Cardiac Cycle Flashcards

Question

Frank-starling law

Answer 1

As EDV increases, stroke volume increases due to increased cardiomyocyte stretch and therefore a more forceful contraction This is because the amount of tension (force of muscle contraction during systole) depends on the resting length of the sarcomere, which is dependent on the amount of blood that fills the ventricles during diastole. The length of the sarcomere determines the amount of overlap between the actin and myosin filaments and so the number of cross-bridges that can form. Low end diastolic volume reduces sarcomere stretching, so fewer myosin heads bind to actin- leading to weaker contraction. However, too much sarcomere stretching prevents optimal overlapping between actin and myosin also reducing the force of contraction.

Answer 2

• the pressure that the chambers of the heart must generate in order to eject blood out of the heart • Affected by systemic vascular resistance and and pulmonary vascular resistance • Occurs during systole • Depends on arterial blood pressure and vascular tone • Afterload is a pressure

Answer 3

Blood pressure Cardiac output Systemic vascular resistance Left ventricular volume Aortic vessel pressure Aortic valve resistance

Answer 4

Troponin C

Answer 5

Vasodilation of the afferent arterioles and vasoconstriction of the efferent arterioles ANP is released by the atria in response to increased ECF volume stretching the atria. It acts to increase GFR,which increases sodium and water excretion via the kidney

Answer 6

lowers blood pressure, primarily by vasodilation and the inhibition of sodium reabsorption by the kidney, the latter having a diuretic effect. Increased natriuresis Decreased vasoconstriction in response to stimuli Inhibition of renin and ADH Lowering of systolic blood pressure

Answer 7

Target the endopeptidase inhibitors responsible for breaking down ANP Treatment for Advanced, treatment-refractory heart failure

Answer 8

Arterial diastolic pressure/ (1/3 * pulse pressure) Eg 140/80 mmHg 80/(1/3* 140-80) = 100mmHg

Answer 9

200-400 ms

Answer 10

An action potential steadily increases the membrane potential of a cardiomyocyte When the membrane potential reaches -70mV (the threshold value), it triggers the opening of Na+ channels in the membrane This leads to rapid influx of Na+ into the cell, leading to a sharp rise in membrane potential (depolarisation) Some L-type Ca2+ channels also open, so Ca2+ also moves into cell

Answer 11

Once membrane potential reaches +40mV, Na+ channels close Simultaneously, K+ channels open , leading to efflux of K+ out of the cell Actions causes a slight decrease in membrane potential

Answer 12

K+ channels remain open , leading to continued efflux of K+ ions Ca2+ channels also open, leading to influx of Ca2+ Ca2+ and K+ movement counteract each other- leading to a plateau

Answer 13

Ca2+ channels close but K+ channels remain open with increasing channel permeability Efflux of K+ causes rapid decrease in membrane potential

Answer 14

Na+/K+ pump restores membrane potential to -90mV by moving 3 Na+ out and 2 K+ in Also leaky K+ and Na+ channels which help to restore membrane potential

Answer 15

Mixed Na+/K+ current instead of only one ion type Activated by hyperpolarisation (rather than depolarisation) Very slow kinetics compared with other currents

Answer 16

Phase 4 depolarisation Absence of fast sodium channels, phase 0 mediated by sodium channels Slower action potential upstroke with a lower amplitude

Answer 17

Mixture of Na+ and K+ current which is activated by hyperpolarisation at low voltages (around -60/-70 mV) At end of each SAN action potential, membrane potential decreases due to repolarisation Once threshold is reached, funny current is activated (phase 4 depolarisation) Leads to inward current of Na+/K+ which restarts diastolic depolarisation phase Provides automaticity for pacemaker cells as occurs at end stage, allowing continuous generation of action potentials

Answer 18

Vasodilation and transient increase in blood flow that occurs n response to tissue ischaemia as occurs in coronary thrombosis, tissue hypoxia and metabolic waste accumulation Level of blood flow after vessel occlusion is greater than before

Answer 19

Arterioles to ensure blood slows down before entering capillaries to allow for optimal oxygen exchange

Answer 20

Haemorrhage due to a reduced circulating volume and so reduced mean systemic filling pressure

Answer 21

Weak pulse Rapid heartbeat Pale skin

Answer 22

[(Diastolic blood pressure x 2) + systolic blood pressure] / 3

Answer 23

Mid to late diastole Systole Early diastole

Answer 24

when the pressure in the atria and ventricular are the same • filling temporarily stops.

