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YR2 BCS Study Points SEM 1 > Block 2 - Cardiovascular > Flashcards

Block 2 - Cardiovascular Flashcards

1
Q

What is the Cardiac Cycle?

  • Electrical activity?
  • Mechanical activity?
  • Pressure differences?
  • Volume changes?
A

Cardiac Cycle: Events associated with blood flow through the heart during a single complete heartbeat

  • Electrical Activity: Summed activity of many cardiac cells, depolarisation and repolarisation detected by ECG
  • Mechanical Activity: Contraction (systole) and relaxation (diastole) of myocardium
  • Pressure Differences: Due to contraction and/or venous return
  • Volume Changes: Due to blood flow down pressure gradient and unidirectional heart valves which prevent back flow
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1
Q

What are the 6 Phases the Cardiac Cycle?

A

Phases of the Cardiac Cycle:

  1. Ventricular filling (late diastole)
  2. Atrial contraction (atrial systole)
  3. Isovolumetric ventricular contraction (ventricular systole)
  4. Ventricular ejection (ventricular systole)
  5. Isovolumetric ventricular relaxation (early ventricular diastole)
  6. Ventricular filling (late diastole)
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2
Q

What are the mechanics of Cardiac muscle contraction?

A

Mechanics of Cardiac Muscle Contraction:

  1. Excitation: Trigger for contraction is myocardial cell AP firing which is caused by spread of depolarisation from pacemaker cell AP firing (myogenic control)
  2. Excitation-Contraction Coupling: Triggering of contraction by gap junctions, AP firing, extracellular Ca2+ entry and Ca2+ binding to troponin.
    1. Current spreads to myocardial cell via gap junctions → AP travels along plasma membrane and down T-tubules → Voltage-gated Ca2+ channels open → Ca2+ entry → Ca2+-induced Ca2+ release from SR via ryanodine receptors → Ca2+ binds to troponin → Exposes myosin-binding sites on actin → Crossbridge cycling (contraction)
  3. Contraction: Crossbridge cycling (faster than smooth but slower than skeletal muscle)
  4. Relaxation: Removal of Ca2+ from cytosol Ca2+ dissociates from troponin → Ca2+ pumped into SR (active transport) AND Ca2+ transported out of cell by Ca2+/Na+ exchanger (antiport) driven by Na+ concentration gradient maintained by Na+/K+ ATPase pump

Repolarisation of cardiac muscle is an active process!!

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3
Q

Review the mechanisms responsible for the generation and distribution of action potentials in cardiac muscle.

  • 5 steps in the Generation/Distribution of APs in Cardiac Muscle?
A

Generation/Distribution of APs in Cardiac Muscle: Pacemaker Cells → Conduction Fibres → Myocardial Cells

  1. SA node (sets the rhythm) fires an AP and depolarisation spreads to adjacent cells through gap junctions
  2. As APs spread across the atria (atrial depolarisation), they encounter the fibrous skeleton of the heart at the AV junction. This barricade prevents the transfer of electrical signals from the atria to the ventricles. The AV node is the only pathway (internodal pathways) through which APs can reach the contractile fibers of the ventricles.
  3. The electrical signal passes through the AV node (holds the rhythm). The AV node delays the transmission of APs slightly by slowing conduction through the nodal cells, allowing the atria to complete their contraction before ventricular contraction begins.
  4. APs spread through the bundle of His (AV bundle) and bundle branches to the apex of the heart
  5. The Purkinje fibers transmit impulses very rapidly, so that all contractile cells in the apex contract nearly simultaneously, allowing depolarisation of the ventricles
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4
Q

Predict the effect of altered electrolyte or permeability changes on the cardiac muscle action potential.

  • What is the distribution of sodium, calcium and potassium in the cellular spaces?
A

Electrolytes:

  • Sodium: Predominantly extracellular (disturbances affect the QRS complex)
  • Calcium: Predominantly extracellular (disturbances affect the QT interval)
  • Potassium: Predominantly intracellular (disturbances affect T waves)
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5
Q

What is the Effect on Myocardial Cells of different electrolyte imbalances?

A
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6
Q

How does an ECG look in hypokalemia and hyperkalemia?

A
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7
Q

Review the function of the cardiac conducting system and atrioventricular ring.

  • What is the Cardiac Conduction System?
  • 6 steps in pathway of cardiac conduction system?
  • Why are electrical signals from the atria not conducted directly into the ventricles?
A

Cardiac Conduction System: Specialised cardiac muscle cells that initiate and send signals to the myocardium for contraction of the atria and ventricles

  1. SA Node: Starts the rhythm
  2. Internodal Pathway: Atrial depolarisation and contraction
  3. AV Node: Holds the rhythm
  4. Bundle of His: Ventricular septum depolarisation and contraction
  5. Bundle Branches: Ventricular septum and apex depolarisation and contraction
  6. Purkinje Fibres: Ventricular depolarisation and contraction

NB: If electrical signals from the atria were conducted directly into the ventricles, the ventricles would start contracting at the top. Then blood would be squeezed downward and would become trapped in the bottom of the ventricles. The apex-to-base contraction squeezes blood toward the arterial openings at the base of the heart.

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8
Q

What are the 2 Functions of Atrioventricular Ring?

A

Function of Atrioventricular Ring:

  1. Allows attachment of muscular fibers of the atria and ventricles, and the attachment of the bicuspid and tricuspid valves
  2. Acts as insulator (dense connective tissue does not conduct electricity), forcing electrical signals from SA node to follow internodal pathway to AV node (prevents the transfer of electrical signals from the atria to the ventricles). The AV node is the only electrical conduit from the atria to the ventricles through the cardiac skeleton.
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9
Q

Review the electrophysiology and interpretation of the ECG.

  • What do each of the waves/segments represent?
A

Electrophysiology of ECG:

  • P Wave: Atrial depolarisation
  • PR Segment: AV nodal delay
  • Q Wave: Interventricular septum depolarisation
  • R Wave: Bulk of ventricular depolarisation
  • S Wave: Left lateral ventricular base depolarisation
  • QRS Wave: Ventricular depolarisation
  • ST Segment: Period of zero potential between ventricular depolarisation and repolarisation
  • T Wave: Ventricular repolarisation
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10
Q

What are the 7 steps in ECG Interpretation?

  • What are the 2 methods for determining HR?
  • How do you know if they are in Sinus rhythm?
  • What is the normal range for PR interval?
  • What is the normal range for QRS duration?
  • What is the normal range for QT interval?
  • Which leads do we look at to assess axis?
  • Normal range for ST segment? Where is it measured to and from?
  • Normal ranges for P, Q, T Waves?
    *
A

ECG Interpretation

  1. Patient Identification (Name, Date and Age)
  2. Calibration: 25mm/sec and 10mm/mV
  3. Rate (Heart Rate):
    1. Method 1: Count number of R waves within a 10 second strip and multiply by 6
    2. Method 2: 300 divide number of large squares between 2 R waves
    3. Bradycardia < 60bpm & Tachycardia > 100bpm
  4. Rhythm and Intervals (PR, QRS Complex and QT):
    1. Sinus Rhythm: P wave before every QRS complex
    2. Is the rhythm regular or irregular? If irregular, is it regularly or irregularly irregular?
    3. PR Interval: < 200ms
    4. QRS Duration: 80-120ms
    5. QT Interval: Dependent on rate
  5. Axis:
    1. Normal: Points down and left like apex (positive deflections in leads I, II and III)
    2. Right: Deviation points to right hip (negative deflection in lead I, positive in II and III)
    3. Left: Deviation points to left arm (positive deflection in lead I and aVL, negative in II and III)
    4. The normal QRS axis should be between -30 and +90 degrees.
    5. If the QRS complex is upright (positive) in both lead I and aVF, then the axis is normal
  6. Segments (ST and PR):
    1. ST Segment: 0.06-0.08 seconds (2 small boxes)
    2. Measured from J Point to start of T wave
    3. Normal: Isoelectric and horizontal
    4. Abnormal: Elevated/depressed and upsloping/ down-sloping
  7. Waves (P, QRS, T, U)
    1. P Wave: 0.08 seconds (2 small boxes)
    2. Q Wave: Less than 0.04 seconds (1 small box)
    3. T Wave: O.16 seconds (4 small boxes)
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11
Q

Relate the ECG leads to the coronary arteries and areas of the heart.

  • Lateral area?
  • Inferior area?
  • Anterior area?
  • Anteroseptal area?
  • Right Atrium and LV Cavity?
A

Relating Leads to Areas of Heart:

Lateral Area (Circumflex Artery) → I, aVL, V5 and V6

Inferior Area (RCA) → II, III and aVF

Anterior Area (LAD) → V1, V2, V3 and V4

Anteroseptal Area (LAD) → V1 and V2

Right Atrium and LV Cavity (RCA/LAD) → V1 and aVR

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12
Q

What are the causes of cardiac arrhythmia? (STRIDES)

A

Arrhythmia: Abnormality of the cardiac rhythm (non-sinus cardiac rhythm)

Causes (STRIDES):

  • Structural heart change such as cardiomyopathy or congenital heart defects
  • Thyroid disease, thrombus, trauma, tamponade or tension pneumothorax
  • Rheumatic heart disease and other valvular diseases
  • Ischaemic heart disease, inflammation of myocardium or endocardium, injury from a heart attack
  • Drugs (pro-rhythmic) and diabetes
  • Electrolyte disturbance
  • Social drugs including nicotine, alcohol, caffeine and cocaine or SNS activity
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13
Q

Describe the underlying pathophysiology of cardiac arrhythmia in terms of abnormal impulse formation and a. automaticity.

  • 4 factors that contribute?
  • 4 examples of arrhythmias caused by abnormal impulse formation due to automaticity?
A

Underlying Pathophysiology of Cardiac Arrhythmias

1. Abnormal Impulse Formation - a. Automaticity:

  • Accelerated generation of an AP by either normal pacemaker tissue (enhanced normal automaticity) or by abnormal tissue within the myocardium (abnormal automaticity)
  • Previously suppressed pacemakers in the atrium, AV node, or ventricle can assume pacemaker control of the cardiac rhythm if the SA node pacemaker becomes slow or unable to generate an impulse or if impulses generated by the SA node are unable to activate the surrounding atrial myocardium
  • Increased SNS input or withdrawal of PNS input (exercise, beta agonist medications) results in higher sinus rates whilst decreased SNS input or increased PNS input (beta blockers, digoxin) leads to lower sinus rates
  • Factors: The discharge rate of normal or abnormal pacemakers may be accelerated by:
    1. Drugs
    2. Various forms of cardiac disease
    3. Reduction in extracellular K+
    4. Alterations of ANS tone
  • Examples:
    1. Sinus tachycardia
    2. Atrial tachycardia
    3. Escape rhythms
    4. Accelerated AV nodal (junctional) rhythms
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14
Q

Describe the underlying pathophysiology of cardiac arrhythmia in terms of abnormal impulse formation and b. Triggered activity.

  • What are EADs and DADs?
  • 6 factors that contribute?
  • 7 examples of arrhythmias caused by abnormal impulse formation due to triggered activity?
A

Underlying Pathophysiology of Cardiac Arrhythmias

1. Abnormal Impulse Formation - b. Triggered Activity:

  • Heart cells contract twice, although they only have been activated once
  • Myocardial damage and electrical instability in the myocardial cell membrane can result in oscillations (after-depolarisations) of the transmembrane potential at the end of the AP, which may reach threshold potential and produce an arrhythmia
  • Classified as early after-depolarisations (EADs) if repolarisation during phase 2 and/or phase 3 of the cardiac AP is interrupted, or delayed afterdepolarisations (DADs) if it occurs after full repolarisation
  • Factors:
    1. Catecholamines
    2. Electrolyte disturbances
    3. Hypoxia
    4. Acidosis
    5. Some medications
    6. Digoxin toxicity
  • Examples:
    1. Torsade de Pointes
    2. Atrial tachycardia
    3. Digitalis toxicity-induced tachycardia
    4. Accelerated ventricular rhythms in the setting of AMI
    5. Reperfusion-induced arrhythmias
    6. Right ventricular outflow tract VT
    7. Exercise-induced VT
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15
Q

Describe the underlying pathophysiology of cardiac arrhythmia in terms of abnormal impulse conduction and b. Conduction delay.

