stimulus for VMC
outputs of VMC
Stimulation of VMC causes stimulation of sympathetic and inhibition of parasympathetic
nervous system (vagus) and vice versa.
c)
Regulation of BP
1) baroreceptors reflex
2) atrial low pressure / cardio-pulmonary
reflex
3) chemo receptor reflex
4) CNS-Ischemic reflex
5) abdominal compression reflex
6) stress relaxation and reverse stress
relaxation
7) capillary fluid shift mechanism
d)
pressure back to normal. But this reflex is not very powerful controller of arterial blood
pressure. Still it is important as it is stimulated at low pressure and helps in preventing
further fall in blood pressure.
4) CNS-Ischemic reflex
When blood flow to the vasomotor centre in the brain stem is decreased enough to cause
nutritional deficiency (i.e. cerebral ischemia) the neurons in the vasomotor centre are
strongly excited. This is due to accumulation of CO2, lactic acid locally near the vasomotor
centre. Excitation of vasomotor centre causes strong sympathetic stimulation leading to
vasoconstriction leading to increase in blood pressure. Peripheral vessels become totally
occluded at certain areas, e.g. kidneys. This most powerful response that activates
sympathetic vasoconstrictor system strongly is called as CNS ischemic response. It is
initiated when blood pressure falls below 60 mm Hg. This acts as an emergency arterial
pressure control system. If rise of pressure does not relieve CNS ischemia, neuronal cells
begin to suffer and within 3 to 10 minutes become totally inactive.
Example of CNS-Ischemic reflex is Cushing reaction- When CSF pressure rises and becomes
equal to arterial pressure; it compresses the arteries in the brain and cuts off the blood
supply to the brain. This initiates the CNS ischemic response. This causes rise in blood
pressure. When blood pressure becomes greater than CSF pressure, blood flows through
the vessels of brain and ischemia is relieved. Blood pressure comes to equilibrium at a new
level. This effect is called Cushing reaction. It protects the vital centers in the brain.
When blood volume and pressure is low the vessel constricts over a small volume and
pressure inside rises, this is termed reverse stress relaxation.
powerful mechanism, iii) work on infinite gain principle means makes 100% correction in BP.
Other mechanisms
11) Some role is played by other hormones like ANP, ADH, adrenaline etc especially in
emergency conditions.
14) Some role by local vasoconstrictors like - endothelins (ET1,2), serotonin
15) And some role by local vasodilators- NO, PGE2, histamine, bradykinin
e)
Experimental studies
one kidney Goldblatts hypertensionWhen one kidney is removed and a constrictor is placed on the renal artery of the remaining
kidney, then within few minutes arterial pressure begins to rise and continues to rise for
several days. The hypertension produced in this way is called one kidney Goldblatts
hypertension. The early rise in blood pressure is due to renin-angiotensin vasoconstrictor
mechanism. The second rise is caused by fluid retention.
two kidney Goldblatts hypertensionHypertension that develops when the artery to one kidney is constricted while artery to the
other kidney is still normal is called two kidney Goldblatts hypertension.
f)
Measurement of BP
Treatment
-life style-Drugs- There are many antihypertensive drugs. The common drugs are:
-Which decrease the activity of sympathetic nervous system, e.g. beta blockers.
-Which decrease tubular absorption of salt and water, e.g. diuretics
-Which block the action of renin-angiotensin, e.g. angiotensin converting enzyme inhibitors.
-Drugs paralyzing the smooth muscle of renal vasculature, e.g. calcium channel blockers
a)
b)
Physiological
Pathological
(Clinical)
Factors increasing heart rate (cause of tachycardia- heart rate 100 /mt or
more)- fever, anemia, hypoxia, hyperthyroidism
Factors decreasing heart rate (cause of bradycardia- heart rate 60 /mt or
less)- hypothyroidism, hypothermia, increase BP, increase ICP, drugs
c)
Shock
a)
Definition of shock
Inadequate blood flow to body cells specially vital organs heart / brain
b)
Causes of shock
Shock caused by reduced cardiac output
1) Hypovolumic shock. There is decrease in blood volume due to any cause, e.g.
hemorrhagic shock (injury, fracture), dehydration shock (diarrhea, vomiting, excess
sweating, and burns), and surgical shock.
2) Cardiogenic shock, due to decreased pmping ability of the heart because of cardiac
abnormalities, e.g. myocardial infarction, toxic states of heart, severe heart valve
dysfunction, heart arrhythmias.
3) Obstructive shock, caused by obstructive blood flow, e.g. tension pneumothorax,
pulmonary embolism, cardiac tumor, etc.
4) Neurogenic shock, caused by general or spinal anesthesia, brain damage, emotional
fainting.