Answer 25

1. left atrium and ventricle are both relaxed, but atrial pressure is slightly higher than ventricular pressure because the atrium is filling with blood that is entering from the veins. 2. AV valve is held open by this pressure difference, and blood entering the atrium from the pulmonary veins continues on into the ventricle 3. aortic valve is closed because the aortic pressure is higher than the ventricular pressure- Throughout diastole, the aortic pressure is slowly decreasing because blood is moving out of the arteries and through the vascular system. 4. ventricular pressure is increasing slightly because blood is entering the relaxed ventricle from the atrium, thereby expanding the ventricular volume. 5. Near the end of diastole, the SA node discharges and the atria depolarize, as signified by the P wave of the ECG. 6. Contraction of the atrium causes an increase in atrial pressure- increased atrial pressure forces a small additional volume of blood into the ventricle, sometimes referred to as the “atrial augmentation.” 7. end of ventricular diastole, so the amount of blood in the ventricle at this time is called the end-diastolic volume (EDV).

Answer 26

AV valve open Semi-lunar valves closed

Answer 27

Contraction of the atrium causes an increase in atrial pressure- increased atrial pressure forces a small additional volume of blood into the ventricle

Answer 28

end of ventricular diastole, so the amount of blood in the ventricle at this time is called the end-diastolic volume (EDV).

Answer 29

1. From the AV node, the wave of depolarization passes into and throughout the ventricular tissue—as signified by the QRS complex of the ECG—and this triggers ventricular contraction. 2. As the ventricle contracts, ventricular pressure increases rapidly; almost immediately, this pressure exceeds the atrial pressure. 3. This change in pressure gradient forces the AV valve to close; this prevents the backflow of blood into the atrium. 4. Because the aortic pressure still exceeds the ventricular pressure at this time, the aortic valve remains closed and the ventricle cannot empty despite its contraction. For a brief time, then, all valves are closed during this phase of isovolumetric ventricular contraction. Backward bulging of the closed AV valves causes a small upward deflection in the atrial pressure wave. 5. This brief phase ends when the rapidly increasing ventricular pressure exceeds aortic pressure. 6. The pressure gradient now forces the aortic valve to open, and ventricular ejection begins. 7. The ventricular volume curve shows that ejection is rapid at first and then slows down. 8. The amount of blood remaining in the ventricle after ejection is called the end-systolic volume (ESV). 9. As blood flows into the aorta, the aortic pressure increases along with the ventricular pressure. Throughout ejection, very small pressure differences exist between the ventricle and aorta because the open aortic valve offers little resistance to flow. 10. Note that peak ventricular and aortic pressures are reached before the end of ventricular ejection; that is, these pressures start to decrease during the last part of systole despite continued ventricular contraction. This is because the strength of ventricular contraction diminishes during the last part of systole. 11. This force reduction is demonstrated by the reduced rate of blood ejection during the last part of systole. 12. The volume and pressure in the aorta decrease as the rate of blood ejection from the ventricles becomes slower than the rate at which blood drains out of the arteries into the tissues.

Answer 30

aortic pressure still exceeds the ventricular pressure at this time, the aortic valve remains closed and the ventricle cannot empty despite its contraction. For a brief time, then, all valves are closed during this phase of isovolumetric ventricular contraction. Backward bulging of the closed AV valves causes a small upward deflection in the atrial pressure wave.

Answer 31

The amount of blood remaining in the ventricle after ejection

Answer 32

1. As the ventricles relax, the ventricular pressure decreases below aortic pressure, which remains significantly increased due to the volume of blood that just entered. The change in the pressure gradient forces the aortic valve to close. The combination of elastic recoil of the aorta and blood rebounding against the valve causes a rebound of aortic pressure called the dicrotic notch. 2. The AV valve also remains closed because the ventricular pressure is still higher than atrial pressure. For a brief time, then, all valves are again closed during this phase of isovolumetric ventricular relaxation. 3. This phase ends as the rapidly decreasing ventricular pressure decreases below atrial pressure. 4. This change in pressure gradient results in the opening of the AV valve. 5. Venous blood that had accumulated in the atrium since the AV valve closed flows rapidly into the ventricles. 6. The rate of blood flow is enhanced during this initial filling phase by a rapid decrease in ventricular pressure. This occurs because the ventricle’s previous contraction compressed the elastic elements of the chamber in such a way that the ventricle actually tends to recoil outward once systole is over. This expansion, in turn, lowers ventricular pressure more rapidly than would otherwise occur and may even create a negative (subatmospheric) pressure. Thus, some energy is stored within the myocardium during contraction, and its release during the subsequent relaxation aids filling.

