CVR🫁💓

Question 1

What is Gastrulation?

Answer 1

Mass movement and invagination of the blastula to form three layers – ectoderm, mesoderm (middle layer) and endoderm

Question 2

What forms from the ectoderm?

Answer 2

Skin, nervous system, neural crest (which contributes to cardiac outflow, coronary arteries)

Question 3

What does the mesoderm form?

Answer 3

All types of muscle, most system, kidneys, blood, bone, cardiovascular system

Question 4

What does the endoderm form?

Answer 4

Gastrointestinal tract (inc liver, pancreas, but not smooth muscle), endocrine organs

Question 5

What are the two heart fields and what do they give rise to?

Answer 5

First heart field - gives rise to early structures
Second heart field - gives rise to more advanced things

FHF – future left ventricle
SHF – outflow tract,
future right ventricle,
atria

Question 6

List some cardiac transcription factors

Answer 6

Nkx2.5, GATA, Hand, Tbx, MEF2, Pitx2, Fog-1

Question 7

What are the stages of cardiac formation?

Answer 7

1.Formation of the primitive heart tube
2.Cardiac looping
3.Cardiac septation

Question 8

Describe formation of the primitive heart tube

Answer 8

In week 3, cells form horseshoe shape called the cardiogenic region. Day 19- 2 endocardial tubes form and fuse on day 21 to form a primitive heart tube.

Question 9

What is the bulbis cordis?

Answer 9

Forms most of the right ventricle and parts of the outflow tracts for the aorta and pulmonary trunk

Question 10

What does the primitive ventricle become?

Answer 10

Most of the left ventricle

Question 11

What does the primitive atrium become?

Answer 11

The anterior parts of the right and left atria

Question 12

What does the sinus venosus in the left and right horns become?

Answer 12

The superior vena cava and part of the right atrium

Question 13

Describe cardiac looping

Answer 13

-Bulbis cordis moves inferiorly, anteriorly and to the embryo’s right
-The primitive ventricle moves to the embryo’s left side
-The primitive atrium and sinus venosus move superiorly and posteriorly
-The sinus venosus is now posterior to the primitive atrium

Question 14

Describe cardiac septation

Answer 14

• The one atrium and ventricle are connected by the atrioventricular canal
  -Blood exits through the truncus arteriosus
  -Endocardial cushions grow from sides of AV canal to partition into 2 separate openings
  -At the same time the AV canal is being repositioned to the right side of the heart
  -Superior and inferior endocardial cushions fuse to form right and left AV canals
• Now blood passes through both of them

Question 15

How does the heart know to have a left orientated ventricle?

Answer 15

Cilliary motion at the node pushes the protein nodal towards the left. A cascade of transcription factors (e.g. Lefty, Pitx2, Fog-1) transduce looping

Question 16

Describe arterial system

Answer 16

Conduits of blood; physical properties (elastic arteries) increase efficiency whilst regulatory control (muscular arteries) control distribution

Question 17

What are Elastic arteries?

Answer 17

Major distribution vessels (aorta, brachiocephalic, carotids, subclavian, pulmonary)

Question 18

What are muscular arteries?

Answer 18

Main distributing branches

Question 19

What are arterioles?

Answer 19

Terminal branches (<300mm diameter)

Question 20

Describe the capillaries

Answer 20

The functional part of the circulation
Blood flow regulated by precapillary sphincters
Between 3-40 microns in diameter
Three types of capillary; continuous (most common), fenestrated (kidney, small intestine, endocrine glands), discontinuous (liver sinusoids)

Question 21

Describe the venous system

Answer 21

Return blood to the heart
System of valves allows “muscular pumping”
Some peristaltic movement

Question 22

What is the innermost layer of the artery/veins?

Answer 22

Tunica intima ( endothelium basement membrane)

Question 23

Second layer of arteries/veins

Answer 23

Tunica media (vascular smooth muscle cells)

Question 24

Third layer of arteries/veins

Answer 24

Internal elastic lamina

Question 25

Fourth layer of arteries/veins

Answer 25

Tunica adventitia (fibroblasts)

Question 26

Outer layer of arteries/veins

Answer 26

External elastic lamina

Question 27

What do you call capillaries that supply blood vessles?

Answer 27

Vasa vasorum

Question 28

What are blood islands and when do they form?

Answer 28

Extraembryonic mesoderm Core of hemoblasts surrounded by Endothelial cells Formed on day 17

Question 29

When does vasculogenesis occur and what is it?

Answer 29

Day 18, formation of a central vessel in the latreral mesoderm

Question 30

What is angiogenesis?

Answer 30

Driven by angiogenic growth factors and takes place via proliferation and sprouting from day 18 onwards other mesodermal cells are recruited to form the structure

Question 31

What drives embryonic vessel development?

Answer 31

Angiogenic growth factors – vascular endothelial growth factor, angiopoietin 1 & 2 Repulsive signals – Plexin / semaphorin signalling, ephrin / Eph interactions Attractive signals

Question 32

What do 1st and 2nd aortic arches become?

Answer 32

Become minor head vessels 1st – small part of maxillary 2nd - artery to stapedius

Question 33

What do the 3rd aortic arches become?

Answer 33

Portion between 3rd and 4th arch disappears Become common carotid arteries, and proximal internal carotid arteries Distal internal carotids come from extension of dorsal aortae

Question 34

What do the right dorsal aorta and right 4th aortic arch become?

Answer 34

R dorsal aorta looses connections with midline aorta and 6th arch, remaining connected to R 4th arch Acquires branch 7th cervical intersegmental artery, which grows into R upper limb Right subclavian artery is derived from right 4th arch, right dorsal aorta, and right 7th intersegmental artery

Question 35

What do the 6th aortic arches become?

Answer 35

Right arch may form part of pulmonary trunk Left arch forms ductus arteriosus – communication between pulmonary artery and aorta

Question 36

Describe an erythrocyte

Answer 36

-2-3 million produced and released from marrow/second -Lifespan 120 days -Anucleate biconcave discs -Haemoglobin to carry oxygen -Millions of antigens on surface (several hundred are blood group antigens)

Question 37

What is different about the antigens on red blood cells?

Answer 37

They have antigens against the other blood groups even though they have never been in contact with them

Question 38

What is the antigen that all red blood cells have?

Answer 38

H- antigen, this is the only one on blood group O but A and B have an extra sugar chain on it

Question 39

Describe ABO antibodies

Answer 39

-Theorised they develop against environmental antigens -Infants <3 months produce few if any antibodies (maternal prior to this) -First true ABO antibodies > 3 months -Maximal title 5-10 years -Titre decreases with age -Mix of IgG and IgM -IgM mainly for group A and B -Wide thermal range means they are reactive at 37C

Question 40

What determines your blood group?

Answer 40

The antigens show the blood group that you are. The antibodies are the against the group(s) that you don't have antigens for. E.g group A has A antigens and B antibodies

Question 41

What are rhesus antigens

Answer 41

-> 45 different Rh antigens -2 genes, Chromosome 1 -RHD – codes for Rh D -RHCE – codes for Rh C and Rh E -Highly immunogenic Can cause haemolytic transfusion reactions and haemolytic disease of the fetus and newborn (HDFN)

Question 42

What is the most important rhesus antigen to look at?

Answer 42

Rhesus D

Question 43

When do you have rhesus antibodies?

Answer 43

Only when you come into contact with the other rhesus D antigen

Question 44

What is Haemolytic disease of the fetus/newborn (HDFN)?

Answer 44

-Rh D sensitization most common cause -Develop anti-Rh antibodies -Severe fetal anaemia -Hydrops fetalis

Question 45

How is HDFN prevented?

Answer 45

-Detect mothers at risk -Maternal fetal free DNA -Anti D prophylaxis

Question 46

How to test for ABO and Rh D grouping?

Answer 46

Forward typing and reverse typing

Question 47

Describe forward typing

Answer 47

-Mix patient's red blood cells with a solution of either A of B antibodies -If the blood cells agglutinate, or clump together, it means the sample has reacted with one of the antibodies and so is the opposite blood group

Question 48

Describe reverse typing

Answer 48

-Mix plasma from patient with known red cells and see if they clump together -Positive is a line at the top of the gel

Question 49

What is cross matching blood?

Answer 49

Units of blood deemed suitable chosen from stocks available: Either exact match (e.g. A+ for A+) OR ‘Compatible” blood (e.g. O- for A+) Mix recipient serum with donor RBCS - indirect antiglobulin test

Question 50

What does the indirect antiglobulin test test for?

Answer 50

Blood grouping for ABO and Rhesus D Detects antibodies in patient’s serum

Question 51

Describe direct antiglobulin test

Answer 51

Detects antibodies on patient’s red cells ? Autoimmune haemolysis ? Transfusion reaction ? Haemolysis due to fetal/maternal group incompatibility

Question 52

Who can donate blood?

Answer 52

-17-65 years old -Body weight 50-158kg -Donors screened to highlight those at risk of infectious diseases -Also screened for health, lifestyle, travel, medical history, medications

Question 53

Temporary exclusion criteria to donate blood

Answer 53

Travel Tattoos/Body piercings Lifestyle

Question 54

Permanent exclusion criteria for donating blood

Answer 54

-Certain diseases -Received blood products or organ/tissue transplant since 1980 -Notified at risk of vCJD

Question 55

What can you donate?

Answer 55

Whole blood Apheresis

Question 56

What is Apheresis?

Answer 56

Blood removed and externally separated into Plasma, Platelets

Question 57

Mandatory tests for blood from blood donors

Answer 57

Hep B Hep C Hep E HIV Syphilis HTLV Groups and antibodies

Question 58

Describe separation and storage of the blood donated

Answer 58

-Whole blood donated into closed system bags -Blood centrifuged to packed red cells, Buffy coat and plasma -Plasma only kept from male donors -Plasma frozen (FFP) or processed to cryoprecipitate -Red cells passed through leucodepletion filter and suspended in additive -Buffy coats pooled with matching ABO and D type and then leucodepleted to make platelets

Question 59

What is a buffy coat and where is it found?

Answer 59

The buffy coat is the fraction of an anticoagulated blood sample that contains most of the white blood cells and platelets following centrifugation Buffy coat is situated in between the plasma and erythrocytes.

Question 60

What is done with red cells

Answer 60

Stored at 4degrees celsius, shelf life 35 days Some units irradiated to eliminate risk of transfusion-associated graft vs host disease

Question 61

Indications for needing a rbc transfusion

Answer 61

Severe anaemia (not purely iron deficiency)

Question 62

What is the transfusion threshold?

Answer 62

Haemoglobin <70 g/L or <80 g/L + symptoms Transfuse 1 unit and recheck FBC (unless massive transfusion needed) Emergency stocks of O Rh D- available in certain hospital areas

Question 63

Features of platelet donation

Answer 63

Most units pooled from 4 donations Some single-donor apheresis units Stored at 22oC with constant agitation, 7 day shelf life

Question 64

Indications for giving platelets

Answer 64

Thrombocytopaenia and bleeding Severe thrombocytopaenia < 10 due to marrow failure (150-450)

Question 65

Transfusion threshold of platelets (NICE)

Answer 65

(all values x10 to the power 9) <10 if asymptomatic and not bleeding <30 if minor bleeding <50 if significant bleeding <100 if critical site bleeding (brain, eye) Part of massive transfusion protocol ABO type still important (units contain ABO antibodies

Question 66

Describe fresh frozen plasma donation and transfusion protocal

Answer 66

From whole donations or apheresis Patients born > 1996 can only receive plasma from low vCJD risk (not UK plasma) Single donor packs have variable amounts of clotting factors. Pooled donations can be more standardized

Question 67

Indications for plasma transfusion

Answer 67

Multiple clotting factor deficiencies and bleeding (DIC) Some single clotting factor deficiencies where no concentrate available

Question 68

Describe the process of cryoprecipitate transfusion

Answer 68

Made by thawing FFP to 4oC and skimming off fibrinogen rich layer Used in DIC with bleeding, and in massive transfusion Therapeutic dose: 2 packs (each pooled from 5 plasma donations)

Question 69

What is immunoglobulin made from?

Answer 69

Made from large pools of donor plasma

Question 70

Describe normal IVIg

Answer 70

Contains Ab to viruses common in population Used to treat immune conditions e.g. ITP

Question 71

Describe specific IVIg

Answer 71

From selected patients Known high AB levels to particular infections/conditions Anti D immunoglobulin used in pregnancy VZV immunoglobulin in severe infection

Question 72

When/why do you give granulocytes?

