Nice to see “U” again

Facts about U wave.

The origin of the U wave is still in question, although most authorities correlate the U wave with electrophysiologic events called "afterdepolarizations" in the ventricles.

U waves are usually best seen in the right precordial leads especially V2 and V3.

Differential Diagnosis of U Wave Abnormalities

 Prominent upright U waves

 Sinus bradycardia accentuates the U wave

 Hypokalemia (remember the triad of ST segment depression, low amplitude T waves, and prominent U waves)

 Quinidine and other type 1A antiarrhythmics

 CNS disease with long QT intervals (often the T and U fuse to form a giant "T-U fusion wave")

LVH (right precordial leads with deep S waves)

Mitral valve prolapse (some cases)

Hyperthyroidism

Negative or "inverted" U waves

 Ischemic heart disease (often indicating left main or LAD disease)  Myocardial infarction (in leads with pathologic Q waves)

 During episode of acute ischemia (angina or exercise-induced ischemia)

 Post extrasystolic in patients with coronary heart disease

 During coronary artery spasm (Prinzmetal's angina)

 Nonischemic causes  Some cases of LVH or RVH (usually in leads with prominent R waves)

 Some patients with LQTS (see below: Lead V6 shows giant negative TU fusion wave in patient with LQTS; a prominent upright U wave is seen

in Lead V1)

CSF circulation

Sites where the heart sound are heard

Mitral area: 1st heart sound Tricuspid area: 3rd and 4th heart soundAortic area: 2nd heart soundPulmonary area: 2nd heart sound

Murmur Abnormal heart sounds are called murmur.  Causes 1.Narrowing of valve or stenosis. 2. Incompetence (dilation) of valve. 3.Congenital defect: atrial septal defect, ventricular septal defect. 4. Increased flow through the normal valve. 

Bruits Murmur that are produced outside heart in vascular system are called bruits.  

AUSCULTATION

Process of listening for sound within body usually sounds of thoracic or abdominal viscera by stethoscope.

PULSE

Pulse is rhythmic dilation and elongation of arterial wall passively produced by pressure change duringventricular systole and diastole. Normal range: 60—90beats/min Average 72beats/min.

Normal pulse

Normal pulse tracing is called catacrotic pulse. Pulse has upstroke and down stroke wave.  •The upstroke wave is ‘P’ and has no secondary wave. It is called percussion wave.•Near the middle of down stroke there is sharp depression called dicrotic notch (D).•This dicrotic notch is followed by small wave called dicrotic wave (d).

Pulse wave transmission

P or percussion wave It is the wave from starting of the wave upto dicrotic notch It coincides with ventricular systole. 

Dicrotic notch It is due to sharp fall of arterial pressure. It is due to rolling back of aortic blood to left ventricle at the beginning of ventricular diastole.  

 ATRIAL PULSE DEPENDS UPON

1. Intermittent discharge of blood from contracting left ventricles.2. Resistance to the blood flow in its passage from arterioles into capillaries.3.The elasticity of vessels wall.

Components of examination of Pulse 

Rate: pulse/min, normally coincide with heart rate. Different in premature contraction.

Rhythm: Each beats are at equidistant or not.

Volume: Depends upon stroke volume. More the stroke volume more volume of pulse.

Condition of vessel wall: By feeling pulse we can know condition of blood vessels. Soft and easily compressible pulse indicates: low CO.

Hard and not compressible pulse indicates atherosclerosis.

Character: normal or abnormal, anacrotic (aortic stenosis), water hammer etc.

Radio femoral delay Co-actation of aorta.

Site of feeling a pulse1.Arterial pulse

Radial BrachialAxillary

CarotidFemoralPoplitealPost. Tibial arteryArteria dorsalis pedis

 

2. Venous pulse Jugular vein only can be seen but not felt.

Procedure of feeling arterial pulse

Pulse is felt by placing three finger side by side on radial artery. Fingers are index, middle and ring finger.

Pulse character Abnormal pulse

 Anacrotic pulse: slow rising pulse When secondary wave is found in upstroke of pulse tracing then it is called anacrotic pulse Cause: aortic stenosis

Collapsing pulse (water hammer pulse): It is characterize by rapid upstroke and descend of pulse wave. Cause: Aortic Incompetence, PDA, Arteriovenous fistula.