  • What causes it?
  • 7 Factors contributing to the pathophysiology?
  • 2 Examples of arrhythmias caused by this underlying pathophysiology?
A

Underlying Pathophysiology of Cardiac Arrhythmias

2. Abnormal Impulse Conduction - a. Conduction Delay

  • Slowed or blocked conduction through the myocardium due to damage to the conduction pathway
  • Factors:
    1. Cardiomyopathy
    2. Thrombosis
    3. Myocarditis
    4. Valvulitis
    5. Endocarditis
    6. Ischemia
    7. Scar tissue
  • Examples:
    1. AV conduction blocks
    2. Bundle branch blocks
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16
Q

Describe the underlying pathophysiology of cardiac arrhythmia in terms of abnormal impulse conduction and b. Conduction delay.

  • What causes it?
  • Factors contributing to the pathophysiology?
  • 7 Examples of arrhythmias caused by this underlying pathophysiology?
A

Underlying Pathophysiology of Cardiac Arrhythmias

2. Abnormal Impulse Conduction - b. Reentry (or Circuit Movements):

  • The mechanism occurs when a ring of cardiac tissue surrounds an inexcitable core (scarred myocardium)
  • Tachycardia is initiated if an ectopic beat finds one limb refractory resulting in unidirectional block, and the other limb excitable.
  • Provided conduction through the excitable limb is slow enough, the other limb will have recovered and will allow retrograde activation to complete the re-entry loop
  • If the time to conduct around the ring is longer than the recovery times (refractory periods) of the tissue within the ring, circus movement will be maintained, producing a run of tachycardia
  • Factors:
    • Injury/damage to myocardium such as ischemia, scar tissue or inflammation
  • Examples:
    1. Regular paroxysmal tachycardias
    2. Atrial fibrillation
    3. Atrial flutter
    4. AV nodal reentry
    5. AV reentry involving a bypass tract
    6. Ventricular tachycardia after MI with the presence of left ventricular scar
    7. Ventricular fibrillation
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17
Q

Describe the Classification of Arrhythmias?

A

Classification of Arrhythmias

Supraventricular:

  • Bradycardia (HR < 60bpm)
    1. Sinus Bradycardia or Arrest
    2. AV Block 1st Degree
    3. AV Block 2nd Degree
    4. AV Block 3rd Degree
  • Tachycardia (HR > 100bpm)
    1. Sinus Tachycardia
    2. Supraventricular Tachycardia
    3. Atrial Fibrillation
    4. Atrial Flutter
    5. Wolff-Parkinson-White Syndrome
  • Ventricular:
    1. Torsades de Pointes
    2. Ventricular Tachycardia
    3. Ventricular Fibrillation
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18
Q

Describe the basic principles of non-pharmacological management of arrhythmias.

A

Basic Principles:

  • Remove extrinsic/underlying cause
  • Stabilise patient
  • Reduce risk of side effects and consequences
  • Long-term monitoring and management

NB: VF and pulseless VT are shockable rhythms!!

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19
Q

What is the Valsalva manoeuvre? Mechanism? Use in arrhythmias?

A
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20
Q

Describe the pharmacology of anti-arrhythmic drugs.

  • Difference between Rate and Rhythm control drugs?
  • Rate control drugs
    • 5 Advantages & 2 Disadvantages
  • Rhythm control drugs
    • 4 Advantages & 2 Disadvantages
A

Pharmacology of anti-arrhythmic drugs

  • Rate Control: AV nodal slowing agents
  • Rhythm Control: Anti-arrhythmic drugs
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21
Q

What is the Vaughan Williams Classification of Anti-Arrhythmic Agents?

A
  • IA - Rhythm Control → Sodium Channel Blocker
  • IB - Rhythm Control → Sodium Channel Blocker
  • IC - Rhythm Control → Sodium Channel Blocker
  • II - Rate Control → Beta Blockers (Adrenergic)
  • III - Rhythm Control → Potassium channel blocker
  • IV - Rate Control → Calcium channel blocker
  • Not Classified
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22
Q

Discuss the Basic Mechanism, Comments and Examples of each of the classes of Anti-Arrhythmic Agents (Vaughan Williams Classification).

A
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23
Q

Describe the pharmacology of anti-arrhythmic drugs.

A
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24
Q

Discuss the Basic Mechanism, Comments and Examples of each of the classes of Anti-Arrhythmic Agents (Vaughan Williams Classification).

  • What do Class Ia agents do to the cardiac AP?
  • What do Class Ib agents do to the cardiac AP?
  • What do Class Ic agents do to the cardiac AP?
  • Where do Class II predominately act?
  • What do Class III agents do to the cardiac AP?
  • Where do Class IV predominately act?
A
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25
Q

Which class of anti-arrhythmic drug is used for the following arrhythmias?

A
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26
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Atrial fibrillation?
A

Atrial Fibrillation:

  1. NO discrete P WAVES!!
  2. Chaotic rhythm
  3. Irregular QRS
  4. Narrow QRS
  5. Irregularly Irregular
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27
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Atrial flutter?
A

Atrial Flutter:

  1. Look in V1 for regular waves
  2. Regularly Irregular
  3. Saw-tooth “F” waves
  4. Narrow QRS
  5. Pattern can be 2:1 or 4.1
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28
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Ventricular fibrillation?
A
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29
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • 1st degree AV Block?
A
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30
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • 2nd degree AV block - Mobitz type I (Wenckebach)?
A
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31
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • 2nd degree AV block - Mobitz type II?
A
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32
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • 3rd degree (complete) AV block?
A
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33
Q

What is Atrial natriuretic peptide?

What is B-type (brain) natriuretic peptide?

A
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34
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Right Bundle Branch Block? (4 characteristics)
A

Right Bundle Branch Block on ECG

  1. QRS duration > 0.12 seconds (3 x small squares)
  2. RSR’(“M”) in V1 and V2 with R’ > R
  3. Slurred S wave in lead I, aVL, V5, and V6
  4. Drop of Q
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35
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Left Bundle Branch Block? (3 characteristics)
A

Left Bundle Branch Block on ECG

  1. QRS duration > 0.12 seconds (3 x small squares)
  2. Broad RSR’(“M”) in I, aVL, V5, and V6
  3. Broad, dominant, monomorphic S wave in V1 and V2

Treat as MI until proven otherwise!

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36
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Wolff-Parkinson White Syndrome? (4 characteristics)
A

Wolff-Parkinson White Syndrome on ECG

  1. Characterised by attacks of rapid heart rate (pre-excitation syndrome)
  2. ECG may not always show tachycardia
  3. Short PR interval
  4. A delta wave (slurring of the upstroke of the QRS complex)
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37
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Supraventricular Tachycardia? (2 characteristics)
A

Supraventricular Tachycardia on ECG

  1. Narrow complex (regular)
  2. No visible P waves (buried in QRS)
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38
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Ventricular Tachycardia? (3 characteristics)
A

Ventricular Tachycardia on ECG

  1. Bizarre morphology
  2. Regular, wide, rapid complex tachycardia = Emergency!
  3. Monomorphic (QRS complex symmetrical) or polymorphic (QRS complex not symmetrical such as with Torsades)
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39
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Atrial Ectopic / Premature Atrial Contraction? (4 characteristics)
  • What are 4 frequently seen ectopic patterns?
A

Atrial Ectopic / Premature Atrial Contraction on ECG

  1. Extra (premature) heart beat
  2. An abnormal (non-sinus) P wave is followed by a QRS complex
  3. P wave typically has a different morphology and axis to the sinus P waves
  4. The abnormal P wave may be hidden in the preceding T wave, producing a “peaked” or “camel hump” appearance

Frequent Ectopy Patterns:

  1. Bigeminy (normal, ectopic, normal, ectopic)
  2. Trigeminy (normal, normal, ectopic)
  3. Couplets (two ectopics in a row)
  4. Triplets (three in a row)
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40
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Ventricular Ectopic? (5 characteristics)
A

Ventricular Ectopic beats on ECG

  1. Extra (premature) heart beat
  2. Broad QRS complex (≥ 120 ms) with abnormal morphology
  3. Premature beat that occurs earlier than would be expected for the next sinus impulse
  4. Usually followed by a full compensatory pause
  5. Discordant ST segment and T wave changes
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41
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Torsades de Pointes? (3 characteristics)
  • Which patients do we see this in?
A

Torsades de Pointes on ECG

  1. Characteristic “twisting” morphology
  2. Like a party streamer
  3. Regularly irregular
  • In patients with known long QT syndrome*
  • Emergency!*
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42
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Left Ventricular Hypertrophy? (3 characteristics)
A

Left Ventricular Hypertrophy on ECG

  1. Larger complexes (thicker muscle) Left axis deviation
  2. Deep S in V2, R in V5
  3. ST depression laterally
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43
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Myocardial Ischaemia? (2 characteristics)
A

Myocardial Ischaemia on ECG

  1. ST depression (at rest ECG normalises)
  2. T wave inversion
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44
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Myocardial Ischaemia?
    • STEMI? (3)
    • NSTEMI? (2)
    • Old Infarct? (2)
A

Myocardial Infarction on ECG

  • ST elevation (starts at J point)
  • ECG can be normal at start until tissue death
  • STEMI:
    1. Persistent elevation >1mm in 2 limb leads
    2. Persistent elevation > 2mm in 2 contiguous chest leads
    3. New LBBB
  • NSTEMI
    1. ST depression > 0.5mm
    2. T wave inversion > 2mm
  • Old Infarct (Death of Muscle)
    1. Q waves where there is no contraction (persist long term)
    2. T wave inversion
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45
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Pericarditis? (2 characteristics)
A

Pericarditis on ECG

  1. Diffuse ST elevation (diffuse pericardial inflammation)
  2. Will change over days not minutes (unlike STEMI)
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46
Q

Demonstrate skills in identifying and interpreting common abnormalities in ECG.

  • Pacemakers? (1 characteristic)
A

Pacemakers on ECG

  1. Spike then LBBB pattern (RV pacing)
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47
Q

What are the 8 clinical features of atrial fibrillation? Explain each.

A
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48
Q

Apply clinical reasoning to determine the physical and psychological causes of palpitations.

  • Differentials for palpations?
A
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49
Q

Apply clinical reasoning to determine the physical and psychological causes of palpitations.

A
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50
Q

Demonstrate skills in interpretation of cardiac symptoms and signs.

A
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51
Q

Demonstrate skills in interpretation of cardiac symptoms and signs.

A
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52
Q

Demonstrate skills in interpretation of cardiac symptoms and signs.

A
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53
Q

Demonstrate skills in interpretation of cardiac symptoms and signs.

A
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54
Q

Describe the relationships between cardiac presentations and anxiety.

