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Biology > Chapter 5 The Heart and Monitoring Heart Function > Flashcards

Chapter 5 The Heart and Monitoring Heart Function Flashcards

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1
Q

Why do multicellular organisms need a mass transport system?

A

Multicellular organisms need a mass transport system because:
-there is a higher demand for nutrients and greater production of waste
-higher metabolic rate
-more active organisms which means that there is a larger number of cells respiring very quickly so a greater demand for oxygen, glucose and carbon dioxide
-the SA:V is too low for diffusion to deliver nutrients at an appropriate rate nor remove wastes at a suitable rate
-hence a transport system is needed to ensure the demand of all individual cells is met

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2
Q

The Cardiac cycle: Atrial systole (and ventricle diastole)

A

During atrial systole muscles in the atrial walls contract, whereas muscles in the ventricle walls relax. This causes an increase in atrial pressure and a decrease in atrial volume, forcing the atrioventricular valves open. Blood is forced into the ventricles.

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3
Q

Ventricular systole

A

During ventricular systole muscles in the ventricle walls contract only once waves of excitation pass through the Purkyne fibres, whereas muscles in the atrial walls relax. This causes an increase in ventricular pressure and a decrease in ventricular volume, forcing the atrioventricular valves closed and the semi lunar valves open. Blood is forced into the arteries.

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4
Q

Complete cardiac diastole (ventricular and atria diastole)

A

-Both atria and ventricles relax
-higher pressure in pulmonary artery and aorta so semi lunar valves close to prevent backflow of blood into ventricles
atria fill with blood (increasing their pressure) due to higher pressure in the vena cava and pulmonary vein
ventricles continue to relax so pressure in atria is greater than pressure in ventricles
AV valves open and blood flows passively into ventricles
process continues

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5
Q

When will valves open?

A

Valves open when the pressure behind them is greater than the pressure in front of them.

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6
Q

Explain how valves close

A

Valves close when pressure in front of the valve is greater than the pressure behind.

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7
Q

Control of the cardiac cycle

A

Electrical impulse is generated at sinoatrial node (SAN)
Electrical impulses sent across atrial walls.
Muscles in atrial walls contract
Layers of non-conducting collagen tissue between atria and ventricles prevents wave of excitation passing directly to ventricles.
AVN receives impulse which causes a slight delay to ensure the atria have stopped contracting before the ventricles contract.
Electrical impulse is sent down bundle of His.
Impulse sent to perkinje fibres.
Electrical impulse arrives at apex of the heart.
At apex, Purkyne fibres spread out through both ventricle walls. Waves of excitation triggers simultaneous contraction of ventricles starting at the apex ( to allow more efficient emptying of ventricles) ventricular systole occurs from the bottom of the heart upwards

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8
Q

Explanation for when the calculated value is greater than the critical value

A

Calculated value is greater than the critical value
degrees freedom
there is a less than 5% probability that the difference between mean pulse rate…and… is due to chance.
rejecting the null hypothesis.
there is a statistically significant difference between…

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9
Q

Explanation of calculated value

A

Calculated value is less than the critical value
degrees freedom
there is a more than 5% probability that the difference between…and…
accept the null hypothesis
there is not a statistically significant difference between…and…

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10
Q

Cardiac Muscle of the heart

A

-myogenic
-muscle contracts in regular rhythm
does not fatigue
-specialised striated muscle
-fibres are branched and uninucleated
-cardiac muscle cells interconnect resulting in simultaneously contraction
intermediate contraction speed and intermediate length of contraction
cardiomyocytes supplied with oxygen and glucose by coronary artery if it becomes blocked—-> heart attack

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11
Q

Function of aorta

A

-carries oxygenated blood at (high pressure as it has to force the blood over a large distance hence overall there is higher resistance within the blood vessels) from left ventricle to the body

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12
Q

function of pulmonary artery

A

-carries deoxygenated blood from right ventricle to the lungs

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13
Q

function of pulmonary vein

A

-carries oxygenated blood from lungs to right atrium

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14
Q

Function of atria

A

-contract to generate a force to move blood at low pressure into the ventricles
pressure is low as walls of atria are thin (less cardiac muscle)
Both atria always contract simultaneously

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15
Q

Function of carotid arteries

A

-blood vessels that carry oxygen-rich blood to the head, brain and face

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16
Q

Function of ventricles

A

-contract to generate a force to move blood at high pressure out of the heart
Pressure is high as LV is thickest (most cardiac muscle)
LV: Forces oxygenated blood into aorta at high pressure
RV: forces deoxygenated blood into the pulmonary artery at lower pressure than LV as if it was the same, the pressure would be too high and would rupture the alveoli.
Both ventricles contract simultaneously

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17
Q

Function of semilunar valves

A

AORTIC valve: found between LV and aorta so prevents backflow of blood from aorta to LV during ventricular diastole
PULMONARY valve: found between the RV and the pulmonary artery so prevents backflow of blood from pulmonary to RV during ventricular diastole.

