Cardiology Physiology Flashcards

Question

When would you give fibrates?

Answer 1

Second line  - Statins not tolerated (after 3 tries of statin + dose reduction)  - Combined with other lipid - Lowering drugs in severe treatment resistant dyslipidemia   - Considered in mixed dyslipidemia (raised TG + low HDL)  - Low HDL and high risk of atheromatous disease (T2DM)

Answer 2

- Myositis (especially if renal impairment)  | - GI disturbances

Answer 3

- Avoid in ALD ≈ increased risk of myositis |  - Contraindicated in hepatic and renal insufficiency

Answer 4

Inhibit transport protein for cholesterol in brush border of enterocytes (NPC1L1) in duodenum ≈ reduce intestinal cholesterol absorption

Answer 5

``` - GI symptoms  - Nausea   - Abdominal bloating   - Constipation  - Diarrhoea ```

Answer 6

- Contraindicated in pregnancy and lactation

Answer 7

Binds bile acid ≈ inhibit cholesterol absorption  - Sequesters bile acids in intestine ≈ X enterohepatic recirculation ≈ increase metabolism of endogenous cholesterol into bile acids

Answer 8

Third line, statins or ezetimibe or fibrates not tolerated. | - FH

Answer 9

- Nausea  - Abdominal bloating  - Constipation   - Diarrhoea

Answer 10

- Taste + texture of colestyramine ≈ reduced adherence  - Interferes with absorption of other drugs (lipid-soluble) + vitamins (DEAK)  - Contraindication in complete biliary obstruction  

Answer 11

Diacylglycerol acyltransferase-2 (DGAT2) inhibitor ≈ Inhibit production of VLDL; lower LDL; lower TG; increase HDL-cholesterol ≈ control of dyslipidemia

Answer 12

Combination or 4th line   - In combination with statins  - Statins not tolerated + other lipid-lowering medicines not tolerated (fibronates, bile acid sequestrates, ezetimibe)   - HDL raising agent  

Answer 13

``` - Flushing  - Itching  - Nausea   - Numbness and tingling  - Worsening of gout  - Diabetes   - Angina ```

Answer 14

- Regular blood tests ≈ LFTs (potential hepatotoxicity)  - Increase GI bleeding + infection rates  - Contraindication in peptic ulcer disease + arterial bleeding

Answer 15

PCSK9i ≈ X cleavage of LDLr ≈ X LDLr shedding ≈ LDL uptake and metabolism

Answer 16

5th line or Severity  - All therapies not tolerated (statins, ezetimibe, fibrates, bile acid sequestrates, nicotinic cid)  - Familial hypercholesterolaemia

Answer 17

- Nausea  - Back and joint pain  - Soreness or itchiness

Answer 18

- Specialist only

Answer 19

1) Ciclosporin (systemic) ≈ severe + monitor   Explanation: Ciclosporin ≈ markedly increases exposure to atorvastatin ≈ myopathy (rhabdomyolysis) + renal failure. Atorvastatin ≈ increase exposure to ciclosporin slightly.   ``` Action:   - Close monitoring  - Avoid concurrent use   - Safety net with myopathy symptoms to report if experienced by pt   - Reduce dose to 10mg daily ``` 2) Clarithromycin (systemic) ≈ severe + monitor   Explanation: Clarithromycin ≈ moderately increases atorvastatin exposure ≈ rhabdomyolysis risk. Previous rhabdomyolysis reported in patient taking Action:   - Temporarily remove statin or reduce dose dose (< 20mg PO).   - Reduce dose ≈ <20mg daily  - Safety net with myopathy symptoms to report if experiences by pt 3) Grapefruit juice (systemic) ≈ mild + adjust    Explanation: Large volumes of grapefruit juice (≈ furanocoumarins) ≈ increase atorvastatin exposure ≈ smaller amounts + separate administration by 12 hours to reduce effects    Action:  - Avoid large volumes of grapefruit juice (1.2L)   - Safety net: Advise patients to report rhabdomyolysis symptoms - Muscle pain, tenderness or weakness

Answer 20

- Check adherence  - Exclude + manage common secondary causes of dyslipidemia: excess alcohol, uncontrolled diabetes, hypothyroidism, liver disease, nephrotic syndrome  - Consider Ddx - Specialist referral

Answer 21

> 20 ASSIGN SCORE

Answer 22

- Bulk flow of materials: gases, nutrients, hormones and waste  - Temperature regulation  - Homeostasis  - Host defence  - Reproduction

Answer 23

- Heart: pump ≈ blood flow in closed system   - Arterial system: conductance system of oxygenated blood away from heart  - Microcirculation: nutrient transfer, waste and water occurs  - Venous system: capacity vessels storing and returning deoxygenated blood to the heart

Answer 24

CVS is parallel, not series, as blood must be able to bypass organs ≈ less metabolic demand ≈ require less perfusion and venous return occurs in opposite flow  

Answer 25

Independent regulation of blood flow to different organs which can adapt to metabolic demands of the tissues  - Independent regulation of blood flow  - Adapts to metabolic demands of tissues

Answer 26

Hypoxia ≈ ischaemia ≈ necrosis

Answer 27

- Brain ≈ 13%  - Heart ≈ 4%  - Skeletal muscle ≈ 20%  - Skin ≈ 9%  - Kidneys ≈ 20%  - Abdominal organs ≈ 24%  - Other ≈ 10%