5) Anaphylactic shock, an allergic reaction which causes marked venous and arteriolar
dilatation and increased capillary permeability due to release of histamine or histamine like
substances.
c)
Stages of shock
1. Non-progressive stage (compensated stages).
Following circulatory compensatory mechanisms (- feedback mechanisms) eventually cause
d)
1.
2.
3.
4.
5.
e)
Treatment of shock
-Blood or plasma transfusion. If the shock is due to hemorrhage transfusion of blood is the
best therapy. If shock if due to plasma loss, plasma or appropriate electrolytic solution can
correct the shock. Plasma substitute such as dextran can be used.
-Saline. Less effective.
2. Sympathomimetic drugs
They mimic sympathetic stimulation. They are most useful in neurogenic and anaphylactic
shock. They are not useful in hemorrhagic shock.
3. Other therapies
-Head low position
-Oxygen
-Glucocorticoids: They are useful because they increase the strength of heart in last stages
of shock, by stabilizing lysosomal membranes they prevent release of enzymes of cells and
help in metabolism of glucose by the severely damaged cells.
f)
Hemorrhage
-Uncompensated stage (due to + feedback mechanisms) in this stage vicious cycle starts.
shock itself leads shock finally death
4) Treatmenti) Fluid replacement therapy- in hemorrhage transfusion of blood is the best therapy.
ii) Other therapies- -Head low position, oxygen, glucocorticoids
Definition and effects-Failure of the heart to pump enough blood to satisfy the needs of the
body is called cardiac failure. It may be manifested in two ways:
-forward failure or decrease in cardiac output which causes weakness or fainting.
-By damming of blood in the veins behind the left causing pulmonary edema and dyspnea or
behind the right heart causing peripheral edema.
Causes -Acute or chronically progressive coronary artery disease, Malfunction of heart
valves, Congenital abnormalities of the heart, Severe hypertension.
Types of shock
left and right sided failure
In large number of patients with acute failure, left sided failure predominates over right
sided failure leading to unilateral left sided failure. Very rarely there is unilateral right sided
failure. When there is predominant left heart failure, right heart pumps normal quantity of
blood to the lungs but blood is not pumped out of lungs into the systemic circulation
because of left sided failure. This causes increased volume of blood to be retained in the
lungs, increased pulmonary capillary pressure (pulmonary vascular congestion) and
pulmonary edema.
Acute stage of compensated failure- When there is sudden damage to the heart as in
myocardial infarction, pumping ability of the heart is immediately depressed. This causes
reduction in cardiac output to as low as 2 1/min. It also causes damming of blood in the
veins resulting into increased systemic venous pressure so that right atrial pressure rises to 4
mm Hg. This low cardiac output still sustains life but is associated with fainting.
When cardiac output becomes low, different circulatory reflexes are activated within 30
seconds, e.g. baroreceptor reflex, chemoreceptor reflex, CNS ischemic response, reflexes
originating in heart. Due to these reflexes, there is strong sympathetic stimulation within
few seconds which causes
Direct effect on the heart. If musculature of the heart is diffusely damaged but still
functional, it strengthens the musculature. Or if the part of the muscle has become non-
functional, normal muscle is stimulated and compensates for non-functional muscle. Thus
heart becomes a stronger pump. Sympathetic stimulation also causes increased tone in the
blood vessels, especially the veins. This results into increased venous return. This, in turn,
increases the pumping ability of the heart increasing cardiac output to about 4.2 1/min
adequate to sustain life.
Chronic stage of compensated failure- After the few minutes of acute attack, a prolonged
secondary state begins which causes: (a) retention of fluid by the kidneys, and (b)
progressive recovery of the heart.
-Retention of fluid by the kidneys. Decreased cardiac output decreases the urine output and
therefore causes retention of fluid and increase in blood volume. When it is moderate, it
helps in compensating the diminished pumping ability of the heart. It increases mean
systemic filling pressure causing flow of blood towards the heart. Secondly it distends the
veins, reduces the venous resistance and increases the flow of blood towards the heart.
If cardiac pumping ability is greatly reduced (less than 25 to 50% of normal) then blood flow
to kidneys is greatly reduced and there is low urinary output. Also there is retention of
excess fluid but it has no beneficial effect on circulation as heart is already pumping at its
maximal ability. This leads to development of edema which is detrimental.
-Progressive recovery of the heart. Heart gradually recovers because of new collateral blood
supply and hypertrophy of undamaged musculature. This is achieved ordinarily within 5 to 7
weeks.
Thus there is compensation for the damage (compensated heart failure) and person has
normal resting cardiac output but if he performs heavy exercise, pumping ability of the heart
cannot be increased to a desired level and symptoms of acute failure may return, i.e. cardiac
reserve is reduced in compensated heart failure.
This is treated by: (i) strengthen the heart by giving cardiotonic drugs, (ii) by administering
diuretic drugs and (iii) by diet (by reducing salt and water intake)