CVS Physiology MBBS 1st Year: Conducting System, Cardiac Cycle, ECG

Cardiovascular System (CVS) is one of the most important systems studied in first-year MBBS physiology. It explains how the heart pumps blood and how vessels maintain circulation to deliver oxygen, nutrients, and hormones throughout the body. A clear understanding of CVS helps students connect basic physiology with clinical conditions they will encounter later.

In CVS Physiology MBBS 1st Year, students learn key concepts such as the heart’s electrical conducting system, cardiac cycle, heart sounds, ECG interpretation, cardiac output, and blood pressure regulation. Topics like hypertension and circulatory shock further show how these mechanisms apply in real-life medical practice, making this unit both exam-focused and clinically relevant.

CVS Physiology MBBS 1st Year

The Cardiovascular System is a crucial topic for examinations, often featuring Long Questions, Case Studies, Short Notes, and MCQs. Thorough preparation is key to excelling in this subject.

I. CVS Major Topics: Heart & Circulation

The Cardiovascular System is primarily divided into two major components:

1. Heart (Cardio):

• Cardiac Cycle

• Cardiac Output

• ECG (Electrocardiogram)

2. Circulation (Vascular System):

• Blood Pressure (mainly regulation)

• Circulatory Shock

II. Recommended Short Notes in CVS

• Conducting System

• Pacemaker Potential (Strong feeling for this being an exam question in many universities.)

• Heart Block

• Heart Sounds

• Starling's Equilibrium (in Circulation)

• Coronary Circulation

• Cardiovascular Changes during Exercise

Conducting System of the Heart

The conducting system orchestrates the electrical impulse spread that causes systole (contraction) and diastole (relaxation).

A. Parts of the Conducting System

1. SA Node (Sinoatrial Node)

2. Internodal Pathways

3. AV Node (Atrioventricular Node)

4. Bundle of His

5. Right & Left Bundle Branches

6. Purkinje Fibers

B. Description of Conducting System Parts

1. SA Node (Sinoatrial Node):

• Location: Superior-lateral wall of the right atrium.

• Composition: Modified muscle cells and specialized P cells.

• Function: The normal pacemaker (natural pacemaker) of the heart.

2. Internodal Pathways:

• Connect the SA Node with the AV Node.

• Three pathways: Anterior (includes Bachmann's Bundle to left atrium), Middle (Wenckebach's Bundle), Posterior (Thorel's Bundle).

3. AV Node (Atrioventricular Node):

• Function: The only gateway for impulses from SA Node to reach ventricles.

• Key Characteristics: Least diameter, least gap junctions, resulting in the slowest conduction velocity.

• Physiological Significance: Causes AV nodal delay, ensuring atrial excitation precedes ventricular excitation.

4. Bundle of His:

• Arises from the AV Node, branches into Left and Right Bundle Branches.

• Impulse enters the left ventricle first, then crosses to the right ventricle.

5. Purkinje Fibers:

• Key Characteristics: More gap junctions, high cell diameter, resulting in the fastest conduction velocity.

• Function: Rapidly spreads impulse from apex to base of the heart.

C. Origin and Spread of the Cardiac Impulse

• 0 seconds: Impulse starts in the SA Node.

• 0.07 seconds: Reaches the AV Node.

• 0.08 seconds: Reaches the Left Atrium (Bachmann's bundle).

• 0.16 seconds: Reaches the Bundle of His (after AV nodal delay).

• 0.19 seconds: Reaches the Apex of the heart.

• 0.22 seconds: Base of the Right Ventricle depolarizes.

• 0.23 seconds: Base of the Left Ventricle depolarizes.

D. SA Node as the Pacemaker of the Heart

The SA Node is the pacemaker due to two properties:

1. Autorehythmicity (Self-Excitation): Spontaneously depolarizes to threshold after every repolarization.

2. Most Rapid Repolarization and Recovery: Exhibits the fastest repolarization and recovery, leading to the highest impulse discharge frequency (60-100 bpm), preventing other parts from firing.

• (Memory Tip: When asked why the SA Node is the pacemaker, explain these two properties, not just that impulses start there.)

E. Action Potential in the SA Node (Pacemaker Potential)

Pacemaker potential (prepotential) is a high-priority short note question. SA Node and AV Node are slow response type cells.

• Definition: The potential that spontaneously rises to threshold after every repolarization, allowing for automatic depolarization.