  • Anxiety Presentations?
    • Emotional
    • Cardiac
    • Respiratory
    • Gastrointestinal
    • Temperature
    • Somatic
    • General
  • Relationship to Cardiac presentation?
A

Anxiety Presentation:

  • Emotional: Excessive and persistent worry, nervousness, fatigue and restless
  • Cardiac: Palpitations, increased heart rate, dizziness, chest pain or discomfort
  • Respiratory: Shortness of breath, difficulty breathing, choking sensation, hyperventilation
  • Gastrointestinal: Abdominal churning, nausea, diarrhoea
  • Temperature: Chills, hot flushes, sweating
  • Somatic: Tremor, tension, shaking, numbness & tingling
  • General: Sense of impending doom, hyperarousal, ANS hyperactivity, weak, having t rouble concentrating and sleeping, and having the urge to avoid things (avoidance behaviour) that trigger anxiety

Relationship to Cardiac Presentation:

  1. Threat is perceived by amygdala
  2. Threat is processed by hypothalamus which activates SNS
  3. SNS is activated and releases adrenaline and noradrenaline which will have systemic effects
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55
Q

List the steps involved in the Development of Atherosclerosis? (12 steps)

  • 3 examples of causes of endothelial injury to arteries?
  • What does endothelial dysfunction cause? What binds here?
  • Describe how this causes inflammation?
  • What are foam cells?
  • How is a fatty streak formed? What binds to it?
  • What forms the fibrous cap around the fatty streak?
  • Role of calcium?
A

Development of Atherosclerosis (RECAP): Fatty Streak → Atheroma → Fibrous Plaque → Occlusion/Rupture

  1. Endothelial injury due to irritants such as LDL, chemicals from smoking or hypertension.
  2. Endothelial dysfunction resulting in increased permeability, leukocyte adhesion, monocyte adhesion and emigration.
  3. LDL bind to receptor on endothelial cells surface and are internalised to under the tunica intima.
  4. Monocytes follow the LDL into the endothelium and break them down via oxidation (inflammation).
  5. If monocytes ingest too many LDL and cholesterol, they will die and become foam cells that remain deposited under the endothelium.
  6. Monocytes secrete pro-inflammatory cytokines for the recruitment of more monocytes, which ingest more LDL and become foam cells, forming a fatty streak.
  7. The fatty streak is thrombogenic, and platelets can bind to the damaged endothelium secreting platelet derived growth factor (PDGF).
  8. PDGF encourages recruitment, proliferation and growth of smooth muscle cells to the tunica intima.
  9. Smooth muscle cells secrete collagen, proteoglycans, elastin fibrous cells that form a fibrous cap around the fatty streak (fatty streak and fibrous cap are referred to as plaque).
  10. Calcium is also deposited in the fatty streak as the fibrous cap prevents its removal by HDL.
  11. Calcium crystalises and stiffens blood vessels walls.
  12. Consequently, the fibrous cap can rupture and expose underlying foam cells to blood giving rise to a thrombus (blood clot). Thrombosis can lead to aneurysm, occlusion, ischemia and infarction whilst progressive plaque growth can lead to stenosis.
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56
Q

Review the Gross Anatomy of the Coronary Arteries and which parts of the heart they supply.

  • Pathway of blood flow from aorta?
  • RCA?
  • RPDA?
  • RMA?
  • LCA?
  • LAD?
  • Left Circumflex?
  • Left Obtuse Marginal Artery?
A

Gross Anatomy of the Coronary Arteries: Aorta → Aortic Sinuses → Coronary Ostio (Openings in Aorta) → Left and Right Coronary Arteries

  • Right Coronary Artery: Supplies SA node, right atrium and ventricle
  • Right Posterior Descending Artery: Supplies AV node, interventricular septum and right and left ventricles
  • Right Marginal Artery: Supplies the right ventricle and apex
  • Left Coronary Artery: Branches into left circumflex artery and LAD
  • Left Anterior Descending Artery: Supplies interventricular septum, left ventricle and some of right ventricle
  • Left Circumflex Artery: Supplies left atrium and ventricle
  • Left Obtuse Marginal Artery: Supplies left ventricle
  • NB: Both the anterior and posterior descending arteries follow the anterior/posterior interventricular groove towards the apex of the heart where they generally anastomose
  • NB: Right coronary artery and left circumflex artery travel along left/right atrioventricular grooves
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57
Q
A
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58
Q

What are Macroscopic features of Normal Coronary Arteries (5) vs. Atherosclerosis (7)?

A

MACROSCOPIC FEATURES

  • Normal Coronary Arteries
    1. Wide lumen
    2. No occluded blood flow
    3. Lumen not encroached by plaques
    4. Undisturbed arterial walls (no deposits, inflammation, clots or narrowing)
    5. Smooth endothelial surface
  • Atherosclerosis
    1. Reduced lumen size
    2. Fatty streaks (flat yellow spots to elongated streaks)
    3. Tunica intima thickening
    4. Fibrous plaques (white-yellow and encroach on the lumen) seen on intimal surface
    5. Calcium deposits (white granules)
    6. Superimposed thrombus (red-brown) over ulcerated plaques
    7. Patchy eccentric lesions (not circumferential)
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59
Q

What are Microscopic features of Normal Coronary Arteries (3) vs. Atherosclerosis (3)?

A

MICROSCOPIC FEATURES/HISTOLOGY

  • Normal Coronary Arteries
    1. Normal tunica intima (layer of flattened endothelial cells)
    2. Normal tunica media (bulk middle layer of smooth muscle cells and elastin)
    3. Normal adventitia (thin outer layer of connective tissue)
  • Atherosclerosis
    1. Superficial fibrous cap composed of smooth muscle cells and dense collagen and elastin
    2. Beneath cap is infiltration of macrophages, T cells, and smooth muscle cells
    3. Deep to cap is necrotic core with cholesterol, (lipid), dead cell debris, foam cells and fibrin
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60
Q

Describe the mechanisms responsible for the development of myocardial ischaemia and their consequences.

  1. Atheroma
  2. Thrombosis
  3. Embolus
  4. Vasospasm
  5. Coronary arteritis
  6. Anaemia
A
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61
Q

Describe the mechanisms responsible for the development of myocardial ischaemia and their consequences.

  1. Atheroma
  2. Thrombosis
  3. Embolus
  4. Vasospasm
  5. Coronary arteritis
  6. Anaemia
A
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62
Q

What are the 2 types of disease?

A

Types of Disease:

  1. Congenital Disease
  2. Acquired Disease (Traumatic, Inflammatory, Degenerative and Neoplastic)
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63
Q
  • What are the 2 types of Myocardial Diseases?
  • 2 Pericardial Diseases?
  • 4 Neoplasms?
A

Myocardial Diseases:

  1. Myocarditis (Inflammatory)
    1. Infective Myocarditis
    2. Immune Myocarditis
    3. Idiopathic Myocarditis
  2. Cardiomyopathy (Degenerative)
    1. Dilated Cardiomyopathy
    2. Hypertrophic Cardiomyopathy
    3. Restrictive Cardiomyopathy
    4. Secondary Cardiomyopathy

Pericardial Diseases:

  1. Pericarditis
  2. Cardiac Tamponade

Neoplasms

  1. Atrial Myxoma
  2. Rhabdomyoma
  3. Angiosarcoma
  4. Metastases
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64
Q

What is Myocarditis?

  • Infective Myocarditis?
    • Most common causes?
  • Immune Myocarditis?
    • Causes?
  • 2 causes of Idiopathic myocarditis?
A

Myocardial Diseases:

Myocarditis (Inflammatory): Primary inflammation of the myocardium, pathologically seen as myocyte necrosis and inflammatory cell infiltration.

  • Infective Myocarditis: Viruses most common causes (e.g. Coxsackie A and B, ECHO, Influenza, HIV and CMV), but can be caused by bacteria (Chlamydia, Rickettsia, Meningococcus, Diphtheria and Borrelia), fungi (candida), helminths (Trichinella) or protozoa (Chaga’s disease and Toxoplasmosis).
  • Immune Myocarditis: Can occur post-viral or post-bacterial infection through cross-reactivity and development of an autoimmune condition. Also due to systemic immune disease (SLE, rheumatic fever or polymyositis), drug hypersensitivity (antibiotics, diuretics, antihypertensives) and transplant rejection.
  • Idiopathic Myocarditis: Due to sarcoidosis and giant cell myocarditis
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65
Q

What is Cardiomyopathy?

  • Dilated Cardiomyopathy? Causes?
  • Hypertrophic Cardiomyopathy? Causes?
  • Restrictive Cardiomyopathy? Causes?
  • Causes of Secondary Cardiomyopathy?
A

Cardiomyopathy (Degenerative): A disorder in which the heart muscle is structurally (wall thickness and chamber size) and functionally (mechanical and electrical) abnormal. Primary myopathy can be genetic, whilst secondary myopathy is due to many causes including toxins, metabolic, drugs, infiltrates, depositions, neuromuscular.

  1. Dilated Cardiomyopathy: Dilation and impaired contraction of one or both ventricles (dilation can result in increased mass and eccentric hypertrophy). Common causes are viral myocarditis (Coxsackie virus) and genetics, but can also occur with drugs, alcohol and pregnancy
  2. Hypertrophic Cardiomyopathy: Increased ventricular wall thickness or mass not caused by pathologic loading conditions. Common causes are athletics and intense endurance training and genetics (mutations in genes coding for sarcomere proteins)
  3. Restrictive Cardiomyopathy: Nondilated ventricles with increased ventriuclar stiffness and impaired ventricular diastolic filling. Can occur idiopathically or due to amyloid, radiation fibrosis, sarcoidosis and metastatic tumours.
  4. Secondary Cardiomyopathy: Caused by cardiotoxic drugs, catecholamine excess, iron overload and thyroid disease
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66
Q

DILATED CARDIOMYOPATHY vs. HYPERTROPHIC CARDIOMYOPATHY?

A

Figure 12.30 Causes and consequences of dilated and hypertrophic cardiomyopathy. Some dilated cardiomyopathies and virtually all hypertrophic cardiomyopathies are genetic in origin. The genetic causes of dilated cardiomyopathy involve mutations in any of a wide range of genes. They encode proteins predominantly of the cytoskeleton, but also the sarcomere, mitochondria, and nuclear envelope. In contrast, all of the mutated genes that cause hypertrophic cardiomyopathy encode proteins of the sarcomere. Although these two forms of cardiomyopathy differ greatly in subcellular basis and morphologic phenotypes, they share a common set of clinical complications. LV, left ventricle.

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67
Q

Pericardial Diseases

  • What is Pericarditis? Classifications? Causes?
  • What is Cardiac tamponade? Causes?
A

Pericardial Diseases:

Pericarditis: Inflammation of the pericardium classified according to the composition of the fluid that accumulates around the heart (serous, fibrinous, purulent or haemorrhagic). Caused commonly by viral infection, but can also be due to bacterial infection, autoimmune conditions, post-MI, chest trauma, cancer or idiopathic.

Cardiac Tamponade: Compression of the heart caused by fluid collecting in the sac surrounding the heart (pericardial cavity). Caused by pericarditis, chest trauma, complications of cardiac surgery, cancer, kidney failure, connective tissues diseases, hypothyroidism and aortic ruptures.

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68
Q

Neoplasms of the Heart

  • What is Atrial Myxoma?
  • What is Rhabdomyoma?
  • What is Angiosarcoma?
  • Metastases?
A

Neoplasms of the Heart:

Atrial Myxoma: Rare heart disorder in which a rare tumour grows in the left heart chamber

Rhabdomyoma: Benign tumour of striated muscle

Angiosarcoma: Rare type of cancer that forms in the lining of the blood vessels and lymph vessels

Metastases: More common than primary cardiac tumours. Pericardial are most common, followed by epicardial and myocardial metastases. Can manifest as a lung mass or mediastinal mass with direct invasion of the adjacent heart, as a central mass extending into the left atrium via the pulmonary veins, as pericardial effusion and nodularity, or as myocardial nodules.

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69
Q

Describe and classify the clinical presentations of Ischaemic Heart Disease (IHD).

  • What is the definition of IHD? 2 types of causes?
A

Definition of IHD: Disturbance in myocardial O2 supply and demand

Decreased Supply: Due to mechanical obstruction (atheroma, thrombosis, spasm, stenosis), or decreased flow of oxygenated blood to myocardium such as with anaemia, hypoxia, hypotension, tachycardia (shortened diastole) and carboxyhaemoglobulinaemia (carbon monoxide poisoning)

Increased Demand: Due to increased cardiac output such as with hyperthyroidism or thyrotoxicosis, or myocardial hypertrophy such as from aortic stenosis or hypertension.

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70
Q

Classification of IHD?

A
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71
Q

Describe the progressive manifestations of ischaemic heart disease.

A
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72
Q

Compare the blood vessel lumen in:

  • a. Stable angina pectoris
  • b. Unstable angina pectoris
  • c. STEMI
A
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73
Q

What are 6 Clinical Features of IHD? Give explanations for each of them.

A

Clinical Features of IHD

  1. Chest Pain (Central) → Pain/Tightness/Pressure/Discomfort, Radiation to Jaw/Shoulder/Neck, On exertion (SA) or at rest (USA)
  2. Dyspnoea/Shortness of Breath
  3. Reduced Exercise Tolerance
  4. Sense of Impending Doom
  5. Palpitations
  6. Sweating
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74
Q

List the fixed and potentially changeable risk factors for coronary disease?

A
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75
Q

Outline the complications of Ischaemic Heart Disease (IHD).

