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100 Cards in this Set
- Front
- Back
- 3rd side (hint)
Location of the SA and AV nodes? |
SA - At the junction of the SVC and the right atria
AV - right posterior part of the interatrial septum |
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How many atrial bundles of purkinji type fibers are there? |
3
Anterior Middle - tract of Wenckebach Posterior - tract of Thorel |
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Name the components of the conducting system of the heart. |
SA node - atrial conducting bundles and atrial muscle - AV node - bundle of His - this splits the left bb off and continues as the right -- ventricular muscle depolarisation
The left BV then splits into the anterior and posterior fascicles |
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Describe the innervation of the heart by the autonomic nervous system. |
PSNS - via vagus nerve - right --SA node, left -- AV node - ACh - endocardial in location
SNS - stellar ganglion - NA - epicardial in location
Each system can inhibit the other one |
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Draw the currents/ electrical potentials of the pace maker cells and ventricular muscle cells. |
Phases 0-4 |
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Describe the phases of of an action potential through a cardiac myocyte.
Name the channels / ion currents responsible for each phase. |
Phase 0 - rapid depolarisation (Na I channels) Phase 1 - initial rapid repolarization (inactivation of Na channels) Phase 2 - plateau (slow Ca channels Phase 3 - slow repolarization (K efflux) Phase 4 - resting membrane potential |
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Resting membrane potential of cardiac myocytes? |
-90mv |
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Describe the ACTION POTENTIAL through a pacemaker cell. |
Self initiating AP. Resting potential at -60Mv Slow depolarisation to -40 via T type Ca2+ channels until threshold reached then opening of L (long) Ca2+ channels. Then K channels open causing an efflux and repolarization. Then opening of the h or f (funny) channel - permeable to Na and K which leads into the beginning of phase 0 again |
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What is the affect of vagal stimulation on the cardiac pacemaker ? |
Opening of a special set of K channels which slows the depolarisation effect of the funny current -- and hence prolongs the period prior to depolarisation ie reduces firing of SA node and slows transmission through the AV node
It also slows Ca opening - decreases spontaneous firing rate |
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SNS effect on pacemaker cells? |
NA released - binds beta 1 receptors - increase c AMP - increase opening of L-type Ca2+ channels - increasing rapidity of depolarisation |
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Describe the effects of digoxin on the heart. |
Inhibits Na/K ATPase Increases contractility in systolic heart failure - increase CO Also works like vagal tone on the heart reducing the number of transmissions via the AV node. Used in AF |
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Which part of the cardiac tissue passes action potentials the fastest ? Ie conduction speed |
Purkinje - 4 m/s
<< atria, ventricles, bundle of his 1
<< SA + AV nodes 0.05 |
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Normal length of intervals
PR QSR QT |
PR - 0.12 - 0.2 - Atrioventricular conduction
QRS - max 0.1 - ventricular depolarisation
QT - 0.43 - ventricular actionHey Lydia,
More problems with the quiz... Please direct me to someone else, I'm just not sure who these questions are suppose to go to.
Question 3 - Both contraction of the ciliary body and contraction of the sphincter muscle of the iris causing miosis increase aqueous flow and the text states both mechanisms allow for treatment of glaucoma - therefore it seems unfair to have both options as separate answers within a question, rather than having them combined as the text presents it?
Question 6 - States that Beta 2 agonists can cause hyperglycaemia in diabetics but on page 143 it says Beta receptors increase insulin release and alpha 2 reduce secretion - so therefore wouldnt alpha 2 increase hyperglycaemia
Sorry - Im just confused by the answers! potential |
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Negative QRS is normal in which leads ? |
aVR, V1/2 |
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Inverted T wave normal in ? |
aVR |
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What is the normal cardiac axis? |
-30 to + 110 |
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What is Stokes- Adams syndrome? |
Periods of cerebral ischemia causing dizziness and fainting / syncope secondary to heart block and low HR |
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Describe type 2 heart block? |
Type 1 Mobitz - Wenckebach - prolonging PR then beat is dropped due to progressive AV Block
Type 2 Mobitz - NO lengthening before a beat is dropped - usually due to structure damage below the AV node |
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Channels affected in congenital long QT? |
K channels and Na channels |
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Describe the physiology of wolf Parkinson's white. |
Accessory pathway - bundle of Kent. Usually the AP - passes via both pathways to the ventricles causing a short PR and a slurred upstroke of the ventricles as the AP passes faster down the accessory pathway.
