The Heart as a Pump

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  • Created by: LBCW0502
  • Created on: 16-01-19 14:06
What does the structure of the heart muscle consist of?
Left/right atria. Left/right ventricles. Mitral valve, pulmonic valve, aortic valve. Myocardium. Aorta. Vena cava. Pulmonary artery/vein
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Why is the muscle on the left ventricle thicker?
To have sufficient force to pump the oxygenated blood to the rest of the body
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Which chambers in the heart contain oxygenated blood?
Left atrium and left ventricle
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Which chambers in the heart contain deoxygenated blood?
Right atrium and right ventricle
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The heart muscle is made up of which type of cells?
Myocardium is made up of cardiomyoctyes - terminally differentiated, cannot regenerate, forms a scar when damaged (can lead to heart failure/affects pump function)
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Neonatal cardiomyocytes can divide once or twice in how many days?
In the first 5 days
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Describe the regulation of excitation-contraction coupling (1)
Muscle contraction is a Ca 2+ dependent phenomenon. Depolarisation of muscle cell, open L-type Ca 2+ channel. Ca enters cell. Activate ryr. Release of Ca 2+ from sarcoplasmic reticulum (for muscle contraction (CICR)). Regulation bidirectional
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Describe the regulation of excitation-contraction coupling (2)
More Ca2+, more muscle contraction. Ca oscillates between cytosol and SR (reuptake SR Ca ATPase, pump also regulated)
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Describe the regulation of excitation-contraction coupling (3)
HR/force of contraction regulated by e.g. adrenaline (sympathetic) in b1 receptors (AC, PKA, cAMP, increase Ca into cell, more contraction) or ACh (parasympathetic) in mAChRs.
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Describe the mechanism involved in ischaemia
Blood supplied to myocardium blocked (clot in coronary artery). Drop in ATP conc. Inhibit ATPase pumps. Disregulation of Ca homeostasis. Ca ATPase, Na-K pump. Build up of Ca in cell (kill cell). Na-Ca reverses (Na out of cell, more Ca into cell)
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Describe features of length tension relationships in skeletal muscle
Optimal sarcomere (contractile unit repeated) length to generate force of contraction, maximum overlap of actin/myosin filaments. Short sarcomere (thin filaments overlap, no contact with thick filaments). Long sarcomere (no contact of filaments)
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Describe features of length tension relationships in cardiac muscle
Similar to skeletal muscle (striated muscle). Normal operating range with force generating (important for heart failure/myocardial wall stretched/not contracting properly). Optimal sarcomere length ~2.2 microns
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What are the possible explanations other than filament overlap? (1)
Stretch dependent sensitivity of troponin C (thin filament, movement to allow myosin head to bind to actin, stretch/increase Ca2+ sensitivity) to Ca 2+. Phosphorylation (response to neurostimulation/agonists e.g. noradrenaline)
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What are the possible explanations other than filament overlap? (2)
Decreasing inter-filament spacing facilitating cross-bridge formation when myocytes are stretched
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If the muscle is sensitive to stretch, what does this mean?
Responsive to preload and afterload (preload and afterload give indications about heart failure)
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What is preload?
Larger volume filled in ventricle, muscle wall stretched (preload), muscle has to contract to eject volume of blood from ventricles (degree of stretching). Increased diastolic volume
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What is afterload?
Resistance/force against muscle is contracting (increased aortic pressure). Ventricle contracts to point where aortic valve opens. Pump against aortic pressure. Increased afterload indicates hypertension (work harder to eject blood into aorta)
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What does an increased preload link to? (1)
Increased resting length (linked to speed of contraction/time, as a function of initial resting length). Contracted length is the same regardless of preload. Ventricle contracts to fixed point (due to sarcomere length/physical limits of filaments)
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What does an increased preload link to? (2)
Stretch muscle, faster contraction/decrease in length. Stronger force of contraction (graph). Preload affects speed of contraction in order to maintain cardiac output
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What is the Frank-Starling mechanism? (1)
Link between systemic/pulmonary circulations. If preload in right ventricle increases, the output in left ventricle increases (balance). Decreased preload detected by baroreceptors (rebalance system/increase). Regulate CO/total peripheral resistance
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What is the Frank-Starling mechanism? (2)
If there is an imbalance in output from the R and L sides (R > L) then filling of L ventricle increases (pumps less blood than R, to increase output). R receives less blood leading to decrease output (rebalance output)
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What is the Frank-Starling curve (1)
Measure in vivo. Stroke volume vs left ventricular end diastolic pressure. Normal heart, LVEDP increases/stroke volume increases (due to stretch mechanism, contraction). Increase in afterload (aortic pressure), stroke volume decreases for same LVEDP.
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What is the Frank-Starling curve (2)
Decrease in afterload leads to larger stroke volume for same LVEDP
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What is the cardiac cycle?
Relationship between volume and pressure. Diastole (relaxation). Systole (contraction)
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What is isovolumetric ventricular contraction? (1)
Occurs at the end of diastole. Pressure in left ventricle reaches point at end of filling. Pressure in LV > pressure in atrium. Mitral valve closes. Atrium relaxes. Aortic valve closed (aortic pressure > LV pressure)
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What is isovolumetric ventricular contraction? (2)
Ventricle contracts, no change in volume (valves are still closed). Generation of pressure. Pressure in LV > pressure in aortic (aortic valve opens). Leads to ejection phase
