Cardiac Cycle

Question 1

What are the four major stages in the cardiac cycle?

Answer 1

1. Atrial systole – Drives blood into the ventricles
2. Early ventricular systole – closes the AV valve
3. Late ventricular systole – pressure rises driving open the semilunar aortic valve – driving blood out through the aorta
4. Ventricular diastole – relaxation

Question 2

What is the repetitive sequence of events in each heart beat?

Answer 2

1. Flow into atria, continuous except when they contract. Inflow leads to pressure rise.
2. 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

3. Atrial systole - completes filling of ventricles.
4. Ventricular systole (atrial diastole). Pressure rise closes A-V valves, opens aortic and pulmonary valves.
5. Ventricular diastole – causes closure of aortic and pulmonary valves.

Question 3

What are the four sounds generated by the heart? What are the associated with?

Answer 3

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

Question 4

What does the following graph show (ventricular volume changes)?

Answer 4

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?

Question 5

Why is the elasticity in the aorta important?

Answer 5

Elastic recoil/pulsatile contraction - Helps maintain pressure in arterial system during diastole - (pressure drops only about one third from systolic B.P.)

Question 6

What are the definitions of stroke volume and ejection fraciton?

Answer 6

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.

Question 7

How does systemic arterial pressure remain high during the cardiac cycle?

Answer 7

Systemic arterial pressure remains high throughout cycle due to elasticity of the vessel walls and peripheral resistance.

Question 8

How do we define cardiac output?

Answer 8

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.

Question 9

What is the effect of an increasing heart rate on cardiac output in a exercise and resting state?

Answer 9

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

Question 10

What is stroke volume dependent on?

Answer 10

Stroke volume is directly proportionate to diastolic filling

Increased diastolic filing increases diastolic end volume and contractility (increased stretch)

Question 11

What is the frank-starling mechanism?

Answer 11

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

Question 12

What is peripheral resistance? WHat happens when peripheral resistance is too high?

Answer 12

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

Question 13

Why do increases (within a range) of peripheral resistance no decrease cardiac output?

Answer 13

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

Question 14

What is the difference between pulmonary and systemic blood pressure?

Answer 14

Systemic - 120/80

Pulmonary - 20/10

Question 15

Describe the excitation pathway in the heart (step-by-step).

Answer 15

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

Question 16

What is the connective tissue dividing the atria/ventricles called? What function does it perform?

Answer 16

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

Question 17

How can electrical signals propagate through the heart without the need of neurons?

Answer 17

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)

Question 18

Outline the ion balance responsible for driving SA node depolarisation and hyperpolarisation. What effect does noradrenaline and acetyl choline?

Answer 18

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

Question 19

What are six differences between cardiac and skeletal muscle action potentials/electrical activity?

Answer 19

1. Neuroggenic vs. myogenic - Skeletal muscles is neurogenic (needs NS input) vs. cardiac muscle is cardiogenic (generates action potentials spontaneously)
2. Action potential length - Cardiac muscles have a long action potential when compared to skeletal muscle (10 fold difference in length)
3. 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.
4. 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
5. 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).

Question 20

Summary of the currents responsible for cardiac action potentials?

Answer 20

Question 21

How does the excitation and contraction coupling differ between skeletal and cardiac muscle?

Answer 21

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)

Question 22

How are ECGs recorded? What is positive and negative deflection?

Answer 22

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)

Question 23

How many electrodes are normally placed on an ECG?

Answer 23

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)

Question 24

Why do leads located on the left ventricle (e.g. V5 and V6) produce a stronger signal?

Answer 24

Left side of the heart is bigger - more depolarisation = greater signal

Question 25

What are the two types of limb leads?

Answer 25

Coronal plane/Limb Leads 1. Bipolar leads - I, II, III 2. Unipolar - aVL, aVR, aVF

Question 26

What are the different signals examine by the bipolar and unipolar limb leads?

Answer 26

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

Question 27

What is the QRS axis? What is a normal axis? What are the two types of deviation?

Answer 27

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)

Question 28

At what angle do all the limb lead signals travel?

Answer 28

Question 29

How can limb leads 1, 2 and 3 be used to calculate the hearts QRS axis?

Answer 29

Look at the leads 1, 2 and 3 on the ECG and examine their deflection - used to determine QRS axis

Question 30

For the following 3 ECGs, is there an axis deviation?

Answer 30

Question 31

Before looking at an ECG, what must you do?

Answer 31

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

Question 32

What is the normal paper speed of an ECG?

Answer 32

Paper speed = 25mm per second Therefore one large box (5mm) corresponds to 0.2 seconds

Question 33

What are the three main waves of the ECG? What do they represent?

Answer 33

Question 34

What are the normal times for the PR, QRS and QT intervals?

Answer 34

PR = 0.12-0.20sec QRS = <0.12s QTc = <0.440s (m), 0.460s (f) - Q wave to end of T wave

Question 35

What does the PR interval tell you? What do abnormalities tell you?

Answer 35

PR interval – time to conduct through atrio-ventricular node/bundle of His Mainly dictated by AVN delay a) Too short - bypass b) Too long - blockage How to calculate - Count the number of boxes between beginning of P wave to the beginning of the Q wave

Question 36

What does the QRS interval tell you? What do abnormalities tell you?

