D4 The heart Flashcards

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1
Q

what is cardiac muscle?

A

striated muscle found in the wall of the heart

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2
Q

what is the structure of the cardiac muscle

A
  • thick and thin muscle fibres with myofibrils
  • cell nuclei in centre
  • rich in mitochondria and glycogen granules
  • “all or none” effect – once activated, max contraction
  • long refractory period (cannot contract again)
  • intercalated discs
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3
Q

how does the cardiac muscle structure ensure that the contraction/systole of the heart is seperated by a rest/diastole

A

long refractory period of cardiac muscle = cannot contract for a second time

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4
Q

in cardiac muscle structure: what are intercalated discs?

A
  • transverse cross-bands
  • attachment site between cardiac muscle cells
  • contain adhering junctions (gap junctions – arrays of densely packed protein channels that permit intercellular passage of ions and small molecules)
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5
Q

what do intercalated discs do? (cardiac muscle)

A
  • allows communication between cells
  • allows electrical impulses to pass rapidly from cell to cell, so the linked cells contract almost simultaneously
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6
Q

what are gap junctions (cardiac muscle)

A
  • arrays of densely packed protein channels that permit intercellular passage of ions and small molecules
  • electrical activation of the heart requires cell-cell transfer of current thru these
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7
Q

4 similarities between cardiac muscle and skeletal muscle

A
  1. SARCOLEMMA (a membrane that surrounds and encloses muscle fibres) + from which transverse tubules tunnel in and around sarcomeres
  2. SARCOPLASMIC RECTICULUM – modified form of ER
  3. STRIATED in appearance + similar arrangement of actin and myosin filaments
  4. all muscle tissue consists of FIBRES that can SHORTEN by a HALF to a THIRD of their length
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8
Q

differences between cardiac muscles and skeletal muscle 7

A
  1. C much shorter and wider than S
    *2. C have a single nucleus, S multicellular
  2. C are branching and joined end to end in a complex 3D network, ?
    *4.C many mitochondria, makes up more of cell vol vs S
  3. C have transverse tubular system consistings of wider invaginations of the cell surface than S (C more abundant branching sarcoplasmic recticulum)
    *6. C contract even in absence of stimulation by a nerve, not voluntary (unlike S)
  4. C is unique to heart (unlike S)
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9
Q

how does the structure of cardiac muslce cells (CMC) allow for propogation of stimuli throughout the heart wall 4

A
  1. intercalated discs at junctions between CMC
  2. direct electrical coupling between cells – allows waves of depolarisation to pass thru – syncing contraction of the muscle (As if in a single cell)
  3. cardiac muscle fibres form an interconnected network
  4. CSC network of walls of atria – seperate from that of ventricles = transmission delay
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10
Q

define the cardiac cycle

A

The sequence of events of a heartbeat, by which blood is pumped around the body.

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11
Q

two stages of cardiac cycle

A
  1. systole – contraction of heart muscle
  2. diastole – relaxation of heart muscle
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12
Q

what is a myogenic activity, and how is the heart an example

A
  • no need for nerve stimulus
  • heart beats rhythmically throughout life without need to be stimulated by and external nerve
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13
Q

what triggers heartbeats in hearts (they are myogenic!) and how

A

the sinoatrial node/’pacemaker’
- a network of specialised, self-excitable cardiac muscle fibres
- located in the right atrial wall
- each elec charge is propped thru the network of muscle fibres in both atria walls (via gap junctions in the intercalated discs)
- muscle of both atrial walls contract simultaneously (atrial systole)

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14
Q

what is the function of the atrioventricular node

A

picks up the signal originating from the SAN (it cannot pass directly from the atria to the ventricles)
- at the base of right atrium

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15
Q

why is there a delay at the atriovetricular node (Essentially AV node structure vs SA node structure)

