Cardiac Cycle Flashcards
What are the four major stages in the cardiac cycle?
- Atrial systole – Drives blood into the ventricles
- Early ventricular systole – closes the AV valve
- Late ventricular systole – pressure rises driving open the semilunar aortic valve – driving blood out through the aorta
- Ventricular diastole – relaxation
What is the repetitive sequence of events in each heart beat?
- Flow into atria, continuous except when they contract. Inflow leads to pressure rise.
- Opening of A-V valves - Flow to ventricles.
Note - High degree of passive flow into the atria – sufficient to maintain adequate blood flow except for during exercise
- Atrial systole - completes filling of ventricles.
- Ventricular systole (atrial diastole). Pressure rise closes A-V valves, opens aortic and pulmonary valves.
- Ventricular diastole – causes closure of aortic and pulmonary valves.
What are the four sounds generated by the heart? What are the associated with?
1st Heart Sound - Closing of AV valves (Lub).
2nd Heart Sound - Closing of semilunar valves (Dub).
3rd Heart Sound - Early diastole of young and trained athletes. Normally absent after middle age. Sounds like “Kentu..cky”. Termed the ventricular gallop. Re- emergence in later life indicates abnormality (e.g. heart failure)
4th Heart Sound – Caused by turbulent blood flow, due to stiffening of walls of left ventricle. Occurs prior to 1st heart sound. Atrial gallop
Note – Tachycardia, 3 + 4 indistinguishable = Summation Gallop
What does the following graph show (ventricular volume changes)?
Shows the changes in ventricular volume during the different phases
At rest - that passive filling of the ventricles is a major contributer and active (atria contract) is a minor contributer
Change when exercising?
Why is the elasticity in the aorta important?
Elastic recoil/pulsatile contraction - Helps maintain pressure in arterial system during diastole - (pressure drops only about one third from systolic B.P.)
What are the definitions of stroke volume and ejection fraciton?
Stroke volume = volume of blood pumped by each ventricle per beat (≏ 75ml) - may double during exercise.
Ejection fraction = % volume pumped out. Ejection fraction = 55-60% (exercise 80%).
In heart failure may be 20%.
Note - The chambers do not empty completely.
How does systemic arterial pressure remain high during the cardiac cycle?
Systemic arterial pressure remains high throughout cycle due to elasticity of the vessel walls and peripheral resistance.
How do we define cardiac output?
Cardiac output is the volume blood pumped per minute (by each ventricle).
Cardiac output = Heart rate x Stroke volume
~5000ml/min ~70/min ~75ml
At rest C.O. = 5 l/min
In exercise > 25 l/min as heart rate increases 2-3 fold and stroke volume increases 2 fold.
What is the effect of an increasing heart rate on cardiac output in a exercise and resting state?
Changes in cardiac output with increasing HR – increases in the exercised state
This is not the case when resting – this is due to low amounts of venous return when in the rested state.
Hence, this shows the importance of adequate venous return to maintain the ventricles filled
What is stroke volume dependent on?
Stroke volume is directly proportionate to diastolic filling
Increased diastolic filing increases diastolic end volume and contractility (increased stretch)
What is the frank-starling mechanism?
Relates stroke volume or cardiac output with end diastolic volume
More blood delivered to the heart - increased stretch - increase contractility – more is pumped
Left and right side balance – one side pumps more the other stretches/pumps more
What is peripheral resistance? WHat happens when peripheral resistance is too high?
Peripheral Resistance (Afterload) = Resistance to blood flow away from the heart
Altered by dilation or constriction of blood vessels (mainly pre-ecapillary resistance arteries - arterioles).
Cardiac Output = Blood pressure/Peripheral Resistance
Increase resistance - reduces cardiac output
Extensive increases in peripheral resistance results in heart failure
Why do increases (within a range) of peripheral resistance no decrease cardiac output?
Basically - increased peripheral resistance - decrease CO - leads to higher end diastolic volume (increased residual ventricular volume) - leads to greater starling forces in following contraction - in turn increasing CO
What is the difference between pulmonary and systemic blood pressure?
Systemic - 120/80
Pulmonary - 20/10
Describe the excitation pathway in the heart (step-by-step).
