Cardiovascular and Respiratory

Question 1

Descibe the layers of the heart.

Answer 1

Epicardium- Outermost layer, formed by visceral layer of pericardium, contains pericardial fluid, lined by simple squamous cells, fat and connective tissue
Myocardium- Middle layer, cardiac muscle, involuntary and striated (blockage of coronary artery can lead to mi)
Subendocardium- layer between, loose connective tissue, contains purkinje fibres
Endocardium- innermost layer, lines cavities and valves of heart, loose connective tissue and simple squamous, regulates contraction. (endocarditis- inflamation of this layer, can cause heart murmers)

Question 2

Describe the branches of the aortic arc

Answer 2

Brachiocephalic trunk> right subclavian and right common carotid
Left common carotid
Left subclavian artery

Question 3

Describe the cellular anatomy and function of the cardiac muscle and nodal cells

Answer 3

Cardiac muscle
- rectangular shape, single nucleus, striated, communicate via intercelated discs
- present in myocardium
Nodal cells
There are 2 notable nodal cells within the heart- The sinoatrial node is a group of cells located in the right atrial wall which have the ability to spontaneously depolarise (pace maker cells). The atrioventricular node is located in the interatrial wall.
An excitation signal (an action potential) is created by the sinoatrial (SA) node.
The wave of excitation spreads across the atria, causing them to contract.
Upon reaching the atrioventricular (AV) node, the signal is delayed.
It is then conducted into the bundle of His, down the interventricular septum.
The bundle of His and the Purkinje fibres spread the wave impulses along the ventricles, causing them to contract.

Question 4

Explain excitation- contraction coupling

Answer 4

Mechanism which links activation of call and contraction of cell:

• membrane depolarisation, receptor operated ion channels, activation of second messenger systems, result in cellular contraction due to an increase in intracellular calcium levels.
• Calcium increases and binds to CAM receptor, this activates MLCK which phosphorylates myosin using an ATP molecule allowing myosin and actin to interact.

Question 5

Explain the autonomic innervation of the heart: Sympathetic

Answer 5

Fibres exit the medulla and decend the spinal cord and synapse with short pre-ganglionic neurons that then synapse onto sympathetic ganglia. post-ganglionic cells then synapse onto target cells in the heart. Increase the rate of depolarisation. Noraepinephrine.

Question 6

Explain the autonomic innervation of the heart: Parasympathetic.

Answer 6

Parasympathetic innervation occurs via the vagus nerve which leaves the brainstem via the medulla as a long preganglionic efferent fibres. Synapse with short postganglionic fibres in tissue. Uses ACh as a neurotransmitter.

Question 7

Define Inotropy

Answer 7

Changes in force of muscle contractions.

Question 8

Define Lusitropy

Answer 8

Relaxation of the heart muscles and chambers

Question 9

Define Chronotropy

Answer 9

Rate of muscular contraction.

Question 10

Explain the role of baroreceptors and chemoreceptors in cardiac function.

Answer 10

Baroreceptors: located in the aortic arc and carotid sinuses. Provide information to the NTS regarding blood pressure so that autonomic innervation can be altered
Chemoreceptors: Peripheral: carotid bodies and aorta, Central: medullary neurons, provide information on PO2 (fall= hypoxemia) and PCO2 (rise= hypercapnia)
- leads to enhanced sympathetic outflow.

Question 11

Define Starlings law of the heart and the anrep effect.

Answer 11

Starling’s law on the heart states that increased pressure leads to reduced flow. The anrep effect is when an increase in afterload of the heart leads to and increase in ventricular intropy.

Question 12

Discuss the relationship between ventricular volume and pressure generation.

Answer 12

Increased ventricular volume leads to stretch on the cardiac muscle in the walls of the heart. This stretch generates force which leads to an increase in pressure for systole.

Question 13

Describe the effects of increased arterial pressure on cardiac function

Answer 13

An increase in resistance leads to the muscles of the heart to work harder. This leads to an increase in the thickness of the muscular wall of the heart and a reduced ventricular volume as a result. This eventually leads to a decrease in cardiac output: breathlessness, fatigue.

