This PPT includes reguation of temperature,respiration and gross pictorial description of cardiac cycle and and cardiac output withits pedodontic implications

1. REGULATION OF
TEMPERATURE,RESPIRATION
AND CARDIAC OUTPUT AND
ITS IMPLICATIONS IN
PEDODONTICS
KARISHMA.S
I MDS
R.V Dental college

2. CONTENTS
 Introduction
 Regulation of body temperature
 Regulation of respiration
 Cardiac cycle
 Regulation of cardiac output
 Clinical considerations
 Conclusion
 References

3. INTRODUCTION
“Homeostasis” refers to the maintainance of constant
Internal environment of the body.
 FEEDBACK SIGNALLING
1.Positive feedback
2.Negative feedback

4. REGULATION OF BODY
TEMPERATURE

5.  Depending on maintainance of body temperature:
-Homeothermic
-Poikilothermic
 Normal body temperature
(35.80C-37.30C)
CORE
RECTAL
ORAL
AXILLARY
SKIN/SURFACE
ZONE OF THERMAL NEUTRALITY-describes a
range of temperatures of the immediate
environment in which a standard healthy adult
can maintain normal body temperature without
needing to use energy above and beyond normal
basal metabolic rate.

6. VARIATIONS OF BODY TEMPERATURE
 AGE
 SEX
 DIURNAL VARIATON
 AFTER MEALS
 EXERCISE
 SLEEP
 EMOTION
 MENSTRUAL CYCLE
 HYPERTHEMIA/HYPOTHERMIA

7. HEAT BALANCE
HEAT GAIN
-METABOLIC
ACTIVITIES
-MUSCULAR ACTIVITY
-ROLE OF HORMONES
-RADIATION OF HEAT
FROM ENVIRONMENT
-SHIVERING
HEAT LOSS
-CONDUCTION
-RADIATION
-CONVECTION
-EVAPORATION
-PANTING

9. REGULATION OF BODY TEMPERATURE
HYPOTHALAMUS
HEAT GAIN CENTRE HEAT LOSS CENTRE
SITUATED IN POSTERIOR
HYPOTHALAMUS
SITUATED IN PREOPTIC NUCLEUS
OF ANTERIOR HYPOTHALAMUS
SITUATED IN POSTERIOR
HYPOTHALAMUS
SITUATED IN PREOPTIC NUCLEUS
OF ANTERIOR HYPOTHALAMUS

11. CLINICAL ASPECTS
CLASSIFICATION
• Low grade fever-38-
CLASSIFICATION:
• Mild-35-330c/95-
HYPERTHERMIA HYPOTHERMIA

12. IN EXTREME CONDITIONS

13. Febrile Convulsions
 Seizures (fits or convulsions) occurring in children aged
6 months to 5 years
 Associated with fever, without other underlying cause
such as CNS infection or electrolyte imbalance.
 As temperature of neuronal tissue could increase the rate
and magnitude of neuronal firing leading to seizures
 Fever involves the release of cytokines
and other inflammatory mediators in the
body and within the brain itself. Certain
cytokines, and specifically interleukin
(IL)-1β, enhance neuronal excitability.

14. REGULATION OF TEMPERATURE IN NEWBORNS
-Lipolysis of brown fat
-BMR is high
-Artificial means of providing warmth
-Underdeveloped thermoregulatory system.
-Lacks behavioural adjustment
-Surface area to proportion to its body
weight is greater, so they lose body heat
more speedily

15. HYPOTHERMIA DURING GENERAL ANESTHESIA
IN CHILDREN
 High ratio of body surface area
over body weight
 An underdeveloped
thermoregulatory system
 Lack of subcutaneous pad of fat
and limited ability of
compensatory thermogenesis
from brown fat
PRE MATURE BABIES
 Need for incubators
 Decreased subcutaneous fat
 Low supply of brown fat
 Reduced metabolic rate
 Large surface area to body
mass ratio

16. Body temperature increases during pediatric full mouth rehabilitation
surgery under general anesthesia.
Chuang YS, Li CH, Cherng CH Journal of Dental Sciences. 2015 Dec 31;10(4):372-5.
Abstract :. This study reports gradually increased body temperature in pediatric
patients receiving full mouth rehabilitation surgery.
Materials and methods: Following institutional review board approval, the medical records of
pediatric patients who received full mouth rehabilitation surgery from 2011 through 2012 were
collected. The body temperatures (preoperative, periodic during operation, and postoperative
5 hours and 12 hours) and the maximum differences in temperature change during operation
were recorded.
Results: A total of 34 patients were enrolled in this study. An increase in body temperature was
found. The mean standard deviation of the difference in temperature change was found to
be 2.50 1.17C. A significant positive correlation was noted (r Z 0.464, P Z 0.006) between
the maximum temperature changes and the operation duration. At 12 hours after operation,
no patients were reported to have a tympanic temperature >37.5C.
Conclusion: Body temperature transiently increased during pediatric full mouth rehabilitation
surgery. The increase in body temperature was associated with operation duration. The etiology
is uncertain. Continuous body temperature monitoring and the application of both heating
and cooling devices during pediatric full mouth rehabilitation surgery should be mandatory.