Overview - SA node - AV node - left and right bundle branches - Purkinje fibres
Sinus rhythm = heart rate controlled by
S.A. node, rest rate approx. 72 beats/min (wide variation).
Step by step:
1. SA node intiates action potential
2. Action potential activates atria.
3. Atrial A.P. activates A.-V. node
4. A.V. node introduces pause - small cells, slow conduction velocity - introduces delay of 0.1 sec - allows ventricular filling
5. A.V. node sends an electrical signal down the bundle of his down into the left and right bundle branches (left - has an anterior and posterior fascicle)
6. Signal continues through Purkinje fibres
What is the connective tissue dividing the atria/ventricles called? What function does it perform?
Cardiac/Fibrous skeleton
Connective tissue between the atria and ventricles that block spread of electrical signals between atria and ventricles – allows nodes to control electrical signals
How can electrical signals propagate through the heart without the need of neurons?
Cardiac muscle is ‘myogenic’ – it generates its own action potentials.
Action potentials develop spontaneously at the sino-atrial node.
A.P. conducted from cell to cell via intercalated discs which have gap (or nexus) junctions (channels that allow propagation of electrical signals)
Outline the ion balance responsible for driving SA node depolarisation and hyperpolarisation. What effect does noradrenaline and acetyl choline?
Pacemaker potential due to:↑gCa,↑gNa,↓gK
Action potential upstroke due to: ↑gCa
Repolarisation due to: ↑gK, ↓gCa
Hyperpolarisation drives depolarisation of pacemaker cells (increase in Na and Ca) –> depolarisation drives activation of gK channels in turn driving hyperpolarisation
Effects of…
Noradrenaline - ↑gNa ↑gCa - increases heart rate
Acetyl choline - ↑ gK, ↓ gCa - decreases heart rate
What are six differences between cardiac and skeletal muscle action potentials/electrical activity?
- Neuroggenic vs. myogenic - Skeletal muscles is neurogenic (needs NS input) vs. cardiac muscle is cardiogenic (generates action potentials spontaneously)
- Action potential length - Cardiac muscles have a long action potential when compared to skeletal muscle (10 fold difference in length)
-
Duration - Action potential controls duration of cardiac muscle contraction/force of contraction whereas in skeletal muscle it only acts as a trigger
4.Simple vs. Complex - Ion currents during action potential - skeletal = simple vs. cardiac = complex - refers to the fact that gNa drives depolarisation and gCa drives contraction in cardiac muscle cells, whereas, skeletal muscle solely relies on gNa. - Source of Ca - Ca is released from the sarcoplasmic reticulum but for heart cells, Ca entry from outside is also needed (‘Ca induced Ca release’) - cardiac muscle relies more on extracellular
-
Relaxation (Ca reduction)
a) Uptake of Ca by sacroplasmic reticulum. - via an ATP driven Ca pump (same as skeletal)
b) Exit of Ca from cell (cardiac exclusive)
- An ATP driven Ca pump (weak).
- Na-Ca exchange protein (energy from Na entry gradient).
Summary of the currents responsible for cardiac action potentials?
How does the excitation and contraction coupling differ between skeletal and cardiac muscle?
Skeletal
1. Action potential drives Ca+ release from SR
- Covalent association between dihydropyridine receptor (membrane) and ryanodine receptor subtype 1 (RyR1) (sarcoplasmic reticulum)
2. Ca2+ binds to troponin - 4 Ca++ troponin
3. Drives cross-bridge cycling
Cardiac
1. Calcium-induced calcium release involving the voltage-gated
calcium channels and ryanodine receptor subtype 2 (RyR2)
How are ECGs recorded? What is positive and negative deflection?
Electrical impulse (wave of depolarisation) picked up by placing electrodes on patient - The voltage change is sensed by measuring the current change
Positive deflection - If the electrical impulse travels towards the electrode this results in a positive deflection (upward signal)
Negative deflection - If the impulse travels away from the electrode this results in a negative deflection (downward signal)
How many electrodes are normally placed on an ECG?
6 chest electrodes - Called V1-6 or C1-C6
4 limb electrodes - Right arm & leg + Left arm and leg
Note - right leg electrode is neutral (dummy electrode)
Why do leads located on the left ventricle (e.g. V5 and V6) produce a stronger signal?
Left side of the heart is bigger - more depolarisation = greater signal
What are the two types of limb leads?
