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.
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 muscle (The Guyton and Hall Physiology)Maryam Fida
In the heart there is Atrial muscle and Ventricular muscle which are separated from each other by the fibrous AV Rings containing Valves.
ATRIAL MUSCLE: thin walled. There are two sheets, superficial and deep sheet. Superficial sheet is common over both atria. Deep sheet is separate for each atrium. Muscle fibers in the deep sheet are at right angle to the muscle fibers in the superficial sheet.
FUNCTIONS OF THE ATRIUM:
1. Receive venous blood from large veins. So atria act as reservoir.
2. Conduct the blood into the ventricles.
3. Atrial contraction is responsible for last 25 % of ventricular filling.
4. In the right atrium there is SA Node(Pace maker) and AV node.
5. In the wall of the atria, there are low pressure stretch receptors and these are involved in various reflexes like brain bridge reflex and left atrial reflex.
6. Atria also produce a hormone i.e. Atrial Natriuretic Hormone. Whenever NaCl increases in ECF, it causes release of ANH which causes natriuresis.
VENTRICULAR MUSCLE:
Much thicker than atrial muscle. Thickness of right ventricle wall is 3-4 mm and thickness of left ventricle is 8 – 12 mm.
1.Involuntary
2.Has cross striations
3.Each cardiac muscle fiber consists of a number of cardiac cells, united at ends in series. Where as in skeletal muscle each muscle fiber is individual cell.
4.Cardiac muscle cells are branching and interdigitate.
5.Single central nucleus in each cell.
6. Atrial muscle and ventricular muscle act as separate functional syncytium and impulses from atria are conducted to ventricles through the AV Node and AV Bundle.
7. Sarcoplasmic system is present. In skeletal muscle triad is at the junction of A and I bands. In cardiac muscle T Tubules are much large and thus in cardiac muscle if we take a section it may form a diad or a triad. And these diads and triads are present at the level of Z Disks.
8.Between adjacent cardiac cells there are side to side and end to end connections and these are the intercellular junctions. These junctions are Gap Junctions. Or intercalated discs
9.When one part of myocardium is excited the whole muscle is excited.
10.Whole myocardium obeys all or none law as a whole.
11.No spike potential but action potential with plateau.
12.Has got long refractory period.
Absolute refractory period in ventricular muscle is 250 – 300 milli sec.
In atrial muscle Absolute refractory period is 150 milli sec
Because of long refractory period cardiac muscle cannot be tetanized.
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.
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 muscle (The Guyton and Hall Physiology)Maryam Fida
In the heart there is Atrial muscle and Ventricular muscle which are separated from each other by the fibrous AV Rings containing Valves.
ATRIAL MUSCLE: thin walled. There are two sheets, superficial and deep sheet. Superficial sheet is common over both atria. Deep sheet is separate for each atrium. Muscle fibers in the deep sheet are at right angle to the muscle fibers in the superficial sheet.
FUNCTIONS OF THE ATRIUM:
1. Receive venous blood from large veins. So atria act as reservoir.
2. Conduct the blood into the ventricles.
3. Atrial contraction is responsible for last 25 % of ventricular filling.
4. In the right atrium there is SA Node(Pace maker) and AV node.
5. In the wall of the atria, there are low pressure stretch receptors and these are involved in various reflexes like brain bridge reflex and left atrial reflex.
6. Atria also produce a hormone i.e. Atrial Natriuretic Hormone. Whenever NaCl increases in ECF, it causes release of ANH which causes natriuresis.
VENTRICULAR MUSCLE:
Much thicker than atrial muscle. Thickness of right ventricle wall is 3-4 mm and thickness of left ventricle is 8 – 12 mm.
1.Involuntary
2.Has cross striations
3.Each cardiac muscle fiber consists of a number of cardiac cells, united at ends in series. Where as in skeletal muscle each muscle fiber is individual cell.
4.Cardiac muscle cells are branching and interdigitate.
5.Single central nucleus in each cell.
6. Atrial muscle and ventricular muscle act as separate functional syncytium and impulses from atria are conducted to ventricles through the AV Node and AV Bundle.
7. Sarcoplasmic system is present. In skeletal muscle triad is at the junction of A and I bands. In cardiac muscle T Tubules are much large and thus in cardiac muscle if we take a section it may form a diad or a triad. And these diads and triads are present at the level of Z Disks.
8.Between adjacent cardiac cells there are side to side and end to end connections and these are the intercellular junctions. These junctions are Gap Junctions. Or intercalated discs
9.When one part of myocardium is excited the whole muscle is excited.
10.Whole myocardium obeys all or none law as a whole.
11.No spike potential but action potential with plateau.
12.Has got long refractory period.
Absolute refractory period in ventricular muscle is 250 – 300 milli sec.
In atrial muscle Absolute refractory period is 150 milli sec
Because of long refractory period cardiac muscle cannot be tetanized.
