Week #5 Flashcards

Question

What are the movements of respiration and which muscles contribute

Answer 1

* Diaphragm is the main muscle of respiration and contracts the thorax vertically to expand it * Intercostal muscles also contribute * Elevation of the upper ribs (ribs 1-7) changes AP dimension of the thorax—i.e. the ribs are connected to the thorax and pulling ribs upward will expand in that direction as the ribs are not horizontal-pump hundle movements * Lower ribs don’t articulate with the sternum so when they are elevated the middle of the shafts move laterally and expand the lateral part of the thorax—bucket handle movement

Answer 2

* The pericardium is connected to the central tendon of the diaphragm * When the diaphragm contracts on inspiration this pericardial sac can stop the diaphragm from descending. * Pericardial sac is positioned in the middle mediastinum

Answer 3

* Outer fibrous pericardium * And inner serous pericardium * Parietal layer lines internal aspect of the fibrous pericardium * And then the visceral layer lining surface of the heart * Arrangement creates pericardial cavity between these two layers—visceral and parietal * Potential space only—couple of mls—not a large volume * Friction free surface for the heart to move * Friction free glide

Answer 4

* atria are thin walled receiving chambers * internal aspect of the anterior part of the right atrium are lined with ridges—**musculi pectinati** * posterior surface is smooth—**sinus venarum** * **Crista terminalis**—clear defined point where the musculi pectinati end and the sinus venarum starts. * Superior Vena cava returns blood from head, neck and upper thorax—no valve * And the inferior Vena cava—returns through the central tendon—remember it goes through the **diaphragm at T8** * Remember that the central tendon is adherent with the pericardium so the moment the IVC pierces the diaphragm it empties into the atrium * Rudimentary valve associated with the IVC opening * This will lead us to the fossa ovalis * Which in utero would have opened into the left atrium because the baby is not breathing air—i.e. blood is already oxygenated so we bypass the pulmonary circulation and just pump through the body * Eventually this seals off—can see it in left and right atrium. * Coronary Sinus is the venous drainage form the heart itself.

Answer 5

* Anterior wall has been flapped down * Thicker walls * Large number of muscular ridging—**trabeculae carnae** * At the outflow tract just before the pulmonary trunk begins is a smooth area that does not have the trabeculae carnae and this area is the conus arteriosus/infundibulum. (note every other area has trabeculae carnae, posteriorly and anteriorly. * Three specialised (atypical) trabeculae carnae are called papillary muscles where their base is connected to the wall but apex projects into the centre * From the apex of each we have a series of chordae tendinae which connect the apex of the papillary muscles with the tricuspid valve * Remember that the papillary muscle are just an extension of the trabeculae carnae—i.e. contract together

Answer 6

* Looking into left ventricle on left and left atrium on right * Left ventricle has the thickest wall overall—pumping into systemic—higher pressure than pulmonary circulation * Bi-cuspid atrioventricular valve—mitral valve—mostly cut away—has the chordae tendinae and papillary muscles * Left atrium simply thin walled and smooth with 4 openings for the 4 pulmonary veins * Ear like appendage heading around to anterior surface of the heart

Answer 7

* Pair of atrioventricular valves * Rings surrounding * And pair of lunar valves * Coronets surround pulmonary and aortic valves * This structure anchors atria and ventricular muscles separately. * 2 separate muscle masses—separated in their attachment to the fibrous skeleton. Atrial muscle mass forming the atrial chamber and the ventricle muscle mass—separated by fibrous and so are separated from AP passing between them—need something to jump this gap

Answer 8

* Tricuspid on right and bicuspid (mitral) on left * 3 cusps * anterior * posterior * septal * Ventricular surface is rough and has attachment of the chordae tendinae * The chordae tendinae connects to two adjacent cusps separately and the pulls them together to close the valve