Pulsus bisferiens (double peak): Combination of slow rising pulse and collapsing pulse. Cause: Aortic Stenosis and Aortic Regurgitation

Pulsus paradoxus: Pulse volume smaller during inspiration and larger during expiration. Causes: Cardiac temponade (pericardial effusion), severe acute asthma.

Pulsus alterans: The amplitude of pulse become alternately large and small. Cause: Left ventricular failure

SINUS ARRYTHMIA When the frequency of pulse is increased during inspiration and fall during expiration, it is called sinus arrhythmia.

Found in children but less commonly in adult.It occurs due to alteration of vagal tone during inspiration.Normal phenomenon.

Blood pressure:

BP means force exerted by blood against any unit area of the vessel wall.

 BP is also defined as lateral pressure exerted by blood on the vessels wall by its contained blood while flowing through it.

Blood pressure 50 mm Hg, means that force exerted on the wall is sufficient to push a column of mercury against gravity up to 50 mm high.

 1 mm Hg of mercury pressure equals to 13.6 mm of water.of mercury is 13.6 times specific gravity than that of water.

 Blood pressure = Cardiac Output X Peripheral Resistance

Importance of BP:

1. It is essential for the flow of blood through the circulatory tree. 2. It provides the motive force for filtration through the capillary bed which is essential for a.Tissue nutrition b. Formation of urine c. Formation of lymph  

 

Basal blood pressure:It is lowest blood pressure necessary for maintaining blood flow sufficient for the need of body at rest.

Causal blood pressure Any pressure that is recorded under ordinary circumstances of life is called casual BP.

Types of blood pressure 

1.Systolic BP

It is maximum pressure in the artery during systole.100-140 mm HgAverage 120mmHg

 

2. Diastolic BPIt is minimum pressure in the artery during diastole.60-90 mmHg.Average 80mmHg.

 

3.Pulse pressure It is difference between systolic and diastolic pressure.

30-40 mmHg 

4. Mean pressure It is diastolic pressure plus one third of pulse pressure 78-98mmHg

Significance of different types of BP

Systolic pressure indicates1.The extend of work done by heart2.The force with which heart is working3.The degree of pressure, which the arterial wall has to withstand.

Diastolic pressure 1.It indicates the constant load against which the heart works

2.Increased diastolic pressure indicates that the heart is approaching to failure.

Pulse pressure It indicates the cardiac output.

Physiological variation of blood pressure   Age: With increasing age BP increases Infant 60/30 mmHg 1 year 80/40 3year 100/60 20 year 120/80 45 year 145/90

70 year 170/95 

Sex: In female BP is slightly lower

Exercise: In heavy exercise systolic BP increases

Diurnal variation: During daytime pressure rises up to 2 o clock then there is a slight fall

During sleep: During sleep there is fall of BP by 15-20 mmHgAfter meal: BP risesEmotion and excitement: Raises systolic BPRespiration: During inspiration BP fall and increases during expiration.

Factors controlling the blood pressure 1. Cardiac Output, which depend on Blood volume Venous return

Force of contraction HR 

2. Peripheral resistance, which depend upon Elasticity of arterial wall Velocity of blood Viscosity of blood

Regulation of blood pressure

1. Nervous regulation2. Humoral regulation

1. Short-term regulation

A. Mechanism acting within seconds

    I. Baroreceptor feedback mechanism      II. Chemoreceptor feedback mechanism III. Central nervous system ischaemia mechanism

B. Mechanism acting within minutes

I. Renin angiotensin vasoconstrictor mechanism II. Capillary fluid shift mechanism III. Stress relaxation changes in vasculature

Baroreceptor mechanism  

Baroreceptor are spray like nerve ending which are stimulated when stretched (Stretch receptor).

Location: In wall of internal carotid artery above the bifurcation In the wall of arch of aorta. 

When blood pressure increased When blood pressure rises above a critical value, the baroreceptor are stimulated ( the stimulation reaches maximum when pressure is 180 mm Hg)

↓ Impulse is carried by Hering’s nerve and Glossopharyngeal nerve to tractus solitarius

↓ This impulse cause inhibition of vasomotor center and excitation of Vagal center

↓ Vasodilatation of peripheral vessels Slowing of heart rate and force of contraction

↓ Both these effect decrease the blood pressure back toward normal level.  

Decrease in blood pressure

When blood pressure falls ↓

Baroreceptor remain inactive ↓

No inhibition to vasomotor center No excitation to vagal center

↓Blood pressure increase back to normal

 As baroreceptor system opposes either increase or decrease in original arterial pressure it is called pressure buffer system.