17. REGULATION OF RESPIRATION

18. Mechanism of regulation of respiration:
 Nervous/neural mechanism
 Chemical mechanism
 Respiration is a reflex process.but it can be controlled
voluntarily,but only for a short period of about 40
seconds,at the end of that period the person is forced to
breath
 Altered pattern of respiration is brought back to normal
within a short time by some regulatory mechanisms in the
body

19. NERVOUS MECHANISM
RESPIRATORY CENTERS:
(a)Medullary centers:
Dorsal respiration group of Neurons
Ventral respiration group of neurons
(b)Pontine centers
Pneumotaxic center
Apneustic center

20. DORSAL RESPIRATION GROUP OF NEURONS
 Situatedin nucleus of tractus solitarius present in upper part of
medulla oblongata.
 All neurons are inspiratory neurons.
Function: It is responsible for basic rhythm of respiration.
VENTRAL RESPIRATION GROUP OF NEURONS
 It is situated in medulla oblongata anterior and lateral to the
inspiratory center.
 It is formed by neurons of nucleus ambiguous and nucleus retro
ambiguous.
Function: This center is inactive during quiet breathing and become
active during forced breathing.during forced breathing the neurons
activate both inspiratory and expiratory muscles.

21. PONTINE CENTRES
PNEUMOTAXIC CENTER:
 It is situated in dorsolateral part of reticular formation of upper Pons.
 It is formed by nucleus parabrachialis.
Function: It controls medullary respiratory centers,particularly the
inspiratory center through apneustic center.
 It always controls the activity of inspiratory center so that duration of
inspiration is controlled, due to which the inspiration
stops and expiration starts.
APNUESTIC CENTER:
 It is situated in reticular formation of lower Pons.
Function: this center increases depth of inspiration by
acting directly on the inspiratory center

22. CONNECTIONS OF RESPIRATORY CENTRES
Efferent pathway:
-phrenic
-intercoastal nerve
Afferent pathway:
impulses from peripheral chemo
and baro receptors are carried to the
respiratory centers by branches of
GLOSSOPHARYNGEAL and VAGUS nerves.
 Vagal nerve fibers also carry impulses
from stretch receptors
 Respiratory centers receive various
impulses from various parts of the body
and regulate accordingly.

23. INTEGRATION OF RESPIRATORY CENTERS
A)Role of medullary centers
-Rhythmic discharge of inspiratory impulses
-Inspiratory ramp
B) Role of pontine centers:
-regulates the medullary centers
-apneustic accelerates dorsal group
-pneumotaxic inhibits apneustic
C)Pre-Botzinger complex:
- In animals
-group of neurons in ventolateral part of medulla.
-pacemakers for rhythmic respiration.

24. FACTORS AFFECTING RESPIRATORY CENTERS
 Hering-Breuer Inflation Reflex
 Hering-Breuer Deflation Reflex
 J-receptor Reflex
 Irritants Reflexes
 Baroreceptors Reflex
 Other influences (mediated via
hypothalamus)

25.  Over-Inflation of lungs→ stimulation of slowly adapting
stretch receptors in smooth muscles of large & small airways
→afferent vagal signals → inhibitory to medullary and
pontine inspiratory network →termination of inspiration.
 This reflex in not important in normal
adults. It is more important &
powerful in neonates.
Hering-Breuer Inflation Reflex

26. Hering-Breuer Deflation Reflex
Deep expiration → Deflation of the lungs → ↓activity of previous
slowly adapting stretch receptors or stimulate other
propioceptors in respiratory muscle → decreasing afferent vagal
signals to respiratory centres→ increase in the activity of
inspiratory neurons →↑ rate of breathing

27.  Present in wall of alveoli and have close contact with
pulmonary capillaries.
 Pulmonary emboli or oedema or congestion →
stimulation of juxtapulmonary-capillaries receptors
→impulses along vagal afferent → respiratory centre →
rapid shallow breathing.
 These receptors are responsible for hyperventilation in
patients affected by pulmonary congestion.
J-receptor Reflex