Question 14

Describe the anatomy of the blood and how this can be altered in blood disorders

Answer 14

Blood is a connective tissue which circulates the body. Its contents can be split categorically into white blood cells (the immune cells of the body), red blood cells, platelets and plasma (liquid part of blood). Imbalances and disorders in these cells can lead to a variety of different diseases.

Question 15

Explain blood typing and the importance of cross matching.

Answer 15

Blood cells contain antigens on the surface of their membranes. Individuals may express A antigens, B antigens, both (AB) or O (no antigens). Blood cells also either have a rhesus antigen and are therefor labeled + or - dependent on its presence. It is important that when giving indivudals a blood transfusion their blood is crossmatched to the donors blood. If the donors blood pocesses antigens which are not present in the recipients blood it can result in a rapid immune response which can be fatal.

Question 16

Explain a companant of blood which can be altered in a disorder.

Answer 16

Sickle Cell aneamia

• autosomal recessive mutation on chromosome 11.
• Results in disfunction of haemoglobin, low iron levels
• cells appear shriveled and stiff, can lead to clotting
• can’t carry oxygen well
• Easy fatigue

Question 17

List the causes, symptoms, treatment and prognosis of sickle cell aneamia

Answer 17

Symptoms
- clotting of blood
- poor circulation
- fatigue
Treatment
- antibiotics, blood transfusion,
- bone marrow transplant
- gene therapy
Prognosis
- Many people living with disease now living past 50 due to advances in medical care and treatment.

Question 18

Describe the stages of blood clotting.

Answer 18

Vasoconstriction
- Mediated by contraction of vascular smooth muscle, reduced flow results in less blood loss, immediate sympathetic reflex. More vasoconstrictors are released due to platelet activation
Formation of Platelet Plug
- Damage to the endothelial cells that line blood vessels exposes collagen. Platelets adhere to collagen and aggregate at the sites of damage. Enhanced by platelet activation factor.
Coagulation
- clot is formed

Question 19

Explain the molecular mechanisms that underlie these stages and explain why this is important.

Answer 19

Platelets contain alpha and dense granules enclosed in a membrane with several glycoprotein receptors (Ib, Ia, IIb, IIIa)
Platelet aggregation is suppressed by non-thrombogenic surface of endothelium (produces prostacylin and nitric oxide)
Von Willebrand factor is a large glycoprotein produced by endothelial cells at a site of injury. Binds to collagen and causes platelet activation.
Activation of platelets leads to the release of granular contents (ADP and phospholipids) which promote further aggregation,
Serotonin and thromboxine released which promote vasoconstriction.
ADP leads to the association of glycoproteins which bind to fibrinigoen to form active complexes.
Enzyme cascade is formed with extrinsic and intrinsic pathways which converts fibrinogen into fibrin by the enzyme thrombin.
(All clotting factors exist in inactive zymogens which are activated by proteolysis)
Thrombin is part of a negative feedback pathway (anti-thrombin)

Question 20

Describe nodal and non- nodal cardiac action potentials.

Answer 20

Nodal
- sometimes referred to as a slow response
- undergo spontaneous depolarisation
- depolarisation phase is slower and have shorter action potential
- 3 phases: Depolarisation (increased calcium and decreased K conductancies), Repolarisation (increased K and decreased Ca conductancy), Spontaneous depolarisation (‘funny’ currents through slow Na+ channels, increase calcium and decrease K+ conductancy)
- Calcium channel blockers often used to treat high heart rate.
Non- Nodal
- Fast response APs
- atrial and ventricular myocytes, Purkinje system in ventricles
- 5 phases: 0-4, Rapid depolarisation (Increased Na+ and decreased K+),
Initial repolarisation (decreased Na+ and increased K+), Plateu phase (Increased calcium conductancy), Repolarisation (K+ increase, Ca+ decrease), Resting Potential (K+ increase, decreased Na+ and Ca+)
- antiiarythmic drugs often target the ion channels to stabilise contraction rate.

Question 21

Explain the main ion channels involved in cardiac action potentials

Answer 21

Sodium, Calcium and potassium voltage gated channels.
Influx of sodium in depolarisation stage causes calcium channels to open, membrane voltage changes and moves more towards the equilibrium potential of K+. Ca and Na+ channels close and K+ opens returning to the resting state.