  • Day 1-3 Post MI? (4)
  • Day 3-5 Post-MI? (5)
  • Day 5-10 Post-MI? (3)
  • Day 10 + Post-MI? (2)
A

Complications of IHD:

  • Stable Angina
  • Unstable Angina
  • Acute Myocardial Infarction (STEMI/NSTEMI)
  • Mortality
  • Day 1-3 Post MI:
    1. Cardiac Dysrhythmia
    2. Pericarditis (Early) or Dressler’s Syndrome (Delayed)
    3. AV Block
    4. Cardiogenic Shock
  • Day 3-5 Post-MI:
    1. Ventricular Free Wall Rupture
    2. Ventricular Septal Rupture
    3. Papillary Muscle Rupture
    4. Acute Mitral/Tricuspid Regurgitation
    5. Ventricular Pseudoaneurysm
  • Day 5-10 Post-MI:
    1. Ventricular Mural Thrombus
    2. Atrial Thrombus
    3. DVT and Pulmonary Embolism
  • Day 10 + Post-MI:
    1. Congestive Heart Failure
    2. Ventricular Aneurysm (VF or VT)
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76
Q

What investigations should be performed for suspected stable angina?

  • What would you seen on ECG?
  • 3 functional imaging techniques?
A
77
Q

What investigations should be performed for suspected Acute Coronary Syndrome (Unstable Angina + MI)?

  • What would you see on ECG?
  • 2 types of anatomical assessment?
  • 3 blood biomarkers?
A
78
Q

What is the management for Stable Angina?

  • 4 general points?
  • 5 specifics? (meds)
A

Management of Stable Angina

General:

  1. Treat underlying conditions (i.e. anaemia or hyperthyroidism)
  2. Manage co-morbidities (i.e. diabetes or hypertension)
  3. Evaluate risk factors and reduce risk where possible
  4. Symptomatic treatment should be started with the vasodilator sublingual or buccal nitrate to relieve acute episodes of stable angina

Specifics

  1. Nitrates: For coronary vasodilation
  2. β-Blockers and/or Ca2+ Channel Blockers: To prevent acute episodes
  3. Statins: To reduce cholesterol
  4. Aspirin: Anti-platelet
  5. ACE Inhibitor: To treat other conditions (i.e. hypertension, heart failure, chronic kidney disease)
79
Q

What is the management for Acute Coronary Syndrome (Unstable Angina + MI)?

  • 3 general points?
  • 7 specifics?
  • 2 Revascularisation methods?
A

Management for Acute Coronary Syndrome

General:

  1. Same as with Angina
  2. High-Risk Patients: Require urgent coronary angiography and intervention
  3. Low-Risk Patients: Managed with oral aspirin, clopidogrel, beta-blockers and nitrates

Specifics

  1. Analgesic: Such as morphine for pain management
  2. Oxygen: For hypoxia, as needed
  3. Nitrates: For coronary vasodilation
  4. Anti-Platelet Agents: Such as aspirin and clopidogrel to reduce risk of MI or death
  5. Antithrombins: Such as heparin to reduce risk of MI or death
  6. β-Blockers: To reduce myocardial ischaemia by blocking circulating catecholamines, reducing HR and BP, reducing myocardial oxygen consumption
  7. Plaque Stabilisation Agents: HMG-CoA reductase inhibitor drugs (statins) and ACE inhibitors are routinely administered to produce plaque stabilization, improve vascular and myocardial remodelling, and reduce future cardiovascular events

Revascularisation:

  1. Percutaneous Coronary Intervention (PCI)
  2. Coronary Artery Bypass Grafting (CABG)
80
Q

What is Primary, Secondary and Tertiary Prevention? Examples of each for IHD?

A
81
Q

Describe the role of invasive treatment approaches to coronary artery disease: coronary artery angioplasty and coronary artery surgery.

A
82
Q

What are the ECG Features of Myocardial Ischaemia?

A

ECG Features of Myocardial Ischaemia:

  1. ST depression (at rest ECG normalises)
  2. T wave inversion
83
Q

What are the ECG Features of Myocardial Infarction?

  • STEMI? (3)
  • NSTEMI? (2)
  • Old Infarct? (2)
A

ECG Features of Myocardial Infarction

  • ST elevation (starts at J point)
  • ECG can be normal at start until tissue death
  • STEMI:
    1. Persistent elevation >1mm in 2 limb leads
    2. Persistent elevation >2mm in 2 contiguous chest leads
    3. New LBBB
  • NSTEMI
    1. ST depression > 0.5mm
    2. T wave inversion > 2mm
  • Old Infarct (Death of Muscle)
    1. Pathological Q waves where there is no contraction (persist long term)
    2. T wave inversion (can correct long-term)
84
Q

What are the ECG Features of Myocardial Infarction?

  • STEMI? (3)
  • NSTEMI? (2)
  • Old Infarct? (2)
A

ECG Features of Myocardial Infarction

  • ST elevation (starts at J point)
  • ECG can be normal at start until tissue death
  • STEMI:
    1. Persistent elevation >1mm in 2 limb leads
    2. Persistent elevation >2mm in 2 contiguous chest leads
    3. New LBBB
  • NSTEMI
    1. ST depression > 0.5mm
    2. T wave inversion > 2mm
  • Old Infarct (Death of Muscle)
    1. Pathological Q waves where there is no contraction (persist long term)
    2. T wave inversion (can correct long-term)
85
Q

What are the 7 Cardiac Ultrasound Features of Myocardial Ischaemia?

A

Cardiac Ultrasound Features of Myocardial Ischaemia:

  1. Abnormal wall motion due to damaged/dead tissue
  2. Decrease in myocardial thickening due to damage and necrosis
  3. Decrease in valve movements of heart due to damage
  4. May have abnormal wall thickness or chamber size due to underlying hypertrophy
  5. May have reduced ejection fraction due to damage to heart muscle
  6. May have altered diastolic or systolic motion
  7. Perhaps post-complications such as thrombus, valve disease, aneurysm or rupture
86
Q

What is Dyspnoea?

What is Orthopnoea?

What is Paroxysmal Nocturnal Dyspnoea?

A

Dyspnoea: Sensation of difficult or uncomfortable breathing (subjective experience perceived by the patient)

Orthopnoea: Dyspnoea that develops when a patient is supine, occurs because in an upright position the patient’s interstitial oedema is redistributed

Paroxysmal Nocturnal Dyspnoea: Severe dyspnoea that wakes the patient from sleep so that he or she is forced to get up gasping for breath. This occurs because of a sudden failure of LV output with an acute rise in pulmonary venous and capillary pressures which leads to transudation of fluid into the interstitial tissues, increasing the work of breathing

87
Q

What are 6 mechanisms underlying the Pathophysiological Basis Dyspnoea?

A
88
Q

Differentials for Dyspnoea?

  • Respiratory?
  • Cardiovascular?
  • Other?
A
89
Q

What are the differentials for dyspnoea based on time course of onset:

  • Seconds to minutes favours?
  • Hours or days favours?
  • Weeks or longer favours?
A
90
Q

What are the differentials for dyspnoea based on:

  • Presence of pleuritic chest pain?
  • Absence of chest pain?
  • Presence of central chest pain?
  • Presence of cough and wheeze?
A
91
Q

What are the distinguishing features between dyspneoa due to heart disease and lung disease?

  • Hx?
  • Development?
  • Present at rest?
  • Dry vs. productive?
  • Exacerbated by infection or not?
A
92
Q

What are the the features of Chest Pain that favour:

  • Angina? (6)
  • Pericarditis or Pleurisy? (6)
  • Esophageal (acid) reflux pain? (6)
A
93
Q

What are the the features of Chest Pain that favour:

  • Myocardial Infarction? (6)
  • Angina? (6)
  • Aortic dissection? (3)
  • Chest wall pain? (5)
A
94
Q

Describe the pathophysiology of heart failure.

  • What is a normal ejection fraction? Below normal? Low?
  • What is Heart Failure with Reduced Ejection Fraction (HFrEF)?
    • 4 Causes?
  • What is Heart Failure with Preserved Ejection Fraction (HFpEF)?
    • 3 causes?
A

Heart Failure with Reduced Ejection Fraction (HFrEF): Pump dysfunction (systolic HF)

  • Dysfunction: Inadequate emptying of ventricles during systole resulting in decreased EF ( ≤ 40)
  • Causes:
    1. Decreased contractility/force of contraction due to myocardial infarction or myocarditis
    2. Decreased blood supply to the heart due to coronary artery disease
    3. Increased afterload due to hypertension
    4. Impaired mechanical function due to valve disease

Heart Failure with Preserved Ejection Fraction (HFpEF): Filling dysfunction (diastolic HF)

  • Dysfunction: Inadequate relaxation and filling of ventricles during diastole, leading to decreased EDV and SV and resulting in preserved EF ( ≥ 50)
  • Causes:
    1. Restrictive cardiomyopathy e.g. amyloidosis or sarcoidosis)
    2. Valve disease
    3. Hypertension
95
Q
  • What causes Pressure overload of the heart? (3)
    • 2 Examples?
  • What causes Volume overload of the heart? (3)
    • 3 Examples?
A
96
Q

Describe the Pathophysiology of Left Sided Heart Failure (Systolic Dysfunction).

  • What are 4 causes of left sided heart failure due to systolic dysfunction?
A

Left Sided Heart Failure Pathophysiology:

Overall: Decreased LV contractility or EDV → Decreases SV → Decreases CO → Not enough blood is pumped into systemic circulation to meed body’s demands → Blood backs up into lungs → Pulmonary congestion/oedema → Pulmonary hypertension

Systolic Dysfunction: LV can’t pump well so EF decreased (many different causes)

  1. Dilated Cardiomyopathies
  2. Mitral/Aortic Regurgitation
  3. Myocardial Infarction
  4. Severe Hypertension/Advanced Aortic Stenosis
97
Q

How do Dilated Cardiomyopathies cause Left Sided Heart Failure due to Systolic Dysfunction?

A

LEFT SIDED HEART FAILURE - SYSTOLIC DYSFUNCTION

Dilated Cardiomyopathies: Progressive dilation of LV via eccentric hypertrophy → Increased EDV → Increased contractility at first (Frank Starling Law) → Eventual weakening and thinning → Decreased LV contractility

98
Q

How does Mitral/Aortic regurgitation cause Left Sided Heart Failure due to Systolic Dysfunction?

A

LEFT SIDED HEART FAILURE - SYSTOLIC DYSFUNCTION

Mitral/Aortic Regurgitation: Chronic LV volume overload → Progressive dilation of LV via eccentric hypertrophy → Increased EDV → Increased contractility at first (Frank Starling Law) → Eventual weakening and thinning → Decreased LV contractility

99
Q

How does Myocardial Infarction cause Left Sided Heart Failure due to Systolic Dysfunction?

A

LEFT SIDED HEART FAILURE - SYSTOLIC DYSFUNCTION

Myocardial Infarction: Necrotic non-functional myocytes (non-conductive, non-contractile) → Decreased LV contractility

100
Q

How does Advanced Aortic Stenosis cause Left Sided Heart Failure due to Systolic Dysfunction?

A

LEFT SIDED HEART FAILURE - SYSTOLIC DYSFUNCTION

Advanced Aortic Stenosis: Increased TPR → Increased LV afterload → Chronic LV pressure overload → Concentric LV hypertrophy → Increased O2 demand BUT squeezed coronary arteries and reduced supply → Decreased LV contractility

101
Q

Describe the Pathophysiology of Left Sided Heart Failure (Diastolic Dysfunction).

  • What are 6 causes of left sided heart failure due to systolic dysfunction?
A

Left Sided Heart Failure Pathophysiology:

Diastolic Dysfunction: LV can’t fill well so EF preserved (many different causes)

  1. Cardiac Tamponade/Myocardial Ischemia/Hypertrophic Cardiomyopathy: Decreased LV relaxation and/or diastolic filling → Decreased EDV
  2. Myocardial Fibrosis/Restrictive Cardiomyopathy/Hypertrophic Cardiomyopathy: Increased LV wall stiffness → Reduction in LV compliance -> Decreased EDV
102
Q

How does Severe Hypertension cause Left Sided Heart Failure due to Systolic Dysfunction?

