cardiovascular respiratory system Flashcards
what determines cardiac output?
- heart rate
- stroke volume
stroke volume x heart rate
what is the normal range for heart rate?
60-100 beats per minute (bpm)
what is the heart rate established by?
sinoatrial node (SAN)
what is the sinoatrial node and where is it found?
cluster of pacemaker cells which sits in the right atrium
what is the normal SAN pacing rate?
100 beats per minute
where does the atrioventricular node (AVN) sit?
above the ventricular septum at the junction between the atria and the ventricles
what does the avn do?
pass on the impulse from the atria to the ventricles
what is the delay in AVN conduction and why is this important?
delay of about 0.15 seconds, allowing the atria to finish contracting and the atrioventricular valves to close before the ventricles start to contract – this prevents blood from regurgitating back into the atria during ventricular contraction
what does the autonomic nervous system do to the heart?
induces the force of contraction of the heart and its heart rate, and controls the peripheral resistance of blood vessels
what nerve supplies parasympathetic input to the heart?
vagus nerves
what does a parasympathetic input do to the heart?
decrease in heart and contraction force
what does sympathetic input do to the heart?
increases heart rate and the force of contraction
what are baroreceptors?
located in the carotid sinus and aortic arch and detect changes in stretch and tension in the arterial wall and changes in arterial pressure
what happens if baroreceptors detect an increase in arterial pressure?
the parasympathetic pathway is activated, vagus nerves carry impulses so heart rate is reduced, vasodilation occurs to reduce arterial pressure
what happens if baroreceptors detect an decrease in arterial pressure?
the sympathetic pathway is activated, heart rate is increased and vasoconstriction occurs to increase arterial pressure
what does adrenaline do to heart rate and where is it released from?
increases heart rate
released from the medulla of adrenal glands
what is stroke volume?
the difference between the end diastolic volume (EDV), the volume of blood in the heart at the end of diastole, and the end systolic volume (ESV) the volume remaining in the heart at the end of systole ie the amount of blood that is expelled with each heartbeat
what can affect stroke volume?
- central venous pressure (CVP)
- Total Peripheral Resistance (TPR)
what is the central venous pressure?
blood pressure in the vena cava as it enters the right atrium
what does the central venous pressure reflect?
the volume of blood returning to the heart and therefore the volume of blood the heart pumps back into the arteries
why does an increase in the CVP increase stroke volume up to a certain point?
- more blood enters the heart during diastole, leading to an increase in end diastolic volume (EDV)
- increased filling of the heart leads to increased ventricular contraction and thus a decrease in end systolic volume (ESV), due to Starling’s Law
what is preload?
diastolic filling pressure
what is the total peripheral resistance?
the pressure in the arteries that blood must overcome as it passes through them, and thus dictates how easy it is for the heart to expel blood (afterload)
what is Starling’s Law?
the more the heart chambers fill, the stronger the ventricular contraction, and therefore the greater the stroke volume
how does an increase in central venous pressure result in an increase in stroke volume?
as the heart chamber fills and stretches, it creates more regions of overlap for actin-myosin cross-bridges to form, allowing for a greater force of contraction
how is a large concentration gradient maintained in capillaries?
via a constant blood flow to allow rapid exchange of molecules with the tissue
how is a thin diffusion distance maintained across capillaries?
as the endothelium of the capillaries is just one cell thick and measures a few micrometres in diameter
what is blood hydrostatic pressure?
the pressure exerted by blood in the capillaries against the capillary wall that forces fluid out of the capillary
what is the oncotic pressure?
the pressure exerted by proteins in the blood, mostly by albumin in the capillaries, that pulls fluid into the blood
what is venous return?
the flow of blood back to the heart
what are veins?
low-pressure, low-resistance vessels, which carry blood back to the heart from organs
what is venous pressure affected by?
- the rate of blood entering the veins
- the rate at which heart pumps out blood
how does cardiac output affect venous pressure?
increased cardiac ouput decreases venous pressure as blood is rapidly pumped out of veins, whereas lowered cardiac output backs up the venous system increasing blood volume and venous pressure
what is the skeletal muscle pump?
muscles, eg quadriceps, contracting to squeeze veins and therefore increasing venous pressure, forcing the vein’s valves to open, allowing more blood to flow back to the heart
what are some non-respiratory functions o f the lungs?
- host defence
- speech
- vomiting
- defecation
what are the types of lung host defences?
- intrinsic
- innate defence
- adaptive immunity
what is intrinsic defence?
always present: physical and chemical. apoptosis, autophagy, RNA silencing, antiviral proteins
what is innate defence?
induced by infection (interferon, cytokines, macrophages, NK cells
what is adaptive immunity?
tailored to a pathogen (T cell, B cells)
give some examples of chemical epithelial barriers (chemical barriers produced by epithelial cells)?
- antiproteinases
- anti-fungal peptides
- anti-microbial peptides
- antiviral proteins
- opsins
what type of barrier is mucus?
physical barrier
what is the purpose of coughing?
expulsive reflex action that protects the lungs and respiratory passages from foreign bodies
what are some causes of coughing?
- irritants
- conditions like COPD
- infections like influenza
what is sneezing?
involuntary expulsion of air containing irritants from the nose
what are some causes of sneezing?
- irritation of nasal mucosa
- excess fluid in the airway
can airway epithelium replair?
sometimes can completely repair
what is plasticity in cells?
when cells can change cell types
how much blood does the heart pump around the body
every minute at rest?
around 5L of blood
what is the normal pressure in the aorta?
120/80 mmHg
when do the ventricles fill with blood?
- during diastole (heart relaxation)
- atrial systole (contraction of the atria)
what happens during the filling phase of the cardiac cycle?
- blood flows from the vena cava and pulmonary veins into the atria, and passively fill the ventricles.