• Phases and Ionic Basis:

1. Repolarization: Primarily due to Potassium (K+) exit.

2. Initiation of Prepotential: K+ exit stops, K+ accumulates inside.

3. Sustained Prepotential Rise: Influx of Sodium (Na+) via HCN ("funny current") channels.

4. Reaching Threshold: Calcium (Ca2+) entry via T-type calcium channels.

5. Depolarization: Completed by Calcium (Ca2+) influx via L-type calcium channels.

F. Impulse Conduction - Additional Details

• AV Nodal Delay: The slowest conducting part, synchronizing atrial and ventricular contractions.

• Bundle of His: Impulse enters the Left Bundle Branch first, then crosses the septum to the Right Bundle Branch. This left-to-right spread is responsible for the Q wave on the ECG.

• Purkinje Fibers (Spread within Ventricles): Impulse spreads from Apex to Base and Endocardium to Epicardium.

• Last Parts to Depolarize: Epicardium of the base of the Left Ventricle, Pulmonary Conus, Uppermost part of the Interventricular Septum.

• Repolarization Spread: Occurs in reverse: Base to Apex and Epicardium to Endocardium. The Apical Endocardium is the last part to repolarize.

G. Action Potential in the Purkinje Fiber / Ventricular Muscle Fiber

This is a common short note or practical question. These are fast response type cells.

• Phase 0 (Rapid Upstroke): Influx of Sodium (Na+) via fast sodium channels.

• Phase 1 (Early Repolarization): Brief Potassium (K+) exit.

• Phase 2 (Plateau Phase): Slow, sustained influx of Calcium (Ca2+) via L-type calcium channels, balancing K+ exit.

• Phase 3 (Delayed Repolarization): Ca2+ channels close, continued Potassium (K+) exit.

• Phase 4 (Resting Membrane Potential): Maintained by K+ leakage channels.

H. Clinical Significance of the Plateau Phase: Why Heart Muscle Cannot Be Tetanized

• The plateau phase causes a long action potential duration (200-300 ms) and a long refractory period.

• This long refractory period makes it impossible to stimulate the heart muscle at high frequencies, thus preventing its tetanization.

• (Memory Tip: Tetanus is a sustained muscle contraction, like a prolonged hand cramp after writing intensely, which occurs in skeletal muscle but is prevented in cardiac muscle.)

Cardiac Cycle

The cardiac cycle is a favorite and essential question for many professors.

A. Required Elements for Cardiac Cycle Discussion

• Events (mechanical and electrical)

• Pressure and Volume Changes (atrial, ventricular)

• Heart Sounds

B. Definition and Duration

• Definition: The sequence of changes in the heart's four chambers during one heartbeat, repeated cyclically.

• Duration: At a normal heart rate (72 bpm), one beat lasts 0.8 seconds.

• [VERBAL EMPHASIS]: When the HEART RATE goes INCREASING, CARDIAC CYCLE DURATION goes DECREASING.

C. Events in the Cardiac Cycle

The two fundamental events are Systole (contraction) and Diastole (relaxation).

• Atrial Systole: 0.1 seconds

• Atrial Diastole: 0.7 seconds

• Ventricular Systole: 0.3 seconds

• Ventricular Diastole: 0.5 seconds

• [VERBAL EMPHASIS]: At HIGHER HEART RATES, VENTRICULAR DIASTOLE SUFFERS MORE. This disproportionate shortening of diastole at high heart rates limits filling time.

D. Atrial Events

1. Atrial Systole:

• Duration: 0.1 seconds.

• Action: Atria contract and pump blood into the ventricles.

• Contraction: Initially strong (dynamic), then weaker (adynamic). This is a Myotonic Contraction.

2. Atrial Diastole:

• Duration: 0.7 seconds.

• Action: Atria relax and receive blood from vena cava (right) and pulmonary veins (left).

E. Ventricular Events

1. Ventricular Systole:

• Duration: 0.3 seconds.

• Phases:

• Onset of Contraction: Ventricular pressure rises above atrial pressure, causing AV valves to close and producing the First Heart Sound (S1).

• Isovolumic Contraction: All four valves are closed. Ventricles contract, volume remains constant, pressure rises rapidly.

• Ejection Phase: Ventricular pressure opens semilunar valves. Blood is ejected rapidly, then reduced. Ventricular contraction is Otonoc contraction (initially weak, then stronger).