Answer 72

Used very rarely Effectiveness controversial Severely neutropaenic patients with life threatening bacterial infections Must be irradiated (to kill T cells)

Question 73

Describe single factor concentrates

Answer 73

Factor VIII for severe haemophilia A (recombinant version – no risk of viral or prion transmission) Fibrinogen concentrate (Factor I)

Question 74

Describe prothrombin complex concentrate (Beriplex/Octaplex)

Answer 74

Multiple factors Rapid reversal of warfarin

Question 75

Important things to remember for the safe delivery of blood

Answer 75

Patient identification 2 sample rule Hand-written patient details Blood selected and serologically cross matched

Question 76

Common mistakes with blood transfusion

Answer 76

Patient identification errors are most common Wrong blood in wrong tube Lab errors are much less common Blood transfusion delayed Too much blood transfused

Question 77

How to avoid blood transfusion?

Answer 77

Optimise patients with planned surgical procedures pre-op Use of EPO-stimulating drugs In renal failure In patients with cancers Intraoperative cell salvage IV iron for severe iron deficiency Some patients may tolerate lower haemoglobin concentrations and not require transfusion at all

Question 78

How safe is blood transfusion?

Answer 78

Blood transfusion now very safe Heavily regulated and monitored (SHOT, MHRA) Potential risk of viral transmission now extremely low Hep B < 1:1,200,000 Hep C < 1:7,000,000 HIV < 1:28,000,000 Transfusion-related GvHD Risk reduced by leucodepletion and irradiation Problems more likely after blood leaves the lab

Question 79

What happens with ABO incompatability?

Answer 79

Rapid intravascular haemolysis Cytokine release Acute renal failure and shock DIC Can be rapidly fatal

Question 80

Treatment for haemolytic reactions

Answer 80

STOP transfusion immediately Fluid resuscitate Send to the lab Must be reported to SHOT

Question 81

Describe bacterial contamination of blood products

Answer 81

Most commonly with platelets (still v. rare) Symptoms very soon after transfusion starts Fever and rigors Hypotension Shock Inspection of unit may show abnormal colouration/cloudiness

Question 82

What is Transfusion related lung injury?

Answer 82

Ab in donor blood reacts with recipient’s pulmonary epithelium/neutrophils Inflammation causes plasma to leak into alveoli

Question 83

Symptoms of TRALI

Answer 83

SOB Cough with frothy sputum Hypotension Fevers

Question 84

What is Transfusion related circulatory overload (TACO)?

Answer 84

-Acute/worsening pulmonary oedema within 6 hours of transfusion -Older patients more at risk

Question 85

Symptoms of TACO

Answer 85

Respiratory distress Evidence of positive fluid balance Raised blood pressure

Question 86

How many big squares on an ECG is equal to 1mV?

Answer 86

2 big squares

Question 87

How do you calculate rate from an ECG?

Answer 87

Rate (bpm) = 300/no. of large squares between cardiac cycles or Rate (bpm) = 300/no. of large squares between cardiac cycles

Question 88

What does positive deflection mean?

Answer 88

Line on ECG goes up Shows net current flow towards the leas

Question 89

What is the Baseline (isoelectric point)?

Answer 89

No net current flow in direction towards the lead

Question 90

What is negative deflection?

Answer 90

Line on ECG goes down Net current flow away from the lead

Question 91

What is the P wave?

Answer 91

Depolarisation of the Atria

Question 92

What is the QRS complex?

Answer 92

Ventricular depolarisation

Question 93

What is the T wave?

Answer 93

The repolarisation of the ventricles

Question 94

What is atrial fibrillation?

Answer 94

Random atrial activity Random ventricular capture Irregularly irregular rhythm

Question 95

What is atrial flutter?

Answer 95

Organised atrial activity ~300/min Ventricular capture at ratio to atrial rate (usually 2:1 so 150 bpm) Usually regular Can be irregular if ratio varies

Question 96

What is the normal PR interval length?

Answer 96

120-200ms ( 3-5 small squares)

Question 97

What does an elongated PR interval show?

Answer 97

Delayed AV conduction Heart block

Question 98

What does a short PR interval show?

Answer 98

Wolff-Parkinson-White-Syndrome

Question 99

What does a longer QRS complex show?

Answer 99

QRS>120 ms Bundle branch block most common cause

Question 100

What is a QT interval?

Answer 100

Measure of time to ventricular repolarization Time from onset of QRS to end of T

Question 101

What are the normal values of the QT interval?

Answer 101

Men 350-440 ms Women 350-460 ms

Question 102

What is an ECG electrode?

Answer 102

Physical connection to patient in order to measure potential at that point 10 electrodes to record a 12 lead ECG

Question 103

What is an ECG lead?

Answer 103

Graphical representation of electrical activity in a particular ‘vector’ Calculated by the machine from electrode signals 12 leads for a 12 lead ECG (I-III, aVL, aVF, aVR, V1-6)

Question 104

What are bipolar leads?

Answer 104

Measures the potential difference (voltage) between two electrodes One electrode designated positive, the other negative

Question 105

What are Unipolar leads?

Answer 105

Measures the potential difference (voltage) between two electrodes One electrode designated positive, the other negative

Question 106

What does the right leg electrode do?

Answer 106

Neutral electrode - Reduces artefact – not directly involved in ECG measurement

Question 107

Describe Lead I

Answer 107

Bipolar lead Designated so that the positive electrode is the left arm and the negative electrode is the right arm So if current is flowing from right to left then there will be positive deflection If the other way around then it will be negative deflection Tells us what is happening in that direction

Question 108

Describe lead II

Answer 108

Right arm is negative electrode and left leg is positive electrode If current flows towards the left leg then there will be positive deflection If opposite way around then negative deflection

Question 109

Describe Lead II

Answer 109

Left leg is the positive electrode and the left arm is the negative electrode If the current flows from the arm to the leg then it is positive deflection, if the other way around then it is negative deflection

Question 110

What degrees are all of the leads represented as?

Answer 110

Lead I- 0 Lead II- +60 Lead III- +120

Question 111

What is a normal axis?

Answer 111

Positive towards leads 1 and 2 In the axis range of -30 to +90

Question 112

What are AVL, AVF and AVR?

Answer 112

Unipolar leads

Question 113

What axis are the aVL, aVF and aVR leads at?

Answer 113

aVL-> -30 aVF-> +90 aVR-> -150

Question 114

Is the QRS deflection negative or positive for aVR?

Answer 114

Negative

Question 115

What does lead I positive and lead II negative mean?

Answer 115

Left axis deviation

Question 116

What does lead I negative and lead II positive mean?

Answer 116

Right axis deviation

Question 117

What does the right coronary artery supply?

Answer 117

Inferior LV wall

Question 118

What does the left circumflex artery supply?

Answer 118

Lateral LV wall

Question 119

What does the left anterior descending artery supply?

Answer 119

Anterior LV wall

Question 120

In which leads does a problem with the inferior wall show?

Answer 120

Lead II, lead III and aVF

Question 121

What leads are used to see electrical activity in the transverse plane?

Answer 121

Chest leads (which are unipolar) V1-V6

Question 122

What area of the heart do leads V1 and V2 show electrical activity for?

Answer 122

Septal wall

Question 123

What area of the heart do leads V3 and V4 show electrical activity for?

Answer 123

Anterior wall

Question 124

What area of the heart do leads V5 and V6 supply?

Answer 124

Lateral wall

Question 125

What does ST elevation show?

Answer 125

Blocked major coronary artery

Question 126

Describe the membrane of the heart muscle

Answer 126

Normally only permeable to K+ Potential determined only by ions that can cross membrane

Question 127

Describe negative membrane potential

Answer 127

K+ ions diffuse outwards (high to low concentration) Anions cannot follow Excess of anions inside the cell Generates negative potential inside the cell

Question 128

What are the ion concentrations in the extracellular fluid (mmol/L)?

Answer 128

Na+ -> 145 K+ -> 4 Ca2+ -> 2 Cl- -> 120

Question 129

What are the ion concentrations in the intracellular fluid?

Answer 129

Na+ -> 14 K+ -> 135 Ca2+ -> 0.0001 Cl- -> 4

Question 130

Describe Myocyte membrane pumps

Answer 130

K+ pumped IN to cells Na+ and Ca2+ pumped OUT of cells Against their electrical and concentration gradients Therefore requires active transport (Na+-K+ pump) Requires ATP for energy

Question 131

Describe phase 4 (resting phase)

Answer 131

Sodium forced out by Na/K ATPases. Generates a concentration gradient and therefore a voltage The setup is now complete, everything from here on relies on passive movement of ions down their gradients.

Question 132

Describe phase 0 (depolarisation)

Answer 132

Large number of Na+ ions enter the cell, causing the charge to increase from -90mv to +20mV = (more) DEPOLARISATION

Question 133

Describe phase 1 (initial repolarisation)

Answer 133

Transient outward current of K+ ions leaving the cell causing a small repolarization

Question 134

Describe phase 2 (plateau)

Answer 134

Calcium channels open, causing calcium to enter the cell and MAINTAIN depolarized state

Question 135

Describe phase 3 (repolarisation)

Answer 135

Outward K+ current causes repolarization back to resting potential

Question 136

Describe action potential propagation

Answer 136

Local depolarization activates nearby Na+ channels Action potential spreads across membrane Gap junctions allow cell-to-cell conduction and propagation of action potential through whole myocardium

Question 137

What does electrical stimulation stimulate the release of to allow for muscle contraction?

Answer 137

CALCIUM Contraction of the heart muscle requires (appropriately-timed) delivery of Ca2+ ions to the cytoplasm Also known as “Excitation-contraction coupling”

Question 138

Describe step 1 of Excitation-Contraction coupling

Answer 138

Step 1: Calcium influx through surface ion channels

Question 139

Describe step 2 of Excitation-Contraction coupling

Answer 139

Step 2: Amplification of [Ca2+]i with NaCa Intracellular Calcium concentration Na Ca = Sodium calcium counter transporter 3 sodium, 1 calcium

Question 140

Describe step 3 of Excitation-Contraction coupling

Answer 140

Step 3: Calcium-induced Calcium Release CICR SR = calcium store Various pumps on surface of the SR maintain this concentration RyR on surface of SR. Activated by calcium, causes sustained calcium release

Question 141

Describe the Troponin-Tropomyosin-Actin-Complex

Answer 141

Calcium binds to troponin Conformational change in tropomyosin reveals myosin binding sites Myosin head cross-links with actin Myosin head pivots causing muscle contraction

Question 142

What are the specialist conduction tissues?

Answer 142

SAN AVN His / Purkinje system

Question 143

Describe the ventricle voltage/time graph for the SAN

Answer 143

Upsloping Phase 4 Less rapid phase 0 No discernable phase 1 / 2 Upsloping Phase 4 Less rapid phase 0 No discernable phase 1 / 2

Question 144

Describe the drift of the ventricle voltage/time graph for the SAN

Answer 144

Sinus node potential drifts towards threshold The steeper the drift, the faster the pacemaker

Question 145

What is the phase 4 slope affected by?

Answer 145

Autonomic tone Drugs Hypoxia Electrolytes Age

Question 146

What does sympathetic stimulation do?

Answer 146

Increases heart rate (positively chronotropic) Increases force of contraction (positively inotropic) Increases cardiac output

Question 147

What does parasympathetic stimulation do?

Answer 147

Decreases heart rate (negatively chronotropic) Decreases force of contraction (negatively inotropic) Decreases cardiac output

Question 148

Describe sympathetic control of heart rate

Answer 148

Adrenaline and noradrenaline + type 1 beta adrenoreceptors Increases adenylyl cyclase  increases cAMP

Question 149

What happens to the heart with increased sympathetic stimulation?

Answer 149

Increases heart rate (up to 180-250 bpm) Increases force of contraction Large increase in cardiac output (by up to 200%)

Question 150

What happens to the heart with decreased sympathetic stimulation?

Answer 150

Decreases heart rate and force of contraction Decreases cardiac output (by up to 30%)

Question 151

What is parasympathetic stimulation of the heartrate controlled by?

Answer 151

Acetylcholine M2 receptors – inhibit adenyl cyclase  reduced cAMP

Question 152

What happens to the heart with increased parasympathetic stimulation?

Answer 152

Decreased heart rate (temporary pause or as low as 30-40 bpm) Decreased force of contraction Decreased cardiac output (by up to 50%)

Question 153

What happens to the heart with decreased parasympathetic stimulation?

Answer 153

Increased heart rate

Question 154

What does the AV node do?