A
  • cells of AV node take longer to get excited than the SA node
  • smaller diameter of AV cells = slowing conduction results
  • fewer sodium ion channels in membranes of AV + more negative resting potential
  • fewer gap junctions in intercalated discs in AV
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16
Q

what is the purpose of the delay of transmission in the AV node

A
  • gives atria time to contract fully (= more blood to ventricles)
  • prevents atria and ventricles from contracting simultaneously
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17
Q

very long but coordination of the heartbeat full prose

A
  1. The beat of the heart is initiated in the sinoatrial node (SA)
  2. Signals from the SA that cause contraction cannot pass directly from A to V –> Instead the impulse spreads along the A to the atrioventricular node (AV), from where it spreads to the V. There is a DELAY between the arrival and passing on of a stimulus at the AV. This delay allows time for atrial systole before the atrioventricular (tricuspid and bicuspid or mitral) valves close. The blood therefore leaves the atria to the ventricles when the atrial systole occurs.
  3. The blood is now in the ventricles and the atrioventricular valves are closed. In the interventricular walls there are specialised fibres grouped to form a bundle called Bundle of His. This bundle splits into two branches that go to the left and right ventricles, leading to other specialised cells called Purkinje fibres.
  4. Conducting fibres ensure coordinated contraction of the entire ventricle wall. The ventricules contract. Blood then flows out of the heart as the semilunar (pulmonary and aortic) valves open and give access to the aorta and pulmonary artery.
  5. The heart is now relaxed.
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18
Q

outline contraction of ventricle wall (involving conducting fibres)

A
  1. From the atrioventricular node, a bundle of fibres (the AV bundle) conducts the signal into the ventricles
    to a point where it splits into right and left branches.
  2. Purkinje fibres deliver the signal to the base of each ventricle via conducting fibres – these ensure coordinated contraction of entire ventricle walls (ventricular systole)
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19
Q

how do conducting fibres speed up contraction of ventricular walls

A

○ large diameter
○ numerous voltage-gated sodium ion channels
○ well supplied with mitochondria + glycogen store – provides direct source of glucose for respiration

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20
Q

when do heart valves close

A

when theres a tendency for blood to flow in the opposite direction
- determined by relative pressures

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20
Q

what instrument is used to hear heart sound

A

stethoscope

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21
Q

what causes the lub sound

A

the simultaneous closure of AV valves

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22
Q

what causes the dub sound

A

closure of semilunar valves in ventricular diastole

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23
Q

who invented the stethoscope?

A

RENE LANNECIN IN 1819

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24
Q

how was the stethoscope revoluntaionary

A

gave access for the first time to body noises eg breathing, heart valves
- learning normal and abnormal breathing sounds = diagnosis of pulmonary ailments

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25
Q

why are the rhythms of pacemaker cells considered myogenic (of muscle origin) and not neurogenic (of neural origin)

A

pacemaker cells have their own intrinsic rhythms of activity – as one action potential is completed, immediately after another is generated in the membrane (even without nerve impulse)

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26
Q

define heart rate

A

the number of times the heart contracts in one minute (beats per minute)

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27
Q

how can a pulse be felt

A

ventricular contractions = wave of blood thru arteries = expansion of artieries = pulse

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28
Q

normal heartbreat ranges between ___ and ____ beats per minute

A

50 and 100

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29
Q

what controls the heartbeat?

A

Sinoatrial node (SA node)
- but can be affected by nervous, hormonal, etc factors

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30
Q

process for measuring heart rate in the neck

A
  1. press on one side of the neck with the index and middle fingers
  2. hence measuring the cartoid artery
  3. count number of beats per minute
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31
Q

process of measuring heart rate inside of wrist

A
  1. using index and middle finger from other hand
  2. count number of beats in one minute
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32
Q

name 10 factors that increase heart rate

A

gender
physical activity
body size
temperature
altitude
posture
stress
eating
sodium and calcium ions in blood
drugs

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33
Q

2 factors that decrease heart rate + how?

