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BLOOD PRESSUREBLOOD PRESSURE
It is the lateral pressure exerted by blood It is the lateral pressure exerted by blood on the wall of the blood vessel during its on the wall of the blood vessel during its flow.flow.
SBP,DBP,PP,MBP.SBP,DBP,PP,MBP. Measurement-Types of instruments-1.Dial Measurement-Types of instruments-1.Dial
manometer.2.Mercury manometer.2.Mercury manometer.3.Electronic manometer.manometer.3.Electronic manometer.
Methods- Palpatory, Auscultatory, Methods- Palpatory, Auscultatory, Oscillatory.Oscillatory.
Systolic pr-120mm Hg(110-140)mm HgSystolic pr-120mm Hg(110-140)mm Hg
Diastolic pr-80mmHg(60-80)mmHgDiastolic pr-80mmHg(60-80)mmHg
Pulse Pr=40mmHgPulse Pr=40mmHg
Mean Arterial Pr=93mmHgMean Arterial Pr=93mmHg
Lateral PrLateral Pr
Total Pr (Perfusion - Pr)Total Pr (Perfusion - Pr)
Normal value AdultNormal value Adult
PressurePressureVelocity- pressure relation-figVelocity- pressure relation-fig
Definition of pressureDefinition of pressure
Total pressure studyTotal pressure study
Lateral pressure study figLateral pressure study fig
Bernoulli, principleBernoulli, principle
(Total pr/Perfusion pr) E=LP+pV2/2(Total pr/Perfusion pr) E=LP+pV2/2
LP=Lateral prLP=Lateral pr
P=rho=density of bloodP=rho=density of blood
V=velocity of BFV=velocity of BF
PHYSIOLOGICAL VARIATIONPHYSIOLOGICAL VARIATION AGE – Increases with age.AGE – Increases with age. SEX – Less in female before menopause. Progesterone SEX – Less in female before menopause. Progesterone
relaxes vascular smooth muscle, Estrogen prevents relaxes vascular smooth muscle, Estrogen prevents atherosclerosis.atherosclerosis.
Body built-obeseBody built-obese Diurnal -Diurnal - DIET – Increases after food intake.DIET – Increases after food intake. SLEEP - DecreasesSLEEP - Decreases POSTURE – Standing decreases.POSTURE – Standing decreases. TEMPERATURE – Hot decreases, Cold IncreasesTEMPERATURE – Hot decreases, Cold Increases PREGNANCY-Pulse pressure increases.PREGNANCY-Pulse pressure increases. ExerciseExercise Fear,anxiety,Fear,anxiety, EmotionEmotion Mental StressMental Stress
Age variationAge variation
Age Systolic mmHg Diastolic mmHg
New born 40 ---
1month-1 year 90 ---
Puberty 120 80
>50 years 140 85
>70Years 150 85
>80years 160 90
EXERCISE & BLOOD EXERCISE & BLOOD PRESSUREPRESSURE
Effect of exerciseEffect of exercise
Variant Effect Cause
Heart rate Chrono/Iono/bath/dromo
Symp.Stim/releaseof catecholamines/decrease vagal tone/Increase Temp
Cardiac output Normal-5l/mt increase to25l/mt
Increase cotractility/VREnhanced
Coronary Blood flow Normal-@250ml/mt increase to1L/mt
Beta recepter mediated coronary V.DilatatiHypoxia/Hypercapnia /acidosis
BP-SystolicBP-Diastolic
IncreaseDecrease
Increase of CODecrease PR
Pulse Pressure Increase More gap in SBP/DBP
DIRECT METHODDIRECT METHOD
INDIRECT METHODINDIRECT METHOD
KOROTKOFF SOUNDSKOROTKOFF SOUNDS
PHASE I – FAINT TAP GRADUALLY PHASE I – FAINT TAP GRADUALLY CLEAR AND LOUDER.CLEAR AND LOUDER.
PHASE II – MURMURISH.PHASE II – MURMURISH. PHASE III – CLEAR AND LOUDER.PHASE III – CLEAR AND LOUDER. PHASE IV – MUFFLINGPHASE IV – MUFFLING PHASE V – DISAPPEARANCE. PHASE V – DISAPPEARANCE.
FACTORS AFFECTING BPFACTORS AFFECTING BP
Blood pressure = C.O X PR So all factors which Blood pressure = C.O X PR So all factors which affect this 2 things affect BP.affect this 2 things affect BP.
C.O –Preload, After load, Heart rate, Myocardial C.O –Preload, After load, Heart rate, Myocardial contractility. contractility.
Peripheral resistance – Diameter of blood Peripheral resistance – Diameter of blood vessel, Viscosity. Vasoconstriction increases PR vessel, Viscosity. Vasoconstriction increases PR & Vasodilatation decreases it.& Vasodilatation decreases it.
Viscosity increases- Polycythaemia, Viscosity increases- Polycythaemia, Hyperprotinaemia, H-Altitude, Decrease temp.Hyperprotinaemia, H-Altitude, Decrease temp.
