The cardiac cycle begins with an electrical impulse from the sinoatrial node that causes atrial contraction. This is followed by a delayed impulse from the atrioventricular node that causes ventricular contraction. The cycle involves electrical and mechanical events represented by the ECG. Cardiac function is controlled by the autonomic nervous system and hormones. Parasympathetic stimulation decreases heart rate while sympathetic stimulation increases it. Important cardiac reflexes maintain homeostasis by regulating heart rate and contractility in response to pressure and chemical sensors.
Assessment of haemodynamics a critically ill patient and its management has always been a matter if debate. Over time a lot of studies and therapeutic interventions have been carried out. This presentation is a review of such interventions and their impact on the outcome.
Neuromuscular monitoring, also known as train of four monitoring, is a technique used during recovery from the application of general anesthesia to objectively determine how well a patient's muscles are able to function. It involves the application of electrical stimulation to nerves and recording of muscle response using, for example, an acceleromyograph. Neuromuscular monitoring is typically used when neuromuscular-blocking drugs have been part of the general anesthesia and the doctor wishes to avoid postoperative residual curarization (PORC) in the patient, that is, the residual paralysis of muscles stemming from these drugs.
Anticoagulants, antiplatelet drugs and anesthesiaRajesh Munigial
It is a presentation on anticoagulants and antiplatelets in anesthesia , starting from basis of coagulation , its tests and dugs and anesthetic implications
Based on latest ASRA (AMERICAN SOCIETY OF REGIONAL ANESTHESIA GUIDELINES)
Intro to Hypoxic pulmonary vasoconstriction Arun Shetty
Hypoxic pulmonary vasoconstriction, a seldom heard phenomenon but very effective physiologic property which helps lungs utilise ventilation to the maximum
A patient with pacemaker presents a complex challenge to the attending anaesthesiologist. The mode of management will be according to the type of pacemaker implanted. This presentation discusses in brief the peri-operative consideration in a patient with pacemaker.
Assessment of haemodynamics a critically ill patient and its management has always been a matter if debate. Over time a lot of studies and therapeutic interventions have been carried out. This presentation is a review of such interventions and their impact on the outcome.
Neuromuscular monitoring, also known as train of four monitoring, is a technique used during recovery from the application of general anesthesia to objectively determine how well a patient's muscles are able to function. It involves the application of electrical stimulation to nerves and recording of muscle response using, for example, an acceleromyograph. Neuromuscular monitoring is typically used when neuromuscular-blocking drugs have been part of the general anesthesia and the doctor wishes to avoid postoperative residual curarization (PORC) in the patient, that is, the residual paralysis of muscles stemming from these drugs.
Anticoagulants, antiplatelet drugs and anesthesiaRajesh Munigial
It is a presentation on anticoagulants and antiplatelets in anesthesia , starting from basis of coagulation , its tests and dugs and anesthetic implications
Based on latest ASRA (AMERICAN SOCIETY OF REGIONAL ANESTHESIA GUIDELINES)
Intro to Hypoxic pulmonary vasoconstriction Arun Shetty
Hypoxic pulmonary vasoconstriction, a seldom heard phenomenon but very effective physiologic property which helps lungs utilise ventilation to the maximum
A patient with pacemaker presents a complex challenge to the attending anaesthesiologist. The mode of management will be according to the type of pacemaker implanted. This presentation discusses in brief the peri-operative consideration in a patient with pacemaker.
This presentation gives you a brief, understandable, captivating and presentable idea on the physiology of blood pressure regulation both on hypertension and hypotension cases.