Answer 28

``` Structure ≈ function   Consider:  - Elasticity  - Smooth muscle   - Fibrous tissue  - Wall thickness  - Diameter (lumen) ``` - Aorta: highly elastic + little smooth muscle with more fibrous tissue; large diameter ≈ elastic + reduced vasoconstriction ≈ smooth blood flow + high blood flow - Artery: elastic tissue + smooth muscle; thick wall + lumen ≈ elasticity to smooth pulsatile flow + vasoconstriction to change lumen diameter; + blood flow - Arteriole: elastic tissue + smooth muscle ≈ ∆ lumen diameter via vasoconstriction + smooth pulsatile flow to reduce pressure at capillaries - Vein ≈ little elastic tissue with little smooth muscle + large lumen ≈ little vasoconstriction + transport blood under low pressure - Venule: No elastic tissue + no smooth muscle; thin wall ≈ transport blood under low pressure from capillaries via venous system into larger, true veins - Capillary: thin (one-cell thick) + no elastic tissue ≈ diffusion of substances

Answer 29

BP reference set-point —> MAP —> baroreceptors —> feedback signal —> brain medulla vasomotor centres (reference set point) —> SNS (via sympathetic cardiac nerve impulses if low BP) / PSNS (via vagus nerve if high BP) —> effectors ≈ BV + heart (or kidneys) —> ∆ MAP

Answer 30

Situation: High BP —> Increased carotid sinus nerve impulses and vagus nerve impulses —> Medulla oblongata —> Reduced sympathetic cardiac nerve impulses and increased parasympathetic = HR, inotropy and vasoconstriction reduced

Answer 31

Changes from pulsatile due to elastic recoil of blood vessels such as aorta and muscular arteries compared to smoothened out flow rate by variable muscular walls in tunica media which alter their vasomotor tone to increase laminar flow rate for adequate perfusion at capillary beds which have high resistance due to being one cell thick

Answer 32

Time continuous variable graph showing changes in blood pressure and the pulse pressure indicated by the difference between systolic and diastolic pressure;  Pulse pressure = SBP - DBP MAP = 1/3 (SBP-DBP) + DBP

Answer 33

average pressure in patient arteries during one cardiac cycle MABP = DBP + 1/3 PP (SBP - DBP)

Answer 34

Standing ≈ increase P by 1mmHg for 1.36cm below surface ≈ 90mmHg by feet  - Increase P as you go down ≈ 1.36cm = 1mHg  - 100mmHg @ heart level   - Leg oedema ≈ 10-20% of blood volume within 15-30 minutes

Answer 35

Physiologically functioning measures ≈ venous valves + venous pump ≈ venous return

Answer 36

Supine to standing ≈ 500ml blood from upper body to legs ≈ reduce venous return ≈ reduced CO ≈ reduced BP ≈ reflex vasoconstriction in legs to facilitate venous return and end-diastolic volume is lagging..few s to function Decreased BP —> decreased baroreceptor activity —> integration of afferent info into brainstem —> increased sympathetic and decreased parasympathetic tone —> increased peripheral vascular resistance, heart rate, vasoconstriction and increased CO to restore BP

Answer 37

relationship between volume of blood and pressure generated by presence of the volume and property of vessel undergoing deformation  

Answer 38

1) Non-compliant: rigid tubes resist expansion when internal pressure rises. Big change in P due to small change in V   E.g. Capillaries + arterioles (smaller so easier to become non-compliant) 2) Compliant: Elastic walls ≈ swell when internal pressure rises. Big change in V with little changes in P E.g. arteries, veins

Answer 39

Compliance decreases in both age and vasoconstriction as more rigid ≈ little change in volume causes a larger change in pressure  

Answer 40

Physical law stating tension within wall of a vessel with partial pressure depends on the radius of the sphere (thickness)   T = PR

Answer 41

1) Control of blood flow: - Low tension required to oppose blood pressure in arterioles   - Smooth muscle control of arteriole and precapillary sphincters are sites of tissue blood flow regulation 2) Capillaries - Extremely thin and still withstand pressure ≈ T = PR so radius is low + pressure is reduced thus less tension generated ≈ less muscular wall required to overcome tension produced  - Thin walls required for exchange process 3) Aneurysm - Pressure either side of bulge equilibrates and so does pressure in weakening of wall ≈ greater tension as pressure is the same; weakening wall (radius increases and P is the same) ≈ consistently swell and eventually burst

Answer 42

- Radius (directly proportional) - Pressure gradient (directly proportional) - Length of the vessel (indirectly proportional) - Thickness of the fluid (indirectly proportional)  - Viscosity

Answer 43

∆D (∆r) —> reduce flow rate as increase resistance —> as Poiseulle’s Law shows  R = (π)r4/8nl —> therefore small reduction of radius/diameter ≈ large change in resistance as radius is to the power of 4—> increase R  

Answer 44

viscosity of plasma and water remains constant but whole blood changes according to haematocrit  - More Hct ≈ more viscosity

Answer 45

Reduced viscosity ≈ increased blood flow velocity as blood is a thixotropic fluid (energy put in to make it move) ≈ less energy required to make it move

Answer 46

AP = CO x TPR

Answer 47

1) Neural  Vasoconstrictor: sympathetic nerves  Vasodilator: NO-releasing nerves  2) Hormonal:   Vasoconstrictor: adrenaline, angiotensin II, vasopressin    Vasodilator: adrenaline, atrial-natriuretic peptide 3) Local:    Vasoconstrictor: myogenic response, endothelin-1   Vasodilator: reduced oxygen, K+, CO2, H+, adenosine, nitric oxide, bradykinin

Answer 48

1) Laminar fluid flow  - Fluid molecules travel in layers  - Middle layer encounters least resistance cf outer layers ≈ shear force 2) Turbulent flow:   - Disrupts flow ≈ increased resistance

Answer 49

Used to indicate whether flow is likely to be laminar or turbulent - given system there is critical value for Re above which turbulence is highly likely   Re = (velocity) x (radius of vessel) / viscosity

Answer 50

- high velocity flow   - large diameter vessels  - low blood viscosity  - abnormal vessel wall

Answer 51

Cardiomyocytes contain intercalated discs @ Z-line ≈ connected via GAP junctions (connexin hexamer ≈ connexon) ≈ flow of AP and ions simultaneously ≈ influx of Calcium via CaVg channels ≈ syncytium ≈ simultaneous, synchronised depolarisation ≈ synchronised contraction of cardiac tissue

Answer 52

Pacemaker cells ≈ self-excitable (autorythmic) ≈ SAN in RA (by sulcus terminalis, between SVC and coronary sinus) ≈ myogenic ≈ determines HR ≈ chronotropy  

Answer 53

1) Pacemaker potentials  - Spontaneous depolarisation  - Slow depolarisation  - Driven by calcium slowly   2) Non-pacemaker potentials   - Rapid depolarisation   - Driven by sodium rapidly and prolonged by calcium   3) His-Purkinje potentials   - Rapid depolarisation  - Spontaneous depolarisation  - Driven by sodium rapidly and prolonged by calcium

Answer 54

Phase 1: @ - 60mV ≈ Funny currents (If) ≈ pacemaker potential + T-type Calcium channels ≈ threshold + depolarisation  - Funny currents (If): -60mV ≈ F-type Na+ channels open at more negative membrane potentials (-60mV) ≈ gNa+ in (‘funny currents’) and K+ channels close ≈ gK+ reduced ≈ pacemaker potential   - T-type Ca2+ channels open @ -50mV ≈ gCa++ increases ≈ Ca2+ in ≈ depolarisation    Phase 2: @ -40mV Slower, sustained depolarisation via L-type Ca2+ channels ≈ gCa++ increases ≈ Ca++ in  - Calcium influx via L-type calcium channels ≈ depolarisation    Phase 3: Repolarisation  - @ +20mV KVg channels open ≈ increased gK+ ≈ increased conductance ≈ repolarisation as potassium efflux occurs - CaVg L-type close ≈ reduce gCa++ ≈ reduced depolarisation + repolarisation  

Answer 55

Phase 0:   - Rapid depolarisation due to NaVg opening at -75mV ≈ gNa+ ≈ Na+ in   Phase 1:  - NaVg close ≈ reduced gNa+   Phase 2:   - L-type CaVg open @ 10mV ≈ gCa++ ≈ Ca++ in ≈ plateau   Phase 3:   - Rapid repolarisation: gCa++ ≈ increased IC Ca++ ≈ K+ channels open ≈ gK+ efflux   - L-type CaVg close ≈ reduced gCa++    Phase 4:  - Stable resting membrane potential where gK+ > gNa+ (50:1)

Answer 56

Cellular hypoxia ≈ depolarises the cell ≈ ∆ phase 3 hyper-polarisation ≈ reduced pacemaker rate ≈ bradycardia

Answer 57

1) PSNS: Vagus nerve (CN X) —> SAN + AVN  - ACh @ M2R ≈ Gai ≈ reduce cAMP ≈ reduce rate of phase 0 depolarisation + hyperpolarise membrane potential (= increase extent + duration of opening of K+ channels ≈ increase gK+)   2) SNS: Sympathetic chain ≈ sympathetic nerves —> atria + ventricles  - NA @ ß1R ≈ Gas ≈ increase cAMP ≈ increase rate of phase 0 depolarisation ≈ increase gCa++ + increase gNa+ via funny channels

Answer 58

Coordinated electrical activity: pacemaker activity of SAN (RA) ≈ initiate process ≈ depolarisation spreads due to functional syncytium (electrically connected via GAP junctions) ≈ SAN in RA —> internodal pathway + interatrial pathway —> AVN (critical delay ≈ atrioventricular flow) —> L + R Bundle of His (interatrial septa) —> Purkinje fibres

Answer 59

SAN (90) > AVN (60) > BoH (50) > PF (40) > V (30) SAN = 'pacemaker'

Answer 60

Conduction measured in m/s as it is a speed of distance/time (m/s)   - SAN to AVN ≈ 1m/s (internodal pathways) ≈ 0.03s   - Internodal pathways ≈ 1m/s   - Atrial + Ventricle fibres ≈ 0.3-0.5m/s   - AVN delay ≈ 0.09s    - Penetrating portion delay ≈ 0.04s   - AVN + BoH ≈ 0.01m/s    - PF ≈ 1.5-4m/s

Answer 61

Equilateral triangle with heart at centre formed by three bipolar limb leads   - Lead I: positive electrode on left arm + negative electrode on right arm ≈ potential difference between two arms    - Lead II: positive electrode on left leg and negative electrode on right arm    - Lead III: positive electrode on left leg and negative electrode on left arm   - Reference electrode: Electrode on right leg ≈ reference electrode for recording purposes   

Answer 62

Einthoven’s triangle (equilateral) ≈ broken apart + collapsed + superimposed over heart ≈ axial reference system - Positive electrode for lead I (Left arm) ≈ 0º relative to heart (along horizontal axis between LA and RA)  - Positive electrode for lead II (RA-LL) axis: +60º cf to heart - Positive electrode for lead III (LA-LL): +120º cf to heart

Answer 63

1) Current (proportional to tissue mass)   | 2) Direction of signal

Answer 64

E x CosƟ (= observed signal)    E = electrical event    Ɵ = angle between event + ECG lead

Answer 65

Smallest angle ≈ greater observed signal

Answer 66

P wave ≈ impulse travelling within AVN (conduction velocity retarded) + in BoH

Answer 67

Prolonged duration of QRS complex ≈ > 0.12-0.20s ≈ impairment of conduction within ventricles ≈ e.g. bundle branch blocks or abnormal pacemaker site (ventricular foci)

Answer 68

ST segment ≈ isoelectric period between S and T waves ≈ time when both ventricles completely depolarised ≈ plateau phase of ventricular action potentials

Answer 69

DDx of ventricular ischaemia or hypoxia e.g. myocardial infarction as ST segment elevated (STEMI) or depressed (NSTEMI)

Answer 70

Last cells to depolarise are the first to repolarise (subepicardial region cf subendocardial region) ≈ repolarisation waves orientated opposite to depolarisation waves ≈ repolarisation moving away from positive recording electrode ≈ positive voltage

Answer 71

T wave (0.12s) > QRS complex (0.12-20s) ≈ repolarisation wave does not use high-velocity bundle-branch of BoH or PFs cf cell-cell conduction ≈ conduction of repolarisation slower than depolarisation

Answer 72

Prolonged QT interval ≈ some types of tachyarrythmias  - Must distinguish if QT interval is excessively long

Answer 73

Ischaemia ≈ inadequate supply of oxygen to heart ≈ chest pain (angina)  - ‘Severe crushing’   - Retrosternal pressure;  - Radiation: Chest, arms, neck + jaw

Answer 74

```  Triggers/exacerbations:  - Exertion  - Cold  - Excitement  - GTN/Rest ``` Chemical factors (K+, H+ and adenosine) ≈ local vasodilation factors + sensitising soup ≈ increase blood flow + pain

Answer 75

1. P Wave: Atrial depolarisation = < 0.12s + < 0.25mV • Positive in leads I and II • Inverted in aVR • Isoelectric after P wave as impulse travels within fibrous septa with velocity retarded

Answer 76

2. QRS Complex: Ventricular Depolarisation = 0.08-0.12s • Q wave is septal depolarisation from L --> R • R wave is ventricular depolarisation • S wave is ventricular depolarisation

Answer 77

3. T Wave: Ventricular repolarization • Can have early take off T wave in young person • Inverted in VR and V1 and V2 in young

Answer 78

PR Interval: Atrial Depolarisation = 0.12-0.20s | • Lengthened in AVN Delay

Answer 79

QRS Complex: Ventricular Depolarisation = 0.08-0.12s

Answer 80

QT Interval: Ventricular depolarisation + Repolarisation

Answer 81

Treatment to reduce chest pain symptoms + treatment to prolong survival ``` 1) Reduce chest pain symptoms:  - ß-blockers   - Nitrates  - Calcium channel antagonists  - Nirocandil  - Ivabradine  - Ranolazine ``` 2) Prolong survival:   - ß-blockers  - Aspirin  - Statins  - ACEi  - ARBs

Answer 82

Heart perfused (coronary blood flow to myocardium) best during diastole. In systole P rises in ventricle ≈ P of LV > P of aorta ≈ semilunar valve opens ≈ blood out ≈ P in aorta rises in systole then P in aorta and LV reduces ≈ P of LV > aorta ≈ aortic valve shuts ≈ diastole ≈ LV pressure reduces in diastole but aorta P reduces slowly + aortic valve shut ≈ retrograde flow ≈ blood flows via Ostia in aortic sinus into RCA and LCA ≈ cycle repeats

Answer 83

Period of time for coronary flow during diastole whereby aortic P > ventricular P ≈ blood flow via coronary sinus into RCA + LCA

Answer 84

1) Increased HR (= narrow coronary window): increased rate ≈ tachycardia ≈ reduced diastolic filling time due to increased systole ≈ narrow coronary window   2) Aortic stenosis/ increased residual volume (increased EDV, reducing pressure difference): increased volume ≈ increased pressure in left ventricle ≈ reduced pressure difference between aortic P and ventricular P ≈ reduced coronary window 3) Mitral valve stenosis or Aortic regurgitation (reduced diastolic volume): Reduced diastolic arterial P thus pressure difference reduced OR retrograde blood flow from aorta and reduced P in diastole ≈ reduced coronary window

Answer 85

Tissue demand ≈ increase arteriolar radius ≈ blood flow - Metabolic control: Myocyte produces local vasodilator byproducts (e.g. adenosine) ≈ vascular SMCs relax (potentially via intermediate produced by endothelial cells)

Answer 86

- Coronary ischaemia: Atherosclerosis ≈ coronary ischaemia ≈ angina (stable angina); ≈ infarction (≈ unstable angina) ≈ MI - Sudden ischaemia: Thrombosis ≈ stenosis/occlusion ≈ ischaemia (≈ unstable angina) ≈ myocardial infarction - Coronary spasms: Oscillatory narrowing of arteries ≈ variant ischaemia ≈ variant angina due to hypoxia

Answer 87

Ischaemia ≈ cellular calcium overload ≈ cell death + dysrhythmias  

Answer 88

Atherosclerotic plaque build up ≈ atherosclerotic changes ≈ reduce diameter/radius of artery (stenosis) ≈ length and viscosity remain same (denominator) however radius reduced significantly ≈ radius to power of 4 = significantly amplified ≈ significant reduction in flow rate ≈ reduced blood flow ≈ hypoperfusion ≈ ischaemia ≈ infarction (calcium toxicity ≈ cardiomyocyte death)

Answer 89

1) Printzmetal’s Variant Angina: Vasospasm ≈ coronary spasm supply ischaemia   - Coronary artery spasm  - Uncommon  - Incomplete understanding; sometimes associated with atherosclerosis 2) Unstable angina: Thrombus ≈ supply ischaemia - Thrombus around ruptured atheromatous plague (unstable atheromatous plaque) w/o complete occlusion of vessel (similar to MI) - Occurs at rest/ low exertion; less exertion required cf stable angina 3) Stable angina: Fixed stenosis ≈ demand ischaemia - Fixed stenosis of coronary arteries - Predictable chest pain on exertion - Treat: Reduce workload of heart ≈ reduce oxygen requirement  - Use drugs to prolong survival: aspirin, statins and ACEi

Answer 90

- Chest pain: retrosternal, heaviness, pressure, weight, burning, tightness   - Radiation: shoulder-tip pain, neck, jaw, inner arms, epigastrium, band-like discomfort  - Relieved: remove exertion + GTN (glyceryl trinitrate) spray + after 10 minutes