Baroreceptor are unimportant in controlling blood pressure for long term because baroreceptor reset to the pressure that they are exposed after 1 or 2 day.

Chemoreceptor mechanismChemoreceptor are chemosensitive cells They are sensitive to lack of oxygen and to excess of H ion and CO2  Location: Carotid bodies in bifurcation of internal carotid arteries Aortic bodies in arch of aorta  When blood pressure falls  ↓

There is decrease in blood supply to all tissue of body. So there is decrease in blood supply to chemoreceptor. Decrease blood supply means decrease oxygen conc. and increase CO2 conc.

↓  Decrease supply of oxygen and presence of more carbon dioxide and H+ in chemoreceptor Stimulates these receptor

↓ Impulse are carried by Hering’s and glossopharyngeal nerve to vasomotor center ‘   ↓ Which excites vasomoto pressure center

↓ Increase blood pressure back to normal

CNS ischaemia mechanism  

Decrease blood pressure ↓

Decrease blood supply to vasomotor center in brain ↓ 

Cause nutritional deficiency and decrease Carbondioxide removal   ↓

This leads to cerebral ischaemia  ↓

Cause stimulation of vasomotor sympathetic system  ↓

Increase BP back to normal

Mechanism acting within minutes  

Works only after few minutes following an acute arterial pressure change, mostly activated within 30 min to several hours.

 

1. Capillary fluid shift mechanism

2. Stress relaxation mechanism

Capillary fluid shift mechanism 

When BP increases

Increase capillary hydrostatic pressure   ↓

This cause increase fluid loss out of circulation into the tissue  ↓

This reduce ECF volume   ↓

This reduces blood volume  ↓

Reduces CO  ↓

Reduces BP back to normal   

Capillary fluid shift mechanism (cont)

When BP falls

Decrease in Capillary hydrostatic pressure

  ↓

Capillary absorbs fluid from tissue

  ↓

Increase blood volume

  ↓

Increase CO

  ↓

Increase BP back to normal

Stress relaxation mechanism  

When pressure in blood vessels becomes too high  ↓

This Stress the blood vessels  ↓

This process keeps on stretching wall more and more  ↓

This stretch of wall of vessels cause fall of pressure toward normalVessel achieves a larger diameter.

 This continuing stretch of vessels is called “stress relaxation”

Poiseuille’s law flow across the tube

Q= pai P r4/ 8nl

D= 1 flow 1ml/minD= 2 flow 16ml/minD= 4 flow 256ml/min.

Long-term control mechanism

1. Renal body fluid mechanism2. Renin angiotensin mechanism

Renal body fluid mechanism  

Increase in BP  ↓

Increase renal output of salt and water (Pressure diuresis and pressure natriuresis) ↓ Decrease ECF volume ↓ Decrease Blood volume ↓

Decrease Cardiac output ↓ Decrease BP back to normal   

When blood pressure decrease

Decrease renal water and salt output ↓

Increase ECF volume ↓

Increase blood volume ↓

Increase venous return to heart ↓

Increase Cardiac output ↓

Increase blood pressure to normal

Importance of salt in renal body fluid system for arterial pressure regulation  

Excess salt in body fluid   ↓

Increases osmolality of body fluid  ↓

This stimulate thirst center  ↓

Person drinks water to dilutes ECF salt to normal \  ↓

Increase ECF volume  ↓

Increase BP   Increase salt -increase osmolality in ECF

↓ Stimulates hypothalamic posterior pituitary glands

  ↓Increases ADH secretion

  ↓ ADH stimulates kidney to reabsorb large quantity of water  ↓ Decreasing urinary loss of water  ↓

Increase ECF volume

Renin angiotensin mechanism

Renin is small protein enzyme released by the juxtaglomerular cell of kidney when arterial BP falls too low.

 

Renin is synthesized and stored in an inactive form called prorenin injuxtaglomerular cell of kidney. When arterial pressure decrease in kidney prorenin molecules split and releases renin.

  Decrease BP

  ↓ J G cells secrete Renin, which is released in blood   ↓

Renin causes conversion of Angiotensiongen (plasma protein) into Angiotensin IAngiotensin I is converted to Angiotensin II by Angiotensin converting enzyme (ACE) located in endothelium of lungs vessels.

