mapleson circuits used in anesthesia practice, are in their way out but it is as important to know the mechanism with which the gases flow to and fro through them.
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.
Humidifiers in anaesthesia and critical careTuhin Mistry
Humidification of inhaled gases has been standard of care during mechanical ventilation in anaesthesia and intensive care. Active & Passive humidification devices have rapidly evolved. basic knowledge of the mechanisms of action of each of these devices, as well as their advantages and disadvantages, becomes a necessity for anaesthesiologists and intensivists.
Human heart anatomy and physiology Part -1Ritu Sharma
The heart is the pump responsible for maintaining adequate circulation of oxygenated blood around the vascular network of the body. It is a four-chamber pump, with the right side receiving deoxygenated blood from the body at low presure and pumping it to the lungs (the pulmonary circulation) and the left side receiving oxygenated blood from the lungs and pumping it at high pressure around the body (the systemic circulation).
mapleson circuits used in anesthesia practice, are in their way out but it is as important to know the mechanism with which the gases flow to and fro through them.
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.
Humidifiers in anaesthesia and critical careTuhin Mistry
Humidification of inhaled gases has been standard of care during mechanical ventilation in anaesthesia and intensive care. Active & Passive humidification devices have rapidly evolved. basic knowledge of the mechanisms of action of each of these devices, as well as their advantages and disadvantages, becomes a necessity for anaesthesiologists and intensivists.
Human heart anatomy and physiology Part -1Ritu Sharma
The heart is the pump responsible for maintaining adequate circulation of oxygenated blood around the vascular network of the body. It is a four-chamber pump, with the right side receiving deoxygenated blood from the body at low presure and pumping it to the lungs (the pulmonary circulation) and the left side receiving oxygenated blood from the lungs and pumping it at high pressure around the body (the systemic circulation).
Hey Guys
im happy you are enjoying my content. please subscribe to my channel on youtube as i will make more videos soon. https://bit.ly/2XXNyTT
thank you as you subscribe.
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.
Anatomy and physiology of the cardiac system
The electrocardiogram a, curves and interpretation of the first and second heart sounds. Generation of action potential within the myocardium ,the gap junctions and how they propagate electrical pilese from sinoatrial mode and ectopoic heartbeat.
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
Francesca Gottschalk - How can education support child empowerment.pptxEduSkills OECD
Francesca Gottschalk from the OECD’s Centre for Educational Research and Innovation presents at the Ask an Expert Webinar: How can education support child empowerment?
Introduction to AI for Nonprofits with Tapp NetworkTechSoup
Dive into the world of AI! Experts Jon Hill and Tareq Monaur will guide you through AI's role in enhancing nonprofit websites and basic marketing strategies, making it easy to understand and apply.
Palestine last event orientationfvgnh .pptxRaedMohamed3
An EFL lesson about the current events in Palestine. It is intended to be for intermediate students who wish to increase their listening skills through a short lesson in power point.
Operation “Blue Star” is the only event in the history of Independent India where the state went into war with its own people. Even after about 40 years it is not clear if it was culmination of states anger over people of the region, a political game of power or start of dictatorial chapter in the democratic setup.
The people of Punjab felt alienated from main stream due to denial of their just demands during a long democratic struggle since independence. As it happen all over the word, it led to militant struggle with great loss of lives of military, police and civilian personnel. Killing of Indira Gandhi and massacre of innocent Sikhs in Delhi and other India cities was also associated with this movement.
The French Revolution, which began in 1789, was a period of radical social and political upheaval in France. It marked the decline of absolute monarchies, the rise of secular and democratic republics, and the eventual rise of Napoleon Bonaparte. This revolutionary period is crucial in understanding the transition from feudalism to modernity in Europe.
For more information, visit-www.vavaclasses.com
2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
How to Make a Field invisible in Odoo 17Celine George
It is possible to hide or invisible some fields in odoo. Commonly using “invisible” attribute in the field definition to invisible the fields. This slide will show how to make a field invisible in odoo 17.
3. Transport and distribute essential substances
to the tissues.
Remove metabolic byproducts.
Adjustment of oxygen and nutrient supply in
different physiologic states.
Regulation of body temperature.
Humoral communication.
