This document provides an overview of cardiovascular physiology. It begins with a brief history of the field and introduces the concept of the heart as a pump. It then discusses the anatomy of the heart including the chambers, valves, conduction system, and cardiac muscle structure. Next, it covers the autorhythmic pacemaker cells, cardiac action potentials, excitation-contraction coupling, and the cardiac cycle. It also discusses neural and hormonal control of the heart, coronary circulation, hemodynamic calculations, and cardiac reflexes.
Describe events in cardiac cycle.
Describe atrial, ventricular and aortic pressure changes during cardiac cycle.
Describe the changes in ventricular volume & stroke volume during cardiac cycle.
Relate ECG changes to the phases of cardiac cycle.
Describe the functions of cardiac valves and relate their state to the production of heart sounds during cardiac cycle.
med_students0
Describe events in cardiac cycle.
Describe atrial, ventricular and aortic pressure changes during cardiac cycle.
Describe the changes in ventricular volume & stroke volume during cardiac cycle.
Relate ECG changes to the phases of cardiac cycle.
Describe the functions of cardiac valves and relate their state to the production of heart sounds during cardiac cycle.
med_students0
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
Cardiac output by Dr. Amruta Nitin Kumbhar Assistant Professor, Dept. of Phys...Physiology Dept
Definition of cardiac output and related terms
Measurement of cardiac output
Variations in cardiac output
Regulation of cardiac output
Cardiac output control mechanisms
Role of heart rate in control of cardiac output
Integrated control of cardiac output
Heart–lung preparation
CVS physiology, all details with explanation easy to recall physiology of cardiovascular system. based on Ganong's Review of Medical Physiology. all the high-yield facts are there.
Conductive system of heart by Dr. Pandian M Pandian M
The student will be able to: (MUST KNOW)
Name the parts of conducting system of the heart.
Appreciate the importance of AV nodal delay.
Explain the mechanism of AV nodal delay.
Give the conduction velocity in different cardiac tissues.
Understand the propagation of electrical impulse in conducting system of heart.
Heart rate by Pandian M, Tutor, Dept of Physiology, DYPMCKOP,MHPandian M
Heart rate
Regulation of heart rate
Vasomotor center – cardiac center
Motor (efferent) nerve fibers to heart
Factors affecting vasomotor center
Applied
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
Cardiac output by Dr. Amruta Nitin Kumbhar Assistant Professor, Dept. of Phys...Physiology Dept
Definition of cardiac output and related terms
Measurement of cardiac output
Variations in cardiac output
Regulation of cardiac output
Cardiac output control mechanisms
Role of heart rate in control of cardiac output
Integrated control of cardiac output
Heart–lung preparation
CVS physiology, all details with explanation easy to recall physiology of cardiovascular system. based on Ganong's Review of Medical Physiology. all the high-yield facts are there.
Conductive system of heart by Dr. Pandian M Pandian M
The student will be able to: (MUST KNOW)
Name the parts of conducting system of the heart.
Appreciate the importance of AV nodal delay.
Explain the mechanism of AV nodal delay.
Give the conduction velocity in different cardiac tissues.
Understand the propagation of electrical impulse in conducting system of heart.
Heart rate by Pandian M, Tutor, Dept of Physiology, DYPMCKOP,MHPandian M
Heart rate
Regulation of heart rate
Vasomotor center – cardiac center
Motor (efferent) nerve fibers to heart
Factors affecting vasomotor center
Applied
Cardiac muscle has three types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are (1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels
Depolarization: First, the action potential of cardiac muscle is caused almost entirely by sudden opening of large numbers of so-called fast sodium channels that allow tremendous numbers of sodium ions to enter the cardiac muscle fiber from the extracellular fluid. These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close. After depolarization, there's a brief repolarization that takes place with the efflux of potassium through fast acting potassium channels.
Plateau: Secondly, another entirely different population of slow calcium channels, which are also called calcium-sodium channels. This second population of channels differs from the fast sodium channels in that they are slower to open and, even more important, remain open for several tenths of a second. During this time, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fiber, and this maintains a prolonged period of depolarization, causing the plateau in the action potential.