- ventricles fill with blood at a steadily decreasing rate, until the ventricles’ pressure is equal to that in the veins
- during atrial systole the atria contract squeezing blood into the ventricles, closing the atrioventricular valves.
what is isovolumetric contraction of the cardiac cycle?
the heart valves are shut as the ventricles contract, causing a build-up of pressure but no change in
volume of blood within the
ventricles
what is the outflow phase of the cardiac cycle?
ventricles’ pressure exceeds the pressure in the aorta/pulmonary trunk so the semilunar valves open and blood is pumped from the heart into the great arteries
what causes the semilunar valves to close?
at the end of ventricular systole, the ventricles relax reducing their pressure below the aorta, closing the
valves. backflow of blood also closes the valves
what is isovolumetric relaxation?
the ventricles relax, ready to re-fill with blood in the next filling phase. the volume of blood within the ventricles remains the same as the atrioventricular valves has not opened yet
what is a “lub” sound from?
occurs at the end of the filling phase when the atrioventricular valves snap shut
what is a “dub” sound from?
occurs at the end of the outflow phase when the outflow valves snap shut
what is Starling’s law?
as the volume of the left ventricle increases (more passive filling, preload), the greater the myocyte stretches and the more forceful the systolic contraction, increasing left ventricular stroke volume
what supplies parasympathetic input to the heart?
vagus nerve (CNX)
what does parasympathetic innervation do to the heart?
slows down heart rate and reduces the force of contraction
how do parasympathetic fibres decrease heart rate?
releases acetylcholine which binds opens up potassium channels, making it harder to reach the threshold for depolarisation
what does sympathetic innervation do to the heart?
innervates the SAN and AVN; increasing the heart rate and increasing the force of contraction
how do sympathetic fibres increase heart rate?
releases noradrenaline
where are baroreceptors located?
aortic arch and carotid sinus
how do baroreceptors detect a change in blood pressure?
they are sensitive to changes in stretch and tension in the arterial wall
what nerve carries impulses from the carotid sinus to the CNS?
glossopharyngeal nerve (IX)
what nerve carries impulses from the aortic arch to the CNS?
vagus (X)
what happens if an increase in arterial pressure is detected by baroreceptors?
parasympathetic pathway is activated, impulses are carried to the CNS and back via the
vagus to reduce heart rate and bring on vasodilation to reduce arterial pressure
what happens if an decrease in arterial pressure is detected by baroreceptors?
sympathetic pathway is activated causing increased heart rate and vasoconstriction to increase blood pressure
what is the purpose of the electrocardiogram?
trace the electrical activity in cardiac tissue
what are the most common types of lead ECGs?
3 lead and 12 lead
what does a ‘lead’ mean?
a view of the heart
how many physical electrodes are there in a 12 lead ECG?
10
how many chest electrodes are there in a 12 lead ECG?
6 chest electrodes (V1-V6)
how many limb electrodes are there in a 12 lead ECG?
4
why is having many leads beneficial?
useful in visualising the electrical activity of the heart from different views, and therefore to localise pathology
what time frame does a small square on an ECG represent?
0.04 secs
what time frame does a large square on an ECG represent?
0.2 secs
how many small squares is in a large square in an ECG?
5
what time frame does 5 large squares on an ECG represent?
1 second
what time frame does 300 large squares on an ECG represent?
1 minute
what does depolarisation towards an electrode give on the ECG race?
a positive complex (upwards)
what does depolarisation away from an electrode give on the ECG race?
a negative complex (downwards)
what does repolarisation towards an electrode give on the ECG race?
a negative complex (downwards)
what does repolarisation away from an electrode give on the ECG race?
a positive complex (upwards)
what does the P wave represent?
atrial depolarisation, as a small upwards inflection as the atria and small and depolarisation is moving towards the lead
what does the QRS complex wave represent?
ventricular depolarisation; large upwards inflection and atrial repolarisation
what does the T wave represent?
ventricular repolarisation
what is ST elevation indicative of?
myocardial infarction, as the ventricles are not relaxing and therefore filling as much, reducing cardiac output
what is STEMI?
ST elevation myocardial infarction
what leads to ST elevation?
as the tissue dies it becomes leaky to electrolytes, leading to a partial depolarisation during the ventricular repolarisation period (ST segment
what are gap junctions?
clusters of intercellular channels that allow direct diffusion of ions and small molecules between adjacent cells (used in action potentials)
what is the resting membrane potential (phase 4) and how is it maintained?
-70mV
at rest K+ channels are open, therefore resting membrane potential tends towards the equilibrium potential for K+ (EK), which is roughly -70mV
what is the process of the ventricles getting depolarised (phase 0)?
as depolarisation spreads across the cells, voltage-gated Na+ channels open leading to an influx of Na+ (then a greater influx due to increased depolarisation; positive feedback)
what is phase 1 of
ventricular action potentials?
transient K+ channels open and repolarise the cell
what is phase 2 of
ventricular action potential?
plateau phase
L-type Ca2+ channels open and Ca2+ enters the cell, leading to a plateau balance with the K+
what happens during the plateau phase of ventricular contractions?
Ca2+ pass through the L-type Ca2+ channels , triggering the release of Ca2+ from the sarcoplasmic reticulum into the cell, which binds to troponin, which moves tropomyosin away from myosin allowing the actin head to access the myosin head binding site and allowing contractions
what happens during phase 3
ventricular contraction?
repolarisation
Ca2+ channels close and K+ repolarises the cell. Na+ channels will begin to recover from inactivation as the membrane potential becomes more negative. ATP is needed to break cross bridges so myosin can move along and muscle can relax. Ca++ returns to sarcoplasmic reticulum
how many phases are there in
ventricular action potentials?
(phases 0-4 inclusive)
what enables a refractory period?
in phase 0, Na+ channels become inactivated almost immediately after opening and can only recover from inactivation to enter the closed state at very negative membrane potentials (after repolarisation). new action potentials can only be generated after phase 3, but usually during pathology
what is the resting membrane potential of the pacemaker cells in the heart and how is this maintained?