Tachyarrhythmias occur with atrial ectopic which find their way down one of the pathways and uses the other one to re-enter the atria and set up a circuit. |
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Effect of hyperkalaemia on the cardiac action potential? |
Hyperkalaemia - increases the ECF K+ and increases the resting membrane potential from -90mv to <-75mv --> reduces Vmax (rate of rise) + reduces the threshold potential
And also increases the activity of k channels - shortens plateau, faster depolarisation = shorter AP
Ie 1. Reduced RMP 2. Reduced Vmax 3. Shortened AP duration |
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ECG changes with hyperkalaemia. |
Early - > 5.5 - peaked T waves, narrow,
> 6.5 - peaked T waves, prolonged P, PR, QRS, reduction in Vmax
> 7 - no atrial activity, broad QRS, sinoventricular rhythm
> 8 - sine wave - rapidly degenerates into asystole or VF |
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How does calcium stablise the myocardium? |
1. Restores Vmax - despite the reduced resting membrane potential --> hence prevents
2. Restores the gap between RMP and threshold potential which normalizes excitability
3. Boosts calcium dependent excitation and conduction in SAN and AVN in severe hyperkalaemia |
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Normal cardiac output? |
4-6 L /min |
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Normal cardiac output? |
4-6 L /min |
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What is cardiac index?
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CO/ BSA 2.4-3.8L/ min2 |
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Describe the role of NO - nitric oxide in endothelium. |
Shear stress or chemicals (ACh or bradykinin) activate receptors in the cells --> |
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What does endothelin do to the blood vessels? |
Construction when injury occurs - part of clotting |
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Location of main arterial baroreceptors ? |
Origin of internal carotid artery - glossopharyngeal CN Aortic arch - vagus |
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Which of the following are incorrect: 1. The SA node is the normal cardiac pacemaker as it has the highest normal frequency of firing 2. The SA node is located in the right posterior portion of the interatrial septum 3. The AV node is located at the junction of the superior vena cava and right atrium 4. There are 3 bundles of fibers that connect the SA node and AV node - anterior/middle/posterior 5. SA node --> internodal pathways --> AV node --> Bundle of His --> Common bundle --> Right BB + Left BB --> LAF + LPF ... purkinje system |
2. The SA node is located in the right posterior portion of the interatrial septum 3. The AV node is located at the junction of the superior vena cava and right atrium Both incorrect --> the other way around |
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Which of the following are incorrect: 1. A fibrous tissue ring separates the atria and ventricles 2. The right vagus mainly supplies the SA node and the left vagus supplies the AV node 3. Most SNS fibers travel via the Stellate ganglion 4. Inhibition of SNS via Presynaptic ACh; Inhibition of PSNS via Neuropeptide Y 5. Noradrenergic fibers are endocardial where as vagal fibers are epicardial |
5. Noradrenergic fibers are endocardial where as vagal fibers are epicardial - incorrect - other way around |
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Which of the following are incorrect: 1. Resting membrane potential of the heart = -70mV 2. Depolarisation spreads rapidly due to the presence of gap junctions 3. The phases of membrane potential, 0 - rapid depolarisation; 1 - initial rapid repolarisation, 2 - plateau, 3 - slow repolarisation, 4 - resting membrane potential 4. Initial depolarisation is due to Na+ channels 5. Initial rapid repolarisation is due to inactivation of Na channels |
1. Resting membrane potential of the heart = -70mV --> incorrect === -90mV |
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Describe the events in the depolarisation in a single cardiac myocyte. |
0 - Rapid depolarisation -- Na+ influx 1 - Initial rapid repolarisation -- Inactivation of Na+ 2 - Plateau - Ca2+ influx 3 - Slow repolarisation -- Net K+ influx 4 - Resting membrane potential |
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What channel allows for the pacemaker activity of the heart and depolarisation? |