A

Severe Hypertension: Increased TPR → Increased LV afterload → Chronic LV pressure overload → Concentric LV hypertrophy → Increased O2 demand BUT squeezed coronary arteries and reduced supply → Decreased LV contractility

103
Q

How does Cardiac Tamponade/Myocardial Ischemia/Hypertrophic Cardiomyopathy cause Left Sided Heart Failure due to Diastolic Dysfunction?

A

LEFT SIDED HEART FAILURE - DIASTOLIC DYSFUNCTION

Cardiac Tamponade/Myocardial Ischemia/Hypertrophic Cardiomyopathy: Decreased LV relaxation and/or diastolic filling → Decreased EDV

104
Q

How does Restrictive Cardiomyopathy cause Left Sided Heart Failure due to Diastolic Dysfunction?

A

LEFT SIDED HEART FAILURE - DIASTOLIC DYSFUNCTION

Myocardial Fibrosis/Restrictive Cardiomyopathy/Hypertrophic Cardiomyopathy: Increased LV wall stiffness → Reduction in LV compliance → Decreased EDV

105
Q

Describe the Overall Pathophysiology of Right Sided Heart Failure (Systolic Dysfunction).

A

Right Sided Heart Failure Pathophysiology:

Overall: Decreased RV contractility → Decreases SV → Decreases RV CO → Increased RA pressure → Blood backs up into systemic venous vasculature (elevated JVP) → Hydrostatic pressure and bulk flow pushes fluid out of capillaries into systemic tissues (pitting oedema) and congestion of fluid in liver and spleen (hepatosplenomegaly). RV also still needs to pump against high afterload → RV pressure overload → Concentric RV hypertrophy → Further decrease of pumping ability

NB: Cor Pulmonale is RV hypertrophy, dilation, and/or dysfunction due to pulmonary hypertension secondary to pulmonary disease (COPD, pulmonary fibrosis, upper airway obstruction, obstructive sleep apnoea, obesity-hypoventilation syndrome or chest wall irregularities such as kyphoscoliosis)

106
Q

What are some causes of Right Sided Heart Failure (Systolic Dysfunction).

  • 4 cardiac diseases?
  • 3 Diseases of Lung Parenchyma?
  • 2 Diseases of Pulmonary Vasculature?
A

Right Sided Heart Failure Pathophysiology:

  • Cardiac Disease (Systolic HF)
    1. Dilated Cardiomyopathies
    2. Tricuspid Regurgitation
    3. Myocardial Infarction
    4. Pulmonic Valve Stenosis
  • Diseases of Lung Parenchyma: Results in Cor Pulmonale HF
    1. COPD
    2. Interstitial Lung Disease
    3. Chronic Infection
  • Diseases of Pulmonary Vasculature: Results in Cor Pulmonale HF
    1. Embolism
    2. Pulmonary Hypertension
107
Q

How do Dilated Cardiomyopathies cause Right Sided Heart Failure?

A

RIGHT SIDED HEART FAILURE

Dilated Cardiomyopathies: Progressive dilation of RV via eccentric hypertrophy → Increased EDV → Increased contractility at first (Frank Starling Law) -> Eventual weakening and thinning → Decreased RV contractility

108
Q

How does Tricuspid Regurgitation cause Right Sided Heart Failure?

A

RIGHT SIDED HEART FAILURE

Tricuspid Regurgitation: Chronic RV volume overload → Progressive dilation of RV via eccentric hypertrophy → Increased EDV → Increased contractility at first (Frank Starling Law) → Eventual weakening and thinning → Decreased RV contractility

109
Q

How does Myocardial Infarction cause Right Sided Heart Failure?

How does Pulmonic Valve Stenosis cause Right Sided Heart Failure?

How does Left Heart Failure cause Right Sided Heart Failure?

A

RIGHT SIDED HEART FAILURE

  • Myocardial Infarction: Non-functional myocytes → Decreased RV contractility
  • Pulmonic Valve Stenosis: Increased TPR → Increased RV afterload → Chronic RV pressure overload → Concentric RV hypertrophy → Decreased RV contractility
  • Left Heart Failure: Pulmonary hypertension → Chronic increased RV afterload → Chronic RV pressure overload → Concentric RV hypertrophy → Decreased RV contractility
110
Q

How do diseases of lung parenchyma result in right sided heart failure?

A

RIGHT SIDED HEART FAILURE

Diseases of Lung Parenchyma: Results in Cor Pulmonale HF

COPD, Interstitial Lung Disease, Chronic Infection: Pulmonary vasoconstriction → Increased pulmonary hypertension → Chronic increased RV afterload → Concentric RV hypertrophy → Decreased RV contractility

111
Q

How do diseases of pulmonary vasculature result in right sided heart failure?

A

RIGHT SIDED HEART FAILURE

Diseases of Pulmonary Vasculature: Results in Cor Pulmonale HF

Embolism or Pulmonary Hypertension: Chronic increased RV afterload → Concentric RV hypertrophy → Decreased RV contractility

112
Q

What is Biventricular Heart Failure?

A

Biventricular Heart Failure: Heart failure in which both the LV and RV are affected (usually due to LV failure) resulting in backward and forward heart failure

113
Q

What are the Clinical Signs and Symptoms of Heart Failure?

  • Both? (4)
  • Left Sided HF? (8)
  • Right Sided HF? (7)
A

Clinical Signs and Symptoms of Heart Failure

  • Both
    1. Diaphoresis, Tachycardia, Tachypnoea (Compensatory SNS Stimulation due to reduced CO)
    2. Cool Clammy Peripheries (Reduced CO and Peripheral Vasoconstriction)
    3. Dyspnoea (Exertional and/or Rest) and Reduced Exercise Tolerance
    4. Fatigue
  • Left Sided Heart Failure
    1. Pulmonary Oedema
    2. Orthopnoea and Paroxysmal Nocturnal Dyspnoea
    3. Bilateral Basal Lung Crackles (Pulmonary Oedema)
    4. Pink (Whitish) Frothy Sputum and Cough
    5. Lung Congestion and Pleural Effusion (Dullness to Percussion)
    6. Confusion (Poor Perfusion to Brain)
    7. Syncope and Presyncope
    8. Nocturia (Increased Fluid Retention due to RAAS)
  • Right Sided Heart Failure
    1. Peripheral Oedema
    2. Elevated JVP
    3. Pitting Oedema (Ankles/Sacrum)
    4. Ascites and Abdominal Bloating (Dullness to Percussion)
    5. Hepatosplenomegaly and RUQ
    6. Discomfort
    7. Weight Gain (Fluid Retention)
114
Q

Complications of Heart Failure?

  • Left Sided? (5)
  • Right Sided? (5)
A

Complications of Left Sided Heart Failure

  1. Arrhythmias
  2. Pulmonary Oedema
  3. Pulmonary Hemorrhage (Congested Capillaries Burst)
  4. Pleural Effusion
  5. Renal Insufficiency (Reduced Perfusion)

Complications of Left Sided Heart Failure

  1. Arrhythmias
  2. Eventual Failure of Left Heart Tricuspid Regurgitation
  3. Peripheral Oedema
  4. Congestive Hepatopathy
  5. Cardiac Cirrhosis and Liver Failure Cardiac Cachexia
115
Q

Describe the Neurohormonal Activation in the Pathophysiology of Left Heart Failure?

A
116
Q

What are 9 Signs of Left Heart Failure of Chest Xray? Mechanisms?

A

Features of Left Heart Failure on CXR

  1. Cardiomegaly
  2. Cephalization
  3. Perihilar Haze
  4. Peribronchial cuffing
  5. Kerley-B lines
  6. Opacified/White Interlobular fissures
  7. Pleural effusion
  8. Air bronchogram
  9. Widespread airspace opacificity
117
Q

Outline the clinical approach to the patient with a bacteraemia but no obvious clinical focus on initial presentation.

  • What is Bacteraemia?
  • 5 Clinical Features?
  • Basic Clinical Approach?
  • Suspected Conditions based on Clinical Features?
A

Clinical Approach to Fever of Unknown Origin: Think infection, autoimmune, inflammation or neoplasm

  • Bacteraemia: The transient presence of bacteria in the blood (usually asymptomatic) caused by local infection or trauma
  • Clinical Features:
    1. Fever, chills
    2. Rigors
    3. Anorexia
    4. Tiredness/Lethargy
    5. Delirium (elderly)
  • Clinical Approach
    1. History
    2. Examination
    3. Investigation
    4. Differentials List
118
Q

Describe the gram stain findings of common organisms and know the common clinical foci of infection with each organism.

A
119
Q

Describe the gram stain findings of common organisms and know the common clinical foci of infection with each organism.

A
120
Q

Describe the gram stain findings of common organisms and know the common clinical foci of infection with each organism.

A
121
Q

Define:

  • Pyrexia of unknown origin (PUO)
  • Bacteremia
  • Septicemia
  • Sepsis
  • Severe Sepsis
  • Septic Shock
A

Pyrexia of Unknown Origin: A fever of 38.3°C or greater for at least 3 weeks with no identified cause after three days of hospital evaluation or three outpatient visits, commonly due to infections, neoplasms or connective tissue disorders.

Bacteraemia: The transient presence of bacteria in the blood (usually asymptomatic) caused by local infection, wounds or trauma, which can lead to infection, sepsis or both.

Septicaemia/Blood Posioning: The presence and multiplication of bacteria in the blood caused by spread of infections throughout the body, including the lungs, abdomen, and urinary tract, which can quickly progress to sepsis.

Sepsis: Term used to describe the signs and symptoms of a systemic inflammatory response syndrome (SIRS) to a localised primary site of infection.

Severe Sepsis: The presence of the sepsis syndrome (presence of either a positive blood culture or clinical features of fever, tachypnoea, tachycardia, suspected infection), complicated by organ dysfunction, hypotension or hypoperfusion and manifested by low blood pressure, oliguria, hypoxia, acute confusion and lactic acidosis.

Septic Shock: Defined as the sepsis syndrome plus organ dysfunction and hypotension unresponsive to adequate fluid replacement.

122
Q

Compare Bacteraemia and Septicaemia in terms of:

  • Definition?
  • Severity?
  • Amounts of bacteria present in the blood?
  • Source?
  • Toxin produced?
  • Symptoms?
  • Tx required?
  • Strains of bacteria?
A
123
Q

What are 4 Mechanisms of Antibiotic Resistance with examples for each?

  • 4 ways they prevent entry of the antibiotic?
  • 3 ways they destroy the antibiotic?
  • 4 ways they change the structure of the antibiotic target?
  • 2 ways they overproduce the target?
A

Mechanisms of Antibiotic Resistance:

  • 1) Prevent Entry of the Antibiotic
    1. Lack of entry transporter
    2. Decreased membrane permeability
    3. Efflux pumps (i.e. PmrA in S. pneumonia, NorA in S. aureus, ArcB in E.coli and MexB in P.aeruginosa)
    4. Porin channel reduction
  • 2) Destroy the Antibiotic
    1. Enzymatic inhibition or degradation (i.e. penicillinases produced by S.aureus)
    2. B-lactamases (intrinsic in anaerobes and common in gram-negatives and ESBLs)
    3. AmpC cephalosporinase (inducible with antibiotic use)
  • 3) Change the Structure of the Antibiotic Target
    1. Point mutations (ribosomal subunits or DNA changes)
    2. Change surface proteins/antigens (i.e. S. pneumonia lowers affinity of PBPs to Penicillin G)
    3. Plasmid mediated resistance genes (i.e. Van A gene in VRE/VRSA, TEM gene in gram negative rod that creates an enzyme that hydrolyses penicillins, Mec A gene in MRSA for resistance to B-lactams)
    4. Alter target site on ribosome to prevent antibiotic from binding (i.e. S. pneumoniae causes erythhromycin ribosomal methylase)
  • 3) Overproduce the Target
    1. FolA gene and overproduction of DHFR and DHPS to become resistant to co-trimoxazole
    2. Overproduction of PBPs
124
Q

Describe the development of antimicrobial resistance.

A
125
Q

What are the Mechanisms of Staphylococci Spp. Resistance?