4. 67% IN THE SYST. VEINS/VENULES
5% IN THE SYSTEMIC CAPILLARIES
11% IN THE SYSTEMIC ARTERIES
5% IN PULMONARY VEINS
3% IN PULMONARY ARTERIES
4% IN PULMONARY CAPILLARIES
5% IN HEART ATRIA/VENTRICLES
10. The intrinsic conduction system of the
heart Sinoatrial (SA) node
- impulse spreads through atria
-100 b.min-1
Atrioventricular (AV) node
- impulse delayed for 0.1sec
internodal
pathway
Ventricular contraction - time
course approx 0.22 secs
*Contraction of the atria*
Bundle of His -
branches -
Purkinje fibers
• A wringing effect starts at the apex following the same pathway as
wave of excitation atria ejecting some blood superiorly
11. Normal pacemaker of the heart
Self excitatory nature
• less negative Er
• leaky membrane to Na+/Ca++
• only slow Ca++/Na+ channels operational
• spontaneously depolarizes at fastest rate
Overdrive suppression
• contracts feebly
12. Delays the wave of depolarization from
entering the ventricle
• Allows the atria to contract slightly ahead of the
ventricles (.1 sec. delay)
Slow conduction velocity due to small
diameter fibers
In absence of SA node, AV node may act
as pacemaker but at a slower rate
13. Sympathetic nerves (release noradrenaline):
Left nerves supply atrial and ventricular muscle
Right nerves supply pacemaker and conduction
system
Effects:
Positive inotropic effect - increase contractility of
muscle
Positive chronotropic effect – increase in rate of
rise of pacemaker potential
Shorten conduction delay in AV node and increase
rate of relaxation
14. Parasympathetic innervation to the heart is
carried by the vagal nerves
These have their effects by releasing
acetylcholine (ACh)
Vagal stimulation produces bradycardia via 2
effects:
• 1. Rate of upward drift of the pacemaker potential is
slowed
• 2. Initial pacemaker potential becomes more negative
(hyperpolarised)
15.
16. Blood flow
left ventricle = 80/ml/min/100g
right ventricle = 40 ml/min/100g
atria = 20 ml/min/100g
*Flow can increase 4-fold
Capillary density - all capillaries open
Very high O2 extraction: (A-V)02 = 14
ml 02/dl
VO2 = 12 ml/min/100g ----> very high
17. to cardiac work
• influenced by
a) systolic pressure
b) heart rate
c) stroke volume
• increases achieved primarily by hyperemia
• 40% due to oxidation of carbohydrates, 60% fatty
acids
18. contraction (systole) leads to compression of
intramural vessels and reduction in flow
pressure inside left ventricle can exceed aortic
pressure during systole
vessel compression greatest in endocardium,
decreases toward epicardium
O2 demand and flow/g is greatest in
endocardium
LV coronary flow decreases as HR increases
since diastole shorter
20. Tachycardia: HR
time in systole
metabolic activity
vessel compression
vasodilation
Bradycardia: HR
time in systole vessel compression
metabolic activity vasoconstriction
21. Tissue oxygenation is major regulator
of vascular tone (adenosine, tiss pO2)
Essentially all capillaries are open to
flow (O2 diffusion distance)
Flow regulation occurs at arterioles
VO2 limited by blood flow (max O2
extraction)
22. AUTOREGULATION OF CBF - extremely good over wide
pressure range (50-150 mm Hg)
REACTIVE HYPEREMIA - peak flow reached after only 15
second occlusion
FUNCTIONAL HYPEREMIA - very tight coupling between
02 demand (V02) and 02 delivery (blood flow)
HYPOXEMIC HYPEREMIA - very sensitive to changes in
arterial oxygen saturation
METABOLIC MECHANISMS ( eg, adenosine) account for
above
IntrinsicVasoregulation-CoronaryCirculation
23. in coronary arteries, -adrenergic
receptors mediate vasoconstriction while
-adrenergic mediate vasodilation
sympathetic stimulation elicits vasodilation
because increases in contractility and HR
elevate VO2 metabolic vasodilation
parasympathetic stimulation elicits small
increment in CBF
24. Continuous capillaries - all perfused;
large surface area for exchange
Most exchange occurs during diastole
(when blood flow is greatest)
Tissue pressure = 15 mm Hg during diastole
Tissue pressure rises with ventricular
pressure during systole; greatest increase
is in endocardium
25. Syncytium = many acting as one
Due to presence of intercalated discs
• low resistance pathways connecting cardiac cells
end to end
• presence of gap junctions
27. STRUCTURE OF A MYOCARDIAL CELL
Mitochondria Sarcolemma
T-tubule
SR
Fibrils
28. In response to action potentials, the levels of
calcium within cardiac muscle rises
Some Ca2+ binds to troponin C, which exists on the
thin actin filaments
This exposes binding sites on the actin filaments
The thick myosin filaments have heads that can flip
These heads (powered by ATP) attach to the actin
binding sites
Myosin heads flip, and the myosin and actin
filaments slide over one another = contraction
29. Link between electrical excitation and
muscle contraction is calcium ions
AP causes sarcoplasmic [Ca2+] to rise from
0.1 M to 2 M in 10msec
Some Ca2+ binds to troponin C to activate
contraction proteins
Intact cell level of free Ca2+ during
excitation is 1-10 M
Typical concn of 2 M only gives partial
activation
If [Ca2+] increased (e.g. by adrenaline), get
more activation, and more contraction
30. Under normal conditions, not all of the contractile
cross-bridges are activated
Can activate more by:
• (a) the length-tension relationship or
• (b) chemically-induced rises in Ca2+ (e.g.