Angiotensin II has following effects:

1.It cause vasoconstriction of arteriole and veins which increase peripheral resistance---increase BP

2.It help to secrete aldosterone from adrenals-Aldosterone increase salt retention, which in turn increase water reabsorption---- increase ECF volume --- increase blood pressure.

3.Angiotensin II itself can also cause salt and water retention by directly acting on kidney.  

Renin persists in blood for 30min to 1 hour. Angiotensin I is weak but angiotensin II is strong vasoconstrictor.

Angiotensin II persists in blood for 1-2 min, because it is rapidly inactivated by multiple blood enzymes collectively called “ Angiotensinase”.

On the other hand increase blood pressure cause decrease Renin secretion that also decrease the function of angiotensin. So salt and water output of kidney increases which cause decrease ECF volume and ultimately causes decrease blood pressure back to normal.

 

RENIN

Mesangial Cells

Macula Densa

Granular Cells

Measurement of blood pressure

1.Direct method  2.Indirect method a. Palpatory method: can measure only systolic b. Auscultatory method

Turbulence

Turbulent flow means that the blood flows in all the directions within the artery with intermixing. Laminar flow pattern is lost. Due to this turbulent flow the a sound is heard with each pulsation.

Kortkoff sound

Blood flow through the smooth blood vessels produce normally no sounds.

But if the artery is partially occluded by inflated cuff then it creates turbulence of blood flow, the jet of blood through the partially occluded vessel sets up the vibration and produce sound called

kortkoff sound.  

It has four different stages

1. Tapping sound: sudden appearance of faint but clear tapping sound-systolic pressure

2.Loud sound: On decreasing the pressure for (10mmHg) the sound becomes loud.

3.Dull sound: Further decreasing the pressure (10-15mmHg) the sound becomes dull.

4. Muffle sound: Further decreasing the pressure (10-15mm Hg) the sound becomes muffled and gradually disappear .The point at which the muffled sound appears/disappear

coincides with diastolic blood pressure.

How to measure blood pressure

1. Patient should be relaxed, arm supported at thelevel of heart, clothing removed from arm.

2. Cuff neatly applied, correct size (should cover at least 2/3 of the circumference), no leaks.

3. Manometer upright, well supported, if aneroid regularly calibrated.

4. Operator check systolic pressure by palpation, release pressure , avoid parallax error.

1. The blood pressure should be measured in both arms, patient in lying or sitting and standing positions. (postural hypotension).

2. Report as 130/90 mmHg, right/left arm, sitting/ standing.

Hypertension (HTN)

HTN is a clinical condition characterized by persistent rise of blood pressure above the normal range. Normal BP 120/80mm Hg(100-140/60-90).Pre HTN 120-140/80-90 mm HgStage I HTN 140-160/ 90-100 mmHgStage II HTN > 160/100mm Hg

 

Effects of HTN 

1.Excess workload on heart lead to early heart failure, it is a risk factor for CAD.2.High pressure sometimes rupture major blood vessels in brain followed by death of major

portion of brain which is called stroke, which causes paralysis.3.High pressure almost causes multiple hemorrhages in kidney producing many area of renal

destruction and eventually renal failure.4.Hypertensive retinopathy.

Types

1.Primary / essential HTN 2.Secondary HTN 

Essential HTN HTN for which no specific cause Is known.

Secondary HTN It is due to some specific disease like

Renal diseaseCoarctation of aorta PheochromocytomaCushing syndrome

 

Volume loading HTN HTN, which occurs due to excess ECF volume. It is due to salt intake or salt retention by kidney 

Vasoconstrictor HTNIt is due to continuous infusion of vasoconstrictor agent into blood or by excess secretion of vasoconstrictor from endocrine glands

The vasoconstrictors are Angiotensin IINorepinephrineEpinephrine

Shock

Topics coveredconcept of shockDefinitionClassificationDescription of each typeCauses of each typeSign symptoms First aidFurther treatmentDetailed pathophysiology

Shock and syncope

Shock refers to reduction to peripheral tissue perfusion.

Syncope: Partial or complete loss of consciousness with interruption of awareness of oneself and ones surroundings. When the loss of consciousness is temporary and there is spontaneous recovery, it is referred to as syncope or, in nonmedical quarters, fainting. Syncope accounts for one in every 30 visits to an emergency room. It is pronounced sin-ko-pea.

