Phsyiology Flashcards

Question

What do the P wave, QRS complex and T wave represent?

Answer 1

P wave = atrial depolarisation QRS complex = ventricular depolarisation T wave = ventricular repolarisation

Answer 2

A fib: - random atrial activity - random ventricular capture - irregularly irregular rhythm Flutter: - organised atrial activity - 300/min - ventricular capture at ratio to atrial rate (2:1 = 150bpm) - Usually regular/ irregular if ratio varies

Answer 3

Allow atria to contract before ventricular systole 120-200ms (3-5 squares) Long - suggests heart block 1st degree Delayed AV conduction

Answer 4

Electrode •Physical connection to patient in order to measure potential at that point •10 electrodes to record a 12 lead ECG Lead •Graphical representation of electrical activity in a particular ‘vector’ •Calculated by the machine from electrode signals

Answer 5

Bipolar lead •Measures the potential difference (voltage) between two electrodes •One electrode designated positive, the other negative •Unipolar lead •Measures the potential difference (voltage) between an electrode (positive) and a combined reference electrode (negative) •Sometimes known as augmented leads

Answer 6

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

Answer 7

Membrane of heart muscle cell •Normally only permeable to K+ •Potential determined only by ions that can cross membrane

Answer 8

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

Answer 9

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

Answer 10

E= 60log (conc outside/conc inside)

Answer 11

Phase 4 - resting potential Phase 0 - depolarisation - Na+ Phase 1 - Initial repolarization - K+ Phase 2 - plateau - Ca+/K+ Phase 3 - repolarisation - K+ Phase 4 - maintenance of resting potential

Answer 12

Contraction of the heart muscles requires delivery of Ca2+ ions to the cytoplasm

Answer 13

Step 1: Ca influx Step 2: Amplification of Ca with Na Step 3: Ca induced Ca release

Answer 14

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

Answer 15

- SAN - AVN - His/purkinje system

Answer 16

- autonomic tone - drugs - hypoxia - electrolytes - age

Answer 17

Sympathetic stimulation •Increases heart rate (positively chronotropic) •Increases force of contraction (positively inotropic) •Increases cardiac output •Parasympathetic stimulation •Decreases heart rate (negatively chronotropic) •Decreases force of contraction (negatively inotropic) •Increases cardiac output

Answer 18

Controlled by: •Adrenaline and noradrenaline + type 1 beta adrenoreceptors •Increases adenylyl cyclase  increases cAMP

Answer 19

•Controlled by: •Acetylcholine •M2 receptors – inhibit adenyl cyclase  reduced cAMP

Answer 20

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

Answer 21

•Prevents excessively frequent contraction •Allows adequate time for heart to fill

Answer 22

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

Answer 23

Shape change Smooth discoid- speculated +psuedopodia - increases SA - increases possibility of cell-cell interactions

Answer 24

•Platelet activation •Increases number of receptors •Increases affinity of receptor for fibrinogen •Fibrinogen links receptors, binding platelets together (platelet aggregation) •Also known as integrin aIIbb3

Answer 25

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

Answer 26

Inhibits amplification pathway

Answer 27

This leads to: •Shape change •Cross-linking of GPIIb/IIIa •Platelet aggregation

Answer 28

Converted into prostaglandins by COX

Answer 29

COX-1 Mediates GI mucosal integrity Thromboxane A2-mediated platelet aggregation COX-2 Mediates inflammation Involved in prostacyclin production, which inhibits platelet aggregation and affects renal function

Answer 30

Aspirin Low dose aspirin inhibits COX-1 and high dose aspirin inhibits both COX-1 and COX-2

Answer 31

ADP activates P2Y1 -Causes platelet activation -Results in GPIIb/IIIa fibrinogen cross-linking and aggregation ADP activates P2Y12 -Sustains platelet activation and aggregation

Answer 32

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

Answer 33

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

Answer 34

Inhibition of translocase and activation of scramblase leads to expression of aminophospholipids on the outer platelet membane, which allows assembly of prothrombinase complex and generation of thrombin

Answer 35

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

Answer 36

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

Answer 37

5 big squares = 1s

Answer 38

Positive Negative Baseline

Answer 39

Pacemaker of the heart

Answer 40

Less than 120ms (3 small squares) Prolonged - bundle branch block most common cause - issues with ventricles William marrow ?