Answer 33

The AV valve also remains closed because the ventricular pressure is still higher than atrial pressure. For a brief time, then, all valves are again closed during this phase of isovolumetric ventricular relaxation. - This phase ends as the rapidly decreasing ventricular pressure decreases below atrial pressure.

Answer 34

The combination of elastic recoil of the aorta and blood rebounding against the valve causes a rebound of aortic pressure

Answer 35

34/10 mmHg

Answer 36

Needed for fetal circulation

Answer 37

Males: 220 - age in years = maximum heart rate Females: 200 - age in years = max heart rate

Answer 38

When AV valve closed

Answer 39

When semilunar valve closed

Answer 40

Increase volume of blood within the ventricle Slushing in Caused by turbulent flow into the ventricles and detected near end of first one third of diastole (rapid ventricular filling) Fluid backing up, as in cardiac failure

Answer 41

Just after atrial contraction at the end of diastole and immediately before S1 A stiff wall With the atrial systole Non compliant ventricles

Answer 42

Sarcomeres within myofibrils shorten as the Z discs are pulled closer together 1. An action potential arrives- depolarisation of the membrane by Na+, causing Ca2+ to diffuse into the neurone 2. The Ca2+ causes vesicles containing ACh to fuse with the presynaptic membrane and release ACh by exocytosis 3. ACh diffuses across the synoptic cleft and binds to receptors in the sarcolemma, causing Na+ channels to open 4. Na+ diffuse into the sarcolemma, depolarising the membrane and generating an action potential that spreads down the T-tubules 5. L-type Ca2+ channels open and trigger Ca2+ diffuse out of the sarcoplasmic reticulum into the cytosol 6. This trigger Ca2+ binds to and opens ryanodine receptor Ca2+ channels in the sarcoplasmic reticulum membrane 7. Ca2+ flows into the cytosol, increasing the Ca2+ concentration 8. Ca2+ bind to troponin (TnC) molecules, stimulating them to change shape. This causes troponin and tropomyosin proteins to change position on the actin filaments, exposing myosin-binding sites. 9. The globular heads of the myosin molecules bind with these sites, forming cross-bridges between the two filaments after linkage of calcium and TnC, and deactivation of tropomyosin and TnI 10. The formation of cross-bridges causes the myosin heads to spontaneously bend (releasing ADP and Pi) pulling the actin filaments towards the centre of the sarcomere (i.e. closer together- 10nm) - power stroke 11. ATP binds to the myosin head, producing a change in shape that causes the myosin heads to be released from the actin filaments 12. ATPhydrolase hydrolyses ATP to ADP and Pi which causes the myosin head to cock back to its original position 13. The myosin head can then bind to new binding sites on the actin closer to the Z disc. The process repeats until the muscle is fully contracted 14. Later on, Ca2+-ATPase pumps return Ca2+ to the sarcoplasmic reticulum 15. Ca2+-ATPase pumps and Na+/Ca2+ exchangers remove Ca2+ from the cell 16. Membrane is depolarised when K+ exits to end the action potential

Answer 43

• 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 44

• 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 45

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

Answer 46

• 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.) • heads are 43nm apart • Alpha myosin and beta myosin.

Answer 47

giant protein, greater than 1 µm in length, that functions as a molecular spring that is responsible for the passive elasticity of muscle

Answer 48

• provision of passive force • stability of the myosin filaments • stability of sarcomeres on the descending limb of the force–length relationship

Answer 49

Hydrolyses ATP interacts with actin

Answer 50

Activates myosin ATP Interacts with myosin

Answer 51

Modulates actin-myosin filaments

Answer 52

Binds Ca2+

Answer 53

Inhibits actin-myosin interaction

Answer 54

Binds troponin complex to thin filament

Answer 55

the region of the sarcomere occupied by the thick filaments.

