Cardio Vascular System Regulatory Mechanism YouTube Lecture Handouts

Get top class preparation for competitive exams right from your home: get questions, notes, tests, video lectures and more- for all subjects of your exam.

Get video tutorial on: Examrace YouTube Channel

Illustration: Cardio Vascular System Regulatory Mechanism YouTube Lecture Handouts

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
Illustration: Systemic Mechanical Neural
Illustration: Systemic Mechanical Neural

Effect of Sympathetic Stimulation

On:

  • Heart
    • + ve chronotropic effect increase in Heart rate,
    • + ve inotropic is increase in force of contraction
    • + ve Dromotropic is Conductivity
    • + ve Bethmotropic is Contractility
  • 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

Illustration: 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

  • 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
  • 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

  • Hypovolemic
  • Cardiogenic
  • Distributive
  • 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
Illustration: Causes
Illustration: Causes
Illustration: Causes

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

  • Correcting the cause
  • 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
Illustration: General Measures
Illustration: General Measures

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:

  • 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
  • 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
Illustration: Experimental Hypertension

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

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.
Illustration: Coronary Supply

Resting Coronary Flow

  • About 4 to 5% of total cardiac output i.e.. ~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.
Illustration: Anastomosis- 2 Types

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

  • 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
  • Capillary density of cardiac muscles is 10 - 15 times that of skeletal muscles about 3000 - 4000/mm2
  • Myocardium has very high oxygen consumption
  • 8 ml/min/100 gm. at rest
  • extraction nearly 100% during exercise
  • 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
Illustration: Phasic Changes in Coronary Blood Flow
Illustration: Phasic Changes in Coronary Blood Flow

Factors Affecting Coronary Circulation

  • Mean Aortic pressure
  • Cardiac output
  • Metabolic factors
  • Exercise
  • Nervous stimulation

Control of Coronary Flow

  • Local control: Autoregulation most important
  • 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 that will increase blood flow Parasymp. ↓HR & force of contraction 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 … ~5 L/min.
  • Heavy exercise … ~25 L/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
    • Increase in Juglar venous pressure
    • Edema in feet (pedal edema)
    • Ascites
    • 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
Illustration: Clinical Procedures
Illustration: Clinical Procedures
Illustration: Clinical Procedures
Illustration: Clinical Procedures
Illustration: Clinical Procedures

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 i.e.. Intermittent contraction of metarterioles & precapillary sphincter
Illustration: Salient Features
Illustration: Salient Features

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
Illustration: Types of Capillaries
Illustration: Types of Capillaries

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
Illustration: Functions

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

Illustration: Heart Transplant
Illustration: Heart Transplant

Ectopic Foci

Illustration: Ectopic Foci

Ventricular Extrasystole

Illustration: Ventricular Extrasystole

Abnormal ECG

Findings in ant. Infarct

Image of Abnormal ECGImage of Abnormal ECG
TimeChangesLeads
Hrs aft. Inf.ST ele.

ST dep.

I, aVL &

II, III& aVF

Hrs to daysQ waveI, aVL, &V
WeeksQ wave & QS complex persists

ST Seg. Becomes Isoelectric

T wave inverted
Late yearsQS complex persists,T wave normal
Illustration: Abnormal ECG
Illustration: Abnormal ECG
Illustration: Abnormal ECG
Illustration: Abnormal ECG
Illustration: Abnormal ECG
Illustration: Abnormal ECG
Illustration: Abnormal ECG

Pacemaker Potential

Illustration: Pacemaker Potential
Illustration: Pacemaker Potential

II degree A-V block showing occasional failure

Illustration: Pacemaker Potential
Illustration: Pacemaker Potential

P-R Interval Prolonged

Illustration: P-R Interval Prolonged
Illustration: P-R Interval Prolonged

Ectopic Foci

Illustration: Ectopic Foci
Illustration: Ectopic Foci
Illustration: Ectopic Foci
Illustration: Ectopic Foci
Illustration: Ectopic Foci
Illustration: Ectopic Foci

CV- Regulatory Mechanisms

Special mechanisms

  • Tubuloglomerular feedback
  • Role of concentration of CO2 and H+ controlling blood flow to brain
Illustration: CV- Regulatory Mechanisms
Illustration: CV- Regulatory Mechanisms
Illustration: CV- Regulatory Mechanisms

Ven. Paraoxysmal Tachy

Illustration: Ven. Paraoxysmal Tachy

Ventricular Extrasystole

Illustration: Ventricular Extrasystole

Atrial Paroxysmal Tachycardia

Illustration: Atrial Paroxysmal Tachycardia

Atrial Extrasystole

Illustration: Atrial Extrasystole