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17
Q

Function of Atrio-ventricular valves

A

Right atrioventricular valve:
prevents backflow of blood from RV to RA during ventricular systole.
closes when pressure in RV is greater than the pressure in RA
ensures deoxygenated blood flows into pulmonary artery.
Left atrioventricular valves: prevents backflow of blood from LV to LA during ventricular systole.
closes when the pressure of LV is greater than pressure of LA
ensures oxygenated blood flows into the aorta

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17
Q

Function of septum

A

-separates RHS from LHS so keeps oxygenated blood separated from deoxygenated blood

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18
Q

Function of vena cava

A

-carries deoxygenated blood from the body to RA
superior vena cava delivers deoxygenated blood from head
Inferior vena cava delivers oxygenated blood from rest of body

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18
Q

Function of chordae tendinae

A

-holds valves in place
-attaches valves to muscle wall of the ventricles
-prevents valves inverting when under pressure (during ventricular systole)

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19
Q

Function of Bundle of His and Purkyne fibres

A

Bundle of His is located in septum and Purkyne fibres located in walls of ventricles
AVN stimulates Bundle of His
Bundle of His conducts wave of excitation to apex of heart

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19
Q

Stroke volume

A

volume of blood pumped out of LV during each cardiac cycle

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19
Q

Cardiac Output

A

volume of blood pumped out of the LV each minute

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19
Q

Heart rate

A

number of beats per minute

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19
Q

Equation for CO

A

CO=SVXHR (cm cubed min -1)

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19
Q

Measuring pulse rate

A

Count number of beats in an artery in 30s and then double (less prone to counting errors so more accurate)

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19
Q

What is pulse?

A

distension of artery wall as blood surges through artery with ventricular systole, followed by elastic recoil of artery wall during ventricular diastole

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20
Q

Different places to measure pulse

A

radial artery-wrist
femoral artery-groin
carotid artery-neck
temporal artery-temples
Need to use place where artery is close to the surface of skin and passes over bone

21
Q

Advantages of measuring pulse rate by counting

A

-quick
-easy
-little equipment and skill needed

22
Q

Why does heart rate increase during strenuous exercise?

A

-skeletal muscles contract at a higher rate
-higher demand for oxygen and glucose
-volume of blood being circulated needs to increase dramatically
HR and Sv both increase
heart muscle contracts more strongly—>greater contraction—>greater force of ejection
skeletal muscles also contract more frequently—-> veins compressed more by skeletal muscles—-> greater venous return (to remove lactic acid, carbon dioxide, heat from contracting muscles)

23
Q

Factors that affect heart rate

A

Age= HR decreases with age
Genetics= tendency for lower HR/higher HR inherited
diseases= some affect HR CF increases HR

24
Q

Lifestyle factors that affect heart rate

A

-PAL——> as increased physical activity level, increased HR Training decreases resting HR due to increased SV and so some cardiac output achieved at lower HR
Smoking=nicotine=increases HR as stimulates release of neurotransmitter noradrenaline which increases electrical activity of SAN
Diet=diet rich in fruit and veg decrease heart rate, diets rich in saturated lipids increase heart rate

25
Q

What would happen if both ventricles contract at the same time?

A

If both ventricles contracted at the same time:
-the V would generate a higher pressure than the A
-forcing the A-V valves to shut
-Blood in the A would consequently not enter the V
-Blood will be forced back into the veins
-placing strain on the heart
and decrease the volume of blood moved through the heart
-less blood would be oxygenated
-poorer transport system and gas exchange

26
Q

What is the SAN?

A

-a pacemaker
-patch of non-conducting tissue
-myogenic so does not require an input from the brain
-starts the wave of excitation which generates the electrical activity causing the atria to contract.

27
Q

What are the 2 nerves that regulate the heart rate?

A

-accelerator nerve (sympathetic nervous system)=this nerve uses noradrenaline as neurotransmitter which increases the HR.
-vagus nerve (parasympathetic neurotransmitter)= this nerve uses acetycholine as neurotransmitter which decreases HR.
The neurotransmitter adrenaline also regulates HR.

