Cardio Vascular System Regulatory Mechanism Youtube Lecture Handouts
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Image of Cardiovascular Regulating Mechanisms
Image of Cardiovascular Regulating Mechanisms
Cardiovascular Regulating or Control Mechanisms
The basic mechanisms involved are:
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Systemic Regulation
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Neural
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Humoral
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Local Regulation
Systemic Mechanical Neural
Includes:
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Medullary cardiovascular control centre
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ANS supply to heart and blood vessels
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Afferent to medullary centers
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Role of skeletal nerves and muscles

Image of Systemic Mechanical Neural
Image of Systemic Mechanical Neural

Image of Autonomic Cardiovascular Control
Image of Autonomic Cardiovascular Control
Effect of Sympathetic Stimulation
On: 1. Heart
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+ve chronotropic effect increase in Heart rate,
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+ve inotropic is increase in force of contraction
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+ve Dromotropic is Conductivity
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+ve Bethmotropic is Contractility
2. Peripheral vascular system
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Vasoconstriction &
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Vasodilatation
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Both are achieved by increasing or decreasing number of impulses in the concerned nerve
Sympathetic Vasodilatation
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By reduction in sympathetic tone
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Parasympathetic vasodilator nerves
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Axon Reflex (dorsal root vasodilatation)
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Sympathetic cholinergic vasodilator
Axon Reflex
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Local response
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Does not depend on CNS
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Antidromic conduction
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At nerve endings substance P is released & it produces vasodilatation
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(Read Triple Response)
Axon Reflex

Image of Axon Reflex
Image of Axon Reflex
Cholinergic Vasodilators
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Neurotransmitter is Acetylcholine
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Vasodilatation
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Eg. Skeletal muscles, liver, heart, lungs
Systemic Reg.-Humoral Mech
Includes:
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Circulating vasodialotors-
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Kinins
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VIP (vasoactive intestinal peptide) and
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NP (atrial natriuretic peptide)
Circulating Vasoconstrictors-
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Epinephrine
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N.E.
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Angiotensin II
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ADH (Vasopressin or antidiuretic hormone)
Role of Ions
Ions:
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Calcium- vasoconstrictor
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Potassium- vasodilator
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vasodilator
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vasodilator sp. in brain
Local Mechanisms
It includes:
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Autoregulation
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Local vasoconstrictors
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Role of endothelium
Nitric Oxide
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Is endothelium derived relaxing factor
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It is potent vasodilator
Endothelins:
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Formed by endothelium
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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
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Increase heart rate & force of con.
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Most peripheral vessels contract except Cerebral, Coronaries & Vessels of active muscles
2. Venous return:
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Contraction of muscular walls of vein
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Contraction of other venous reservoirs
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↑venous return
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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
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Decreased blood volume
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Causes:
Hemorrhage- External or internal blood loss
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Dehydration-
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Skin------Burns (plasma loss)
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Kidneys--DM. Diabetes Insipid us
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GIT------ Diarrhoea or vomiting
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Traumatic shock - Is special type of hypovolaemic shock which is associated with neurogenic shock caused by severe pain
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Pain inhibits vasomotor centre
2. Cardiogenic Shock
Inadequate cardiac output
Causes:
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Myocardial Ischemia
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Cardiac arrhythmias
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Congestive heart failure
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Severe valvular dysfunctions
3. Distributive Shock / Warm or Low Resistance Shock
Increased capacity of circulating system due to vasodilatation
Three types
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Anaphylactic- histamine in sensitive persons causes vasodilatation as well there is increase in capillary permeability
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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
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Impairment of ventricular filling due to some external pressure on heart
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Pericardial tamponade (pressure caused by bleeding in the pericardium)
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Tension pneumothorax
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Constrictive pericarditis
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Pulmonary embolism