2. Ventricular Diastole:

• Duration: 0.5 seconds.

• Overlap: Most ventricular diastole (4 of 5 parts) overlaps with atrial diastole, allowing 80% of ventricular filling to occur passively. The last part coincides with atrial systole, actively filling the final 20%.

• Phases:

• Proto Diastole: Ventricular pressure falls; blood starts flowing back from aorta/pulmonary artery.

• Isovolumic Relaxation: Semilunar valves close to prevent backflow, producing the Second Heart Sound (S2). All four valves are closed. Volume remains constant, pressure falls rapidly.

• Ventricular Filling Phase: Ventricular pressure falls below atrial pressure, AV valves open.

• First Rapid Filling: Initial gush of blood, may produce Third Heart Sound (S3).

• Diastasis: Period of slow, dull filling.

• Last Rapid Filling (Atrial Kick): Coincides with atrial systole, may produce Fourth Heart Sound (S4) (Atrial Sound).

F. Atrial Pressure Changes (Jugular Venous Pulse - JVP)

Atrial pressure changes involve three upward waves (A, C, V) and two downward slopes (x, y):

• A Wave: Caused by Atrial systole (contraction).

• C Wave: Caused by Bulging backward of the tricuspid valve during ventricular isovolumic contraction.

• X Downslope: Caused by ventricular ejection and tricuspid valve returning to normal position.

• V Wave: Caused by Accumulation of venous blood in the right atrium during ventricular isovolumic relaxation.

• Y Downslope: Caused by the tricuspid valve opening, allowing blood to flow into the ventricle.

• (Memory Tip: A Wave = Atrial Systole; C Wave = Isovolumic Contraction (bulging back); V Wave = Venous filling (against closed valve during isovolumic relaxation).)

G. Left Ventricular Pressure-Volume (LVPV) Loop

The LVPV loop plots Left Ventricular Volume against Pressure.

• Phase 1: Ventricular Filling: Volume increases (50 mL to 130 mL - End Diastolic Volume, EDV); pressure does not change significantly.

• Phase 2: Isovolumic Contraction: Volume constant; pressure rises sharply (up to 120-130 mmHg).

• Phase 3: Ejection: Volume decreases (130 mL to 50 mL - End Systolic Volume, ESV); Stroke Volume = 80 mL. Pressure remains high.

• Phase 4: Isovolumic Relaxation: Volume constant (50 mL); pressure falls sharply.

• Clinical Significance:

• Width of the loop indicates Stroke Volume.

• Height of the loop indicates Afterload.

• EDV point indicates Preload.

H. Heart Sounds

Heart sounds have valvular, muscular, and vascular/blood components.

1. First Heart Sound (S1):

• Timing: Onset of ventricular systole.

• Cause: Closure of the AV valves (Mitral and Tricuspid).

• Heard: Best in Mitral and Tricuspid areas; corresponds with carotid pulse.

2. Second Heart Sound (S2):

• Timing: Onset of ventricular diastole.

• Cause: Closure of the semilunar valves (Aortic and Pulmonary).

• Heard: Best in Aortic and Pulmonary areas; occurs between carotid pulsations.

3. Third Heart Sound (S3): Caused by first rapid filling of the ventricles.

4. Fourth Heart Sound (S4): Caused by last rapid filling of the ventricles (atrial systole/kick), also called Atrial Sound.

• Adventitious Sounds: Foreign sounds like Murmurs, often due to valvular heart diseases (Stenosis or Regurgitation).

Electrocardiogram (ECG)

The ECG is the graphic record of the electrical activity of the heart from the body surface.

A. ECG Leads

Leads view heart activity from various directions.

• Bipolar Limb Leads: Lead I, Lead II, Lead III. (Einthoven's Law: Lead II = Lead I + Lead III). Lead II usually shows highest amplitude.

• Unipolar Limb Leads: aVR, aVL, aVF.

• Chest Leads: V1 to V6.

• 12-Lead ECG System: 3 bipolar + 9 unipolar leads.

B. Heart Rate Calculation from ECG

Heart Rate (bpm) = 1500 / RR Interval (in mm).

• 1500 mm/min is ECG paper speed (25 mm/s * 60 s/min).

• RR Interval is distance between two successive R waves.

C. ECG Waves and Their Representation

• P Wave: Represents Atrial depolarization. Duration ~0.1 seconds. P Mitrale (notched P wave) indicates left atrial hypertrophy. Atrial repolarization is usually masked by the QRS complex.