Answer 154

Transmits cardiac impulse between atria and ventricles Delays impulse Allows atria to empty blood into ventricles Fewer gap junctions AV fibres are smaller than atrial fibres Limits dangerous tachycardias

Question 155

Describe the conduction of the heart

Answer 155

Velocity of conduction Faster in specialised fibres Atrial and ventricular muscle fibres: 0.3 to 0.5 m/s Purkinje Fibers: 4m/s

Question 156

Describe the His-Purkinje system

Answer 156

AV node -> ventricles Rapid conduction To allow coordinated ventricular contraction Very large fibres High permeability at gap junctions

Question 157

What is automaticity?

Answer 157

Spontaneous discharge rate of heart muscle cells decreases down the heart SAN (usually) fastest Ventricular myocardium slowest

Question 158

Describe the refractory period

Answer 158

Resting state= closed -> open via depolarisation Open -> closed and inactivatable via automatic Closed and inactivatable -> resting state via repolarisation

Question 159

Describe the normal refractory period

Answer 159

Normal refractory period of ventricle approx 0.25s Less for atria than for ventricles

Question 160

Describe the heart muscle during the refractory period

Answer 160

Refractory to further stimulation during the action potential Fast Na+ +/- slow Ca2+ channels closed (inactivating gates)

Question 161

What does the refractory period do?

Answer 161

Prevents excessively frequent contraction Allows adequate time for heart to fill

Question 162

What happens after an absolute refractory period?

Answer 162

After absolute refractory period Some Na+ channels still inactivated K+ channels still open Only strong stimuli can cause action potentials Affected by heart rate

Question 163

What is the importance of platelets in disease?

Answer 163

Thrombosis - Formation of clot (thrombus) inside blood vessel - Platelets have a central role in arterial thrombosis Heart attack (myocardial infarction) Stroke Sudden death Antiplatelet medications can be life-saving

Question 164

What is atherogenesis and atherothrombosis?

Answer 164

Atherogenesis- Formation of fatty deposits in the arteries These fatty deposits then form fibrous plaque and atherosclerotic plaque Atherothrombosis- the rupture of the fatty deposits and plaque causing a blockage of the artery

Question 165

Why do we need blood flow control?

Answer 165

Maintain blood flow Maintain arterial pressure Distribute blood flow Auto-regulate/homeostasis Function normally Prevent catastrophe! (maladapt in disease)

Question 166

What are platelets?

Answer 166

Fragments of megakaryocytes in bone marrow

Question 167

Describe platelet shape change

Answer 167

Activation -> Shape change Smooth discoid -> spiculated + pseudopodia Increases surface area Increases possibility of cell-cell interactions

Question 168

What is on the surface of the platelets?

Answer 168

Glycoprotein IIb/IIIa (GPIIb/IIIa) receptor (aka integrin aIIbb3) 50,000 to 100,000 copies on resting platelet

Question 169

Describe platelet activation in terms of the Glycoprotein IIb/IIIa (GPIIb/IIIa) receptor

Answer 169

Increases number of receptors Increases affinity of receptor for fibrinogen Fibrinogen links receptors, binding platelets together (platelet aggregation)

Question 170

What happens after atherosclerotic plaque rupture?

Answer 170

Platelets adhere to damaged vessel wall Collagen receptors bind to subendothelial collagen which is exposed by endothelial damage GPIIb/IIIa also binds to von Willebrand factor (VWF) which is attached to collagen Soluble agonists are also released and activate platelets

Question 171

What is shear flow?

Answer 171

Blood flow across vessel walls causes shear force

Question 172

What is Von Willebrand factor?

Answer 172

It is a blood glycoprotein that promotes hemostasis (process to prevent bleeding), specifically, platelet adhesion. Initially adheres to endothelial cell, then is rolled until it forms stable adhesion activation

Question 173

How do platelets get activated?

Answer 173

Many different agonists can cause platelet activation incl- collagen, thrombin, thromboxane, ADP This leads to: Shape change Cross-linking of GPIIb/IIIa Platelet aggregation

Question 174

What does aspirin do?

Answer 174

It inhibits an amplification pathway Low dose aspirin inhibits COX-1 and high dose aspirin inhibits both COX-1 and COX-2

Question 175

What does arachidonic acid do?

Answer 175

Converted into prostaglandins by COX

Question 176

What does Cyclooxygenase 1 (COX-1) do?

Answer 176

Mediates GI mucosal integrity Thromboxane A2-mediated platelet aggregation

Question 177

What does Cyclooxygenase 2 (COX-2) do?

Answer 177

Mediates inflammation Involved in prostacyclin production, which inhibits platelet aggregation and affects renal function

Question 178

What does ADP do in platelets

Answer 178

Platelet purinergic receptors Platelet P2Y Receptors- P2Y1 and P2Y12 Different G proteins link to different signalling pathways

Question 179

What does P2Y1 do?

Answer 179

Activates phospholipase C which produces protein kinase C and Ca2+ Initiation of aggregation Shape change Causes platelet activation Results in GPIIb/IIIa fibrinogen cross-linking and aggregation

Question 180

What does P2Y12 do?

Answer 180

Produces P13 kinase and adenylate cyclase Adenylate cyclase then produces cAMP Amplification of platelet activation, aggregation and granule release Sustains platelet activation and aggregation

Question 181

How is the platelet activation amplified?

Answer 181

ADP causes platelet activation via P2Y receptors Dense granules release ADP, which causes further activation Activation of GPIIb/IIIa also amplifies platelet activation

Question 182

How does thrombin affect platelet activation?

Answer 182

Thrombin activates protease-activated receptors (PAR) on platelets This leads to platelet activation and release of ADP, which amplifies this activation

Question 183

Platelet procoagulant activity mediated by changes to membrane lipid bilayer

Answer 183

Platelet activation occurs e.g thrombin activating PAR1 This leads to Ca2+ being released from intracellular stores This inhibits translocase and activates scramblase which leads to the expression of aminophospholipids on the outer platelet membrane, which allows assembly of prothrombinase complex and generation of thrombin

Question 184

Describe the mechanisms of platelet activation?

Answer 184

Platelet procoagulant activity: activated platelets catalyse thrombin generation, creating an amplification loop that also links with coagulation (the production of fibrin)

Question 185

Describe a platelet-fibrin clot

Answer 185

Fibrin strands that surround red blood cells and platelets

Question 186

What is the Fibrinolytic system?

Answer 186

A dynamic interaction between fibrinolytic and anti-fibrinolytic factors is designed to maintain homeostasis i.e. haemostasis without thrombosis

Question 187

Mechanism of the fibrinolytic system

Answer 187

Endothelium releases tPA which cleaves plasminogen to plasmin - regulated by PAI-1 to form tPA/PAI Plasmin cleaves fibrin to fibrin degradation products- regulated by antiplasmin to form plasmin: antiplasmin complex

Question 188

Platelet alpha granules

Answer 188

Mediate expression of surface P-selectin and release of inflammatory mediators

Question 189

Platelets and inflammation

Answer 189

Platelets have pro-inflammatory and prothrombotic interactions with leukocytes and release inflammatory mediators from alpha granules

Question 190

How do monocytes interact with platelets in inflammation?

Answer 190

Cytokines e.g. chemotactic molecules Proteolytic Enzymes Pro-thrombotic molecules : Tissue factor Adhesion Molecules e.g. PSGL-1

Question 191

How do platelets interact with monocytes in inflammation?

Answer 191

Inflammatory mediators Adhesion Molecules e.g. P-Selectin Coagulation Factors

Question 192

What drugs are anticoagulants?

Answer 192

HEPARINS FONDAPARINUX BIVALIRUDIN RIVAROXABAN APIXABAN DABIGATRAN EDOXABAN

Question 193

What is aortal-mitro continuity

Answer 193

means that endocarditis can spread

Question 194

Main components of the myocardium

Answer 194

Contractile tissue, Connective tissue, fibrous frame, specialised conduction system

Question 195

What does the pumping action of the heart depend on?

Answer 195

The pumping action of the heart depends on interactions between the contractile proteins in its muscular walls.

Question 196

What does the Cardiac Myocyte do?

Answer 196

-The pumping action of the heart depends on interactions between the contractile proteins in its muscular walls. -The interactions transform the chemical energy derived from ATP into the mechanical work that moves blood under pressure from the great veins into the pulmonary artery, and from the pulmonary veins into the aorta. -The contractile proteins are activated by a signalling process called excitation-contraction coupling.

Question 197

When does the excitation-contraction coupling begin and end?

Answer 197

Excitation-contraction coupling begins when the action potential depolarizes the cell and ends when ionized calcium (Ca2+) that appears within the cytosol binds to the Ca2+ receptor of the contractile apparatus.

Question 198

Is movement of Ca2+ passive or active?

Answer 198

Movement of Ca2+ into the cytosol is a passive (downhill) process mediated by Ca2+ channels.

Question 199

When does the heart relax?

Answer 199

The heart relaxes when ion exchangers and pumps transport Ca2+ uphill, out of the cytosol.

Question 200

All or nothing phenomenon

Answer 200

Either the heart muscle contracts fully or doesn't contract at all there is no in between

Question 201

Key features of the myocyte cell

Answer 201

-Filled with cross-striated myofibrils. -Plasma membrane regulates excitation-contraction coupling and relaxation. -Plasma membrane separates the cytosol from extra-cellular space and sarcoplasmic reticulum. -Mitochondria: ATP, aerobic metabolism and oxidative phosphorylation.

Question 202

Does the relaxation process of the myocardium expend energy?

Answer 202

Relaxation process of the heart expends energy just like contraction

Question 203

What does the heart rely on during aerobic metabolism?

Answer 203

Free fatty acids

Question 204

What does the myocardium rely on for energy during hypoxia?

Answer 204

There is no FFA metabolism, thus anaerobic metabolism ensues. This relied on metabolising glucose (anaerobically) producing energy sufficient to maintain the survival of the affected muscle without contraction.

Question 205

How are contractile proteins arranged?

Answer 205

In a regular array of thick and thin filaments (The so called Myofibrils).

Question 206

What is the A-band?

Answer 206

The region of the sarcomere occupied by the thick filaments

Question 207

What is the I-band?

Answer 207

It is occupied only by thin filaments that extend toward the centre of the sarcomere from the Z-lines. It also contains tropomyosin and the troponins.

Question 208

Where are the Z lines?

Answer 208

Z lines bisect each I-band.

Question 209

Describe the sarcomere

Answer 209

-The functional unit of the contractile apparatus, -The sarcomere is defined as the region between a pair of Z-lines, -The sarcomere contains two half I-bands and one A-band.

Question 210

Describe the sarcoplasmic reticulum

Answer 210

A membrane network that surrounds the contractile proteins, The sarcoplasmic reticulum consists of the sarcotubular network at the centre of the sarcomere and the subsarcolemmal cisternae (which abut the T-tubules and the sarcolemma).

Question 211

What is the transverse tubular system (T-tubule)?

Answer 211

Is lined by a membrane that is continuous with the sarcolemma, so that the lumen of the T-tubules carries the extracellular space toward the centre of the myocardial cell.

Question 212

Describe contraction of the myocardium

Answer 212

Sliding of actin over myosin by ATP hydrolysis through the action of ATPase in the head of the myosin molecule. These heads form the crossbridges that interact with actin, after linkage between calcium and TnC, and deactivation of tropomyosin and TnI.

Question 213

Describe the features of myosin

Answer 213

2 heavy chains, also responsible for the dual heads. 4 light chains. The heads are perpendicular on the thick filament at rest, and bend towards the centre of the sarcomere during contraction (row.) alpha myosin and beta myosin.

Question 214

Describe the features of actin

Answer 214

Globular protein. Double-stranded macromolecular helix (G). Both form the F actin.

Question 215

Describe the features of tropomyosin

Answer 215

Globular protein. Double-stranded macromolecular helix (G). Both form the F actin.

Question 216

What does troponin I do?

Answer 216

With tropomyosin inhibit actin and myosin interaction.

Question 217

What does Troponin T do?

Answer 217

binds troponin complex to tropomyosin.

Question 218

What does troponin C do?

Answer 218

High affinity calcium binding sites, signalling contraction. Drives TnI away from Actin, allowing its interaction with myosin

Question 219

What is in a contractile unit?

Answer 219

Z, I, A and H zones, Myosin, Actin, Tropomyosin, Troponins, Titins, Calcium, ATP, Crossbridges.

Question 220

How is the contractile cycle controlled

Answer 220

Calcium ions- more means more contraction as more myosin binding sites are exposed Troponin phosphorylation Myosin ATPase

Question 221

What are the three basic events in the cardiac cycle?

Answer 221

- LV contraction, - LV relaxation, - LV filling.

Question 222

What are the steps in LV contraction?

Answer 222

- Isovolumic contraction - Maximal ejection

Question 223

What are the steps in LV relaxation?