With hyperpolarisation --> the FUNNY channel - H channel - Permeable to Na+ & K+ H current allows for slow depolarisation It then reaches a threshold and opens CALCIUM T type channels (transient) = prepotential --> then L type channels (long lasting) --> impulse |
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Which of the following are incorrect: 1. Atrial and ventricular muscle fibers do not have prepotentials and only discharge spontaneously when injured 2. The depolarisation in pacemaker cells is due to rapid influx of Na channels 3. Prepotentials in pacemakers is due to T type Ca2+ channels 4. ACh hyperpolarises the pacemaker cells via opening K channels = slowly of opening Ca2+ channels 5. ACh mediates its effects via M2 receptors --> increase cAMP |
5. ACh mediates its effects via M2 receptors --> increase cAMP - incorrect - DECREASE cAMP |
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How does Noradrenaline increase the firing rate of cardiac myocytes? |
NA --> B1 receptors --> increased cAMP --> facilitates opening of L type Ca2+ channels --> increasing the Ca2+ influx and hence the rapidity of depolarisation of pacemaker cells - faster depolarisations then the next one can occur quicker |
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Which of the following are incorrect? 1. There is AV nodal delay of 0.5s 2. The Purkinje system has the fastest conduction rate of 4m/s, the SA and AV nodes are the slowest 3. On an ECG the T wave represents ventricular repolarisation 4. Normal PR interval = 0.12 - 0.20 sec 5. Normal QRS < 0.1 sec 5. |
1. There is AV nodal delay of 0.5s - incorrect - 0.1 seconds |
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Inverted T wave is normal in which part of the ECG? |
aVR and V1 |
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Which of the following are incorrect? 1. The base is the heart is formed by the ventricles 2. There is no Q wave in V2 and V3 3. Normal Axis is from -30 to +110 4. Stokes Adams syndrome is cerebral ischemia resulting in dizziness and fainting due to low ventricular rate 5. RAD is suggestive of RVH |
2. There is no Q wave in V2 and V3 - incorrect - V1/V2 |
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Second degree heart block Describe type 1/2. |
Mobitz 1 - Progressive lengthening of PR then beat dropped - Wenckebach Mobitz 2 - Fixed prolonged PR interval, with beat dropped |
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How is a left anterior hemiblock demonstrated on an ECG? |
Left anterior hemiblock = Left axis deviation |
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How is a left posterior hemiblock demonstrated on the ECG? |
Left posterior hemiblock = RAD |
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Main signs of hyperkalaemia on ECG? |
Tall peaked t waves >8.5 - broad, slurred QRS, no atrial activity seen resting membrane potential decreases with increasing ECF K+ = muscle becomes unexcitable |
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Main signs of hypokalaemia on ECG>? |
u wave Long PR ST depession T wave inversion |
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In complete heart block 1. fainting may occur because the atria are unable to pump blood into the ventricles. 2. ventricular fibrillation is common. 3. the atrial rate is lower than the ventricular rate. 4. fainting may occur because of prolonged periods during which the ventricles fail to contract. |
4. fainting may occur because of prolonged periods during which the ventricles fail to contract. --> correct |
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Currents caused by opening of which of the following channelscontribute to the repolarization phase of the action potential ofventricular muscle fibers? A. Na+ channels B. Cl− channels C. Ca2+ channels D. K+ channels E. HCO3− channels |
D. K+ channels |
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Which of the following are incorrect regarding the heart? 1. Contraction of a myocyte lasts 50ms 2. Diastolic Pressure refers to the lowest pressure during diastole 3. In systolic heart failure the CO is preserved 4. 50% of ventricular filling occurs passively 5. beta blockers have been shown to reduce mortality in heart failure |
3. In systolic heart failure the CO is preserved - incorrect - CO is reduced; preserved in diastolic failure 4. 50% of ventricular filling occurs passively- incorrect - 70% |
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What mechanical event is linked to diastole? |