- -55mV
- 3Na+/ 2 K+ in, K+ always flowing out through leaky K+ channels
what causes the membrane potential of the cardiac pacemaker cells to rise?
the membrane is also permeable to Ca2+ and Na+ through their leaky channel membranes, which increases the membrane potential?
what happens when the threshold membrane potential has been reached and what is this threshold?
- -40mV
- voltage-gated calcium channels open, allowing Ca2+ to influx in and depolarise the membrane
what happens during pacemaker cell repolarisation?
- Ca2+ voltage gated inactivate
- K+ channels open, there is an efflux of K+ ions out of the cells
what is the impact of parasympathetic activity on cardiac pacemaker cells and how do they work?
acetylcholine acts on the SAN which lengthens the interval between pacemaker potentials, hence slowing heart rate
what is the impact of sympathetic activity on cardiac pacemaker cells and how do they work?
releases noradrenaline which shortens the interval between impulses by making the pacemaker potential steeper, hence increasing the heart rate
where are calcium ions released from?
the sarcoplasmic reticulum
describe the stages in calcium induced calcium release
- membrane depolarisation opens voltage-operated calcium channels. releasing calcium ions
- calcium bonds to ryanodine receptors on the sarcoplasmic reticulum which induces conformational changes in a Ca2+ channel associated with the ryanodine receptor
- ryanodine receptors acre activated which opens them and releases Ca2+ from the SR stores- ‘calcium spark’
what happens after calcium induced calcium release?
after the calcium spike occurs, calcium binds to troponin-C which moves the tropomyosin away from the actin binding site thus exposing it and initiating cross-bridge binding
describe the process of the sliding filament model of contraction?
- calcium binds to troponin-C, which moves tropomyosin away from myosin
- the actin binds to the myosin head, which releases ADP and an inorganic phosphate
- the myosin head pivots and bends, pulling on actin and moving it causing muscle contraction
- a new molecule of ATP binds to the myosin head, causing it to detach from the actin
how is calcium removed after a stimulus is removed?
by re-entering the sarcoplasmic reticulum via a SERCA (sarco(endo)plasmic reticulum calcium-ATPase) channel at the expense of an ATP molecule
what is the lifespan of platelets?
7-10 days
what is the normal platelet count?
150-400 x 109/L
where are platelets distributed?
70% in the blood, 30% in the stream
what are platelets made from?
fragments of megakaryocytes that come off as they travel through the blood vessel
what type of granules so platelets contain?
alpha-granules and dense granules
what do alpha granules contain?
proteins of high molecular weight, including von Willebrand Factor (vWF), factor V and fibrinogen
what do dense granules contain?
low molecular weight molecules such as ATP, ADP, serotonin, and calcium ions
what is the function of platelets?
formation of blood clots at the site of bleeding
what are the three main stages in the formation of a blood clot?
adhesion, activation and aggregation
what is the adhesion step in the formation of a blood clot?
- the injured blood vessel wall exposes its underlying endothelium and collagen fibres.
- exposed collagen fibres bind vWF released from the damaged endothelium, which in turn binds to vWF receptors on platelets to promote adhesion.
- the exposed collagen itself also promotes platelet binding.
- the clotting cascade
what is the activation stage of blood clotting?
platelet activation results in a morphological change on the membrane surface of the platelet, increasing the surface area and preparing it for aggregation
what is the aggregation stage of blood clotting?
platelets bind to vWF and fibrinogen. fibrinogen facilitates the formation of crosslinks between platelets, aiding platelet aggregation to form a platelet plug
what type of receptors do platelets have on their surfaces?
agonist and adhesion receptors
what do agonist receptors do?
recognise stimulatory molecules e.g. collagen, thrombin, and ADP
what do adhesion receptors do?
promote the adhesion of platelets to other platelets, the vessel wall or leucocytes
what triggers the extrinsic pathway for the coagulation cascade?
external trauma which causes blood to escape the circulation
what triggers the intrinsic pathway for the coagulation cascade?
internal damage to the vessel wall
describe the extrinsic pathway to the coagulation cascade
- damage to the blood vessel means that factor VII exits the circulation into surrounding tissues
- factor VII gets converted to factor VIIa
- factor VIIa gets converted to factor X
describe the intrinsic pathway of the coagulation cascade?
- XII turns gets converted to XIIa
- XI gets converted to XIa
- IX gets converted to IXa
- X gets converted to Xa
what is the common pathway for coagulation?
the extrinsic and intrinsic pathways converge, and X
converts prothrombin to thrombin. thrombin con
verts fibrinogen into fibrin which are insoluble and are stabilised by factor XIIII
what is fibrinolysis?
fibrin is dissolved leading to the consequent dissolution of the clot, degrading the thrombus
what type of blood supply reaches the lungs?
- pulmonary
- bronchial
what do bronchial arteries do?
supply blood to the lung architecture
what is the difference between the pulmonary and systemic wall?
systemic is thicker
what is the difference between the pulmonary and systemic muscularisation?
systemic has more significant muscularisation
how is pulmonary arterial pressure measured?
cardiac output x pulmonary
vascular resistance (ohms law)
how is vascular resistance measured?
(8 x L x viscosity)/ (pi r^4)
why does cardiac output increase but pulmonary arterial pressure not increase as much?
increased cardiac vessels are recruited which helps to reduce pressure
what are the two types of respiratory failure?
type I and II
what is type I respiratory failure?
pO2 <8kPA (low) and pCO2 < 6kPA (low-normal)
what is type II respiratory failure?
pO2 <8kPA (low) and pCO2 > 6kPA (high)
what causes type I respiratory failure?
embolisms
what causes type II respiratory failure?
hypoventilation
what causes low oxygen levels?
- hyperventilation
- diffusion impairments
- V/Q mismatch
- shunt
what can cause diffusion impairments?