1. ION CHANNELS
2. ION CHANNEL RECEPTORS- PRINCIPLES
3. STRUCTURE OF ION CHANNEL RECEPTORS
4. VOLTAGE GATED ION CHANNELS
5. LIGAND GATED ION CHANNELS
6. THANKS
Etiopathogenesis and pharmacotherapy of arrhythmia
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
DRUGS AFFECTING THE SODIUM CHANNEL BOTH BLOCKER AND OPENERS, STRUCTURE OF SODIUM CHANNEL AND ITS LOCATION. SODIUM CHANNEL GATTING MECHANISM BY WITCH THEY ACTING. TYPES OF SODIUM CHANNEL AND ITS FUCTIONS. THEIR THERAPEUTIC APPLICATION WITH EXAMPLES OF DRUGS.
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.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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
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.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
- 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
- Link to NephroTube website: www.NephroTube.com
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13. Ion channels are also sub-classified by their mechanism of
gating:
Voltage dependent, ligand-dependent, and mechano-
sensitive gating.
• Voltage-gated ion channels change their conductance in
response to variations in membrane potential.
• Voltagedependent gating is the commonest mechanism of
gating observed in ion channels.
• A majority of ion channels open in response to
depolarization.
• The pacemaker current channel (If channel) opens in
response to membrane hyperpolarization.
• The steepness of the voltage dependence of opening or
activation varies between channels.
14. Ion channels have 2 mechanism of closure.
• Certain channels like the Na+ and Ca2+ channels enters a
closed inactivated state during maintained depolarization.
• To regain their ability to open, the channel must undergo a
recovery process at hyperpolarized potentials.
• The inactivated state may also be accessed from the closed
state.
• Inactivation is the basis for refractoriness in cardiac muscle
and is fundamental for the prevention of premature re-
excitation.
• If the membrane potential is abruptly returned to its
hyperpolarized (resting) value while the channel is open, it
closes by deactivation, a reversal of the normal activation
process.
15. Ligand-dependent gating is the second major gating mechanism of cardiac
ion channels.
• The most thoroughly studied channel of this class is the acetylcholine
(Ach)-activated K channel.
• Acetylcholine binds to the M-2 muscarinic receptor and activates a G
protein–signaling pathway, culminating in the release of the subunits Gαi
and Gβγ.
• The Gβγ subunit activates an inward-rectifying K channel, IKAch that
abbreviates the action potential and decreases the slope of diastolic
depolarization in pacemaker cells.
• IKAch channels are most abundant in the atria and the SA and
atrioventricular nodes.
• IKAch activation is a part of the mechanism of the vagal control of the heart.
• The ATP-sensitive K+ channel, also termed the ADP-activated K+ channel, is
a ligand-gated channel distributed abundantly in all regions of the heart
Editor's Notes
The Cardiac Action Potential
The normal sequence and synchronous contraction of the atria and ventricles require the rapid activation of groups of cardiac cells. An activation mechanism must enable rapid changes in heart rate and also respond to the changes in autonomic tone. The propagating cardiac action potential fulfils these roles.
Phase 4, or the resting potential, is stable at 90 Mv in normal working myocardial cells.
2. Phase 0 is the phase of rapid depolarization. The membrane potential shifts into positive voltage range. This phase is central to rapid propagation of the cardiac impulse (conduction velocity, 1 m/s).
3. Phase 1 is a phase of rapid repolarization. This phase sets the potential for the next phase of the action potential.
4. Phase 2, a plateau phase, is the longest phase. It is unique among excitable cells and marks the phase of calcium entry into the cell.
5. Phase 3 is the phase of rapid repolarization that restores the membrane potential to its resting value.
Ion channels are pore-forming membrane proteins whose function is establishing a resting membrane potential, shaping action potentials and other
electrical signals by gating the flow of ions across the cell membrane, controlling the flow of ions across membranes, and regulating cell volume.
They are often described as narrow, water-filled tunnels that accept only specific type of ions. This characteristic is called selective permeability.
Ion channels are integral membrane proteins, formed as assemblies of several proteins.
Such "multi-subunit" assemblies usually make a circular arrangement of identical or homologous proteins closely packed around a water-filled pore through the plane of the lipid bilayer membrane.
Ion channels are different from other transporter
proteins:
The rate of ion transport through the channel is
very high (often 106 ions per second or above).
Ions pass through channels down their
electrochemical gradient, which is a function of ion
concentration and membrane potential,
"downhill", without the input of metabolic energy (e.g. Adenosine triphosphate, active transport mechanisms, co-transport mechanisms).
Phase 2 (plateau) represents a balance between the depolarizing Ltype inward Ca2+ current (ICa,L) and the repolarizing ultra-rapidly (IKur), rapidly (IKr), and slowly (IKs) activating delayed outward rectifying currents.