Repolarization: When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential.
Properties of cm, plateau potential & pacemaker by Pandian M this PPT for I ...Pandian M
Describe the properties of cardiac muscle including its morphology, electrical, mechanical and metabolic functionsSLOs: After attending lecture & studying the assigned materials, the student will: 1.Describe the general features of cardiac muscle.2.Discuss the light and electron microscopic appearance of cardiac muscle, characteristic features of sarcotubular system.3.Enlist the electrical properties of heart muscle.4.Explain the phases of cardiac muscle action potential5.Explain the nodal action potential.6.Differentiate between cardiac muscle A.P. and nodal A.P., effect of nervous innervation and ions on AP.7.Enumerate and explain the mechanical properties of heart muscle, metabolic functions, characteristic features.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
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2. Introduction
• In 1628, Willam Harvey ,first advanced the concept of
circulation with” heart” as generator for circulation.
• Modern concept includes heart as a pump and cellular
aspects of cardiomyocyte and its regulation by neural and
hormonal control.
3. Heart as pump
• To create the “pump” we have to understand the Functional
Anatomy
–Chambers
–Valves
–Intrinsic Conduction System
–Cardiac muscle
4. Anatomy of the Heart
Chambers
• 4 chambers
– 2 Atria
– 2 Ventricles
• 2 systems
– Pulmonary
– Systemic
5. Structure
• Specific architectural order of cardiac
muscles provides basis for heart to
function as pump.
• Ellipsoid shape of LV is result of spiral
bundles of cardiac muscle
• Orientation of muscle bundle is
longitudnal in subepicardium
circufrential in middle and again
longitudnal in subendocardium.
• This orientation allows LV to eject blood
in cork screw type beging from base
and ending at apex. Thus completely
emptying the ventricle.
• Twisted LV function as pulling force
during diastole.
6. Valves
• Function is to prevent backflow
– Atrioventricular Valves
• Prevent backflow to the atria
• Prolapse is prevented by the chordae tendinae
– Tensioned by the papillary muscles
– Semilunar Valves
• Prevent backflow into ventricles
7. Intrinsic Conduction System
• Consists of “pacemaker”
cells and conduction
pathways
• Coordinate the contraction
of the atria and ventricles
8. Functional Anatomy of the Heart
Cardiac Muscle
• Characteristics
– Striated
– Short branched cells
– Uninucleate
– Intercalated discs
– T-tubules larger and
over z-discs
9. Autorhythmic Cells (Pacemaker Cells)
• Characteristics of
Pacemaker Cells
– Smaller than contractile
cells
– Don’t contain many
myofibrils
– No organized sarcomere
structure
• do not contribute to the
contractile force of the heart
normal contractile
myocardial cell
conduction myofibers
SA node cell
AV node cells
10. Autorhythmic Cells (Pacemaker Cells)
• Characteristics of Pacemaker Cells
– Unstable membrane potential
• “bottoms out” at -60mV
• “drifts upward” to -40mV, forming a pacemaker potential
– Myogenic
• The upward “drift” allows the membrane to reach threshold potential (-40mV) by itself
• This is due to
1. Slow leakage of K+
out & faster leakage Na+
in
» Causes slow depolarization
» Occurs through If channels (f=funny) that open at negative membrane potentials and
start closing as membrane approaches threshold potential
2. Ca2+
channels opening as membrane approaches threshold
» At threshold additional Ca2+
ion channels open causing more rapid depolarization
» These deactivate shortly after and
3. Slow K+
channels open as membrane depolarizes causing an
efflux of K+
and a repolarization of membrane
12. NEURAL CONTROL OF HEART
• Altering Activity of Pacemaker Cells
– Sympathetic activity
• NE and E increase If channel activity
– Binds to β1 adrenergic receptors which activate cAMP and
increase If channel open time
– Causes more rapid pacemaker potential and faster rate of action
potentials
Sympathetic Activity Summary:
increased chronotropic effects
↑heart rate
increased dromotropic effects
↑conduction of APs