Syncope

Syncope is due to a temporary reduction in blood flow and therefore a shortage of oxygen to the brain. This leads to lightheadedness or a "black out" episode, a loss of consciousness. Temporary impairment of the blood supply to the brain can be caused by heart conditions and by conditions that do not directly involve the heart:

ShockShock is a Cardiovascular Derangement in

1. Deliver Oxygen and Metabolic Substrates

2. Remove Products of Cellular Metabolism

3. Thermoregulation

Definition:A physiological state characterized by a significant, systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery and insufficient removal of cellular metabolic products, resulting in tissue injury.

Classification of Shock

•Hypovolemic

•Septic/Inflammatory

•Cardiogenic (Intrinsic, compressive & Obstructive)

•Neurogenic

•Anaphylactic

CAUSES

Shock can be caused by any condition that reduces blood flow, including:

1.Heart problems (such as heart attack) or heart failure).

2.Low blood volume (as with heavy bleeding or dehydration).

3.Changes in blood vessels (as with infection or severe allergic

reactions).

SYMPTOMS

Dizziness, light-headedness, or faintness.Profuse sweating, moist, pale skin Rapid but weak pulseShallow breathing Chest painUnconsciousness

Hypovolemic Shock

•Decreased preload->small ventricular end-diastolic volumes -> inadequate cardiac generation of pressure and flow

•Causes:

-- bleeding: trauma, GI bleeding, ruptured aneurysms, hemorrhagic pancreatitis

-- protracted vomiting or diarrhea, severe burn

-- adrenal insufficiency; diabetes insipidus-- dehydration

-- third spacing: intestinal obstruction, pancreatitis, cirrhosis

Hypovolemic Shock Signs & Symptoms: Hypotension, Tachycardia, Oliguria,

Diminished Pulses.

Markers: monitor UOP,CVP, BP, HR, Hct,CO, lactic acid and PCWP

Treatment: ABCs, IVF (crystalloid), Transfusion,stop ongoing Blood Loss

Patients on β-blockers, spinal shock & athletes may not be tachycardic

Septic/Inflammatory Shock

Mechanism: release of inflammatory mediators leading to

1. Disruption of the microvascular endothelium

2. Cutaneous arteriolar dilation and sequestration of blood in cutaneous venules and small veins

Causes:

1. Anaphylaxis, drug, toxin reactions

2. Trauma: crush injuries, major fractures, major burns.

3. infection/sepsis: G(-/+ ) speticemia, pneumonia, peritonitis, meningitis, cholangitis, pyelonephritis, necrotic tissue, pancreatitis, wet gangrene, toxic shock syndrome, etc.

Septic/Inflammatory ShockSigns: Early– warm vasodilation, often adequate urine output, febrile, tachypneic.

Late-- vasoconstriction, hypotension, oliguria,

altered mental status.

Monitor/findings: Early—hyperglycemia, respiratory alkylosis, hemoconcentration, WBC typically normal or low. Late – Leukocytosis, lactic acidosis Very Late– Disseminated Intravascular Coagulation & Multi-Organ System Failure.

Tx : ABCs, IVF, Blood cx, Drainage (ie abscess) pressors.

Cardiogenic ShockMechanism: Intrinsic abnormality of heart -> inability to deliver blood into the vasculature with adequate power

Causes:

1. Cardiac: myocardial ischemia, myocardial infarction, cardiomyopathy, myocardiditis

2. Mechanical: cardiac valvular insufficiency, papillary muscle rupture, septal defects, aortic stenosis

3. Arrythmias: bradyarrythmias (heart block), tachyarrythmias (atrial fibrillation, atrial flutter, ventricular fibrillation)

4. Obstructive disorders: PE, tension peneumothorax, pericardial tamponade, constrictive pericaditis, severe pulmonary hypertension.

Cardiogenic Shock

Characterized by high preload (CVP) with low CO Signs/SXS: Dyspnea, rales, loud P2 gallop, low BP, oliguria Monitor/findings: CXR pulm venous congestion, elevated CVP,

Low CO. Tx: CHF– diuretics & vasodilators +/- pressors. LV failure – pressors, decrease afterload, intraaortic ballon pump & ventricular assist device.

