the heart Flashcards

1
Q

what is the circulatory system and the two types

A
  • link exchange surfaces (lungs) with cells throughout the body
  • open: heart, gross blood vessels, released straight into tissues (small animals, not efficient)
  • closed: more complex (mammals), muscular pump (heart), arteries, veins and capillaries
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2
Q

what are the advantages of a closed circulatory system

A
  • nutrient delivery and waste removal is more rapid (kidney, liver, lungs)
  • resistant control selectively directs blood (maintain BP, vasoconstriction / dilation)
  • cellular elements aid in transport (albumin)
  • support higher levels of metabolic activities than open (mammals)
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3
Q

describe the evolution of the heart

A
  • from 2 to 4 chambers
  • increase separation of blood flow to gas exchange organs and rest of body
  • fish: 2 chambers, 1 atria and 1 ventricle, 2 capillary beds
  • reptile: 3 chambers, mixed blood (low conc. oxygen)
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4
Q

what does double circulation mean

A
  • maintains BP in the organs
  • oxygen rich and oxygen poor blood are pumped separately from right and left side of heart
  • systemic: oxygen rich delivers oxygens to this circuit, HBP
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5
Q

describe the actions of the heart (5)

A
  • cardiac cycle: contracts and releases in a rhythmic code
  • systole: pumping / contraction, ejects blood into circulation
  • diastole: relaxation / filling
  • beats per day: 100,000 times (does not fatigue)
  • resting: muscles work hard, twice as hard as leg muscles of a sprinter, even at rest
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6
Q

describe basic heart anatomy

A
  • size of fist, 250-350g, 4 chambers
  • middle of thoracic cavity, mediastinum between 2-5 intercostal rib space (12-14cm)
  • oblique
  • point of maximal intensity (5th intercostal space, feel vibration)
  • left side of diaphragm (left lung = smaller)
  • pericardium: sac like structure
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7
Q

describe in detail the pericardium and its two layers (outer most)

A
  • fibrous: superficial, external, tough, dense, connective, protects heart, prevents overfilling, anchors to surrounding structures
  • serous: deep, thin, slippery, two layers, pericardial cavity in-between, parietal / visceral
  • parietal: internal surface of fibrous pericardium
  • pericardial cavity: film of serous fluid, mobility without friction (cardiac tamponade -excess fluid, blockage)
  • visceral / epicardium: integral part of heart wall
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8
Q

what are the walls of the heart made of

A
  • epicardium: visceral layer of serous pericardium, contains fat deposits
  • myocardium: thickness, circular / spiral bundles of cardiac muscle cells (allows squeezing / ejection), contracting layer, connective tissue (fibrous skeleton, stability, bones of heart)
  • endocardium: flat, same tissue as BV, squamous endothelium, continuous with BV
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9
Q

describe microscopic anatomy of cardiac muscle

A
  • striated, short, fat, branched, interconnected, multi / uni nucleate
  • t tubules: surround myofibrils, conduct impulses from surface of cell to sarcolemma and sarcoplasmic reticulum
  • sarcoplasmic reticulum: similar to skeletal
  • mitochondria: numerous, 25-35% of volume (no fatigue)
  • intercalated discs: junctions, anchor adjacent cells (desmosomes - prevent separation during contraction)(gap - connection / pores, electrically couple)
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10
Q

what BV supply the heart muscle

A

coronary arteries:
- left: branches into circumflex artery (LV) and anterior interventricular artery
- right: branches into right marginal artery (RV) and posterior interventricular artery
- posterior / anterior interventricular merge at apex - anastomoses
- coronary sinus: large vein in the centre of heart, empties blood from coronary arteries into RA
cardiac veins:
- great cardiac vein: left of heart
- small / middle / anterior cardiac veins

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11
Q

what are examples of blockage of coronary circulation

A
  • angina pectoris: not enough oxygen during exercise, thoracic pain, transient deficiency in blood delivery to myocardium, spasms of CA, cells weakened
  • myocardial infarction: heart attack, complete / prolonged coronary blockage, myocardial cells die, cell death = replaced with scar tissue (weakened)
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12
Q

what are the chambers of the heart

A
  • two atria: right / left
  • two ventricles: right (thinner) / left (thicker)
  • interatrial septum
  • interventricular septum
  • internal wall (not smooth)
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13
Q

what are the valves of the heart and their functions

A
  • atrioventricular (AV): prevent back flow into atria when ventricles contract (mitral / tricuspid)
  • semilunar (SL): prevent back flow into ventricles when pumping (aortic and pulmonary), three curses
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14
Q

describe the pathway of blood flow through the heart

A

superior / inferior vana cava - right atrium - tricuspid valve - right ventricle - pulmonary SL. valve - pulmonary trunk - pulmonary artery - lungs - pulmonary veins - left atrium - bicuspid valve - left ventricle - aortic SL valve - aorta - body tissue / coronary arteries (heart tissue, cardiac veins, coronary sinus

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15
Q

what differences are there in foetal circulation

A
  • ductus arteriosus: connects pulmonary artery with descending aorta (doesn’t go to lungs), right V strengthens - becomes ligamentum arteriosum
  • ductus venosus: connects umbilical vein to inferior vena cava (oxygenated blood by passes liver) - becomes ligamentum venosum
  • foreman ovale: hold in interatrial septum, shunts highly oxygenated blood from RA to LA - closes to form fossa ovalis
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16
Q

what are the sounds of the heart

A
  • lub dub (closing of valves)
  • first: AV valves close, beginning of systole
  • second: SL valves close, beginning of diastole
17
Q

what is a pulse and where are they found

A
  • not heart beat
  • direct measure of heart beat caused by movement of waves of pressure through vascular system due to contraction of muscles
  • higher in newborns
  • carotid (neck), femoral (gluteus maximus), brachial (anterior elbow), radial (wrist)
18
Q

what is heart muscle called the differences in electrical activation of the heart in comparison to skeletal cells