28. Irritant receptors are present in the bronchioles.these are
stimulated by irritants(ammonia,sulphur dioxide) → afferent
impulses to resp centres through vagus → produces
hyperventilation with bronchiospasm → prevents further
entry of irritants
Irritant Reflexes

29. Baroreceptor Reflex
Acute change in blood pressure →
stimulation of baroreceptors →afferent
signals via X & IX → inhibitory to
respiratory centre → decrease rate &
depth of respiration → ↓venous return
→ ↓COP → ↓ABP

30. Other Influences from higher centers
hypothalamus & limbic system
Temperature: Increases respiratory rate
Pain: Sudden pain decreases, prolonged
pain increases rate
Alcohol: Decreases rate
Exercise: increases breathing rate (higher cortical
centers)

31. CHEMICAL MECHANISM
Operated through chemo receptors.
Chemoreceptors have sensory nerve endings,which give response to
chemical change in blood
Chemoreceptors are stimulated by changes in the blood such as
-hypoxia(decreased PO2
-hypercapnia(increased PCO2)
-increased hydrogen ion concentration
TYPES OF CHEMORECEPTORS:
-Central chemoreceptors
-Peripheral chemoreceptors

32. Central Chemoreceptors/chemo sensitive area
 Present in the brain
hence are central
 Situated in the deeper
part of medulla
oblongata, close to the
dorsal respiratory group
of neurons

33. Peripheral Chemoreceptor Pathway
 The carotid & aortic bodies are
sensitive to
-Fall in PaO2,
-An increase in PaCO2 or H+
concentration
 They maximally stimulated when
PaO2 decreases below
50-60mm Hg
 They detect changes in dissolved
O2 but not in the O2 that is bound
to Hb.
Peripheral
chemoreceptors are
the only sensors
detecting a fall in
PO2

35. IMPLICATION OF RESPIRATORY REGULATION
IN PEDODONTICS
 High peripheral airway resistance
in children younger than 5 years
of age (airway diseases) „
 Low ratio of functional residual
capacity to total lung capacity
(low reserve)
 Narrow airway in children(greater
risk of airway obstruction from
small foreign bodies. )
 Infants dependent on
diaphragm(Diaphragms could
fatigue and infants could become
apneic)
RESPIRATORY RATES
1.Infants - 40 -60/min
2.Toddler- 24- 40/min
3.Pre schooler- 22 -34/min
4.School- 18-30/min
5.Adolescent – 12 -16/min

36.  Infants are nose breathers.(especially first 4-6 months infants breathe
through nose only. Care must be taken during blockade)
 Relatively larger tongue and smaller oral cavity
(tongue is more likely to obstruct the airway than in the adult. This
makes it essential that there is correct positioning of the head jaw to
open the airway.)
 Trachea is more cartilaginous and
soft and is comparatively shorter than
that of the adult, which increases the
risk of dislodgement of the
endotracheal tube.

37.  Breathing: The ribs of the infant are positioned more
horizontally than those of the adult. This means that with
inspiration the ribs only move up, and not up-and-out, like the
adult rib cage. This limits the capacity to increase tidal
volumes.

38. DENTAL CONSIDERATIONS
The common chronic childhood respiratory diseases
which have the potential for associated dental
morbidity include:
 Obstructive sleep apnoea,
 Asthma
 Bronchopulmonary dysplasia (chronic neonatal
lung disease

39. ASTHMA:
Clinical manifestation Constriction of bronchi, coughing,
wheezing, chest tightness, and shortness of breath
Oral manifestation
 Increased caries risk, enamel defects
 Increased gingivitis and periodontal disease risk; •
 Higher rates of malocclusion and increased: overjet,
overbite, posterior crossbite; high palatal vault
 Oral candidiasis,
 Xerostomia,
Some reports indicate that dental materials may
exacerbate asthma including dentifrices, fissure
sealants, tooth enamel dust, methyl methacrylate,
fluoride trays, and cotton rolls and use of latex gloves

40. OBSTRUCTIVE SLEEP APNOEA-
CRANIOFACIAL ANOMALIES MAINLY
 retrognathic mandible,
 narrow palate,
 large neck circumference,
 long soft palate
 tonsillar hypertrophy,
 nasal septal deviation
 relative macroglossia
 Xerostomia

41.  Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease
that affects newborns and infants. It results from damage to the lungs
caused by mechanical ventilation (respirator) and long-term use of
oxygen. Most infants recover from BPD, but some may have long-term
breathing difficulty.
 BPD risk is highest in premature infants with low birth weight (less
than 4.5 pounds). These premature babies don’t have fully developed
lungs when they’re born
Bronchopulmonary dysplasia (chronic neonatal lung
disease

