Cardio Vascular System Regulatory Mechanism Youtube Lecture Handouts

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Cardiovascular Regulating or Control Mechanisms

The basic mechanisms involved are:

• Systemic Regulation

• Neural

• Humoral

• Local Regulation

Systemic Mechanical Neural

Includes:

• Medullary cardiovascular control centre

• ANS supply to heart and blood vessels

• Afferent to medullary centers

• Role of skeletal nerves and muscles

Effect of Sympathetic Stimulation

On: 1. Heart

• +ve chronotropic effect increase in Heart rate,

• +ve inotropic is increase in force of contraction

• +ve Dromotropic is Conductivity

• +ve Bethmotropic is Contractility

2. Peripheral vascular system

• Vasoconstriction &

• Vasodilatation

• Both are achieved by increasing or decreasing number of impulses in the concerned nerve

Sympathetic Vasodilatation

• By reduction in sympathetic tone

• Parasympathetic vasodilator nerves

• Axon Reflex (dorsal root vasodilatation)

• Sympathetic cholinergic vasodilator

Axon Reflex

• Local response

• Does not depend on CNS

• Antidromic conduction

• At nerve endings substance P is released & it produces vasodilatation

• (Read Triple Response)

Axon Reflex

Cholinergic Vasodilators

• Neurotransmitter is Acetylcholine

• Vasodilatation

• Eg. Skeletal muscles, liver, heart, lungs

Systemic Reg.-Humoral Mech

Includes:

• Circulating vasodialotors-

• Kinins

• VIP (vasoactive intestinal peptide) and

• NP (atrial natriuretic peptide)

Circulating Vasoconstrictors-

• Epinephrine

• N.E.

• Angiotensin II

• ADH (Vasopressin or antidiuretic hormone)

Role of Ions

Ions:

• Calcium- vasoconstrictor

• Potassium- vasodilator

• vasodilator

• vasodilator sp. in brain

Local Mechanisms

It includes:

• Autoregulation

• Local vasoconstrictors

• Role of endothelium

Nitric Oxide

• Is endothelium derived relaxing factor

• It is potent vasodilator

Endothelins:

• Formed by endothelium

• Produce vasoconstriction

Changes During Muscle Exercise

1. Mass sympa. Discharge: while signals are transmitted from cerebral cortex to muscles they are also transmitted to VMC

• Increase heart rate & force of con.

• Most peripheral vessels contract except Cerebral, Coronaries & Vessels of active muscles

2. Venous return:

• Contraction of muscular walls of vein

• Contraction of other venous reservoirs

• ↑venous return

• Increase in cardiac output

CVS- SHOCK

Definition: Is a condition characterized by INADEQUATE TISSUE PERFUSION

Types –4 types

1. Hypovolemic

2. Cardiogenic

3. Distributive

4. Obstructive

1. Hypovolemic Shock /Cold Shock

• Decreased blood volume

• Causes:

  Hemorrhage- External or internal blood loss

• Dehydration-

  • Skin------Burns (plasma loss)

  • Kidneys--DM. Diabetes Insipid us

  • GIT------ Diarrhoea or vomiting

• Traumatic shock - Is special type of hypovolaemic shock which is associated with neurogenic shock caused by severe pain

• Pain inhibits vasomotor centre

2. Cardiogenic Shock

Inadequate cardiac output

Causes:

• Myocardial Ischemia

• Cardiac arrhythmias

• Congestive heart failure

• Severe valvular dysfunctions

3. Distributive Shock / Warm or Low Resistance Shock

Increased capacity of circulating system due to vasodilatation

Three types

• Anaphylactic- histamine in sensitive persons causes vasodilatation as well there is increase in capillary permeability

• Septic - Septicemia is a condition in which bacteria circulate & multiply in the blood & release toxic products. (Toxins sp. Gram –ve bacteria)

High fever & vascular smooth muscle paralysis causes vasodilatation

Neurogenic- caused by

↓ Symp. Tone,

↑ Vagal tone as in vasovagal syncope or emotional fainting

4. Obstructive Shock

Causes

• Impairment of ventricular filling due to some external pressure on heart

• Pericardial tamponade (pressure caused by bleeding in the pericardium)

• Tension pneumothorax

• Constrictive pericarditis

• Pulmonary embolism

Stages of Shock

Three Stages

• Stage I/ non progressive (compensated)

• Stage II-progressive (non-compensated)

• Stage III-refractory (irreversible)

Non Progressive Shock

• Moderate reduction in cardiac output

• 10 to 15 % blood loss has no significant effect

• All compensatory mechanisms come into action and blood pressure comes back to normal. Compensatory Mechanisms operate by –ve feedback.