Answer 56

occupied only by thin filaments that extend toward the centre of the sarcomere from the Z-lines. It also contains tropomyosin and the troponins.

Answer 57

bisect each I-band.

Answer 58

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

Answer 59

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

Answer 60

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.

Answer 61

always maximally contracts The cardiac sarcomere must function near the upper limit of their maximal length (LMAX) = 2.2 um

Answer 62

Mesenchyma

Answer 63

1. 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. 2. Movement of Ca2+ into the cytosol is a passive (downhill) process mediated by Ca2+ channels. 3. The heart relaxes when ion exchangers and pumps transport Ca2+ uphill, out of the cytosol.

Answer 64

Free fatty acids

Answer 65

Adjacent cells are joined end to end at structures called intercalated disks, within which are desmosomes that hold the cells together and to which the myofibrils are attached. Also found within the intercalated disks are gap junctions similar to those found in single-unit smooth muscle.

Answer 66

-2 -> +12 cmH2O

Answer 67

Heart failure Cardiogenic shock Obstructive shock High circulating volume Positive end-expiratory pressure ventilation eg CPAP

Answer 68

Hypovolaemic shock Distributive shock

Answer 69

Predictor of left ventricular systolic function (Stroke volume/ end diastolic volume) x100

Answer 70

Nitric oxide, cytokines Autonomic innervation

Answer 71

Vasoconstrictor peptides Bind to g-protein coupled receptors Endothelin-1 is most potent Secreted by vascular endothelium High levels associated with heart and renal failure

Answer 72

Nitric oxide formed via oxidation of nitrogen atoms contained with L-arginine by NO synthase

Answer 73

Activation of guanylate cyclase Increased intracellular cGMP Downstream cellular processes

Answer 74

Vasodilation Increased vascular permeability (Increases local immune cell migration to site of infection but may lead to septic shock via reduced vascular resistance and low BP)

Answer 75

Tissue oxygen delivery = pulmonary oxygen absorption + pulmonary artery oxygen before gas exchange

Answer 76

ECG or Doppler ultrasound

Answer 77

the pressure required to fill the ventricle to the same diastolic volume.

Answer 78

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 79

• low resistance conduits • Elastic • Cushion systole • Maintain blood flow to organs during diastole

Answer 80

• principal site of resistance to vascular flow • TPR = total arteriolar resistance • Determined by local, neural and hormonal factors • Major role in determining arterial pressure and distributing flow to tissues/organs • Vascular smooth muscle determines radius • VSM contracts → decrease radius (vasoconstriction) → increases resistance → decrease flow • VSM relaxes → increases radius (vasodilation) → decreases resistance → increase flow • myogenic tone- VSM never completely relaxed

Answer 81

• 40000km and large area → slow flow • Allows time for nutrient/waste exchange • Plasma or interstitial fluid flow determines the distribution of ECF between these compartments • Flow also determined by arteriolar resistance and number of open pre-capillary sphincters

Answer 82

• compliant • Low resistance consists • Capacitance vessels • Up to 70% of blood volume but only 10mmHg • Valves aid venous return against gravity • Skeletal muscle/ respiratory pump aids return • SNA mediated vasoconstriction maintains VR/VP

Answer 83

• fluid/ protein excess filtered from capillaries • Return of the interstitial fluid to CV system via thoracic duct and left subclavian vein • Uni-directional flow aided by smooth muscle in lymphatic vessels; skeletal muscle pump; respiratory pump

Answer 84

using brachial artery (convenient to compress and level of heart): sounds (Korotkoff) 0. > systolic pressure = no flow, no sounds 1. Systolic pressure = high velocity = tap 2-4. Between S and D = thus 5. Diastolic pressure = sounds disappear

Answer 85

• short term regulation of bp (minute-minute control) • New baseline formed of arterial pressure as deviated from the normal baseline for more than a few days • Can lead to hypertension if new baseline is higher

Answer 86

• atria, ventricles and pulmonary artery • When stimulated, decreased vasoconstrictor and decreased bp • Decreased release of angiotensin, aldosterone and vasopressin leads to fluid loss