42. CARDIAC CYCLE

43.  Events of cardiac cycle are classified into 2 divisions :
-SYSTOLE
-DIASTOLE
 The subdivision of systole and diastole are:
SYSTOLE:
Isometric contraction - 0.05 sec
Ejection period - 0.22 sec
DIASTOLE:
Protodiastole - 0.04sec
Isometric relaxation - 0.08sec
Rapid filling - 0.11sec
Slow filling - 0.19sec
Last rapid filling
(or) Atrial systole - 0.11sec

45. REGULATION OF CARDIAC OUTPUT

46. CARDIAC OUTPUT:
Amount of blood pumped out from each ventricle. Usually refers to left
ventricular output through aorta
Cardiac output = Heart Rate X Stroke Volume
VENOUS RETURN:
It is the quantity of blood flowing from the veins into the right atrium
each minute.
Venous Return = Cardiac Output

47.  Stroke volume- 70ml(60-80ml when 72 beats/min)
 Minute volume-stroke volumeXheart rate(5 lts/ventricle/min)
 Cardiac index-amount of blood pumped per
ventricle/minute/sq mt of body surface area.

48. VARIATIONS IN CARDIAC OUTPUT
PHYSIOLOGICAL:
 Age
 Sex
 Body build
 Diurnal variation
 Environmental temperature
 Emotional conditions
 Sleep
 Exercise
PATHOLOGICAL:
 Increase in cardiac output
-fever
-anemia
-hyperthyroidism
 Decrease in cardiac output
-hypothyroidism
-atrial fibrillation
-congestive cardiac failure
-shock

49. DISTRIBUTION OF CARDIAC OUTPUT
 The whole amount of blood pumped out by right ventricle goes to
lungs, whereas by left ventricle is distributed to different parts of
body.
 The heart which pumps the blood to all the organs receives the
least amount of blood

50. FACTORS MAINTAINING CARDIAC OUTPUT
1)VENOUS RETURN
-Respiratory pump
-Muscle pump
-Gravity
-Venous pressure
-Sympathetic tone
2)FORCE OF CONTRACTION
3)HEART RATE
4)PERIPHERAL RESISTANCE

51. VENOUS RETURN:
-Respiratory pump
-Muscle pump
-Gravity
-Venous pressure
-Sympathetic tone

52. Role Of Frank-Starling Mechanism
Frank-Starling Law:
It states that “ Within physiologic limits, the heart pumps all the
blood that returns to it by the way of veins.”
Increased Venous Return
Cardiac muscles stretches to greater length
Ventricular muscle contracts with greater force
Increased Cardiac Output

53. EFFECTS
Stronger Contractions:
Increased heart volume stretches muscles and causes
stronger contraction.
Heart Rate:
Stretch increases heart rate as well.
S-A Node:
Direct effect on rhythmicity of the node to increase heart rate
as much as 10-15%.
Bainbridge Reflex:
It gives reflexes to the vasomotor center and then back to
the heart by the way of sympathetic nerves and vagi,
increases the heart rate

54. FORCE OF CONTRACTION
Preload-Stretching of muscle fibre at the end of diastole just
before contraction
 Depends upon venous return and ventricular filling
 Force of contraction and cardiac output are directly
proportional
Afterload-Force against which the ventricles must contract
and eject the blood
 Force is determined by arterial pressure
 Force in left ventricle is determined by aortic
pressure and in right by pressure in pulmonary
artery
 Force of contraction and cardiac output are
inversely proportional

55. HEART RATE
Cardiac output is directly proportional to heart rate.
Regulated by nervous mechanism having 3 components:-
1)Vasomotor center(cardio-acceleratory and
cardio-inhibitory areas)
2)Motor nerve fibers to the heart
(parasympathetic and sympathetic
3)Sensory nerve fibers from the heart
(inferior cervical sympathetic nerve)

56. PERIPHERAL RESISTANCE
 Resistance offered to the blood flow at the peripheral blood vessels.
Resistance= pressure gradient/volume of blood flow
 Inversely proportional to cardiac output
Three important factors determine:
1.Radius of blood vessel
2.Pressure gradient
3.Viscosity of the blood

57. IMPLICATION OF CARDIAC OUTPUT IN CHILDREN
 At birth, the neonatal myocyte is not fully developed; making the
heart less able to respond to volume loading with an increased
cardiac output.
 Neonatal cardiac output is significantly dependent on heart rate,
indicating they have less preload reserve. Blood pressure continues
to rise throughout childhood.
 Fixed-stroke volume: to increase cardiac output, infants are limited
to increasing their heart rate as they are unable to increase stroke
volume.