• QRS Complex: Represents Ventricular depolarization. Duration ~0.08 to 0.1 seconds.

• Q Wave: First negative deflection, septal depolarization.

• R Wave: First positive deflection, depolarization towards apex.

• S Wave: Second negative deflection, depolarization towards base.

• T Wave: Represents Ventricular repolarization.

D. ECG Intervals and Segments

1. PR Interval:

• Definition: Onset of P wave to onset of R wave.

• Normal: 0.12 to 0.20 seconds.

• Significance: Reflects AV Nodal Delay.

• Applied Aspect: Heart Block (AV Block):

• First Degree: Prolonged PR interval (>0.24s). All impulses conducted, but delayed.

• Second Degree (Incomplete): Some impulses blocked.

• Mobitz Type I (Wenckebach): Progressively lengthening PR interval until a QRS is dropped.

• Mobitz Type II: Fixed PR interval, but periodic dropped QRS complexes.

• Third Degree (Complete): No impulses cross AV node. P waves and QRS complexes (idioventricular rhythm) are independent.

2. ST Segment:

• Definition: End of S wave to start of T wave.

• Nature: Isoelectric (flat line).

• Significance: All ventricular muscle fibers are fully depolarized.

3. J Point: The point at the end of the S wave, used as a baseline for measuring amplitudes.

4. QT Interval:

• Definition: Beginning of Q wave to end of T wave.

• Normal: 0.4 to 0.43 seconds.

• Significance: Total time for ventricular depolarization and repolarization (Ventricular Activation Time).

E. ECG Changes in Myocardial Infarction (MI) - Applied Aspect

• Acute MI:

• Hyperacute Phase: ST segment elevation.

• Subacute Phase: ST segment returns, often with ST segment depression and T wave inversion.

• Old Infarction: Shows a characteristic QS pattern (deep Q wave, then S wave).

Cardiac Output

Cardiac Output (CO) is a common LAQ.

Introduction & Definition

• Cardiac Output (CO): Amount of blood pumped by the heart (left ventricle) in 1 minute.

• Normal: 5 Liters per minute.

• Formula: Cardiac Output = Stroke Volume × Heart Rate

• Stroke Volume (SV): Blood ejected in one beat (70-90 mL).

• Heart Rate (HR): (72 bpm).

• Cardiac Index (CI): CO per square meter of Body Surface Area (BSA). Normal: ~3 L/min/m².

Factors Determining Cardiac Output

Determined by Stroke Volume and Heart Rate.

1. Stroke Volume

Depends on the strength of ventricular contraction.

• A. Intrinsic Determination (Heterometric Regulation):

• Concept: Strength controlled by changing ventricular muscle fiber length.

• Frank-Starling Law: More the venous return, more the ventricular filling (increased EDV/Preload), stronger the contraction, and higher the stroke volume.

• Stroke Volume is directly proportional to Preload (EDV) and inversely proportional to Afterload (aortic pressure).

• Factors Determining Venous Return: Skeletal muscle pump, Respiratory pump.

• B. Extrinsic Determination (Homeometric Regulation):

• Concept: Strength controlled without changing fiber length (at constant EDV).

• Positive Inotropism (increased myocardial contractility): Caused by sympathetic discharge, catecholamines, cardiac glycosides (e.g., Digitalis).

2. Heart Rate

Increased HR generally increases CO, but effects on SV vary:

• HR 72-130 bpm: Increases SV (due to Staircase Effect).

• HR 130-160 bpm: SV remains constant, CO still increases.

• HR > 160 bpm: SV decreases significantly, CO may suffer.

• Bainbridge Reflex: Rapid IV saline increases right atrial filling, causing sudden HR increase.

Five Fundamental Properties of Cardiac Muscle

1. Chronotropic Effect: Effect on Heart Rate (Memory Tip: Chrono has 'R' like heart Rate.)

• Sympathetic: Positive (increase HR). Vagus: Negative (decrease HR).

2. Dromotropic Effect: Effect on Conduction Speed (Memory Tip: Dromo has 'D' like conDuction speeD.)

• Sympathetic: Positive. Vagus: Negative.

3. Inotropic Effect: Effect on Contractility.

• Sympathetic: Positive (ventricular). Vagus: No effect on ventricular contractility.