Answer 9

* Base is attached to internal surface of the wall of the vessel and the apices meet in the centre * Anterior, posterior, and left and right (aortic is labelled correctly) * When ventricle contracts blood is pushed through the pulmonary and aortic valve when the pressure increases to above the pressure in the vessels. And then when we get a decrease in pressure in the ventricles then the valves just close off. * In the aortic valve the coronary arteries arise and then these arteries deliver blood to the heart

Answer 10

* SA node in the right atrium and right at the top of the crista terminalis * The AV node is also in the right atrium * The bundle of His is what allows the conduction system to bridge across the fibrous skeleton and then bundled branches (purkinje fibres) take the AP down to the ventricles

Answer 11

* The cardiac plexus is situated at the base of the heart and is divided into a superficial and deep part. It receives branches from the vagus and sympathetic trunk

Answer 12

* The very first branches of the aorta * They emerge onto the anterior surface of the heart either side of pulmonary trunk * Right coronary artery descends in the anterior atrioventricular groove (coronary groove) * There is a marginal branch that comes of the right coronary artery which runs along inferior border of the anterior portion of the hear * And the right coronary artery will give off another branch that leads to the left coronary artery and runs along the posterior interventricular groove * In 60% of cases we will see a branch come off the start of the right coronary artery and then run between ascending aorta and right atrial appendage to supply the SA node and in 90% of cases the right coronary artery will also supply the AV node * Left coronary artery also starts at the anterior of the heart but then splits into circumflex branch and an anterior interventricular branch. * The circumflex branch moves posteriorly and then meets with the right coronary artery in the posterior atrioventricular groove * May be other branches also

Answer 13

* Two fibre system * pre-ganglionic and post ganglionic * Pre-ganglionic neurons release ACh which acts on the post ganglionic neurons and this results in ACh release and action on MuscR which result in slowing of HR, through action on the SA node and AV node * The parasympathetic nervous sytem is constently acting upon the heart slow HR-evident through the application of "atropine" a parasympathetic blocker

Answer 14

* two fibre system * pre ganglionic fibres release ACh which acts on Nicotinic receptors, they then act to release NA which acts on Beta and alpha adrenoceptors * Innervates the SA node, conducting tiussue and myocardial cells * Increase HR and increase contractile force (positive ionotrope) * When blocked by propranolol the HR decreases a bit indicatign that sympathetic fibres are not that actie at rest

Answer 15

* The parasympathetic nervous system

Answer 16

* The SA node is the key cell type that regulate rate and if we block the autonomic nerved the cells will depolerise at 100bpm * Resting membrane potential of -60 * At resting there is a bit of Na and a bit of Ca leaking down an electrochemical gradient (i.e. the cell is negatively charged compared to the extracellular environment) * Eventualy the Na and Ca leaking reaches a threshold and Ca then floods in. * And then we get repolerisation--i.e. opening of the pottasium channel

Answer 17

* ACh acts on muscurinic **M2 receptors** (G-protein coupled) * decreases cAMP leading to opening K+ channels * leads to hyperpolarisation K+ leaves and slows Na and Ca influx * So now it takes longer for the cells to reach threshold (phase 4)

Answer 18

* Acitavation of **Beta1 Adrenoceptors** (G-protein coupled) increases cAMP production leads to opening of Ca channels * Ca entry speeds up rate of firing * Increases the slope of phase 4 depolarisation * increases rate of firing of SA node and more rapid conduction AV node * can trigger dysrythmia if pushed too hard

Answer 19

* The ventricular myocyte AP has a stable resting membrane potential. * Phase 0-depolerization-Na in * Phase 1-rapid repolerisation-K out * Phase 2 plateu-Ca in K out * Phase 3-repolerisation K out * Phase 4-stable membrane potential

Answer 20

* Shortness of breath, fainting, fatigue, chest pain

Answer 21

* Altered impulse formation * Automaticity of pacemaker cells * Abnormal generation of action potentials at sites other than the SA node * Altered impulse conduction * Conduction block * Ventricles adopt own slower rate * Re-entry * Extra beats increase rate * Triggered activity * Early or late after-depolarisations * Excess sympathetic activation

