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The development of cardiorespiratory disease > PBL 48 > Flashcards

PBL 48 Flashcards

1
Q

Explain the action potential through the SAN/AVN

A

Phase 4:

  • Pacemaker Na+ influx (If)
  • Ca2+ channels recover from inactivation
  • Pumps restore ion gradients

Phase 0:
- Ca2+ influx

Phase 3:

  • Ca2+ channels inactivate
  • Delayed K+ efflux
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2
Q

Explain the action potential through myocytes

A
  1. Phase 4: RESTING POTENTIAL
    - Na+ and Ca2+ channels recover from inactivation
    - Pumps restore ion gradients
  2. Phase 0: RAPID UPSTROKE
    - Na+ influx
  3. Phase 1: EARLY RAPID REPOLARISATION
    - Na+ channel inactivation
    - Fast K+ efflux = depolarisation
  4. Phase 2: PLATEAU
    - Ca2+ influx and K+ efflux balance each other out
  5. Phase 3: FINAL REPOLARISATION
    - Ca2+ channels inactivate
    - Delayed K+ efflux
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3
Q

Explain the process of cardiac contraction (cardiac cycle)

A
  1. Atrial contraction (atrial systole begins)
    - Atrial contraction increases pressure in the atria, this causes the rest of the blood to enter the ventricles
  2. Isovolumic contraction
    - Contraction of the ventricles begins which closes the AV valves due to pressure build up
  3. Ventricular contraction
  4. Ventricular ejection
    - Ventricular pressure is now high enough to open the SL valves causing blood to leave the ventricles
  5. Isovolumic relaxation
    - Ventricles relax and pressure begins to drop causing the SL valves to close and blood to enter the coronary circulation.
    - Blood also begins to enter the atria
  6. Ventricular filling
    - Both sets of atria are relaxed and passive ventricular filling occurs
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4
Q

What is the Vaughan-Williams classification of drugs?

A

A method of classifying anti-arrhythmic drugs

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5
Q

Explain the different classes of vaughan-williams classes

A

Class I: SODIUM CHANNEL BLOCKERS (1a, 1b and 1c)

Class II: Beta blockers

Class III: Potassium channel blockers

Class IV: Calcium channel blockers

Class V: Agents that work by other or unknown mechanisms

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6
Q

Explain the difference between class 1 agents and their effects on the AP

A
  • Sodium channel
    1a: moderate reduction in phase 0 slope, reduced AP duration and increased effective refractory period

1b: small reduction in phase 0 slope, reduced AP duration and decreased effective refractory period
1c: PRONOUNCED reduction in phase 0 slope, no effect on AP duration or effective refractory period

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7
Q

Examples and side effects of class 1a sodium channel blockers

A

Quinidine, disopyramide, procainamide

  • Side effects: tachycardia, dry mouth, urinary retention, blurred vision and constipation
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8
Q

Examples and side effects of class 1b sodium channel blockers

A

Lidocaine, phenytoin, mexiletine

Side effects: tachycardia, dry mouth, urinary retention, blurred vision and constipation

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9
Q

Examples and side effects of class 1c sodium channel blockers

A

Flecainide and propafenone

Side effects: tachycardia, dry mouth, urinary retention, blurred vision and constipation

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10
Q

Explain the mechanism of class 1a medications and when are they used

A

Mechanism: inhibits sodium influx through cell membrane, causes slowing of the rate and amplitude of initial rapid depolarisation, reduces cell excitability and conduction velocity

  • Used in treatment of life-threatening ventricular arrhythmias, restoration of normal sinus rhythm and treatment of AF and flutter
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11
Q

Explain the mechanism of class 1b agents and when they are used

A

Mechanism: inhibits sodium influx through cell membrane, causes slowing of the rate and amplitude of initial rapid depolarisation, reduces cell excitability and conduction velocity

  • Used for atrial/ventricular fibrillation, atrial flutter and ventricular tachycardia
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12
Q

Explain the mechanism of class 1c agents and when they are used

A

Mechanism: inhibits sodium influx through cell membrane, causes slowing of the rate and amplitude of initial rapid depolarisation, reduces cell excitability and conduction velocity

  • Used in treatment of paroxysmal and persistent AF
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13
Q

Which patients are beta-blockers contraindicated in?

