The Heart as a Pump Flashcards
What causes the P wave in an ECG?
Atrial contraction (depolarisation of atria)
What causes the QRS complex in an ECG?
Ventricular excitation/contraction
What causes the T wave in an ECG?
Ventricular recovery - repolarisation of Vs
What are intervals on an ECG?
Measure how long electrical events occur
Intervals on ECG?
-PR interval
-QT interval
Segments on ECG?
-PR segment
-ST segment
Label the waves, segments, intervals on this ECG.
Why doesn’t anything between AV node –> purkinje fibres give a wave on ECG?
Not strong enough firing
Give the stages on an ECG.
-P wave
-PR interval
-PR segment
-QRS complex
-QT interval
-ST segment
-T wave
Summarise what causes each of:
-P wave
-PR interval
-QRS complex
-ST segment
-T wave
-QT interval
What are 1, 2 & 3?
What are the 2 types of contraction in cardiac muscles?
-Isometric
-Isotonic
What does isotonic mean in cardiac contraction?
-Same tension
-Changing length
What does isometric mean in cardiac contraction?
-Same length
-Changing tension
What are the 2 types of elements in cardiac muscle?
-Contractile
-Elastic
When does isometric contraction occur?
-If load is too heavy to move
–> contraction causes tension (changing tension) in elastic elements, but NO muscle shortening (same length)
When does isotonic contraction occur?
-If load can be moved
–> muscle tension increased high enough to match load = muscle shortens (change in length)
Apply isometric contraction to cardiac contraction.
-Pressure increase in elastic elements of ventricular cardiac muscle
= partial contraction of contractile elements (changing tension)
-NO external shortening yet (same length) as tension not yet matched load (arterial pressure)
–> valves stay shut - no blood ejected
Apply isotonic contraction to cardiac contraction.
-Pressure increase in elastic elements of ventricular cardiac muscle
= contraction causes tension (pressure) in the ventricles, so matches load (pressure in arteries)
= muscle shortens & load moves (valves open & blood ejected)
-Isotonic phase equates to ventricular ejection in heart
Name these 5 stages of the cardiac contraction cycle.
1 = atrial ejection
2 = ventricular contraction/depolarisation
3 = ventricular ejection
4 = isovolumetric ventricular relaxation
5 = atrial contraction/depolarisation/ventricular filling
Describe the 5 stages of the ‘cardiac cycle’/cardiac contraction in relation to ECG.
A - heart is relaxed - fills w/ blood passively - into atria & some into ventricles (passive)
What is the length-tension relationship of muscles?
-Amount of force in contraction - vs muscle can generate in contraction depends on initial length of sarcomere
-Long sarcomere length = no interaction between actin & myosin (no cross-bridges) = no force generated
-As decrease sarcomere length - actin gradually interacts more & more with myosin as the length shortens (increased no. cross-bridges/overlap) = amount of force generated increases with decreased sarcomere length
What is responsible for determining how many cross-bridges actually form during muscle contraction?
Intracellular [Ca2+]
What are muscle cells of heart called?
Myocardial cells
What occurs at this max tension of myocardial cells?
Max overlap of thick (myosin) & thin filaments (actin) - any shorter/longer sarcomere lengths & tension generated will be less than max - too short & the opposite actin filaments will overlap - distorts myosin (fewer cross-bridges)
–> initial increase in force as sarcomere length decreases but then at max force then continued sarcomere shortening decreases force
Summarise the length-tension relationship.
-Higher initial sarcomere length = greater contraction force –> but only up to max tension (limit)
-After limit - increase in sarcomere length decreases force of contraction
How does the length-tension relationship link to myocardial cells?
Inc pressure in vs reflects tension of muscle fibres/sarcomeres (= stretched - get longer)
What is the systolic pressure-volume of ventricles?
-Systolic –> higher vol of blood in vs - more tension - so higher pressure
-Tension reflects pressure (pressing against walls of vs)
-Contraction generated = relative to level of pressure caused (& so the vol of blood in vs too - as vol influences pressure)
What is end-diastolic ventricular volume?
-Vol of blood in ventricles at end of diastole (relaxation - when are filling) before contraction of ventricles
- end d vol increases = increases v pressure against walls (passive mechanisms)
-Pressure inc reflects tension inc of muscle fibres (as vs = stretched)
–> graph shows ventricular pressure & vol relationship in diastole of vs - as vol inc - pressure does too
Give a flow diagram to represent how the Frank-Sterling mechanism equalises the output between the right and left sides of the heart.
Pulmonary circulation (deoxy blood, heart –> lungs) & systemic circulation (oxy blood, lungs –> heart) is kept same
How does preload affect stroke volume?