Answer 22

1. Na+ channel blockers-reduce phase 0 slope and peak of ventricular action potential: * 1a moderate block * 1b weak block * 1c strong block 2. Beta-adrencoceptor antagonism-decrease rate and conduction (SA node) 3. K+ channel blockade-delay phase 3 of ventricular action potnetial and prolong APD 4. Ca2+ channel blockade-most effective at SA and AV nodes-reduce rate and conduction

Answer 23

* Predominatly used for **ventricle arrythmias** * Class 1a lengthens the repoleraisation and so lengthens the effective refactory period-this class is probably the one that is most effective at the SA node AV node dysrythmias but they are all mostly for ventricular AP modification * Can get many different side effects at different doses * effective does is 2-3 ug/ml * Na+ channel blockers will have many systemic effects * 4ug/ml Lip and tongue numbness 5ug/ml Light headedness 7ug/ml Visual disturbance 8ug/ml Muscular twitching 10ug/ml Convulsions 15ug/ml Coma 20ug/ml Respiratory arrest 25ug/ml Cardiovascular depression

Answer 24

* Prevent β₁-adrenoceptor effects on SA & AV nodes * Decrease sinus rate, conduction velocity & aberrant pacemaker activity * Also have membrane satbilising effects on the Purkinje fibres and so they can also block sodium channels * Adverse effects * Bradycardia, reduced exercise capacity, AV conduction block, hypotension * Bronchoconstriction(poor selectivity?), Hypoglycaemia

Answer 25

* prolong cardiac action potnetial * slow phase 3 repolarisation * decrease incidnece of re-entry * increase risk of triggered events * So mainly used for ventricular re-entry dysrythmias but may also trigger these events too * Amiodarone is also shown to block Na+, Ca2+ and B-adrenoceptors * reversible photosensitisation, skin discolouration and hypothyroidism * pulmonary fibrosis with long term use

Answer 26

* Cardioselective-act preferentialy on SA and AV node and have effects on the initiation of AP. * Can also slow connduction and increase refactory period * Facial flushing, peripheral oedema, dizziness,bradycardia, headache, nausea

Answer 27

* BP\> than 140/90 mmHg * risk factor for * stroke, TIA * MI, Ischaemic heart disease, CHF * aortic aneurism, retinal heamorrhage * renal failure * death * Multifactorial disease * often no known cause * Risk factors * smoking, diet, weight, stress * Treatment benefirs are **unequivocal** * less morbidity * fewer deaths

Answer 28

* Smoking * Diet * Weight * Stress

Answer 29

* Baroreceptors sense the pressure change and signals to the brainstem. * Sympathetic nervous activation * Noradrenaline is released which can act on alpha1 adrenoceptors to constrict blood vessels, increase cardiac output with B1 adrenoceptors. * NA also acts on **B1 adrenoceptors in the kidney** which secretes Renin * Activates AngII and causes increased constriction of blood vessels though AT1 receptors. * AngII also works on kidney to conserve water and perhaps direct effects on the heart too

Answer 30

* Angiotensin system inhibitors * Beta-adrenoceptor antagonists * calcium channel blockers-blood vessels also have L type calcium channels and regulate tone of arteries-calcium influx leads to vessel constriction * Diuretics

Answer 31

* Renin works on angiotensinogen which makes angiotensin I and then ACE converts to AngII and then that acts on AT1 receptors and causes vasoconstriction and release of **aldesterone** which acts on the kidney and casue salt and water retention * AngII also causes increase of Sympathetic nerve activity-**positive feedback** * ACE inhibitors are called **"prils"** * prevent conversion of AngI to AngII * Reduce vascular tone * Reduce aldosterone production * Reduce cardiac hypertrophy * through reducing further sympathetic nerve activation **Adverse effects** * Most of the side effects due to the fact that ACE inhibitors also prevent the breackdown of bradykinin by ACE (ACE is a kininase) (bradykinin is a vasodilator and also involvged in the pain responses) * First-dose hypotension * Dry cough * Loss of taste * Hyperkalaemia (+ thiazide diuretic) * always prescribed with a diuretic to control hyperkaaemia * Acute renal failure * Itching, rash, angio-oedema * Foetal malformations