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
HEART RATE
REGULATION OF HEART RATE
VASOMOTOR CENTER – CARDIAC CENTER
MOTOR (EFFERENT) NERVE FIBERS TO HEART
FACTORS AFFECTING VASOMOTOR CENTER
for all medical & health care students
Heart rate by Pandian M, Tutor, Dept of Physiology, DYPMCKOP,MH. This ppt for...Pandian M
Heart rate
Regulation of heart rate
Vasomotor center – cardiac center
Motor (efferent) nerve fibers to heart
Factors affecting vasomotor center
Applied
Similar to Cardiac Cycle and Anaesthetic Implications (20)
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
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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2. CARDIAC CYCLE
• SEQUENCE OF ELECTRICAL AND MECHANICAL
EVENTS DURING THE COURSE OF A SINGLE
HEARTBEAT
• BEGINS WITH THE INITIATION OF HEART BEAT
• CARDIAC PACEMAKER TISSUES HAVE
AUTOMATICITY AND RHYTHMICITY
• SA Node is the natural pacemaker
• it generates impulses at the highest frequency
3. Electrical Events
• Electrical events in cardiac cycle are represented by the ECG
• ECG is the result of differences in the electrical potential
generated by the heart at the sites of lead placement
• The action potential generated by the SA node, travels to Both
atrium causing atrial systole, causing P wave of ECG
4. • AV node is situated at the junction of the Atrial septum and
Ventricular septum.
• AV node is distally connected to the Bundle of HIS
• It is responsible for slow conduction
• delay between the Atrial and Ventricular contraction
occurs here
• Represented by the PR interval on ECG
Electrical Events
5. • Bundle of HIS divides into the left and right bundle branches
• terminates into the Purkinje finer system which supplies the
individual cardiomyocytes
• These fibres spread depolarisation to ventricular
myocardium
• Depicted by the QRS complex on the ECG
• depolarisation is followed by ventricular repolarisation and
depicted by T wave on ECG.
Electrical Events
8. • When ventricular chamber fills, AV valves leaflets are pushed
upwards
• Closure of AV valves, leads to start of ventricular systole depicted by
R wave on ECG
• Ventricular systole has 2 parts
• Isometric/ Isovolumic contraction
• Ventricular ejection
• Electrical impulse -> Bundle of HIS and purkinje fibres -> Ventricular
myocardium contracts -> Increased Intraventricular pressure
• If Intraventricular pressure >> PA and Aortic pressure —> Opening
of PA and Aortic valves -> Ventricular ejection (2nd part of VS)
Mechanical Events of Cardiac Cycle
9. • Ventricular ejection has 2 phases
• Rapid ejection - maximal forward flow, maximal PA
and Aortic pressure
• Reduced ejection - as the flow, PA and Aortic
pressure taper towards the end of systole
• Pressure in both ventricles reduces as blood is ejected out
Mechanical Events of Cardiac Cycle
10. • Ventricular diastole occurs with the closure of PA and Aortic valves
• VD has two phases
• Initial Isometric / Isovolumic relaxation phase
• Repolarisation of ventricular myocardial
• T wave on the ECG
• Late phase
• Rapid decrease in the intraventricular pressure till it
decreases to less than RT and LT atrial pressures
• AV valve reopens
• Cycle repeats
Mechanical Events of Cardiac Cycle
11. Control of Cardiac Function
• Two regulators - Neural and Hormonal
• Major neural component is the Autonomic Nervous
System - sympathetic and parasympathetic components
• both provide opposing input to regulate cardiac function
12. Sympathetic Nervous
System effects
• Primary neurotransmitter is Nor-Epinephrine
• it has positive chronotropic (rate), inotropic (contractility)
and lusitropic (relaxation) effects
13. Parasympathetic Nervous
System
• Major neurotransmitter is Acetylcholine
• It has more direct inhibitory effect on Atria
• Negative modulatory effect on ventricles
14. Control of cardiac function
• Both Nor-Epinephrine and Acetylcholine bind to Seven-