Answer 41

Measure of time to ventricular repolarisation Onset of QRS end of T Men - 350-440ms Women 350-460ms

Answer 42

+ve electrode at +ve source = positive deflection Current flow towards lead +ve electrode at -ve source = negative deflection Current flow away from lead

Answer 43

Neutral electrode - reduces artefact - not directly involved in ECG measurement

Answer 44

LV contraction - isovolumetric contraction - maximal ejection LV relaxation - start relaxation and reduced ejection - isovolumetric relaxation - Rapid LV filling and suction - Slow LV filling (diastasis) - atrial booster

Answer 45

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

Answer 46

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

Answer 47

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

Answer 48

Physio: 1. Isovolumetric contraction 2. Maximal ejection Cardio: 1. M1 to A2 2. Only part of isovolumetric contraction (includes maximal and reduced ejection phases)

Answer 49

Physiologic 1. Reduced ejection 2. Isovolumetric relaxation 3. Filling phases Cardio 1. A2 to M1 interval (filling phases included)

Answer 50

Load present before LV contraction has started

Answer 51

Load after ventricle starts to contract

Answer 52

Difference between LAp and LV diastolic pressure

Answer 53

The cardiac sarcomere must function near the upper limit of their maximal length (LMAX) = 2.2 m. •The physiologic LV volume changes are affected when the sarcomere lengthens from 85% of LMAX to LMAX! ? •Steep relationship: length-dependent activation. In the cardiac sarcomere, at 80% of the optimal length, only 10% of the maximal force is produced!

Answer 54

Increasing diastolic heart volume, leads to increased velocity and force of contraction (Frank 1895). •This is the positive inotropic effect.

Answer 55

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

Answer 56

Elasticity, is the myocardial ability to recover its normal shape after removal of systolic stress.

Answer 57

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

Answer 58

Diastolic distensibility is the pressure required to fill the ventricle to the same diastolic volume.

Answer 59

The pressure-volume loop reflects contractility in the end-systolic pressure volume relationship, while compliance is reflected at the end diastolic pressure volume relationship.

Answer 60

Iso = the same (Greek), •Metric = length (Greek), •Tonic = contractile force (Greek), •The force-velocity curve may be a combination of initial isometric conditions followed by isotonic contraction. •The isometric conditions can be found during isovolumic contraction, isotonic contraction is totally impossible in the heart, given the constantly changing load.

Answer 61

Contractile tissue, •Connective tissue, •Fibrous frame, •Specialised conduction system.

Answer 62

Contractile tissue, •Connective tissue, •Fibrous frame, •Specialised conduction system.

Answer 63

The pumping action of the heart depends on interactions between the contractile proteins in its muscular walls. The interactions transform the chemical energy derived from ATP into the mechanical work that moves blood under pressure from the great veins into the pulmonary artery, and from the pulmonary veins into the aorta. The contractile proteins are activated by a signalling process called excitation-contraction coupling. Excitation-contraction coupling begins when the action potential depolarizes the cell and ends when ionized calcium (Ca2+) that appears within the cytosol binds to the Ca2+ receptor of the contractile apparatus. Movement of Ca2+ into the cytosol is a passive (downhill) process mediated by Ca2+ channels. The heart relaxes when ion exchangers and pumps transport Ca2+ uphill, out of the cytosol.

Answer 64

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

Answer 65

Relies on free fatty acids during aerobic metabolism (efficient energy production) •During hypoxia, there is no FFA metabolism, thus anaerobic metabolism ensues. This relied on metabolising glucose (anaerobically) producing energy sufficient to maintain the survival of the affected muscle without contraction.

Answer 66

Contractile proteins are arranged in a regular array of thick and thin filaments (The so called Myofibrils). •A-band: the region of the sarcomere occupied by the thick filaments. •I-band: is occupied only by thin filaments that extend toward the centre of the sarcomere from the Z-lines. It also contains tropomyosin and the troponins. •Z lines bisect each I-band.

Answer 67

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

Answer 68

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

Answer 69

The transverse tubular system (T-tubule) is lined by a membrane that is continuous with the sarcolemma, so that the lumen of the T-tubules carries the extracellular space toward the center of the myocardial cell. •Mitochondria.

Answer 70

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

Answer 71

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

Answer 72

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

Answer 73

Elongated molecule, made of two helical peptide chains. •It occupies each of the longitudinal grooves between the two actin strands. •Regulates the interaction between the other three!

Answer 74

I: with tropomyosin inhibit actin and myosin interaction. •T: binds troponin complex to tropomyosin. •C: high affinity calcium binding sites, signalling contraction. •The latter bond, drives TnI away from Actin, allowing its interaction with myosin.