Answer 32

* Block the AT1 and AT2 receptors * Clinically they block the vasoconstriction effects of AngII working to constrict the blood vessels * But also reduce aldesterone release as well * Reduce vasoconstricttion * Reduce aldosterone * Reduce cardiac hypertrophy * Reduce sympathetic activity **Adverse effects** * still get hyperkaleamia so still need thiazide diuretic * this is due to blocking of aldesterone release due to the fact that aldesterone promotes K secretion into the urine * headache and diziness

Answer 33

* pregnancy * bilateral renal stenosis * impaired renal function already, dont want to make it worse by inhibitng theprimary regulatating system of the kidneys * angioneurotic oedema

Answer 34

* called "olols" * Mechanism * Reduce cardiac output * Rate, contractility * Reduce renin release * Blood volume, TPR **Side effects** * Cold extremities * could be due to the reflex constriction of peripheral arteries due to blood volume reduction * could also be due to the blocking of the B2 adrenoceptors that cause vasodilation in blood vessels * Fatigue * reduced exercise capacity due to reduced CO * Beta-2 blockade of receptors in arteries supplying muscles limiting vasodilation and thus blood supply * Dreams, Insomnia-related to lipid solubility * Bronchoconstriction-Beta-2 adrenoceptors in bronchus-**contradicated in asthma**

Answer 35

* Inhibit voltage-gated L-type Ca2+ channels in myocardium and vasculature * Two subclasses that are either more cardio selective or more vascular selective * Reduce cardiac/vascular contractility * Reduce vascular resistance **Side effects** * oedema, flusing and headache, all due to the increased dilatation, headaches increased cerebral pressure etc * also the L-type calcium channel blockers that are are more cardio-selective can give a bradycardia * More vascular selective drugs can result in a reflex tachycardia

Answer 36

* Inhibit Na+ and Cl- transporter in the distal convoluted tubule and causes reduced reabsorption * We get increased water and Na and Cl loss * lower blood volume and stroke volume and blood pressure * can get K loss as well and so are also pprescribed with ACE inhibitors and AngII antagonists **Side effects** * loss of K+

Answer 37

1. Epicardium (outer layer) a simple squamous epithelium, subepicardial connective tissue, blood vessels, fat, nervous tissue 2. Myocardium-muscle cells and capillaries 3. Endocardium (inner layer) an endothelial layer, subendocardial connective tissue, conducting tissue

Answer 38

* Cells are small * They have a central nucleus * Form branching fibres * Joined by intercalated discs

Answer 39

* Gap junctions are at intercalted discs are there to electrically connect the cells and coordiante beating. * However, the gap junctions only co-ordinate electrical activity on a local level * To co-ordinate contraction of different chambers a separate conducting system is needed – Purkinje fibres

Answer 40

* fastest * SA node * AV node SA node is the fastest though and the AV node follows unless the SA node expires and the AV node must take over

Answer 41

* Modified cardiac muscle cells - larger * Limited contractile machinery * Full of glycogen * Form bundles in subendocardium

Answer 42

* tunica intima * tunica media * tunica adventitia

Answer 43

* Comprosed of a monolayer of squamous epithelium (endothelium) * This sits on basal lamina and is supported by a thin layer of connective tissue

Answer 44

* Actively inhibit clotting by secreting inhibitors * Prime underlying connective tissue with Von Willebrand's factor (activates clotting)-so when there is rupture of the vessel there is clotting * Release vasoactive substances like endothelin (vasoconstrictor) and nitric oxide (vasodilator) which act on underlying smooth muscle

