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Cardiovascular Block > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What is the normal sinus rhythm?

A
  • 60-100 bpm in adults and a consistent, smooth pattern on the ECG.
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2
Q

explain 1st degree heart block

A
  • First-degree heart block is caused by prolonged conduction of electrical activity through the AV node. It can be identified on the ECG by finding a PR interval >200ms.
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3
Q

explain Mobitz type 1 second degree heart block

A

o Mobitz type 1 is a type of second-degree heart block that is usually due to reversible conduction block at the AV node it is characterized by progressive lengthening of the PR interval which results in a P-wave that fails to conduct a QRS.

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4
Q

explain mobitz type 2 second degree heart block? what causes it? what does the QRS complex usually look like?

A

o Mobitz type 2 is a type of second-degree heart AV block where there are intermittent non-conducted P-waves. The PR interval is constant. It is usually caused by a conduction system failure, especially in the His-Purkinje system. In most cases, there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/bifascicular block.

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5
Q

what indicates a broad QRS on an ECG?

A

QRS longer than 0.12 seconds, three small boxes

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6
Q

what indicates a narrow (normal) QRS on an ECG?

A

QRS less than 0.12 seconds, < 3 small boxes.

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7
Q

explain third-degree heart block
ECG patter?

A
  • Complete (third-degree) heart block occurs when atrial impulses fail to be conducted to the ventricles.
  • P waves are not associated with QRS complex.
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8
Q

how might patients with 3rd degree heart block present? and what does the ECG show?

A
  • Patients may present with syncope or cardiac arrest. ECG shows severe bradycardia and dissociation between the P waves and QRS complex.
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9
Q

describe atrial fibrillation? what does the ECG show? what is the pulse like?

A
  • Atrial fibrillation occurs when there is uncoordinated atrial contraction, typically at approximately 300-600 bpm. Delay at the atrioventricular node means that only some of the atrial impulses are conducted to the ventricles, resulting in an irregular ventricular response. There is no P-wave on surface ECG > fibrillary activity. Irregularly irregular pulse.
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10
Q

what is atrial flutter? what is the typical pattern on an ECG?

A
  • Atrial flutter is caused by an aberrant macro-circuit within the right atrium which cycles at 300bpm. This circuit activates the AV node but because this node has a relatively long refractory period it is not able to conduct impulses down the His-Purkinje system at such a fast rate. Instead, there is a degree of block meaning that only 2:1, 3:1, 4:1 or rarely 5:1 atrial impulses are conducted to the ventricle. Typical sawtooth pattern of P-wave on the surface ECG
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11
Q

explain supraventricular tachycardia

A
  • A tachycardia that occurs above the ventricles.
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12
Q

describe Wolff-Parkinson-White syndrome

A
  • WPW syndrome is caused by a congenital accessory electrical pathway which connects the atria to the ventricles bypassing the AV node. This accessory pathway leads to the potential for re-entrant circuits to form leading to supraventricular tachycardias.
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13
Q

describe ventricular fibrillation? what type of rhythm? what are the QRS complexes like?

A
  • Ventricular fibrillation is an irregular broad complex tachycardia. This is always a pulseless rhythm. The QRS complexes are polymorphic and irregular.
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14
Q

describe ventricular tachycardia. what will the ECG show?

A
  • Ventricular tachycardia refers to fast rhythm disturbances that occur in the ventricles. ECG will show absent P-waves plus regular broad QRS complexes QRS complexes occurring frequently and rapidly.
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15
Q

what medication can be used to treat life-threatening ventricular tachycardia or fibrillation?

A
  • Class III potassium channel blockers such as amiodarone are used for life-threatening ventricular tachycardia or fibrillation.
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16
Q

discuss amiodarone

A

o Used for VT and occasionally supraventricular tachycardia.
o Many interactions with other drugs, particularly digoxin.
o Has striking side effect profile:
 Thyroid (hypo or hyper).
 Pulmonary fibrosis.
 Slate grey pigmentation.
 Corneal deposits.
 LFT abnormalities.

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17
Q

explain sinus arrest

A
  • Sinus arrest is a type of arrhythmia that occurs when the SA node fails to generate an electrical impulse or stops functioning altogether. This can result in a pause in the heartbeat, which can last for several seconds or even longer.
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18
Q

what are atrial ectopic beats?

A
  • Atrial ectopic beats occur when an electrical impulse originates in the atria before it is supposed to. This causes the atria to contract prematurely, creating an extra heartbeat.
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19
Q

what are ventricular ectopic beats?