A
  • ASTHMA (they cause bronchoconstriction)
  • COPD
  • HYPOTENSION
  • METABOLIC DISORDERS
  • PVD
  • UNCONTROLLED HEART FAILURE
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14
Q

Mechanism of potassium channel blockers

A
  • Prevent K+ efflux which therefore prolongs the duration of APs by prolonging phase 3
  • Since they do not affect sodium channels, conduction velocity is not decrease
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15
Q

In which patients are potassium channel blockers contraindicated in?

A
  • Severe conduction disturbances
  • Sinus node disease
  • Iodine sensitivity
  • SAN heart block
  • Sinus bradycardia
  • Thyroid dysfunction
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16
Q

Side effects of potassium channel blockers

A 
Hypotension
Nausea
Dizziness
Headaches
Arrhythmias
Hepatic disorders
Respiratory disorders
Skin reactions
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17
Q

Examples of potassium channel blockers

A

Amiodarone

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18
Q

Mechanism of calcium channel blockers

A

Bind and inhibit non-dihydropyridine calcium channels which decreases conduction through the AVN and shortens plateau phase of AP
- This reduces heart contractility

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19
Q

Dihydropyridine vs non-dihydropyridine calcium channel blockers: difference in mechanism

A

Dihydropyridine: block calcium channels located in the muscle cells of the heart and arterial blood vessels, thereby reducing the entry of calcium ions into the cell = THEY HAVE VASODILATORY ACTIONS ON VASCULAR SMOOTH MUSCLE (used for hypertension etc)

Non-dihydropyridine: Shorten conduction through the AVN to prolong the plateau phase of the AP = ACT PRIMARILY ON THE HEART (used for arrhythmias and heart-related pathologies)

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20
Q

Examples of dihydropyridine vs non-dihydropyridine calcium channel blockers

A

Dihydropyridines: amlodipine, nifedipine, felodipine, nicardiPINE

Non-dihydropyridines: Verapamil, diltiazem

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21
Q

In which patients are calcium channel blockers contraindicated

A

Patients with:

  • Heart failure
  • Impaired LV function
  • Hypotension
  • SA block
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22
Q

Side effects of calcium channel blockers

A
  • Peripheral oedema
  • Abdo pain
  • Dizziness
  • Drowsiness
  • Flushing
  • Nausea
  • Palpitations
  • Skin reactions
  • Tachycardia
  • Vomiting
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23
Q

Examples of Non-DHPR calcium channel blockers

A

Verapamil

Diltiazem

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24
Q

What is an ectopic pacemaker

A
  • An excitable group of cells which cause premature heartbeats outside the normally functioning SAN
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25
Q

Role of ectopic pacemakers

A

They can either cause additional beats of the heart or take over the normal pacemaker activity of the SAN, leading to cases of tachycardia or bradycardia, depending on their location and electrical conditions

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26
Q

How can ectopic pacemakers be seen on ECGs

A

Change in shape of the QRS complex and prolonged duration (>0.1s) as more time is required for the entire ventricle to become depolarised

27
Q

Why is normal ectopic pacemaker activity suppressed?

A

By the SAN because it provides higher impulses and faster electrical activity

28
Q

In which circumstances do ectopic pacemakers take over natural heart rhythm?

A

Malfunctioning SAN or an ectopic foci

29
Q

When ectopic pacemaker activity takes over natural heart rhythm, what symptoms can you present with?

A
  • Perception of a missed heart beat
  • Palpitations
  • Feeling faint
30
Q

What are causes of instances in which the ectopic pacemaker takes over the natural heart rhythm?

A
  1. Increased local parasympathetic activity
  2. Elevated sympathetic output
  3. Over-stimulation from drugs
  4. Cardiac ischaemia
  5. Infection
  6. Sinus venosis and atrial defects
  7. SA node dysfunction (1st degree block)
  8. SAN blockage
  9. AVN blockage (3rd degree block)
31
Q

Where are atrial, junctional and ventricular pacemakers located?

A
  • Atrial = within atria
  • Junctional = near the AVN and septum
  • Ventricular = within the ventricles
32
Q

In simple terms, what is an MI

A

An extremely dangerous condition caused by a lack of blood flow to the heart muscle, blockage of the CORONARY ARTERIES

33
Q

What is a cardiac arrest?