Progressive Shock

• 15 to 25 % of blood loss

• Vicious cycle of cardiovascular deterioration sets because of +ve feedback mechanisms. They lead to

• Cardiac depression

• Vasomotor failure

• Sludged blood

• capillary permeability

• Release of toxins from ischemic tissues.

• Timely therapeutic intervention is essential. Otherwise it will progress to refractory shock

Refractory Shock/ Irreversible Shock

All therapeutic interventions are usually ineffective & eventually patient dies

Causes:

• Depletion of high energy phosphate compounds like ATP in body cells, especially liver & heart

• Necrosis of cells especially near venous end of capillaries, liver, kidneys, lungs & heart are mainly affected

• Acute tubular necrosis leads to renal failure & uraemic death

• Deterioration of lungs may lead to Shock Lung Syndrome

Treatment

AIM

1. Correcting the cause

2. Helping Physiological Compensatory Mechanisms

• General management

• Replacement therapy

• Sympathomimetic drugs

• Oxygen therapy

• Glucocorticoids

General Measures

• Room temp. --- should not be worm, as sweating & vasodilatation can aggravate shock

• Raising the foot end of the patient’s bed by 6 to 12’’ (Trendelenburg position) promotes venous return specially helpful in hemorrhagic & neurogenic shock

Replacement Therapy

• Haemorrhagic Shock---Transfusion

  • Whole blood

  • If not available Dextran can be used

• Burns ---Plasma or Dextran

  In dehydration IV infusion of ringer or any other appropriate solution should be used

Sympathomimetic Drugs

• Not useful in Haemorrhagic shock

  Symp. System is already very active

• Especially useful in Neurogenic & Anaphylactic Shock

• Dopamine is drug of choice

• Epinephrine or Norepinephrine may also be used

Glucocorticoids

Particularly useful in Anaphylactic shock

Syncopes

Hypertension

Can be

• Experimental – Induced in laboratories

• Clinical

Experimental Hypertension

Can be:

1. One kidney Gold blatt’s Hyper. One kidney removed, a constrictor is placed on the renal artery of remaining kidney

The BP ↑ initial ↑ is by Renin -Angiotensin mec. The second rise is due to fluid retention

2. Two kidney Gold blatt’s Hypert.

• Artery of one kidney clamped

• Artery of other kidney is normal

• An increase in BP. Renin remains high through out

Hypertension

Definition: persistent high BP

• Systolic > 140 Diastolic > 90 mmHg

  Type: 2 types

• Primary or essential- no underlying disease

• A strong hereditary tendency

Essential Hypt

Treatment:

• 1 Diuretics in sub diuretic doses

• 2 Ca ⁺⁺ channel blockers

• 3 β blockers

• 4 ACE inhibitors

• 5 Clonidines

Secondary Hypertension

• Is secondary to some underlying disease

• Treat the underlying cause

Other Types of Hypt

• Systolic Hypt- Definition: only systolic BP is high diastolic may be normal, sub normal or high. Pulse pressure is high

• Neurogenic Hypt.-acute hypt. Caused by strong stimulation of Symp. Nerves. Repeated attacks of stimulation may lead to permanent hypert.

Complications of Hypertension

If left untreated can lead to following lethal effects

• Coronary heart disease, heart attack, heart failure

• Brain haemorrhages, infarcts

• Renal failure, uremia & death.

Blood Supply to Heart

From:

• Coronaries

• Only about 75 to 100 µgm of inner endocardial surface can obtain nutrients from blood present in heart chambers.

Coronary Circulation

Heart is supplied by two coronaries

• Rt. coronary

• Lt. Coronary

Rt. coronary continues as post. Inter -ventricular or post. Descending branch

Left coronary

St. Supplied by Rt. Coronary

Are:

• Rt. Ventricle

• Rt. Atria

• Post. Part of left ventricle

• Post. Part of interventricular septum

• Major part of conducting system of heart including SAN

St. Supplied by Lt. Coronary

Are:

• Lt. atrium

• Ant. Part of Lt. ventricle

• Ant. Part of inter ventricular Septum

• A part of the Lt. branch of bundle of HIS

Coronary Supply

Predominant supply

• 50%----Rt. coronary art.

• 20%----Lt. Coronary art.

• 30%----Equal by two art.

Resting Coronary Flow

• About 4 to 5 % of total cardiac output ie. ~ 225 ml/min

• 0.7 or 0.8 ml/gm of heart muscles

Collateral Circulation in Heart

• Are not true End arteries- normally coronaries function as end arteries. Almost no communication exist among large arteries

• Anastomosis are present among small vessels 20 to 250 µm dia.