Answer 223

- Start of relaxation and reduced ejection - Isovolumic relaxation - Rapid LV filling and LV suction - Slow LV filling (diastasis) - Atrial booster

Question 224

Describe ventricular contraction (systole)

Answer 224

Wave of depolarisation arrives, Opens the L-calcium tubule, {ECG: Peak of R}, Ca2+ arrive at the contractile proteins, LVp rises > LAp: MV closes: M1 of the 1st HS, LVp rises (isovolumic contraction) > Aop, AoV opens and Ejection starts.

Question 225

Describe ventricular relaxation (diastole)

Answer 225

LVp peaks then decreases. Influence of phosphorylated phospholambdan, cytosolic calcium is taken up into the SR. “phase of reduced ejection”. Ao flow is maintained by aortic distensibility. LVp < Ao p, Ao. valve closes, A2 of the 2nd HS. “isovolumic relaxation”, then “MV opens”.

Question 226

Describe ventricular filling

Answer 226

LVp < LAp, MV opens, Rapid (E) filling starts. Ventricular suction (active diastolic relaxation), may also contribute to E filling (esp. ex. ?S3). Diastasis (separation): LVp=LAp, filling temporarily stops. Filling is renewed when A contraction (booster), raises LAp creating a pressure gradient.(path, S4)

Question 227

Describe physiologic systole

Answer 227

1. Isovolumic contraction, 2. Maximal ejection

Question 228

Describe cardiologic systole

Answer 228

1. From M1 to A2, 2. Only part of isovolumic contraction (includes maximal and reduced ejection phases)

Question 229

Physiologic Diastole

Answer 229

1. Reduced ejection 2. Isovolumic relaxation 3. Filling phases

Question 230

Describe cardiologic Diastole

Answer 230

1. A2 to M1 interval (filling phases included)

Question 231

What is preload?

Answer 231

The load present before the left ventricular contraction has started

Question 232

What is afterload?

Answer 232

Is the load after the ventricle starts to contract

Question 233

What is Starling's law of the heart?

Answer 233

Within physiologic limits, the larger the volume of the heart, the greater the energy of its contraction and the amount of chemical change at each contraction.

Question 234

What is LV filling pressure?

Answer 234

Is the difference between LAp and LV diastolic pressure

Question 235

Atrial augmentation

Answer 235

Atrial contraction pushes the remainder of the blood at the end of diastole

Question 236

What is the Force-length interaction?

Answer 236

The force produced by the skeletal muscle declines when the sarcomere is less than the optimal length (Actin’s projection from Z disc “1m” X 2). In the cardiac sarcomere, at 80% of the optimal length, only 10% of the maximal force is produced!

Question 237

What is All or none on a cellular level?

Answer 237

The cardiac sarcomere must function near the upper limit of their maximal length (LMAX) = 2.2 m. The physiologic LV volume changes are affected when the sarcomere lengthens from 85% of LMAX to LMAX! Steep relationship: length-dependent activation.

Question 238

What is the Frank and isovolumic contraction?

Answer 238

The heart can, during the cycle, increase and decrease the pressure even if the volume is fixed. Increasing diastolic heart volume, leads to increased velocity and force of contraction (Frank 1895). This is the positive inotropic effect. Ino: Fibre (Greek); tropus: move (Greek).

Question 239

What is contractility?

Answer 239

(inotropic state): the state of the heart which enables it to increase its contraction velocity, to achieve higher pressure, when contractility is increased (independent of load)

Question 240

What is elasticity?

Answer 240

Is the myocardial ability to recover its normal shape after removal of systolic stress.

Question 241

What is compliance?

Answer 241

Is the relationship between the change in stress and the resultant strain.(dP/dV).

Question 242

What is Diastolic distensibility?

Answer 242

The pressure required to fill the ventricle to the same diastolic volume.

Question 243

What does the pressure volume loop reflect?

Answer 243

contractility in the end-systolic pressure volume relationship

Question 244

When is compliance reflected?

Answer 244

At the end diastolic pressure volume relationship

Question 245

Describe the blood flow through the organs

Answer 245

Heart 4% Other 3.5%Bronchi 2%Thyroid 1%Adrenal 0.5Heart 4%Other 3.5%Bronchi 2%Thyroid 1%Adrenal 0.5%

Question 246

Where is most of the blood volume?

Answer 246

Small veins and venules- 43% Large systemic veins- 20% Pulmonary circulation- 12% Heart- 10% Systemic arteries- 10% Capillaries- 5%

Question 247

Important features of the arteries

Answer 247

Low resistance conduits Elastic Cushion systole Maintain blood flow to organs during diastole

Question 248

Describe features of arterioles and their function

Answer 248

Principal site of resistance to vascular flow Therefore, TPR = Total Arteriolar Resistance Determined by local, neural and hormonal factors Major role in determining arterial pressure Major role in distributing flow to tissue/organs

Question 249

Describe TPR

Answer 249

Basically arteriolar resistance Vascular smooth muscle (VSM) determines radius VSM Contracts = ↓Radius = ↑Resistance ↓Flow VSM Relaxes = ↑Radius = ↓Resistance ↑Flow Or Vasoconstriction and Vasodilatation VSM never completely relaxed = myogenic tone Independent of pressure driving it

Question 250

Describe capillaries

Answer 250

40,000km and large area = slow flow Allows time for nutrient/waste exchange Plasma or interstitial fluid flow determines the distribution of ECF between these compartments Flow also determined by Arteriolar resistance No. of open pre-capillary sphincters

Question 251

Features of veins

Answer 251

Compliant Low resistance conduits Capacitance vessels Up to 70% of blood volume but only 10mmHg Valves aid venous return (VR) against gravity Skeletal muscle/Respiratory pump aids return SNS mediated vasoconstriction maintains VR/VP

Question 252

Describe the lymphatic system

Answer 252

Fluid/protein excess filtered from capillaries Return of this interstitial fluid to CV system Thoracic duct; left subclavian vein Uni-directional flow aided

Question 253

What is the lymphatic unidirectional flow aided by?

Answer 253

Smooth muscle in lymphatic vessels Skeletal muscle pump Respiratory pump

Question 254

Equation for cardiac output

Answer 254

Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)

Question 255

What is the blood pressure equation?

Answer 255

Blood pressure = CO x Total Peripheral Resistance (TPR) (like Ohm’s law: V=IR)

Question 256

What is Ohm's law?

Answer 256

Flow= pressure gradient/resistance

Question 257

What is Poiseuille's equation?

Answer 257

Delta P= 8uLQ/ pi r4

Question 258

What is the equation for pulse pressure?

Answer 258

Pulse pressure (PP) = Systolic – Diastolic Pressure

Question 259

What is the equation for mean arterial pressure?

Answer 259

Mean Arterial Pressure (MAP)= Diastolic Pressure + 1/3 PP

Question 260

What governs flow?

Answer 260

Ohm's law and Poiseuille's equation

Question 261

What is Frank-Starling mechanism?

Answer 261

How the heart responds to volume SV increases as End-Diastolic Volume increases Due to Length-Tension (L-T) relationship of muscle ↑EDV = ↑Stretch = ↑Force of contraction Cardiac muscle at rest is NOT at its optimum length ↑Venous return = ↑EDV = ↑SV = ↑CO (even if HR constant)

Question 262

How does stroke volume change in the frank-starling mechanism?

Question 263

How does blood volume affect circulation?

Answer 263

Venous return important beat to beat (FS mechanism) Blood volume is an important long term moderator BV = Na+, H20 Controlling water and sodium conc: Renin-Angiotensin-Aldosterone system; ADH; Adrenals and kidneys

Question 264

What is the goal of control of circulation?

Answer 264

Maintain blood flow! CO = SV x HR This needs pressure to push blood through peripheral resistance MAP = CO x TPR

Question 265

What is blood pressure?

Answer 265

Pressure of blood within and against the arteries

Question 266

What is systolic pressure?

Answer 266

Highest, when ventricles contract (100-150mmHg)

Question 267

What is diastolic blood pressure?

Answer 267

Lowest, when ventricles relax (not zero, due to aortic valve and aortic elasticity .. 60-90mmHg)

Question 268

Equation for mean arterial pressure

Answer 268

Mean arterial pressure = D + 1/3(S-D)

Question 269

How to measure blood pressure?

Answer 269

Measured using a sphygmomanometer Using brachial artery Convenient to compress Level of heart

Question 270

Sounds at each

Answer 270

0) > Systolic Pressure = no flow, no sounds- 1) Systolic pressure = high velocity = tap 2-4) Between S and D = thud 5) Diastolic pressure = sounds disappear

Question 271

Components of BP control

Answer 271

Autoregulation Local mediators Humoral factors Baroreceptors Central (neural) control

Question 272

What is Myogenic Autoregulation?

Answer 272

Stretch of vascular smooth muscle Contraction until diameter is normalised or slightly reduced

Question 273

Describe the variation of autoregulation

Answer 273

Intrinsic ability of an organ Constant flow despite perfusion pressure changes Renal/Cerebral/Coronary = Excellent Skeletal Muscle/Splanchnic = Moderate Cutaneous = Poor

Question 274

Brain and heart

Answer 274

intrinsic control dominates to maintain BF to vital organs

Question 275

Skin

Answer 275

BF is important in general vasoconstrictor response and also in responses to temperature (extrinsic) via hypothalamus

Answer 276

: dual effects: at rest, vasoconstrictor (extrinsic) tone is dominant; upon exercise, intrinsic mechanisms predominate

Question 277

Local humoural factors

Answer 277

Vasoconstrictors and vasodilators

Question 278

Vasoconstrictors examples

Answer 278

Endothelin-1 Internal Blood Pressure (myogenic contraction

Question 279

Vasodilators examples

Answer 279

Hypoxia Adenosine Bradykinin NO K+, CO2, H+ Tissue breakdown products

Question 280

How does endothelium control blood pressure

Answer 280

Control functions Essential for control of the circulation Nitric Oxide (NO) = potent vasodilator Prostacyclin = potent vasodilator Endothelin = potent vasoconstrictor

Question 281

Nitric oxide and Prostacyclin

Answer 281

The powerful local vasodilators Produced in endothelium

Question 282

Endothelin

Answer 282

Powerful vasoconstrictors

Question 283

Circulating hormonal factors

Answer 283

Vasoconstrictors: Epinephrine (skin), Angiotensin II, Vasopressin Vasodilators: Epinephrine (muscle), Atrial Natriuretic Peptide

Question 284

What are baroreceptors

Answer 284

see slides

Question 285

Arterial baroreceptors

Answer 285

Key role in short-term regulation of BP; minute to minute control, response to exercise, haemorrhage If arterial pressure deviates from ‘norm’ for more than a few days they ‘adapt’/’reset’ to new baseline pressure eg. in hypertension The major factor in long-term BP control is blood volume (Na+, H20)

Question 286

What are cardiopulmonary barorecteptors

Answer 286

Atria, ventricles, PA stretch: Secretion of ANP ↓vasoconstrictor centre in medulla, ↓ BP; and ↓release angiotensin, aldosterone & vasopressin (ADH), fluid loss Blood volume regulation

Question 287

Central neural control loop

Answer 287

See slide

Question 288

Describe the main neural influences on the medulla

Answer 288

Baroreceptors, Chemoreceptors, Hypothalamus, Cerebral cortex, Skin, Changes in blood [O2] and [CO2]

Question 289

Other higher centres

Answer 289

CV reflexes also require hypothalamus and pons Stimulation of anterior hypothalamus ↓ BP and HR; The reverse with posterolateral hypothalamus Hypothalamus also important in regulation of skin blood flow in response to temperature

Question 290

How does the cerebral cortex affect blood flow and pressure?