Question 22

Define autoregulation within the heart.

Answer 22

Autoregulation refers to the intrinsic regulation of blood flow despite changes in perfusion pressures. For example when blood flow is reduced to an organ it drops for a breif amount of time and then returns to resting state.

Question 23

List the differences between myogenic and metabolic theories of autoregulation.

Answer 23

There are different theories of autoregulation.
Myogenic
- Intrinsic to smooth muscle action
- reactive hyperaemia- when blood flow is inadequate there is an increase in contraction and vasodilation.
Metabolic
- blood flow linked to the metabolic activity of cells, increase in muscle contraction leads to increased flow (reactive hyperaemia), actively metabolising cells thought to release vasoactive substances which cause dilation. Hypoxia- causes vasodilation (not in pulmonary circulation). Tissue metabolites and ions:Adenosine: formation increases during hypoxia, important in regulating coronory blood flow.

Question 24

Describe the experiments demonstrating autoregulation.

Answer 24

• Cutting blood flow to an area can demonstrate myogenic response- vasodilation occurs to deliver more blood.
• Aletering the metabolic activity of a tissue via stimulation and recording changes in pressure, flow etc…

Question 25

Describe the functional and anatomical specialisations of coronary and cerebral vascular beds.

Answer 25

Coronary vascular beds have a large capillary density and endothelial area to reduce diffusion distance.
Cerebral beds have a high density and low diffusion difference. Circular system (circle of willus) which allows for continue of flow despite blockage of one carotid artery.

Question 26

Explain the transport of O2 in the blood and influencing factors.

Answer 26

O2 can be transported attatched to heamoglobin and dissolved in plasma.
- The amount of O2 dissolved in the blood is proportional to the partial pressure of the gas (Henry’s law). It can be calculated via the calculation: solubility constant (0.03 at body temp.) x PO2.
- Most O2 is transported connected to haemoglobin. 4 s.u., polypeptide, haem group, 2a and 2B. O2 in molecular form binds usely to O2.
- O2 saturation is the ratio of bound O2 in relation to what can be bound.
- Things that can shift the affinity curve: L- high affinity, R- low affinity: decrease in temp= L, increase in pH=L, decrease in DPG= L. vice versa.
Bohr Effect- Elevated PO2 shifts to R, H+ binds to Hb decreasing its affinity.
- Myoglobin found in muscle: binds to 1 O2, high affinity curve.

Question 27

Explain the transport of CO2 in the blood and influencing factors

Answer 27

CO2 can travel as a bicarbonate, carbamino acids or dissolved in the blood

• Carbamino compounds: combination of CO2 with a terminal amine groups, can only readily bind to lysine and arginine in RBCs.
• CO2 dissolves spontaneously in water to form bicarbonate (slowly in plasma- more likely to occur in RBCs). RBCs contain the enzyme carbonic anhydrase which catalyses the reaction.

Question 28

Compare the pattern of breathing at rest/ at high intensity exercise.

Answer 28

Inspiration is active at rest utilizing the diaphragm (phrenic nerve), and experation is passive at rest ocurring due to elastic recoil and changes in pressure. At high intensity exercise both insperation and experation is active utilising the intercostal muscles, chest muscles and the diaphragm working to force air in and out of the lungs.

Question 29

Describe the functional anatomy of the respiratory system.

Answer 29

The functional aspect of the respiratory system can be split anatomically into the conducting zone which consists of the nose, pharynx, larynx, trachea, bronchi, bronchioles and terminal bronchioles (goblet cells- mucus, ciliated cells), and the respiratory zone which contains the respiratory bronchioles, alveoli etc…

Question 30

Describe the role of alveolar, intrapleural, transpulmonary and translung pressures in the mechanics of breathing.

Answer 30

Alveolar pressure begins at 0, expansion of the thorax causes the pleural pressure to become negative. This causes the pilmonary pressure to increase and the lungs to expand accordingly. Alveolar pressure becomes negative resulting in inspiration of air.
The pleural and transpulomonary pressure return to normal and elastic recoil takes place. The alveolar pressure increases and becomes greater than the atmospheric pressure expelling the air from the lungs.

Question 31

Describe the ventilation- perfusion mismatch.