increased inotropic effects
↑contractility
Sympathetic Activity Summary:
increased chronotropic effects
↑heart rate
increased dromotropic effects
↑conduction of APs
increased inotropic effects
↑contractility
13. Autorhythmic Cells (Pacemaker Cells)
• Altering Activity of Pacemaker Cells
– Parasympathetic activity
• ACh binds to muscarinic receptors M2(distributed more in atria)
– Increases K+
permeability and decreases Ca2+
permeability =
hyperpolarizing the membrane
» Longer time to threshold = slower rate of action potentials
Parasympathetic Activity
Summary:
decreased chronotropic effects
↓heart rate
decreased dromotropic effects
↓ conduction of APs
decreased inotropic effects
↓ contractility
Parasympathetic Activity
Summary:
decreased chronotropic effects
↓heart rate
decreased dromotropic effects
↓ conduction of APs
decreased inotropic effects
↓ contractility
14. Hormonal control on heart
• Angiotensin II – growth & function
• AT1- adult heart ,+ve chrono iono
Cardiac hypertrophy & heart failure
• ATII- anti proliferative ,predominent fetal heart
Ischemia injury upregulation
• ANP , BNP - P-V overload
Chronic heart failure increases - predictor of mortality
15. Conduction system
• The special conductive system of the heart:
• SA node – Keith-Flack´s node (1907) – pacemaker – in the
posterior wall of the right atrium (at the junction of superior
venacava with RA)
• Internodal tracts of: 1. Bachman
2. Wenckebacnh
3. Thorel
16. • AV node – (secondary centre of automatic function)
Conduction in AV node is slow – delay of 0.1 s),
velocity of conduction 20 mm/s.
• Physiological role: It allows time for the atria to empty their contents into
the ventricles before ventricle contraction begins.
• His bundle (v- 4-5 m/s),spread in 0.08-0.1 sec
Right/left bundle branches, Purkinje system
• Very large fibers. This allows quick - immediate transmission of the cardiac
impulse throughout the entire ventricular system.
• Depolarisation starts at left side of interventricular septum and moves
right ---then down the septum to apex.last depolarised are posteriorbasal
portion of heart pul cous.
• Excitation of the myocardium from endocardium to epicardium
18. Cardiac muscle
• Special aspects
– Intercalated discs
• Highly convoluted and interdigitated junctions
– Joint adjacent cells with
» Desmosomes & fascia adherens
– Allow for synticial activity
» With gap junctions
– More mitochondria than skeletal muscle
– Less sarcoplasmic reticulum
• Ca2+
also influxes from ECF reducing storage
need
– Larger t-tubules
• Internally branching
19. Action Potential
– The action potential of a contractile cell
• Ca2+
plays a major role again
• Action potential is longer in duration than a “normal” action
potential due to Ca2+
entry
• Phases
4 – resting membrane potential @ -90mV
0 – depolarization
» Due to gap junctions or conduction fiber action
» Voltage gated Na+
channels open… close at 20mV
1 – temporary repolarization
» Open K+
channels allow some K+
to leave the cell
2 – plateau phase
» Voltage gated Ca2+
channels are fully open (started during
initial depolarization)
3 – repolarization
» Ca2+ channels close and K+ permeability increases as
slower activated K+ channels open, causing a quick
repolarization
22. Myocardial Physiology
Contractile Cells
• Plateau phase prevents summation due to
the elongated refractory period
• No summation capacity = no tetanus
– Which would be fatal
24. Excitaion Contraction Coupling
• Initiation
– Action potential via pacemaker cells to conduction
fibers
• Excitation-Contraction Coupling
1. Starts with CICR (Ca2+
induced Ca2+
release)
• AP spreads along sarcolemma
• T-tubules contain voltage gated L-type Ca2+
channels which open upon depolarization
• Ca2+
entrance into myocardial cell and opens RyR
(ryanodine receptors) Ca2+
release channels
• Release of Ca2+
from SR causes a Ca2+
“spark”
• Multiple sparks form a Ca2+
signal
25. • Excitation-Contraction Coupling cont…
2. Ca2+
signal (Ca2+
from SR and ECF) binds to troponin to
initiate conformational changes in thin actin filament
3. Myosin head rotate, move the attached actin and
shorten the muscle fibre forming power stroke