transmembrane-spanning G protein coupled receptors
• at rest, the heart has a tonic level of Parasympathetic
cardiac nerve firing and little (if any) Sympathetic activity
• during exercise / stress - sympathetic influence prominent
15. • Parasympathetic innervation of heart is by Vagus nerve
• Supraventricular tissue receives more intense vagal innervation
than ventricles
• Parasympathetic target neuroeffectors are muscarinic receptors
in heart - M2
• Activation of M2
• Reduces pacemaker activity
• slows AV conduction
• Directly reduces atrial contractile force
• inhibitory modulation of ventricle contractile force
16. •Sympathetic innervation is more prominent in ventricles than atria
•Nor-epinephrine stimulates Adrenergic receptors AdRs in the heart
•AdRs two types - Alpha and Beta
•both are G protein coupled receptors
•Effectors are -
•Adenylyl cyclase (AC)
•L-type calcium current (iCA)
•Phospholipase β (PLC-β)
•Intracellular signals are
•DAG - Diacetylglycerol
•Inositol 1,4,5 triphosphate IP3
•Protein Kinase C (PKC)
•cAMP
•Protein Kinase A
•Mitogen activated protein kinase MAPK
17. • Three types of β adrenoceptors are - β1, β2, β3
• β1 predominant in both atria and ventricles
• β2 substantial in atria and 20% in ventricles
• β3 in human ventricles
• Two types of ⍺ adrenoceptors - ⍺1 and ⍺2
• ⍺1 has 3 subtypes - ⍺1A, ⍺1B and ⍺1D
• ⍺1A is responsible for cardiac hypertrophy
18. Hormonal Control of Cardiac function
• Hormonal influence is either direct or indirect
• Direct hormones are those produced by the cardiac myocytes
• Indirect hormones are those produced by other tissues and
delivered to the heart
• Most hormones are plasma membrane G-protein coupled
receptors (GPCR)
• Non- GPCR include
• Natriuretic peptide receptors
• Glucocorticoid and Mineralocorticoid receptors
19. • Cardiac hormones are polypeptides secreted by cardiac tissues
• Natriuretic peptides, Aldosterone and Adrenomedullin secreted by cardiomyocytes
along with Angiotensin II
• Renin angiotensin system most important regulators of cardiovascular physiology,
cardiac growth and function.
• Angiotensin II has 2 receptors - AT1 and AT2 both in the heart
• AT1 stimulation induces Positive chronotropic and inotropic effects
• Activation of AT1 -> Cardiac hypertrophy -> heart failure and adverse remodelling
of myocardium
• AT2 mediates cell growth and proliferation of cardiomyocytes, fibroblasts
• induces growth factors aldosterone and catecholamines
• AT2 activation - counter regulatory and antiproliferative
• ACE inhibitors block AT1 receptor activty
21. Sex Steroid Hormones
• Estradiol - 17β E2
• cardiac contractility is intense in premenopausal women than in men of
similar age group
• withdrawal of HRT in post menopausal women, significantly reduces
cardiac contractility
• Estradiol bind and act on oestrogen receptors ER⍺ and ERβ
• Estrogen has vasodilatory effect due to stimulation of vascular
endothelial nitric oxide synthase -> lower systolic BP in premenopausal
women
• Testosterone has opposite effect
22. Cardiac Reflexes
• These are fast acting reflex loops between the heart and CNS that contribute to regulation of cardiac function
and maintenance of physiologic homeostasis
• Cardiac receptors are linked to the CNS by myelinated and unmyelinated afferent fibres, that travel along the
vagus nerve.
• Intracardiac Receptors are situated in - Atrium, Ventricles, Pericardium and coronary arteries
• Extracardiac receptors located in the great vessels and carotid artery
• They are
1. Baroreceptor Reflex (carotid Sinus reflex)
2. Chemoreceptor reflex
3. Bainbridge reflex
4. Bezold-Jarisch reflex
5. Valsalva manoeuvre
6. Cushing reflex
7. Oculocardiac reflex
23. Baroreceptor Reflex
• also known as the Carotid Sinus reflex
• responsible for maintenance of arterial blood pressure.
• utilises negative feedback loop, to maintain arterial pressure
around a preset value.