Answer 290

Stimulation usually ↑ vasoconstriction Emotion can ↑ vasodilatation and depressor responses eg. blushing, fainting. Effects mediated via medulla but some directly

Question 291

WHat do central chemoreceptors do

Answer 291

Chemosensitive regions in medulla ↑PaCO2 = vasoconstriction, ↑peripheral resistance, ↑BP ↓PaCO2 = ↓medullary tonic activity, ↓BP Similar changes with ↑ and ↓ pH PaO2 less effect on medulla; Moderate ↓ = vasoconstriction; Severe ↓ = general depression Effects of PaO2 mainly via peripheral chemoreceptors

Question 292

Short term BP control

Answer 292

Baroreceptors ↑BP ⇒ ↑Firing ⇒ ↑PNS/↓SNS ⇒ ↓CO/TPR = ↓BP

Question 293

Long term BP control

Answer 293

Volume of blood Na+, H20, Renin-Angiotensin-Aldosterone and ADH

Question 294

Key central effectors are peripheral

Answer 294

Blood vessels (vasodilatation and vasoconstriction: affects TPR) Heart (rate and contractility: CO = HR x SV) Kidney (fluid balance: longer term control)

Question 295

Homeostasis

Answer 295

See slide

Question 296

Physiological relevance of blood pressure

Answer 296

Cold Standing up Running Lifting Injury Blood loss

Question 297

Pathological relevance of blood pressure

Answer 297

Fainting Orthostatic hypotension POTS Heart failure Hypovolaemic shock Cardiogenic shock Heart block Cushing’s syndrome Respiratory failure General anaesthetic

Question 298

Fainting

Answer 298

Aetiology = emotion, heat, standing, dehydration Symptoms = nausea, air hunger, sweating Physiology = Fall in HR and Venous Pooling (X nerve) Signs = Collapse due to ↓ CO HR falls, CO falls, BP falls, perfusion to brain reduced ‘Neuro-cardiogenic syncope’ = Faint! Treatment = lay supine and elevate limbs to ↑VR Frank-Starling leads to improved SV and CO Long term: fluids, salt .. Midodrine (α agonist) Lifestyle adaptation

Question 299

Blood loss

Answer 299

Perfusion to brain must be maintained Local vasoconstriction Maintain CO/BP by ↑HR Sympathetic outflow Widespread cutaneous vasoconstriction Eventually .. SHOCK (BP↓, Pulse↑, organ hypoperfusion) and death Treat: rapid volume replacement EARLY

Question 300

Orthostatic hypotension

Answer 300

Aetiology = standing quickly, too long, dehydration, hot room Symptoms = lightheaded, sweating, syncope Physiology = Fall in BP and Venous Pooling (X nerve) Failure to reflexly maintain BP and HR Perfusion to brain reduced Treatment = lay supine and elevate limbs to ↑VR Frank-Starling leads to improved SV and CO Investigate: Lying/ standing BP; tilt test Common cause: BP drugs, B blockers, vasodilators Lifestyle adaptation

Question 301

Postural orthostatic tachycardia syndrome (POTS)

Answer 301

Standing Palpitation, dizzy, near syncope, sweating, debilitating Physiology = Excess tachycardia response Investigate = Tilt test HR↑ >40bpm; BP usually OK Not well understood

Question 302

Describe the nose

Answer 302

Most superior portion of the respiratory tract Multiple functions -Temperature of inspired air (0.25 second -contact) -Humidity (75-80% RH) -Filter function -Defence function Cilia take inhaled particulates backwards to be swallowed Splinted open

Question 303

What does the anterior nares open into?

Answer 303

The enlarged vestibule - Skin lined -Stiff hairs Surface area of the nose -Doubled by turbinates

Answer 304

Superior meatus- under superior turbinate -Olfactory epithelium -Cribriform plate -Sphenoid sinus Middle meatus- under middle turbinate -Sinus openings Inferior meatus- under inferior turbinate -Nasolacrimal duct On the lateral nasal wall

Question 305

Describe the paranasal sinuses

Answer 305

Pneumatised areas of the; -Frontal -Maxillary -Ethmoid -Sphenoid bones Arranged in pairs Evagination of mucous membrane from the nasal cavity Extension of the mucosa into the sinus

Question 306

Describe the frontal sinuses

Answer 306

Within frontal bone Midline septum Over orbit and across superciliary arch Nerve supply – ophthalmic division of V nerve

Question 307

Describe the maxillary sinuses

Answer 307

Located within the body of the maxilla Pyramidal shape Open into the middle meatus Hiatus semilunaris

Question 308

Where is each part of the maxillary sinuses?

Answer 308

Base – lateral wall of the nose Apex – zygomatic process of the maxilla Roof – floor of the orbit Floor – alveolar process

Question 309

Describe the ethmoid sinuses

Answer 309

Between the eyes Labyrinth of air cells Semilunar hiatus of the middle meatus Nerve supply - ophthalmic and maxillary V nerve (trigeminal nerve)

Question 310

Describe the sphenoid sinuses

Answer 310

Medial to the cavernous sinus Carotid artery, III,IV, V, VI Inferior to optic canal, dura and pituitary gland Empties into sphenoethmoidal recess, lateral to the attachment of the nasal septum Nerve supply – ophthalmic V

Question 311

Describe the pharynx

Answer 311

Fibromuscular tube lined with epithelium Squamous and columnar ciliated, mucous glands Skull base  C6  Oesophagus Anterior  Nasal Cavities, mouth and larynx Nasopharynx Oropharynx Laryngopharynx (hypopharynx)

Question 312

Describe the nasopharynx

Answer 312

Bounded by -base of skull -Sphenoid rostrum -C Spine -Posterior nose (choana) -Inferiorly at soft palate opens to oropharynx Eustachian tube orifices (lateral wall) Supply air to middle ear Pharyngeal tonsils on posterior wall

Question 313

Soft palate anteriorly Palatine tonsils on the lateral walls Palatoglossal folds Palatopharyngeal folds Inferiorly to the hyoid bone

Answer 313

Soft palate anteriorly Palatine tonsils on the lateral walls Palatoglossal folds Palatopharyngeal folds Inferiorly to the hyoid bone

Question 314

Describe the larynx

Answer 314

Valvular function Prevents liquids and food from entering lung Rigid structure 9 cartilages Multiple muscles Arytenoid cartilages rotate on the cricoid cartilage to change vocal cords Vocal cords approximate anteriorly

Question 315

What are the laryngeal cartilages?

Answer 315

Single Double -Epiglottis -Cuneiform -Thyroid -Corniculate -Cricoid -Arytenoid

Question 316

Describe laryngeal innervation

Answer 316

The vagus (X) -Superior laryngeal nerve -Recurrent laryngeal nerve

Question 317

Describe the superior laryngeal nerve

Answer 317

-Inferior ganglion -Lateral pharyngeal wall -Divides into -Internal -Sensation -External -Cricothyroid muscle

Question 318

Describe the recurrent laryngeal nerve

Answer 318

All muscles except cricothyroid R and L different Left lateral to arch of aorta, loops under aorta, ascends between trachea and oesophagus Right R Subclavian artery, plane between trachea and oesophagus

Question 319

Describe the main features of gas exchange

Answer 319

20m2 gas exchange area per lung Minute ventilation approx 5 litres Cardiac output approx 5 litres per minute Regional differences in ventilation and perfusion (blood supply) 600 million alveoli

Question 320

lower respiratory structure

Answer 320

-Main airways: Trachea Main Bronchi Lobar Bronchi Segmental branches Respiratory Bronchiole Terminal Bronchiole Alveolar Ducts and Alveoli -Pleura

Question 321

Angle of Louis

Question 322

Describe the trachea

Answer 322

Larynx to carina (5th thoracic vertebra, T5) Oval in cross section Pseudo stratified, ciliated, columnar epithelium Goblet cells Semicircular cartilages Mobile (3 cm and 1cm, superior and inferior) Sensory innervation- recurrent laryngeal nerve

Question 323

Describe the bronchi

Answer 323

Left and Right main bronchi Sharp division between these The carina R main bronchus more vertically disposed 1-2.5cm long, related to the R pulmonary artery L main bronchus 5cm long, related to the aortic arch

Question 324

Describe the Lobar bronchi

Answer 324

Lobar Bronchi (normal) -Right -Upper lobe -Middle lobe -Lower lobe -Left -Upper lobe and lingular -Lower lobe

Question 325

What are the left segmental bronchi?

Answer 325

Upper lobe: Apico-posterior, Anterior Lingular: Superior and Inferior Lower lobe: Apical, Ant, Post, Lat

Question 326

Describe acinus

Answer 326

Distal to the terminal bronchiole Alveoli more profuse with increasing generation of subdivision Ducts are short tubes with multiple alveoli Interconnection between alveoli exist (pores of Kohn)

Question 327

Describe the alveoli

Answer 327

Type I pneumocytes: Pavement Type II pneumocytes: Surfactant producers (keeps alveoli patent) Alveolar macrophage Basement membrane Interstitial tissue Capillary endothelial cells

Question 328

Describe the pleura of the lungs

Answer 328

Visceral: Applied to the lung surface Parietal: Applied to the internal chest wall Each a single cell layer Small amount of fluid between Continuous with each other at lung root Parietal pleura has pain sensation Visceral pleura has only autonomic innervation

Question 329

Describe the blood supply to the lungs

Answer 329

Bronchial and pulmonary circulations Pulmonary circulation L and R pulmonary arteries run from R ventricle 17 orders of branching Elastic (>1mm ) and non elastic Muscular (<1mm ) Arterioles (<0.1mm ) Capillaries

Question 330

How much

Answer 330

Requirement to move 5 litres / minute of inspired gas [cardiac output 5 litres / min]

Question 331

What is the respiratory pump?

Answer 331

Generation of negative intra-alveolar pressure Inspiration active requirement to generate flow Bones, muscles, pleura, peripheral nerves, airways all involved Bony structures support respiratory muscles and protect lungs Rib movements; pump handle and water handle

Question 332

What are the muscles of respiration?

Answer 332

Inspiration Largely quiet and due to diaphragm (C3/4/5) contraction External intercostals (nerve roots at each level) Expiration Passive during quiet breathing

Question 333

Describe the pleura

Answer 333

2 layers, visceral and parietal Potential space only between these, few millilitres of fluid

Question 334

Describe the nerves of the respiratory pump

Answer 334

-Sensory; -Sensory receptors assessing flow, stretch etc.. -C fibres -Afferent via vagus nerve (10th cranial nerve) -Autonomic sympathetic, parasympathetic balance

Question 335

What is static lungs

Answer 335

Both chest wall and lungs have elastic properties, and a resting (unstressed) volume Changing this volume requires force Release of this force leads to a return to the resting volume Pleural plays an important role linking chest wall and lungs

Question 336

what is needed at the alveoli

Answer 336

ventilation and perfusion

Question 337

Ventilation

Answer 337

Bulk flow in the airways allows O2 and CO2 movement Large surface area required, with minimal distance for gases to move across. Total combined surface area for gas exchange 50-100 m2 300,000,000 alveoli per lung

Question 338

Dead space

Answer 338

Volume of air not contributing to ventilation Anatomic; Approx 150mls Alveolar; Approx 25mls Physiological (Anatomic+Alveolar) = 175mls

Question 339

Describe circulation in the bronchi

Answer 339

Blood supply to the lung; branches of the bronchial arteries Paired branches arising laterally to supply bronchial and peri-bronchial tissue and visceral pleura Systemic pressures (i.e. LV/aortic pressures) Venous drainage; bronchial veins draining ultimately into the superior vena cava

Question 340

Describe pulmonary circulation

Answer 340

Left and right pulmonary arteries run from right ventricle Low(er) pressure system (i.e. RV / pulmonary artery pressures) 17 orders of branching Elastic (>1mm ) and non elastic Muscular (<1mm ) Arterioles (<0.1mm ) Capillaries

Question 342

Describe alveolar perfusion

Answer 342

1000 capillaries per alveolus Each erythrocyte may come into contact with multiple alveoli Erythrocyte thickness an important component of the distance across which gas has to be moved At rest, 25% the way through capillary, haemoglobin is fully saturated

Question 343

What does alveolar perfusion depend on?

Answer 343

Pulmonary artery pressure Pulmonary venous pressure Alveolar pressure Capillaries at the most dependent parts of the lung are preferentially perfused with blood at rest

Question 344

What is hypoxic pulmonary vasoconstriction

Answer 344

Matching ventilation and perfusion important Pulmonary vessels have high capacity for cardiac output 30% of total capacity at rest Recruiting of alveoli occurs as a consequence of exercise

Question 345

Nomenclature of pulmonary physiology

Answer 345

PaCO2- arterial CO2 PACO2- Alveolar CO2 PaO2- arterial O2 PACO2- Alveolar O2 PiO2- Pressure of inspired oxygen

Answer 346

PaCO2=kVco2/VA Normally PaCO2= 4-6 KPa

Question 347

Ways that CO2 is carried

Question 348

Physiological causes of a high CO2

Question 349

Alveolar gas equation

Answer 349

PAO2= PiO2-PaCO2/R R=Respiratory Quotient [ratio of Vol CO2 released/Vol O2 absorbed, assume = 0.8]

Question 350

Causes of low PaO2

Answer 350

Alveolar hypoventilation Reduced PiO2 Ventilation/perfusion mismatching (V/Q) Diffusion abnormality

Question 351

Describe O2/Hb dissociation curve non linear

Answer 351

Sigmoid shape As each O2 molecule binds, it alters the conformation of haemoglobin, making subsequent binding easier (cooperative binding) Varying influences 2,3 diphosphoglyceric acid H+ Temperature CO2

Question 352

Describe acid base control in the blood

Answer 352

Body maintains close control of pH to ensure optimal function (e.g. enzymatic cellular reactions) Dissolved CO2/carbonic acid/respiratory system interface crucial to the maintenance of this control pH normally 7.40 H+ concentration 40nmol/l [34-44 nmol/l]

Question 353

Measures you can get from a blood gas

Answer 353

PaCO2- arterial CO2 PaO2- arterial O2

Question 354

How does the body control acid/base levels?