-Higher preload (longer initial muscle/sarcomere length due to EDV - stretches) = inc pressure/tension (length-tension relationship) = greater force of contraction as more cross-bridges (systole) = more blood ejected (vol) = inc SV
-Lower preload (shorter initial muscle/sarcomere length due to EDV - stretches) = dec pressure/tension = lower force of contraction as fewer cross-bridges (systole) = less blood ejected (vol) = dec SV
How does contractility affect stroke volume?
-Inotropic effect - NS’s effects on contractility
+ve = increase in contractility - stimulates inc in contraction force of myocardial cells - more blood ejected - SV inc (SYMP NS)
-ve = decrease in contractility - stimulates dec in contraction of myocardial cells - less blood ejected - SV dec (PARASYMP NS)
What happens during haemorrhage?
-Dec venous return (as has left body)
-Dec EDV
-Dec SV (Starling’s law)
Mechanism to maintain arterial pressure (so stay conscious):
-Symp response = +ve inotropic (larger force of contraction)
= inc in SV
-CO = HR x SV (mechanism aims to maintain CO as blood falls)
-Large tachycardia (v. fast HR) - BUT = reduced filling time of vs (reduced EDV) - so SV can fall!
How does the sympathetic NS increase the force of contraction in +ve inotropism?
-Nor/adrenaline from symp NS binds to β1 adrenoreceptors (on myocyte membs) = GPCR
-alpha subunit splits off from beta & gamma
-alpha subunit binds to adenylyl cyclase = activated
-Adenylyl cyclase converts ATP —> cAMP
-cAMP - activates protein kinase A (PKA)
-PKA - phosphorylates L-type Ca2+ channels = more Ca2+ influx = so more Ca2+ induced Ca2+ release from SR = more troponin C moved out myosin binding site on actin = stronger contraction force (more cross bridge cycling)
*Relaxation (diastole) = faster due to increased Ca2+ pumped back (faster) into SR - due to phosphorylation of phospholamban - reduces cytosolic Ca2+
*Increased Ca2+ stored in SR for next release (next AP)
*Next beat can happen sooner and will be stronger –> as Ca2+ influx from memb & SR will occur
Link it all together:
1 = Why is the length-tension relationship important in myocardial cells/heart muscle cells?
2 = How - what is the mechanism of this?
3 = How does volume, pressure, tension, stroke volume in ventricular systole & diastole relate?
1 = It equalises/maintains the output by right side (pulmonary circulation) & left side (systemic circulation) –> output of both vs is kept equal
-If not equal - would get blood accumulation in lungs (if output of left higher than right output - see image)
2 = If input of blood increases in 1 side of heart (increased venous return) = increases EDV (as more blood moves into vs when relaxed) = increases stretch of ventricular musculature (sarcomere length increases) = decreased side-by-side distance between actin & myosin (move closer) = more cross-bridge interaction = muscle contracts with more force = increases stroke vol (more blood ejected by v) –> this will have same effect on other ventricle
3 = inc DSV = inc pressure/stretching/tension = inc SV –> means systole (contraction) has occurred with more force (to eject v’s blood - SV)
How to calculate the ejection fraction?
How is cardiac output calculated?
(i.e., total vol of blood ejected by v per unit time)
Calculation for cardiac output - including units?
Describe the stages in this ventricular pressure-volume loop.
*1–>2 = isovolumetric ventricular contraction (systole):
-V full of blood (diastole just finished) at 1 (which is atrial contraction/systole)
-Vol in v = EDV
-Vs contracts = inc pressure (but all valves closed)
-Mitral/bi & tri valves close
*2–>3 = ventricular ejection:
-At 2 v pressure exceeds arteries = SL valves open
(Orange dashed line shows systolic press-vol curve)
-Rest of v contraction = used to eject blood via arteries (SV)
-Pressure remains high - vs still contracting
*3–>4 = isovolumetric relaxation
-End of systole at 3 - vs relax
-V pressure dec below arteries = SL valves close
-Vol remains constant (isovolumetric) @ ESV as all valves are shut
*4–>1 = ventricular filling
-At 4 v press below atria = bi/tri vales open
-Vs passively fill with blood due to atrial contraction
-Press in atria above vs = bi/tri valves open - so vs fill with more blood (actively)
Why have these changes to the ventricular pressure-volume loops occurred?
A:
-Increased EDV (as higher venous return) = 1
-Constant afterload & contractility
B:
-Increased aortic pressure = inc afterload
-LV must eject blood @ higher pressure to exceed aortic pressure - in isovolumetric contraction = 2
-Ventricular ejection 2–>3 - but less blood is ejected due to inc afterload (lower SV) - ESV is higher (remaining blood) = 3 & 4
C:
-Greater tension/pressure in systole = 2
-So more blood ejected (inc SV & ejection fraction - less blood remains in vs - lower ESV) = 3 & 4
Fill in.