• also, capable of establishing a prevailing set point for arterial
blood pressure, when the preset value has been reset
because of chronic HTN
24. Chemoreceptor Reflex
• Located in carotid bodies and aortic body
• respond to change in pH status and blood O2 tension
• PaO2 < 50mmHg or Acidosis stimulates chemoreceptors
• Impulse conducted via Nerve of Hering (branch of glossopharyngeal nerve), Vagus ->
chemosensitive area of medulla
• Response -
• Stimulation of respiratory centres, increased ventilatory drive
• Activation of parasympathetic system
• Reduction in heart rate, myocardial contractility
• Persistent hypoxia - CNS directly stimulated, increased sympathetic activity
25. Bainbridge Reflex
• Elicited by stretch receptors in the Right atrial wall and
Cavoatrial junction
• increased right sided filling pressure -> vagal afferent signals
to cardiovascular centre in medulla
• inhibits parasympathetic activity -> increases heart rate
• HR also increases by direct effect on SA node by stretching
of atrium
• Changes are dependent on the underlying HR before
stimulation
26. Bezold-Jarisch Reflex
• Responds to noxious ventricular stimuli sensed by chemoreceptors
and mechanoreceptors in the LV wall
• Induces triad of Hypotension, Bradycardia, Coronary Artery dilatation
• as it induces bradycardia, it is thought of as cardioprotective
• Vagal afferent type C fibres
• Implicated in CV conditions such as MI, thrombosis, revascularisation,
syncope
• Modulated by Natriuretic peptide receptors - ANP, BNP
• Reflex is less pronounced in patients with cardiac hypertrophy, atrial
fibrillation
27. Valsalva Maneuver
• Forced expiration against a closed glottis -> increased
intrathoracic pressure, increased CVP and decreased venous
return
• Cardiac output, blood pressure decreased after valsalva
• Baroreceptors sense this decrease -> Cause increase in HR,
myocardial contractility through sympathetic stimulation
• when glottis opens, venous return increases -> Heart
vigorously contracts -> increased SBP -> baroreceptor reflex
will stimulate parasympathetic efferent pathways to the heart
28. Cushing Reflex
• it is a result of cerebral ischemia caused by increased ICP
• at the medullary vasomotor centre induces Initial activation
of sympathetic nervous system
• increase in HR, arterial blood pressure, myocardial
contractility to improve cerebral perfusion
• reflex bradycardia will follow
29. Oculocardiac reflexes
• provoked by pressure applied on the globe of the eye / traction on
the surrounding structures
• stretch receptors located in the extra ocular muscles
• activation will send afferents through long and short ciliary nerves
which merge with ophthalmic division of trigeminal nerve at ciliary
ganglion
• trigeminal nerve -> gasserian ganglion -> increased
parasympathetic tone and subsequent bradycardia
• administer atropine or glycopyrrolate prior to surgery reduces
incidence of bradycardia
Starts with Blood returning from Systemic and Pulmonary circulation into the Right and Left Atria respectively
once atrial blood volume increases, Pressure in Atrium increases
If / When atrial pressure exceeds ventricular pressure, AV valves (mitral and tricuspid) open
70% ventricular filling occurs by Passive flow from atrium to ventricle
30% occurs during atrial systole / Atrial Kick
Depolarisation of SA node -> Atrial Systole -> P wave on ECG
Changes in arterial blood pressure are monitored by circumferential and longitudinal stretch receptors located in carotid sinus and aortic arch
Nucleus solitarius receives impulses from stretch receptors -> via afferents of vagus and glossopharyngeal nerve
Stretch receptors activated if Systemic blood pressure > 170mmHg
Response to stimulation -> Decreased sympathetic activity -> Decrease in cardiac contractility, Heart rate and vascular tone
Activation of parasympathetic system -> Reduces heart rate and myocardial contractility
Reverse happens with onset of HYPOTENSION
This reflex plays an important role during acute blood loss and shock
Reflex is useless when SBP < 50mm Hg
Hormones alter baroreceptor reflexes
Volatile aesthetics inhibit HR component
Ca channel blockers, ACE inhibitors, Phospodiesterase inhibitors lessen the blood pressure raising effect of this reflex
these interfere with peripheral vasculature or CNS signalling pathways