noradrenaline from sympathetic nerves, or
circulating adrenaline)
31. Inotropic = strengthening
Catecholamines increase the amount of Ca2+
stored in the SR (a rise in the Ca2+ current
during the plateau of the AP)
Uptake back into the SR is also upregulated,
meaning the muscle relaxes faster, and
preserves the diastolic filling period
Three mechanisms regulate contractile force:
• The size of the Ca2+ current
• Affinity of contractile proteins for Ca2+ (depends on
stretch)
• Degree of actin-myosin overlap (also depends on
stretch)
32. A small population of heart cells have
the ability to spontaneously depolarize –
autorhythmic.
The most important group of such cells
makes up the sinoatrial node (SA node).
• SA functions as our pacemaker..
33. The cells of the SA node do not maintain a
“normal” resting potential because Ca++ is
constantly leaking into the cell through slow
calcium channels = pacemaker potential.
The potential starts at ~ -60 mV and
gradually depolarizes to ~ -40 mV, which
triggers the opening of fast calcium channels
and maybe voltage-gated Na+ channels.
The membrane potential rapidly shoots up to
~ +20 mV = depolarization..
36. Repolarization begins when K+ voltage-gated
gates open and K+ rushes out of the cell.
A new pacemaker potential begins when the
potential reaches ~ -60 mV.
Adjacent myocardial cells begin depolarizing
because of the influx of cations (probably
Ca++) through the gap junctions.
At threshold, Na+ gates open and Na+ rushes
into the cell.
The membrane is depolarized to ~ +15 mV.
37. Unlike noncardiac cells, repolarization
does not begin immediately.
Instead the potential difference is
maintained for ~ 200 – 300 ms by the slow
diffusion of Ca++ into the cell which
balances the outward diffusion of K+. This
is the plateau phase.
Once the cell has slowly repolarized to
threshold, K+ gates open and the cell is
quickly repolarized to resting potential of ~
-90 mV..
38.
39. This wave of depolarization spreads
throughout the atrial myocardium but cannot
reach the ventricular myocardium because
of the fibrous skeleton.
The only electrical connection between the
myocardia is in the AV node to AV bundle to
bundle of His to Purkinje fibers.
The specialized cells in the AV bundle
conduct the impulse very slowly.
This time delay allows the atria to complete
systole before the ventricles begin systole..
40. The electrical activity occurring in the
heart can be monitored with the ECG
(EKG).
Each cardiac cycle produces three distinct
waves; P, QRS, and T.
The waves represent changes in potential
between two different regions of the
surface of the heart.
The waves do not represent APs in
individual cardiac cells nor do they
represent the flow of blood through the
heart..
41. The impulse then travels to the AV
bundle, located in the superior
interventricular septum.
The AV bundle then splits into left and
right bundle branches, which continue
as Purkinje fibers.
Conduction System Animation..
44. SINGLE VENTRICULAR ACTION POTENTIAL
ECG
P
Q S
T
R
1 mV
Repolarization of ventricles
Depolarization of ventricles
Depolarization of atria
ENDOCARDIAL FIBER
EPICARDIAL FIBER
ATRIAL
FIBER
45. SINGLE VENTRICULAR ACTION POTENTIAL
ECG
P
Q S
T
R
1 mV
Repolarization of ventricles
Depolarization of ventricles
Depolarization of atria
ENDOCARDIAL FIBER
EPICARDIAL FIBER
ATRIAL
FIBER
49. Cardiac Cycle
All events which occur between two consecutive
heartbeats.