ECG = P wave Mechanical: Isovolumetric relaxation of the ventricles with closed valves. Once Ventricular P < Atrial P - AV valves open. Blood flows into the ventricles ~70% then pumped by atrial systole. These valves then close |
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What occurs during systole? |
Beginning = AV valves close - 1st heart sound Isovolumetric contraction against closed aortic/pulmonary valves until P > aorta (80mmHg)/pulmonary artery (10mmHg). Valves open --> Ejection of blood until P falls below aortic and valves close again = P2 sound ECG - QRS complex |
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Which of the following are incorrect: 1. S1 corresponds to closure of the AV valves; S2 corresponds to the closure of the semilunar valves 2. Peak pressure in the Pulmonary artery is ~25mmHg 3. Normal Stroke volume =150ml 4. End Diastolic volume = 130ml 5. End systolic volume = 50ml |
3. Normal Stroke volume =150ml - incorrect ---> 80-90ml |
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Normal ejection fraction? |
65% Stroke volume ~ 80-90ml EDV = 130ml ESV = 40-50ml |
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Order the following events: Isovolumetric contraction Right ventricular ejection phase Left ventricular ejection phase Atrial systole AV closure Left ventricular depolarisation Right ventricular depolarisation |
Atrial systole AV closure Left ventricular depolarisation Right ventricular depolarisation Isovolumetric contraction Right ventricular ejection phase (due to low Pulmonary Pressure to overcome) Left ventricular ejection phase |
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Draw the normal pressure volume loop for the left ventricle |
d-a = diastolic filling a AV valves close a-b = isovolumetric contraction b = aortic valve opens b-c = Ventricular ejection c = aortic valve closing c-d = isovolumetric relaxation |
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Which of the following is incorrect: 1. Ventricles can theoretically contract at a rate of 400bps 2. The maximal AV conduction is 230bps 3. The heart cannot be tetanized 4. 5. |
Note - rates >230 are usually due to paroxysmal VT; AV node refractory period causes the maximal conduction rate |
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What are the terms total electromechanical systole (QS2), preejection period (PEP) and left ventricular ejection time (LVET) refer to? |
total electromechanical systole (QS2) - time from beginning of QRS to closure of Aortic valve (S2) preejection period (PEP) - QS2 - LVET = PEP (period of isovolumetric contraction) left ventricular ejection time (LVET) - Period from the carotid pressure rise to the dicrotic notch |
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A collapsing pulse is associated with ? Other names? |
Aortic insufficiency Corrigan or water-hammer pulse |
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What is the dicrotic notch? |
The dicrotic notch is a small oscillation on the falling phaseof the pulse wave caused by vibrations set up when the aortic shuts. Only visible on a pressure wave recording |
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The beginning of systole is signified by ? End of Systole? |
Beginning: The R wave on the QRS Closure closure of the AV valves (S1) End: Semilunar valves closing (S2) End of T wave |
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Draw a normal JVP |
A - Atrial systole C - Tricuspid Closure + bulging of valve due to ventricular contraction X slope - Atrial relaXation V - Venous atrial filling then tricuspid opens Y slope - Atrial emptying passive |
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Timing of 4th heart sound? |
Atrial systole due to blood pushed from atria into ventricle - hitting stiff non-compliant ventricle --> HTN, hypertrophy |
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timing of 3rd heart sound? |
Following 3rd heart sound in early/mid diastole Heart failure |
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Which of the following are incorrect: 1. Duration of a cardiac AP = 0.15-0.25ms 2. Duration of skeletal muscle AP = 0.007ms 3. Absolute refractory period of Cardiac muscle > skeletal muscle 4. Venous pressure falls during expiration as a result of increased negative intrathoracic pressure 5. The V wave in the JVP is due to the rise in atrial pressure prior to tricuspid opening |
4. Venous pressure falls during expiration as a result of increased negative intrathoracic pressure - incorrect - during INSPIRATION = Negative pressure |