Neurogenic Shock

Causes:

1. Spinal cord injury

2. Regional anesthesia

3. Drugs

4. Neurological disorders

Mechanism: Loss of autonomic innervation of the cardiovascular system (arterioles, venules, small veins, including the heart)

Anaphylactic shock

Bee or wasp sting, drugs as penicillin Antigen antibody mediated type 1 hypersensitivity

reaction, systemic, in a previously sensitized person. Ag + Ab mast cell, basophils-release inflamatory

mediators, as histamine, leukotrines, serotonine, TXA2, prostaglandins.

Typical early phase and late phase reactions. Widespread vasodilatation leading to shock. Renal, pulmonary and other system effects.

Monitoring Adjuncts in Shock

Sphyngomanometry

Pulse Oximeter

Arterial Line

Central Venous Line

First Aid

* Check the person's airway, breathing, and circulation. If necessary, begin rescue breathing and CPR.

Even if the person is able to breathe on his or her own, continue to check rate of breathing at least every 5 minutes until help arrives.

If the person is conscious and DOES NOT have an injury to the head, leg, neck, or spine, place the person in the shock position.

First Aid

Lay the person on the back and elevate the legs about 12 inches. DO NOT elevate the head. If raising the legs will cause pain or

potential harm, leave the person lying flat. Give appropriate first aid for any wounds, injuries, or illnesses. Keep the person warm and comfortable. Loosen tight clothing.

Shock position

The position that has the head and torso (trunk) supine and the lower extremities elevated 6" to 12". This helps to increase blood flow to the brain; also referred to as the modified Trendelenburg's position.

IF THE PERSON VOMITS OR DROOLS

Turn the head to one side so he or she will not choke. Do this as long as there is NO suspicion of spinal injury.

If a spinal injury is suspected, "log roll" him or her instead. Keep the person's head, neck and back in line and roll him or her as a unit.

Do Not   

DO NOT give the person anything by mouth, including anything to eat or drink.

DO NOT move the person with a known or suspected spinal injury.

DO NOT wait for milder shock symptoms to worsen before calling for emergency medical help.

Prevention

Learn ways to prevent heart disease, falls, injuries, dehydration, and other causes of shock.

If you have a known allergy (for example, to insect bites or stings), carry an epinephrine pen.

SHOCK

Once someone is already in shock, the sooner shock is treated, the less damage there may be to the person's vital organs (like the kidney, liver, and brain).

Early first aid and emergency medical help can save a life.

Pathophysiology of shock

changes of tissues organs function ， metabolism ， and structures

Causes ↓Shock = hypoperfusion of microcirculation ↓ humoral factors ↑

Shock is an acute, systemic fundamental pathologic process in microcirculatory disorder of perfusion .

(adrenaline, noradrenaline , angiotensin II, histamine etc.)

Pale face

Pale, cold and clammy skin→cyanosis

Dysphoria →Apathy or coma

rapid pulse→weakened pulse

BP(-)→BP↓

oliguriaa→anuria

CausesClinical Manifestations

early phaseserious phase

Pathogenesis and typical

changes of shock

According to the different changes of

microcirculation, the typical shock is

usually divided into three phases :

Ischemic hypoxia phase (Early phase of shock or Compensated phase)

phase of stagnant hypoxia (phase of shock or Decompensated phase)

phase of microcirculatory failure (Late phase of shock or Refractory phase of shock or phase of Disseminated

Intravascular Coagulation)

Leads to

Microcirculation is the blood circulation between the arterioles and venules. between arterioles and venules.

Straight pathwayarteriovenous shunt

True capillary pathway

后微动脉

venule

true capillary A-Vshunt

Precapillarysphincter arteriole

postarteriole

Precapillary resistance = arteriole +Postarteriole + Precapillary sphincter

postcapillary resistance = venule+microvenule

后微动脉

venule

true capillary A-Vshunt

Precapillarysphincter arteriole

postarteriole

β

α

α

α

α

receptor

Precapillary resistance “control ” microcirculatory perfusion volume.

postcapillary resistance “control ”Volume flowing out.

Except heart and brain, alpha and β receptors are distributed in the microvasculature.

Vasodilatory factors : 1 Noradrenaline and adrenaline + β receptors 2 Histamine , kinin , serotonin. 3 Local metabolites (H+ ion, lactic acid.)

Factors causing Vasoconstriction :

1 Activation of sympathetic NS2 Noradrenaline and adrenaline + α receptors3 Angiotensin II, Vasopressin,TXA2 etc.

To be continued----

Pathophysiology of shock.