Systole: simultaneous contraction of the two
ventricles creating pressure to pump blood to the
lungs and body.
Diastole: resting phase immediately after systole
and lasts about 0.5s assuming one complete
cycle takes 0.8s.
52. Volume of blood
pumped/min. by each
ventricle.
• Pumping ability of the
heart is a function of
the beats/ min. and
the volume of blood
ejected per beat.
CO = SV x HR
• Total blood volume
averages about 5.5
liters.
Each ventricle pumps
the equivalent of the
total blood volume
each min. (resting
conditions).
53. The total amount of blood pumped by the left
ventricle in one minute (Q)
Q = SV x HR
Average cardiac output at rest is 5-6 litres,
during exercise it can exceed 30 litres in a
trained endurance athlete.
54. Without neuronal influences, the
heart beats according to the
rhythm set by SA node.
Regulation of HR (chronotropic
effect):
• May be + or – effect.
Autonomic control:
• Sympathetic and parasympathetic
nerve fibers to the heart modify the
rate of spontaneous depolarization.
• Innervate the SA node.
NE and Epi stimulate opening of
Na+/Ca2+ channel.
ACH promotes opening of K+ channel.
Major means by which cardiac rate
is regulated.
Cardiac control center (medulla):
• Coordinates activity of
autonomic innervation.
55. Blood ejected from left ventricle - not all blood is
ejected, the amount of blood remaining is called
end-systolic volume.
Stroke Volume = end-
diastolic volume - end-systolic volume
56. Stroke volume is regulated by 3
variables:
• EDV:
Volume of blood in the ventricles at the end of
diastole.
• Total peripheral resistance (TPR):
Frictional resistance or impedance to blood flow in
the arteries.
• Contractility:
Strength of ventricular contraction.
57. Workload on the heart prior to contraction
(preload).
• SV directly proportional to preload.
Increase in EDV results in an increase in SV.
• SV directly proportional to contractility.
Strength of contraction varies directly with
EDV.
Ejection fraction:
• SV/ EDV.
Normally is 60%.
Clinical diagnostic tool.
58. Total Peripheral Resistance:
• Impedance to the ejection of blood from ventricle.
• Afterload.
In order to eject blood, pressure generated in the ventricle
must be greater than pressure in the arteries.
• Pressure in arteries before ventricle contracts is a
function of TPR.
SV inversely proportional to TPR.
• Greater the TPR, the lower the SV.
59. Relationship between
EDV, contraction
strength, and SV.
Intrinsic mechanism:
• Varying degree of
stretching of
myocardium by EDV.
• As EDV increases:
Myocardium is
increasingly
stretched.
Contracts more
forcefully.
60. As the ventricles
fill, the
myocardium
stretches; This
increases the
number of
interaction
between actin
and myosin.
Allows more
force to develop.
Explains how the
heart can adjust
to rise in TPR.
61. Contractility:
• Strength of contraction
at any given fiber
length.
Depends upon
sympathoadrenal
system:
• NE and Epi produce an
increase in contractile
strength.
+ inotropic effect:
More Ca2+ available to
sarcomeres.
62. Parasympathetic
stimulation:
- chronotropic effect.
Does not directly
influence contraction
strength.
CO affected 2
ways:
• + inotropic effect
on contractility.
• + chronotropic
effect on HR.
63. Return of blood to the
heart via veins.
Venous pressure is
driving force for return
of blood to the heart.
Veins have thinner
walls, thus higher
compliance.
• Capacitance vessels.
2/3 blood volume is
in veins.
EDV, SV, and CO are
controlled by factors
which affect venous
return.
70. CARDIAC OUTPUT (Q) =
VO2
[O2]a - [O2]v
250 ml/min
20 ml% - 15 ml%
=
= 5 L/min
.
Q = HR x SV
.
SV =
Q
HR
.
=
5 L/min
70 beats/min
= 0.0714 L or 71.4 ml
CARDIAC INDEX = Q
m2 body surface
area
.