4. At the end of power stroke ATP binds to now exposed
site on myosin head and causes detachment from actin
5. ATP is hydrolysed and adp binds to myosin head the
energy produced is used for pi
26. Contraction
– Same as skeletal muscle,
• Length tension relationships exist
– Strongest contraction generated
when stretched between 80 &
100% of maximum (physiological
range)
The filling of chambers
with blood causes stretching
27. • Relaxation
– Ca2+
is transported back into
the SR and
– Ca2+
is transported out of the
cell by a facilitated Na+
/Ca2+
exchanger (NCX)
– As ICF Ca2+
levels drop,
interactions between
myosin/actin are stopped
– Sarcomere lengthens
28. Cardiac Cycle
Coordinating the activity
• Cardiac cycle is the sequence of events as
blood enters the atria, leaves the ventricles
and then starts over
• Synchronizing this is the Intrinsic Electrical
Conduction System
• Influencing the rate (chronotropy &
dromotropy) is done by the sympathetic and
parasympathetic divisions of the ANS
29. Cardiac Cycle
Coordinating the activity
• The electrical system gives rise to electrical changes
(depolarization/repolarization) that is transmitted through
isotonic body fluids and is recordable
– The ECG!
• A recording of electrical activity
• Can be mapped to the cardiac cycle
30. Waves:
•P – atrial depolarization (0.1 – 0.3 mV, 0.1 s)
•QRS – ventricular depolarization (atrial repolarization)
•Q – initial depolarization (His bundle, branches)
•R – activation of major portion of ventricular myocardium
•S - late activation of posterobasal portion of the LV mass and the pulmonary
conus
•T – ventricular repolarization
•U – repolarization of the papillary muscles
31. The duration of the waves, intervals and segments
•P – wave 0.1 s
•PQ – interval 0.16 s
•PQ – segment 0.06 – 0.1 s
•QRS complex 0.05 – 0.1 s
•QT interval 0.2 – 0.4
•QT segment 0.12
•T wave 0.16
32.
33. ECG MONITORING INTRAOPERATIVELY
• 3 lead system is most basic- 3 electrodes Rt arm Lt arm Lt leg
• Its adequate for monitoring Arrythymias but limited use to identify ischemias
• We use modified 3 lead system where electrodes are placed on chest wall which
helps in monitoring of ischemias and improved detection of arrythymias(taller P
waves)
• Modified lead systems
Central subclavicular system- one electrode in Rt clavicular one in v5
34. • Only single lead is used V5 has 75%
sensitivity
• V4 has 61 %
• V4 + V5 has 90%
• V4 + V5 +II has 96% (BEST)
35. Cardiac Cycle
• Duration – 0.8 sec
• Systole = period of contraction atrial - 0.1 sec ventricular 0.3 sec
• Diastole = period of relaxation atrial 0.7 sec ventricular 0.5 sec
• Phases of the cardiac cycle
1. Diastole
• Both atria and ventricles in diastole
• Blood is filling both atria and ventricles due to low pressure conditions
Mechanisms of the filling:
a) residual energy from the left ventricle
b) Negative“ intrathoracic (interpleural) pressure
Ventricular fillling
1)Period of rapid filling (first 1/3 of the diastolic time)
2)Period of slow filling – diastasis (next 1/3)
3) Atrial systole (last 1/3) + 20-30 % of the filling of the ventricles
36. Cardiac Cycle
Phases
2. Atrial Systole ( 0.1 sec)
• Completes ventricular filling
3. Isovolumetric Ventricular Contraction (0.05 sec)
• Increased pressure in the ventricles causes the AV valves to close…
– Creates the first heart sound (lub)
• Atria go back to diastole
• No blood flow as semilunar valves are closed as well
4. Ventricular Ejection
• Intraventricular pressure overcomes aortic pressure and pulmonary
pressure
– Semilunar valves open
– Blood is ejected - Rapid ejection and Reduced Ejection
37. 5. Ventricular Relaxation(Diastole)
Protodiastole
The ventricular pressure falls to a value below that in aorta, closing of
the semilunar valves
– Semilunar valves close = second heart sound (dup)
Isovolumetric relaxation
Pressure still hasn’t dropped enough to open AV valves so volume
remains same (isovolumetric)
Rapid filling Phase
Reduced Filling Phase (Diastasis)
41. CORONARY CIRCULATION
• 250 ml/ min exercise 1000ml/min
• Rt Coronary Ar – RA, RV, IVS,SA node & Conducting system except lt
bundle.
