Cardiology Flashcards

1
Q

Definition of heart failure?

A

Failure of the body to maintain a cardiac output that can accommodate metabolic demands.

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2
Q

5 main causes of heart failure?

A
Coronary artery disease
Hypertension
Valvular heart disease
Cardiomyopathy
Cor Pulmonale
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3
Q

How to calculate Cardiac Output?

A

Heart Rate x Stroke Volume

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4
Q

Three main components of the neurohormonal component of cardiovascular regulation?

A

RAAS system
Sympathetic nervous system
Vasopressin (ADH)

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5
Q

Role of the sympathetic nervous system in Heart Failure?

A

Increased cardiac sympathetic activity activates β₁ β₂ and α₁ leads to increased cardiac toxicity and arrhythmias.

Increased sympathetic activity to the kidneys leads to stimulation of α₁, and β₁ (Leading to activation of RAAS) Increased BP

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6
Q

What is hBNP?

A

Brain Natriuretic Peptide

Predominantly found in cardiac ventricles

vasodilatory and Diuretic properties.

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7
Q

Effects of hBNP?

A

Dilation of veins and arteries

Decreased Noradrenaline and aldosterone

Increased Diuresis & Natriuresis

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8
Q

Some endothelium derived Vasodilators?

A

NO

Bradykinin

Prostacyclin

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9
Q

Endothelium derived vasoconstrictor?

A

Endothelin I

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10
Q

Symptoms (NOT SIGNS) of Left Ventricular Failure?

A

Dyspnoea on exertion

Nocturnal Dyspnoea

Orthopnoea (SOB when lying flat)

Cough

Haemoptysis (coughing up blood)

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11
Q

Signs (NOT SYMPTOMS) of Left ventricular

A

Basal Lung Crackles

Tachycardia

S3 Gallop (heart sound)

Pleural effusion

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12
Q

Right ventricular failure Symptoms (not signs)?

A

Abdominal pain

Anorexia

Nausea

Bloating

swelling

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13
Q

Right Ventricular failure Signs (not symptoms)?

A

Peripheral oedema

Jugular venous distension

Hepato-jugular reflex

Hepatomegaly

Ascites

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14
Q

Class I, II, II and IV classifications of heart failure?

A

I: No symptoms with ordinary activity

II: Slight limitation with physical activity

III: Marked limitation with physical activity

IV: Unable to carry out any physical activity with discomfort, symptoms may be present at rest.

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15
Q

5 year mortality rate after heart failure diagnosis?

A

50%

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16
Q

Diagnostic techniques used to evaluate New onset heart failure?

A

ECG

Chest X-Ray

Blood-Test

Echocardiography

17
Q

Uses of Diuretics in heart failure?

A

Used to Relieve fluid retention

Decrease Bloop Pressure

Improved exercise tolerance

Facilitate the use of other drugs used for heart failure

18
Q

Drugs to use in Heart failure?

A

Diuretics

ACE inhibitors

Angiotensin Receptor Blockers

Beta-Blockers

Aldosterone antagonists

Digitalis Glycosides

19
Q

What is automaticity in pacemaker cells?

A

A pacemakers cell’s ability to spontaneously depolarise, and propagate an Action potential.

20
Q

Where do sympathetic and parasympathetic innervation act in the heart?

A

SA node, pretty much no effect on lower pacemakers.

21
Q

What are the three pacemakers of the heart?

A
SA node (normal)
- 60-100 min-1

AV node
- 40-60 min-1

Purkinje fibres
- 20-40 min-1

22
Q

Three main mechanisms leading to the generation of arrhythmias?

A

Enhanced automaticity

Re-Entry

After depolarisation

23
Q

How can enhanced automaticity generate an arrhythmia?

A

If a lower pacemaker becomes faster than a higher pacemaker then this one will start to take over and the heart will not contract rhythmically.

24
Q

How can re-entry generate an arrhythmia?

A
  1. Slow conduction causes a short refractory period and this means the myocyte is able to receive new impulses
  2. There is rapid conduction and a long refractory period meaning the myocyte cannot receive new impulses

If there are two pathways next to each other firstly the beat cannot gain entry to the rapid conduction pathway as it has not recover and so will travel down the slow one, when it reaches the end of the slow it can now travel back up the rapid one and will cause a circular pathway of contraction.

25
Q

Examples of re-entry arrhythmias?

A

Macro-reentry: Wolf-Parkinson White

Micro-reentry: Atrial fibrillation

26
Q

What can arrhythmias present with?

A

Syncope (blackouts)
Palpitations
Angina
Dyspnoea

27
Q

What four things do you use to clinically classify arrhythmias?

A

Heart rate (tchy/bradycardic)
Rhythm (regular/irregular)
Site (supraventricular/ventricular)
QRS complex of an ECG (narrow/broad)

28
Q

How can you tell whether an arrhythmia is supraventricular or ventricular?

A

Supraventricular if the QRS is narrow.

29
Q

Types of atrial ectopic beats?

A

Isolated ectopic beat

Atrial tachycardia

Atrial flutter (atria not really beating)

Atrial fibrillation (atria not contracting at all)

30
Q

What does it mean in an ECG if the p-wave is negative?

A

That the AV node is depolarising from the bottom up

31
Q

Examples of ventricular ectopic beats?

A

Ventricular tachycardia

Ventricular fibrillation (dead unless defibrillated)

Heart block

32
Q

Types of heart Block?

A

First Degree: AV node very slow to conduct resulting in very long PR interval

Second degree:

  • Mobitz I: Some P waves are generated but not conducted
  • Mobitz II: This is pathological, not every P-wave is conducted but there is a rhythm to which ones are and a set PR interval.

Third degree heart block: No conduction to ventricles at all, the purkinje fibres become the pacemakers

33
Q

What’s asystole?

A

No heart contraction.

34
Q

Four main anti-arrhythmic drug classes?

A

Sodium channel blockers
Beta adrenoceptor blockers
Potassium channel blockers
Calcium channel blockers

35
Q

Mechanism of action of beta-adrenoceptor blockers?

A

Suppression of abnormal pacemakers

36
Q

Mechanism of action of potassium channel blockers?

A

Tissue remains in refractory period for longer

37
Q

Mechanism of calcium-channel blockers?

A

Decrease automaticity in supraventricular tissues.

38
Q

5 things to look out for during a CV examination, when measuring someone’s pulse?

A
Volume
Rate
Character
Rhythm
Quality
39
Q

What are the changes to the ECG in a STEMI?

A

ST elevation

Deep Q wave

Negative T wave in late STEMI