Answer 354

Blood and tissue buffers important Carbonic acid / bicarbonate buffer in particular CO2 under predominant respiratory control (rapid) HCO3- under predominant renal control (less rapid) The respiratory system is able to compensate for increased carbonic acid production, but; Elimination of fixed acids requires a functioning renal system

Question 355

Carbonic acid equilibrium

Answer 355

CO2 + H2O <-> H2CO3 <-> H+ + HCO3- Carbonic anhydrase

Question 356

Henderson-Hasselbalch equation

Answer 356

pH=6.1 + log10[[HCO3-]/[0.03*PCO2]]

Question 357

when co2 increases

Answer 357

In order to keep pH at 7.4, log of the ratio must equal 1.3 As PaCO2 rises (respiratory failure) HCO3- must also rise (renal compensatory mechanism) to allow this- as the pH lowers

Question 358

Four main acid base disorders

Answer 358

Respiratory acidosis, respiratory alkalosis, metabolic acidosis, metabolic alkalosis

Question 359

Functions of the lung?

Answer 359

Respiration: Ventilation and gas exchange: O2, CO2, pH, warming and humidifying Non-respiratory functions: Synthesis, activation and inactivation of vasoactive substances, hormones, neuropeptides Lung defence: complement activation, leucocyte recruitment, host defence proteins, cytokines and growth factors Speech, vomiting, defecation.

Question 360

Intrinsic host defences

Answer 360

Always present: Physical and chemical. Apoptosis, autophagy, RNA silencing, antiviral proteins

Question 361

Innate defence

Answer 361

induced by infection (Interferon, cytokines, macrophages, NK cells)

Question 362

Adaptive immunity

Answer 362

Tailored to a pathogen (T cell, B cells)

Question 363

What is epithelium?

Answer 363

A tissue composed of cells that line the cavities and surfaces of structures throughout the body. Many glands are also formed from epithelial tissue. It lies on top of connective tissue, and the two layers are separated by a basement membrane.

Question 364

What is respiratory epithelium?

Answer 364

serves to moisten and protect the airways. It also functions as a barrier to potential pathogens and foreign particles, preventing infection and tissue injury by action of the mucociliary escalator.

Question 365

Chemical epithelial barriers

Answer 365

antiproteinases anti-fungal peptides anti-microbial peptides Antiviral proteins Opsins

Question 366

Describe mucous and it's functions

Answer 366

Airway mucus is a viscoelastic gel containing water, carbohydrates, proteins, and lipids. It is the secretory product of the mucous cells (the goblet cells of the airway surface epithelium and the submucosal glands). Mucus protects the epithelium from foreign material and from fluid loss Mucus is transported from the lower respiratory tract into the pharynx by air flow and mucociliary clearance.

Question 367

What do cilia do in the lungs?

Answer 367

Beat to move mucus up the airways

Question 368

What is a cough and what causes it?

Answer 368

A cough is an expulsive reflex that protects the lungs and respiratory passages from foreign bodies Causes of cough: 1. Irritants- smokes, fumes, dusts ect 2. Diseased conditions like COPD, tumours,ect 3. Infections(influenza)

Question 369

How does a cough happen

Answer 369

Defence reflex so afferent and efferent pathways Afferent

Question 370

What is a sneeze and what causes it?

Answer 370

Sneeze is defined as the involuntary expulsion of air containing irritants from the nose Causes of sneeze: 1. Irritation of nasal mucosa 2. Excess fluid in airway

Question 371

Why can injury to airway epithelium repair its self and how?

Answer 371

Injury-> Spreading and dedifferentiation->cell migration->cell proliferation ->redifferentiation -> regeneration This is because it exhibits a level of functional plasticity

Question 372

What happens when epithelial changes go wrong?

Answer 372

We get pulmonary diseases Underpin many obstructive lung diseases

Question 373

What are mucus plugs/inflammation?

Answer 373

Mucus and inflammatory cells blocking airways

Question 374

Key facts about the pulmonary and bronchial circulation

Answer 374

Unique dual blood supply of the lungs Pulmonary Circulation From Right Ventricle 100% of blood flow Bronchial Circulation 2% of Left Ventricular Output

Question 375

Describe the pulmonary circulation system

Answer 375

Receives 100% of cardiac output (4.5-8L/min.) Red cell transit time ≈5 seconds. 280 billion capillaries & 300 million alveoli. Surface area for gas exchange 50 – 100 m2

Question 376

Pulmonary arteries features

Answer 376

Vessel wall-> thin Muscularization-> minor Need for redistribution-> not in normal state

Question 377

Systemic arteries features

Answer 377

Vessel wall-> thick Muscularization-> significant Need for redistribution-> yes

Question 378

Pressures of pulmonary circulation (mmHg)

Answer 378

RA 5 RV 25/0 PA 25/8

Question 379

Pressures of the systemic circulation

Answer 379

LA 5 LV 120/0 Aorta 120/80

Question 380

How do you measure wedge pressure

Question 381

What is Ohm's law?

Answer 381

Voltage across circuit = Current x Resistance V = I R Pressure across circuit = Cardiac Output x Resistance mPAP – PAWP = CO x PVR mPAP (mean pulmonary arterial pressure), PAWP (pulmonary arterial wedge pressure left atrial pressure), CO (cardiac output) PVR (pulmonary vascular resistance)

Question 382

What is pouiseuille's law?

Answer 382

Resistance = (8 x L x viscosity)/(π r4) A small change in radius can have a big impact on it

Question 383

exercise

Answer 383

mPAP – PAWP = CO x PVR On exercise CO increases significantly but mPAP remains stable/increases slightly because of recruitment and distention in response to increased pulmonary artery pressure

Question 384

What are the pO2 and pCO2 values for type I and type II respiratory failure?

Answer 384

Type I Respiratory Failure pO2 < 8 kPA pCO2 <6 kPA Type II Respiratory Failure pO2 < 8 kPA pCO2 >6 kPA

Question 385

Causes of hypoxaemia

Answer 385

Hypoventilation Diffusion Impairment Shunting V/Q mismatch

Question 386

What is hypoventilation and what are the causes?

Answer 386

Type II Respiratory Failure pO2 < 8 kPA pCO2 >6 kPA Failure to ventilate the alveoli Causes: Muscular weakness Obesity Loss of respiratory drive

Question 387

Different causes of diffusion of impairment

Answer 387

Gaseous Diffusion Pulmonary Oedema Blood Diffusion Anaemia Membrane Diffusion Interstitial Fibrosis

Question 390

Abbreviations for lung physiology measures

Answer 390

TLC- total lung capacity VC- vital capacity RV- residual volume TV- tidal volume FRC- functional residual capacity

Question 391

Measured values of lung capacity

Answer 391

FEV1- Forced expiratory volume in one second FVC- Forced vital capacity- All the air to residual volume Flow volume curve Peak Expiratory Flow (PEF) Lung volumes Transfer factor estimates [Compliance]

Question 392

Forced expiration

Answer 392

Most of the air comes out in the first second Breathe in to total lung capacity (TLC) Exhale as fast as possible to residual volume (RV) Volume produced is the vital capacity (FVC) Volume time graph looks like a sharp increase in the first second then it plateaus

Question 393

Peak flow

Answer 393

1/10th of a second in Can see it on a flow volume graph Single measure of highest flow during expiration Peak flow meter, spirometer Gives reading in litres/minute (L/min) Very effort dependent May be measured over time, by giving a patient a PEF meter and chart

Question 394

Flow volume graph for forced expiration

Answer 394

Take the exact same procedure Re-plot the data showing flow as a function of volume PEF; peak flow FEF25; flow at point when 25% of total volume to be exhaled has been exhaled FVC; forced vital capacity

Question 395

What are lung volumes?

Answer 395

Expiratory procedures only measure VC, not RV Various other ways to measure RV and TLC are needed These include; Gas dilution Body box (total body plethysmography; shown in picture)

Question 396

Describe gas dilution

Answer 396

Measurement of all air in the lungs that communicates with the airways Does not measure air in non-communicating bullae Gas dilution techniques use either closed-circuit helium dilution or open-circuit nitrogen washout

Question 397

Total body/ body box plethysmography

Answer 397

Alterative method of measuring lung volume, (Boyle's law), including gas trapped in bullae. From the FRC, patient “pants” with an open glottis against a closed shutter to produce changes in the box pressure proportionate to the volume of air in the chest The volume measured (TGV) represents the lung volume at which the shutter was closed FRC, inspiratory capacity, expiratory reserve volume, vital capacity all measured From these volumes and capacities, the residual volume and total lung capacity can be calculated TLC = VC+RV

Question 398

Transfer estimates

Answer 398

Carbon monoxide used to estimate TLCO, as has high affinity for haemoglobin Single 10 second breath-holding technique 10% helium, 0.3% carbon monoxide, 21% oxygen, remainder nitrogen. Alveolar sample obtained; DLCO is calculated from the total volume of the lung, breath-hold time, and the initial and final alveolar concentrations of carbon monoxide.

Question 399

What is TLco an overall measure of the interaction of?

Answer 399

alveolar surface area alveolar capillary perfusion physical properties of the alveolar capillary interface capillary volume haemoglobin concentration, and the reaction rate of carbon monoxide and hemoglobin.

Question 400

Regression equations

Question 401

Abnormal FEV1 values

Answer 401

Forced expiratory volume in one second in litres Good overall assessment of lung health Compare with predicted value 80% or greater “normal” Above the lower limit of normal for that patient (LLN) Above mean minus 1.645 SD

Question 402

Abnormal FVC values

Answer 402

Compare with predicted value 80% or greater “normal” Above the lower limit of normal for that patient (LLN) Above mean minus 1.645 SD Low value indicates likely Airways Restriction 🫁

Question 403

Abnormal FEV1/ FVC ratio

Answer 403

There is a predicted ratio for each individual, but.. Abnormal ratio < 0.70 = airways obstruction [Can also use the LLN* for each individual patient] *Lower limit of normal

Question 404

Asthma physiology changes

Answer 404

FEV1- Normal or reduced FVC- Normal PEF- Typically variable, increased diurnal variation of 20% MEF- Low, typically 'scalloped' shape to the flow volume curve TLC- High or normal TLco and Kco- Normal or elevated eNO- High RAW- High when airway narrowing present

Question 405

Asthma typical blood gases

Answer 405

PaO2 Normal PaCO2 Low pH Normal or elevated HCO3- Normal

Question 406

COPD characteristics

Answer 406

COPD is a progressive condition Typified by wheeze and shortness of breath on exercise, progressively worse with time Intermittent exacerbations Typified by airways obstruction and lack of significant PEF variation Typified by reduced mid expiratory flows Typified by partial or poor response to treatments

Answer 407

FEV1- Reduced significantly FVC- May be normal or reduced PEF- Typically not variable MEF- low typical scalloped shaped to the flow volume curve DLco and Kco- low eNO- normal RAW- high

Question 408

COPD typical blood gases

Answer 408

PaO2 Low PaCO2 High in type 2 respiratory failure Low in type 1 respiratory failure pH Normal HCO3- May be elevated if chronic acidosis

Question 409

Asbestosis (pulmonary fibrosis due to asbestos) changes to values

Answer 409

FEV1- Reduced significantly FVC- Reduced significantly PEF- Typically not variable MEF- Low or normal TLC- Reduced Dlco and Kco- Low eNO- Normal RAW- no typical change

Question 410

Asbestosis typical blood gases

Answer 410

PaO2 Low PaCO2 Low pH Normal HCO3- Low

Question 411

What is the requirement for respiration?

Answer 411

Ensure haemoglobin is as close to full saturation with oxygen as possible Efficient use of energy resource Regulate PaCO2 carefully variations in CO2 and small variations in pH can alter physiological function quite widely

Question 412

Breathing is automatic so...

Answer 412

No conscious effort for the basic rhythm Rate and depth under additional influences Depends on cyclical excitation and control of many muscles Upper airway, lower airway, diaphragm, chest wall Near linear activity Increase thoracic volume

Question 413

What is taking a breath dependent on?