Coronal plane/Limb Leads
- Bipolar leads - I, II, III
- Unipolar - aVL, aVR, aVF
What are the different signals examine by the bipolar and unipolar limb leads?
Bipolar Limb Leads
Lead 1 - left arm to right arm
Lead 2 - left arm to right leg
Lead 3 - right arm to left leg
Unipolar Limb Leads
aVL - signals to the left shoulder
aVF – signals to the feet
aVR – signals to the right shoulder
What is the QRS axis? What is a normal axis? What are the two types of deviation?
The QRS axis represents the net overall direction of the heart’s electrical activity.
Abnormalities of axis can hint at:
1. Ventricular/structural abnormality
2. Conduction abnormality (i.e. hemiblocks)
Normal QRS axis is defined as ranging from -30°to +90°
-30° to -90° is referred to as a left axis deviation (LAD)
+90° to +180° is referred to as a right axis deviation (RAD)
At what angle do all the limb lead signals travel?
How can limb leads 1, 2 and 3 be used to calculate the hearts QRS axis?
Look at the leads 1, 2 and 3 on the ECG and examine their deflection - used to determine QRS axis
For the following 3 ECGs, is there an axis deviation?
Before looking at an ECG, what must you do?
Look for reference pulse which should be the rectangular wave on the left of the paper.
Normal calibration should be 10mm tall (10 small boxes) = 1mV
What is the normal paper speed of an ECG?
Paper speed = 25mm per second
Therefore one large box (5mm) corresponds to
0.2 seconds
What are the three main waves of the ECG? What do they represent?
What are the normal times for the PR, QRS and QT intervals?
PR = 0.12-0.20sec
QRS = <0.12s
QTc = <0.440s (m), 0.460s (f) - Q wave to end of T wave
What do the following two ECGs show (think PR)?
Top - Prolonged PR interval – first degree heart block
Bottom - Wolff-Parkinson-White syndrome - PR interval is shortened (less than 3 boxes) and slurred up-stroke in R wave – indicates that there is an alternative pathway by which the electrical impulse is by-passing the AV node
Important to identify - as rapid conduction, if patient as atrial fibrillation, potentially leading to ventricular fibrillation or cardiac arrest
How can the QRS complex indicate ventricular hypertophy?
Ventricular hypertrophy - largely caused by hypertension
Abnormally tall R wave in leads closest to the left ventricle (V5 and V6) and in S-wave in V1
Criteria hypertrophy - R wave in V5 or V6 plus S-wave in V1 is greater 35mm
What happens to the QRS complex during right bundle branch block (RBBB)?
RBBB in V1
- No change in initial impulse travel
small r wave - signals travels first to LBB
- Impulse depolarizes LV creating an s wave
- But RV depolarizes late creating an r’ wave
- Hence RSR’ pattern (‘M’ shape) created
‘MaRRoW’ pattern
- Result in an increased duration of the QRS complex - exceed 0.12 seconds (three small boxes)
What happens to the QRS complex during light bundle branch block (LBBB)?
LBBB in V1
- Initial deflection altered since travels right to left now
- Q wave/ negative deflection - RV depolarizes unopposed
- May produce small r wave
- Travels across septum to depolarize LV - deep S wave
- W pattern in V1 - ‘WiLLiaM’ pattern
- V1 and V6 will be recipricol - sit in opposite directions
Note - ST segments are not interpretable in left bundle branch block
Which of the following shows a RBBB and LBBB?
Left - QRS duration is prolonged (more than 3 small boxes) and RSR’ shape = right bundle branch block
Right - V1 W shape plus V1 and V6 are reciprocal
What does ST elevation or depression indicate?
ST segement:
Begins at the END of the QRS complex
And ends with the BEGINNING of the T wave.
Normally an ISOELECTRIC line
ST segment elevation or depression could indicate myocardial ischaemia or infarction
How can the location of an infarction be identified based on ST elevation/depression?
Leads effected can indicate where the infarction is taking place:
I and AVL – Lateral
II, III, aVF – inferior
V1 and V2 – septal
V3 and V4 – anterior
V5 and V6.- lateral
Lateral = Left Circumflex – lateral aspect
Inferior aspect - Right Coronary artery
Anterior - Left anterior descending
What does the following ECG with an ST elevation indicate?