Answer 91

Atypical angina (2/3) or silent myocardial ischaemia + angina (1/3) - absent of chest pain   ``` Silent myocardial ischaemia:  - Women   - Elderly  - Transplanted hearts  - Diabetes (autonomic neuropathy) ```

Answer 92

Anti-anginal drugs ≈ reduce metabolic demand of heart ≈ reduced oxygen requirement ≈ reduced % of ischaemia precipitating angina - Pre-load ≈ ∆ volume filling heart: ventricles are compliant so large change in volume ≈ small change in P   - After-load: ∆ volume leaving heart e.g. vasodilation ≈ reduce aortic after load pressures   - Metabolic demand: reduce sympathetic drive + increase PSNS tone; reduce contraction rate (chronotropy)

Answer 93

1) Vasodilators: organic nitrates; nirocandil, calcium antagonists  - Reduce preload or after load   2) Slow heart rate: ß-blockers + ivabradine  and r - Reduce metabolic demand of the muscle

Answer 94

Initial stretching of cardiomyocytes prior to contraction ≈ muscle sarcomere length - HR - Atrial contractility - Ventricular compliance - Venous return - Aortic pressure

Answer 95

Load heart must eject blood against ≈ closely related to aortic pressure ``` σ = ventricular wall stress  P = Pressure   r = radius  h = wall thickness ``` Factors: - Aortic pressure - TPR

Answer 96

Functional hypertrophy (e.g. LV) ≈ increased sarcomere units per area ≈ thickened wall ≈ increase h; P x r remains same ≈ reduced ventricular wall stress ≈ reduced after load as sarcomere units share tension (P x r)

Answer 97

Increase after load ≈ Frank-Starling curve down ≈ reduce SV h/e increased left-ventricular end-diastolic pressure (LVEDP).   - Increase in after-load ≈ decreased velocity in fibre shortening (force-velocity relationship) ≈ reduced rate of volume ejection ≈ more blood left within ventral ≈ end-systolic volume increased (increased pressure)

Answer 98

Decrease arterial pressure ≈ decreased after-load ≈ ventricle requires less P to open aortic valve (reduced pressure gradient aorta:LV) ≈ valve open ejection velocity increased (b/c decreased after load ≈ increased velocity of cardiac fibre shortening) ≈ increased ejection volume ≈ reduced ESV ≈ less blood in LV added to by ventricular systole ≈ reduced EDV ≈ decrease in EDV < decrease in ESV thus SV increased (SV = EDV - ESV)

Answer 99

Afterload increase ≈ reduced SV ≈ increase LVEDP ≈ end-systolic volume increased (incomplete ejection due to decreased velocity in fibre shortening) ≈ residual volume ≈ residual volume added to end-diastolic volume ≈ secondarily increases pre-load via Frank-Starling Law

Answer 100

Parasympathetic input ≈ vagus nerve (CNX) ≈ ACh at muscarinic receptors (M2) target cells ≈ decrease slope of pacemaker potential ≈ negative chronotropic effect ≈ decrease HR

Answer 101

Reduced parasympathetic tone + Increased sympathetic tone via sympathetic trunk ≈ Reduced inhibition via ACh at M2r + NA @ ß1 adrenoceptors ≈ increase slope of pacemaker potential ≈ positive chronotropic effect + positive inotropic effect ≈ increase HR and force of contraction

Answer 102

1) ß-blockers  (Bisoprolol, Atenolol)  2) Calcium antagonists   (Amlodipine; Lercanidipine; Diltiazem; Verapamil) 3) Organic nitrates (GTN, isosorbide mononitrate)   4) Potassium channel activators (Nicorandil)    5) Other (Ivabradine; Ranolazine)

Answer 103

ß1 antagonist in heart + kidneys --> reduce Gas --> reduce cAMP --> reduce PK --> reduce chronotropy and inotropy and antidysrhythmic action

Answer 104

- Bradycardia - Confusion - Dizziness - Dry eye - Dyspnoea - Erectile Dysfunction - Fatigue - Nausea - Peripheral coldness - Visual impairment - Syncope

Answer 105

X opening of L-type CaVg ≈ block Ca2+ entry ≈ inhibit calcium entry upon depolarisation ≈ reduce chronotropy + inotropy --> reduce after-load + dilate coronary vessels

Answer 106

Headache (cerebral flow) Constipation (reduced GI flow) Flushing/heat Ankle oedema (increased diameter causes reduced P --> FS Fluid Exchange)

Answer 107

Metabolised to NO ≈ relax SMCs ≈ vasodilation ≈ increased flow to meet demand ≈ reduce preload and EDV (less F-S mechanism) + dilation of collateral coronary vessels (higher [NO]) to reduce afterload

Answer 108

K+-ATPase activation (efflux) ≈ hyperpolarization ≈ reduced contraction of smooth muscle ≈ reduced afterload (increase EF) + reduced venous return (EDV)

Answer 109

Headaches Dizziness Flushing

Answer 110

Inhibit F-type channels ≈ reduce If ≈ Reduce Na+ ≈ reduce pacemaker activity

Answer 111

Inhibit Na+ channel ≈ indirectly stop Ca2+ in cardiac

Answer 112

Umbrella term for syndrome, collection of symptoms, due to decreased blood flow in coronary arteries (ischaemia) ≈ unstable angina of coronary artery disease/STEMI/NSTEMI

Answer 113

1) Unstable angina:  - Variable ECG changes   - Normal CTn 2) Non-ST elevation myocardial infarction (NSTEMI): - Variable ECG changes   - Elevated CTn 3) ST elevation myocardial infarction (STEMI):  - ECG meeting STEMI criteria   - Elevated CTn

Answer 114

```  1) Modifiable  - Smoking (pack years)   - BP: diagnosed when? Treated or untreated?  - Cholesterol  - Diabetes  - Weight/diet/lifestyle   ``` 2) Non-modifiable   - FH (M < 55 ; F < 60)  - Sex  - Ethnicity  

Answer 115

* PCx: Pain; Dyspnoea; Palpitation; Syncope; Ankle oedema; Calf pain; Syncope * HPCx: SOCRATES + other Sx * PMHx: Illness + investigations ≈ CVD; HTN; DM; HCL; Rheumatic fever; Murmur; CT disease * DHx: OTC, P, Illicit, Allergies ≈ OTC; NSAIDs; Herbal; Illicit * FHx: Premature death (F = 60; M = 55); Sudden unexplained death; FH; Thrombophilia * SHx: Smoking, Alcohol, Illicit drugs occupation, stress, domestic situation * SEx: Cardiology; Respiratory; GI; Renal; Liver; MSK; Neurology; Dermatology * ICE

Answer 116

SOCRATES * Site: Chest/ Epigastrium/ R or L hypochondrium/R or L lumbar/ Umbilical/ R or L iliac region/ Hypogastrium * Onset: Day/Gradual/Sudden/Precipitants/Similar Sx * Character: Sharp/Stabbing/Heavy/Crushing/Ache * Radiation: Arms/Back/Neck/Jaw/Abdomen * Associated Sx: Nausea/Sweating/Dizziness/Dyspnea/Fever/Cough/Anorexia/Ankle oedema/Dysarthria * Time and duration: Pattern; Time of day; Associated activity; Regularity/Irregularity * Exacerbating and relieving factors: Medication/Moving/Breathing/Eating/Resting/Position/Stress * Severity: 1-10 pain scale

Answer 117

* Intro + ID * Consent * Manage set-up: 45º * End-of-bed inspection: Condition; Sweaty; Pale; SOB; Deformities/Syndromes; Fomites * Hands: Temperature; Capillary refill; Palmar surface; Dorsal surface; Nails (clubbing) * Head/Face: Mouth; Eyelids; Iris; Fundi * Pulses: Radial (collapsing?); Brachial; Carotid * Blood pressure • JVP ± abdominojugular test • Inspect pericardium: Deformity; Pulsations; Scars; Dilated vessels • Palpate precordium: Heaves; Thrills • Auscultation: A (2nd ICS RHS); P (2nd ICS LHS), T (4th ICS LHS), M (5th MCL LHS) - Repeat with bell - Accentuation maneuver: forward + expiration (aortic) and LHS + expiration (mitral) • Lung bases: crackles/consolidation * Inspect lower limbs: Temperature; Colour; Skin; Hair; Amputations; Ulcers * Palpation: Pulses (Femoral; Popliteal; Tibialis Posterior; Dorsalis Pedis); Temperature; Capillary refill time; Peripheral oedema * Buerger’s Test: 45º  lower  reactive hyperemia * Close consultation: Thank; Explain findings; Answer questions

Answer 118

* ECG: STEMI (ST raised ≈ < 2-2.5mm in two contiguous ECG leads) * Glucose: Normal or elevated plasma glucose (hyperglycemia common in setting of acute MI) * Cardiac Troponin: Elevated > 99th percentile of reference limit * FBC: Normal range but can vary – raised CRP * U+E: Normal but can vary – electrolyte disturbances; eGFR recorded early on * Serum lipids: Normal or elevated * ABG: SaO2 < 90%  O2 * CXR: PE; Cardiomegaly; Pacemaker; Clear lung fields; Normal cardiac contour * Echocardiogram: LV changes; valvular defects; RV changes; Pericardial effusion; LV mural thrombus

Answer 119

* ß-Blockers: Bisoprolol, Atenolol * CCBs: Amlodipine, Lercanidipine; Diltiazem, Verapamil * Nitrates: GTN, Isosorbide mononitrate * Potassium channel activators: Nicorandil * HCN channel blockers: Ivabradine * Other: Ranolazine

Answer 120

* Aspirin: 300mg PO * Anti-platelet (P2Y12 inhibitor): Clopidogrel 75mg PO OD * Anti-emetic: Metoclopramide * Analgesia: IV Morphine * Oxygen: if SpO2 < 94% * IV Nitrate (GTN) • Coronary reperfusion therapy: PCI or Thrombolysis (streptokinase)

Answer 121

* Bulk flow of materials * Temperature regulation * Homeostasis * Host defense * Reproduction

Answer 122

1) Pulmonary: RH to lungs  - PSP: 30mmHg  - PDP: 12mmHg    | 2) Systemic: LH to rest of body  - SBP: 120mmHg  - DBP: 70mmHg

Answer 123

* Anterior (sternocostal): RV + RA + LV    * Inferior (diaphragmatic): RV + LV  - Separated from base by coronary sinus    * Base (posterior): LA

Answer 124

* Right margin (R pulmonary): RA * Left margin (L pulmonary): LV + left auricle  - Cardiac impression in L lung * Inferior margin: RV + LV  

Answer 125

* R 3rd CC * R 6th CC * L 2nd CC * L 5th CC Concept: LA --> RV: 2, 3, 5, 6

Answer 126

* Heart tube folds in embryological development * Invaginates into serous pericardium with outer fibrous sac * Ventral looping * Sinus formation (Transverse sinus: arteriovenous plane; Oblique: potential space posterior to LA)

Answer 127

* SVC + IVC + CS + smallest cardiac vein opens into * Atrium proper (smooth surface) * Right auricle (ridges) * Crista terminalis: separates RA from R Auricle from SVC and IVC opening * Limbus of fossa ovalis: RHS of IA septum ≈ site of foramen ovale * Pectinate muscles: ridged inner surface ≈ power for contraction w/o thickening cardiac wall * Tricuspid AV valve: 3 cusps, base of each cusp attached to annulus fibrosus ≈ blood flows forward and medially through valve

Answer 128

* Pulmonary veins x4 open into * Atrium proper (smooth surface) * Left Auricle (ridges) * Pectinate muscles: ridged inner surface ≈ power for contraction w/o thickening cardiac wall  * Falx septi: depressed area on LHS of IA septum by fusion of valve of foramen ovale * Mitral (bicuspid valve): 2 cusps with base of each valve attached to annulus fibrosus; blood flows towards apex of heart

Answer 129

* Pulmonary valve: 3 semilunar cusps - on free edge, nodule of semilunar cusp ≈ each cusp has pulmonary sinus ≈ helps closure of pulmonary valves after systole * Chorda tendinea: fibrous cords extending between papillary muscles + AV cusps ≈ prevent exertion of cusps ≈ prevent regurgitation of blood into atria during ventricular systole; one papillary muscle to more than one cusp * Papillary muscles: 3 ≈ attaching to chorda tendinea attaching to cusps; named relative to position (anterior, posterior and septal) * Trabecula carnea: irregular muscular ridges ≈ thick, course, muscular bundles * Septomarginal trabecula (moderator band): bridge between IV s eptum + anterior papillary muscle ≈ carry R Bundle branch of AV bundle of cardiac conduction system ≈ passes from septum to base of anterior pituitary muscle ≈ contractile impulses reach ≈ contract in synchrony   * Infundibulum (conus arteriosus): leads to pulmonary trunk ≈ blood flows upwards, backwards and to the left through this valve ≈ promotes laminar flow

Answer 130

* Trabecula carneae: irregular muscular ridges * Papillary muscles: 2 ≈ attaching to chorda tendinea attaching to cusps; named relative to position (anterolateral and posteromedial)  * Chorda tendinea: fibrous cords extending between papillary muscles + AV cusps ≈ prevent exertion of cusps ≈ prevent regurgitation of blood into atria during ventricular systole; one papillary muscle to more than one cusp   * Aortic valve: 3 semilunar cusps ≈ ≈ superior surfaces of cusps and aortic wall bear aortic sinuses ≈ origination for coronary arteries * Aortic vestibule: leads to aorta ≈ blood flows upwards, backwards and to the right ≈ laminar flow

Answer 131

* Superior Vena Cava: R 3rd CC and sternum; Avalvular; intervenous tubercle (black) * Inferior Vena Cava: Valve of IVC (X retrograde flow) * Cardiac Sinus: Valve of CS (= X retrograde flow)

Answer 132

* Fibrous ring with connecting areas  structural + functional support * 4 rings (= annulus fibrosus) surround valves * 2 trigones (R+L) between four rings and membranous portions of IA, IV and AV septa Functions of fibrous skeleton: • Cusp attachment • O+I for atrial and ventricular muscles • Insulate atria from ventricles  independent atrial and ventricular contractions

Answer 133

1) Endocardium • Endothelium • Line inner surfaces and valves • Oxygenated directly from blood in chambers 2) Myocardium • Spiral and circular muscle fibres • Originate and insert into fibrous skeleton (annulus fibrosus + trigones) • Atrial musculature --> pectinate muscles • Ventricular musculature --> trabeculae carneae, papillary muscles + septomarginal trabeculae 3) Epicardium • Visceral layer of serous pericardium

Answer 134

* S1: 1st heart sound --> closure of AV valves at systole | * S2: 2nd heart sound --> closure of semilunar valves at diastole

Answer 135

* Aortic Valve: R 3rd ICS * Pulmonary Valve: L 3rd ICS * Tricuspid Valve: R 4th ICS * Mitral valve: R 4th CC

Answer 136

* Aortic valve: 2nd R ICS for S2 * Pulmonary valve: 2nd L ICS for S2 * Tricuspid valve: 4th L ICS for S1 * Mitral valve: 5th L ICS for S1

Answer 137

