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MS1 > Week 4 Cardiology > Flashcards

Week 4 Cardiology Flashcards

1
Q

Depression Vs Cardiac Blues

A
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2
Q

Infective triggers for inflammatory heart disease

A

Bacterial, fungal, viral, parasitic

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3
Q

Non-Infective causes of inflammatory heart disease

A

Often autoimmune disease
Also hypersensitivity to medications, toxins or allergens

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4
Q

Endocarditis

A

Inflammation of the endocardium; characterised by vegetations composed of platelets, fibrin, microorganisms, and inflammatory cells, affects heart valves.

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5
Q

Myocarditis

A

Inflammation of the myocardium, presenting with myocardial necrosis or fibrosis,

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6
Q

Pericarditis

A

Inflammation of the pericardium, often presents with sharp pleuritic chest pain, pericardial effusion, and diffuse ST-elevation on ECG. Also elevated serum Troponin levels

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7
Q

Rheumatic heart disease

cause, effects, symptoms

A

-starts from Sterptococcus group a infection
-antibodies mistakenly attack and damage heart tissues especially valves
-causes scaring and inflammation or heart valves leading to stenosis (narrowing) or leaking (regurgitation)``
Symptoms include: Dyspnoea, Chest Pain, Fatigue and palpations

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8
Q

SA node location

A

Between superior venal cava and right atrium

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9
Q

AV node location

A

Border between right atrium and Right ventricle

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10
Q

Bundle of His location

A

Within the right atrium

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11
Q

Bundle branches location

A

In the subendocardial layer of the intraventicular septum

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12
Q

Cardiac Conduction system

A
  1. Resting membrane potential of -70mV
  2. Slow influx of Na+ deploarises membrane
  3. T-Type Ca2+ channels open, resulting in further depolarisation
  4. L-Type Ca2+ channels open, further depolarisation
  5. Membrane potential exceeds thresholds action potential occurs
  6. K+ channels open, efflux of K+ ions initiates hyper polarisation
  7. Hyper polarisation opens If (funny) Channels, resulting in slow influx of Na+ (restarts)
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13
Q

Pacemaker cells

A

Located in the SA and AV nodes, these cells generate spontaneous action potentials that initiate the heart’s electrical activity.

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14
Q

Cardiomyocytes

A

The muscle cells of the heart, responsible for the contractile force that pumps blood throughout the body.
Also allow propagation of electrical signals

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15
Q

Heart electrical signal propagation

A
  1. Electrical signal originates in SA
  2. Signal rapidly spreads across atria, causing atrial contraction
  3. Impulse reaches AV node, where it is briefly delayed, allowing ventricles to fill
  4. Signal travels down bundle of his, bundle branches and then to the Purkinje fibres that disturbed the signals through the ventricular myocardium
  5. Ventricular contraction
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16
Q

Excitation-Contraction Coupling

A
  1. Action poetical depolarise the sarcolemma (Cardiomyocyte Cell Membrane)
  2. Triggers opening of voltage gated L type calcium channels —> Ca2+ enters cell
  3. Induces further realse of Ca2+ from Sacroplasmic reticulum
  4. Intracellular Ca2+ binds to troponin, exposing actin binding sites for myosin, leading to muscle contraction
  5. Relaxation as Ca2+ is pumped out of the cell
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17
Q

Phase 0 of action potential in Cardiac cells

A

Depolarisation
- Initiated by rapid influx of sodium ions through voltage gated Na+ channels leading to sharp rise in membrane potential

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18
Q

Phase 1 Of Action potential in Cardiac cells

A

Initial Repolairsation
- Occurs as Na+ channels close and transient outward potassium (K+) channels
open, causing a brief, partial repolarisation.

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19
Q

Phase 2 of action potentials in cardiac cells

A

Plateau phase
- is characterised by a balance between the inward flow of calcium (Ca2+) ions through
L-type Ca2+ channels and the outward flow of K+, maintaining a prolonged depolarised state crucial for muscle
contraction.

20
Q

Phase 3 of action potentials in Cardiac Cells

A

Repolarisation
- happens as Ca2+ channels close and delayed rectifier K+ channels open, allowing K+
to exit the cell and restoring the membrane potential toward its resting state.

21
Q

Phase 4 of action potentials in cardiac cells

A

Resting Potential
- Na+/K+ pump keeps membrane at a stable, negative resting potential until next action potential

22
Q

Modification of Action Potential generation in the SA node

A
  • Without control would do 100-110 action potentials per min
  • Parasympathetic NS works as a break
  • Acetylcholine is released from Parasympathetic nerve fibres and travels along the vagus nerve to reduce heart rate
23
Q

Parasympathetic stimulation of cardiac action potentials

A

increases K+ currents and causes hyperpolarisation and slows depolarisation (i.e. moves the membrane potential away from the threshold).

24
Q

Sympathetic stimulation of cardiac action potentials

A

increases Ca2+ currents and causes faster depolarisation (i.e., the membrane potential is moved closer to the threshold).