Answer 36

QRS duration – time for ventricular depolarisation Inform you on.. Patterns of conduction disease though Bundles - RBBB - right branch bundle block - LBBB - left branch bundle block

Question 37

What does the ST interval tell you? What do abnormalities tell you?

Answer 37

ST segment – start of ventricular repolarisation (should be isoelectric) Hence.... If there is ST elevation --> possible acute infarction or pericarditis, repolarisation abnormalities If there is ST depression --> Ischaemia, LV strain (LVH)

Question 38

What do the following two ECGs show (think PR)?

Answer 38

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

Question 39

How can the QRS complex indicate ventricular hypertophy?

Answer 39

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

Question 40

Outline the normal conduction path in the ventricles.

Answer 40

Normal Conduction 1. Fibers of LBB begin conduction 2. Impulse travels across interventricular septum from left to right, causing... a) small r wave in V1 b) small q wave in V6 3. Signal then travels across ventricles causing depolarization of both RV + LV Note - LV contributes most to complex - Deep s wave V1 - Tall r wave V6

Question 41

What happens to the QRS complex during right bundle branch block (RBBB)?

Answer 41

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)

Question 42

What happens to the QRS complex during light bundle branch block (LBBB)?

Answer 42

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

Question 43

Which of the following shows a RBBB and LBBB?

Answer 43

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

Question 44

What does ST elevation or depression indicate?

Answer 44

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**

Question 45

How can the location of an infarction be identified based on ST elevation/depression?

Answer 45

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

Question 46

What does the following ECG with an ST elevation indicate?

Answer 46

Leads V2, V3 and V4 - Anterior ST elevation - Left anterior descending occlusion -

Question 47

What does the following ECG with an ST elevation indicate?

Answer 47

ST elevation – leads 2, 3 and AVF – inferior leads - Occlusion of the right coronary artery

Question 48

What happens when there is widespread ST elevation/depression across many leads of an ECG?

Answer 48

Indicates widespread Ischaemia Likely Left main stem obstruction

Question 49

When using an ECG, how can you calculate the heart rate when the cardiac rhythm is regular?

Answer 49

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

Question 50

When using an ECG, how can you calculate the heart rate when the cardiac rhythm is irregular?

Answer 50

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

Question 51

What is bradyarrhythmia and tachyarrhythmia?

Answer 51

**Bradyarrhythmia** Any abnormality of cardiac rhythm resulting in a slow heart rate (heart block, slow AF) (c.f. sinus brady) HR < 60bpm **Tachyarrhythmia** Any abnormality of cardiac rhythm resulting in a fast heart rate (SVT, uncontrolled AF/ Flutter, VT) (c.f. sinus tachy) HR > 100bpm

Question 52

What are the causes of bradyarrhythmias?

Answer 52

Heart Block 1st degree 2nd degree 3rd degree HB

Question 53

What is 1st degree heart block? How can it be recognised?

Answer 53

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

Question 54

What is 2nd degree (Mobitz I) heart block? How can it be recognised?

Answer 54

2nd degree AV Block (“Mobitz I” also called “Wenckebach”): 1. Irregular Rhythm 2. PR interval continues to lengthen until a QRS is missing (non-conducted sinus beat) 3. PR interval is NOT CONSTANT 4. Rhythm is usually benign unless associated with underlying pathology, (i.e. MI)

Question 55

What is 2nd degree (Mobitz II) heart block? How can it be recognised?

Answer 55

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

Question 56

What is 3rd degree AV block/complete heart block? How can it be recognised?

Answer 56

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

Question 57

What type of heart block does this ECG show?

Answer 57

ECG shows 1st degree heart block - constant increase in PR interval

Question 58

What type of heart block does this ECG show?

Answer 58

2nd degree - Mobitz type 1 - PR interval becomes consistently longer until QRS disappears

Question 59

What type of heart block does this ECG show?

Answer 59

P waves are not associated with QRS complexes – example of complete heart block

Question 60

What are the two broad types of tachyarrhythmias?

Answer 60

**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

Question 61

What does atrial fibrillation and atrial flutter look like on an ECG?

Answer 61

**Atrial fibrillation** – most common narrow complex tachycardia – narrow + no obvious P waves **Atrial flutter** – irregular – narrow QRS and characteristic saw tooth pattern

Question 62

What does a supra-ventricular tachycardia (SVT) look like?

Answer 62

Supraventricular tachycardia – narrow complex tachycardia Could either be due to.... 1. AVNRT - Atrioventricular nodal reentrant tachycardia (AVNRT) 2. AVRT - Atrioventricular reentrant tachycardia

Question 63

What does ventricular tachycardia look like?

Answer 63

Broad complex tachycardia - QRS complexes are broad, regular and fast - life threatening

Question 64

What does ventricular fibrillation look like?

Answer 64

Ventricular fibrillation – broad complex – electrical activity is completely disorganized – associated with cardiac arrest

Question 65

How to approach an ECG?

Answer 65

Be systematic! 1. Rate 2. Rhythm 3. Axis 4. Go through the heart cycle a) P wave b) PR interval c) QRS duration and morphology d) T wave and (QT interval)