Leads V2, V3 and V4 - Anterior ST elevation - Left anterior descending occlusion -
What does the following ECG with an ST elevation indicate?
ST elevation – leads 2, 3 and AVF – inferior leads - Occlusion of the right coronary artery
What happens when there is widespread ST elevation/depression across many leads of an ECG?
Indicates widespread Ischaemia
Likely Left main stem obstruction
When using an ECG, how can you calculate the heart rate when the cardiac rhythm is regular?
If the cardiac rhythm is REGULAR
- Count the number of large squares between R waves (RR interval)
- Rate = 300 divided by number of large squares between R waves
When using an ECG, how can you calculate the heart rate when the cardiac rhythm is irregular?
If the cardiac rhythm is IRREGULAR
Use rhythm strip at the bottom of 12-lead ECG
Rhythm strip is a 10 second recording of the heart
Rate = number of QRS complexes multiplied by 6
What is 1st degree heart block? How can it be recognised?
1st degree AV Block:
1. Regular Rhythm
2. PR interval > .20 seconds (5 small boxes/1 large box) and is CONSTANT
3. Causes: IHD, conduction system disease, seen in healthy children or athletes
4. Usually does not require treatment
What is 2nd degree (Mobitz I) heart block? How can it be recognised?
2nd degree AV Block (“Mobitz I” also called “Wenckebach”):
- Irregular Rhythm
- PR interval continues to lengthen until a QRS is missing (non-conducted sinus beat)
- PR interval is NOT CONSTANT
- Rhythm is usually benign unless associated with underlying pathology, (i.e. MI)
What is 2nd degree (Mobitz II) heart block? How can it be recognised?
2nd degree AV Block (“Mobitz II”):
Features
1. Irregular Rhythm
2. QRS complexes may be wide (greater than .12 seconds)
3. Non-conducted sinus impulses appear at irregular intervals
4. PR interval is constant
Implications
- Rhythm is somewhat dangerous as the block is lower in the conduction system (BB level)
- May cause syncope or may deteriorate into complete heart block (3rd degree block)
- It’s appearance in the setting of an acute MI identifies a high risk patient
- Cause: IHD, fibrosis of the conduction system
- Treatment: pacemaker
What is 3rd degree AV block/complete heart block? How can it be recognised?
3rd degree AV Block (“Complete Heart Block”):
Features
- Atria and ventricles beat independent of one another (AV dissociation)
- QRS’s have their own rhythm, P-waves have their own rhythm
Implications
- May be caused by inferior MI and it’s presence worsens the prognosis
- May cause syncopal symptoms or angina, especially if ventricular rate is low
- Treatment: usually requires pacemaker +/- temporary pacing/ isoprenaline
What type of heart block does this ECG show?
ECG shows 1st degree heart block - constant increase in PR interval
What type of heart block does this ECG show?
2nd degree - Mobitz type 1 - PR interval becomes consistently longer until QRS disappears
What type of heart block does this ECG show?
P waves are not associated with QRS complexes – example of complete heart block
What are the two broad types of tachyarrhythmias?
Narrow complex tachycardia (QRS duration - less than 0.12s)
- Uncontrolled (ie “fast”) Atrial Fibrillation or Flutter
- Atrial tachycardia
- AVNRT/ AVRT
- Basically originating from the atria
Broad complex tachycardia (QRS duration more than 0.12 s)
- Ventricular tachycardia
- Ventricular fibrillation
- Basically orginating from the ventricles
What does atrial fibrillation and atrial flutter look like on an ECG?
Atrial fibrillation – most common narrow complex tachycardia – narrow + no obvious P waves
Atrial flutter – irregular – narrow QRS and characteristic saw tooth pattern
What does a supra-ventricular tachycardia (SVT) look like?
Supraventricular tachycardia – narrow complex tachycardia
Could either be due to….
1. AVNRT - Atrioventricular nodal reentrant tachycardia (AVNRT)
2. AVRT - Atrioventricular reentrant tachycardia
What does ventricular tachycardia look like?
Broad complex tachycardia - QRS complexes are broad, regular and fast - life threatening
What does ventricular fibrillation look like?
Ventricular fibrillation – broad complex – electrical activity is completely disorganized – associated with cardiac arrest