Answer 413

CO2 levels

Question 414

Basic breathing rhythm -Pons

Answer 414

Pneumotaxic and Apneustic Centres

Question 415

Basic breathing rhythm in medulla oblongata

Answer 415

Phasic discharge of action potentials Two main groups Dorsal respiratory group (DRG) Ventral respiratory group (VRG)

Question 416

When are the DRG and VRG active?

Answer 416

DRG; predominantly active during inspiration VRG; active in both inspiration and expiration Each are bilateral, and project into the bulbo-spinal motor neuron pools and interconnect

Question 417

Describe the central pattern generator

Answer 417

Neural network (interneurons) Located within DRG/VRG Precise functional locations not known Start, stop and resetting of an integrator of background ventilatory drive

Question 418

Describe Inspiration

Answer 418

Progressive increase in inspiratory muscle activation Lungs fill at a constant rate until tidal volume achieved End of inspiration, rapid decrease in excitation of the respiratory muscles

Question 419

Describe expiration

Answer 419

Largely passive due to elastic recoil of thoracic wall First part of expiration; active slowing with some inspiratory muscle activity With increased demands, further muscle activity recruited Expiration can be become active also; with additional abdominal wall muscle activity

Question 420

What is the impact of chemoreceptors in the respiratory system?

Answer 420

Central (60% influence from PaCO2) and peripheral (40% influence from PaCO2) Stimulated by [H+] concentration and gas partial pressures in arterial blood Brainstem [primary influence is PaCO2] Carotids and aorta [PaCO2, PaO2 and pH] Significant interaction

Question 421

What are the central chemoreceptors

Answer 421

Located in brainstem Pontomedullary junction Not within the DRG/VRG complex Sensitive to PaCO2 of blood perfusing brain Blood brain barrier relatively impermeable to H+ and HCO3- PaCO2 preferentially diffuses into CSF

Question 422

Where are the peripheral chemoreceptors?

Answer 422

Carotid bodies Bifurcation of the common carotid (IX) cranial nerve afferents Aortic bodies Ascending aorta Vagal (X) nerve afferents

Question 423

What are the peripheral chemoreceptors?

Answer 423

Responsible for [all] ventilatory response to hypoxia (reduced PaO2) Generally not sensitive across normal PaO2 ranges When exposed to hypoxia, type I cells release stored neurotransmitters that stimulate the cuplike endings of the carotid sinus nerve Linear response to PaCO2 Interactions between responses [Poison (e.g. cyanide) and blood pressure responsive]

Question 424

What are the lung receptors and what do they do?

Answer 424

Stretch, J and irritant Afferents; vagus (X) Combination of slow and fast adapting receptors Assist with lung volumes and responses to noxious inhaled agents

Question 425

What are stretch lung receptors?

Answer 425

Smooth muscle of conducting airways Sense lung volume, slowly adapting

Question 426

What are irritant lung receptors?

Answer 426

Larger conducting airways Rapidly adapting [cough, gasp]

Question 427

J; juxtapulmonary capillary lung receptors

Answer 427

Pulmonary and bronchial C fibres

Question 428

Airway receptors in the nose, nasopharynx and larynx

Answer 428

Chemo and mechano receptors Some appear to sense and monitor flow Stimulation of these receptors appears to inhibit the central controller

Question 429

Airway receptors in the pharynx

Answer 429

Receptors that appear to be activated by swallowing respiratory activity stops during swallowing protecting against the risk of aspiration of food or liquid

Question 430

Describe muscle proprioceptors

Answer 430

Joint, tendon and muscle spindle receptors Intercostal muscles > > diaphragm Important roles in perception of breathing effort

Question 431

What happens in ascent

Answer 431

Ascending; PiO2 falls (FiO2 remains constant) Decreased PAO2 Decreased PaO2 Peripheral chemoreceptors fire (e.g carotid) Activates increased ventilation (VA) Increased PAO2 Increased PaO2

Question 432

CO2 elimination equation

Answer 432

PaCO2=kVco2/ VA

Question 433

How is CO2 carried

Question 434

Physiological causes of high CO2

Question 435

Causes of low PaO2

Answer 435

Alveolar hyperventilation Reduced PiO2

Question 436

PAO2 normal value

Answer 436

20KPa-6KPa/0.8= 20

Question 437

Resp failure blood gases

Answer 437

PaO2 <8KPa <60mmHg [10.5 - 13.5] PaCO2 >6.5KPa >49mmHg [4.7 – 6.5]

Question 438

Hypoxaemia

Answer 438

decrease in pp of oxygen in the blood

Question 439

What is Hypoxia

Answer 439

Reduced level of tissue oxygenation

Question 440

Respiratory failure type I

Answer 440

PaO2- Low (hypoxaemia) PaCO2- Low/Normal (hypocapnia/normal)

Answer 441

PaCO2- low (

Question 442

types of time course for resp failure

Answer 442

Acute, rapidly For example; opiate overdose, trauma, pulmonary embolism Chronic, over a period of time For example; COPD, fibrosing lung disease

Question 443

Resp failure type 1 mechanisms

Answer 443

Most pulmonary and cardiac causes produce type I failure Hypoxia Mismatching of ventilation and perfusion Shunting Diffusion impairment Alveolar hypoventilation Similar effects on tissues seen with; Anaemia, carbon monoxide poisoning, methaemoglobinaemia

Question 444

Treatments for resp failure type I

Answer 444

Airway patency Oxygen delivery Many differing systems Increasing FiO2 Primary cause (e.g. antibiotics for pneumonia

Question 445

common cause of both type 1 and type 2

Answer 445

COPD

Question 446

Respiratory failure; type II mechanisms

Answer 446

Lack of respiratory drive Excess workload Bellows failure

Question 447

clinical features of hypoxia

Answer 447

Central Cyanosis Oral cavity May not be obvious in anaemic patients Irritability Reduced intellectual function Reduced consciousness

Question 448

Clinical features of hypercapnia

Answer 448

Irritability Headache Papilloedema Warm skin Bounding pulse Confusion Somnolence Coma

Question 449

Respiratory failure type II treatments

Answer 449

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

Question 450

How to measure exhaled nitric oxide and what does it show?

Answer 450

Simple measure of nitric oxide in exhaled breath Simple machines able to do this Measured in ppb Generally increased in asthma Not “diagnostic” A reflection of eosinophilic airway inflammation High >50ppb, normal <25ppb

Question 451

Asthma and occupation

Answer 451

15% of asthma is due to occupation common causes High molecular allergens: latex, wood, animals and fish Low molecular allergens:Glutaraldehyde Isocyanates Paints Metal working fluids Metals

Question 452

What is the prevalence of asthma?

Answer 452

5-16% of people worldwide have asthma Wide variation between countries Increase in prevalence second half of the 20th century Now plateaued mostly US study; Poorer individuals, African-Americans Many studies identify a wide range of risk factors

Question 453

How is asthma affected by the environment?

Answer 453

Pollens, Infectious agents and microorganisms, Fungi, pets, air pollution All aggrivate/ cause asthma

Answer 454

silica, coal grain cotton cadmium

Question 455

What is hypersensitivity pneumonitis?

Answer 455

is an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled agents Acute, sub acute and chronic forms (fibrotic, non fibrotic) Immune complex related disease Antigen reacts with antibody Normally IgG response Very significant environmental influences; farmers lung, bird fanciers lung, metal working fluids

Question 456

CF genotype classification

Answer 456

Class I: no functional CFTR protein is made (e.g. G542X) Class II: CFTR protein is made but it is mis-folded (e.g. F508del) Class III: CFTR protein is formed into a channel but it does not open properly (e.g. G551D) Class IV: CFTR protein is formed into a channel but chloride ions do not cross the channel properly (e.g. R347P) Class V: CFTR protein is not made in sufficient quantities (e.g. A455E) Class VI: CFTR protein with decreased cell surface stability (e.g. 120del123) More than 2000 CF - causing CFTR mutations have been found Most common of which is F508del [a class II mutation found in up to 80% to 90% of patients]

Question 457

CF prevention management

Answer 457

Segregation Surveillance – frequent review minimum every 3 months Airway clearance – physio & exercise Nutrition – pancreatic enzymes, diet high calorie & fat, supplements including vitamins, percutaneous feeding Psychosocial support

Question 458

CF prevention drugs

Answer 458

Suppression of chronic infections – antibiotic nebulisation Bronchodilation – salbutamol nebulisation Anti inflammatory – azithromycin, corticosteroids Diabetes – insulin treatment Vaccinations – influenza, pneumococcal, SARS CoV 2

Question 459

Describe CF rescue antibiotics

Answer 459

2 week course IV antibiotics Home vs hospital Issues with frequent antibiotics Allergies Renal impairment Resistance Access problems If antibiotics are needed frequently then a port can be put in

Question 460

Genotype directed therapies for cystic fibrosis

Answer 460

Small-molecule agents facilitate defective CFTR processing or function Ivacaftor in G551D (6%) and other specific mutations Improved lung function (FEV1), BMI, QoL Orkambi in F508del – only licensed for compassionate use in UK Mixed outcomes Gene therapy – further research needed as significant problems with delivery

Question 461

How does Ivacaftor (Kalydeco) work?

Answer 461

CFTR potentiator - potentiates chloride secretion via increased CFTR channel opening time Class III mutations

Question 462

How does lumacaftor (Orkambi) work?

Answer 462

Lumacaftor is a CFTR corrector - corrects cellular misprocessing of CFTR (e.g. folding) to facilitate transport from the endoplasmic reticulum Class II mutation - F508del/F508del

Question 463

Describe some challenges with treating CF

Answer 463

- Adherence to treatment - High treatment burden - High cost of certain treatments - Allergies/intolerances to treatment - Different infectious organisms and their resistance to drugs

Question 464

Describe Alpha-1 antitrypsin deficiency (AATD)

Answer 464

Autosomal recessive genetic disorder 80 different mutations of SERPINEA1 gene on chromosome 14 Serum antiprotease M phenotype normal and healthy S and Z phenotypes major disease associations Leads to: Early onset emphysema and bronchiectasis Unopposed action of neutrophil elastase in the lung

Question 465

Autonomic nervous system

Answer 465

The peripheral autonomic nervous system divides into sympathetic and parasympathetic branches, which typically have opposing effects The autonomic nervous system conveys all outputs from the CNS to the body, except for skeletal muscular control Two nerves in series, the pre- and post-ganglionic fibres The parasympathetic ganglia are near their targets with short post-ganglionic nerves, whereas the sympathetic ganglia are near the spinal cord with longer post-ganglionic fibres

Question 467

Parasympathetic bronchoconstriction

Answer 467

Vagus nerve neurons terminate in the parasympathetic ganglia in the airway wall Short post-synaptic nerve fibres reach the muscle and release acetylcholine (ACh), which acts on muscarinic receptors of the M3 subtype on the muscle cells This stimulates airway smooth muscle constriction

Question 468

Anti muscularinics

Answer 468

Ipratropium bromide (Atrovent) can be used as inhaled treatment to relax airways in asthma and COPD, but is a short acting antimuscarinic (SAMA) SAMA less widely used since long acting muscarinic antagonists (LAMAs) were developed Ipratropium is still used in high dose in nebulisers as part of acute management of severe asthma and COPD

Question 469

LAMAs

Answer 469

Have long duration of action (many hours), often given once daily (tiotropium) Increase bronchodilatation and relieve breathlessness in asthma and COPD Seem to reduce acute attacks (exacerbations) as well Have other benefits, e.g. on parasympathetic regulation of mucus production

Question 470

Sympathetic regulation of the bronchi

Answer 470

Sympathetic NS Regulates the fight-and-flight response Nerve fibres release noradrenaline which activates adrenergic receptors, of which there are two main types (alpha/beta) Nerve fibres in humans mainly innervate the blood vessels, but airway smooth muscle cells have adrenergic receptors (beta) Activation of beta2 receptors on the airway smooth muscle causes muscle relaxation (by activating adenylate cyclase, raising cyclic AMP)

Question 471

What are SABAs and LABAs?