- pulmonary oedema
- membrane diffusion, interstitial fibrosis
- blood diffusion e.g. anaemia
why is there more perfusion in the alveoli at the bottom of the lung?
the alveolar pressure is less than the
venous and arteriole
what is v/q?
ventilation/perfusion
what is cyanosis?
body turning blue as haemoglobin has a low saturation of oxygen
what is eisenmenger syndrome?
the development of pulmonary hypertension (high blood pressure in the lungs) due to an untreated congenital heart defect e.g. ventricular septal defect
where does pulmonary embolism start?
in the legs
what factors increase the likelihood of thrombosis?
- circulatory statis (not moving)
- endothelial injury
- hypercoaglable
what is airway resistance?
the degree of resistance to air flow through the respiratory tract during inspiration and expiration
why is the total resistance greater in the trachea and larger bronchi as opposed to bronchioles despite the larger diameter?
smaller airways are in larger numbers running in parallel which reduces the total resistance to airflow
what does sympathetic innervation do to bronchial smooth muscle and airway diameter? and by what mechanism?
relaxes bronchial smooth muscle which increases airway diameter to allow more airflow. noradrenaline form adrenal glands act on adrenal medulla to release adrenaline which acts on B2 receptors on airways smooth muscle
what does parasympathetic innervation do to bronchial smooth muscle and airway diameter and by what mechanism?
increases smooth muscle contraction to reduce diameter (bronchoconstriction) through the vagus nerve where acetyl-choline acts on M3 receptors
what is radial traction?
during expiration, elastic fibres of the surrounding alveoli pull on small airways to hold them open and prevent them from collapsing
what is laminar flow?
the state of flow in which air moves through a tube in parallel layers, with no disruption between the layers, and the central layers flowing with the greatest velocity
what is turbulent flow?
when air is not flowing in parallel layers, and direction, velocity and pressure within the flow of air become chaotic
why do the intercostal muscles and diaphragm would need to work harder to expand and contract the lungs in turbulent flow?
turbulence leads to the need for a much greater difference in pressure to move the air
what is FEV1?
forced expiratory volume in one second
what is FVC?
forced vital capacity
what is gas dilution
what is plethysmography?
measures changes in volume in different parts of the body. the test may be done to check for blood clots in the arms and legs. It is also done to measure how much air you can hold in your lungs
how are transfer estimates carried out and what do they measure?
a person is given some carbon monoxide to breathe in, ad the amount breathed out is measured which allows to estimate the overall function of the lung, eg haemoglobin concentration, alveolar surface area and capillary
volume
what is considered normal for forced expiratory volume in one second in litres
80% or greater is considered normal
what is airways restriction? in what conditions may this happnen?
forced vital capacity FVC is less than 80% of predicted. pulmonary fibrosis
what is forced vital capacity?
the amount of air that can be forcibly exhaled from your lungs after taking the deepest breath possible measured using spiriometry
what is airways obstruction and in what conditions will this happen?
forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) ratio is less than 0.7. asthma and COPD
does the urge to breathe come from oxygen or carbon dioxide levels?
carbon dioxide levels; when holding breathe oxygen saturation increases and reaches 100%, but the blood pH decreases due to CO2 which gives the urge to breathe in order to remove it
what the pons?
pneumotaxic and apneustic centre
what is the medulla?
phasic discharge of action potential
when is DRG active?
predominately active during inspiration
when is VRG active?
active in both inspiration and expiration
what happens when a diaphragm that is already flat contracts?
it shortens
what do central chemoreceptors do?
detect CO2 concentrations
what do peripheral chemoreceptors do?
measure CO2 and oxygen and pH
where are central chemoreceptors located?
in the brainstem, pontomedullary junction, stimulate ventilation
what blood vessels supply the pericardium?
pericardiacophrenic arteries
what blood vessels supply the diaphragm?
pericardiacophrenic arteries
what do internal jugular veins do?
drains the head and the neck
what drains the pericardium and the diaphragm?
pericardiacophrenic veins
what are vagus nerves also known as?
cranial nerves X
what is the concentration of O2 and CO2 in respiratory failure?
PaO2 is low <8kPa
PaCO2 may be elevated >6.8 kPa
what is hypoxaemia?
a decrease in the partial pressure of oxygen in the blood
what is hypoxia?
a reduced level of tissue oxygenation
what happens to the PaO2 and PaCO2 in type 1 respiratory failure?
low PaO2 (hypoxaemia)
low/normal PaCO2 (hypocapnia)
what happens to the PaO2 and PaCO2 in type 2 respiratory failure?
low PaO2 (hypoxaemia)
high PaCO2 (hypercapnia)
is type I or 2 respiratory failure more common?
type 1
what causes hypoxia in type 1 respiratory failure?
- mismatching of ventilation and perfusion
- shunting
- dffusion impairment
- alveolar hypoventilation
what are some type I respiratory failure treatments?
- airway patency
- oxygen delivery
- increasing FiO2
- primary cause (e.g. antibiotics for pneumonia)
where is type 2 respiratory failure commonly found?
COPD
what are some symptoms of hypercapnia?
- rritability
- headache
- papilloedema
- warm skin
- pounding pulse
6.confusion - somnolence
- coma
what are some type 2 respiratory failure treatments?
Airway patency
Oxygen delivery
Primary cause (e.g. antibiotics for pneumonia)
Treatment with O2 may be more difficult
For example; COPD patients rely on hypoxia to
stimulate respiration
assisted ventilation
what is a good indicator for eosinophilic respiratory inflammation?
exhaled nitric oxide test
what percentage of asthma is related to occupation?
15%
what are some occupational causes of asthma?
HMW, Grain, Wood, Animals, fish
Latex, Glutaraldehyde, Isocyanates, Paints, Metal working fluids
Metals
infectious agents, fungi, pets, air pollutants
what % of the population have asthma?
5-16%
is asthma variable amongst countries?
yes, as it is influenced by the quality of the air breathed in
what metal exposure is associated with emphysema development?
cadmium
what % of COPD is related to occupation?
