Practical 2 Flashcards
Intrinsic stimulation
Internal stimulation that makes the heart beat by itself
Autorhythmic cells
Specialized, noncontractile cells that cause interinsic stimulation
Intrinsic conduction system
1) Initiates the action potential that causes contraction of cardiac muscle fibers
2) Provides a pathway for conduction the action potential to all cardiac muscle fibers
Extrinsic stimulation
Only increase or decrease intrinsic pace
Electrocardiograph
Recods electrical charges in the heart
Electrocardiogram (ECG,EKG)
Chart recording of electrical events that occur before each heartbeat
P wave
First wave; small, upward direction; represents atrial depolarization; occurs immediately before the atria contract
QRS complex
Short downward Q - tall upward R - medium downward S; represents ventricular depolarization; occurs just before the ventricles contract
T wave
medium, upward deflection; represents ventricular repolarization and occurs just before the ventricles relax
P-Q interval
interval between the beginning of the P wave until the beginning of the Q wave; represents the time interval between the beginning of conraction of the atrium and the beginning of the contraction of the ventricle
Q-T interval
Interval of time between the start of Q to the end of T wave; represents the time interval from the beginning of ventricuar depolarization until the end of ventricular repolarization - ventricles are contracting
S-T segment
Segment from the end of the S to the beginning of the T wave; it represents the time the ventricular fibers are fully deploarized
Normal sinus rhythm
Heart rate of 60-100 beats/min
Tachycardia
Heart rate above 100 beats/min
Bradycardia
Heart rates below 60 beats/min
Cardiac cycle
(# of squares counted) x 0.04 sec/mm
Heart block
Could be produced by cardiac damage to the AV node or AV bundle. Associated with P-Q interval
Complete heart block
Results in the ventricles depolarizing independently from the atria
Right or left bundle branch block
QRS complex longer than 0.12 sec. Two ventricles do not contract simultaneously.
Myocardial damage
Lengthens normal interval of QR interval of 0.38 sec.
What causes air to move into our lungs when we breath
the movement of the ribs
What is the action of the diaphragm during inhalation
Contraction
Bronchoscopy
Endoscopic technique of visualizing inside of airways
What is the purpose of physiotherapy on lungs
move the mucus
Alveoli
Millions of tiny air sacs where gases are exchanged
How does oxygen in the alveolus get into the bloodstream in the lungs?
Diffusion of oxygen from alveolus into the bloodstream
How does carbon dioxide get out of the bloodstream?
Breathing out makes carbon move from bloodstream to outside
What is the genetic problem in the lungs of someone with Cystic Fibrosis
The proteins don’t work properly and the mucus is thicker
How is the progress of cystic fibrosis monitored?
Weight, height. Peak flow meter to see how blocked airways are
How does drug Pulmozyme work in cystic fibrosis patients
Helps mucus in lungs liquify to help cough it up. Chops up lung molecules
Pneumonia
Acute inflammation of the alveoli. The subsequent immune response causes fluid leakage and cellular accumulation (exudate) in the alveoli
Histological description of Smoker’s Lung
Dark and mottled. Black deposits, appear more flattened
Histological description of Emphysema
Damaged alveoli. Disconnected/disjointed
How does emphysema affect gas exchange between lungs and pulmonary capillaries?
Alveoli themselves are damaged
Main function of the respiratory system
Brings needed oxygen into lungs and eliminates CO2
What are the two serous membranes surrounding each lung?
Visceral and Parietal pleura
What is inside the pleural cavity
Pleural/serous fluid
Pleural fluid
Lubricates and facilitates breathing
What anatomical structures make up the “Bronchial Tree”?
Terminal, Main, later, segmental bronchae, cartilage, smooth muscle
How are bronchioles different from the other structures of the bronchial tree?
Walls contain more smooth muscle
What anatomical structures are part of the conduction zone?
Terminal bronchioles
What anatomical structures are part of the respiratory zone?
Alveoli, alveolar duct, alveolar sac
What is surfactant and how does it function in an alveolus?