A

Mechanisms of Staphylococci Spp. Resistance: Acquired via plasmid transfer via bacterial conjugation (horizontal gene transfer) or spontaneous gene mutation and positive selection.

126
Q

Review anatomy and physiology of heart valves and supporting structures.

  • What are the 2 types of heart valves?
  • Which have chordae tendinae and which don’t?
A

Types of Valves:

  1. Semilunar Valves (Pulmonary and Aortic): Three semilunar cusps of dense connective tissue covered by endothelium with no chordae tendineae
  2. Atrioventricular Valves (Tricuspid and Mitral): Triangular-shaped cusps of dense connective tissue covered by endothelium with chordae tendineae attached to free edges
  • Chordae Tendineae: Attach to cusps of the right tricuspid valve and the left mitral valve to prevent them going back into the atrium
  • Papillary Muscles: Pulls on chordae when ventricle contracts to assist
127
Q

Review anatomy and physiology of heart valves and supporting structures.

  • What is the Triscuspid valve? Which chambers does it connect?
  • Leaflets?
  • Which coronary artery surrounds it?
  • Appearance on ECHO?
A

Anatomy of Heart Valves:

Tricuspid Valve (Right Atrium → Ventricle):

  • Three thin leaflets (anterior, posterior and septal) built for low pressure
  • Multiple chordae and 3-5 papillary muscles (less arranged than the mitral valve)
  • Septal attachments
  • AV junction on medial side of tricuspid annulus near septum
  • Prone to regurgitation from annular and RV dilatation
  • Surrounded by the RCA
  • More apically oriented (towards apex) than mitral on ECHO
128
Q

Review anatomy and physiology of heart valves and supporting structures.

  • What is the Pulmonary valve? Which chambers does it connect?
  • Leaflets?
  • Coronary arteries?
  • Regurgitation?
A

Pulmonary Valve (Right Ventricle → Pulmonary Trunk):

  • Three leaflets (right, left and anterior cusps)
  • No coronary arteries
  • Pulmonary stenosis and/or regurgitation usually congenital
129
Q

Review anatomy and physiology of heart valves and supporting structures.

  • What is the Mitral/Bicuspid valve? Which chambers does it connect?
  • Leaflets?
  • Papillary muscles?
  • Septal attachments?
A

Mitral/Bicuspid Valve (Left Atrium → Ventricle):

  • Two leaflets (anterior and posterior)
  • Two papillary muscles (medial and lateral)
  • No septal attachments
  • Anterior leaflet has as one scallop
  • Posterior leaflet has three scallops (P1, P2, P3 with P1 lateral)
  • Looks like smiley face when open
  • Double kick action for passive flow, diastasis and atrial contraction
  • Medial to the mitral valve is the cardiac crux, the right heart and the conducting system
  • Posterior to the mitral valve is the annulus and pericardial space
130
Q

Review anatomy and physiology of heart valves and supporting structures.

  • What is the Aortic valve? Which chambers does it connect?
  • Leaflets?
  • Coronary arteries?
  • Sound?
A

Aortic Valve (Left Ventricle → Aorta):

  • Three leaflets (right coronary, left coronary and non-coronary cusps)
  • Two coronary arteries in the aortic sinuses
  • Looks like Mercedes sign when closed
  • “Crescendo-decrescendo” blood flow as it increases to peak systole than decreases
  • Anterior to the annulus is the right ventricle (best seen on ECHO)
  • Medial is the right atrium, posterior is the left atrium/mitral valve and lateral is left atrium
131
Q

Surface anatomy for auscultation of the heart valves?

A

Auscultation of Valves:

Aortic Valve Auscultation Point: Right 2nd intercostal space right parasternal edge

Pulmonary Valve Auscultation Point: Left 2nd intercostal space next to sternum

Tricuspid Valve Auscultation Point: Left 4th or 5th intercostal space next to sternum

Mitral Valve Auscultation Point: Left 5th intercostal space at midclavicular line

132
Q

Describe the Physiology of Heart Valves. What happens during:

  • Isovolumetric Contraction
  • Ventricular Contraction and Ejection
  • Isovolumetric Relaxation
  • Ventricular Filling
  • Atrial Contraction
A
133
Q

What are the 5 basic causes of valvular pathology?

A

Basic Causes of Valvular Pathology:

  1. Congenital: Valvular abnormalities
  2. Traumatic: Valve rupture
  3. Infective: Infective endocarditis
  4. Immune: Valvular disease
  5. Degenerative: Age-related changes
134
Q

Predict the key pathophysiological effects of valvular heart disease and relate these to clinical symptoms and signs.

  • What are the Pathophysiological Effects and Clinical Signs and Symptoms (8) of MITRAL REGURGITATION?
A

Valvular Heart Disease - Mitral Regurgitation

  • Pathophysiological Effects: Increased LV EDV → Backflow of Blood from LV → Increased LA Volume → LV and LA Dilation → LV Dysfunction → Reduced CO → CHF and Pulmonary HTN → RV Failure
    • NB: Volume dilates first and then hypertrophies later due to increased filling pressure
  • Clinical Signs and Symptoms
    1. Can be present for many years before symptoms appear
    2. Signs of pulmonary oedema
    3. Signs of peripheral oedema
    4. Palpitations (AF and Increased SV)
    5. Fatigue, lethargy, syncope and presyncope (reduced CO)
    6. Displaced apex
    7. Pansystolic murmur at apex to axillar
    8. Apical systolic thrill
135
Q

What are 11 Causes of Mitral Regurgitation

A

Causes of Mitral Regurgitation

  1. Valve Degeneration: Calcification*, rheumatic**, endocarditis or connective tissue disorders
  2. Dilated Fibrous Ring: Marfan’s or LVF
  3. Fixed Fibrous Ring: Calcification
  4. Leaflet Retraction: Carcinoid syndrome or rheumatic disease
  5. Leaflet Perforation: Infective endocarditis or surgery
  6. Leaflet Prolapse: Mitral valve prolapse (MVP)
  7. Long Chordae Tendinae: MVP Syndrome
  8. Short Chordae Tendinae: Rheumatic or post-MI displacement and leaflet tethering
  9. Ruptured Chordae Tendinae: Downward vegetation growth
  10. Ischaemic/Ruptured/Fibrotic Papillary Muscles: MI and post-MI
  11. Ventricular Abnormalities: Dilated cardiomyopathy or post-MI necrosis and fibrosis
136
Q
  • 1 Cause of Mitral Stenosis?
  • 1 Cause of Mitral Prolapse?
  • 2 Causes of Aortic Stenosis?
A

Mitral Stenosis → Rheumatic Heart Disease

Mitral Prolapse → MVP/Barlow’s/Floppy Valve Syndrome: Connective tissue disorder causing weakened connective tissue of mitral valve, leads to translucent billowing parachute-like leaflets and lengthening and thinning of chordae tendinae

Aortic Stenosis → Congenital: Bicuspid or unicuspid valve & Valve Degeneration: Calcification (old age) or rheumatic

137
Q

6 Causes of Aortic Regurgitation?

A

Causes of Aortic Regurgitation

  1. Congenital: Quadricuspid, bicuspid or prolapsed valve
  2. Valve Degeneration: Calcification, endocarditis, rheumatic or trauma
  3. Cusp Perforation: Infective endocarditis and trauma (chest blow)
  4. Cusp Retraction: Rheumatic valvular disease, carcinoid valvular disease, syphilis and bicuspid aortic stenosis with prolapse of smaller cusp under bigger one
  5. Aortic Root Dilation: Aortic aneurysm, syphilis, rheumatic arthritis, ankylosing spondylitis, giant cell aortitis, Reiter’s syndrome
  6. Aortic Wall Weakening: Marfan’s syndrome, idiopathic and Osteogenic Imperfecta
138
Q
  • 2 Causes of Tricuspid Stenosis and Regurgitation?
  • 1 Cause of Pulmonary Stenosis and Regurgitation?
A
  • Tricuspid Stenosis and Regurgitation
    1. Congenital
    2. Valve Degeneration: Rheumatic or infective endocarditis from IV drug use
  • Pulmonary Stenosis and Regurgitation
    1. Congenital
  • * Calcification normally occurs at the age of 75 or greater, but bicuspid aortic valve can calcify in children ** Rheumatic disease usually results in fusion of cusps resulting in small rigid opening*
  • NB: Diagnosis of valvular disease is through clinical assessment, ECHO and angiography*
139
Q

Outline the pathophysiology of rheumatic heart disease following rheumatic fever.

10 steps

A

Pathophysiology of Rheumatic Fever and Heart Disease:

  1. Exposure to Group A streptococcal bacteria (i.e. S. pyogenes).
  2. Infection with Group A streptococcal bacteria (presents as pharyngitis and sore throat or skin sores).
  3. Host immune system develops delayed autoimmune reaction triggered by molecular mimicry and antigen cross-reactivity between the cell wall M proteins of the infecting S. pyogenes and cardiac myosin and laminin
  4. Activation of auto-reactive lymphocytes
  5. Tissue injury and inflammation, valvular injury and neuronal cell surface targeting leading to cell signalling and dopamine release (Sydenham’s chorea)
  6. Acute Rheumatic Fever (joint swelling and pain (migratory polyarthritis), carditis (myocardial Aschoff body), fever, heart problems, chorea (jerky movements), erythema marginatum (skin rash) and subcutaneous painless nodules on elbows, wrists, knees, ankles and near spine)
  7. Recurrent infection and acute rheumatic fever
  8. Chronic permanent damage to one or more heart valves (stretched and/or scarred) that remains after the episodes of acute rheumatic fever is resolved
  9. Rheumatic Heart Disease that presents with mitral leaflet thickening, commissural fusion and shortening and thickening and fusion of chordae and papillary muscles
  10. Complication of rheumatic heart disease such as valvular disease, heart failure, arrythmias (AF), stroke, endocarditis and pregnancy complications.
140
Q

What are the major criteria for acute rheumatic fever? (Jones)

A
141
Q

What are the major and minor criteria for acute rheumatic fever?

A
142
Q

Predict the key pathophysiological effects of valvular heart disease and relate these to clinical symptoms and signs.

  • What are the Pathophysiological Effects and Clinical Signs and Symptoms (7) of MITRAL STENOSIS?
A

Valvular Heart Disease - Mitral Stenosis

  • Pathophysiological Effects: Obstruction to LV → Increased LA Pressure (Protected LV) → LA Dilatation → Increased Pulmonary Vascular Resistance → Pulmonary HTN and RV Failure → Eventual LV Decreased EDV → Reduced CO and CHF
  • Clinical Signs & Symptoms
    1. No symptoms until the valve is moderately stenosed
    2. Signs of pulmonary oedema
    3. Signs of peripheral oedema
    4. Palpitations (AF)
    5. RV heave
    6. Opening snap and loud S1 sound Mid-diastolic rumble at apex
    7. Mitral facies (rosy cheeks/blue tongue)
143
Q

Compare Mitral Regurgitation and Mitral Stenosis in terms of:

  • Pulse?
  • Apex?
  • Sounds?
  • Murmurs?
  • Mitral Stenosis → Face? RV?
A
144
Q

Predict the key pathophysiological effects of valvular heart disease and relate these to clinical symptoms and signs.

  • What are the Pathophysiological Effects and Clinical Signs and Symptoms (6) of AORTIC REGURGITATION?
A

Valvular Heart Disease - Aortic Regurgitation

  • Pathophysiological Effects: Backflow of Blood from Aorta → Increased LV Volume → LV Dilation → LV Dysfunction → Reduced CO
  • Clinical Signs & Symptoms
    1. Significant symptoms occur late and do not develop until LV failure
    2. Signs of pulmonary oedema Syncope and angina (reduced CO) Palpitations (increased LV size)
    3. Displaced apex
    4. Collapsing pulse
    5. Wide pulse pressure
    6. Decrescendo early-diastolic murmur
145
Q

Predict the key pathophysiological effects of valvular heart disease and relate these to clinical symptoms and signs.