Answer 87

• Chemosensitive regions in medulla • high PaCO2 →vasoconstriction- high peripheral resistance and high blood pressure • Low PaCO2 → low medullary tonic activity this low bp • Similar changes with high and low pH • PaO2 has less effect on medullar- moderate reduction in PaO2 = vasoconstriction / severe decrease = general depression • Effects of PaO2 mainly regulated by peripheral PaO2

Answer 88

• Baroreceptors • ↑BP ⇒ ↑Firing ⇒ ↑PNS/↓SNS ⇒ ↓CO/TPR = ↓BP

Answer 89

• Volume of blood • Na+, H20, Renin-Angiotensin-Aldosterone and ADH

Answer 90

• very sensitive to PO2 decrease as well as PCO2 increase and pH decrease • Increased sympathetic outflow- results in increased TPR • chemoreceptors involved in control of breathing • Decreased PO2 decreases the parasympathetic output to the heart → increase heart rate →increase CO

Answer 91

• most sensitive to CO2 and pH • Less so to O2 • Increased firing leads to sympathetic outflow • Arterial vasoconstriction in skeletal muscle, renal and splanchnic system • Increased TPR

Answer 92

• Baroreceptors • Chemoreceptors • Hypothalamus • Cerebral cortex • Skin • Changes in blood [O2] and [CO2]

Answer 93

• Stimulation of anterior hypothalamus ↓ BP and HR; • The reverse with posterolateral hypothalamus • Hypothalamus also important in regulation of skin blood flow in response to temperature • Cerebral cortex can affect blood flow & pressure. • Stimulation usually ↑ vasoconstriction • Emotion can ↑ vasodilatation and depressor responses eg. blushing, fainting. Effects mediated via medulla but some directly

Answer 94

• found in carotid sinus and aortic arch primarily • Secondary found in veins, myocardium and pulmonary vessels • Afferent- glossopharyngeal nerve to medulla • Efferent- sympathetic and vagus X • Firing range proportional to medulla • Increased bp sensed by Baroreceptors which is then sent via the glossopharyngeal (IX) to the medulla where there is increased firing which results in stimulation of parasympathetic (X) nerve and decrease in sympathetic stimulation • Results in decrease CO and TPR- BP = CO x TPR

Answer 95

• epinephrine- acts on alpha receptors • Angiotensin II • vasopressin

Answer 96

• epinephrine - acts on beta receptors • Atrial natriuretic peptide (ANP)

Answer 97

• intrinsic ability of an organ • Constant flow despite perfusion pressure changes • Renal/cerebral/coronary = excellent • Skeletal muscle/splanchnic = moderate • Cutaneous = poor • Brain and heart: intrinsic control dominates to maintain BF to vital organs • Skin: BF is important in general vasoconstrictor response and also in responses to temperature (extrinsic) via hypothalamus • Skeletal muscle: dual effects: -at rest, vasoconstrictor (extrinsic) tone is dominant -upon exercise, intrinsic mechanisms predominate

Answer 98

1. Ohm’s law- flow = pressure gradient / resistance 2. Poiseuille’s equation- flow is inversely proportional Radius ^4

Answer 99

Mechanism that allows vascular resistance to be adjusted to maintain a constant blood flow in an organ across a pre-determined range of arterial pressures Seen in the kidneys and brain (as constant perfusion is essential for the organs)

Answer 100

Stroke volume and preload

Answer 101

Increased systolic pressure, stroke volume, stroke work and heart rate Decreased end-systolic and end-diastolic volume (as more blood ejected from the heart)

Answer 102

B-type natriuretic peptide (BNP) Hormone produced and secreted by ventricular cardiomyocytes when excessively stretched and so unable to pump blood as effectively

Answer 103

Largest and closest to heart Elastin in media/externa——-> expand and recoil to absorb pressure

Answer 104

Thick muscular walls Includes coronary arteries

Answer 105

Arteriolar resistance Pre-capillary sphincters Plasma/ISF flow

Answer 106

Respiratory pump-diaphragm contraction

Answer 107

72 bpm 60-100 bpm

Answer 108

Stroke volume/ end-diastolic volume = 65%

Answer 109

Blood flow = velocity x cross-sectional area of vessel

Answer 110

100-150 mmHg

Answer 111

60-90 mmHg

Answer 112

High: renal, cerebral, coronary Moderate: skeletal, splanchnic Poor: cutaneous

Answer 113

Endothelin-1

Answer 114

NO, prostacyclin, bradykinin, adenosine, tissue factor

Answer 115

CO2 + H2O ——> H2CO2 ——> H(CO3)- + H+

Answer 116

Less blood pumped by left ventricle ——> blood backs up in pulmonary circulation ——> increases pulmonary pressure ——> pulmonary oedema——> breathless