Answer 45

* Middle layer, consisits if smooth muscle arranged concentrically (or helically) * Contricits the lumen * Decrease in lumenal diameter, increase the resistance- blood pressure up * The smooth muscle secretes the connective tissue in which it is embedded (collagen type III, elastin and ground susbtance) * It can vary from a single layer of smooth muscle to up to 40 to 50 layers * In the situation of atherosclerosis the smooth muscle synthesis can get a bit out of control

Answer 46

* Contains connective tissue (collagen type I and elastin, plus ground substnace), with embedded fibroblasts * Anchors to surrounding tissue * Has own blood supply (vasa vasorum) in larger vessels * blood vessels for blood vessels

Answer 47

* Arteries themselves vary in their structure depending on where they are in the circualtion * genrally arteries have to withstand high, rapidly changing blood pressures * they also regulate the blood pressure by constricting or relaxing * **Elastic arteries** are closest to the heart as they have to withstand the highest blood pressure fluctuations * blood pressure rises during Heart contraction but does not drop to 0 when the heart is in diastole * this is due to the arteries bouncing back (due to there ellastic nature) * blood flow is continuous but pulsatile * **Muscular arteries** are further from the heart * Distribute blood into the tissue * Little elastin in the media * Contractions of the smooth muscle in the media regulates the blood pressure and regulates blood supply to organs

Answer 48

* Arterioles still have all 3 layers but only one layer of smooth muscle in the media * Arterioles can also contract and relax * Because there are so many arterioles they are the main regulators of blood pressure * less than 0.1mm in diameter

Answer 49

* Capillaries arfe often thinner then the diameter of a RBC and so force contact between the vessel wall and the RBCs * capillaries only have a single smooth muscle cell controlling blood flow associated with it * may be a **meta arteriole** between the arterioles and the smooth muscles * capillaries are formed by a single endoothelail cell wrapping around to form a thin tube and sealed with tight junctions * sitting on a basal lamina * sometimes has a pericyte (media) * a few collagen fibres surround the vessel (adventitia) *

Answer 50

* Found in pancreas, intestines and endocrine glands * Diaphragms are not just simple membranes. They contain 8 wedge shaped channels * sometimes the diaphragm is completely missing (like in the kidney)

Answer 51

* Blood from capillaries is collected in the veins * veins carry deoxygenated blood at **low** pressure * contain 70% of the blood * act as a blood resovoir * Has the same layers as arteries * media is thinner, adventitia is thicker (to help withstand hydostatic pressure) * valves to force blood in one direction * assisted by skeletal muscle contractions

Answer 52

* Blood from capillaries collected by venules * equivalent to the capillaries in that they have a pericyte in the media rather than smooth muscle * although later on they do acquire smooth muscle * ussually larger lumen than arterioles * are the site for diapedesis and so express ICAMs and integrins for leukocyte entry into tissue * affected by histmaine and other cytokines

Answer 53

* Subendothelial connective tissue is well developed * adventitia enlarged, often at expense of media * to cope with hydrostatic preessure * sometimes, longitudinal smooth muscle bundles in the adventitia (stiffening)

Answer 54

* capillaries are thin walled and leaky * so lots of fluid can accumulate in the intercellular space so lymphatics drain extracellular fluid back into the circulation * lymphatics also have valves and skeletal muscle contraction which assists in bringing fluid back to large veins in thoracic cavity and abdominal cavity * No red cells, lymph and WBC * Very thin epithelial wall forming endothelium and gaps between allow fluid to come back in and valves are present and so we pump fluid back * large ones look like veins * usually collapsed post mortem

Answer 55

* intimal damage and thickening in the **arteries** * with fibrosis * commonn ageing or with hypertension * Impair arteries so they cannot relax and contract because there is too much collagen * Can narrow lumen and impair blood supply to downstream tissues

Answer 56

* intimal damamge and thickening of the **arterioles** * Smooth muscles have produced too musch matrix and proteins from blood (albumin, Immunoglobulins) can leak across damaged endothelium * known as hylanine arteriolosclerosis **Sequale** * poor blood supply to tissues (ischeamia) * benign nephrosclerosis-ischaemia of the functional units of the kidney due to narrowed arterioles * possibility of microaneurysms and then bleeding * cerebral heamorrhage *