15%
what occupational exposures contribute to COPD?
silica, coal, grain, cotton and cadmium
what causes asthma?
genetic and environmental risks
how common is cystic fibrosis?
1/2500 have it, 1/25 are carrier
where is the genetic defection on cystic fibrosis found?
found on the long arm on chromosome 7
F508del most common mutation causing CF
how does cystic fibrosis cause symptoms?
CTFR protein abnormality (transport protein) leads to dysregulated epithelial fluid transport
how is cystic fibrosis diagnosed?
immunoreactive trypsinogen test in new-borns
how does cystic fibrosis affect the pancreas?
blockage of exocrine ducts, early activation of pancreatic enzymes, and eventual auto-destruction of the exocrine pancreas
Most patients require supplemental pancreatic enzymes
how does cystic fibrosis affect the intestine?
bulky stools can lead to intestinal blockage
how does cystic fibrosis affect the respiratory system?
mucus retention, chronic infection, and inflammation that eventually destroy lung tissue
is there a singular cystic fibrosis mutation?
no, more than 2000 CFTR cystic fibrosis causing mutations have ben found
what is alpha-1 antitrypsin disease?
inherited, monogenic condition resulting in early onset emphysema +/- bronchiectasis
what initiates parasympathetic innervation of the bronchus?
vagus nerve
what is ipratropium bromide (atrovent)
short term muscarinic (blocks parasympathetic actvity acetyl-choline)
how does salbutamol work?
activates beta2 receptors onthe airway smooth muscle causes muscle relaxation by activating a
whats the relationship between levels and pressure
going down 10m increases atmospheric pressure by 1
what is boyles law?
p1v1=p2v2
why is diving hazardous to the lungs?
what is an apnoea dive?
diving whilst holding breath
what is the diving reflex?
when a human holds their breath and submerges in water, the face and nose become wet which in turn causes bradycardia, apnea, and increased peripheral vascular resistance;
what is oxygen toxicity?
when people receive high levels of oxygen (for examples as the pressure increases due to diving) leading to shortness of breath, cough and chest pain
what is nitrogen narcosis?
increased pressure of inspired nitrogen as ambient pressure of air is increasing, increasing coldness and feelings of euphoria
what is decompression illness?
since nitrogen was delivered under high pressure when diving, because it was purely soluble when the person returns to the surface the nitrogen starts bubbling
what is the altitude of the death zone?
above 8000m
what is the Aa difference?
the difference between the oxygen and arteriole oxygen partial pressure usually 1kPa in healthy individuals but greater in unhealthy
what is the treatment of acute mountain sickness or altitude pulmonary oedema?
descend immediately
when is the pseudoglanders phase?
8-17 weeks
what is the ductus arteriosus?
pulmonary trunk linked to the distal arch of aorta by the ductus arteriosus, permitting blood to bypass pulmonary circulation
muscular wall contracts to close after birth (a process mediated by bradykinin)
what is the ductus venosus?
oxygenated blood entering the foetus also needs to bypass the primitive liver. This is achieved by passage through the ductus venosus, which is estimated to shunt around 30% of umbilical blood directly to the inferior vena cava
what is the foramen ovale?
foramen ovale is a passage between the two atria, which is responsible for bypassing the majority of the circulation
what are some adaptive changes at birth?
Fluid squeezed out of lungs by birth process
Adrenaline stress leads to increased surfactant release.
Gas inhaled
Oxygen vasodilates pulmonary arteries
Pulmonary vascular resistance falls
Right atrial pressure falls, closing foramen ovale
Umbilical arteries constrict
Ductus arteriosus constricts
what is pulmonary interstitial emphysema?
lung cysts rupturel aveoli
how is pulmonary interstitial emphysema treated?
Warmth
Surfactant replacement (if intubated)
Oxygen and fluids
Continuous Positive Airway Pressure (maintain lung volumes, reduce work of breathing)
Positive pressure ventilation if needed
what are the layer of the heart (outside to inside)?
fibrous pericardium, parietal serous pericardium, visceral serous pericardium, myocardium, endocardium
how long are systole and diastole?
systole 0.3s and diastole 0.5s
how much blood is ejected from the ventricles with each contraction?
2/3
what is diastasis?
when the pressure within the atria and ventricles begins to even out and the ventricles no longer passively fill
how are blood vessels autoregulated?
intrinsically (increasing diameter) and extrinsically (vasodilation and vasoconstriction)
does the smooth muscle within the blood vessels ever relax?
no
what is hyperaemia?
increased blood flow
what is active hyperaemia?
metabolic response that increases blood flow e.g. exercise
what is reactive hyperaemia?
occluded tissue; after occlusion removed, increased blood flows to it
where are peripheral chemoreceptors found, what are they sensitive to and what is their response?
aortic arch and carotid sinus. detects an increase in CO2, a decrease in pH and a decrease in oxygen. leads to an increase in blood pressure (sympathetic) impulses to pressor region of medulla
where are arterial baroreceptors found, what are they sensitive to and what is their response?
aortic arch and carotid sinus. responsa to an increase in blood pressure. when blood pressure increases firing rate also increases more distil to the baroreceptor. the rate of impulses increase to the depressor (centre medulla) to decrease blood pressure parasympathetic
where are cardiopulmonary baroreceptors found, what are they sensitive to and what is their response?
found in atria, ventricles and pul. artery. responds to an increase in blood volume. when blood volume increases the baroreceptor gets distorted more so more impulses are sent to depressor region of medulla to decrease blood pressure parasympathetic
how is cardiac output calculated?
stroke volume x heart rate
how is blood pressure calculated?
cardiac output x total peripheral resistance
how is pulse pressure calculated?
systolic pressure - diastolic pressure
how is mean arteriole pressure calculated?
diastolic pressure + 1/3 pulse pressure
what is Poiseuille’s law?
flow - (pi x r^4)/ (8 x length x viscosity)
how is flow (I) calculated?
