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Flashcards in Cardiovascular Deck (11):
1

Draw or describe the Frank-Starling law as it applies to the human cardiac muscle. What factors influence the Frank-Starling curve?

1. Frank-Starling law describes the relationship between stroke volume and EDV
- Increasing EDV -> Increases contractility -> Increases SV until a maximum point is reached

2. Curve shifted
- Up/L: Circulating catecholamines, sympathetic nervous system, inotropic drugs (digoxin, glucagon)
- Down/R: Low catecholamines, parasympathetic nervous system, drugs (procainamide), hypoxia, hypercarbia, acidosis, loss of myocardium (IHD, heart failure)

2

Draw and describe an ECG tracing of a single normal heart beat. What features would appear different in a STEMI? Explain the electrophysiological changes that cause the ST segment elevation seen in myocardial infarct. What electrophysiological changes are seen in the late phase of myocardial infarct

1. ECG features
- P wave = Atrial depolarization
- PR interval = AV node conduction
- QRS = Ventricular depolarization
- ST interval = Plateau of ventricular depolarization
- T = Ventricular repolarization
- QT interval = Ventricular action potential

2. ECG changes in STEMI
- ST segment elevation in affected leads
- ST segment depression in reciprocal leads

3. Electrophysiological changes in STEMI
- Immediately post-STEMI within seconds to minutes: Abnormal rapid repolarization -> K+ leak out of cell -> Tissue more +ve -> Current flows out of tissue
- Minutes post-STEMI: Reduced resting membrane potential -> Reduced intracellular K+ -> Tissue more -ve -> Current flows into tissue
- > 30 minutes post-STEMI: Slow depolarization of surrounding normal tissue -> Tissue more +ve -> Current flows out of tissue

4. Late phase of STEMI
- Seen days to weeks post-STEMI
- Tissue infarct established -> Dead tissue electrically silent -> Infarcted area more -ve than other area as does not conduct current -> Q wave on ECG

3

What are the ECG changes in hyperkalemia? How does it change in hypokalemia?

1. ECG changes in hyperkalemia
- Mild: No changes
- Moderate: Tall peaked T waves
- Severe: PR lengthening, P flattening, QRS lengthening, sinusoidal ECG
- Ventricular arrhythmias: VT, VF
- Asystole

2. ECG changes in hypokalemia
- Mild: T flattening
- Moderate: T inversion, ST depression, U wave, PR lengthening

4

Describe the normal cardiac conduction pathway. Draw and describe the action potential of a normal cardiac pacemaker cell.

1. Cardiac conduction pathway
- SA node
- Atria
- AV node -> Short pause
- Bundle of His
- L + R bundle branches
- Anterior + posterior fascicles on the L
- Up the Purkinje fibres
- Ventricles

2. Cardiac pacemaker cell action potential
- Prepotential phase = -60 to -40 = Reduce K efflux and increase Ca influx through T-type Ca channels
- Depolarization phase = -40 to +20 = Opening of L-type Ca channels causing Ca influx
- Repolarization phase = +20 to -60 = Closing of Ca channels, opening of K+ channels causing K efflux

5

Draw and label the normal membrane potential of a normal pacemaker cell. By what mechanisms can tachyarrhythmias be generated? What conditions may predispose to tachyarrhythmias?

1. Pacemaker cell action potential
- Pre-potential phase: Ranging from -60 to -40 mV, due to decreased K+ efflux and opening of T-type Ca channels
- Depolarization phase: Up to +20mV, due to opening of L-type Ca channels
- Repolarization phase: Due to opening of K+ channels

2. Mechanisms leading to tachyarrhythmias
- Increased automaticity (AT, VT)
- Accessory pathway (WPW)
- Re-entry loops (VT)
- Early after-depolarization (Torsades)
- Late after-depolarization (Digoxin toxicity)

3. Predisposing conditions leading to tachyarrhythmias
- IHD
- Cardiac surgery with scar
- Cardiomyopathies -> HOCM
- Cardiac failure -> AF
- Channelopathies -> WPW
- Electrolytes disturbances -> K, Mg, Ca
- Sympathomimetic agents

6

What are the common mechanisms that cause abnormalities of cardiac conduction? Describe the major differences between a ventricular muscle action potential and pacemaker cell potential. How do sympathetic and parasympathetic stimulation change the prepotential?

1. Mechanisms causing abnormalities of cardiac conduction
+ Increased automaticity/pacemaker potential -> AF, AT, VF, VT, ectopic
+ Accessory pathway -> WPW
+ Re-entry loops -> Tachyarrhythmias -> SVT, VT
+ Early after-depolarization -> Torsades
+ Late after-depolarization -> Digoxin toxicity
+ Conduction deficits/delays -> Heart block, bundle branch block
+ Reduced automaticity -> Sick sinus syndrome
+ Prolonged repolarization -> Long QTc syndrome

2. Ventricular AP vs pacemaker potential
- Ventricular:
+ More -ve RMP of -90
+ Fast Na channels causing depolarization
+ Plateau phase
+ No pre-potential phase and automaticity
- Pacemaker cells:
+ More +ve RMP of -60 to -40
+ Slow Ca channels causing depolarization
+ No plateau phase

3. Sympathetic and parasympathetic stimulation on prepotential
- Sympathetic stimulation -> Noradrenaline stimulating B1-receptors -> Increases cAMP -> Increases slope of prepotential and firing rate
- Parasympathetic stimulation -> Acetylcholine binding to M2-receptors -> Decreases cAMP -> Reduces slope of prepotential and firing rate
+ Pre-potential phase and automaticity

7

Please describe or draw a ventricular muscle action potential. How does the ECG relate to the ventricular muscle action potential? Why does tetani not occur in cardiac muscle?