Answer 57

* build up of inflammatory, fibrotic, necrotic and fatty material in arteries * Fibrous and gunky * from the latin for ''hard porridge'' * **Fibrous cap and necrotic lipid core** **Stages of formation** 1. Fatty streak * Collection of foam cells in the **intima** * macrophages that have ingested lipid * very common so not clinically significant 2. Damage, Inflammation, cholesterol and fibrosis 3. Stable atherosclerotic plaque * Fibrous cap * chronic inflammatory cells * necrotic lipid core * likely asymptomatic * can encroach on lumen over time * still have lumen though becasue in the early stage the plaque actually grows outwards 4. Unstable atherosclerotic plaque

Answer 58

* **Dystrophic calcification** * appears in areas of cell degeneration * e.g. tuberculosis, breast lesions, atherosclerosis * **Metastatic clacification** * ussually as a result of kidney disease * serum calcium and phosphate levels are too high * They reach their precipitation threshold and fall out of solution: calcification in blood vessels, kidneys, other

Answer 59

* thinner fibrous caps * or even ulceration * Larger necrotic core * more inflammatory cells * less than 50% stenosis * i.e. likely to be asymptomatic

Answer 60

* APE can be: plaque rupture, haemorrhage into plaque and erosion of endothelium * this can lead to clotting **(thrombosis)** * or the plaque can fly off and clot somewhere else **(thromboembolism)** * or atheroembolism-peice of plaque can fly off and get caught **(atheroembolism)**

Answer 61

* \>70% stenosis

Answer 62

* anuerysm and rupture * result of wall weakening * Occlusion by thrombus * Critical stenosis * blood vessels becomes completely clogged

Answer 63

* Endothelial dysfunction is important in the start of atherosclerosis * normal endothelium does not interact with immune cells * **but if you make it angry then it will be leaky and inflammatory cells will enter etc** * leaky * expresses adhesion molecules * produces cytokines and growth factors * changes from anti-coagulent to pro-coagulent * **Takes up more LDL** * which become oxidised * and then pro-inflammatory * **Allow monocytes into intima** * expression of adhesion molecules * monocytes enter intima and become macrophages * macrophages phagocytose oxidised LDL and produce inflammatory cytokines * Endothelial dysfunction risk factors include * hypertension has a low grade shear effect * smoking has toxic and pro-inflammatory effects * high blood sugar and lipids can damage endothelium

Answer 64

* LDL accumulates in the intima and is oxidises * and then taken up by macrophages and smooth muscle cells * and they becoem foam cells and this stimlates inflammatory cytokines and the production of free radicals * The oxidised LDL is also toxic to the endothelial cells

Answer 65

* T cells help macrophages to call more T cells etc-chronic inflammation * attract more inflammatory cells * more ROS * more cytokines * more MMPs * perpetuates inflammatory cycle

Answer 66

* smooth muscle cells come in and produce collagen when damage occurs to the intima * so produce thick fibrous cap * so probably a good thing so we can wall off the thick necrotic debris * collagen-thicker fibrous cap

Answer 67

* Abnormal dilation of a blood vessel * can also get them in heart * Can get true aneurysm or a false aneurysm * True aneurysm is when the whole wall stretches out-without bursting * can be saccular-one side * fusiform-both sides * False aneurysm is where it has ruptured * dissection * heamatoma * Weak media-lack of blood supply due to inflammation due to atherosclerosis or congenital etc * weak media due to intimal thickening * risk is that the aneurysm can rupture and blood will leak out

Answer 68

* associated with atherosclerosis * inflammatory environment weakens ECM * MMPs * intimal thickening interferes with wall perfusion * Risk of rupture increases above 5cm diameter * often contain thrombus which can embolise

Answer 69

* in cerebral circualtion * weakening of a congenital defect * major cause of subarachnoid haemorrhage