Image of Cardiac Tamponade
Image of Cardiac Tamponade

Image of Cardiogenic Shock
Image of Cardiogenic Shock

Image of Obstructive Shock
Image of Obstructive Shock
Stages of Shock
Three Stages
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Stage I/ non progressive (compensated)
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Stage II-progressive (non-compensated)
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Stage III-refractory (irreversible)
Non Progressive Shock
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Moderate reduction in cardiac output
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10 to 15 % blood loss has no significant effect
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All compensatory mechanisms come into action and blood pressure comes back to normal. Compensatory Mechanisms operate by –ve feedback.
Progressive Shock
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15 to 25 % of blood loss
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Vicious cycle of cardiovascular deterioration sets because of +ve feedback mechanisms. They lead to
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Cardiac depression
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Vasomotor failure
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Sludged blood
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capillary permeability
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Release of toxins from ischemic tissues.
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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:
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Depletion of high energy phosphate compounds like ATP in body cells, especially liver & heart
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Necrosis of cells especially near venous end of capillaries, liver, kidneys, lungs & heart are mainly affected
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Acute tubular necrosis leads to renal failure & uraemic death
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Deterioration of lungs may lead to Shock Lung Syndrome
Treatment
AIM
1. Correcting the cause
2. Helping Physiological Compensatory Mechanisms
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General management
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Replacement therapy
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Sympathomimetic drugs
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Oxygen therapy
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Glucocorticoids
General Measures
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Room temp. --- should not be worm, as sweating & vasodilatation can aggravate shock
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Raising the foot end of the patient’s bed by 6 to 12’’ (Trendelenburg position) promotes venous return specially helpful in hemorrhagic & neurogenic shock

Image of Use a Fan to Lower Temperature
Image of Use A Fan To Lower Temperature

Image of Place the Victim in Shock Position
Image of Place The Victim In Shock Position
Replacement Therapy
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Haemorrhagic Shock---Transfusion
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Whole blood
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If not available Dextran can be used
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Burns ---Plasma or Dextran
In dehydration IV infusion of ringer or any other appropriate solution should be used
Sympathomimetic Drugs
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Not useful in Haemorrhagic shock
Symp. System is already very active
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Especially useful in Neurogenic & Anaphylactic Shock
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Dopamine is drug of choice
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Epinephrine or Norepinephrine may also be used
Glucocorticoids
Particularly useful in Anaphylactic shock
Syncopes
Hypertension
Can be
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Experimental – Induced in laboratories
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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.
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Artery of one kidney clamped
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Artery of other kidney is normal
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An increase in BP. Renin remains high through out

Image of Two Kidney and One Kidney
Image of Two Kidney And One Kidney
Hypertension
Definition: persistent high BP
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Systolic > 140 Diastolic > 90 mmHg
Type: 2 types
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Primary or essential- no underlying disease
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A strong hereditary tendency
Essential Hypt
Treatment:
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1 Diuretics in sub diuretic doses
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2 Ca ++ channel blockers
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3 β blockers
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4 ACE inhibitors
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5 Clonidines
Secondary Hypertension
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Is secondary to some underlying disease
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Treat the underlying cause
Other Types of Hypt
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Systolic Hypt- Definition: only systolic BP is high diastolic may be normal, sub normal or high. Pulse pressure is high
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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
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Coronary heart disease, heart attack, heart failure
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Brain haemorrhages, infarcts
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Renal failure, uremia & death.
Blood Supply to Heart
From:
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Coronaries
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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
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Rt. coronary
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Lt. Coronary
Rt. coronary continues as post. Inter -ventricular or post. Descending branch
Left coronary
St. Supplied by Rt. Coronary
Are:
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Rt. Ventricle
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Rt. Atria
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Post. Part of left ventricle
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Post. Part of interventricular septum
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Major part of conducting system of heart including SAN
St. Supplied by Lt. Coronary
Are:
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Lt. atrium
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Ant. Part of Lt. ventricle
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Ant. Part of inter ventricular Septum
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A part of the Lt. branch of bundle of HIS
Coronary Supply
Predominant supply
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50%----Rt. coronary art.
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20%----Lt. Coronary art.
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30%----Equal by two art.

Image of Coronary Supply
Image of Coronary Supply
Resting Coronary Flow
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About 4 to 5 % of total cardiac output ie. ~ 225 ml/min
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0.7 or 0.8 ml/gm of heart muscles
Collateral Circulation in Heart
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Are not true End arteries- normally coronaries function as end arteries. Almost no communication exist among large arteries
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Anastomosis are present among small vessels 20 to 250 µm dia.
Anastomosis in Coronaries
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They open within few seconds after occlusion of large art. & flow gradually↑
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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
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Cardiac
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Extra cardiac
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Cardiac Ana.- between the branches of two coronaries
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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.

Image of Anastomosis
Image of Anastomosis
Cardiac Veins
Venous drainage
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Lt. atria & lt. ven. ----coronary sinus
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Rt. atria & rt. Ven. ---Ant. cardiac veins
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Small part by---------The besian vessels
Pecularities of Coronary Circulation
1. Makes 5 % of cardiac output--- 250 ml.
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3-6 fold increase during exercise
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Blood flow of lt. ventricle is twice the rt. ventricle
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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
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8 ml/min/100gm. at rest
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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
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During systole pressure falls to very low value, due to compression of intramuscular vessels
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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

Image of Phasic Changes in Coronary Blood Flow
Image of Phasic Changes In Coronary Blood Flow