A
  • myocyte: activation is similar to that of nerve cell
  • self-excitable: all connected to neural cells, , some can cause depolarisation of other cells (activating themselveS), only muscle that can contract without nervous connection
  • motor unit: contract at the same time, single unit
  • length of refractory period: longer (250ms) than in skeletal (2ms), prevent tachycardia (too many beats per minute)
19
Q

how does cardiac muscle contraction occur

A
  1. depolarisation opens the voltage-gated fast Na+ channels in sarcolemma
  2. reversal of membrane potential from -90 mV to +30 mV
  3. depolarisation wave in t-tubules causes the SR to release Ca2+
  4. SR releases more Ca2+ (calcium sparks)
  5. Ca2+ surge prolongs the depolarisation phase (plateau = the cells continue to contract)
  6. Ca2+ channels inactivate and K+ channels open
  7. K+ efflux, which brings the membrane potential back to its resting voltage
  8. Ca2+ pumped back into SR and extracellular space
20
Q

what are the intrinsic and extrinsic features of the heart

A
  • intrinsic: cardiac conduction system, auto rhythmic cells, initiate / distribute impulses to coordinate depolarisation / contraction, without nerve connections
  • extrinsic: nervous connections, ANS, ability to modify activity of heart (increase / decrease HR)
21
Q

what are auto rhythmic cells and how does action potential occur

A
  • pacemaker cells
  • unstable resting potential, slow opening of Na channels (into cell), reduction of negative charge (gradual), never a flat line
  • threshold: depolarisation, Ca channels open (into cell), influx of Ca, rising phase, Na close
  • repolarisation: inactivation of Ca channels, opening of voltage gated K channels (out of cell), negative charge restored
22
Q

describe the sequence of excitation in the heart

A
  • spread of electric current
    1. SA node: pacemaker, right atrial wall, generates impulses about 75x per min (damage = slow HB)
    2. AV node: inferior portion of interA septum, pauses impulses for 0.1 seconds
    3. AV bundle: bundle of His, superior part of interV septum, electrical connection between A and V (problem = contract independently)
    4. right / left bundle branches: pathways, interV septum, carry impulses to apex of heart
    5. purkinje fibres: sub-endocardial conducting network, depolarises contractile cells of both V
23
Q

what is the extrinsic innervation of the heart

A
  • HB modified by ANS (two cardiac centres in medulla)
  • ganglia: parallel to spinal cord in chest and neck (PNS)
  • vagus: 10th cranial nerve, runs to heart, decreases HR and force
  • sympathetic cardiac nerves: increase HR and force of contraction
24
Q

what is the cardioaccelatory centre

A
  • innervates SA and AV nodes, heart muscles and coronary arteries
  • projects to sympathetic neurons in T1-T5
  • pre-ganglionic neurons: synapse with post ganglionic neurons in cervical and upper thoracic sympathetic trunk
  • post-ganglionic fibres: run through cardiac plexus to heart, innervate structures above
25
Q

what is the cardioinhibitory centre

A
  • inhibits SA and AV nodes
  • send impulses to parasympathetic dorsal vagus nucleus in medulla, inhibit impulses to heart via branches of vagus nerves
  • located in most parasympathetic post-ganglionic motor neurons (ganglia of heart and their fibres project heavily to SA and AV nodes)
26
Q

what is electrocardiography

A
  • ECG / EKG
  • recording of electric currents produced by the heart
  • composite of all action potentials generated by nodal and contractile cells at given time
  • P wave: A depolarisation / contraction, initiation = SA node
  • QRS complex: ventricular depolarisation / contraction (after R), begins at apex (complex pathway / bigger muscles hence bigger wave), atrial repolarisation (occurs at same time, not shown)
  • T wave: ventricular repolarisation, begins at apex
  • PR: A depolarisation / contraction (contraction)
  • QT: ventricular depolarisation / repolarisation (contraction)
  • ST: plateau phases of ventricular myocyte’s, ventricular myocardium is depolarised
  • RR: time between heartbeats (0.8-1 sec)
27
Q

what are homeostatic imbalances

A
  • tachycardia: fast HR (>100BPM), may lead to fibrillation, sport activity / fever
  • brachycardia: slow HR (<60BPM), inadequate circulation, endurance training
28
Q

what is ventricular fibrillation

A
  • synchronous ventricular depolarisation is interrupted
  • ventricular cells fire and propagate action potentials randomly
  • destroys pumping action of heart, not a unit
  • death within 3 minutes without defibrillation or CPR
29
Q

what is the role of chemicals in regulation of heart rate

A
  • hormones: epinephrine (enhances HR / contractility), thyroxine (increases HR, enhances effects of norepinephrine and epinephrine)
  • ion conc. (Ca /K), maintained for normal HB, increase Ca = increase HR, increase K = block activity of heart
  • toxins: fever / fighting infection, digitoxin / fox glove (inhibits NaK pump, brachycardia, atrial fibrillation), oleandrin (plant, inhibits NaK pump)
30
Q

what effects does cocaine have on the heart

A
  • stimulates sympathetic nervous system (inhibits catecholamine reuptake)
  • increase HR, BP, block NaK channels, inflammation of heart (myocarditis), cardiomyopathy (disease of heart)
31
Q

how is an ECG measured and what is deflection

A
  • 12 leads / electrodes: placed at various sites of the body

- deflection: vector of depolarisation produces biggest deflection on lead that is parallel to vector