• Lt coronary Ar– LA, LV, IVS(majority) lt bundle
• 70% Rt, 10% Lt dominance.Remaining both – based on posterior
descending ar supply
• Hypoxia main determinant than neural factors
42.
43. Haemodynamic Calculations
• Cardiac output : per unit time.
• Depends on following factors
- HR
- Contractility : frank starling relationship – EDV
- Preload : VR, EDV, Ventricular compliance, diastolic pause, atrial systole
Preload / venous return depends on two factors
Rt atrial pressures ( high pressure low return)
Mean Circulatory Filling Pressures (high pressure more return)
• Mean circulatory filling pressure measured by temporary cessation of cardiac
output and equilbration of peripheral pressures
44. • After load – refers to resistance against which heart has to pump
the blood
• Factors affecting after load are
- mechanical obstruction as aortic stenosis
- systemic blood pressure
- pharmocological intervention like
phenylephrine ,ephedrine
increases syst vascular resistance
45. • Cardiac output measured by
CO = SV* HR
SV calculated by Pressure volume Curves
(EDV-ESV)
• Thermodilution method – pulmonary artery catheter
• Fick’s method
(oxygen consumption / arteriovenous o2 difference x 10)
• Echocardiography
46. • Cardiac output = SV x HR 5-7 L/min
• Cardiac Index = CO/BSA 2.4 L/min
• SV = EDV – ESV 70-90 ml (1ml/kg)
• MAP = CO x SVR 60-90 mm Hg
= 2/3 Diastolic pressure + 1/3 Systolic
• SVR =[( MAP –CVP) /CO ] X 80 800-1200 dynes/s/cm
47. Cardiac Reflexes
Baro receptor Reflex :
• Location Internal carotid ar jst abov bifurcation
• Respond to pressure changes
• If MAP is raised stretch in receptors stimulation of CNS and
decreased sympathetic stimulation results in vasodilatation
• Baroreceptors adapt in 1-3 days to sustained raise in BP.
• Halothane inhibit heart rate increase in Baro receptor reflex
48. ChaemoRecptor reflex:
•Located in carotid and aortic bodies
•Abundant blood supply by nutrient arteries
•Respond to changes in arterial blood oxygen concentration by
detecting the pH changes and paO2
•Don’t respond utill BP< 80 mmHg
•Ventillatory response to hypoxemia (pao2<60) is inhibited by
subanesthetic dose of inhalational anesthetics(0.1 MAC)
49. Bezold Jarsich Reflex
• Dec in Lt Ventricular vol activates receptors that cause
paradoxical bradycardia.
• This compensatory bradycardia is to allow filling of
ventricles,but also deteriorates blood pressure.
• Spinal anesthesia and epidural
50. • BainBridge Reflex:
stretching of atria increases heart rate.
• Cushing reflex :
CNS ischemic response towards raised ICP.
when ICP is raised and equals arterial pressure
cushing reflex improves systemic pressure
above ICP
Triad of cushing reflex is Hypertension ,bradycardia and irregular
respirations.
51. Occulo cardiac reflex
•Pressure on globe provokes the signals through ciliary nerves to
opthalmic nerve to gasserian ganglion increased parasympathetic
stimulation results in bradycardia.
•30-90% incidence during surgery
•Anti muscurinic drugs like glycopyrollate or atropine is useful