Image of Systole (Ejection Phase)
Image of Systole (Ejection Phase)
Factors Affecting Coronary Circulation
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Mean Aortic pressure
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Cardiac output
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Metabolic factors
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Exercise
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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
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Direct effect: by autonomic N.S.
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Sympathetic:
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Extensive coronary innervation
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Transmitter are N.E. & Epinephrine.
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N.E. acts on alpha receptors, causes vasoconstriction, epicardial vessels have preponderance of alpha receptors
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Epinephrine acts on beta receptors of coronary vessels & causes vasodilatation
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Intramuscular arteries are rich in beta receptors
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Overall effect is vasoconstriction
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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
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Nitrous oxide method (kety method): is commonest method based on Fick Principle
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Radionuclides utilization techniques
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Coronary angiographic tech.
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Use of Electromagnetic flow meters
Angina Pectoris
Is pain in pectoral region on exertion?
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Patient gets pain on exertion because the blood supply to heart is not adequate
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Pain is Hot, Pressing & Constricting type & is relieved by rest
Treatment: Vasodialotors
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Most commonly used is Nitroglycerine
Myocardial Infarction
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Damage to muscle caused by occlusion of coronary
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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
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Cardiac failure is almost synonymous to ventricular failure
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Failure of heart to function or to pump adequately
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Resting cardiac output-- ~ 5L/min.
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Heavy exercise ---------- ~ 25L/min.
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Failure can be
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Acute as in myocardial Infarction or
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Chronic failure:
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Left ventricular failure
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Rt. Ven. Failure or
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Biventricular failure
Chronic Heart Failure
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In early stages reserve is encroached.
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No disability at rest & failure is said to be compensated
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However further decrease in ventricular power will lead to decompensated failure & clinical manifestation
Lt. Ven. Failure
Causes:
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Primary ventricular dysfunction
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Heavy load is imposed eg. Hypertension
Clinical picture:
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High pressure in lt. atrium
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Pulmonary congestion
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Crepitations heard on auscultation on chest
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Pulmonary edema result in cough & dyspnea
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Orthopnea: dyspnea in lying position
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Decrease output leads to tissue hypoxia
Rt. Ven. Failure
Causes:
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Vent. Dysfunction
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Overload because of mitral stenosis or parenchymal lung diseases like emphysema or fibrosis
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Rt. Ven. Failure secondary to lung disease is known as core pulmonale
Clinical picture:
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Increase back pressure in Rt. Atrium & systemic veins
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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
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Starts as Lt. or Rt. Ven. Failure
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Ultimately both ven. are involved
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Major features are due to congestion in systemic veins & pulmonary vasculature it is called Congestive Cardiac Failure
In Lt. Vent. Failure: Symptoms Are More
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The patient is very uncomfortable due to cough & difficulty in breathing
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Signs may be absent or may be limited to fine Crepitations.
In Rt. Ven. Failure: Signs Are More
Pt. has
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Prominent Juglar veins
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Raised juglar venous pressure
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Hepatomegaly
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Oedema
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But may have no obvious symptom
High Output Failure
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Paradoxically Cardiac Output is high
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Left to right shunt eg. Fallot Tetralogy. Blood flows from lt. to rt. side so output of rt. Ve. is high & eventually it fails
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Hyperthyroidism high tissue metabolism
Fatal Cardiac Conditions
Causes of death
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Cardiac shock
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Rupture of infarcted area
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Ven. Fibrillation
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Damming of blood on venous system in systemic circulation & specially in lungs can leads to Acute Pulmonary Oedema which can be fatal
Clinical Procedures
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Angioplasty
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Bypass surgeries
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Defibrillator
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Pacemaker

Image of Clinical Procedures
Image of Clinical Procedures

Image of Bypass Grafting
Image of Bypass Grafting

Images of Saphenous Vein Bypass
Images of Saphenous Vein Bypass

Image of Automated External Defibrillator (AED)
Image of Automated External Defibrillator (AED)

Image of Several Thousand Volts for a New Milliseconds
Image of Several Thousand Volts For A New Milliseconds
Capillary Circulation
Salient features:
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Diameter is ~4 to 9 microns.
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Unicellular layer of endothelial cells
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Thin slits (pores) between the cells
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Blood flow is intermittent. Vasomotion ie. Intermittent contraction of metarterioles & precapillary sphincter

Image of Capillary Circulation
Image of Capillary Circulation

Image of Endothelial Cell
Image of Endothelial Cell
Types of Capillaries
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Continuous capillaries-- In the brain junctions are tight & forms blood brain barrier
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Sinusoidal cap.--In the liver pores are wide & even plasma proteins can pass
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Fenestrated cap. -- In kidney small oval windows called fenestrae penetrate through the middle of endothelial cells in addition to cleft or pores