pressure (v)/ resistance (r)
what is Frank Starlings law?
the greater the end diastolic volume (or
ventricular filling) the harder the contraction as the myocytes stretch more to accommodate the greater filling, which increases contraction strength. stroke volume increases and therefore so does cardiac output
what pressure keeps blood in vessels and how?
oncotic pressure, albumin presses on vessel walls and keeps fluid in
what force squeezes blood out of vessels?
hydrostatic pressure (increased pressure within the vessel forces blood out)
how can failing hearts be treated and why?
failing hearts have a decreased cardiac output, can be treated by increasing stroke volume by increasing the volume of extracellular fluid via injections
what are vasodilators?
hypoxia, low pH high CO2, bradykinin, NO, prostacyclin, high K+, acetyl choline, atrial natriuretic peptide
what are vasoconstrictors?
endothelium 1, angiotensin II, ADH, noradrenalin
define stroke volume
ventricular ejection at systole
define cardiac output
ventricular ejection/ unit time
define total peripheral resistance
total peripheral systemic resistance. arterioles (highest)
define preload
amount of myocyte stretch in ventricular filling. a
volume
define afterload
resistance myocytes contract against in
ventricular systole. a resistance
define contractility
how hard the heart beats
define compliance
how easy heart fills in diastole
define frank starlings law
higher EDV leads to harder vent. contraction
define diastolic distensibility
pressure to fill ventricles a diastole to EDV
how are parasympathetic effects carried out on the CVD?
acetyl choline acts on M2 receptors, to decrease heart rate and decrease the force of contraction. less Ca2+ ions enter myocyte, triggering less action potentials decreasing contractility and cardiac output
how are sympathetic effects carried out on the CVD?
noradrenaline acts on B1 receptors to increase heart rate and increase the force of contraction. more Ca2+ ions enter myocyte, triggering more action potentials increasing contractility and cardiac output
what are the two different types of arteries and where are they found?
- elastic: aortic, closer to the heart have more elastic tissue in tunica media, larger lumen as need to withstand greater pressures and maintain constant pressure by quick elastic recoil
- muscular: distil to heart. more muscle in tunica media, smaller lumen. more muscle for vasodilation and vasoconstriction
what are arterioles?
arteries with 3 or less muscle layers in tunica media. where arteries transition towards capillaries. site of most resistance
what is responsible for end diastolic volume?
veins
how do veins return blood to the heart?
- skeletal muscle contractions
- resp muscles need blood so increase venous return
- peristalsis (smooth muscle contraction in HI track neds blood)
what regulates entry of blood into the capillaries?
precapillary sphincters
what are the three types of capillaries?
continuous: fully intact endothelium + basement membrane - tiny molecules pass through
fenestrated: endothelial gaps, basement membrane intact. allows glucose and aa through
discontinuous: huge endo gaps, incomplete basement membrane, whole RBC can fit through
what are the normal pressures in systemic and diastolic vessels? and what happens to the vessels where there is lots of and a lack of oxygen?
pulmonary 25/8 (lower pressure prevents oedma), systemic 120/80. systemic thicker walls. pul, hypoxia is vasoconstriction, systemic hypoxia is
vasodialation
how long do RBCs last for, what hormone stimulates their production and where from, what is their structure and what are young RBCs called?
120 days, erythropoietin (kidney), 2 alpha and 2 beta chains (gamma in foetus), reticulocyte
how long do white blood cells last for, what hormone stimulates their production?
6-10 hours, granulocyte macrophage colary stimulating factor
how long do platelets last for, what hormone stimulates their production?
7-10 days, thrombopoietin
what is serum?
plasma without clotting factors
what is blood made from?
plasma and blood cells (red, white and platelets)
what is haematocrit?
a measurement of the the percentage by volume of red cells in your blood. ~0.45
what is the precursor to all blood cells?
hemocytoblast (pluripotent). the formation of blood cells are haematopoiesis
what is the main function of neutrophils as well as their appearance?
inflammatory response. granulocytes (release primary and secondary granules), multilobed
what is the main function of monocytes as well as their appearance?
immature cells, become macrophages and antigen presenting cells. kidney bean looking nucleus, also large
what is the main function of eosinophils as well as their appearance?
fights parasitic worms. antihistamines (reduce allergic response). pink granules with IgE receptors
what is the main function of basophils as well as their appearance?
produces histamine (increase allergic response). dark blue granules with IgE receptors
what is the main function of lymphocytes as well as their appearance?
cell mediated + innate response. very little cytoplasm, mostly nucleus
what is the precursor cell to platelets?
megakaryocytes
what is endomitosis?
the formation of platelets, where the DNA doubles but the cell does not divide
what do inactive platelets look like?
smooth and discoid
what do active platelets look like?
increased surface area and pseudopoid
what granules does platelets release?
electron dense granules (for energy, ADP, ATP, Ca++, serotonin) and alpha dense granules (mediate scaffolding VWF. fibrinogen, platelet derived growth factor)
what is having too much platelets called and what is the risk?
thrombocytosis, increased risk of spontaneous clots
what is having too little platelets called and what is the risk?
thrombocytopenia (cuts can cause increased bleeding)
what is the first stage to the coagulation cascade?
vascular constriction; endothelium 1 is released from damaged endothelium which causes constriction
what keeps healthy blood vessels open?
prostacyclin and NO
describe the formation of the platelet plug
factor 8 VWF binds to exposed collagen at injured endothelium using GP 1b. platelets adhere to
VWF on collagen via GP IIa/IIIb and become activated. alpha and electron granules are released and more platelets become activated by positive feedback to form a primary platelet plug
what hydrolyses the platelet plug?
tissue plasminogen activator converts plasminogen to plasmin. plasmin eats fibrin and converts it to fibrinogen
what clotting factors are produced in the liver?
all bar VWF
what blood type is the universal acceptor?
AB+
what blood type is the universal donor?