Answer 75

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

Answer 76

Calcium ions, •Troponin phophorylation, •Myosin ATPase.

Answer 77

Protein - location and salient properties 1. Myosin - Thick filament - Hydrolyses ATP, interacts with Actin 2. Actin - Thin filament - Activates myosin ATP, interacts with myosin 3. Tropomyosin - Thin filament - Modulates actin-myosin interaction 4. Troponin C - Thin filament - Binds Ca2+ 5. Troponin I- Thin filament - Inhibits actin-myosin interaction 6. Troponin T - Thin filament - Binds troponin complex to thin filament

Answer 78

Sarcolemma - role in systole (S) - role in diastole (D) 1. Na+ channel - (S)Depolarisation, (S)Opens Ca2+ channels 2. Ca2+ channel - (S)Action potential plateau, (S)Ca2+ -triggered, Ca2+ release 3. Ca2+ pump (PMCA) - (D)Ca2+ removal 4. Na+/Ca2+ exchanger - (S)Ca2+ entry - (D)Ca2+ removal 5. Na+ pump - (D)Repolarisation, (D) Na+ gradient for Na+/Ca2+ exchanger

Answer 79

Transverse tubule 1. Na+ channel - (S)Action potential propagation 2. Ca2+ channel - (S)Ca2+ -triggered Ca2+ release

Answer 80

SR 1. Subsarcolemmal cisternae Ca2+ release channel - (S)Ca2+ release 2. Sarcotubular network’s Ca2+ pump (SERCA) - (D)Ca2+ removal

Answer 81

Myofilaments 1. Actin & myosin - (S)Contraction 2. Troponin C - (S)Ca2+ receptor 3. Other proteins - (S)Allosteric regulation

Answer 82

Contraction of the working cells of the myocardium involves interactions among six proteins: myosin of the thick filament, actin, tropomyosin, and the 3 components of troponin in the thin filament.

Answer 83

•These interactions are controlled by the downhill movement of Ca2+ into the cytosol (excitation-contraction coupling) and active Ca2+ transport out of the cytosol.

Answer 84

•All of these Ca2+ fluxes are highly regulated, which provides for the changes in cardiac muscle chemistry that give rise to changes in myocardial contractility.

Answer 85

The basic three events are: - LV contraction, - LV relaxation, - LV filling.

Answer 86

Wiggers suggested the diagram in 1915. •Lewis added the ECG and the HS in 1920.

Answer 87

LV contraction: - Isovolumic contraction ( b ) - Maximal ejection ( c ) •LV relaxation: - Start of relaxation and reduced ejection ( d ) - Isovolumic relaxation ( e ) - Rapid LV filling and LV suction ( f ) - Slow LV filling (diastasis) ( g ) - Atrial booster ( a ).

Answer 88

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

Answer 89

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

Answer 90

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

Answer 91

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

Answer 92

Physiologic 1. Isovolumetric contraction 2. Maximal ejection Cardiologic systole 1. From M1 to A2 2. Only part of isovolumetric contraction (includes max and reduced ejection phases)

Answer 93

Physiologic - reduced ejection - isovolumetric relaxation - filling phases Cardiologic Diastole - A2 to M1 interval (filling phases included)

Answer 94

Preload: is the load present before LV contraction has started. •Afterload: is the load after the ventricle starts to contract.

Answer 95

Starling 1918: Within physiologic limits, the larger the volume of the heart, the greater the energy of its contraction and the amount of chemical change at each contraction. •LV filling pressure: is the difference between LAp and LV diastolic pressure. •The relationship reaches a plateau.

Answer 96

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

Answer 97

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

Answer 98

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

Answer 99

Contractility (inotropic state): the state of the heart which enables it to increase its contraction velocity, to achieve higher pressure, when contractility is increased (independent of load) •Elasticity, is the myocardial ability to recover its normal shape after removal of systolic stress.

Answer 100

Compliance is the relationship between the change in stress and the resultant strain.(dP/dV). •Diastolic distensibility is the pressure required to fill the ventricle to the same diastolic volume.

Answer 101

The pressure-volume loop reflects contractility in the end-systolic pressure volume relationship, while compliance is reflected at the end diastolic pressure volume relationship.

Answer 102

The force-velocity curve may be a combination of initial isometric conditions followed by isotonic contraction. •The isometric conditions can be found during isovolumic contraction, isotonic contraction is totally impossible in the heart, given the constantly changing load.

Phsyiology Flashcards

(132 cards)