28
Q

Invstigating the effect of exercise and pulse rate

A

IV= Age, gender, BMI, diet, training programme- shoud be at least 10 subjects (individual people)
DV= heart rate (or recovery rate)
CV= agae, gender, diet, level or intensity of training, PAL, BMI (unless these are the independent variable obviously)

29
Q

Health and safety for experiment on investigating effect of exercise and pulse rate

A

-ensure no subject has serious health conditions like asthma

30
Q

Processing data

A

-calculate mean to reduce the effect of any anamalous results

-calculate standard deviation to asses reliability of data
-size of SD indicates the spread of the data about the mean and the smaller the standard deviation, the more reliable data
Standard error=SD/ square root of N
-calculate t-test: to determine if there is a significant difference between the mean values for each IV category
state null hypothesis: there is no significant difference between the mean HR for “IV category” and the mean HR for “IV Category 2”

31
Q

What do ECGs measure?

A

ECGs measure spread of electrical excitation through heart through electrocardiography
-doesn’t directly measure electrical activity of the heart but measures small electrical differences in skin which occur as a result of the electrical activity of the heart

32
Q

Why are there no risks to electrocardiograms?

A

-no risks as this procedure monitors the electrical impulses and does not emit electricity
-no risk of shock

33
Q

Function of P wave

A

-wave of excitation passing over atroa walls (depolarisation of atria resulting in atria contraction)

34
Q

Function of QRS wave

A

wave of excitation passing over ventricle walls (depolarisation of ventricles)

35
Q

Function of T wave

A

repolarisation of ventricles

36
Q

Q——-T

A

Contraction time

37
Q

T——Q

A

filling time (ventricles are relaxed)

38
Q

What does height of wave indicate?

A

-indicates how much electrical charge is passing through the heart: bigger the wave: more electrical charge:stronger connection

39
Q

How to recognise a heart attack?

A

-chest pain, heavy crushing pressure, tightness, squeezing in the centre of the chest, pain travelling from chest to arms, jaw, neck, back and abdomen
-lightheaded or dizziness
-profuse sweating
-shortness of breath
-cold ashen looking skin and blue lips
-rapid and weak pulse which may be irregular
nausa or vomitting
anxiety
coughing
unexpected collapse

40
Q

How to assist someone having a heart attack

A

-call 999-inform ambulance control that it is a suspected heart attack
make person rest while waiting for an ambulance
sit person in W position-sitting up at about 75 degrees to ground with knees bent
300mg aspirin
medication for angina
monitor constantly and record pulse and breathing rate

41
Q

Treatment of cardiac arrest

A

-if person becomes unconscious follwing suspected heart attack they may be in cardiac arrest
-usually occurs as a result of ventricular fibrilation
results in no effective blood circulation
appear not to be breathing
not moving
don’t respond to any stimulation such as being touched or spoken to

42
Q

How to perfom CPR (Cardiopulmonary resuscitation)

A

-check airway and for breathing by tilting head back
carry out chest compressions on adult
place heel of your hand on the sternum at the centre of the person’s chest
place your other hand on top of your other hand and interlock fingers
using your body weight, keep your elbows locked straight and press straight down vertically
press down firmly and quickly by 4-5 cm and then relax
after each compression release all pressure on the person’s chestwithout lsoing contact between the hands and sternum
aim to do chest compresions at a rate of 100-120 compressions a minute
repeat x30 then give mouth to mouth resuscitation twice
repeat this 30:2 ratio until an ambulance arrives

43
Q

What happens during a cardiac arrest?

A

-supply of blood to region of cardiac muscle is disrupted
-area of cardiac muscle does not receive sufficient oxygen
-cardiac muscle in atrial or ventricular walls contract rapidly and irregularly
-ventricles do not fill fully as no ventricular diastole to allow filling
-blood isnt pumped out of ventricles
patient stops breathing due to lack of oxygen supply

44
Q

Using a defibrillator

A

-use an automated external defibrillator
-AED=Safe, portable elctrical device
-AED helps to establish a regular heartbeat during cardiac arrest by monitoring the person’s heartbeat and giving them an eectrical shock if necessary
-apply two electrodes pads to chest
-pads placed in diagonal line across chest with heart position in the middle
-reading on machine shows if heart is fibrillating
-if it is then AED applies electrical discharge
-stops the chaotic electrical activity of fibrillation and allows heart to restore regular rhythm determined by SAN.