  • What are the Pathophysiological Effects and Clinical Signs and Symptoms (7) of AORTIC STENOSIS?
A

Valvular Heart Disease - Aortic Stenosis

  • Pathophysiological Effects: Outflow Obstruction → Increased LV Afterload → Increased LV Pressure → LV Hypertrophy → LV Dysfunction → Reduced CO → LV Failure → Pulmonary HTN and RV Failure
  • Clinical Signs & Symptoms
    1. No symptoms until aortic stenosis is moderately severe
    2. Exercise-induced syncope, angina, dyspnoea (muscle outgrows oxygen supply)
    3. Signs of pulmonary oedema
    4. Signs of peripheral oedema
    5. Systolic thrill
    6. Systolic ejection click
    7. Mid-systolic crescendo-decrescendo murmur radiating to carotids
146
Q

Compare Aortic Stenosis and Aortic Regurgitation in terms of:

  • Pulse?
  • Apex?
  • Sounds?
  • Murmurs?
A
147
Q

Predict the key pathophysiological effects of valvular heart disease and relate these to clinical symptoms and signs.

  • What are the Pathophysiological Effects and Clinical Signs and Symptoms (3) of TRICUSPID REGURGITATION?
A

Valvular Heart Disease - Tricuspid Regurgitation

  • Pathophysiological Effects: Backflow of Blood from RV → Increased RA Volume → RV and RA Dilation → RV Dysfunction → Systemic Venous Congestion
  • Clinical Signs & Symptoms
    1. Signs of peripheral oedema
    2. Palpitations (AF)
    3. A blowing pansystolic murmur, best heard on inspiration at the lower left sternal edge
148
Q

Predict the key pathophysiological effects of valvular heart disease and relate these to clinical symptoms and signs.

  • What are the Pathophysiological Effects and Clinical Signs and Symptoms (3) of TRICUSPID STENOSIS?
A

Valvular Heart Disease - Tricuspid Stenosis

  • Pathophysiological Effects: Obstruction to RV → Increased RA Pressure → RA Hypertrophy → Systemic Venous Congestion → Eventual Heart Failure and Reduced CO
  • Clinical Signs & Symptoms
    1. Signs of peripheral oedema
    2. Pre-systolic pulsation felt over liver
    3. A rumbling mid-diastolic murmur heard best at the lower left sternal edge and is louder on inspiration
149
Q

Predict the key pathophysiological effects of valvular heart disease and relate these to clinical symptoms and signs.

  • What are the Pathophysiological Effects and Clinical Signs and Symptoms (2) of PULMONARY REGURGITATION?
A

Valvular Heart Disease - Pulomary Regurgitation

  • Pathophysiological Effects: Backflow of Blood from Pulmonary Trunk → Increased RV Volume → RV Dilation → RV Dysfunction → Systemic Venous Congestion
  • Clinical Signs & Symptoms
    1. Usually causes no symptoms
    2. A decrescendo early-diastolic murmur, beginning with the pulmonary component of the second sound that is difficult to distinguish from the murmur of aortic regurgitation
150
Q

Predict the key pathophysiological effects of valvular heart disease and relate these to clinical symptoms and signs.

  • What are the Pathophysiological Effects and Clinical Signs and Symptoms (2) of PULMONARY STENOSIS?
A

Valvular Heart Disease - Pulmonary Stenosis

  • Pathophysiological Effects: Outflow Obstruction → Increased RV Afterload → Increased RV Pressure → RV Hypertrophy → RV Dysfunction → RV Failure → Systemic Venous Congestion and Heart Failure
  • Clinical Signs & Symptoms
    1. Severe pulmonary obstruction is incompatible with life, but lesser degrees of obstruction give rise to symptoms
    2. Fatigue and syncope
    3. Signs of peripheral oedema
    4. RV heave
    5. A harsh mid-systolic ejection murmur, best heard on inspiration, to the left of the sternum in the 2ICS
151
Q

What are the Pathological Features (3) and Complications (8) of:

Infective Endocarditis?

A

Valvular Heart Diseases - Infective Endocarditis

  • Pathological Features
    1. Valvular Vegetations
    2. Perivalvular Abscesses
    3. Impaired Valve Function
  • Complications
    1. Heart murmur, heart valve damage and heart failure
    2. Stroke
    3. Paralysis or paresis
    4. Seizure
    5. Abscesses that develop in the heart, brain, lungs and other organs
    6. Pulmonary embolism
    7. Kidney damage
    8. Enlarged spleen
152
Q

What are the Pathological Features (4) and Complications (6) of:

Valve Stenosis?

A

Valvular Heart Diseases - Valve Stenosis

  • Pathological Features
    1. Narrowed Valve Opening
    2. Calcification
    3. Fibrotic Scarring
    4. Abnormal No. of Cusps/Leaflets
  • Complications
    1. Depends on Site of Valve Damage
    2. LV dysfunction and failure Pulmonary HTN and oedema RV dysfunction and failure
    3. Peripheral oedema
    4. Heart failure
    5. Atrial fibrillation and arrhythmias
    6. Stroke (due to dilated ventricle and transmural thrombus)
153
Q

What are the Pathological Features (6) and Complications of:

Valve Regurgitation?

A

Valvular Heart Diseases - Valve Regurgitation

  • Pathological Features
    1. Impaired Closure of Valve Calcification
    2. Fibrotic Scarring Stretched/Dilated Chamber
    3. Cusp/Leaflet Perforation, Retraction or Prolapse
    4. Short, Long or Ruptured Chordae Tendinae
    5. Ischemic/Ruptured/Fibrotic Papillary Muscles
    6. Vessel Dilation or Wall Weakening
  • Complications
    1. Depends on Site of Valve Damage
    2. As above
154
Q

Outline the principles of primary prophylaxis and secondary prophylaxis (prevention of further episodes of acute rheumatic fever leading to rheumatic heart disease) of acute rheumatic fever.

  • Primordial Prevention? (2)
  • Primary Prevention? (2)
  • Secondary Prevention? (2)
  • Tertiary Prevention? (4)
A

Acute Rheumatic Fever Prevention

  • Primordial Prevention:
    • Reduce overcrowding
    • Improve respiratory and skin hygiene
  • Primary Prevention:
    • Treatment of Group A Streptococcal infection
    • Develop Group A Streptococcal vaccine (not yet developed)
  • Secondary Prevention:
    • Antibiotic prophylaxis (about every 3.5-4 weeks up to the age of 25 or further if necessary)
    • Regular ECHO to detect asymptomatic rheumatic heart disease cases
  • Tertiary Prevention:
    • Medical management of heart failure and complications of rheumatic heart disease
    • Access to surgical interventions for valve lesion
    • ECHO screening of high-risk groups for rheumatic heart disease
    • Access to dental care, contraception and regular clinical review
155
Q

List the risk factors for infective endocarditis (e.g. rheumatic heart disease, prosthetic valves) = 15

A

Infective Endocarditis: An endovascular infection of cardiovascular structures, including cardiac valves, atrial and ventricular endocardium, large intrathoracic vessels and intracardiac foreign bodies (i.e. prosthetic valves, pacemaker leads and surgical conduits).

Risk Factors for Infective Endocarditis:

  1. Infection
  2. Poor dental hygiene
  3. Recent dental treatment
  4. Intravenous drug use
  5. Tattoos and body piercings
  6. Soft tissue infections
  7. Intravascular devices
  8. Cardiac surgery
  9. Permanent pacemakers
  10. Prosthetic heart valves
  11. Co-morbidities such as structural, valvular, rheumatic or congenital heart disease
  12. Chronic hemodialysis
  13. HIV infection
  14. Immunosuppression
  15. History of endocarditis
156
Q

Outline the pathology of infective endocarditis.

A

Pathology of Infective Endocarditis:

  • The presence of organisms in the bloodstream (episode of bacteremia)
  • Abnormal cardiac endothelium facilitating their adherence and growth
    1. Endothelial damage can be due to aberrant jet streams and turbulent flow in the setting of diseased cardiac valves and septal defects or direct trauma from intravascular devices
    2. Damaged endocardium promotes platelet and fibrin deposition which allows organisms to adhere and grow, leading to an infected vegetation
    3. Aortic and mitral valves are most commonly involved in infective endocarditis apart from intravenous drug users in whom right-sided lesions are more common
157
Q

Outline the microbiology of infective endocarditis.

A

Microbiology of Infective Endocarditis:

  • Streptococci spp. (50-80% of Cases): S. viridans normally found in the upper aerodigestive tract, may disseminate during tonsillectomy, dental extraction, dental cleaning resulting in bacteremia. S. viridans causes subacute and chronic bacterial endocarditis.
  • Staphylococci spp. (20-30% of Subacute and 50% of Acute Cases): S. aureus and S. epidermidis common in patients with indwelling central venous catheters, IVDA, diabetes, chronic haemodialysis and prosthetic valve endocarditis. Staphylococcal endocarditis can affect functionally normal native valves and cause extensive tissue damage and septic emboli. Prosthetic valve endocarditis is mainly due to coagulase negative staphylococci (S. epidermidis). S. aureus causes acute bacterial endocarditis.
  • Enterococci spp. (5-15% of Cases): S. faecalis, S. bovis and S. faecium
  • HACEK Organisms: Haemophilus parainfluenza, Haemophilus aphrophilus, Actinobacillus (Haemophilus) actinomycetemcomitans, Cardiobacterium hominis, Eikenella species, and Kingella species
  • Less Common Organisms: Candida, Aspergillus, Histoplasma, and Brucella (common in IVDA, alcoholics, and patients with prosthetic heart valves)
158
Q

What are the Manifestations of Infective Endocarditis?

  • Systemic Inflammatory Effects? (9)
  • Vascular Phenomena? (4)
  • Immunological Phenomena? (3)
A

Manifestations of Infective Endocarditis

  • Systemic Inflammatory Effects
    1. Fever (with no obvious source)
    2. Elevated CRP and ESR Increased WCC
    3. Anaemia
    4. Haemolysis
    5. Microscopic haematuria
    6. Other markers (lactate, low platelets, renal impairment, low complement)
    7. Arthralgia
    8. Malaise
    9. Splenomegaly and tender spleen Weight loss
  • Vascular Phenomena
    1. Emboli
    2. Janeway lesions (blanching non painful erythematous lesions on palms and soles)
    3. Splinter hemorrhages (nail and conjunctiva)
    4. Skin petechiae
  • Immunological Phenomena
    1. Osler’s Nodes (painful nodules on fingertips)
    2. Roth Spots (retinal hemorrhages)
    3. Glomerulonephritis (haematuria)

NB: Vascular effects are due to septic emboli whilst immunological effects are due to immune complex depositions

NB: Other manifestations also include murmurs, dyspnoea and chest pain

159
Q

What are 8 complications of Infective Endocarditis?

A

Infective Endocarditis - Complications: Depends on valve and exact location of vegetation

  1. Heart problems such as heart murmur, heart valve damage and heart failure
  2. Stroke
  3. Paralysis or paresis
  4. Seizure
  5. Abscesses that develop in the heart, brain, lungs and other organs
  6. Pulmonary embolism
  7. Kidney damage
  8. Enlarged spleen
160
Q

Outline the prophylaxis (7) and prevention (5) of infective endocarditis.

A

Prophylaxis and Prevention of Infective Endocarditis:

  1. Antibiotic Prophylaxis:
    1. Prosthetic heart valves
    2. Congenital heart disease or surgery
    3. Prior endocarditis
    4. Heart transplant
    5. Rheumatic heart disease in indigenous patients
    6. Tooth extraction or reimplantatio
    7. Periodontal procedures or dental surgery such as implants
  2. Avoid high risk behaviours (IV drug use or tattoos)
  3. Maintain good dental hygiene
  4. Identify and treat underlying bacteraemia early
  5. Manage comorbidities such as HIV and structural, valvular, rheumatic or congenital heart disease
161
Q

What are the Diagnostic Criteria for Infective Endocarditis?

(Modified DUKE Criteria)

A

Diagnosis of Infective Endocarditis: Modified DUKE Criteria

  • Major Criteria: Positive blood cultures (before antibiotics administered) and/or cardiac imaging (transoesophageal imaging) showing vegetation, abscess or other signs
  • Minor Criteria:
    1. Predisposing factors such as valve replacement or intravenous drug use
    2. Fever greater than 38 degrees
    3. Vascular phenomena such as emboli, haemorrhages, or Janeway lesions
    4. Immunological phenomena such as Osler’s nodes, Roth’s spots and rheumatoid fever
162
Q

Diagnostic Criteria for:

  • Definite IE?
  • Possible IE?
  • Rejected IE?
A
163
Q

List common antibiotics used for infective endocarditis.