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Which of the following are incorrect: 1. The first heart sound is soft during bradycardia due to well filling of the ventricles and the leaflets float closed 2. Physiological splitting of the second heart sound occurs during expiration 3. Murmurs are caused by turbulent blood flow ie with high velocity 4. 5. |
2. Physiological splitting of the second heart sound occurs during expiration - incorrect - during EXPIRATION |
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Methods of measuring CO in humans? |
1. ECHO + doppler 2. Direct Fick method - 02 up take 3. Indicator dilution method - ie thermodilution |
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Factors affecting cardiac output? |
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Normal stroke volume at rest? |
70ml |
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Normal cardiac output ? |
Stroke volume x heart rate = Cardiac output Ie 70ml x 70bpm = 4900ml ~ 5L /min |
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What is cardiac index? |
a relation between CO and BSA NORMAL = 3.2L Output/min/m2 BSA |
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Describe the effect of the following on Cardiac Output: 1. Sleep 2. Anxiety/stress 3. Eating 4. Sitting or standing from lying 5. Rapid arrhythmias 6. Pregnancy 7. Exercise 8. High temperature |
1. Sleep - Nil 2. Anxiety/stress - ↑ 3. Eating - ↑ (30%) 4. Sitting or standing from lying - ↓ 5. Rapid arrhythmias - ↓ 6. Pregnancy - ↑ 7. Exercise - ↑ (700%) 8. High temperature - ↑ |
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What is Chronotropic, inotropic... |
Chronotropic - Affecting the heart rate Inotropic - Affecting strength of contraction |
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What is preload and afterload? |
Preload - the degree of myocardial stretch - ie filling / EDV Afterload - resistance against which the blood is expelled ie aortic pressure / diastolic P |
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Starlings law of the heart? |
Energy of contraction is proportional to theinitial length of the cardiac muscle fiber Proportional to EDV Starling’s law ofthe heart - demonstrated on the Frank-starling curve which plots ventricular SV vs EDV |
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Factors affecting EDV? |
Shorter diastole = reduced EDV (ie with tachycardia) Raised intrapericardial pressure - ie pericardial effusion or constrictive pericarditis Reduced ventricular compliance - stiff ventricle from infarction, infiltrative diseases Reduced Preload / venous return (standing, paralysis, hypovolaemia) |
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How do catecholamines have positive inotropic effects ? |
NA --> B1 adrenergic receptor --> Gs --> Activation of adenylyl cyclase + ↑ cAMP --> |
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How are caffeine and theophylline positively inotropic? |
Xanthines They inhibit the breakdown of cAMP |
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How is digoxin positively inotropic? |
inhibition of N/K ATPase results in decreased removal of Ca from the cytosol by Na/Ca exchanger |
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What are the main factors affecting myocardial contractility? |
1. Circulating catecholamines ↑ 2. SNS/PSNS nerve impuses 3. Digitalis/other inotropes + pharmacological depressants 4. Hypoxia/hypercapnia/acidosis ↓ 5. Loss of myocardium 6. Intrinsic depression 7. Force-frequency relation (↑ HR = ↑Ca) - mild effect |
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What is the common feature to all forms of shock? |
Inadequate tissue perfusion |
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Physiological changes in trained athletes - cardiac. |
Lower heart rates Greater end systolic ventricular volumes greater stroke volume at rest |
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Which of the following are incorrect: 1. Basal O2 consumption by the beating heart is 9ml/100g/min at rest - little further can be extracted so further increase in requirement requires increased flow 2. Negative pressure within the thorax during inspiration helps increase venous return 3. Active cellular marrow is called red marrow and is the location of erythropoiesis 4. RBC have a much longer half life than WBC 5. Haematopoietic stem cells are uncommitted, totipotent cells capable of producing any cell in the body |