Answer 70

* Blood leaves intima (due to rupture) and gets into the media * Aortic dissection is common and is strongly associated with hypertension * can involve or compress important arteris * can rupture into pericardium * cardiac tamponade * can rupture into thorax * exsanguination

Answer 71

* hyperplasia should cease after a few months of life * through childhood heart undergoes hypertrophy

Answer 72

* Myocadial infarction * Cardiac damage eg myocarditis * Volume overload * pressure overload

Answer 73

* Concentric hypertrophy * increase LV mass * Increase wall thickness * often due to pressure overload * more sarcomers in parallel * Eccentric Hypertrophy * increase LV mass * Normal relative to wall thickness * often due to volume overload * myocyte stretching-more sarcomeres in series * Remodelling * Normal LV mass * Increase in relative wall thickness

Answer 74

* LV hypertrophy (concentric) is meant to compensate for a high pressure afterload * meant to maintain systolic function, cardiac output and LVEDP * LV hypertrophy (eccentric) is compensation for volume overload * meant to increase LVEDV and increase EF * But sometimes with chronic hypertrophy we can get decompensation where LVEDV increases and LVESV increases but ejection fraction decreases * reduced systolic function and cardiac output * LVEDP must increase even more and we end up with cardiac failure

Answer 75

**Environmental** * Concentric-pressure overload, high afterload * hypertension, aortic stenosis * eccentric-volume overload, high preload * mitral and aortic regurgitation, ventricular septal defect * Following myocardial infarction * following cardiac injury * obesity, diabetes, renal failure * Infiltration **Genetic** * Hypertrophic Cardiomyopathy * Fabry's disease *

Answer 76

* Clinical-forceful apex beat, S4, S3 * ECG-tall voltages, T wave inversion * tall QRS due to hypertrophy * CXR * larger heart in eccentric LVH * may be normal size in concentric LVH * Echo * MRI * Cardiac CT

Answer 77

* concentric hypertrophy is the worst at causing mortality following myocardial infarction * LVH is a marker for increasing severity of CVD

Answer 78

* thick muscle is stiff and harder for the ventricle to relax and full with blood so pressure required to fill ventricle is higher. * higher LVEDP required to achieve same LVEDV (preload) * So increased LA and pulmonary vein pressure * can lead to pulmonary congestion * Atrial kick now also more important and this can lead to atrial fibrillation * sensitive to dehydration due to low BP and also sensitive to fluid loading-i.e. pulmonary congestion due to too much fluid

Answer 79

* must treat underlying condition * valves etc * Hypertension * Weight loss

Answer 80

* Pretty mushc the same as LVH eccentric hypertrophy * but used as a term to describe what occurs after myocardial infarction * heart dilates around infarct zone and the rest of the heart also dilates * Though angiotensin has a role as ACE inhibitors seems to prevent remodelling-often with Beta blockers as well

Answer 81

**Causes** * congenital * transposition of the great arteries * Pulmonary hypertension * lung disease * pulmonary embolus * chronic L heart failure * Right heart valves * Pulmonary Stenosis/Regurgitation * Tricuspid Regurgitation

Answer 82

**Cause** * Autosomal dominant * Positive family history * Mutation in genes for sarcomere proteins * \>900 mutations in 12 genes (since 1990) * Most common * Beta cardiac myosin heavy chain * cardiac myosin binding protein * cardiac troponin I and T **What happens** * Hypertrophy of the ventricular septum * cellular hypertrophy * myocyte dissarray * LV outflow tract obstruction * i.e. all the extra muscle get in the way * Diastolic Dysfunction * **Ventriuclar arrythmias-sudden death** * same mutations can cause varied symptoms * symptoms can vary from mild to severe * common cause of sudden death inn athletes *

Answer 83

* large and thickened heart * particularly the right ventricle often becomes smaller after training is stopped but not always *

Answer 84

* Responsible for the cardiac output vs left ventricular end diastolic volume relationship * Responsible for * CO=venous return * Left heart output=right heart output