4. Bathmotropic Effect: Effect on general Excitability (Memory Tip: Taking a bath makes one feel excited.)

• Sympathetic: Positive. Vagus: Negative.

5. Lusitropic Effect: Effect on Relaxibility/Diastolic Function.

• Sympathetic: Positive (improve relaxation). Vagus: No effect.

Factors Influencing Cardiac Output

• A. Physiologic Factors:

• Increased CO: Exercise, anxiety, pregnancy, diet.

• Decreased CO: Sleep, posture changes.

• B. Pathologic Factors:

• Increased CO: Anemia, hyperthyroidism.

• Decreased CO: Cardiogenic shock, hypothyroidism, congestive heart failure.

Heart Failure (Short Notes)

• Definition: Heart fails as a pump, leading to decreased SV and CO.

• Types:

• Right-sided: Blood accumulates in peripheral veins, causing edema (e.g., lower limb swelling) and Hepatoomegaly.

• Left-sided: Blood accumulates in lungs, causing Pulmonary Edema.

• Signs/Symptoms: Breathlessness, edema.

• Treatment: Digitalis.

• Hepatojugular Reflex: Sign of Right-sided Heart Failure; pressing liver forces blood into jugular vein.

Methods of Measurement of Cardiac Output

1. Fick Principle: CO = Oxygen Consumption / Arteriovenous Oxygen Difference.

2. Dye Dilution Method: Injected dye's dilution over time indicates CO.

3. Thermodilution: Similar to dye dilution, using warm saline and temperature change.

4. 2D Echo: Most reliable for measuring stroke volume.

Circulation: Blood Pressure

Blood Pressure Definition

Blood Pressure (BP): The lateral pressure exerted by the moving column of blood on the vessel wall.

Determinants of Blood Pressure

Blood Pressure = Cardiac Output × Total Peripheral Resistance (TPR).

• TPR: Influenced by vessel diameter (especially arterioles).

• Vasoconstriction increases TPR and BP.

• Vasodilation decreases TPR and BP.

Types of Blood Pressure

1. Systolic Blood Pressure (SBP): Highest pressure during ventricular systole; indicates heart's contraction force.

2. Diastolic Blood Pressure (DBP): Lowest pressure during ventricular diastole; indicates peripheral resistance.

3. Pulse Pressure (PP): SBP - DBP; indicates Stroke Volume.

4. Mean Arterial Pressure (MAP): Average pressure over one cardiac cycle.

• Formula: MAP = DBP + (1/3 × Pulse Pressure).

5. Mean Circulatory Filling Pressure (MCFP): Average pressure if heart stops (6-7 mmHg).

Regulation of Blood Pressure

This is a key LAQ.

I. Neural Regulation of Blood Pressure

Involves a reflex arc:

1. Receptors:

• Baroreceptors: In Carotid Sinus and Aortic Arch; detect existing and changing BP.

2. Afferent Nerves:

• From Carotid Sinus: Glossopharyngeal nerve (9th Cranial Nerve).

• From Aortic Arch: Vagus nerve (10th Cranial Nerve).

3. Center (Vasomotor Center in Medulla Oblongata):

• Nucleus of Tractus Solitarius (NTS): Sensory input.

• Rostral Ventrolateral Medulla (RVLM): Vasoconstrictor area; activates sympathetic preganglionic neurons.

• Dorsal Motor Nucleus of 10th Cranial Nerve: Inhibits heart via vagus.

4. Efferent Nerves:

• Sympathetic Nerves: Cause vasoconstriction and increased HR/contractility.

• Parasympathetic Nerves (Vagus): Cause bradycardia and reduced contractility (atrial).

5. Effector Organs: Heart and Blood Vessels.

II. Short-Term Regulation of Blood Pressure

Rapid mechanisms:

1. Baroreflex Mechanism (Baroreceptor Reflex):

• Buffer nerves (9th & 10th cranial nerves) buffer BP fluctuations.

• Speed: Regulates BP in less than 1 second.

• Sensitivity: Carotid baroreceptors (60-180 mmHg); Aortic baroreceptors (90-210 mmHg). Most sensitive around 100 mmHg.

• Resetting: Baroreceptors reset if exposed to a consistent BP for 48 hours.

2. Chemoreceptor Mechanism (Chemoreflex):

• Location: Carotid bodies, aortic bodies.

• Stimulation: Activated when BP falls below 60 mmHg (senses hypoxia).