O-
where are ABO antigens produced and can they cross the placenta?
produced in spleen cannot cross
can rhesus antigens cross the placenta?
yes
what is the most immunogenic rhesus and how will you have the antibodies?
D, if DD or Dd will have antibodies therefore no immune response
what is haemolytic disease of the foetus and new-born?
mother has a child with a DD or Dd man. child is born as Dd, mother makes RhD antibodies against babies antigens but baby is fine. when second baby is born, mothers RhD antibodies attack foetus leading to anaemia and death
how does the AVN delay signals?
there are less gap junctions to allow the electrical signal to pass and the fibre has a smaller diameter
what are the three binding sites on troponin?
myosin, actin and tropomyosin
how do nodal cells become depolarised?
t-type Ca++ allow influx into the cell till threshold of -40mV is met where L type Ca++ open till +10 is reached. VG K+ open and K+ leaves the cell
what is bradycardia?
low heart rate <60bpm
what is tachycardia?
high heart rate >100bpm
what does the right coronary artery supply?
SAN, AVN and post IV septum
what does the right marginal artery supply?
RV, apex
what does the posterior descending artery supply?
RV, LV. post 1/3 IV septum
what does the left coronary artery supply?
left atrium, left ventricle, septum, AV bundle of His
what does the left anterior descending artery supply?
anterior 2/3 IV septum, RV, LV
what does the left marginal artery supply?
left ventricle
what does the circumflex artery supply?
left atrium and left ventricle
what is systolic heart failure?
heart does not pump hard enough
what is diastolic heart failure?
heart doesn’t fill to full
volume
what is left sided heart failure and what does it cause?
blood backs up into the lungs causing pulmonary oedma fluid build up in lungs
what is right sided heart failure and what does it cause?
blood backs up in the rest of the body causing peripheral oedma, mostly in the legs
embryology of the heart
at what level does the trachea bifurcate?
t4
what is the respiratory tree?
trachea to right and left lobar bronchi, to segmental bronchi, terminal bronchioles, respiratory bronchioles, alveolar ducts and sacs
what does the upper airway consist of? conducts air
nasopharynx to terminal bronchioles
what does the lower airway consist of? gas exchange
respiratory bronchioles to alveolar sacs
what is respiratory epithelium?
pseudostratified ciliated columnar epithelium with interspersed goblet cells
what are the accessory muscles that aid in active inspiration?
sternocleidomastoid, serratus anterior, latissimus dorsi
what are the accessory muscles that aid in active expiration?
internal intercostal muscles, abdominal muscles
why is the interpleural space important?
the chest wall has a natural tendency to pull out, and the alveoli a natural tendency to pull in. during inspiration, pathology of the space pre
vents the alveoli from moving out
what is the transpulmonary pressure and its value?
alveolar pressure- interpleural pressure. alveolar pressure is 0, IP pressure is -4 so transpulmonary pressure is 4mmHg
what happens if the transpulmonary pressure decreases?
the lungs move more naturally inwards, parietal pleura remains stuck to chest wall. air flows into interpleural space causing pneumothorax
pontine and medullary centers
what are slow acting stretch receptors?
found in the smooth muscle of the airway, respond to distension. activated at the starts the process of expiration and ends inspiration (myelinated)
what are the three types of lung receptors?
what are rapid acting stretch receptors?
found between airway epithelium, responds to irritants and activated leads to bronchoconstriction (myelinated)
what are j receptors?
found across capillary walls, respond to increased lung pressure due to fluid (embolisms). leads to increased respiration (unmyelinated)
describe peripheral chemoreceptors
found in aortic arch and carotid sinus. sensitive to changes in ppO2 and activated when ppO2<60%. fast response
describe central chemoreceptors
found in medullary and detect changes in ppCO2. constitutes respiratory drive as mixes w water by crossing the blood brain barrier lowering pH. slow response
what is V/Q?
ventilation/perfusion. should be equal. if not hypoxia
what happens when the V/Q
value is high?
areas are ventilated but not perfused well, which is called dead space. can be cause by an embolism (blood clot)
what happens when the V/Q
value is low?
areas are well perfused but not ventilated. can be caused by pulmonary oedma as alveoli are collapsed which leads to blood being shunted
what does the body do when the V/Q value is high?
local bronchoconstriction, where air is diverted to better perfused areas
what does the body do when the V/Q value is low?
hypoxic pulmonary vasoconstriction as blood is diverted to better
ventilated areas
what factors shift the oxygen dissociation curve to the left?
high pH, low CO2, low O2, low DPG
what factors shift the oxygen dissociation curve to the right?
low pH, high CO2, high O2, high DPG
in what ways and proportions is carbon dioxide transported in teh blood?
- dissolved in plasma (10%)
- bound to Hb carbaminohaemoglobin (23%)
- as HCO3- (65%)
normal blood pH?
7.35-7.45
what does hypoventilation cause?
resp acidosis
what does hyperventilation cause?
resp alkalosis
hendson hasselback equation (pH of buffers)
pH = pKa + log10 ([A–]/[HA])
what is Dalton’s law?
total pressure = ppA + ppB +….
what is Boyle’s law?
P1V1=P2V2
what is Henry’s law?
volume of gas dissolved in liquid depends on pp and solubility of it.
conc gradient = solubility coefficient x pp
what is the alveolar gas equation?
PAO2 (alveolar) = PiO2 (inspired oxygen) − (PaCO2÷R). R= 0.8 usually
what is Laplace’s law?
alveolar pressure depends on surface tension and radius
P = 2T/ r
what secretes surfactant?
type ii pneumocytes
what does greater lung compliance mean?
the lungs more readily expand
what determines lung compliance?
surface tension and elasticity of lung tissue
what is hypoxia most commonly caused by?
hypoxaemia (lowered paO2)
what are four causes of hypoxaemia?