Answer 117

1. Respiratory failure or left side heart failure ——> increases pulmonary pressure (hypertension) 2. Harder for right ventricle to pump into pulmonary artery 3. Systolic dysfunction——> RV hypertrophy 4. Decreases filling ——> diastolic dysfunction 5. Blood backs up in systemic circulation 6. Increases central venous pressure ——> peripheral oedema and ascites (abdomen)

Answer 118

Myocardial ability to recover its normal shape after removal of systolic stress

Answer 119

Relationship between change in stress and resultant strain: EDP - EDV relationship

Answer 120

Heart can increase its contraction velocity to increase pressure : ESP - ESV relationship

Answer 121

Pressure required to fill ventricles to same diastolic volume

Answer 122

Blood goes back into atrium ——> preload has normal filling plus what went back into atrium This increases preload ——> ventricle needs increased pressure to overcome resistance ——> hypertrophy

Answer 123

Pressure in V>A —> AV valves shut (R peak) Isovolumic contraction: SL valves remain shut- increase in pressure but same volume QRS complex: ventricular depolarisation

Answer 124

Pressure in V> aortic or pulmonary —> SL valves open As 70% of blood is ejected: Decreases ventricular pressure and ejection force Atrial filling starts Leaves 30% of blood (EDV) ST interval

Answer 125

Isovolumic relaxation: pressure in V (<80mmHg) < aorta so SL valves shut- T wave ends Passive blood flow when AV valves open (85-95% of blood) Rapid filling: pressure in A>V Slow filling (diastasis): pressure in A=V Just after P wave —> atrial booster- contraction (5-15% blood) - PR interval ATRIAL SYSTOLE

Answer 126

1. Nerve impulse reaches NMJ —> Ca2+ release triggers ACh exocytosis (all NMJs are excitatory) —> ACh binds to post synaptic receptor on motor end plate —> Na+ entry into sarcoplasm Produces wave of depolarisation

Answer 127

Concentration of cytosolic Ca2+

Answer 128

• ACh and insulin stimulate calcium release which leads to L-arginine being converted to NO aided by NO synthase

Answer 129

• angiotensin II, vasopressin, cytokines, thrombin, oxidative reactive species, shearing forces all stimulate endothelin-1 production • Big endothelin-1 converted to endothelium-1 by endothelium converting enzyme • Endothelin-1 acts on G coupled proteins which stimulate IP3 and calcium release, resulting in smooth muscle contraction

Answer 130

Dead cardiac muscle- releases troponin- sign of myocardial infarction

Answer 131

acts to increase blood volume and systemic vascular resistance. Renin (released from granular cells in the juxtaglomerular apparatus of the kidney) converts angiotensinogen (protein from the liver) into angiotensinogen 1. ACE then converts it into angiotensin 2- which causes vasoconstriction in systemic circulation and renal microvasculature (constricting the efferent arteriole). ACE also removes bradykinin (a vasodilator) causing further vasoconstriction. Angiotensin 2 increases salt absorption in the kidney through activation of aldosterone, leading to an increase in plasma volume and blood pressure

Answer 132

• The muscle contraction of the heart may weaken due to overloading of the ventricle with blood during diastole. In a healthy individual, an overloading of blood in the ventricle triggers an increases in muscle contraction, to raise the cardiac output. In heart failure, however, this mechanism fails due to weakened cardiac muscles which results in a failure of the heart to pump an adequate amount of blood. • To compensate for the lowered cardiac output, the heart rate rises. This makes the condition worse as the heart muscles require more nutrients to work and the myocardial muscles pump at an increased rate. • Stroke volume reduces as the systole or diastole contractions start to fail. If the volume of blood in the ventricle at the end of systole rises, it means less blood is ejected. If the volume at the end of diastole is decreased, it means less blood is entering the heart during diastole.