Image of Types of Capillaries
Image of Types of Capillaries

Image of Basement Membrane of Types of Capillaries
Image of Basement Membrane of Types of Capillaries
Functions:
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Maintain average pressure & flow through tissues. Necessary for transfer of substances
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Lipid soluble suble sub. Pass through cell mem.
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Water soluble through pores
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Forms tissue fluid

Capillary Pressure and Plasma Colloid Osmotic Pressure
Image of Capillary Pressure And Plasma Colloid Osmotic Pressure
Osmotic Pressure
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Plasma osmotic pressure is exerted by all substances present in it. It is 5000 mmHg
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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:
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↑ Filtration pressure
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↓ Osmotic Press. Gradient across capill.
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↑ Capill. Permeability
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Inadequate lymph flow
Angiogenesis
Is growth of new vessels
Angiogenic factors:
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Endothelial cell growth factor
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Fibroblast growth factor
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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
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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

Image of Heart Transplant
Image of Heart Transplant

Image of Capillary Network
Image of Capillary Network
Ectopic foci

Image of Normal Conduction and Atrial Fibrillation
Image of Normal Conduction And Atrial Fibrillation
Ventricular Extrasystole

Image of Ventricular Extrasystole
Image of Ventricular Extrasystole
Abnormal ECG
Findings in ant. Infarct
Time | Changes | Leads |
Hrs aft. Inf. | ST ele. ST dep. | I, aVL & V3-6 II, III& aVF |
Hrs to days | Q wave | I, aVL, &V5-6 |
Weeks | Q wave & QS complex persists ST Seg. Becomes Isoelectric | T wave inverted |
Late years | QS complex persists, | T wave normal |

Image - 1 of Parasitic Worms
Image - 1 of Parasitic Worms

Image - 2 of Parasitic Worms
Image - 2 of Parasitic Worms

Image of NTS Reflex Arcs
Image of NTS Reflex Arcs

Image of Afferent from BR
Image of Afferent From BR

Image of Direction of Impulse
Image of Direction of Impulse

Image of Reflex Action and Reflex Arc
Image of Reflex Action And Reflex Arc

Image of Orthodromic Conduction
Image of Orthodromic Conduction
Pacemaker Potential

Image of Pacemaker Action Potential
Image of Pacemaker Action Potential

Image of Mid-Clavicular and Mid-Axillary Line
Image of Mid-Clavicular And Mid-Axillary Line
II degree A-V block showing occasional failure

II Degree A-V Block Showing Occasional Failure Image - 1
II Degree A-V Block Showing Occasional Failure Image - 1

II Degree A-V Block Showing Occasional Failure Image - 2
II Degree A-V Block Showing Occasional Failure Image - 2
P-R Interval Prolonged

Image of P-R Interval Prolonged
Image of P-R Interval Prolonged

Orthodromic Conduction and Antidromic Conduction
Image of Orthodromic Conduction And Antidromic Conduction, Direction of Impulse
Ectopic Foci

Image of Normal Sinus Rhythm and Atrial Fibrillation
Image of Normal Sinus Rhythm And Atrial Fibrillation

Normal Heart and Enlarged Heart Due to Cardiomyopathy
Image of Normal Heart And Enlarged Heart Due To Cardiomyopathy

Donor Heart Stitched
Donor heart stitched

Image of Air Line Connects through Skin to Power Console
Image of Air Line Connects Through Skin To Power Console

Image of Capillary Network and Arteriole Structure
Image of Capillary Network And Arteriole Structure

Image of Phasic Coronary Blood Flow and Aortic Pressure
Image of Phasic Coronary Blood Flow And Aortic Pressure
CV- Regulatory Mechanisms
Special mechanisms
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Tubuloglomerular feedback
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Role of concentration of CO2 and H+ controlling blood flow to brain

Image of CV-Regulatory Mechanisms
Image of CV-Regulatory Mechanisms

Image of Pulmonary Capillary
Image of Pulmonary Capillary

Image of Hydrostatic Pressure
Image of Hydrostatic Pressure
Ven. Paraoxysmal Tachy

Image of Ventricular Paraoxysmal Tachycardia
Image of Ventricular Paraoxysmal Tachycardia
Ventricular Extrasystole

Ventricular Extrasystole
Ventricular Extrasystole
Atrial Paroxysmal Tachycardia

Image of Atrial Paroxysmal Tachycardia
Image of Atrial Paroxysmal Tachycardia
Atrial Extrasystole

Image of Atrial Extrasystole
Image of Atrial Extrasystole