- hypoventilation (increased PaCO2)
- diff. impairment (thickening of membrane)
- shunt (septal defect, perfusing unventilated alveoli)
- V/Q mismatch
what is hypercapnia?
increased CO2 levels; caused by hypoventilation and
V/Q mismatch
what is important to consider when giving an asthmatic with type ii respiratory failure oxygen?
giving them O2 causes hyperventilation, which reduces PaCO2, reducing ability to breathe. alveoli collapse breathing ceases leading to death
what is pulse pressure?
the difference between systolic and diastolic pressure
what is Poiseuille law?
small changes in radius leads to a greater change in vascular resistance
8xLxviscosity / πxr4
how can Ohm’s law be translated to arteriole pressure?
mean pulmonary arteriole pressure - mean arteriole wedge pressure = CO x peripheral vascular resistance
what is the normal FEV1/FVC ratio?
0.75
what is the inspiratory reserve volume?
max inhalation in excess of tidal (normal) volume ~2000ml
what is exhalatory reserve volume?
max exhalation excess of normal exhalation ~1250ml
what is tidal volume?
tidal normal breathing ~500ml
what is residual volume?
air in lungs left after max expiration ~1250ml
lung capacity
why does lung compliance decrease with age?
costal cartilages become more stiff and lung elasticity decreases
what is prone with ageing lungs?
V/Q mismatch, lower compliance, weaker immune response, delayed hypercapnia/hypoxia response. lower FEV1 an FVC that could falsely show obstruction
what are some features of the innate immune system?
non specific, inherited and immediate
how do neutrophils kill bacteria?
identify threat. becomes activated by cytokines, adhesion to the site of infection, diaphoresis (neutrophil-neutrophil adhesion) via chemotaxis where the neutrophils move in response to a chemical stimulus, phagocytosis, bacterial killing
what is adaptive immunity?
specific, uses APCs. T+B cells
what do T cells do and what are the types?
directly kills pathogen. cytotoxic t cells bind to CD8 receptors and puncture holes in cell membrane by releasing perforin which empties cell contents. t helper cells induces other cell activation through CD4 receptors
what is the function of B cells?
secrete antibodies to kill pathogen through humoral action
what are the different classes of antibodies Ig’s?
GAMED, G (most abundant), A (breast milk and mucosa) ,M ( first found in infection),E (allergens), D (unknown, may be a B cell activator)
what are the broad classifications of host defences within the lungs?
immune and non immune barriers
what are examples of non immune barriers within the lungs and how do these act as barriers ?
- respiratory epithelium (barrier, antipathogen, mucus).
- mucus (mucos-cillary escalator to be coughed up and swallowed and general protection/ lubrication)
- coughing (air is forced out by a pressure gradient created by the epiglottis closing and thoracic pressure increasing)
what are examples of immune barriers within the lungs and how do these act as barriers ?
alveolar macrophages which represent 95% of all macrophages within the lung that act on a regular basis with minor disturbances. neutrophils are involved in larger response leading to inflammation
what is hypersensitivity?
allergic hyper-response, inflammation of self cells
what is type I hypersensitivity with examples?
IgE receptors bind to basophils which secrete histamine and PGs leading to bronchoconstriction and
vasodilation and inflammation. e.g. asthma and hayfever
what is type II hypersensitivity with examples?
IgM and IgG leads to a cytotoxic response and tissue damage/altered receptors e.g. autoimmune responses
what is type III hypersensitivity with examples?
IgG immune complex formation and deposition e.g. pigeon fancier lung and malt worker’s
what is type IV hypersensitivity with examples?
T cell mediated, delayed response
where are beta type 1 and 2 receptors found?
2 in the lungs (2 lungs) and 1 in the heart (1 heart)
how are respiratory issues treated?
bronchodilation. B2 agonists (salbutamol) and M3 antagonists (ipa/trospium)
how to calculate pressure of inspired gas?
atmospheric gas x fraction of inspired gas
how to calculate partial pressure of arteriole oxygen?
partial pressure of alveolar oxygen - (alveolar/arterial concentration gradient, typically 1)
how to calculate partial pressure of arteriole carbon dioxide?
constant of ventilation of carbon dioxide x alveolar
ventilation
what physiological responses occur with increased altitude?
hypoxia due to less oxygen leading to hyperventilation. lower PaCO2, increase heart rate and increase blood pH (temp alkalosis)
what pathology occurs with increased altitude and what are the symptoms and treatment?
acute mountain sickness (headaches, treated with descent). high altitude pulmonary oedema (oxygen and descent)
what pathology occurs with decreased altitude and what are the symptoms and treatment?
depression sickness (N2 can not be excreted properly leading to bubbles in tissue), inert gas narcosis (N2), CNS oxygen toxicity (too much oxygen), arterial gas embolism (presents 15min after surfacing), pulmonary barotrauma
what is the foramen ovale?
a hole between the left and right atria (upper chambers) of the heart to allow blood to bypass lungs as it is already oxygenated
what is the ductus venosus?
a shunt that allows oxygenated blood in the umbilical vein to bypass the liver and is essential for normal fetal circulation. blood becomes oxygenated in the placenta and travels to the right atrium via umbilical veins through the ductus venosus, then to the inferior vena cava
what is the ductus arteriosus?
embryology of the lungs
a blood vessel that connects the pulmonary artery (main vessel supplying the blood to the lungs) to the aorta (main vessel supplying the blood to the body) to bypass lungs
what do umbilical arteries do and how many are there?
2, carry deoxygenated blood from foetus to the mother
what do umbilical veins do and how many are there?
1, supplies oxygenated blood from the mother to the foetus
what happens during the first breath?
fluid is squeezed out of the lungs and surfactant is produced. air is inhaled and the pul arteries vasodilate
what does the umbilical
vein become?
ligamentum teres
what does the ductus venous become?
ligamentum venosus
what does the ductus arteriosus become?
ligamentum venosus arteriosus
what does the foramen ovale become?
fossa ovale
what are the aortic arches?
a series of six arches that develop consecutively to connect the aortic sac with the paired dorsal aorta