Answer 471

Short-acting (salbutamol) and long-acting (formoterol, salmeterol) beta2 agonists are valuable drugs Given with steroids in asthma, often without steroids in COPD Often given with LAMA in COPD Acute rescue of bronchoconstriction Prevention of bronchoconstriction Reduction in rates of exacerbations

Question 472

Mechanism of action of Beta 2-agonists

Answer 472

Stimulation of β2 adenoreceptors results in activation of adenylate cyclase, increased intracellular cAMP and subsequent airway smooth muscle relaxation

Question 473

Adverse effects of beta2 agonists

Question 474

Describe type I hypersensitivity

Answer 474

Mediators-> IgE antibodies Timing-> immediate (within 1 hour) Examples-> anaphylaxis and hayfever Antigen interacts with IgE bound to mast cells or basophils Degranulation of mediators lead to local effects Histamine the predominant mediator

Question 475

Describe type II hypersensitivity

Answer 475

Mediators-> Cytotoxic antibodies bound to cell antigen Timing-> Hours to days Examples-> Transfusion reactions Goodpastures (Anti GBM disease) Antibodies reacting with antigenic determinants on the host cell membrane Usually IgG or IgM Outcome depends on whether complement is activated and if metabolism of cell is affected

Question 476

Describe type III hypersensitivity

Answer 476

Mediators-> Deposition of immune complexes Timing-> Typically 7-21 days Examples-> Hypersensitivity pneumonitis; lupus; post streptococcal Glomerulonephritis Antigen-immunoglobulin complexes are formed on exposure to the allergen These are deposited in tissues and cause local activation of complement and neutrophil attraction

Question 477

Describe type IV hypersensitivity

Answer 477

Mediators-> T-cells (lymphocytes) Timing-> Days to weeks or months Examples-> Tuberculosis; Stevens-Johnson syndrome T-cell mediated, releasing IL2, IFᵧ and other cytokines Requires primary sensitisation Secondary reaction takes 2-3 days to develop May result from normal immune reaction – if macrophages cannot destroy pathogen, they become giant cells and form granuloma

Question 478

Medical history

Answer 478

Age, Gender, Occupation Presenting complaint History of presenting complaint Previous medical condition Drug history and allergies Social history- hobbies Family history+ extended family history Review of systems

Question 479

Respiratory rate

Answer 479

Ususally 10-12 per minute

Question 480

Units of pressure

Answer 480

1 bar -1000 millibars 760 mmHg / torr 1 atmosphere absolute (ATA) 10 metres of sea water (msw) 33.08 feet of sea water (fsw) 101.3 kilopascals (kPa) 14psi

Question 481

What is Boyle's law and what are its applications?

Answer 481

At a constant temperature the absolute pressure of a fixed mass of gas is inversely proportional to its volume P1V1=P2V2 Applications barotrauma arterial gas embolism gas supplies

Question 482

What is the diving reflex?

Answer 482

When cold water is splashed on someone's face then they might have apnoea bradycardia peripheral vasoconstriction

Question 483

What is Dalton's law?

Answer 483

Total pressure exerted by a mixture of gases is equal to the sum of the pressures that would be exerted by each of the gases if it alone were present and occupied the total volume

Question 484

What are the effects of Dalton's law at sea level and at 10 msw?

Answer 484

At sea level; partial pressure N2 = 0.78 ata, O2 = 0.209 ata At 10 msw; partial pressure N2 = 1.56 ata, O2 = 0.418 ata [Breathing air at 10 msw same PaO2 as breathing 42% O2 at sea level]

Question 485

What is the Lorrain Smith Effect (pulmonary oxygen toxicity)?

Answer 485

PiO2 > 0.5 ATA 100% oxygen -> symptoms in 12 - 24 hours Cough, chest tightness, chest pain, shortness of breath Also a problem with ITU patients Relief with PiO2 < 0.5 ATA Unit of Pulmonary Toxic Dose (UPTD) can be calculated Forced Vital Capacity (FVC) can be useful to monitor

Question 486

Describe CNS Oxygen toxicity

Answer 486

V - Vision (tunnel vision etc) E - Ears (tinnitus) N - Nausea T - Twitching (extremities or facial muscles) I - Irritability D - Dizziness common final (and often the first) sign will be a convulsion ConVENTID

Question 487

What is inert gas narcosis?

Answer 487

Commonest is nitrogen narcosis worsens with increasing pressure first noticed between 30-40 msw Increased PiN2 individual variation influencing factors- cold, anxiety, fatigue, drugs, alcohol and some medications Narcotic potential related to lipid solubility

Question 488

What are the signs and symptoms of inert gas narcosis?

Answer 488

10-30m. - Mild impairment of performance 30-50m. - Over confidence, sense of well being 50-70m - Sleepiness, confusion, dizziness 70-90m. - Loss of memory, stupefaction 90+ - Unconsciousness, death Note: death may occur at much shallower depths

Question 489

What is decompression illness?

Answer 489

N2 poorly soluble Ascent  fall in pressure  fall in solubilty  gas bubbles Type I Cutaneous only Type II Neurologic O2, supportive treatments and urgent recompression

Question 490

Describe arterial gas air embolism

Answer 490

Gas enters circulation via torn pulmonary veins Small transpulmonary pressures can lead to AGE Normally occur within 15 minutes of surfacing Urgent recompression

Question 491

What is pulmonary barotrauma?

Answer 491

Air leaks from burst alveoli: Pneumothorax Pneumomediastinum Subcutaneous emphysema

Question 492

Alveolar gas equation

Answer 492

PAO2 = PiO2 – PaCO2/R** * One version, not taking into account pH2O **R=respiratory quotient, = CO2 produced / O2 consumed A=Alveolar, a=arterial R = 0.8 with a normal diet R approx = 1 with primarily carbohydrate diet R closer to 0.7 with fat rich diets

Question 493

Normal barometric pressure at different altitudes

Answer 493

Barometric pressure Altitude (m) 101 (760) 0 57 (429) 4800 46 (347) see slide 12

Question 494

What is the equation for alveolar arterial O2 difference?

Answer 494

Alveolar Arterial O2 difference Whilst normal pretty complete equilibration of O2, there normally is a small difference between Alveolar and arterial oxygen partial pressure = PAO2 – PaO2 = (approx) 1KPa

Question 495

Normal blood gases

Answer 495

PaO2 10.5 - 13.5 KPa PaCO2 4.5 - 6.0 KPa pH 7.36 - 7.44

Question 496

Describe right shift of the oxygen dissociation curve

Answer 496

Shifts to the right bc you want to deliver the oxygen to the tissues that are metabolically active causes Acidity 2,3 DPG* Increased temperature Increased PCO2 [*2,3 biphosphoglycerate]

Question 497

WHat happens to FiO2 and PiO2 as you ascend?

Answer 497

FiO2 remains constant at approx 0.21 PiO2 falls with altitude

Question 498

Describe the response of the lungs at altitude

Answer 498

Hypoxia leads to.. Hyperventilation at 10000ft altitude Increases minute ventilation Lowers PaCO2 Alkalosis initially Tachycardia Adaptive changes Multiple Alkalosis compensated by renal bicarbonate excretion

Question 499

What is acute mountain sickness?

Answer 499

Recent ascent to over 2500m Lake Louise score  3 Must have a headache and one other symptom

Question 500

What are the risk factors for acute mountain sickness?

Answer 500

Recent travel to over 2500m, after a few hours Sea level normal dwelling Altitude, rate of ascent and previous history of AMS Younger people Descend; the only reliable treatment [o2, recompress, acetazolamide] You should never go up higher if you have AMS

Question 501

What increases risk of high altitude pulmonary oedema?

Answer 501

Unacclimatised individuals Cough, shortness of breath Rapid ascent above 8000ft (2438m) 2-5 days

Question 502

What decre

Answer 502

Risk less if sleeping below 6000ft (1829m) Speed of ascent slower (300-350m/day) Individual susceptibility Exercise Respiratory Tract Infection Incidence 2% at 4000m

Question 503

What are the treatments of pulmonary oedema

Answer 503

O2 Decent urgent Gamow bag Steroids Ca2+ blockers? Sildenafil

Question 504

What are the main features of High Altitude Cerebral Oedema?

Answer 504

Serious AMS not a pre requisite Confusion Behaviour change

Question 505

Treatment for high altitude cerebral oedema?

Answer 505

Immediate descent Symptoms may resolve relatively quickly Gamow bag

Question 506

What to do at different sea level SaO2s

Answer 506

Patients need physiological assessment if they have low O2 levels at sea level

Question 507

Stages of lung development

Answer 507

Embryonic 0-5 weeks Pseudoglandular 5-17 weeks Cannalicular 16-25 weeks Alveolar 25 weeks- term

Question 508

Embryonic

Question 509

Describe the pseudoglandular phase of lung development

Answer 509

5-17 weeks Exocrine gland only Major structural units formed. Angiogenesis Mucous Glands Cartilage Smooth Muscle Cilia Lung fluid

Question 510

Describe canalicular phase

Answer 510

16-25 weeks. Distal Architecture Vascularisation i.e formation of capillary bed Respiratory bronchioles. Alveolar ducts.  Terminal sacs

Question 511

Describe alveolarisation from 25 weeks to birth

Answer 511

Alveolar sacs Type 1 and Type 2 cells Alveoli simple with thick interstitium

Question 512

Describe alveolarisation from birth to 3-5 years

Answer 512

Thinning of alveolar membrane and interstitium ↑ complexity of alveoli

Question 513

5-17

Answer 513

Major airways defined Nests of angiogenesis Smaller airways down to respiratory bronchioles

Question 514

16-25

Answer 514

Terminal bronchioles Capillary Beds Alveolar ducts

Question 515

25-40 weeks

Answer 515

Alveolar budding, thinning and complexification

Question 516

What goes wrong in the embryonic phase

Answer 516

Laryngeal, Tracheal and oesophageal atresia,tracheal and bronchial stenosis,pulmonary agenesis

Question 517

What goes wrong in the pseudoglandular phase

Answer 517

Bronchopulmonary sequestration,cystic adenomatoid malformations, alveolar-capillary dysplasia,

Question 518

Things that go wrong in the alveolar phase

Answer 518

Acinar Dysplasia, alveolar capillary dysplasia, Pulmonary hyoplasia

Question 519

What are the types of cystic adenomatoid malformations?

Answer 519

Type 0- Trachebronchial Type 1- Bronchial Type 2- Bronchiolar Type 3- Alveolar duct Type 4- Distal acinar

Question 520

Systemic blood vessles

Answer 520

Purpose: deliver oxygen to hypoxic tissues Hypoxia/acidosis/CO2 is vasodilator Oxygen is vasoconstrictor

Question 521

Pulmonary blood vessles

Answer 521

Purpose: pick up oxygen from oxygenated lung Oxygen is vasodilator Hypoxia/acidosis is vasoconstrictor

Question 522

Describe the important parts of fetal circulation

Answer 522

Lung is not useful organ to fetus PaO2 = 3.2 kPa (31,000 feet) Shunting of blood Right Left via ductus arteriosus High Pulm Vasc Resistance (hypoxia) Tissue resistance (fluid filled) Low systemic resistance (placenta)

Question 523

What is in fetal lungs and why?

Answer 523

Fetal airways are distended with fluid Fluid aids in lung development Actively secreted by lungs

Question 524

Describe the ductus arteriosus

Answer 524

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)

Question 525

What is the ductus venosus?

Answer 525

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

Question 526

Describe the foramen ovale

Answer 526

The foramen ovale is a passage between the two atria, which is responsible for bypassing the majority of the circulation

Question 527

What happens to the ductus arteriosus immediately after birth

Question 528

Describe the ductus venosus after birth

Question 529

WHat happens in the lungs at birth

Answer 529

Fluid squeezed out of lungs by birth process Adrenaline stress leads to increased surfactant release. Gas inhaled

Question 530

What happens in the blood vessels at birth

Answer 530

Oxygen vasodilates pulmonary arteries Pulmonary vascular resistance falls Right atrial pressure falls, closing foramen ovale Umbilical arteries constrict Ductus arteriosus constricts

Answer 531

Switch as left side becomes higher pressure than

Question 532

Different types of surfactant

Answer 532

Surface active phospholipid Phosphatidyl choline Phosphatidyl glycerol Phosphatidyl inositol Surfactant proteins A, B, C, D

Question 533

When is surfactant produced and what does it do?

Answer 533

Virtual abolition of surface tension Allows homogeneous aeration Allows maintenance of functional residual capacity Produced by Type 2 Pneumocytes from 34 weeks gestation Dramatic increase in 2 weeks prior to birth

Question 534

What causes a surfactant deficiency?

Answer 534

Prematurity + Asphyxia + Cold + Stress + Twins Respiratory Distress Syndrome Loss of lung volume Non-compliant lungs Uneven aeration

Question 535

How to treat surfactant deficiency?

Answer 535

Distension of alveoli Steroids Adrenaline

Question 536

What is Pulmonary Interstitial Emphysema?

Answer 536

Lung cysts rupture and let air out of the ruptured alveoli into the interstitium between the alveoli and capillary

Question 537

Management of pulmonary interstitial emphysema

Answer 537

Warmth Surfactant replacement (if intubated) Oxygen and fluids Continuous Positive Airway Pressure (maintain lung volumes, reduce work of breathing) Positive pressure ventilation if needed