A
  1. age: heart muscles cant pump as efficiently
  2. potassium ions: decrease action potentials (hyperkalemia)
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34
Q

how does gender increase heart rate

A

women have slightly smaller hearts = needs to beat at a faster rate than male heart

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35
Q

how does physical activity increase heart rate

A

more blood required in muscles for oxygen supply

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36
Q

how does body size increase heart rate

A

larger ppl have higher heart rate than smaller ppl – blood needs to cover larger area

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37
Q

how does temperature increase heart rate

A

incr temp = vasodilation = increases beats
(also applies to fevers)

38
Q

how does altitude lead to increased heart rate

A

body requires incr oxygen = cardiac output incr

39
Q

how does posture incr heart rate

A

standing heart rate > lying down
- standing = pump against gravity

40
Q

how does stress lead to incr heart rate

A

body produces more epinephrine = accelerated heart rate

41
Q

how does eating lead to incr heart rate

A

more blood needs to be pumped to the stomach and intestines after eating

42
Q

how does sodiu and calcium ions in the blood lead to incr heart rate

A

blood retains more water to dilute ions = needs to pump more

43
Q

how do drugs incr heart rate

A

caffeine and nicotine – stimulants of nervous system and cardiac centres = incr heart rates

44
Q

what should be ensured when designing an investigation working with a human 5

A
  1. subject is reasonably fit
  2. everyone understands and is confident abt the procedures
  3. risk assessment undertaken
  4. no one experiences prolonged discomfort
  5. no medical diagnosis to be made as a result of experiment
45
Q

when to take the pulse when experimenting with heart rate 4

A

after 5-20 mins of rest

after standing upright for 5 mins

immediately after exercise

short intervals until pulse returns to normal

46
Q

the formula for cardiovascular efficiency

A

(duration of exercise x 100) / (recovery pulse x 5.6)
- if used 3 minute step test

47
Q

procedure for the 3 minute step test – to investigate the effect of exercise on heart rate

A
  1. steppnig rate 24 steps per min
  2. step height 45 cm
  3. duration of exercise 3 mins
48
Q

if the SA node becomes diseased or damaged, normal heart rhythm can be restored by ….

A

the surgical implementation of an artificial pacemaker

49
Q

in what situations would a patient need an artificial pacemaker

A
  1. heart does not beat fast enough
  2. system of fibres conducting signals within and between A and V is faulty
50
Q

what does a pacemaker do

A

delivers electrical impulses via electrodes to the heart wall – regulate heart rate

51
Q

what does a pacemaker consist of

A

a battery powered generator (that sends out electrical impulse) + wires with electrodes to connect to heart muscle

52
Q

the procedure of inserting artificial pacemakers 3

A
  1. small cut made on left side of chest
  2. generation placed under skin here
  3. 2 leads to right A / 1 lead to right A and 1 to right V wall
53
Q

what does an ECG do

A

ECG = electrocardiography
- checks the electrical actvity of the heart

54
Q

how are the electrical signals picked up by ECG generated?

A

impulses that originate in the SA node during cardiac cycle generate electrical currents (conducted thru fluids of body as a whole)

55
Q

procedure for ECG 3

A
  1. electrodes attached to patients chest – detect electrical changes
  2. changes produced from muscle electrical activity (bc cardiac conduction in heart)
  3. signals obtained in ECG – amplified in machine, displayed on screen of an oscilloscope
56
Q

what does ECG aid in the diagnosis of

A

cardiovascular disease

57
Q

how to calculate heart beats with an ECG trace

A

internval between sucessive highest peak

58
Q

whats the wave just before the highest spike in the ECG trace

A

SA node electrical activity and contraction of atria

59
Q

whats the highest peak +slight dips before and after on an ECG trace

A

excitation of the ventricles

60
Q

whats the wave after the peak on an ECG trace (larger than the one before)

A

relaxation of ventricles at the end of the contraction

61
Q

what device is used to measure blood pressure

A

sphygmomanometer
sph-yg-mo-man-o-meter

consists of an inflateable cuff and a measuring device

62
Q

mechainal vs digital sphygmomanometer

A

mechanical: measures pressure in ml of mercury
digital: makes oscillometric measurements – cuff pressure used to detect small oscillations in blood flow caused by pulse

63
Q

what is hypertension

A

systolic pressure greater than 140mm Hg
+
diastolic pressure greater than 90 mm Hg

64
Q

name the causes of hypertension 5

A
  1. deposition of fat in arteries and the formation of fibrous tissue
  2. high salt content in diet
  3. smoking
  4. obesity and lack of exercise
  5. excessive alcohol consumption
65
Q

how does obesity and lack of excercise lead to hypertension

A
  • esp abdominal obesity
  • bp falls when weight is lost
65
Q

how does deposition of fat in arteries and formation of fibrous tissue result in hypertension?