``` Arterial: 1. Right Coronary Artery: RA, RV, SAN, AVN, IV septum, small areas of LA and LV • SA Nodal branch • Right marginal artery • Posterior interventricular artery • AV Nodal branch ``` Anastomoses with Left Coronary Artery in coronary sulcus and apex ``` 2. Left Coronary Artery: LA, LV, IV septum • Left Anterior Descending Artery (LAD) • Left Marginal Artery • Left Diagonal Branch • Circumflex Artery ``` Anastomoses with Left Coronary Artery in coronary sulcus and apex Concept: RCA usually ‘dominant’ forming posterior part of interventricular septum

Answer 138

* Coronary Sinus: Receives cardiac venous blood; located in the AV groove; Thebesian valve at joining of right atrium * Great Cardiac Vein (Anterior interventricular vein): Drain anterior LV + RV * Left Marginal Veins: Drain left ventricle into Great Cardiac Vein or Coronary Sinus * Inferior Veins of Left Ventricle (Posterior veins): Drain left ventricle * Middle Cardiac Vein (Posterior interventricular vein): Drains posterior LV + RV draining into Coronary Sinus or directly to Right Atrium * Small Cardiac Vein (Right Cardiac Vein): Drains right ventricle

Answer 139

* Great-Lad: Great Cardiac Vein + Left Anterior Descending (LAD) Artery * Mid-Post: Middle Cardiac Vein + Posterior Interventricular Artery * Small-Margins: Small Cardiac Vein + Right Marginal Artery

Answer 140

• SAN: anterior to SVC opening, superior to crista terminalis  • AVN: postern-inferior part of IA septum, close to opening of coronary sinus   • AV Bundle/ BoH: Runs along membranous part of IV septum + conductive route through the fibrous skeleton • R+L Bundle Branches:  i) Right Bundle Branch: Descends on RHS of IV septum ≈ enters septomarginal trabecula to reach base of anterior papillary muscle ≈ splits into Purkinje fibres spreading out into ventricular walls  ii) Left Bundle Branch: Descends on left side of membranous part of IV septum ≈ splits into Purkinje fibres

Answer 141

• Presynaptic sympathetic fibres T1-5 - Increase chronotropy + inotropy - Dilate coronary arteries • Parasympathetic fibres from Vagus Nerve (CN X) - Decrease chronotropy + inotropy - Vasoconstriction of coronary arteries

Answer 142

1) Hepatic circulation: • Ductus venosus --> Ligamentum venosum 2) Pulmonary circulation • Foramen ovale --> Limbus of fossa ovale/falx septi • Ductus arteriosus --> ligamentum arteriosum

Answer 143

``` Cellular Processes • Action potential • L-type DHP channels open (CaVg) • Ca2+ influx = calcium spark • Calcium binds RyR on SR • Calcium released in Calcium-induced Calcium Release (CICR) • Binds Tpn-C • Reveals binding site on actin • Cross-bridge cycling ``` Concept: Maximum inotropy achieved by SNS input

Answer 144

SNS modification: Catecholamines ≈ ß1 adrenoceptor ≈ Gas ≈ cAMP ≈ PKA ≈ increase calcium from SR and increased calcium stores * A) +Pi to sarcolemmal Ca2+ channel (via protein kinase) ≈ release more Ca2+ from SR * B) +Pi to phospholamban --> reduce inhibition of SR Ca2+-ATPase ≈ sequestration increased for higher cytosolic release of calcium

Answer 145

* Inhibit Na,K-ATPase * Reduced Na+ extrusion * Na+ accumulation * Reduced electrochemical gradient for Ca2+ to diffuse into * Less extracellular calcium * IC Ca2+ and Na+ accumulation * After-depolarisations  arrhythmias

Answer 146

* Absolute Refractory Period (ARP): all NaVg inactivated ≈ no stimuli can trigger AP * Relative Refractory Period (RRP): most NaVg inactivated, some NaVg able to be depolarised ≈ high magnitude stimuli can trigger AP   * Supernormal Period (SNP): majority of NaVg been depolarised but not at low enough levels to return to resting membrane potential ≈ if another AP propagates across cell, increased % that AP occurs

Answer 147

1) Atrial systole 2) Isovolumic contraction 3) Ventricular contraction 4) Isovolumic relaxation 5) Ventricular diastole

Answer 148

* Increase atrial, ventricular and venous pressure   * Increase ventricular volume   * Blood can move retrograde due to no venae cavae valves however inertia of anterograde flowing venous return reduces retrograde flow ECG: P wave ≈ atrial depolarisation ≈ contraction    Pressure: Atria contract to empty following initial pressure gradient-driven atria to ventricle diastole ≈ complete ventricular filling as blood passes through tricuspid AV valve into ventricles • Atrial P > ventricle P ≈ blood filling • Compliant ventricles ≈ fill ≈ increase volume without increase P ≈ compliance  • Atrial contraction ≈ reduced compliance and ventricular P increases   Volume: Ventricle volume increases • 20-25% blood at rest ejected from atria and into ventricles • Final ventricular volume topped up by atrial contraction     Phonocardiogram: S4 ≈ atrial gallop  - LV non-compliant and blood strikes LV

Answer 149

= phase between ventricular systole and opening of semilunar valves - Ventricular pressure rises without a change in volume ≈ isovolumic ≈ ventricular volume remains constant in brief period   ECG: R wave on ECG   Pressure: Earliest rise in ventricular pressure following atrial contraction   Volume: Remains the same   Phonocardiogram: S1  - AV valves shut

Answer 150

- Opening semilunar valves marks onset  - Divided into: rapid ejection (shorter phase) + reduced ejection (longer phase)  - Following reduced ejection period, flow decelerates due to pressure gradient reversal ≈ three waves of venous return: a wave (atrial contraction); c wave (impact of common carotid artery with jugular vein + closure of tricuspid in early ventricular systole); v wave (rise in pressure due to atrial filling) ECG: QRS complex ≈ ventricular depolarisation (rapid ejection) + T wave (reduced ejection) Pressure: Sharp rise in pressure + gradual rise in pressure - Sharp rise in ventricular + aortic pressure ≈ peak ventricular and aortic pressure  - TPR > ventricular pressure ≈ reduced ejection period Volume: Rapid decrease in ventricular volume - Reduced ventricular volume ≈ increased aortic blood flow   - Sharp decrease in atrial pressure at onset of ventricular election from descent of base of heart + consequent stretching of atria  - Peak flow curve coincided with left pressure curve intersecting aortic pressure in ejection   - Reversal of ventricular-aortic pressure gradient in presence of continuous blood flow from LV to aorta is result of potential energy stored in stretched atrial walls ≈ decelerate blood flow from LV to aorta Phonocardiogram: S2 ≈ closure of aortic + pulmonary valves

Answer 151

= Period of time between closure of semilunar valves and opening of AV valves ≈ major fall in ventricular pressure without change in ventricular volume ECG: TP segment ≈ baseline ≈ reference to ST segment election or depression   Pressure: Major fall in pressure    Volume: No change in volume    Phonocardiogram: None

Answer 152

- Ventricular filling after opening of AV valves  - Atrial P > ventricular P ≈ blood flows down pressure gradient into relaxing ventricles ≈ rapid filling phase   ECG: TP segment ≈ baseline ≈ reference to ST segment elevation or depression   Pressure: Decrease in ventricular pressure below left atrial pressure  - Pressure reversal ≈ open mitral valve + tricuspid valve ≈ rapid flow of blood from atria to relaxing ventricles ≈ transient decrease in atrial + ventricular pressure + sharp increase in ventricular volume    Volume: Increase in volume  - Increase in blood flow due to pressure reversal ≈ atrial P > ventricular P ≈ open mitral + tricuspid valve ≈ flow of blood from atria to relaxing ventricles   - Slight increase during diastasis as blood returns from peripheral veins + lungs ≈ slow addition to ventricular filling shown by gradual rise in atrial, ventricular and venous pressure and ventricular volume   Phonocardiogram: S3 ≈ ventricular gallop  - Mitral valve opens ≈ passive filling of left ventricle ≈ large amount of blood striking compliant left ventricle

Answer 153

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

Answer 154

* SV: EDV (Pre-Load: Venous return + Filling Time); ESV (Pre-load: Venous return + filling time; Contractility (ANS); Afterload (Vasodilation) * HR: SNS; PSNS; Hormones; Drugs

Answer 155

• Stroke volume is the ejection fraction (volume of blood) pumped by the left ventricle of the heart in one contraction

Answer 156

• Stroke Volume (SV) = End-Diastolic Volume (EDV) – End-systolic Volume (ESV)

Answer 157