5 L/min
1.6 m2=
= 3.1 L/min/m2
71. The pressure exerted by the blood on the
vessel walls
Expressed by two numbers - systolic and
diastolic
Systolic= highest pressure & corresponds to
ventricle contraction
Diastolic= lowest pressure & represents the
ventricle relaxing
72. Mean arterial pressure = the average
pressure exerted by the blood as it travels
through the arteries:
MAP = 1/3 pulse pressure + diastolic pressure
Generalised constriction of blood vessels
increases blood pressure whereas dilation
decreases blood pressure
Hypertension is a chronic elevation of blood
pressure above normal healthy values
73. Elevated body temperature
• HR increases about 10 beats for every degree F
elevation in body temperature
• Contractile strength will increase temporarily but
prolonged fever can decrease contractile strength
due to exhaustion of metabolic systems
Decreased body temperature
• decreased HR and strength
74. Pressure inside is 35 to 15 mmHg
5% of the blood is in capillaries
exchange of gases, nutrients, and wastes
flow is slow and continuous
76. VASOMOTION = Intermittent flow due to constriction-
relaxation cycles of precapillary shpincters
or arteriolar smooth muscle (5 - 10/min)
AUTOREGULATION OF VASOMOTION:
1. Oxygen Demand Theory (Nutrient Demand Theory)
O2 is needed to support contraction (closure)
2. Vasodilator Theory
Vasodilator substances produced (via O2)
e.g. Adenosine Heart
CO2 Brain
Lactate, H+, K+ Skeletal Muscle
3. Myogenic Activity
77. 3 central priorities of CVS:
1. adequate blood supply to brain & heart
2. “ “ “ to other organs
after brain & heart supply assured
3. control capillary pressure to maintain
tissue volume & composition of interstitial
fluid within reasonable ranges
78. Baroreceptors monitor BP – info from
baroreceptors + info from chemoreceptors
(monitoring CO2 & O2 concentrations & pH of
blood) is transmitted to brain – other sensory
receptors are involved in reflex effects on the
CVS including mechanoreceptors (respond to
mechanical distortion & pressure) &
thermoreceptors (responsive to temperature
changes) = all this info is integrated in a collection
of brain neurons called medullary CV center (at
the level of medulla/pons)
79. Medullary CV center receives info also from
medullary respiratory center, hypothalamus,
amygdala nucleus & cortex – output from
medullary CV center feeds into sym & para
autonomic motor neurons that innervated heart
& smooth muscle of arterioles & veins
Stim. of sympathetic nerves = increases rate &
force of heart contraction & causes
vasoconstriction = marked increase in arterial
BP & CO; in general, the reverse happens
when stim para nerves ending in reduction of
BP & CO
80. 2 functional regions with opposing effects on
BP:
1. stimulation of pressor center results in
sympathetic activation & rise in BP
2. stimulation of depressor center = in parasym.
activity & drop in BP fig 12-42 p. 513
Role played by baroceptors which are widely
distributed in arterial system show increased
rates of firing with increase in BP …
81. unmyelinated barorecptors (mammals, amphibians &
reptiles) respond only to pressures above normal
initiating reflexes that reduce arterial BP
myelinated baroreceptors (only mammals) respond
only to pressures below normal initiating reflexes
that raise BP - many baroreceptors are located in
carotid sinus & in mammals, carotid sinus is a
dilation of internal carotid artery at its origin =
buried in the thin walls are finely branched nerve
endings function as baroreceptors ( inc. in BP stretches
wall of carotid sinus causing an increase in discharge frequency)
82. arterial chemoreceptors located in carotid &
aortic bodies NB in ventilation (later) but also
have some effect on CVS = when blood
perfusing carotid & aortic bodies has high
levels of CO2 or low O2 & pH, arterial
chemoreceptors respond with increase in
discharge frequency which results in peripheral
vasoconstriction & slowing of HR if animal is
not breathing (e.g. submersion)
CO is reduced while birds & mammals are
diving
83. 1. atrial receptors (esp. mechanoreceptors in
atrial walls) &
2. ventricular receptors (nerve endings of both
myelinated {mechanoreceptive &
chemoreceptive} & unmyelinated sensory
afferent fibers imbedded in ventricles) =
together monitor venous pressure & HR to
ensure activity of heart is correlated with
blood inflow from venous system & blood
outflow into arterial system
84. Chronotropic (+ increases) (- decreases)
• Anything that affects heart rate
Dromotropic
• Anything that affects conduction velocity
Inotropic
• Anything that affects strength of contraction
eg. Caffeine would be a + chronotropic agent
(increases heart rate)