A
  • blood flow impeded
  • thickening of artery wall = loss of elasticity = further incr BP
65
Q

how does smoking lead to hypertension

A
  • nicotine – vasoconstricting drug
  • arterioles constrict = BP incr
65
Q

how does excessive alcohol consumption lead to hypertension

A

reversal of alcohol drinking habit has lead to lowered blood pressure

66
Q

how does high salt content in the diet result in hypertension?

A

greater retention of water in the body – vol of blood incr, BP incr

67
Q

name the consequences of hypertension 8

A
  1. damages heart, blood vessels, brain, kidneys
  2. accelerates onset of atherosclerosis
  3. incr workload of heart, makes brain hemorrhage more likely
  4. stroke (reduced supply of blood to brain)
  5. blindness
  6. hardening of arteries
  7. heart attack, failure
  8. kidney failure
68
Q

can hypertension be treated?

A

yes! with drugs
its also a chronic illness that obese ppl can have

69
Q

what iis thrombosis?

A

the formation/presence of a blood clot in a blood vessel

70
Q

what is a thrombus

A

blood clot formed within a blood vessel

71
Q

what is an embolus

A

a thrombus that breaks free and circulates the blood stream (ew)

72
Q

what is atherosclerosis?

A

the cause of thrombosis

73
Q

how is thrombosis caused?

A
  1. caused by damage to arteries, and subsequent formation of scar tissue
  2. buildup of cholesterol and other lipids on scar tissue = plaque
  3. plaque = platelets release clotting factors, clot over plaque = thrombus
  4. thrombus blocks flow of blood to tissues = thrombosis
74
Q

how does thrombosis lead to coronary heart disease

A

thrombut/clot occurs in coronary artery = supply of blood to areas of heart blocked = irregular heartbeat and CHD

75
Q

3 simple steps to atherosclerosis! aka disease of the blood

A
  1. damage to artery walls
  2. raised blood pressure
  3. inflammation and plaque formation at site of fat deposit
76
Q

3 steps for atherosclerosis in arteries but detailed

A
  1. damage to artery walls – fats build up, fibrous tissue laid down with fatty streaks
  2. raised blood pressure: fatty deposits, formation of fibrous tissue: impede blood flow
  3. inflammation and plaque formation at fat deposit: inflammation = artery lining breaks down, circulating blood exposed to deposits = plaques form, cholesterol accumulates, blood platelets = clotting (forming thrombus)
77
Q

consequences of thrombosis (2) (short)

A
  1. heart attack / myocardial infarction
  2. a stroke
78
Q
A
79
Q
A
80
Q

how does thrombosis cause a heart attack 3

A
  1. occurs when embolus swept into coronary artery
  2. blood supply cut off, tissues no oxygen = die
  3. enough heart muscle dies = no longer an effective pump
81
Q

how does thrombosis cause a stroke 3

A
  1. when embolus blocks an artery in the brain
  2. neurons depend on continuous supply of blood for o2 and glucose – no blood supply = death
  3. neurosn cant be replaced = loss of bodily functions controlled by that region
81
Q

what is coronary heart disease

A

decr blood flow and oxygen to heart muscle bc of narrowed heart arteries

81
Q

what is ventricular fibrillation

A

the interruption of the electrical impulses that control heartbeat

82
Q
A
83
Q

how does ventricular fibrillation occur

A

rapid heart beating = low bp (ventricles cant pump hard enough) = symptoms eg chest pain, dizziness, nausea, fainting

84
Q

what equipemtn is used in the event of ventricular defibrillation

A

defibrillator

85
Q

what does a defibrillator do (simple)

A

deliver a theraputic dose of electrical energy to the heart

86
Q

what does a defibrillator do (more detailed)

A

electrical impulse = depolarises heart muscles = reestablish function of natural pacemaker

87
Q

how do automated portable defibrillators work 3

A
  1. analyse existing heart rhythm
  2. diagonse if condition is treatable
  3. adnimister correct electric shock
88
Q

what is the kind of defibrillator you can put in the bodu

A

implantable cardioverter-defibrillator (ICD)
- monitors heart rhythms, sends out shocks when needed to incr/decr heart rhythm