• Effect: Increases BP. Regulates BP in 30-60 mmHg range.

3. CNS Ischemic Response:

• Trigger: Severely decreased cerebral blood flow (BP below 30 mmHg).

• Mechanism: CNS ischemia stimulates vasomotor center, causing dramatic increase in BP (e.g., 20 mmHg to 250 mmHg).

• Significance: "Last ditch" effort to maintain brain perfusion.

• Cushing's Reaction: Variant caused by increased intracranial tension (ICT) compressing cerebral arteries, triggering CNS ischemic response.

IV. Long-Term Regulation (Short Note Topic)

Acts over hours to weeks:

1. Kidney-Body Fluids Mechanism: Kidneys adjust urine output to regulate blood volume and BP.

• BP 60 mmHg: Zero urine output.

• BP 100 mmHg: Normal urine output.

• BP 160 mmHg: Significantly increased urine output.

2. Renin-Angiotensin-Aldosterone System (RAAS):

• Trigger: Decreased blood volume/pressure.

• Steps:

• Kidney JG cells secrete Renin.

• Renin converts Angiotensinogen (liver) to Angiotensin I.

• ACE (lungs) converts Angiotensin I to Angiotensin II.

• Angiotensin II: Potent vasoconstrictor (increases BP), promotes salt/water retention, stimulates Aldosterone secretion from adrenal cortex.

• Aldosterone: Acts on kidneys to increase sodium and water reabsorption, leading to increased blood volume and BP. (Memory Tip: "Angio" means blood vessel, "tensin" refers to tension.)

Hypertension

1. Hypotension

Hypotension is BP generally below 60 mmHg, leading to reduced cerebral blood flow, dizziness, and fainting.

2. Hypertension Definition

Diagnosed when Diastolic BP > 90 mmHg OR Systolic BP > 140 mmHg.

3. Types of Hypertension

• Essential (Primary) Hypertension: 95% of cases; no identifiable secondary cause.

• Secondary Hypertension: 5% of cases; due to an underlying condition (e.g., kidney, heart, endocrine disorders).

4. Degrees of Severity (Hypertension)

• Mild: Diastolic BP 90-104 mmHg.

• Moderate: Diastolic BP 105-115 mmHg.

• Severe: Diastolic BP > 115 mmHg.

• Malignant: Diastolic BP > 130 mmHg with end-organ damage.

5. Management of Hypertension

• Dietary Measures: Salt restriction.

• Medications: Diuretics, Calcium Channel Blockers, ACE Inhibitors, Sympatholytics.

Circulatory Shock

Circulatory shock is a long question topic covering types, stages, signs, and treatment.

1. Definition

Circulatory shock is a condition of decreased cardiac output and decreased blood pressure, leading to hypoperfusion of tissues and organs and their depressed functioning.

2. Types of Circulatory Shock

• Cardiogenic Shock: Caused by heart failure or arrhythmias (heart cannot pump adequately).

• Hypovolemic Shock: Caused by loss of blood volume (hemorrhage) or fluid (diarrhea, vomiting).

• Neurogenic Shock: Caused by nervous system issues, leading to sudden withdrawal of sympathetic support and vagal firing (e.g., severe pain, emotional trauma).

• Anaphylactic Shock: Severe systemic allergic reaction (e.g., antibiotic injection) with histamine release, causing sudden BP drop.

• Septic Shock: Caused by severe infection; characterized by high-grade fever ("warm shock").

3. Stages of Circulatory Shock

1. Compensated Stage: Body's negative feedback mechanisms (baroreflex, chemoreflex, CNS ischemic response) can achieve self-recovery.

2. Progressive Stage: Negative feedback fails, a vicious cycle begins. Treatment is essential for recovery.

3. Irreversible Stage: Even treatment will not cause recovery; recovery is no longer possible.

4. Signs and Symptoms

• Dizziness, Thirst, Tachycardia, Palpitations, Fainting, Dryness of mouth, Thready pulse.

5. Physiological Basis of Treatment

A. Non-Drug Treatment

• Head-low position

• Oxygen administration

• Fluid replacement (oral or IV)

• Plasma expanders

B. Drug Treatment

• Treatment of underlying cause

• Steroids

• Antihistaminics (for anaphylactic shock)

• Antipyretics (for septic shock)

• Injection Adrenaline (Epinephrine): "Brahmastra" or most potent life-saver drug.