Answer 85

* Use JVP as a indirect measure * Use pulmonary artery wedge pressure * Catheter wedged into pulmonary artery will measure the pulmonary venous pressure * so occlude the pulmonary artery and we can measure the left ventricle pressure indirectly

Answer 86

* Hydrostatic pressure pushing out * pressure of the fluid pushing non the capillary wall * osmotic pressure pushing in * Hydrostatic pressure dominates at the arterial end so fluid is pushed out of the capillary * at the venous end osmotic pressure dominates and so fluid is pushed back in * So most of the arterial pressure is lost across the cappilaries

Answer 87

* Increased pressure in the venous system causes fluid to leak out rather than fluid to come back in (through osmotic pressure) * could be due to heart failure * Decreased osmotic pressure * plasma protein loss: renal failure * Blocked lymphatics (fluid leaked into tissues is no longer transported back into tissues) * cancer * Increased capillary permeability * Infection

Answer 88

* if we have more EDP in the left ventricle then that means more pressure pushing fluid out of the pulmonary capillary and and this could lead to congestion

Answer 89

* LVEDP=Preload: LV function * LVEDP=LAP=PVP: Lung capillaries (increase pressure in the capillaries will cause increase fluid leak and potentially pulmonary oedema) * RVEDP=Preload: RV function * RVEDP=RAP=JVP: Peripheral capillaries where increased pressure will cause fluid leak and peripheral oedema

Answer 90

* Cardiac output is less than the body needs * Usually due to decreased CO * rarely due to increased body needs * usually systolic failure * loss of contractility

Answer 91

* The body must retain fluid and increase venous return and increase LV end diastolic pressure. * But if the LVEDP increases too much (i.e. above 20-25mmHg) than the CO does increase but at the expense of the lungs and fluid will build up and leak into the alveoli and patients will present with **shortness of breath**

Answer 92

* venous pressures * arterial pressures

Answer 93

* **Loss of myocardial muscle** * Ischeamic heart disease * Cardiomyopathy * dilated cardiomyopathy where the heart becomes very thin and dilated and heart loses muscle * **Pressure overload** * Aortic stenosis * Hypertension * **Volume overload** * Valve regurgitation * Shunts (e.g. septal defects)

Answer 94

* Left hear failure * shortness of breath-can be very severe * fatigue * tachycardia * Lung crepitations-crackles due to fluid * Right heart failure * Peripheral oedema

Answer 95

* Decreased CO * decreased renal blood flow * activation of the renin/angiotensin/aldesterone system * Fluid, Na+ retension * K+ loss (echanged with Na+) * Angiotensin causes Vasoconstriction (AT1 receptors) * These adaptions result in in more fluid(due to water retention), potential for arrythmia (due to K+ loss) and vasoconstriction leads to higher afterload and makes it harder for the heart to work.

Answer 96

* Increase NA * Initial increase in contractility * long term deleterious effect * vasoconstriction (Beta2 receptors in vessels) * ventricular arrythmia * direct toxic effect of NA on the heart muscle

Answer 97

* Global heart disease * e.g. cardiomyopathy * Specific right heart disease * RV cardiomyopathy * right sided valves; shunts * pericardial disease * pulmonary hypertension (arterial) * Lung disease: cor pulmonale * Pulmonary embolism * Left heart disease * causes high pressure in the LV, LA and Pulmonary venous system * pulmonary venous high pressure causes pulmonary congestion * chronic hypoxia * will lead to physiological response where we get pulmonary vasoconstriction * Endothelin * lead to pulmonary arterial hypertension * right heart failure

Answer 98

* Diuretics (frusemide) * Aldosterone antagonists e.g. spironolactone * Angiotensin convertinf enzyme inhibitors (ACE Inhibitors) captopril, ramipril

Answer 99

* ACE inhibitor

Answer 100

* a angiotensinII receptor antagonist

Week #5 Flashcards

(128 cards)