Physiology Flashcards
7 phases of the cardiac cycle
1) Atrial contraction
2) Isovolumetric contraction
3) Rapid ejection
4) Reduced ejection
5) Isovolumetric relaxation
6) Rapid filling
7) Atrial systole
Intercalated discs
Allow action potential to pass from one cell to another without the need for a synapse
Four stages of cardiac muscle action potential
1) Depolarisation
2) Early repolarisation
3) Plateau phase
4) Final repolarisation
Plateau phase- cells involved and its importance
Plateau phase prevents tetanisation of cells
Has L-type calcium channels involved
**Very slow to open and very slow to close
What prevents the ventricle from contracting top-down?
Annulus fibrosis
Insulating activity
Conduction from SA node
Electrical activity begins at the pacemaker cells at the SA node
Travels from the right atrium to the left atrium
Travels down the Bundle of His
And terminates in Purkinje fibres
Resting potential of cardiac cells
Diagram says -85mV
What happens in each of the four phases of cardiac action potential
1) Depolarisation:
Cardiac cell at its resting potential. Fast Na+ channels open, Na+ comes in and reaches a threshold voltage of -70mV- self-sustaining Na+ current reached
L-type calcium channels open
Overshoots slightly above 0 mV
2) Early repolarisation:
Some K+ channels open and 0 mV reached
3) Plateau phase
L-type calcium channels still open, K+ flows out and this countercurrent maintains voltage at 0 mV
4) Final repolarisation
L-type calcium channels now close and K+ channels outflow exceeds Ca inflow. Resting potential of -85mV reached
SA node action potential
Spontaneous leaky Na+ channels have Na+ flowing in This is called the funny current
RMP is -60mV
At -55mV T-type Ca2+ channels open
At -40mV, threshold voltage, L-type calcium channels open and depolarise to 0mV
Brief plateau phase by K+ channels and then return to normal
Delay at AV node (0.16s) purposes
1) Delay conduction to ventricle, allows atria to contract fully
2) Acts as gate-keeper, limiting the transmission of ventricular stimulation during abnormal atrial rhythms
Chronotropy
Heart rate
Dual innervation of the heart
Parasympathetic NS innervates SA node
Similarly sympthathetic will have different effect on the chronotropy
ECG different components
P wave- atrial depolarisation
QRS complex- ventricular depolarisation
T wave- ventricular repolarisation
Heart block
Failure of stimulation of ventricles following atrial contraction
Time of one cardiac cycle
0.8 s
What causes the opening of the aortic valve
LV pressure increases more than aortic pressure
What causes mitral valve to shut
Ventricular pressure greater than atrial pressure
Normal resting cardiac output
5250 mL/min
CO
Cardiac output
CO = SV x HR
Things that can increase HR
Things that can decrease HR
Positive chronotropic factors
- Sympathetic stimulation
- Drugs
- Hypocalcaemia
- Anaemia
Negative chronotropic factors
- Parasympathetic stimulation
- Hypercalcaemia
- Hypoxia
Things that can affect the stroke volume
Preload
Afterload
Contractility
Frank Starling Law
Amount of blood entering the heart will equal the amount of blood leaving the heart
EDV approximately same as SV
Afterload
Resistance blood must overcome to pump blood to the body
Inversely proportional to the stroke volume
Factors that increase contractility
Factors that decrease contractility
Positive inotropic factors
- Sympathetic stimulation
- Caffeine
- Hypocalcaemia
Negative inotropic factors
- Parasympathetic stimulation
- Hypercalcaemia
- Hypoxia
- Hyperkalaemia
Cardiac work
Defined as the amount of work done by the ventricle to transport a volume of blood from a region of low pressure to a region of high pressure
SV equation
EDV- ESV
What affects stroke volume
EDV and ESV
EDV:
- Venous filling pressure (preload)
- Force of atrial contraction
- Time to fill the ventricle
- Distensibility of the ventricle wall
ESV:
- Afterload
- Force of ventricular contraction
Frank Starling mechanism
Increased venous pressure to the heart increases filling pressure which increases SV
The ability of the heart to change its contractility in response to changes in venous pressure
Length-tension relationship
Increase in length will result in increase in tension (force of contraction)
Resting sarcomere length
1.6 um
What influences preload
Peripheral venous tone
Gravity
Blood volume
Respiratory pump
What does gravity do to preload
Reduces it
Increased inotropy
Increased active tension at a fixed preload
Sympathetic inotropy
Adrenaline and NA bind to B1 receptors
They increase Ca2+ influx by releasing Ca from SR or increasing sensitivity of Ca for Trop C
Effect of hypertrophy on afterload
Hypertrophied ventricle = Low afterload
Afterload’s effect on preload
Increased afterload can cause increased preload
Effects of exercise
1) Increased contractility
2) Increased CO and increased preload
3) Increased afterload
Effect of preload and afterload on the curve
Increased afterload –> increased preload –> curve moves RIGHT
Decreased afterload –> decreased preload –> curve moves LEFT
What sense the arterial pressure
Baroreceptors
Where is the carotid sinus
Bifurcation of internal and external carotid arteries
How do baroreceptors work
They respond to stretching of the arterial wall where if there is an increase in BP, the arterial wall also increases leading to increased AP in the baroreceptors
How does the information from the baroreceptors go to the brain?