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What is ventricular ejection?
Ventricle still contracts to eject the blood into the aorta. Aortic valve is opened. Mitral valve is closed (aortic/mitral values alternate)
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What is isovolumetric ventricular relaxation?
Ventricles are relaxed at the end of systole. Valves still closed, until atrium pressure > ventricular pressure
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What is ventricular filling?
Contraction of atria (atrium pressure > ventricular pressure) leads to opening of mitral valves to allow blood to flow from atria to ventricles
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What are the components of the cardiac cycle graph?
Aortic pressure. Left atrial pressure. Left ventricular pressure. Left ventricular end diastole volume. ECG. Opening/closing of mitral/aortic valves. Heart sounds
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Which side of the heart has a lower pressure?
Right side (pulmonary side of the heart), RA (0-4), RV (25/4), pulmonary artery (25/10)
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What are the pressure readings on the left side of the heart?
Aorta (120/80), LA (8-10), LV (120/10)
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What are the key points based on the left atrial pressure graph in the cardiac cycle
Slight increase in LAP due to bulging of atrial valves inwards (despite being empty). Ventricular contraction with bulging AV valves into atrium. Ventricular ejection (atrial base pulled down. Filling of atrium (mitral valve closed/increase pressure)
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Describe features of a pressure volume loop
Area (stroke work/ejection certain volume). 1. mitral valve opens. 2. diastolic filling. 3. Mitral valve closes. 4. Isovolumetric contraction. 5. aortic valve opens. 6. ejection. 7. aortic valve closes. 8. isovolumetric relaxation. 9. stroke volume
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How does the pressure volume loop change with increased inotropy (increased force of contraction)?
Slight left shift of PV loop, affects end systolic pressure volume relationship (steeper), does not affect end diastolic pressure volume relationship
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How does the pressure volume loop change with a dilated cardiomyopathy (decrease inotropy)?
Defect in muscle (causes ventricle to dilate, larger volume). Shift to the right. LV volume increases. Bigger volume at end of diastole. Can decrease in size due to not contracting properly. Change in both EDPVR/ESPVR
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How does the pressure volume loop change with LV hypertrophy?
Wall of LV becomes thicker. Could give stronger contraction. Volume of ventricular cavity can be smaller (taller PV loop). Size of PV loop decreases in size. Affects filling/stroke volume
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How does the pressure volume loop change with aortic stenosis?
Calcification of aortic valve (stiff/doesn't open or close). Taller PV loop (stronger contraction against aortic valve). Higher pressure generation. Higher volume of blood at the end of systole (doesn't eject blood properly)
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How does the pressure volume loop change with aortic regurgitation?
Valves not closing properly. Blood can go across valve. Ventricle contracts, eject blood into aorta. Diastole, ventricle filling, aortic valves should be closed
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Describe features of the heart sounds (1)
S1 (closure of AV valves). S2 (closure of aortic/pulmonary valves). S1/S2, lub-dub sounds, (aortic valve, large, low frequency, AV valve, high frequency).
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Describe features of the heart sounds (2)
S3 (blood filling in ventricle, tensing of chordae/vibration of tendons, normal in young, abnormal in adults). S4 (atrial systole causing vibration of ventricular wall, more common when ventricular compliance is reduced)
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What is used to measure heart sounds?
Stethoscope (4 areas on the heart to measure heart sounds, valves/chambers). Detection of abnormal sounds before confirming with ultrasound
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What are abnormal heart sounds? (1)
Noises between the main sounds (e.g. aortic insufficiency, aortic valves not opening/closing properly, rushing sound, blood going across valve) - aortic stenosis
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What are abnormal heart sounds? (2)
Mitral insufficiency (noise during filling/diastole phase, valve not opening properly) - mitral stenosis
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What are abnormal heart sounds? (3)
Aortic insufficiency (aortic valves remain open during filling). Mitral insufficiency (mitral valves remain open)
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What is stenosis?
A narrowing that leads to turbulence and associated sounds when blood is flowing through the valve when the valve is open (effects aortic pressure)
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What is insufficiency (or incompetence)?
Incomplete closing of the valve which leads to turbulent flow of blood through the valve when it ought to be closed (effects aortic pressure)
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What is the splitting of the S2 sound?
Normal in young people. During inspiration, increase filling in RV leading to longer ejection. Expands pulmonary blood vessels, reducing filling of LV leading to shorter ejection. Wide split may signal a bundle branch conduction effect
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How do you measure cardiac output? (1)
Fick's principle (measure O2 consumption/breathing and arteriovenous O2 content difference/between pulmonary artery and systemic artery, blood samples, use blood-gas analyser).
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How do you measure cardiac output? (2)
Ultrasound measures diameter of aorta, SA of cross-section of aorta, velocity (cm/s), measure volume of blood being ejected. Stroke volume = velocity x area x time. CO = HR x SV
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Other cards in this set

Card 2

Front

Why is the muscle on the left ventricle thicker?

Back

To have sufficient force to pump the oxygenated blood to the rest of the body

Card 3

Front

Which chambers in the heart contain oxygenated blood?

Back

Preview of the front of card 3

Card 4

Front

Which chambers in the heart contain deoxygenated blood?

Back

Preview of the front of card 4

Card 5

Front

The heart muscle is made up of which type of cells?

Back

Preview of the front of card 5
View more cards

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