25
Q

Atrial Fibralation - ECG findings

A
  • Irregulary Irregular Heart Beat
  • No Discenerable P waves
26
Q

Types of Atrial Fibralation

A
  • Paroxysmal; Spontaneously Terminates (<7 Days)
  • Persistant; Lasts >7 days or requires cardioversion
  • Long Standing Persistant; >12 Months
  • Permanent; continous, attempts to resotre sinus rhythym have been abandonded
27
Q

Atrial Fibralation - Risk Factors

A
  • Age
  • Hypertension
  • Obesity
  • Alcohol Intake
  • Family History
  • Cardiac Disease
28
Q

Atrial Fibralation Symptoms

A
  • Palpitations
  • Dyspnoea
  • Excercise intolerance
  • Fatigue
  • Chest Discomfort
  • Dizziness
  • Syncope
  • NB: ~40% of ppl report no symptoms
29
Q

Treatment of Atrial Fibralation

A
  • Control Heart Rate; <110bpm, done with beta blockers or calcium channel blockers
  • Rythym Control catheta albation + anti coags
  • Anti coags reduce stroke risk
  • Risk Factor Management eg exercise perscription or weight loss
30
Q

Sick Sinus Syndrome

A

Includes:
* Persistent sinus bradycardia
* Sinus arrest or block
* Combinations of SA and AV node abnormalities

31
Q

Common forms of bradyarryhthmia

A
  • Sinus Bradycardia
  • Sinus Arrhythmia
  • Sinus Node Aging
  • Sick Sinus Syndrome
32
Q

Sinus Bradycardia

A

Below 50 BPM
Causes:
* High Vagal tone/ decreased sympathetic tone
* Sinus node dysfunction or remodeling
* Effects of medication
NB: doesn’t matter unless accompanied by other symptoms

33
Q

AV Block

A

Atrial impulse is delayed or not conducted to ventricles
3 Categories
* 1st Degree: prolonged time for conduction (>200ms PR interval)
* 2nd Degree (I): progressive lengthening of conduction until no impulse is conducted
* 2nd Degree (II): Intermittent block of conduction without prior lengthening
* 3rd Degree: Complete dissociation between atrial and ventricular impulses Needs urgent pacemaker, on ECG PR intervals not coupled with QRS

34
Q

Basic management of bradyarrhythmias

A

Pacing using a pacemaker

35
Q

Sudden Cardiac Death

A

A sudden and unexpected death occurring within an hour from the onset of symptoms , or patients found dead within 24hrs of being asymptomatic and assumed to be cardiac arrhythmia or haemodynaic collapse

36
Q

Cardiac causes of SCD

A
  • Coronary Artery disease (CAD) ~70-50%
  • Cardiomyopathies ~15-35%
  • Inherited Arrhythmias ~2-10%
  • Valvular heart disease ~1-5%
37
Q

Reversible causes of SCD (sudden cardiac death)

A

4 H’s & 4T’s
* Hypoxia
* Hypovolaemia
* Hypokalaemia
* Hypothermia/Hyperthermia
* Tension pneumothorax
* Toxins
* Tamponade
* Thrombosis (pulmonary/coronary)

38
Q

Forms of Ventricuar arrhythmia

A

Sustained Ventciular Tachycardia
Non Sustained Ventricular Tachycardia
Polymorphic Ventricular Tachycardia
Torsades de Pointes (Ballerina)

39
Q

Sustained Ventricular Tachycardia

A

Cardiac arrhythmia of more than 3 complexes, more than 100BPM, lasts more than 30s

40
Q

Non Sustained Ventrciular tachycardia

A

Cardiac arrhythmia of >3 consecutive complexes; >100BPM; terminates spontaneously <30s

41
Q

Polymorphic Ventricular Tachycardia

A

Multiform QRS from beat to beat —> indicates ischemia

42
Q

Torasdes de Pointes

A

Long QT segment, polymorphic, twisting of points

43
Q

Diagnoses of Ventricular Arrhythmias

A
  • Heart Rate and regularity
  • JVP
  • Elevated BP
  • Murmurs
  • Oedema
  • Sternotomy scars
    ECG
  • wide QRS complex, not preceded by p waves
44
Q

Vichrow’s triad

A

Atrial Fibralation Leads to:
* Blood Stasis (due to Atrial enlargement and atrail hypocontractility)
* Hypercoaugubility
* Endothelial Damage

This Leads to thrombis formation in the atria, thrombus travels from the atria to the brain causing an ischmeaic stroke

45
Q

CHA2DS2VAS

A
  • Congestive Heart Failure +1
  • Hypertension +1
  • age (75+) +2
  • Diabetes +1
  • Stroke +2
  • Vascular disease +1
  • age (65-74) +1
  • Sex +1

Treat with anticoaugulant at 1 if male, 2 if female

MS1 (12 decks)

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