A

When your heart suddenly stops beating, can be due to an MI or other causes but can prevent blood from reaching vital organs and tissues which can cause damage and death to them

34
Q

Causes of cardiac arrest (Hs and Ts mnemonic)

A

Hs:

  1. Hypovolemia
  2. Hypoxia
  3. H+ (acidosis)
  4. Hyper/hypokalaemia
  5. Hypothermia
  6. Hypoglycaemia

Ts:

  1. Tablets/toxins
  2. Tamponade
  3. Tension pneumothorax
  4. Thrombosis (MI)
  5. Thromboembolism
  6. Trauma
35
Q

What is the leading cause of heart attacks?

A

CHD

36
Q

Blockage of coronary vessels causes ischaemia of the heart, what is the consequence of prolonged myocardial ischaemia?

A

Cardiomyocyte death, beginning from the endocardium and moving towards the epicardium.
- Rapid depression of systolic function

37
Q

Explain the pathophysiology of an MI

A
  1. Atherosclerotic plaque in the coronary vessel
  2. Plaque ruptures
  3. Thrombus forms over atheroma
  4. Cardiomyocyte ischaemia
  5. Pain signals sent to brain
  6. Clot continues to grow – increased chest and left arm pain
  7. Surge of adrenaline causes HR to increase
  8. Cardiomyocytes slow down due to lack of O2 and stop beating, so the rest of the heart has to compensate and beat faster
  9. Cardiomyocyte membrane breakdown due to build-up of toxic waste products from metabolism
  10. Troponin protein leaked which is SPECIFIC to heart muscle cells only - DIAGNOSIS OF MI
    - Lose lots of cardiomyocytes per second, so after around 20 minutes of no treatment, the heart will never beat the same again
  11. Chronic high-grade stenosis of coronary arteries can induce ischaemia which leads to the induction of ventricular arrhythmia, which may lead to ventricular fibrillation, leading to death
  12. Chest pain, shortness of breath, nausea before the event occurs
38
Q

STEMI vs NSTEMI

A

STEMI = complete blockage of the heart, ST elevation on ECG

NSTEMI = partial blockage of the heart, NON-ST elevation on ECG

39
Q

Transmural vs subendocardial infarct

A

Transmural (full thickness) - involves the entire thickness of the left ventricular wall

Subendocardial (subendocardial) - multifocal areas of necrosis confined to the inner third to half of the left ventricular wall

40
Q

Symptoms of an MI

A
  1. Chest pain – heaviness, tightness of squeezing across the chest
  2. Radiated/referred pain - left arm (or right), jaw, neck, back or stomach
  3. Lightheadedness or dizzy
  4. Sweating
  5. SOB
  6. Anxiety
  7. Nausea/vomiting
  8. Coughing/wheezing
41
Q

Explain why pain occurs during an MI

A

Due to a side effect of cardiac muscle having to respire anaerobically due to ischaemia, which produces lactic acid. A build-up of lactic acid subsequently causes pain

42
Q

Risk factors for an MI

A
  1. Age (>45M, >55F)
  2. Smoking
  3. Hypertension
  4. Diabetes
  5. FHx
  6. Hyperlipidaemia
  7. Autoimmune conditions e.g RA or SLE
  8. Illicit drug use
  9. Pre-eclampsia history
  10. Metabolic syndrome
  11. Lack of physical activity
  12. Stress
43
Q

How does the adult heart heal from an infarction?

A

Through formation of a scar, dependent on an inflammatory cascade triggered by alarmins released by dying cells
- RAAS activation and TGFb release causes fibroblast to myofibroblast conversion and also promotes deposition of ECM proteins

44
Q

Complications of an MI

A
  1. Arrhythmias
    - Necrosis of cardiac tissue can damage the electrical conduction system within heart muscle. Leading to abnormal beating and synchronisation of heart rhythm
  2. Heart failure
    - If an MI damages excessive heart muscle, there may not be enough muscle left for the heart to function properly
  3. Sudden cardiac arrest
    - Electrical disturbances can lead to sudden stoppage of the heart
    - Without sudden treatment, an MI can increase the risk of sudden cardiac arrest
45
Q

What is coronary artery disease (CAD)/ischaemic heart disease (IHD)

A

it is an umbrella term for a group of diseases that includes:

  1. Stable angina
  2. Unstable angina
  3. MI
  4. Sudden cardiac death/cardiac arrest
46
Q

What is the leading cause of MI?