``` 1) Intrinsic: F-S Mechanism • Increased EDV • Increased length-tension relationship • Increased inotropy • EDV increased (increased lusitropy too) ``` ``` 2) Extrinsic: SNS • Sympathetic discharge of NA • Increased chronotropy • Reduced filling with EDV • Reduced ESV • SV increased ```

Answer 158

1. EDV (‘pre-load’) • Venous return (increased load -> stretch sarcomeres to optimal 2.2um -> force of contraction -> increased/optimal inotropy) • Filling time • -> ‘Pre-load’ = initial stretching of cardiac myocytes prior to contraction 2. ESV • Pre-load: Venous return + Filling time • Contractility (ANS)

Answer 159

* SNS drive: ∆ vasculature + veins (arterial pulse pump) -> ∆ capacity -> increase venous return -> increase CO * Muscle pumps: Contractions -> open valves * Inspiration -> Diaphragm descends -> increased intraabdominal pressure + reduced intrathoracic pressure -> reduced pressure in intrathoracic veins + increased pressure in intraabdominal veins -> increased pressure difference -> increased venous return * Blood volume: Increased blood volume -> increased venous return

Answer 160

Frank-Starling Mechanism = Length-tension relationship of cardiomyocyte sarcomeres which yields a pressure-volume curve shown in cardiac muscle. ``` Principle: • Increased EDV (pre-load) • Increased sarcomere stretching • Sarcomeres form optimal cross-bridge • Optimal inotropy ```