Anastomosis in Coronaries

• They open within few seconds after occlusion of large art. & flow gradually↑

• If atherosclerosis causes constriction of coronaries slowly over a period of years collaterals develop at the same time so patient does not get acute cardiac problem

Anastomosis- 2 Types

• Cardiac

• Extra cardiac

• Cardiac Ana.- between the branches of two coronaries

• Extra cardiac- between the branches of coronaries and vessels lying near the heart, as: vasa vasora of aorta, vasa vasora of pulmonary arteries, intra –thoracic arteries bronchial arteries etc.

Cardiac Veins

Venous drainage

• Lt. atria & lt. ven. ----coronary sinus

• Rt. atria & rt. Ven. ---Ant. cardiac veins

• Small part by---------The besian vessels

Pecularities of Coronary Circulation

1. Makes 5 % of cardiac output--- 250 ml.

• 3-6 fold increase during exercise

• Blood flow of lt. ventricle is twice the rt. ventricle

• Flow to ventricles is four times the atrial flow

2. Capillary density of cardiac muscles is 10-15 times that of skeletal muscles about 3000-4000/mm²

3. Myocardium has very high oxygen consumption

• 8 ml/min/100gm. at rest

• O2 extraction nearly 100% during exercise

4. Vessels are compressed during systole

Total occlusion of Lt. ventricular vessels may lead to sub endocardial infarct.

Phasic Changes in Coronary Blood Flow

Lt. Ventricle

• During systole pressure falls to very low value, due to compression of intramuscular vessels

• During diastole flow rises because of relaxation of ventricular muscles.

Rt. Ven. Changes are far less as force of contraction of rt. Ventricle is much less

Factors Affecting Coronary Circulation

• Mean Aortic pressure

• Cardiac output

• Metabolic factors

• Exercise

• Nervous stimulation

Control of Coronary Flow

1. local control: Autoregulation most important

2. Nervous control.

Local control:

Release of vasodialotors like adenosine other sub. are Brady kinins, H⁺, CO₂, prostaglandins.

Nervous Control

• Direct effect: by autonomic N.S.

• Sympathetic:

  • Extensive coronary innervation

  • Transmitter are N.E. & Epinephrine.

  • N.E. acts on alpha receptors, causes vasoconstriction, epicardial vessels have preponderance of alpha receptors

  • Epinephrine acts on beta receptors of coronary vessels & causes vasodilatation

  • Intramuscular arteries are rich in beta receptors

  • Overall effect is vasoconstriction

Parasy. Very little vasodilatation

Indirect Effect:

Symp. Stimulation increases heart rate, force of cont. & metabolism of heart, thus induces relative lack of O2 that will increase blood flow Parasymp. ↓HR & force of contraction O2 consumption & leads to vasocons.

Measurement: Of Coronary Blood Flow

• Nitrous oxide method (kety method): is commonest method based on Fick Principle

• Radionuclides utilization techniques

• Coronary angiographic tech.

• Use of Electromagnetic flow meters

Angina Pectoris

Is pain in pectoral region on exertion?

• Patient gets pain on exertion because the blood supply to heart is not adequate

• Pain is Hot, Pressing & Constricting type & is relieved by rest

  Treatment: Vasodialotors

• Most commonly used is Nitroglycerine

Myocardial Infarction

• Damage to muscle caused by occlusion of coronary

• Subendocardial mus. are specially susceptible & often get infarcted without any evidence of infarction in the outer portions

Myocardial Ischaemia

Irreversible damage of cardiac muscle because of poor blood supply

Cardiac Failure

• Cardiac failure is almost synonymous to ventricular failure

• Failure of heart to function or to pump adequately

• Resting cardiac output-- ~ 5L/min.

• Heavy exercise ---------- ~ 25L/min.

• Failure can be

• Acute as in myocardial Infarction or

• Chronic failure:

• Left ventricular failure

• Rt. Ven. Failure or

• Biventricular failure

Chronic Heart Failure

• In early stages reserve is encroached.