A

Atherosclerosis

47
Q

Explain the process of atherosclerosis

A
  1. Begins with endothelial cell injury
  2. Lipoprotein deposition
    - Accumulate in the tunica intima as they pass through the damaged epithelium from the blood
  3. Inflammatory reaction (fatty streak formation)
    - Macrophages ingest lipids (LDL) and convert into foam cells
  4. Smooth muscle cap formation
    - Smooth muscle cells secrete ECM e.g collagen to form a fibrous cap, hardening the artery. Calcium is deposited, hardening the artery
  5. Plaque rupture
    - Exposing foam cells to blood flow, thrombus forms at the site of ruptured plaque, reducing blood flow through the artery. Atherothrombosis
  6. Embolisation
    - If part of the thrombus breaks off and goes down stream
48
Q

Risk factors for atheroma

A
  1. Smoking
  2. Hypertension
  3. Diabetes
  4. Hypercholesterolaemia
  5. Obesity
  6. FHx of CHD
  7. South Asian, African or Afro-Caribbean
  8. Drinking Xs alcohol
  9. Age
  10. Diet
49
Q

Which drugs are used to control atheroma formation?

A

Statins and fibrates

50
Q

Mechanism of statins

A

Inhibit HMG-CoA reductase which plays a role in cholesterol production
- Increases LDL uptake by the liver

51
Q

Mechanism of fibrates

A

Activates PPAR which induces transcription of genes that facilitate lipid metabolism, increases HDL levels

52
Q

Angina can lead to…

A

MI

Stroke

53
Q

How would a patient describe angina?

A

A squeeing in their chest or a heavy weight lying on their chest

54
Q

Symptoms of angina

A
  1. Chest pain - may radiate to arms, neck, jaw, shoulder or back
  2. Dizziness
  3. SOB
  4. Fatigue
  5. Sweating
55
Q

Risk factors for angina

A

Usually caused to due atherosclerosis, so has the same risk factors for this

  1. Poor diet
  2. Age
  3. Lack of exercise
  4. Smoking
  5. FHx
  6. Obesity
  7. Hyperlipidaemia
56
Q

Stable vs unstable angina causes

A
  1. Stable angina is less severe usually triggered by physical activity during which there is inadequate blood supply to the heart muscle
    - Other causes are associated with activation of the sympathetic pathway including emotional stress, cold temperatures, heavy meals and smoking
  2. Unstable angina is more severe and caused by atherosclerotic plaques forming a thrombus. This can suddenly and severely decreased blood flow to your heart muscle
57
Q

What is Prinzmetal’s angina?

A

Type of angina caused by a sudden spasm in a coronary artery, temporarily narrowing the artery and reducing blood flow to the heart

  • Can occur at rest and typically presents overnight
  • Attacks occur in clusters and are associated with emotional stress, vasoconstrictive drugs, and illegal substances e.g. cocaine
58
Q

Pharmacological control of angina

A
  1. Nitrates
  2. Beta blockers
  3. Calcium channel blockers
59
Q

Mechanism of nitrate drugs

A
  • Given once an angina attack has started, most commonly GTN, as a mouth spray or as tablets that dissolve under the tongue
  1. It is a pro-drug which is converted to nitric oxide by mitochondrial aldehyde dehydrogenase
  2. This then activates cGMP
  3. Activation of a cascade of protein kinase-dependent phosphorylation events within smooth muscle
  4. Dephosphorylation of myosin causes relaxation of smooth muscle and increased blood flow in veins, arteries and cardiac tissue
60
Q

Major contraindications of nitrates

A
  1. Hypotensive disorders
  2. Bradycardia
  3. Brain trauma
  4. Pulmonary oedema
  5. Cardiogenic shock
61
Q

Side effects of nitrates

A
  1. Arrhythmias
  2. Asthenia (lack of energy before/without effort)
  3. Cerebral ischaemia
  4. Dizziness
  5. Drowsiness
  6. Flushing
  7. Headaches
  8. Hypotension
  9. Nausea/vomiting
62
Q

Contraindications for beta-blockers

A
  1. PVD
  2. Diabetes
  3. COPD
  4. Asthma
63
Q

Function of calcium channel blockers

A

Inhibits contractile process of the myocardium, causing vasodilatation, increased O2 delivery to the myocardium and decreased resistance/BP/afterload

64
Q

Contraindications of calcium channel blockers

A
  1. Arrhythmias
  2. Heart failure
  3. Bradycardia
  4. 2nd/3rd degree heart block
  5. Sick sinus syndrome

The development of cardiorespiratory disease (23 decks)

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