Answer 161

``` 1) SNS • NA binds ß1 adrenoceptors • Gas • cAMP • PKA • +Pi  1) Phospholamban (reduce extrusion) + 2) Ca2+-ATPase + CaVg (increase calcium spark) • Increased IC [Ca2+] • Increased chronotropy + inotropy + lusitropy ``` ``` 2) PSNS • ACh binds M2R • Gai • Reduced cAMP • Negative chronotropic + inotropic effects ```

Answer 162

* Cardiac Output provides oxygenated blood into systemic circulation for Gaseous Exchange via Diffusion outlined by Fick’s Law * CO = VO2 / (Ca-Cv) - VO2: Volume of oxygen consumed per minute - Ca: Oxygen content of arterial blood - Cv: Oxygen content of venous blood Principle • Cardiac Output (L/min) = Rate of O2 consumption (L/min) (VO2/Ca-Cv)

Answer 163

* Inversely proportional * Decreased compliance -> reduced change of volume/pressure -> stiffer -> increase in systolic pressure + decrease in diastolic pressure -> Increased Pulse Pressure

Answer 164

* Proportional * Increase stroke volume -> blood volume ejected (SV (EF) = EDV – ESV) -> increased systolic pressure (exceeds runoff doubled) + diastolic pressure falls at same rate -> pressure drops to higher than previous DBP -> new SBP – DBP >>

Answer 165

• MABP = DBP + 1/3 PP

Answer 166

* MABP is Constant in Exercise (homeostasis): increased CO + reduced SVR (TPR) * Increased HR + SV = increased CO

Answer 167

* Inflate cuff * Occlusion of brachial artery  no sound * Begin deflating cuff * Listen to sound at cubital fossa * Pressure taken at First Korotkoff Sound (SBP) * Pressure taken when no sound  laminar flow  Fifth Korotkoff Sound (DBP)

Answer 168

* Age: ATHSCL; Calcification ≈ Reduced compliance * Cuff size: narrow ≈ false elevation. 80/40 rule ≈ Length should be 80% circumference of upper arm and Width 40% of upper arm circumference

Answer 169

• Central blood volume increased ≈ increase venous return ≈ increase EDV ≈ F-S Mechanism ≈ increase CO

Answer 170

• Change in total blood volume + Salt retention + Shift in fluid from interstitial space to plasma - Haemorrhage - Fluid loss - Transfer of fluid from plasma to interstitial space • Change in distribution of blood volume + Transmural P + Venous compliance

Answer 171

• Abnormal valve, septal defect or outflow obstruction ≈ turbulent flow ≈ heard on auscultation

Answer 172

• Innocent murmur: turbulent blood flow due to increased velocity of blood - Athletes - Febrile patients - Pregnant women

Answer 173

* Closure of atrioventricular valves   * Atrial pressure increases ≈ final contraction of 20% volume into ventricles ≈ ventricular pressure rises slightly due to increased volume but also mitigated by compliance ≈ Atrial pressure > Ventricular pressure ≈ AV valves close * S1 sound ≈ Lub

Answer 174

* Closure of semilunar valves  * Ventricular pressure increases ≈ contraction ≈ 120mmHg ≈ semilunar valves open as ventricular P > outflow vessel P ≈ reduced volume and pressure in contraction ≈ outflow P (pulmonary artery and aorta) > ventricular P ≈ semilunar valves close * S2 ≈ Dub

Answer 175

Think of which valves are opened in normal cardiac cycle • S1 (mitral and tricuspid valves shut thus turbulent from from regurgitation or from stenosis of outflow valves) • S2 (aortic and pulmonary outflow valves shut thus turbulent flow from regurgitation or from stenosis of AV valves mitral and tricuspid)   

Answer 176

Systole   Open:   • Aortic stenosis • Pulmonary stenosis    Closed: • Mitral regurgitation • Tricuspid regurgitation

Answer 177

Diastole  Open: • Mitral stenosis • Tricuspid stenosis    Closed: • Aortic regurgitation • Pulmonary regurgitation

Answer 178

* Older age * Congenital abnormalities: subvalvular; valvular (Bicuspid); Supravalvular * Rheumatic fever * CKD/HTN

Answer 179

* Calcification (Aortic sclerosis to severe Aortic Stenosis) * Smoking * Hypertension * Diabetes * Dyslipidaemia * Elevated CRP (inflammatory conditions) * Rheumatic Fever • Congenital (bicuspid valves): subvalvular; valvular (bicuspid); supravalvular (Williams Syndrome)

Answer 180

: Damaging stimuli ≈ inflammatory processes ≈ valvular endocardium damaged ≈ Abnormal blood flow across valve + Narrowing of aortic valve ≈ increased afterload ≈ failure to increase CO on demand ≈ LV HCM ≈ increased myocardial O2 requirement ≈ reduced systemic and coronary flow ≈ reduced myocardial oxygen delivery

Answer 181

* SOBE * Dyspnoea * Cx Pain * Exertional presyncope * Insidious onset

Answer 182

* Ejection systolic murmur: crescendo-decrescendo pattern; radiates to carotid; loudest at 2nd ICS RHS (aortic valve auscultation point) and expiration (RILES) * S2 diminished (advanced AS) * Heavy apex beat * Narrow pulse pressure: reduced SBP and DBP remains = ∆PP * Paradoxically split S2 (severe AS, aortic valve so delayed it follows pulmonic valve closure in expiration) * Gallavardin’s Phenomenon: holosystolic murmur at apex of heart occurring in older patients with calcific AS; mimics mitral regurgitation

Answer 183

* ECG: QRS amplitude increased – LV hypertrophy * CXR: Cardiomegaly; Pulmonary oedema (air space opacification, Bat-wing distribution, Kerley B lines * Echocardiogram: Stiff leaflets; Retrograde flow (Doppler); Bernoulli Equation

Answer 184

Bernoulli Equation: ∆P = 4 (V22 - V12) If V1 < 1.5.. ∆P = 4v2 E.g. V1 = 1 cf V2 = 4 thus use ∆P = 4v2 = ∆P = 4(4)2 = 64mmHg

Answer 185

* Mild < 35mmHg * Moderate: 36-64mmHg * Severe > 65mmHg

Answer 186

Pick and Select dependent on Clinically Stable Asymptomatic; Clinically Stable Symptomatic or Clinically Unstable • Echocardiogram: Follow up in 1-5 years • Medicine withdrawal: Vasodilators which exacerbate peak pressure gradient – Nitrates, CCBs, Nicorandil, ACEi, ARBs, Alpha-blockers, Phosphodiesterase inhibitors • Surgical Valve Replacement - ABX for infective endocarditis prophylaxis - Anticoagulation • TAVR - ABX for infective endocarditis prophylaxis - Anticoagulation

Answer 187

* Bicuspid aortic valve * Rheumatic fever * Endocarditis * Connective tissue diseases * Aortitis

Answer 188

* Congenital: Bicuspid aortic valve * Acquired: Valvular - Rheumatic disease - Degenerative - Endocarditis • Acquired: Supravalvular e.g. Aortic Root Dilation - Marfan’s Syndrome - Takayasu’s - Aortitis secondary to syphilis • Acquired: Traumatic

Answer 189

• Change to valvular function ≈ retrograde flow of blood ≈ increase in left ventricular volume + pressure ≈ increase wall tension (Laplace’s Law: T = PR) ≈ hypertrophy (eccentric hypertrophy >) ≈ systolic hypertension 2º to increased stroke volume ≈ volume overload causes increase in left ventricular end-diastolic volume ≈ increase cavity size ≈ systolic dysfunction

Answer 190

* Dyspnoea (SOBE) * Fatigue * Weakness * Orthopnoea * Paroxysmal Nocturnal Dyspnoea * Ankle oedema

Answer 191

* Ankle oedema * Soft S1: Early coaptation of mitral valve leaflets * Soft or absent S2 * Early diastolic murmur; high pitched; heard at 2nd RHS ICS loudest on expiration * Displaced apex beat

Answer 192

* ECG – non-specific but routine and check for myogenic cause * CXR: Cardiomegaly; Pulmonary Oedema * Echocardiogram: Jet of regurgitation, mixed jet stream

Answer 193

* Annual Follow Up * BP management (minimise dilation): inotropes (dobutamine or dopamine) + vasodilators (nitroprusside) * Surgical Valve Replacement * TAVR

Answer 194

* Streptococcal infection | * Female sex

Answer 195

* Rheumatic fever (95%) * SLE * Serotogenic drugs (e.g. Fenfluramine) * Ageing (Mitral annular calcification) * Amyloidosis * Chest radiation • Congenital deformity: Valvular/Subvalvular

Answer 196

Damage ≈ damage to valvular endocardium ≈ inflammatory processes ≈ fibrosis/calcification of valves ≈ reduce valve orifice ≈ increased LA pressure (referred to lungs) + reduced LV filling reducing cardiac output 1) Increased LA pressure ≈ dilated LA (compliance) ≈ increased pulmonary venous pressure ≈ pulmonary congestion 2) Reduced LV filling pressure ≈ reduced cardiac output

Answer 197

* Dyspnoea * Ankle oedema * Orthopnoea * Paroxysmal Nocturnal Dyspnoea * Atrial fibrillation

Answer 198

* Raised JVP (pulmonary HTN or RV failure) * Atrial fibrillation * Low-pitched rumbling apical mid-diastolic murmur (MDM): heard best 5th ICS MCL LHS, expiration (RILEs) * Absence of silence between S1-S2

Answer 199

* ECG: AF, P mitrale (bifid P wave in lead II, upright P waves in lead I) * CXR: LA enlargement (sail sign), pulmonary oedema * Echocardiogram: Thick mitral valve (X Fishmouth view); lack of movement; small valvular orifice

Answer 200

• Follow-up annually * ß-blockers * Cardiac glycosides (Digoxin) * Anticoagulants (DOACs, anti-platelets, anti-coagulants * Surgical mitral valve replacement * Percutaneous Balloon Valvuloplasty (via Femoral Vein)

Answer 201

* Mitral valve prolapse * Rheumatic disease * Infective endocarditis * PMHx: MI, CHD, Ischaemic Heart Disease * HOCM * Drug abuse (anorectic drugs/dopaminergic drugs)

Answer 202

* Rheumatic Fever * Infective endocarditis * Ischaemic papillary muscle dysfunction * Myxomatous prolapse * Prolapse • Congenital: Congenital mitral stenosis (rare***)

Answer 203

Damage to valvular endocardium or myocardium ≈ inflammatory process ≈ failure of mitral valve to close in S1 sound due to patency ≈ regurgitation from LV to LA in systole ≈ dilation of LA + eccentric cardiac (functional) hypertrophy ≈ increase SV to maintain CO ≈ time ≈ LV dysfunction and increased LV end-systolic diameter

Answer 204

* Dyspnoea (SOBE) * Ankle oedema * Orthopnoea

Answer 205

* Atrial Fibrillation * Displaced apex beat * Pan-systolic murmur (S1-S2): loudest at 5th ICS MCL LHS in expiration radiating to axilla

Answer 206

* ECG: AF, P mitrale (bifid P wave in lead II, upright P waves in lead I) * CXR: LA enlargement (sail sign), pulmonary oedema * Echocardiogram: ∆ leaflet structure; regurgitation (jet stream)

Answer 207

• Annual follow-up * Diuretics * ACEi/ARBs * Nitrates: Nitroprusside * Ionotropic agents: Dobutamine/Dopamine * Surgical mitral valve repair * Mitral Valve Replacement * TMVR * Mitraclip procedure

Answer 208

* Rheumatic fever * Left-sided heart failure * Permanent pacemaker

Answer 209

* Rheumatic Fever * 2º RH dilatation * 2º pulmonary hypertension * Marfan’s Syndrome * Tricuspid valve prolapse • Congenital: Valvular (Cleft Valve)

Answer 210

Damage ≈ inflammation ≈ valve is patent and following ‘closure’, allows regurgitation between S1-S2 ≈ RH dilates + elevated RA pressure ≈ Atrial Fibrillation + RV dysfunction/dilation

Answer 211

* Fatigue * Dyspnoea * Peripheral Oedema * Palpitations (Atrial Fibrillation)

Answer 212

* JVP raised * RV heave * Pan-systolic murmur: left sternal edge, loudest in inspiration

Answer 213

* ECG: Atrial Fibrillation, P mitrale * CXR: Cardiomegaly, pleural or pericardial effusion, pacemaker presence * Echocardiogram: valve morphology/function, regurgitation

Answer 214

* Manage underlying condition * Heart Failure Management and Risk Factor Modification * Surgical Valve Replacement

Answer 215

* Rheumatic Fever * GAS Pharyngitis * Metastatic carcinoid tumours

Answer 216

* Rheumatic Fever (RHD) | * Congenital

Answer 217

Damage (e.g. cross-reactivity between GAS and host-valve tissue) ≈ inflammation ≈ fibrosus of annulus and chordae tendineae ≈ overlap ≈ reduced tricuspid flow into RV ≈ RA pressure increases ≈ RA dilation ≈ Increased retrograde flow into IVC, SVC and cardiac veins

Answer 218

* Dyspnoea * Fatigue * Ankle Oedema

Answer 219

* Elevated JVP (prominent A wave in sinus rhythm) | * Diastolic murmur: heard best at 4th ICS LHS and increased by inspiration (RILEs); mid-diastolic murmur

Answer 220

* ECG: Sinus Rhythm vs Atrial Fibrillation * CXR: RA enlargement, pulmonary opacities * Echocardiogram: Elevated tricuspid valve gradient, reduced flow

Answer 221

* Annual Follow-Up * Surgical Tricuspid Valve Replacement * Percutaneous Balloon Valvuloplasty

Answer 222

* Congenital heart disease * Pulmonary stenosis/Valvuloplasty * PMHx endocarditis/Rheumatic Fever/Carcinoid Heart Disease

Answer 223

• Congenital heart disease (Majority): ToF * Left-sided heart failure e.g. Mitral Valve Stenosis * Rheumatic Fever * Endocarditis * Carcinoid Heart Disease * Syphilis * Trauma

Answer 224

Damage to valves ≈ patency ≈ volume overload in RV ≈ Dilation of RV + RV hypertrophy ≈ Equalisation of pulmonary artery pressure and RV pressure in diastole ≈ RV failure with RHS SV reduced ≈ Reduced oxygenation of blood ≈ Oedema, dyspnoea, fatigue

Answer 225

* Dyspnoea * Fatigue * Dizziness * Palpitations * Syncope * Cyanosis

Answer 226

* RV heave | * Low-pitched diastolic murmur: heart best at 4th ICS LHS on inspiration (RILEs) and sat forward

Answer 227

* ECG: Non-specific * CXR: pulmonary artery dilation; RV dilation * Echocardiogram: regurgitant jet; RV dilation

Answer 228

* Medical Management of Heart Failure | * Surgical valve replacement

Answer 229

* Rheumatic Fever * Endocarditis * Carcinoid disease of the Heart • Congenital (majority)

Answer 230

Damage ≈ inflammation/structural change ≈ reduced valve orifice ≈ reduced blood flow from RV to pulmonary artery ≈ increased ESV in RV ≈ RV hypertrophy (concentric and eccentric hypertrophy)

Answer 231

* Chest pain * Syncope * Fatigue * Dyspnoea

Answer 232

* RV heave * Systolic thrill * Ejection Systolic Murmur: Loudest in inspiration + sitting forward at 2nd ICS LHS * Harsh ejection systolic murmur

Answer 233

* ECG * CXR: RV dilatation * Echocardiogram: Reduced flow through valve; valve damage/structural changes Pulmonary stenosis

Answer 234

Aortic sclerosis/stenosis Pulmonary stenosis Patient group: - Pregnancy - Fever - Athletes

Answer 235

Aortic regurgitation Pulmonary regurgitation

Answer 236

Mitral regurgitation Tricuspid regurgitation Ventricular septal defect Mitral prolapse

Answer 237

Mitral stenosis Pulmonary stenosis

Answer 238

* General Anaesthetic | * Midline sternotomy

Answer 239

* LOS * Mortality risk * Morbidity risk * CVI * MI * Haemorrhage * Infection * Pacemaker * Renal failure * Infective endocarditis * Regurgitation * Stenosis

Answer 240

* Biological tissue valve: Attached to mesh framework scaffold * Percutaneous or transapical approach • Indications: Elderly, Frail, Major comorbidities, Risk of Surgery

Answer 241

Advantages: + Minimally-invasive + Lower risk Disadvantage: - New technique - Longevity: Unknown

Answer 242

Mechanical Prosthesis • Longevity • Lower risk of needing repeat surgery * Anticoagulation mandatory * No option for percutaneous intervention in future Bioprosthesis • No anticoagulation required • Option for percutaneous intervention in future * Higher risk of repeat surgery * Less longevity

Answer 243

1) Bicuspid Aortic Valve: Bicuspid, X tricuspid semilunar 2) Atrial Septal Defect: Interatrial septum patent 3) Ventricular Septal Defect: Interventricular septum patent 4) Tetralogy of Falot

Answer 244

Turbulent flow ≈ valve thickening + stiffening ≈ valvular dysfunction (earlier cf degenerative aortic valve disease)

Answer 245

- Passive management  - AVR   - TAVI   - Aortic surgery  

Answer 246

Interatrial septum patent ≈ L atrium P > R atrium P ≈ L to R shunt ≈ reduced efficiency of CO ≈ RH pressure increases ≈ RH dilatation ≈ SOBE, dyspnoea etc

Answer 247

- Surgical closure   | - Percutaneous closure  

Answer 248

Interventricular defect ≈ LV P > RV P ≈ L to R shunt ≈ recirculation of oxygenated blood ≈ RV dilatation + LV hypertrophy

Answer 249

- Surgical closure   | - Percutaneous closure

Answer 250

Pulmonary stenosis, RV hypertrophy, overriding aorta and Ventricular septal defect ≈ constriction of blood outflow tracts + heart working harder ≈ HCM ≈ poor systemic oxygen delivery ≈ intermittent cyanosis (infants), tetralogy spells: cyanotic, sleepy (unresponsive) and irritable ≈ relieved by squatting

Answer 251

 - Tetralogy spells  - Cyanotic   - Tired   - Irritable    

Answer 252

Transannular patch

Answer 253

Stenosis of descending aorta ≈ reduced flow to descending aorta + systemic circulation

Answer 254

1) Valve Dysfunction 2) Ventricular Dysfunction 3) Arrhythmias

Answer 255

1) Valve • Surgical Replacement • TVR • Valvuloplasty 2) Ventricular Dysfunction * ACEi/ARBs * ß-blockers * Diuretics * Cardiac Resynchronisation Therapy: Pacemaker fitted to both ventricles or both SAN and AVN * Left Ventricular Assist Device (LVAD): Mechanical Circulatory Component  pump blood into aorta via circumventing blood outside heart * Transplant: Replace with anatomically and physiologically functioning heart 3) Arrhythmias • ß-blockers • Cardiac glycosides • Anti-arrhythmic * Pacemakers * Implantable Cardiac Defibrillators * Catheter Ablation

Answer 256

Process to prevent and stop bleeding, to keep blood within a damaged blood vessel which involves coagulation, blood changing from a liquid to a solid (gel) which has three steps: vasoconstriction, temporary blockage by platelet plug and blood coagulation (= formation of a fibrin clot). This seals the hole until tissues are repaired.

Answer 257

Simple squamous cells (endothelial cells) lining the interior surface of blood vessels and lymphatic vessels forming a barrier between intravascular volume in the lumen and the rest of the vessel wall

Answer 258

Inhibit platelet aggregation ≈ Reduce haemostasis + aids haemodynamic • Produce thrombomodulin ≈ thrombin control (+ Protein C ≈ Active Protein C ≈ inhibit VIIIa production and Va production) • Produce heparin sulphate ≈ inhibit thrombin production • Release enzymes to degrade platelet granule-derived molecules ≈ Thromboxane • Prostacyclin + NO ≈ Inhibit platelet aggregation + adhesion

Answer 259

Circulating, nuclear fragment of a bone marrow megakaryocytic which functions to maintain integrity of vasculature by producing a platelet plug in the second phase of clotting when attracted by lowered prostacyclin and collagen fragments; TXA2 + serotonin from platelets ≈ vasoconstriction * Nuclear fragments of megakaryocytes * Produced in bone marrow * Stimulated by Thrombopoetin (TPO) ≈ Liver produces TPO * Circulate for 5-10 days * 30% stored in spleen * Destroyed by antibody-mediated macrophage phagocytosis ≈ destruction

Answer 260

a) Platelets in circulation   • Megakaryocytes produced in bone marrow • Pseudopods form from megakaryocytes in endothelium • Platelets bud off of megakaryocytic mixing with RBCs and WBCs in circulation    b) Intrinsic vessel wall damage, exposure of collagen 6, binding GP IIa-IIb + platelet plug     • Breach in endothelium wall ≈ exposes subendothelium   • Prostacyclin levels lower subendothelium cf endothelium + collagen + subendothelial molecules ≈ platelet sticking ≈ platelet plug   • Platelets bind glycoprotein receptor (Gp Ib-Ix) via von Willebrand Factor (vWF) located in association with type VI collagen microfibrils in subendothelium   • TXA2 + serotonin released from ‘activated platelets’ ≈ vasoconstriction ≈ reduce vessel lumen ≈ reduced blood flow ≈ reduced blood loss • Increase platelets adhere to site @ GP IIa-IIb platelet receptor in combination with plasma protein fibrinogen   • Platelets reduced from aggregation + extension along endothelium by in-tact endothelium ≈ endothelial cells produce prostacyclin • Platelets changed shape ≈ release granules from platelet cytoplasm ≈ irreversible aggregation   c) Coagulation plug  • ADP, thrombin, thromboxane A2 released ≈ recruit more platelets  • Thrombin catalyses conversion of soluble fibrinogen to fibrin ≈ stabilise platelet plug

Answer 261

Intrinsic pathway: Initiated on exposure to negatively charged non-endothelial surface e.g. collagen • Results in XII (+Collagen) ≈ XIIa (+ XI) ≈ XIa (+IX) ≈ IXa (+X) —> Xa • Production of Factor Xa ≈ Convergence * Xa (+II) ≈ IIa (Thrombin) * IIa (+I) ≈ Ia (Fibrin)

Answer 262