Viscosity decreases-Anemia, Hypoprotinaemia, Viscosity decreases-Anemia, Hypoprotinaemia, Increase temp.Increase temp.
Determinant of Blood pressureDeterminant of Blood pressure
Central factorsCentral factors--
CO &HRCO &HR
Peripheral factors-Peripheral factors-
1.Periferal resistance1.Periferal resistance
2.Blood volume2.Blood volume
3.Venous return3.Venous return
4.Elastisity of BV4.Elastisity of BV
5.Velocity of flow5.Velocity of flow
6.Diameter of BV6.Diameter of BV
7.Viscosity7.Viscosity
Determinant of Blood PressureDeterminant of Blood Pressure
ResistanceResistance Ohm’slaw=Relation of current/pot diff/resistance=Ohm’slaw=Relation of current/pot diff/resistance=I=pd/rI=pd/rModified Ohms lawModified Ohms lawQ=P/RQ=P/RQ=(P1-P2)/RQ=(P1-P2)/RQ=FlowQ=FlowP=Pressure gradientP=Pressure gradientR=ResistanceR=ResistanceR=(P1-P2)/QR=(P1-P2)/Q Hagen- poiseuille’s law Hagen- poiseuille’s law
Q= Q= (P1-P2)X(P1-P2)Xππr4r4 88ηηll
= ( P1-P2)/ = ( P1-P2)/ (P1-P2)x(P1-P2)x π πr4 r4 = R=8= R=8ηηl/l/ππr4r4 88ηηl l
Medullary cardiovascular control Medullary cardiovascular control centercenter
Concept of Vasomotor ToneConcept of Vasomotor Tone
Innervation of BV—Sympathetic Innervation of BV—Sympathetic dominancedominance
Due to cont.discharge from ILHC of Due to cont.discharge from ILHC of SP.CordSP.Cord
Concept of Vagal ToneConcept of Vagal Tone
Innervation of Heart—Parasympa-Innervation of Heart—Parasympa-dominancedominance
Right VagusRight Vagus
Left VagusLeft Vagus
Method of studyMethod of study----
Dominance of Autonomic toneDominance of Autonomic tone
Innervations of BV-Innervations of BV-
Sympath-Vasoconstrictor fibre-Vaso motor Sympath-Vasoconstrictor fibre-Vaso motor tone.Method of studytone.Method of study
Para sympath Vasodilator fibrePara sympath Vasodilator fibre
Anatomically symp -functionally ParaAnatomically symp -functionally Para
Method of studyMethod of study
Cardiac innervationsCardiac innervations
Symp-T1-T5 ofSymp-T1-T5 of
Parasymp-Vagus (Rt & Lt)Parasymp-Vagus (Rt & Lt)
Method of studyMethod of study
InnervavationInnervavation
Baroreceptor reflexBaroreceptor reflex
REGULATORY MECHANISMSREGULATORY MECHANISMS
REGULATIONREGULATION
These mechanisms try to maintain These mechanisms try to maintain mean B.P within 95-100mmHg.mean B.P within 95-100mmHg.
1.Rapidly acting.1.Rapidly acting. 2.Intermediate.2.Intermediate. 3.Long term.3.Long term. 4.Miscellaneous.4.Miscellaneous.
SHORT TERMSHORT TERM Act within seconds to minutes.Act within seconds to minutes. Control major immediate changes. Control major immediate changes.
Change in posture, Acute blood loss.Change in posture, Acute blood loss. Loss their capacity within days.Loss their capacity within days. Various reflexes.Various reflexes. 1.Baroreceptor reflex.-60-200mmHg.1.Baroreceptor reflex.-60-200mmHg. 2.Chemoreceptor reflex.40-2.Chemoreceptor reflex.40-
100mmHg.100mmHg. 3.CNS Ischemic response.15-3.CNS Ischemic response.15-
50mmHg.50mmHg. 4.Respiratory reflex-Inspi/Expi4.Respiratory reflex-Inspi/Expi
CNS ISCHAEMIC RESPONSECNS ISCHAEMIC RESPONSE
Fall in B.P-20-30mmHg-Decrease Fall in B.P-20-30mmHg-Decrease perfusion to brain-CNS Ischaemia-CO2 perfusion to brain-CNS Ischaemia-CO2 accumulation in VMC-Direct accumulation in VMC-Direct stimulation of VMC (Pressure area)-stimulation of VMC (Pressure area)-Powerful sympathetic discharge all Powerful sympathetic discharge all over body-HR,B.P increase to maintain over body-HR,B.P increase to maintain normal blood supply to brain.normal blood supply to brain.
This mechanism is the final frontier to This mechanism is the final frontier to prevent the death of the person.prevent the death of the person.