Carotid sinus baroreceptors- Innervated by sinus nerve of Hering (Glossopharyngeal nerve)
This synpases with nucleus tractus solitarius
Aortic baroreceptors innervated by the aortic nerve that combines with the vagus nerve
- *Carotid sinus receptors control BP in brain
- *Aortic sinus receptors control systemic BP
Mean arterial pressure
MAP- mean pressure over the entire cardiac cycle
“Driving force” for perfusion through tissue beds
Is mean arterial pressure the average of systolic and diastolic pressures?
No, as they are not of the same duration
Blood pressure (MAP)
P= QR
P- mean arterial pressure
Q- blood flow
R- Resistance (systemic vascular resistance)
BP equation
MAP = CO x SVR
To regulate BP- what three things can you regulate
CO
SVR
Blood volume
What two things affect venous return
Skeletal muscle pump
Respiratory pump
MAP is affected by:
CO
SVR
Blood volume
Distribution of blood between arteries and veins
Systemic vascular resistance depends on:
Size of the lumen
Blood viscosity
Length of the blood length
How is BP measured?
Short-term- Baroreceptors
Long-term- Renin-angiotensin system
How is BP controlled?
Short-term- Baroreceptor reflex
Long-term- Renin/angiotensin/aldosterone hormonal control
Atrial natriuretic peptide
Released by the cells of the atria
Lowers blood pressure by causing vasodilation and promoting loss of salt and water in the urine (lowers blood volume)
Antidiuretic hormone (ADH) or vasopressin
Respond to dehydration or decreased blood volume
Cause vasoconstriction and increased water retention (increases blood volume and increases BP)
Increased cardiac output in relation to venous pressure
Increases venous pressure
There’s two ways of measuring venous pressure: Cardiac function curve and venous pressure curve
In cardiac function curve-
Increased venous pressure leads to increased CO
In venous pressure curve-
Increased CO leads to decreased venous pressure and hence, reduced pre-load
When pressure in right atrium is 0 mmHg, what is the cardiac output
5L/min
What enhances cardiovascular function curve?
- Increased inotropy
- Decreased HR
- Reduced afterload
At zero CO, what is P(ra)?
8 mmHg
Hilum
Renal artery, renal vein and ureter together
Function of the glomerulus
Takes blood and turns it into a filtrate and lets the rest of the blood flow on
Efferent arteriole later on becomes the renal vein
Bowmann’s capsule
Where the filtrate is collected
Glomerular filtration rate and the diameters of afferent and efferent arterioles
Diameter of afferent arteriole is directly proportional to the filtration rate
Diameter of efferent arteriole is indirectly proportional to the filtration rate
Effect of higher pressure on glomerular filtration rate
Increases it
Proximal convulated tubule
Active resorption of glucose, Na+ and AA
Descending part of the Loop of Henle
Only permeable to water- major part of water resorption
Ascending part of Loop of Henle
Thick
Salts are actively pumped out to make the medulla really salty so water can flow out with it
Not permeable to water
Distal convulated tubule
More reabsorption
Ends with a lot of waste that is collected into the collecting duct
Collecting duct
Here, under the influence of ADH
More ADH, collecting duct is more porous and more water leaves- filtrate more concentrated
Three sites of drug regulation in the kidney
1) Glomerulus
2) Distal convulated tubule
3) Collecting duct
Two ways kidneys control BP
1) Cause arteries to constrict
2) Blood volume
How does vasoconstriction occur in the kidneys
Specialised cells (juxtaglomerular cells- BP and macula densa- Na)
When BP drops, filtered Na drops
Juxtaglomerular cells release RENIN
Renin converts angiotensin I to angiotensin II (ACE)
Angiotensin causes blood vessels to constrict and raises BP
How do kidneys cause an increase in blood volume
Angiotensin II stimulates the adrenal gland to release ADH. ADH increases retention of salt and water in the distal tubule, increasing blood volume
Effect of angiotensin II on GFR
Increases it
Pre-capillary sphincter
A band of smooth muscle at the beginning of a capillary which causes blood flow in capillaries to constantly change route
Systemic vasoconstrictors
NA
Serotonin
Vasopressin
Angiotensin II
Systemic vasodilators
Adrenaline
ACh
ANP
Local vasoconstrictors
Serotonin
Endothelin
Local vasodilators
NO
Histamine
Adenosine
Adenosine
Local vasodilator
Released in hypoxic conditions