All correct
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Describe the % of different types of WBC in normal human blood. |
Total - 9000/uL (normal range 4-11000) Neutrophils - 50-70% Eosinophils - 1-4% Basophils - 0.4% Lymphocytes - 20-40% Monocytes - 2-8% |
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Which of the following is incorrect regarding platelets? 1. Half life = 4 days 2. Splenectomy results in thrombocytopaenia 3. Formed from megakaryocytes 4. Normal range 150-500 5. Small granulated bodies, no nuclei |
2. Splenectomy results in thrombocytopaenia - incorrect --> results in thrombocytosis due to reduced clearing |
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The affinity of O2 for Hb is increased by ? |
Alkaline environment Low DPG Low temperature |
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Haemoglobin in the fetus? |
Alpha 2; Gamma 2 --> higher affinity of O2 to allow passage of O2 to the fetus Adult alpha/beta |
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Metabolism of Haemoglobin? |
Hb --> tissue macrophages --> Heme --> biliverdin via heme oxygenase --> bilirubin --> excreted in bile |
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Protein mutation resulting in hereditary spherocytosis? |
Spectrin |
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Order blood types in order of prevalence |
O 45% A 41% B 10% AB 4% US statistics |
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Layers of a vessel wall? |
Intima - with internal elastic lamina Media Adventitia - with external elastic lamina |
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Which of the following is incorrect regarding blood vessels: 1. Arterioles are the resistance vessels due to high SM 2. Veins hold 54% of the blood at any one time 3. Metarterioles feed into arterioles then capillaries 4. Glomerular endothelium have the highest conductivity of all endothelium 5. Brain capillaries have low conductivity |
3. Metarterioles feed into arterioles then capillaries - incorrect - Arterioles --> metarterioles --> capillaries |
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Cross sectional area of the Aorta? Arteries Arterioles Capillaries? |
Aorta - 4.5cm2 Arteries - 20cm2 Arterioles - 400cm2 Capillaries - 4500cm2 |
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Function of pericytes? |
Wrap around capillaries Make BM + ECM Contractile Regulation of endothelial junctions |
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Describe flow in terms of pressure and resistance. |
Flow = Perfusion Presssure/ Resistance |
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How can we determine flow clinically? |
Doppler flow US - reflected back from moving RBC and WBC - the frequency determines the the flow rate |
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Which of the following are incorrect: 1. Blood flow is highest in the center of the blood vessel 2. Critical velocity refers to the velocity at which blood flow becomes turbulent 3. If Reynolds number is >3000 - flow is usually turbulent 4. The velocity of blood in the aorta is high and low in capillaries due to the difference in surface area 5. Velocity is inversely proportional to radius |
5. Velocity is inversely proportional to radius - incorrect - inversely proportional to the 4th power of the radius |
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The capacitance vessels are? |
Veins |
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Normal volume of blood in the heart, lungs, veins and arteries at any one time ? |
Heart - 12% Lungs - 18% Veins >50% Arteries - 8% Capillaries - 5% |
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Estimate of MAP? |
Diastolic + 1/3 (systolic-diastolic) |
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MAP in the foot? 50cm above the head? Heart level? Given MAP =100mmHg |
Foot = 180mmHg
50cm above the head = 62mmHg Heart level = 100 |
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Venous pressure in the foot? Thigh Heart? |
Foot - 80mmHg Thigh - 60mmHg Heart - 0 |
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Which of the following are incorrect regarding blood vessels? 1. Capillary pressure is ~ 32 at the arteriolar end and 15 at the venous end 2. Venous pressure at the ankle is ~ 85-90mmHg 3. Primary hyperaldosteronism is the 2nd most common cause of HTN 4. Essential hypertension causes 88% of HTN |
None - all correct |
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