Answer 31

V= the exchange of air between the lungs and the environment
Q= perfusion (passage of blood through lungs)
V/Q= the amount of air that reaches the alveoli divided by the amount of blood that flows through the capillaries

Question 32

Describe normal partial pressures in terms of V/Q matching.

Answer 32

V/Q is normally ~0.8.
Inspired air has a PO2 150mmHg.
- contents of lung and alveoli have a pressure of around PO2=100, PCO2=40. The partial pressures of venous blood are PO2= 40, PCO2=45 and arterial blood are PO2=100, PCO2= 40.

Mismatch occurs when anything occurs which changes the perfusion of the lungs

Question 33

Describe different mismatches of V/Q

Answer 33

Ventilation obstruction:
alveoli: No CO2 is expelled so the CO2 in the lung increases and O2 decreases, arterial blood is equal to venous blood
Perfusion Obstruction:
Abstruction of venous blood leads to an abundance of O2 in lungs but no experation. drop in CO2 content in lungs and no gradient generation for O2 uptake.

Question 34

Describe ventilatory reflexes which assist the control of respiratory rhythms.

Answer 34

Mechanoreceptors in muscles involved in respiration signal to the NTS on the degree of lung expansion. Can send motor impulses to the diaphragm.
Chemoreceptors in brain and periphery detect changes in pH which increase respiratory rate to increase O2 when required.
The Hering-Breuer reflex is initiated by lung expansion, which excites stretch receptors in the airways. Stimulation of these receptors, which send signals to the medulla by the vagus nerve, shortens inspiratory times as tidal volume (the volume of air inspired) increases, accelerating the frequency of breathing.

Question 35

Describe current research into cardiovascular disease.

Answer 35

Zebra Fish

• Capable of regeneration of heart tissue following damage
• formation of a clot and the presence of erythrocytes, followed by the formation of a fibrin network. At day 9 the cardiomyocytes entered the tissue and contributed to regeneration.
• proliferation rather than hypertrophy

Question 36

Describe the anatomy of valve murmers, the componants involved and the possible treatments.

Answer 36

Occurs due to leakage in the valves of the heart (the tricuspid valve:right atrium and right ventricles, the bicuspid/ mitral valve: left ventricle and atrium, the aortic valve: left ventricle from the aorta, and the pulmonary valve: right ventricle from the pulmonary artery).
Symptoms include light headedness, shortness of breath, cyanosis, episodes of tachycardia and chest pain.
Can be congenital or developed. Infections such as endocarditis can cause valve murmers.
Stenosis, where blood flows back through narrowed or stiff valves within the heart.
Regurgitation where blood leaks through valves which do not close tightly enough.
Pulmonary regurgitation which is a rare condition, the cause is usually pulmonary hypertension (narrowing of pulmonary blood vessels causing increased blood pressure.
Mitral prolapse which involves an abnormality in the closing of the mitral valve.
Treatments involve medications for blood pressure (calcium channel blockers and ACE inhibitors), heart arrythmia and blood thinners. If symptoms persist there are surgical options.

Question 37

Explain the anatomy and physiology of the lungs.

Answer 37

2x lungs
Right is larger (left is above the heart and therefor smaller)
R- contains 3 lobes (superior, inferior and oblique) and 2 fissures seperating them (oblique and horizontal fissure)
L- contains 2 lobes (superior and inferior) seperated by the oblique fissure.

Question 38

Describe common adult and pediatric respiratory conditions.

Answer 38

Pediatric- respiratory distress syndrome in premature babies. Premature babies have an insufficient level of Type 2 surfactant producing simple squamous epithelium. Therefor therefor the surface tension is high leading to difficulty in breathing. Newborns are often put on asperators to force air into the lungs and can cause lung scarring.
COPD is a common adult condition of the lungs. Caused by an accumulation of scar tissue associated with insperation of harmful chemicals (smokers). Scar tissue inhibits the movement of lungs and limits the air intake. Leads to difficulties in breathing. Diseases can be life threatening. Treated with steroids.

Question 39

Discuss current lung function investigations and how they may benifit diagnosis and treatment.