Principles? (4)

A

Common Antibiotics for Infective Endocarditis: Usually 4-6 Weeks of IV therapy (two weeks in hospital)

  1. Broad Spectrum: IV Penicillin (1.8 g 4 hourly) and Gentamicin (4 mg/kg/d) and Vancomycin (MRSA)
  2. Prosthetic Valve or MRSA Risk: Vancomycin
  3. Specific IV Antibiotics: Target to specific bacteria

Principles of Antibiotic Treatment:

  1. Initially start with broad spectrum to relieve fever and signs of sepsis, then change when the exact organism is known
  2. If stable, wait for definitive organism first
  3. If unstable, treat immediately after blood cultures
  4. Once the bug is known, choose the right antibiotic for the bacteria and start intense IV therapy in hospital
164
Q

Outline the mechanisms of fever production. (7)

A

Mechanisms of Fever Production:

  1. Tissue inflammation via infection, trauma, autoimmunity, hemorrhage, tumours, thrombosis and heat stroke
  2. Macrophages or monocytes release pyrogens/cytokines (IL-1B, TNF-a and IL-6)
  3. Cytokines induce cyclooxygenases 2 (COX-2) that convert arachidonic acid into prostaglandins
  4. This results in increased production of prostaglandins in the vascular and perivascular cells of the hypothalamus
  5. Prostaglandins (specifically PGE2) stimulates the production of neurotransmitters
  6. Neurotransmitters reset the temperature set point at a higher level
  7. Increased metabolic rate, rigors and peripheral vasoconstriction help the body generate and conserve heat
165
Q

Describe the Lifecycle of Plasmodium - Exo-Erythrocytic Cycle? (4)

A

Lifecycle of Plasmodium:

Exo-Erythrocytic Cycle

  1. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host
  2. Sporozoites infect liver cells which begins the exo-erythrocytic stage of the life cycle where asexual multiplication occurs
  3. Within hepatocytes sporozoites mature into schizonts in the liver
  4. Schizonts rupture and release merozoites into circulation, ending the exo-erythrocytic cycle

NB: In the case of P. vivax and P. ovale, a few parasites remain dormant in the liver as hypnozoites which may reactivate at any time causing relapsing infection

166
Q

Describe the Lifecycle of Plasmodium - Erythrocytic Cycle? (5)

A

Lifecycle of Plasmodium -** **Erythrocytic Cycle

  1. The merozoites invade RBCs where they undergo another asexual cycle called the erythrocytic cycle
  2. During this stage the merozoites develop to form immature or ring stage trophozoites which then progress to mature trophozoites
  3. The mature trophozoites develop into schizonts
  4. At the end of the erythrocytic cycle, the infected RBCs burst, releasing the merozoites
  5. At this stage, merozoites can either infect new RBCs to begin the erythrocytic cycle again, or they can develop into gametocytes
167
Q

Describe the Lifecycle of Plasmodium - Sporogonic Cycle? (5)

A

Lifecycle of Plasmodium - Sporogonic Cycle

  1. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal, beginning the sporogonic cycle
  2. While in the mosquito’s stomach, the microgametes fertilise the macrogametes generating zygotes
  3. The zygotes become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts
  4. The oocysts grow, rupture, and release sporozoites which go to the mosquito’s salivary glands
  5. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle
168
Q

What is the Epidemiology of Malaria?

A

Epidemiology of Malaria:

  • In 2017, there were 219 million cases of malaria in 90 countries
  • In 2017, malaria deaths reached 435,000
  • Africa carries a disproportionately high share of the global malaria burden. In 2017, the region was home to
  • 92% of malaria cases and 93% of malaria deaths.
  • Malaria endemic areas include Africa, South America, and Asia (tropical and sub-tropical areas)
169
Q

What is the Pathogenesis of Malaria? (7)

A

Pathogenesis of Malaria:

  1. Host becomes infected with Plasmodium sporozoites via a bite from an infected anopheline mosquito
  2. Plasmodium spp. invade RBCs and digest hemoglobin. As hemoglobin is digested, a toxic metabolite hemozoin (a polarizable crystal) is produced.
  3. The intracellular parasites modify the erythrocytes in several ways
    1. They derive energy from anaerobic glycolysis of glucose to lactic acid (hypoglycaemia and lactic acidosis)
    2. Parasites reduce RBC membrane deformability, resulting in hemolysis and accelerated splenic clearance (splenomegaly and anaemia)
    3. Alterations to uninfected RBCs, such as the addition of P. falciparum glycosylphosphatidylinositol (GPI) to the membrane, may play a role in increased clearance of uninfected cells (anaemia)
  4. Once RBCs rupture (according to the parasite life cycle), cell membrane remnants and the hemozoin crystal are phagocytised by circulating macrophages
  5. Activated macrophages release pro-inflammatory cytokines such as TNF-a, IFN-y, IL-1, IL-6 and IL-8
  6. Cytokines results in headache, fever and rigors, nausea and vomiting, diarrhea, anorexia, tiredness, aching joints and muscles, thrombocytopenia, immunosuppression, coagulopathy, and central nervous system manifestations
  7. In P. falciparum malaria, RBCs containing schizonts adhere to the lining of capillaries in the brain, kidneys, gut, liver and other organs which can cause mechanical obstruction and rupture, releasing toxins and stimulating further cytokine release
170
Q

9 Clinical Features of Malaria?

A

Clinical Features of Malaria:

  1. Fever (paroxysmal)
  2. Headache
  3. Malaise
  4. Chills
  5. Fatigue
  6. Abdominal pain
  7. Vomiting and/or diarrhoea
  8. Hepatosplenomegaly
  9. Anaemia
  • Incubation period is 10–21 days, but can be longer
  • In cases with P. vivax and P. ovale, relapses may occur weeks or months after being infected
  • P. falciparum symptoms are more severe and include behavioural changes, confusion, seizures, anaemia, respiratory failure, kidney failure, coma and shock
  • If not treated immediately, P. falciparum malaria can lead to death
171
Q

Prevention for malaria? (3)

A

Prevention:

  1. Antimalarial medication
  2. Anti-mosquito sprays or lotions
  3. Sleeping under a permethrin-treated bed net
172
Q

Discuss causes of fever in travellers, including: a). Malaria; b). Dengue; c). Typhoid; d). Hepatitis; e). Diarrhoeal illness

  • Causative pathogen for each?
  • Route of transmission for each?
A

Causes of Fever in Travellers:

Malaria: Infection with plasmodium spp. (P. falciparum, P. vivax, P. ovale, P.malariae) following a female Anopheles mosquito bite

Dengue: Infection with dengue virus (four different antigenic varieties) transmitted by the daytime-biting Aedes aegypti mosquito or Aedes albopictus mosquito (less common), which breed in standing water in refuse dumps in inner cities in tropical and subtropical areas

Typhoid: Infection with Salmonella Typhi transmitted via faecal-oral route such as with contaminated water or food, or close contact with infected prson

Hepatitis: Infection with Hepatitis A or E virus via faecal-oral route (contaminated food or water) or infection with Hepatitis B, C or D via exchange of blood or body fluids (tattoos, sex, needles, transfusion, mother)

Diarrhoeal Illness: Infection with gastrointestinal pathogen such as S. auerus, B. cereus, C. perfringens, C. botulinum, C. difficile, E. coli, V. cholera, C. jejuni, Salmonella spp., Shigella spp., Rotavirus or Norovirus through contaminated food or water

173
Q

Explain the approaches to diagnosis for each of the common causes of fever in travellers.

A
174
Q

Explain the approaches to diagnosis for each of the common causes of fever in travellers.

A
175
Q

Which infectious diseases are more common in each continent?

A
176
Q
A
177
Q

What are Cardiac Thrills?

What are Cardiac Murmurs?

A

Thrills: Palpable murmurs

Murmurs: Abnormal heart sounds due to turbulent blood flow across heart valves or vascular abnormalities

178
Q
  • Pansystolic = 4
  • Midsystolic = 4
  • Late systolic = 2
  • Early diastolic = 2
  • Mid-diastolic = 5
A
179
Q
  • Presystolic = 3
  • Continuous = 5
A
180
Q

What 6 things should be documented with a cardiac murmur?

A

Cardiac Murmurs

  1. Timing and Duration
  2. Intensity → Crescendo: Increasing intensity, Decrescendo: Decreasing intensity, Crescendo-Decrescendo: Diamond-shaped
  3. Area of Greatest Intensity and Radiation
  4. Grading (Loudness and Harshness): Levine’s Grading System
  5. Presence of a Thrill
  6. Changes During Respiration or with Dynamic Manoeuvres
181
Q

What is the timing and duration of different cardiac murmurs:

  • Systolic Murmur
  • Diastolic Murmur
  • Pan/Holo-Systolic
  • Mid-Systolic
  • Late Systolic
  • Early Diastolic
  • Mid-Diastolic
  • Pre-Systolic
  • Continuous Murmur
A

Cardiac Murmurs - Timing and Duration:

  • Systolic Murmur: Occur between S1 and S2
  • Diastolic Murmur: Occur between S2 and S1
  • Pan/Holo-Systolic: Lasting for all of systole
  • Mid-Systolic: Starts after S1 and ends before S2, in crescendo-decrescendo manner
  • Late Systolic: Starts after S1 and extends up to S2, usually in a crescendo manner
  • Early Diastolic: Starts immediately after S2 and extends through diastole, in a decrescendo manner
  • Mid-Diastolic: Starts later in diastole after S2 and may be short or extend right up to S1
  • Pre-Systolic: Just before S1
  • Continuous Murmur: Lasting for all of diastole and systole
182
Q

What is the area of greatest intensity and radiation for each of the cardiac murmurs?

A

Area of Greatest Intensity and Radiation

183
Q

How are Cardiac Murmurs Graded?

A

Grading (Loudness and Harshness): Levine’s Grading System

  • Grade 1/6: Very soft and not heard at first (often audible only to consultants and to those students who have been told the murmur is present)
  • Grade 2/6: Soft, but can be detected almost immediately by an experienced auscultator
  • Grade 3/6: Moderate, there is no thrill
  • Grade 4/6: Loud, thrill just palpable
  • Grade 5/6: Very loud, thrill easily palpable
  • Grade 6/6: Very, very loud, can be heard even without placing the stethoscope on the chest
184
Q

What are 3 types of added cardiac sounds?

A

Added Sounds:

Extra S3 Sound (“Kentucky”): Low-pitched mid-diastolic sound indicative of increased ventricular filling due to reduced ventricular compliance

Extra S4 Sound (“Tennessee”): Late diastolic sound indicative of increased ventricular filling, due to a high- pressure atrial wave reflected back from a poorly compliant ventricle

Systolic Ejection Click: An early systolic high-pitched sound that is heard over the aortic or pulmonary and left sternal edge areas due to the abrupt doming of the abnormal valve early in systole
Example: Aortic stenosis or pulmonary stenosis

185
Q

Demonstrate familiarity with basic features of cardiac ultrasound examination (and linking with anatomy) showing abnormal valve function.

  • Which 7 features should be assessed on cardiac ultrasound?
A

Features of Cardiac Ultrasound:

  1. Structure of valves
  2. Size of chambers
  3. Wall motion and contraction
  4. Direction and velocity of blood flow (regurgitation/stenosis)
  5. LV wall thickness
  6. E/A Ratio: Marker for the function of the LV and represents the ratio of peak velocity blood flow from gravity in early diastole (the E wave) to peak velocity flow in late diastole caused by atrial contraction (the A wave)
  7. Bernoulli Equation: ∆P = P2-P1 = 4(V22 – V12) which calculates pressure gradient from velocity to assess degree of obstruction of valves (often used for aortic stenosis)
186
Q

Label the heart chambers/valves.

A
187
Q
A
188
Q
A
189
Q
A

YR2 BCS Study Points SEM 1 (7 decks)

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