58.  Smaller vessels / more subcutaneous tissue
It is often extremely difficult to obtain vascular access
in young children and infants, due to the size of their
veins and the increase in subcutaneous tissue during
infancy.
 Relatively healthy cardiovascular system
The cardiovascular system of the infant and child is
generally healthy. So fluid resuscitation is less of a
concern than in adults, where cardiac disease is more
prevalent.

59. Drug consideration
 Inhaled anaesthetic drugs-decrease in heart rate-
decrease cardiac output-depress central nervous
system.
 Precaution to prevent hypotension-
Well hydrated prior to procedure requiring inhaled or
intravenous sedation.

60. CONGENITAL HEART DISEASE- heart disease that children are born
with, usually caused by heart defects that are present at birth.
(e.g. atrial/ventricular septal defects, pulmonary/aortic stenosis
transposition, heart valve abnormalities)
Oral consideration:-
-Infective endocarditis risk from dental treatment
-Post-operative bleeding risk in children with anti-coagulated
status following surgical procedures
-May have oral manifestations caused by co-occurring disorders,
Other concerns:
• Depression/Anxiety
• Genetic and syndromic conditions (~11%) such as Down, Turner, Marfan
and; osteogenesis imperfecta
• Asthma
• Intellectual disabilities

61. Tetralogy of Fallot
 Right ventricular (RV) outflow tract obstruction (RVOTO)
 ventricular septal defect (VSD),
 Aorta dextroposition,
 RV hypertrophy

62. Pediatric Patients with High Pulmonary Arterial Pressure in Congenital Heart Disease Have
Increased Tracheal Diameters Measured by Computed Tomography
NobukoOhashiMD, PhDHidekazuImaiMD, PhDYutakaSeinoMDHiroshiBabaMD, PhD
Objectives:
Determination of the appropriate tracheal tube size using formulas based on age or height
often is inaccurate in pediatric patients with congenital heart disease (CHD), particularly in
those with high pulmonary arterial pressure (PAP). Here, the authors compared tracheal
diameters between pediatric patients with CHD with high PAP and low PAP.
Participants:
Pediatric patients, from birth to 6 months of age, requiring general anesthesia and tracheal
intubation who underwent computed tomography were included. Patients with mean
pulmonary artery pressure >25 mmHg were allocated to the high PAP group, and the
remaining patients were allocated to the low PAP group. The primary outcome was the
tracheal diameter at the cricoid cartilage level, and the secondary goal was to observe whether
the size of the tracheal tube was appropriate compared with that obtained using predictable
formulas based on age or height.
Conclusions:
Pediatric patients with high PAP had larger tracheal diameters than with low PAP and required
larger tracheal tubes compared with the size predicted using formulas based on age or height.

63. General Guidelines: Antibiotic Prophylaxis
• Administer a single dose of antibiotic regimen 30-60 minutes before dental
procedure.
• Dosage may also be administered up to two hours after procedure if not
administered before only in cases when antibiotics are inadvertently not
administered.
• Amoxicillin is preferred oral therapy (50 mg/kg). If allergic, consider use of
Clindamycin (20 mg/kg), Cephalexin (50 mg/kg), or
Azithromycin/Clarithromycin (15 mg/kg)
• Antibiotic prophylaxis recommended for following conditions: * High Risk
includes prosthetic cardiac valves, previous infective endocarditis, and
congenital heart disease (unrepaired cyanotic CHD, including shunts and
conduits, completely repaired cardiac defect with prosthetic material or
device – for 1st 6 months following surgery, repaired CHD with residual
defects at the site or adjacent to the site of a prosthetic patch or device),
cardiac transplant patients who develop valvulopathy)

64. CONCLUSION
It is very necessesary to know about the condition of the child regarding
the general health before initiating any kind of dental procedures which
help in preventing complications to the child and also helps in customizing
the treatment protocol for each child accordingly including the drug
considerations.

65.  TEXTBOOK OF PHYSIOLOGY-SEMBULINGAM
[5TH EDITION]
 TEXTBOOK OF MEDICAL PHYSIOLOGY-GUYTON AND HALL
[11THEDITION]
 REVIEW OF MEDICAL PHYSIOLOGY – WILLIAM F GANONG
[18TH EDITION]
 PEDIATRIC DENTISTRY INFANCY THROUGH ADOLESENCE - PINKHAM
[4TH EDITION]
 INTERNET SOURCES
REFERENCES