1. Ventricular muscle action potential
- Phase 4 = RMP -> - 90mV
- Phase 0 = Depolarization -> Up to +20mV -> Due to opening of fast Na channels -> Na influx
- Phase 1 = Early rapid repolarization -> Due to closing of Na channels and opening of K+ channels -> K+ efflux
- Phase 2 = Plateau -> Due to opening of L-type Ca channels -> Ca influx to balance K efflux
- Phase 3 = Late repolarization -> Due to closing of Ca channels and continued opening of K channels -> Returns cell back to RMP

2. ECG and ventricular muscle action potential
- Phase 0 = Depolarization = QRS complex on ECG
- Phase 2 = Plateau = QT interval on ECG
- Phase 1, 2, 3 = Repolarization = T wave on ECG

3. Tetani does not occur in cardiac muscle due to
- Long duration of AP
- Cardiac muscle still contracting in relative refractory period

8

Describe how the waveforms of an ECG relate to the cardiac cycle. Describe the changes in the L ventricular volume through the cardiac cycle starting from atrial systole.

1. ECG waveforms and cardiac cycle
- Atrial systole = End of P wave to R wave
- Ventricular systole = End of R to T wave

2. Changes in L ventricular volume through the cardiac cycle
A. Atrial systole
- Phase 1 = Atrial contracts -> Small increase in volume of ventricle due to atrial contraction
B. Ventricular systole
- Phase 2 = Isovolumetric contraction -> Mitral valve closes -> Ventricle contracts -> Increase in pressure but NO CHANGE in volume in ventricle (150mls)
- Phase 3 = Ventricular ejection -> Aortic valve opens -> Blood pumped out of ventricle -> Reduce in ventricular volume to 65mls at the end
C. Ventricular diastole
- Phase 4 = Isovolumetric relaxation -> Aortic valve closes -> Ventricle relaxes -> Reduction in pressure but NO CHANGE in volume in ventricle
- Phase 5 = Ventricular filling -> Mitral valve opens -> Passive filling of ventricle -> Increase volume in ventricle

9

Please draw and label the pressure-volume curve of the L ventricle. Describe how the pressure and volume changes in the L ventricle at the onset of systole. Describe how the pressure and volume changes in the L ventricle at the onset of diastole.

1. Pressure-volume curve of L ventricle
- Pressure = Y axis (100, 200)
- Volume = X axis (50, 150)

2. Changes in curve at onset of systole
- Isovolumetric contraction (A - B) = Increase in pressure but no change in volume
- Aortic valve opens (B)
- Ventricular ejection (B - C) = Blood flows out of ventricle, reduce in volume but minimal change in pressure

3. Changes in curve at onset of diastole
- Isovolumetric relaxation (C - D) = Decrease in pressure but no change in volume
- Mitral valve opens (D)
- Ventricular filling (D - A) = Blood flows into ventricle, increase in volume but mild change in pressure

10

What are the determinants of myocardial oxygen consumption? What are the changes in cardiac function with exercise and how are these mediated? What are the physical laws involved? What are the factors that influence contractility? How does decreasing HR improve symptoms of angina? What effect does increase in preload and afterload have on myocardial oxygen demand?

1. Myocardial oxygen consumption determined by
- Wall surface tension
- Heart rate
- Myocardial contractility

2. Exercise
- Increases HR and SV
- Due to sympathetic nervous system stimulation, release of adrenaline
- Increase venous return due to pumping of skeletal muscle

3. Physical laws involved
- Frank Starling law
- La Place law

4. Factors influencing contractility
- Intrinsic function of myocytes -> IHD, cardiomyopathy
- Sympathetic/parasympathetic nervous system stimulation
- Drugs -> +ve (adrenaline, NA, digoxin) or -ve inotrope (antiarrhythmic, CCB, B-blocker)
- Hypoxia -> Reduces contractility
- Hypercarbia -> Reduces contractility
- Acidosis -> Reduces contractility
- Circulating catecholamines

5. Decreasing HR improves angina by
- Reducing myocardial O2 demand
- Allowing more time for coronary perfusion which occurs during diastole

6. Increase in preload and afterload causes increase in myocardial O2 demand
- Ventricular work = SV x MAP
- Increase preload -> Increases SV -> Increases ventricular work and O2 demand
- Increase afterload -> Increase MAP -> Increase ventricular work and O2 demand
- Pressure work/changes in afterload causes more significant increase in O2 demand than volume work/changes in preload

11

What two factors determine cardiac output? What methods can be used to measure cardiac output? What is cardiac preload? What factors affect preload? What is normal SV?

1. Cardiac output (CO) = Stroke volume (SV) x Heart rate (HR)
- SV is determined by preload, afterload and myocardial contractility
- HR is determined by sympathetic and parasympathetic nervous system stimulation

2. Cardiac output measured by
- Fick’s method
- Cardiac Doppler ultrasound

3. Cardiac preload
- Equivalent to end-diastolic volume (EDV)
- Degree of stretch of the heart muscles compared to resting length

4. Factors affecting preload
- Blood volume: Hypovolaemia, dehydration, shock
- Atrial filling: Reduced venous return, impaired venous pump, parasympathetic stimulation causing vasodilation
- Ventricular filling: Diastolic heart failure
- Pericardial: Constrictive pericarditis, tamponade
- Intrapleural: Pneumothorax

5. Normal SV = 70 - 90 mls