Answer 133

lack of relaxation of atria so less passive flow of blood from atria to ventricle

Answer 134

Because these vessels traverse the myocardium, myocardial contraction during systole compresses arterial branches and prevents perfusion. Therefore, coronary perfusion occurs during diastole rather than systole.

Answer 135

• can lead to an often-fatal heart attack know was a widowmaker • LAD artery is the most commonly occluded of the coronary arteries. It provides the major blood supply to the interventricular septum, and thus bundle branches of the conducting system. Hence, blockage of this artery due to coronary artery disease can lead to impairment or death (infarction) of the conducting system. The result is a "block" of impulse conduction between the atria and the ventricles known as "right/left bundle branch block." • Right bundle branch block: left ventricle contracts first → signal carried to right side via Purkinje fibres → right ventricle contracts • Left bundle branch block: right ventricle contacts → left ventricle contracts • Generally results in ST segment elevation in precordial leads and reciprocal ST segment depression in inferior leads • Can cause stable or unstable angina

Answer 136

• may cause infarction of the inferior wall of the left ventricle with or without right ventricular (RV) myocardial infarction (MI), manifested as ST-segment elevations in leads II, III, and aVF. • right coronary artery branches supply the sinus and atrioventricular nodes; hence, blockage in these vessels can lead to conduction abnormalities • causes heart rate to slow until it stops

Answer 137

Fatigue Weakness Shortness of Breath on exertion Shortness of Breath at Rest Cough and wheezing Anorexia / loss of appetite Paroxymal nocturnal dyspnea Nausea Abdominal pain Nocturia

Answer 138

Pulmonary edema Pleural effusion Tachycardia Narrow pulse pressure Cardiomegaly Peripheral edema Jugular vein distension

Answer 139

Fatty streak formation as the result of foam cell accumulation in the vessel wall

Answer 140

Endothelial cell injury

Answer 141

The pressure that would be present in the circulation if the heart was removed and the system was allowed to equilibrate

Answer 142

X-axis = end-diastolic volume Y-axis = stroke volume

Answer 143

Intracellular Ca2+

Answer 144

Hypocalcaemia- causes increased nervous system excitement by lowering threshold for depolarisation as less Ca2+ to block sodium channels and inhibit depolarising

Answer 145

Closure of the aortic valve

Answer 146

Diastole (blood enters ventricles from atria passively) and atrial systole

Answer 147

Cardiomyocytes in the ventricles

Answer 148

In response to stretch caused by increased blood flow in the vernricles

Answer 149

High levels in heart failure as a result of stress on the ventricles

Answer 150

An increase in ventricular pressure and a decrease in atrial pressure causing the AV valve to close

Answer 151

Rightward shift of the curve

Answer 152

Causes curve to shift to the right- decreases haemoglobin’s affinity for oxygen to encourage unloading of oxygen at respiring tissues

Answer 153

Oxygen binding to Hb causes a decreased affinity of Hb for CO2

Answer 154

Elevated right atrial pressure - partially offsets decline in cardiac output by increasing preload = frank-starling law

Answer 155

Total peripheral resistance

Answer 156

Calcium and potassium

Answer 157

Adenosine - acts on A2 receptors of smooth muscle cells

Answer 158

No activation of peripheral chemoreceptors in carotid bodies as respond to dissolved oxygen but oxygen bound to Hb

Answer 159

Change in pressure/resistance

Answer 160

Arterio-venous anastomoses

Answer 161

Up regulation of the sarcolemmal Na+/Ca2+ exchanger resulting in increased efflux of Ca2+ from the cardiomyocyte The transient increase in Ca2+ concentration is reduced so the contraction is weaker

Answer 162

Decreases due to compression of thoracic veins

Answer 163

Impaired conductivity

Answer 164

Inferior myocardial infarction

Answer 165

Increase in aortic pressure upon valve closure- blood rebounds against valve

Answer 166

Right side heart failure - right ventricle must pump blood harder through pulmonary artery

Answer 167

Left heart failure - blood backs up pulmonary system, increasing hydrostatic pressure

Answer 168

Right side heart failure

Answer 169

Left main coronary artery

Answer 170

Reduced blood pressure

Answer 171

Local nitric oxide release overrides central control

Cardiac Cycle Flashcards

(217 cards)