Two types of hyperaemia
Active (increased metabolism)
Reactive (occlusion)
What happens to coronary pressure when aortic pressure is high
Low coronary pressure
During systole, everything is contracting and blood doesn’t flow into coronary arteries
Functions of the conducting zone of the respiratory system
1) Filter
2) Humidify
3) Warm
Conducting zone- respiratory passages that carry air to the site of gas exchange
Respiratory zone- where gas exchange occurs
Functions of the pleura
Reduce friction
Create suction
Compartmentalisation
Boyle’s Law
For air to go into the alveoli, their pressure must reduce below the atmospheric pressure- done through chest expansion
What is the normal pleural pressure
Always has to be negative (-5 cm/H2O) to suck lungs into the chest wall
Expiration increases the pleural pressure close to 0
Definitions of spirometry
Tidal volume- normal quiet breathing
Inspiratory reserve volume- forced inspiratory volume
Inspiratory capacity- maximum volume that can be inspired after normal expiration
Expiratory reserve volume- volume after normal exhalation
Residual volume- Air in the lungs after forced exhalation
Vital capacity- IRV + TV + ERV
Functional residual capacity- ERV + RV
Dead space
Some inspired air doesn’t contribute to gas exchange
Made of anatomical dead space and alveolar dead space
Hence, total dead space
Alveolar ventilation efficiency
Getting more air into the lungs is more effective in getting tissues more oxygenated when compared to increased the frequency
Elastic resistance and non-elastic resistance- name two viscous resistance factors
1) Viscous resistance
2) Diameter of the tube
Compliance
How easily something can be stretched
*Ease with which the lungs expand
Elastance
Tendency to recoil to initial size after distention
What are residual volume and total lung capacity dependent on?
Chest wall
Function of Alveolar Type II cells
Surface tension between air and liquid is inwards, it reduces the diameter and opposes alveolar expansion
These cells produce surfactant that reduces surface tension
Lack of surfactant can cause Infant Respiratory Distress Syndrome (IRDS)
Low compliance
Stiff lung- cannot expand- fibrosis, TB, Pulmonary oedema
High compliance
Floppy lung due to loss of elastic tissue
Extra work is needed to exhale
Emphysema/COPD, Bronchitis
Histamine receptors
H1- increases secretions
H2- increases viscosity
**Mucosal oedema
Airway smooth muscle tone
Airways constrict with:
- Increased ACh
Airways dilate with:
- Decreased ACh
Most common index of resistance
FEV1/FVC
On a flow volume chart- what is positive flow?
Expiration
Causes of restrictive lung disease
Parenchymal
- Sarcoidosis
- Pulmonary fibrosis
- Pneumonia
Extraparenchymal
- Diaphragmatic problems
- Myasthenia gravis
- Lobectomy
- Obesity
- Ankylosing spondylitis
Restrictive lung disease
Reduced lung capacity
Smaller lung volume
Increased flow rate
Increased FEV1/FVC
Obstructive lung disease
Increased resistance causing airway obstruction
Reduced flow rate
Larger lung volume
Reduced FEV1/FVC
Diffusion rate is affected by four things
1) Surface area
2) Concentration gradient
3) Membrane thickness
4) Diffusion constant
How long does it take for gases to reach equilibrium
0.24 s
Limitations to pulmonary gas exchange
Low O2 conc Hypoventilation Diffusion limitations V/Q mismatching Right --> Left shunts
What is VA/Q at rest?
0.84
Dead space
Shunt
Dead space- Impaired perfusion (high VA/Q)
Shunt- Impaired ventilation (low VA/Q)
Autoregulation of arteriole and bronchiole diameter
O2- arteriole (high O2, arterioles dilate)
CO2- bronchiole (high CO2 bronchioles dilate)
**This is to match the mismatched V/Q
Regional differences in Va/Q
Top half of the lungs under perfused
Bottom half of the lungs under ventilated
Two things do this:
1) Hydrostatic pressure (pushing blood into capillary beds)
2) Alveolar expansion (alveoli squished on expiration)
What is the V/Q ratio in pulmonary embolism
HIGH
O2 dissociation factors
More O2 unloaded:
- High temp
- High CO2
- High H+ (low pH)
More O2 loaded
- Low temp
- Low CO2
- Low H+ (high pH)
Where does the dorsal respiratory group feed to?
Nucleus of tractus solitarius
Pneumotaxic centre
Limits inspiration
Controls the switch off point of inspiratory ramp
Hering Breur inflation reflex
Responds to lung stretching too much to switch off the inspiratory ramp
When tidal volume is 3x