Answer 39

Testing lungs ability to empty and fill (spirometry). Testing perfusion capacity (carbon monoxide inhaled and then the blood is tested to see how much carbon monoxide is taken into the blood stream.

Question 40

Discuss the effects of high altitude on the cardiovascular system, respiratory system and metabolism

Answer 40

High altitude induces hypoxia. It directly effects vascular tone of pulmonary and systemic resistance vessels. Chemoreceptor mediated response. Sympathetic activation- increased heart rate, increased cardiac output, myocardial contraction velocity increase and increase of BP. Causes systemic vasodilation but pulmonary constriction to improve ventilation perfusion matches but results in pulmonary hypertension.

Question 41

Discuss the adaptations of high altitude living.

Answer 41

Individuals who live at high altitudes tend to have an increase of cardiac tone which allows for sustained high HR over a lifetime. They have also been shown to have a higher concentration hemoglobin allowing for sufficient oxygen binding.

Question 42

Describe the health risks of exposure to high altitude.

Answer 42

Altitude sickness

• normally after reaching altitudes of more than 3000 metres.
• symptoms include nausea, vomitting, dizziness, difficulty breathing, loss of apetite
• Cerebral and pulmonary edema can occur: capillary leakage, fluid on brain (intracranial pressure increase) and fluid on lungs (pressure on lungs and difficulty breathing). Can be fatal. Believed to be down to neurohumoral and hemodynamic responses elicited by continues hypoxia. This occurs quicker in fast ascents (less time to aclimatise.

Question 43

Explain the sequential development of the foetal heart.

Answer 43

Ectoderm- blood vessels, Mesoderm- lateral plate> splanchnic. wall of heart, blood vessels

• Heart beat begins at 21 days
• development begin days 18/19
• cardiogenic area of mesoderm, elongated cords develop known as cardiogenic cords
• They become hollow (endocardial tubes)
• Day 21- lateral folding occurs joing tubes together
• By day 22 primitive areas of the heart are established: Truncus arteriosus, bulbis cordis, ventricle, atrium, sinus venosis.
• blood flows from sinus venosis
• The bulbus cordis and ventricle grow more rapidly and the heart bends- atrium and sinus venosis appear superior to the truncus arteriosis.
• The sinus venosis goes on to form part of the right atrium, coronary sinus and SA node
• Bulbis cordis goes on to form the R ventricles
• Truncus arteriosis- forms ascending aorta and pulmonary trunk.
• Endocardial cushions form day 28, intratrial septim grows towards endocardial cushions, formation of the interventricular septum, partitioning complete by wk 5.

Question 44

Describe foetal circulation and highlight how it is different from adult circulation

Answer 44

In feotal circulation blood is shunted between atria as oxygen is recieved via maternal circulation.
Septum primum- d33, foreman primum R-L, Prior to foreman primum closure- foreman secundum forms between d38-40. Foreman ovale develops and shunts blood with ductus arteriosis until the decrease of pressure at birth which causes it to close (fossa ovale)

Question 45

Discuss congenital heart defects.

Answer 45

Congenital heart defects make up a large portion of fatal defects in neonates.

• Heart murmers,
• failure of closure of the foreman ovale

Question 46

Discuss sequential development of and functions of the respiratory system.

Answer 46

Develop from endoderm (lining of glands) and mesoderm (walls of tract) during wk 4

• Begins as respiratory diverticulum which is an expansion from the foregut.
• Distal portion becomes tracheal bud which diverges into bronchial buds and become bronchioles. By wk 24 there are 17 orders of branches.
• Pleural sacks develop from the mesoderm.
• wk 16-26 involve the development of respiratory areas. Infants born at the end of this stage have a chance of survival.
• After wk 26 T1 and T2 cells are properly developed.
• By wk 20 there is surfactant but it is not yet sufficient to facilitate breathing

Question 47

Discuss the changes observed in circulation following birth.

Answer 47

Following birth-
Umbillical arteries and veins constrict and become fibrosed, proximal ambillical arteries become superior vessical arteries to urinary bladder, distal umbillical arteries become medial umbillical ligaments, Umbillical vein becomes ligamentum teres, ductus venosis becomes ligamentum venosum, foreman ovale, fossa ovalis, ductus arteriosis become ligamentum arteriosum.