``` 2) Extrinsic pathway: Initiated by tissue factor (TF; Factor III) • Results in VII (+ TF) ≈ VIIa • VIIa (+X) ≈ Xa • Xa (+ II) ≈ IIa (Thrombin) • IIa (+ I) -> Ia (Fibrin) ```

Answer 263

• Protein C: Reduce Factor Va production ≈reduce IIa production) + reduce Factor VIIIa production (≈ reduce Xa production)   - activated by thrombomodulin-thrombin complex   • Co-factor, Factor S: Produce active protein C ≈ Decreased Va and VIIa (+ reduced production)   • Antithrombin: inhibits production of Xa and IIa (thrombin IIa + Xa production from X)    • Heparin cofactor II: inhibits IIa    • Heparin: stimulates antithrombin + heparin cofactor II

Answer 264

System responsible for breaking down clot after clot served purpose in haemostasis which is coordinated by a series of enzymatic reactions. Plasmin is the key driver of the fibrinolytic system.

Answer 265

* Plasminogen (+ tPA) --> Plasmin | * Fibrin (+ Plasmin) --> D-Dimer ± Fibrin Degradation Products (FDP)

Answer 266

* D-Dimer assay | * D-Dimer > FDPs as specific only to fibrin

Answer 267

- FBC - PT - APTT - TCT - Correction tests

Answer 268

1) FBC: platelet count/size/granules but poor assessment of platelet function • Platelet count • Platelet size 2) Prothrombin Time (PT): Ca2+ + plasma (replace that removed by citrate anticoagulant) + brain thromboplastin (≈ TF) ≈ 12-15 seconds cf INR • Extrinsic pathway • Reproducibility • INR Reference point • Monitor liver function: II, VII, IX and X produced in liver • Warfarin therapy monitoring (assess via extrinsic pathway) 3) Activated Partial Thromboplastin Test (APTT): Ca2+ + plasma + kaolin + phospholipids (replace contact factor, collagen) ≈ clotting in 25-36 seconds (more steps in the intrinsic pathway) • Intrinsic pathway • Standard reference point • Monitor heparin therapy 4) Thrombin Clotting Time (TCT): Ca2+ + plasma + thrombin (common pathway) ≈ fibrin --> fibrinogen • Common pathway • Assess presence of fibrinogen • Check for disseminated intravascular coagulation 5) Correction Tests: Mix patient plasma + normal plasma (50:50) --> correction occurs = patient sample deficient in factors • Prolonged PT (>15 s) or APTT (> 36s)

Answer 269

1) Fresh Frozen Plasma (FFP) • Coagulation factors in normal proportion • Dose: 15ml/kg • 200ml plasma from blood • Uses: Liver disease + Severe Haemorrhage 2) Cryoprecipitate (CryoPpt): Concentrated fibrinogen (Factor I), VWF and Factor VIII • Concentrate of Factor I, VWF and Factor VIII • 4º C • Uses: Haemophilia and Severe Haemorrhage

Answer 270

1) Fresh Frozen Plasma (FFP) • Coagulation factors in normal proportion 2) Cryoprecipitate (CryoPpt): Concentrated fibrinogen (Factor I), VWF and Factor VIII • Concentrate of Factor I, VWF and Factor VIII

Answer 271

Warfarin Heparin DOACs Aspirin Clopidogrel

Answer 272

1) Tranexamic Acid: Inhibit tPA --> reduce production of plasmin --> reduced fibrin degradation • Inhibit tPA --> no plasmin production --> no fibrin degradation • IV or Oral

Answer 273

• Uses: Trauma, GI bleeding, post-operative or delivery

Answer 274

Warfarin: Competitive inhibitor of Vitamin K epoxide + Vitamin K reductase -> prevent reduced vitamin K -> reduce production of carboxyglutamate of factors II, VII, IX and X (all hepatic produced) • Inhibit production of reduced vitamin K • Measure by PT (extrinsic pathway)  Factor VII is key in extrinsic pathway

Answer 275

• Uses: DVT, PE, Prosthetic heart valve replacement, Atrial Fibrillation Positives: • Cheap • Measurable effect (INR) • Reversible: Vitamin K or factor concentrate ``` Negatives: • Drug interactions • Slow onset • Unpredictable dose • Regular testing: PT • Haemorrhage risk • Narrow therapeutic window ```

Answer 276

Increased exposure: • Reduce Vitamin K: ABX • P450 enzyme inhibition: ABX, statins, acute alcohol intake • Platelet function ∆: Aspirin, clopidogrel, NSAIDs Decreased exposure: • Enzyme reduction: Rifampicin, Phenytoin, Chronic alcohol intake • High level of vitamin K • Cranberry juice