BARO & CHEMORECEPTORSBARO & CHEMORECEPTORS
Arterial baroreceptorsArterial baroreceptors
Direct stimulationDirect stimulation Hypoxia, HypercapniaHypoxia, Hypercapnia
Stimulatory inputStimulatory inputFrom Cortex via hypothalamusFrom Cortex via hypothalamus
From pain pathway, Joint, Muscle(Somato Sympathetic reflex) linkFrom pain pathway, Joint, Muscle(Somato Sympathetic reflex) link
From carotid, aortic chemoreceptorFrom carotid, aortic chemoreceptor
Inhibitory inputInhibitory inputFrom cortex via hypothalamusFrom cortex via hypothalamus
From lungFrom lung
From BarorecepterFrom Barorecepter
Factors affecting VMCFactors affecting VMC
MEDULLARY CENTERSMEDULLARY CENTERS
BARORECEPTOR REFLEXBARORECEPTOR REFLEX
CHEMORECEPTOR CHEMORECEPTOR CONTROLCONTROL
LONG TERM REGULATIONLONG TERM REGULATION
R.A SYSTEM-(Long term)R.A SYSTEM-(Long term)
1.Epinephrine/Nor epinephrine1.Epinephrine/Nor epinephrine
2.Thyroxin2.Thyroxin
3.Aldosterone3.Aldosterone
4. Vasopressin4. Vasopressin
5. Serotonin/Bradykinin/histamine5. Serotonin/Bradykinin/histamine
6.VIP6.VIP
7.Prostaglandine7.Prostaglandine
8.Acetyl choline8.Acetyl choline
9.ANP9.ANP
Hormonal regulationHormonal regulation
Chemical Physiologic role Source Type
Nitric oxide Paracrine mediator Endothelium Local
Atrial natriuretic peptide
Reduce blood pressure Atrial myocardium, brain
Hormonal
Vasoactive intestinal peptide
Digestive secretion, relax smooth muscle
Neurons Neural, hormonal
Histamine Increase blood flow Mast cells Local, systemic
Epinephrine (2) Enhance local blood flow to skeletal muscle, heart, liver
Adrenal medulla Hormonal
Acetylcholine (muscarinic)
Erection of clitoris, penis Parasympathetic neurons
neural
Bradykinin Increase blood flow via nitric oxide
Multiple tissues Local
Adenosine Enhance blood flow to match metabolism
Hypoxic cells local
Substances that mediate vascular smooth muscle relaxation
Chemical Physiologic role Source Type
NE ( ) Baroreceptor reflex Sympathetic neurons Neural
Endothelin Paracrine Vascular endothelium Local
Serotonin Platelet aggregation, smooth muscle contraction
Neurons, digestive tract, platelets
Local, neural
Substance P Pain, increased capillary permeability
Neurons, digestive tract
Local, neural
Vasopressin Increase blood pressure during hemorrhage
Posterior pituitary Hormonal
Angiotensin II Increase blood pressure Plasma hormone Hormonal
Prostacyclin Minimize blood loss from damaged vessels before coagulation
endothelium local
Substances causing contraction in vascular smooth muscle
Local RegulationLocal Regulation
Local Vasoconstrictors Local Vasodilators
Endothelial originET1,ET2,ET3
MetabolicOrigin
Endothelialorigin
Co2/LactateH+adenosine
NO
If BP Fall< 60mmHgIf BP Fall< 60mmHg
CNS-devoid of o2CNS-devoid of o2
VMC- StimulatedVMC- Stimulated
Vasocnstriction occurVasocnstriction occur
BP stabilised to save lifeBP stabilised to save life
Cushing Reflex-Cushing Reflex-
CNS Ischemic ResponseCNS Ischemic Response
MISCELLANEOUSMISCELLANEOUS 1.Role of sympathetic nerves-Sympathetic nerves 1.Role of sympathetic nerves-Sympathetic nerves
of kidney are stimulated for several weeks-Renal of kidney are stimulated for several weeks-Renal retention of fluid-Chronic rise of B.P. Probable retention of fluid-Chronic rise of B.P. Probable cause of essential hypertension-Increase cause of essential hypertension-Increase sensitivity of kidneys to sympathetic discharge.sensitivity of kidneys to sympathetic discharge.
2.Role of ADH-Direct effect-Large doses-Increase 2.Role of ADH-Direct effect-Large doses-Increase vasoconstriction-Increase B.P.vasoconstriction-Increase B.P.
Indirect effect-Fall in B.P-Decrease atriocaval Indirect effect-Fall in B.P-Decrease atriocaval discharge.- Increase ADH secretion –Fluid discharge.- Increase ADH secretion –Fluid retention-Rise in B.P-(Reverse)retention-Rise in B.P-(Reverse)
So it has both Short term and long term effects.So it has both Short term and long term effects. Corrects 75% fall in B.P in minutes-Corrects 75% fall in B.P in minutes-
VASOCONSTRICTION.VASOCONSTRICTION. Also has long term effect through kidney. Also has long term effect through kidney.
APPLIEDAPPLIED
HYPERTENSION- HYPERTENSION- 1. ESSENTIAL1. ESSENTIAL
2.SECONDARY (Polycythaemia, O.C Pill, 2.SECONDARY (Polycythaemia, O.C Pill, Cons syndrome, Kidney disease, Cons syndrome, Kidney disease, Endocrine, Thyrotoxicosis.)Endocrine, Thyrotoxicosis.)
HYPOTENSION.HYPOTENSION.