• No disability at rest & failure is said to be compensated

• However further decrease in ventricular power will lead to decompensated failure & clinical manifestation

Lt. Ven. Failure

Causes:

• Primary ventricular dysfunction

• Heavy load is imposed eg. Hypertension

Clinical picture:

• High pressure in lt. atrium

• Pulmonary congestion

• Crepitations heard on auscultation on chest

• Pulmonary edema result in cough & dyspnea

• Orthopnea: dyspnea in lying position

• Decrease output leads to tissue hypoxia

Rt. Ven. Failure

Causes:

• Vent. Dysfunction

• Overload because of mitral stenosis or parenchymal lung diseases like emphysema or fibrosis

• Rt. Ven. Failure secondary to lung disease is known as core pulmonale

Clinical picture:

• Increase back pressure in Rt. Atrium & systemic veins

• Venous congestion leads to

1. Increase in Juglar venous pressure

2. Edema in feet (pedal edema)

3. Ascites

4. Pooling of blood in liver leads to enlargement of liver

Biventricular Failure

• Starts as Lt. or Rt. Ven. Failure

• Ultimately both ven. are involved

• Major features are due to congestion in systemic veins & pulmonary vasculature it is called Congestive Cardiac Failure

In Lt. Vent. Failure: Symptoms Are More

• The patient is very uncomfortable due to cough & difficulty in breathing

• Signs may be absent or may be limited to fine Crepitations.

In Rt. Ven. Failure: Signs Are More

Pt. has

• Prominent Juglar veins

• Raised juglar venous pressure

• Hepatomegaly

• Oedema

• But may have no obvious symptom

High Output Failure

• Paradoxically Cardiac Output is high

• Left to right shunt eg. Fallot Tetralogy. Blood flows from lt. to rt. side so output of rt. Ve. is high & eventually it fails

• Hyperthyroidism high tissue metabolism

Fatal Cardiac Conditions

Causes of death

• Cardiac shock

• Rupture of infarcted area

• Ven. Fibrillation

• Damming of blood on venous system in systemic circulation & specially in lungs can leads to Acute Pulmonary Oedema which can be fatal

Clinical Procedures

• Angioplasty

• Bypass surgeries

• Defibrillator

• Pacemaker

Capillary Circulation

Salient features:

• Diameter is ~4 to 9 microns.

• Unicellular layer of endothelial cells

• Thin slits (pores) between the cells

• Blood flow is intermittent. Vasomotion ie. Intermittent contraction of metarterioles & precapillary sphincter

Types of Capillaries

• Continuous capillaries-- In the brain junctions are tight & forms blood brain barrier

• Sinusoidal cap.--In the liver pores are wide & even plasma proteins can pass

• Fenestrated cap. -- In kidney small oval windows called fenestrae penetrate through the middle of endothelial cells in addition to cleft or pores

Functions:

• Maintain average pressure & flow through tissues. Necessary for transfer of substances

• Lipid soluble suble sub. Pass through cell mem.

• Water soluble through pores

• Forms tissue fluid

Osmotic Pressure

• Plasma osmotic pressure is exerted by all substances present in it. It is 5000 mmHg

• Plasma colloidal osmotic pressure. Is exerted by proteins only. It is 25 mm Hg. Is important for fluid exchange

Applied Aspect: Oedema

There is excessive accumulation of fluid in interstitial spaces

Causes:

• ↑ Filtration pressure

• ↓ Osmotic Press. Gradient across capill.

• ↑ Capill. Permeability

• Inadequate lymph flow

Angiogenesis

Is growth of new vessels

Angiogenic factors:

• Endothelial cell growth factor

• Fibroblast growth factor

• Angiotenin

Elephantiasis

Caused by inadequate lymph flow. Seen in filariasis parasitic worms migrate into lymph nodes & obstruct them. It results in marked swelling specially of legs & scrotum

In Lt. Vent. Failure: Symptoms Are More

• The patient is v. uncomfortable due to cough & difficulty in breathing

• Signs may be absent or may be limited to fine Crepitations.

In Rt. Ven. Failure: Signs Are More

Pt. has

• Prominent Juglar veins

• raised juglar venous pressure

• Hepatomegaly

• Oedema

• But may have no obvious symptom

High Output Failure

• Paradoxically Cardiac Output is high

• Left to right shunt eg. Fallot Tetralogy. Blood flows from lt. to rt. side so output of rt. Ve. is high & eventually it fails

• Hyperthyroidism high tissue metabolism

Heart Transplant

Ectopic foci

Ventricular Extrasystole

Abnormal ECG

Findings in ant. Infarct

Pacemaker Potential

II degree A-V block showing occasional failure

P-R Interval Prolonged

Ectopic Foci

CV- Regulatory Mechanisms

Special mechanisms

• Tubuloglomerular feedback

• Role of concentration of CO₂ and H⁺ controlling blood flow to brain

Ven. Paraoxysmal Tachy

Ventricular Extrasystole

Atrial Paroxysmal Tachycardia

Atrial Extrasystole