Answer 277

``` Scoring for risk: CHADSVASc • CHF • HTN • Age (>75) = 2 • DM • Stroke • Vascular Disease • Age (65-74) • Sex Category ```

Answer 278

2) Heparin: Binds anti-thrombin --> reduce Xa + thrombin (IIa) generation • Bind anti-thrombin – Reduce Xa + IIa • Monitor with APTT or fixed dose • Uses: DVT, PE or VTE prophylaxis

Answer 279

Inhibitors of coagulation factor II or X -> decreased factor IIa or Xa • Inhibit X/II -> reduced amount of Xa/IIa -> reduced production of Ia (fibrin) 2 Types: • Direct thrombin inhibitors: Dabigatran • Xa inhibitors: Apixaban, Rivaroxaban and Edoxaban

Answer 280

Benefits: • Limited monitoring needed (renal function must be fine) • Lower bleeding risk: Apixaban • Effective for stroke prevention Negatives: • Shorter half life • Reversal agents are expensive

Answer 281

Aspirin Clopidogrel

Answer 282

1) Aspirin ≈ Irreversible, non-selective COX-1 inhibitor ≈ competitively inhibits arachidonic acid at PGH2 synthase cyclooxygenase active site ≈ reduce formation of PGH2, PGE2 and TXA2 ≈ less platelet aggregation at endothelial surface  

Answer 283

Post-TIA or Post-MI, stroke prevention in AF   

Answer 284

GI bleeding risk, dyspepsia    

Answer 285

inhibit ADP-induced platelet aggregation ≈ anti-platelet drug  • Inhibit ADP-induced platelet aggregation • No reversal agents so effects last for platelet lifespan ≈ 5-10 days  - Can ‘reverse’ with CryoPpt + FFP but takes time   

Answer 286

• Uses e.g.: Recurrent MI prevention, ischaemic stroke, TIAs   

Answer 287

1) Streptokinase or alteplase ≈ tPA ≈ increase activation of plasminogen to plasmin ≈ D-dimer and FDP products  

Answer 288

Stenting and clot removal (thrombectomy) are alternative treatments

Answer 289

Constricting discomfort in the front of the chest, or neck, shoulders, jaw or arms Precipitated by physical exertion Relieved by rest or GTN within 5 minutes

Answer 290

CT Coronary angiography

Answer 291

Beta blockers Calcium channel blockers nitrates

Answer 292

Aspirin Statin Ace-inhibitor Beta-blocker (symptom control and prevention)

Answer 293

Patients who are getting angina in spite of optimal pharmacological treatment (to improve symptoms) Patients with left main stem stenosis and/or multivessel disease (to improve prognosis)

Answer 294

Angina pain not relieved by x2 GTN w/i 15 minutes Pale SOB Nausea Angor animi

Answer 295

Clinical presentation ECG Tpn (serial or high sensitivity)

Answer 296

- Unstable angina - NSTEMI - STEMI

Answer 297

Survival of patient Minimisation of myocardial damage

Answer 298

Aortic stenosis

Answer 299

- Pregnancy - Fever - Anaemia - Thyrotoxicosis - Excessive exercise

Answer 300

Fatigue Dyspnoea(breathlessness) Chest pain Heart Failure Syncope Sudden death

Answer 301

Murmur right upper sternal edge. May be quiet in advanced disease Low amplitude slow rising pulse Low bp – narrow pulse pressure Prominent apex beat Signs of cardiac decompensation (heart failure)

Answer 302

Mechanical Bioprosthetic

Answer 303

Valvular disease Coronary artery disease Hypertension Myocarditis Cardiomyopathy (including alcoholic)

Answer 304

Alleviate symptoms Delay progression Reduce mortality.

Answer 305

Paroxysmal nocturnal dyspnoea or orthopnoea. Ankle oedema Night cough Dyspnoea on exertion

Answer 306

Cardiomegaly Neck vein distension (raised JVP) Rales (crepitations, crackles) Acute pulmonary oedema S3 gallop rhythm

Answer 307

Echocardiogram Bloods: BNP

Answer 308

B. Class I

Answer 309

A. Class II

Answer 310

C. Class III

Answer 311

D. Class IV

Answer 312

- Diuretics (Furosemide) - ß-blockers - ACEi - ARB - MRAs

Answer 313

D. It is an HMG-CoA reductase inhibitor which competitively inhibits the enzyme that catalyses the synthesis of cholesterol, thus lowering cholesterol synthesis

Answer 314

Mechanoreceptors sensitive to change in rate of pressure change and steady/mean pressure

Answer 315

Carotid body baroreceptors + Aortic arch baroreceptors 1. Carotid Body Baroreceptors @ Carotid Artery --> CN IX ≈ NTS (MCVC) 2. Aortic Baroreceptors @ walls of Aorta --> CN X ≈ NTS (MCVC)

Answer 316

Carotid sinus/body receptors > Aortic arch baroreceptors ≈ respond to pressures ranging from 60-180mmHg cf aortic arch receptors have higher threshold pressure and less sensitive than carotid sinus receptors ≈ small ∆ in arterial pressure ≈ ∆ carotid body baroreceptors > aortic arch baroreceptors

Answer 317

Cardiopulmonary baroreceptors ≈ low-pressure receptors ≈ sense central blood volume ≈ stretch of vessel walls (compliance means large volume change causes little pressure change due to compliance) ≈ atria, ventricles, veins and pulmonary vessels

Answer 318

Blood volume reduced ≈ reduced blood pressure ≈ cardiopulmonary baroreceptors detect deviation ≈ SNS increase CO (chronotropy, inotropy, dromotropy, lusitropy) + TPR (arteriolar vasoconstriction + venous vasoconstriction) + PSNS decrease inhibition of CO

Answer 319

Medullary Cardiovascular Control Vasomotor Centre (MCVC)

Answer 320

Adaptation in physiology and pathology ≈  - Exercise  - Hypertension

Answer 321

Baroreceptor reflex ≈ Arterial blood pressure ≈ set-point (or cardiopulmonary baroreceptors) ≈ baroreceptors accustomed ≈ firing rate ≈ Sinus nerve of Hering (Glossopharyngeal nerve CNIX) + Aortic nerve (Vagus nerve CNX) ≈ NTS (MCVC) ≈ effect Increase blood pressure ≈ deviation from set-point ≈ baroreceptors detect increased arterial blood pressure ≈ increased firing rate = increased frequency of impulses ≈ relayed along CNIX and CNX ≈ NTS (MCVC) ≈ PSNS (medial portion of MCVC) > SNS (lateral portion of MCVC) i) Reduced SNS tone ≈ reduced NE at ß1, ß2 and a1 ≈ reduced cardiac output (chronotropy, inotropy, lusitropy, dromotropy) + reduce TPR (reduced arterial constriction + reduced venous constriction)   ii) Increased PSNS tone ≈ increased ACh at M2r ≈ reduced CO (negative inotropy + negative lusitropy)

Answer 322

Decrease blood pressure ≈ deviation from set-point ≈ baroreceptors detect decreased blood pressure ≈ reduced firing rate ≈ reduced frequency of impulses ≈ relayed along CNIX and CNX ≈ NTS (MCVC) ≈ PSNS (medial portion of MCVC) < SNS (lateral portion of MCVC) ≈  i) Increased SNS tone ≈ increased NE @ ß1r + a1r; ß2r ≈ increased CO (chronotropy, lusitropy, inotropy, dromotropy) + increase TPR (arterial constriction + venous constriction) + increase renin secretion from kidney (renal ß2 receptors)

Answer 323

Baroreceptor maintains constant pressure + preserves flow to brain and heart as vasculature of heart and brain do not participate in baroreceptor reflex-mediated changes ≈ no vasoconstrictor effects + perhaps vasodilator effects ≈ not impinged ≈ prevents blood flow falling when pressure falls

Answer 324

Graph with Frequency of impulses (Hz) against arterial blood pressure (mmHg) with curve being sigmoidal  - Increase arterial blood pressure ≈ increase sigmoidal curve RHS ≈ increase Hz of impulses from carotid body    - Decrease arterial blood pressure ≈ decrease sigmoidal curve LHS ≈ decrease Hz of impulses from carotid body

Answer 325

Reduce minute-to-minute variations or arterial pulse shown experimentally by denervation of baroreceptors ≈ oscillating arterial pressure  

Answer 326

Blood Pressure = TPR x CO 1) Heart - SV - HR = CO 2) Peripheral arterioles - TPR

Answer 327

Blood flow to medullary CVCC reduced ≈ Emergency pressure control system - Increased TPR - Increased SNS - Increased Systemic Arterial Pressure

Answer 328

SNS + PSNS + Adrenaline

Answer 329

SNS + EDV + Adrenaline

Answer 330

Venous return = - SNS of veins - BV - Respiratory pump - Skeletal muscle pump

Answer 331

- Blood viscosity | - Arteriolar radius

Answer 332

Control of body fluid volume ≈ blood pressure control via kidneys ≈ renal-body fluid feedback system ≈ arterial pressure increases = urine production increases = diuresis OR arterial pressure decreases ≈ urine production decreases = reduced diuresis

Answer 333

Increased ECF volume ≈ increased blood volume ≈ increased mean circulatory filling pressure ≈ increased venous return of blood to the heart ≈ increased cardiac output ≈  - Autoregulation ≈ increased total peripheral resistance ≈ increased arterial pressure   - Increased arterial pressure ≈ increased urine output

Answer 334

Balanced thus increase pressure ≈ urine output increased cf reduced pressure ≈ urine output decreased

Answer 335

Antidiuretic hormone, arginine vasopressin is a peptide hormone released from the posterior pituitary glad in response to hypovolemia and increased osmotic pressure

Answer 336

Osmotic pressure increased Hypovolemia Hypotension AGT II increased

Answer 337

Dehydration ≈ increased [salt] ≈ ∆ osmolarity ≈ osmoreceptors in Hypothalamus sense ≈ trigger AVP/ADH ≈  1) increase water permeability in renal collecting ducts ≈ blood volume ≈ reduced urine production    2) Vasoconstriction ≈ increase total peripheral resistance

Answer 338

Renin-angiotensin-aldosterone system (RAAS) ≈ blood volume and vascular resistance system influencing CO and arterial pressure

Answer 339

1. Angiotensinogen @ Liver 2. Renin @ JGA cells - Proteolytically cleaves AGTen --> AGT I 3. ACE @ Pulmonary Endothelial cells - > Cleaves AGT I to AGT II 4. AGT II @ numerous sites - Increase TPR @ Peripheral vessels - Increased secretion of ADH @ Posterior Pituitary - Increased aldosterone @ Zona Glomerulosa - Increased efferent vasoconstriction to maintain GFR @ Efferent arteriole of Glomerulus

Answer 340

Atrial-natriuretic peptide ≈ AA peptide synthesised and stored in muscle cells ≈ released in response to stretch of atria + helps oppose effects of RAAS  

Answer 341

Increase as MCVC neurones inhibit firing of preganglionic PSNS ≈ reduced ACh ≈ reduced PSNS tone ≈ increase HR

Answer 342

Decrease as MCVC neurones increase firing of preganglionic PSNS ≈ increased ACh ≈ increased PSNS tone ≈ decrease HR

Answer 343

Transection of spinal cord ≈ ∆ thoracolumbar outflow ≈ reduced basal sympathetic tone on heat and vasculature ≈ reduced ACh from preganglionic neurones ≈ NE from postganglionic sympathetic nerves ≈ reduced binding of ß1 at nodal cells and ventricular cardiomyocytes + reduced NE at a1 + ß2 (a1 predominates) ≈ tonic firing ≈ spinal shock ≈ blood pressure falls

Answer 344

detected by a delta fibres + c delta fibres ≈ afferent neurone ≈ dorsal horn of spinal cord ≈ ascending afferent neurone ≈ spinothalamic tract ≈ synapse in thalamus ≈ integration ≈ efferent SNS output ≈ increase NE at ß1, a1 and ß2 ≈ increase CO, SVR and mean arterial pressure

Answer 345

deep pain c delta fibres ≈ afferent neurone ≈ dorsal horn of spinal cord ≈ ascending afferent neurone ≈ spinothalamic tract ≈ synapse in thalamus ≈ integration ≈ reduced SNS > PSNS ≈ PSNS tone dominates ≈ increased ACh at M2r ≈ reduced CO, reduced SVR and reduced blood pressure ≈ hypotensive response

Answer 346

Bradycardia and hypotension as mimics myocardial ischaemia in the posterior or inferior myocardium

Answer 347

Emotional stress ≈ vasovagal syncope ≈ dramatic drop in chronotropy, cardiac output and SVR

Answer 348

Cold water on face + rise in PCO2:O2 (= pH drop) ≈ detected by thermoreceptors ≈ relayed by Trigeminal nerve; detected by chemoreceptors centrally ≈ relayed to CNS ≈ integrated by CNS ≈ efferent SNS drive + PSNS decline ≈ peripheral vasoconstriction + reduced HR ≈ reduced metabolic demand however cerebral + cardiac arteries remain unaffected ≈ prolong survival

Answer 349

Renal hypoxia +/- reduced Hct ≈ EPO release ≈ bone marrow output increases ≈ erythropoiesis ≈ increase circulating mass of RBCs ≈ increase plasma volume with larger RBC mass

Answer 350

1) Compensated shock (non-progressive): normal CV regulatory mechanisms compensate for initial decrease in CO + arterial pressure ≈ baroreceptor response + hormonal (RAAS + ADH/AVP) ≈ increase HR + SVR ≈ increase CO  E.g. unit of blood 2) Progressive shock: positive-feedback cycle ≈ blood pressure decreases to level below autoregulation of blood flow in heart and brain ≈ organs maintain CV system, (heat and brain) deteriorate due to hypoperfusion.  MOA: Coronary circulation compromised ≈ myocardial contractility reduces ≈ reduced HR + SV ≈ reduced CO; Brain hypoperfusion ≈ deterioration of vasomotor centre in brain ≈ reduce vascular resistance ≈ reduce venous return + SVR ≈ reduce arterial pressure 3) Irreversible shock: Cardiac and cerebral function irreversible ≈ poor tissue oxygen delivery on tissue metabolism ≈ depressed mental function; loss of consciousness; renal failure and generalised muscle weakness

Answer 351

Pulse Pressure = SBP – DBP MAP = 1/3 PP + DBP

Answer 352

Relationship between volume and pressure which is generated by the presence of the volume and property of vessel undergoing deformation Complicance = ∆V/ ∆P

Answer 353

Non-Compliant: Rigid tubes resisting expansion when internal pressure rises - Big change in P with small change in V - Capillaries + Arterioles Compliant: Increase in pressure leading to change in vessel wall and change in volume - Small change in P with large change in V - Arteries + Veins

Answer 354

T = P R Aneurysm: Weakening wall thus radius increases to reduce the tension as P remains the same, may swell until potential rupture.

Answer 355

Capillaries: Extremely thin (low R) and withstand pressure. T = PR and radius is low so pressure reduced prior to blood reaching capillaries to reduce tension. This requires less muscular wall.

Answer 356

Sympathetic Adrenaline AGT II AVP Myogenic response Endothelin-1

Answer 357

NO-releasing nerves Adrenaline ANP ``` Hypoxia K+, CO2, H+ Adenosine NO BK ```

Answer 358

Skeletal: Long fibres; multinucleate; peripheral nucleus; voluntarily controlled; striated Cardiac: short fibres; single nucleus; central nucleus; involuntary; striated; lipofuscin granules Smooth muscle: single nucleus; central nucleus; involuntary; non-striated

Answer 359

``` GI disturbances Rash Insomnia Angio-oedema Myositis ```

Answer 360

GI disturbances | Myositis

Answer 361

GI symptoms

Answer 362

``` Flushing Itching Nausea Numbness and tingling Worsens gout Diabetes Angina ```

Answer 363

``` Nausea Soreness at site Itchiness at site Joint pain Back pain ```

Answer 364

Atorvastatin + Ciclosporin - Close monitoring - Avoid concurrent use - Safety net with myopathy symptoms - Reduce dose -> 10mg Atorvastatin + Clarithromycin - Reduce dose -> 20mg - Safety net with myopathy symptoms

Cardiology Physiology Flashcards

(389 cards)