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:
- 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
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
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
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
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.
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.
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
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
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
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
Time | Changes | Leads |
---|---|---|
Hrs aft. Inf. | ST ele. ST dep. | I, aVL & II, III& aVF |
Hrs to days | Q wave | I, aVL, &V |
Weeks | Q wave & QS complex persists ST Seg. Becomes Isoelectric | T wave inverted |
Late years | QS complex persists, | T wave normal |
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