45
Q

Function of ECGs

A

-measure spread of electrical excitation through heart through the process of electrocardiography
-measures small electrical differences in skin which occur as a result pf the electrical activity of the heart
-changes in peaks can be used to detect and diagnose heart conditions
-no risks generally as procedure monitors the electrical impulses and does not emit electricity so no risk of shock

46
Q

P-wave

A

-wave of excitation passing over atrial walls (depolarisation of atria resulting in atria contraction)

47
Q

QRS

A

-Wave of excitation passing over ventricle walls (depolarisation of ventricles)

48
Q

T wave

A

-repolarisation (recovery) of ventricles (recovery of the atria is masked by the QRS)

49
Q

Q—>T

A

Contraction time

50
Q

T—->Q

A

Filling time (ventricles relaxed)

51
Q

What does the height of wave indicate?

A

height of any wave indicates how much electrical charge is passing through the heart: bigger wave=more electrical charge=stronger contraction

52
Q

ST Segment

A

-beginning of ventricle repolarisation, should be flat

53
Q

PR Interval

A

-delay of AV node to allow filling of ventricles

54
Q

Ventricular fibrillation

A

-no regular pattern to ECG
-muscle in ventricle walls flutter
possibly due to myocardial infarction
-no distinct QRS complex
-victim has no blood circulation
-usually unconscious
almost certainly fatal: causes cardiac arrest
-the person having VF suddenly collapses or fails unconscious, because the brain and muscles have stopped receiving blood from the heart
-immediate use of defibrillator
-may need coronary bypass surgery
-sudden death
-for survivors of VF, complications include: coma, reduced mental acuity, and neurological problems similar to those seen after a stroke

55
Q

Atrial fibrillation (AF)

A

-muscle walls of atria contract arrhythmically
-prevents effective ventricular filling
-no distinct P wave
-P-R interval is not easily identifiable
-abnormalities or damage to heart structure
-high blood pressure
-heart attacks
-coronary heart disease
-abnormal heart valves
-congenital heart defects you’re born with
-hyperthyroidism
-increased risk of stroke
-increased risk of heart failure
-chronic fatigue
-additional heart rhythm problems
-inconsistent blood supply
-uncomfortable
-medication to prevent a stroke
-medication to control a heart rate
-cardioversion= where the heart is given a controlled electrical shock to restore normal rhythm

56
Q

Bradycardia

A

-resting heart rate is very slow
-longer gaps between QRS complexes
-gap between each peak in the trace is very long, causing a long gap between the T-wave and the next P-wave
-P waves and height of QRS peaks are both similar to a normal trace
-defined as resting HR between 40-60bpm
-ECG looks normal except delay between waves of more than one second
-long gap between T wave and next P wave
-sign of an active/healthy person
-could be inactive SAN
-no effect usually
-may cause tiredness due to insufficient blood flow to organs
-artificial pacemaker to replace SAN

57
Q

Tachycardia

A

-resting HR is very high
-shorter gaps between QRS complexes
-defined as resulting HR above 100bpm
-ECG shows very small gap between T wave and P wave of next cardiac cycle
-a reaction to certain medications
-congenital electrical pathway abnormalities in the heart
-congenital abnormalities of heart
-consuming excess alcohol
-coronary artery disease, heart valves disease, heart failure, heart muscle disease, tumours or infections
-hypertension
-hyperthyroidism
-smoking
-certain lung diseases

58
Q

Effect of Tachycardia

A

-rapid HR= less time for the atria and ventricles to fill
-little gap between the T-wave of one cycle and theP-wave of the next
-hence less blood is pumped to the body with each heartbeat
-overtime—> drop in blood pressure
-also increases the workload of the heart—> increasing myocardial oxygen demand

59
Q

Treatment of Tachycardia

A

-varies depending on what caused the condition, the patient’s age and general health
-address the cause of tachycardia
-may try to slow rate (prevent subsequent episodes of tachycardia to reduce risk complications)

60
Q

Myocardial infarction

A

-peaks and troughs of ECG are less distinct and not as regular
S-T portion is higher than normal (ST elevation)
-cause: occlusion of coronary artery following the rupture of an atherosclerotic plaque
-leads to formation of blood clot
-blood supply to part of heart muscle is partly or fully blocked
-cardiac muscle cells deprived of oxygen
-cardiac muscle cells stop contracting
-treatment: aspirin-stops blood from clotting, nito-glycerine-dilates blood vessels, pain relieve pain and is often given intravenously, thrombolytics: break up clots can be given with other anticoagulants
anticoagulants: make blood less likely to form clots

61
Q

Preparation for an ECG

A

-Area of ECG is cleaned with alcohol and dried
-Electrodes are placed over the heart

62
Q

Heart rate equation

A

60/time taken for one heart beat (s)

63
Q

Arrhythmia

A

-irregular heart rate
-varied distance between end of T-wave and P-wave

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