A mixture of phospholipids and lipoproteins which lowers surface tension of alveolar fluid
Anatomical structures that form the respiratory membrane in the lung
Alveolar wall and capillary wall
Pulmonary ventilation
Exchange of air between atmosphere and lungs
Boyle’s law
Pressure and volume are inversely related
What muscles contract during quiet inspiration?
Diaphragm and external intercostal muscles
what additional muscles come into action during deep inspiration?
Sternolcleidomastoid, scalenes
What additional muscles come into action during deep expiration
Internal intercostal muscles, internal + external oblique
Intrapulmonary or intra-alveolar pressure
Pressure within the alveoli. 760 mm Hg is normal
Intrapleural pressure
Pressure within the pleural cavity
What is the effect of surface tension on an alveolus?
Pulls alveoli inward, alveolar wall helps overcome this effect
Intrapleural pressure during inspiration?
Decrease in pressure
Intrapleural pressure during expiration?
Increase in pressure. Returns to negative form
What happens when the thoracic wall is punctures at least to the level of the pleural cavity?
Pneumothorax. Lung collapses
Transpulmonary pressure
Suction to keep lung inflated
What happens to airway resistance when the bronchioles constrict?
Resistance increases, decreased airflow
Mathematical relationship between air flow and resistance?
increase resistance, decreased airflow
Effect of parasympathetic (acetylcholine) stimulation on airflow in the bronchioles?
Increased air flow, relaxation
Effect of histamine application on air flow in bronchioles?
Allergic reaction. Increased airway resistance, decreased air flow harder to breath
Effect of sympathetic (epinephrine) stimulation on bronchioles?
Dilutes bronchioles, decreased airways resistance, increased air flow, adequate gas exchange
Lung compliance
Ease with bags expand
2 factors affecting lung compliance
Stretchability of elastic fibers within lungs, furface tension within alveoli
What happens in an infant’s lungs during respiratory distress syndrone?
Low compliance. Collapsed alveoli resist expansion
With Diaphragm pushed up
- Internal jar volume decreased
- Internal jar pressure increased
- volume of lungs decreased
- out of lungs
With Diaphragm pulled down
- internal jar volume increased
- internal jar pressure decreased
- volume of lungs increased
- into lungs
Bronchial sounds
Produced by air rushing through large respiratory passageways (trachea + bronchi). Both inhalation and exhalation
Vesicular breathing sounds
Result from air filling alveolar sacs and resembles sound of rustling or muffled breeze. Inhalation ONLY
Obstructive pulmonary diseases
Airflow into and out of lungs is reduced/restricted. ex. asthma
Diagnosis of obstructive pulmonary diseases usually requires
measurements of pulmonary flow rates
restrictive pulmonary disease
Person’s ability to inflate and deflate the lungs is reduced, and as a result, lung l=volumes and capacities are below normal.
ex. Pulmonary fibrosis
Restrictive pulmonary diseases are diagnosed by determining
Lung volumes and capacities
Tidal Volume (TV)
Amount of air inhaled or exhaled with each breath under resting conditions - normal quiet breathing: ~500 ml
Inspiratory reserve volume (IRV)
The amount of air that can be forcefully inhaled after a normal tidal volume inhalation: ~3100 ml
Expiratory reserve volume (ERV)
The amount of air tha can be forcefully exhaled after a normal tidal volume exhalation: ~1200 ml
Vital capacity (VC)
The maximum exchangable air in the lungs. Maximum amount of air that can be exhaled after a maximal inhalation. VC = TV + IRV + ERV: ~4800 ml
Minute respiratory volume
= Tidal volume (in liters) x Respirations per minute
Male vital capacity
= (.052) (Height) - (.022)(Age) - 3.60
Female vital capacity
= (.041)(Height) - (.018)(Age) - 2.69
Forced Vital Capacity
Test in which a limit is placed on the length of time a subject has to expel vital capacity air
FEV1
66-83% vital capacity exhaled
FEV2
75-94% vital capacity exhaled
FEV3
78-97% vital capacity exhaled
When Asthmatic exhales their vital capacity maximally, FEV measurements are
all reduced because of heavy mucus secretion and smooth muscle action which reduces airway diameter and increases airway resistance