A
  • Ventricular ectopic beats occur when an electrical impulse originates in the ventricles before it is supposed to. This causes the ventricles to contract prematurely, creating an extra heartbeat.
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20
Q

what are the symptoms of atrial fibrillation?

A

o Palpitations.
o Chest pain.
o Shortness of breath.
o Dizziness.

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21
Q

what are the signs of atrial fibrillation?

A

o An irregular pulse rate with a variable volume pulse.
o A single waveform on the JVP (due to loss of the a-wave > this normally represents atrial contraction).
o An apical to radial pulse deficit (as not all atrial impulses are mechanically conducted to the ventricles. The radial pulse is lower than the apical pulse.
o Auscultation – may be a variable intensity first heart sound.
o Features suggestive of the underlying cause (e.g., hyperthyroidism, alcohol excess, sepsis).
o Features suggestive of complications resulting from the AF (e.g., heart failure).

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22
Q

discuss the investigations of atrial fibrillation

A
  • To confirm the diagnosis, an ECG is performed > absence of P-waves and irregular QRS complex (narrow). Document arrhythmia on ECG – 12 lead, 24-hour recording (or longer), event recorder.
  • Blood tests esp. thyroid function.
  • Echocardiogram.
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23
Q

what does treatment of atrial fibrillation aim to achieve?

A

rate control
rhythm control
anticoagulation?

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24
Q

discuss rate control in atrial fibrillation

A

o A beta-blocker such as bisoprolol or a rate-limiting CCB (e.g., diltiazem) should be the initial monotherapy. Can use class I sodium channel blockers such as flecainide.
o Consider digoxin monotherapy for people with non-paroxysmal AF only if they are sedentary (do no or very little physical exercise).

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25
Q

discuss rhythm control in atrial fibrillation

A

o Electrical cardioversion.
o Pharmacological cardioversion > adenosine.
o Pacemaker and ablation of the AV node (occasionally).
o Substrate modification (only suitable for a minority > paroxysmal) e.g., pulmonary vein isolation, surgical procedures.

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26
Q

discuss anticoagulation treatment in atrial fibrillation

A
  • Consider anticoagulation e.g., NOACs or warfarin- the risk of bleeding must be less than the risk of stroke (CHADS2-Vasc score etc.).
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27
Q

what is electrical cardioversion?

A
  • Electrical cardioversion is a procedure that uses a controlled electric shock to restore normal rhythm of the heart in patients with AF.
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28
Q

what type of congestion is congestive heart failure?

A

generalised acute congestion

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29
Q

what causes congestive heart failure?

A
  • Congestive heart failure occurs when the heart is unable to clear blood from the ventricles > ineffective pump e.g., ischaemia, valvular disease.
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30
Q

pathophysiology of congestive heart failure: what mechanisms occur?

A

o Decreased CO.
o Decreased renal glomerular filtration rate (GFR):
 Activation or RAAS.
 Increased sodium and water retention.
o Increased amount of fluid in the body.
o Increased fluid (overload) in veins (treatment > diuretics).

31
Q

effects of congestive heart failure

A

o Heart cannot clear blood from the ventricles.
o Back pressure, blood dammed back in veins.
o Lungs > pulmonary oedema:
 Left heart failure – blood dams back into lungs.
 Clinically, crepitations in lungs, tachycardia.
o Liver- central venous congestion:
 Right heart failure – blood dams back to systemic circulation.
 Increased JVP, hepatomegaly, peripheral oedema.

32
Q

list the conditions that cause vascular congestion

A
  • Congestive heart failure > causes congestion in lungs and other organs.
  • Liver disease.
  • Kidney disease.
  • Venous insufficiency.
  • Blood clots.
  • Infections.
  • Lymphatic obstruction.
  • Trauma.
  • Tumours.
33
Q

define the term exudate. what is its features? what is it caused by?

A
  • Exudate is a protein-rich fluid that accumulates in tissues as a result of inflammation. It has a high protein content, a high specific gravity, and a cloudy or purulent appearance. Exudate is typically caused by local factors such as infection, trauma or malignancy.
34
Q

define the term transudate. characteristic and appearance? what conditions cause this?

A
  • Transudate is a protein-poor fluid that accumulates in tissues due to a disruption in the balance between hydrostatic and oncotic pressures, without significant inflammation. It has a low protein content, a low specific gravity, and a clear or slightly yellow appearance. Transudate is typically caused by systemic conditions such as heart failure, liver disease, or kidney disease.
35
Q

what are starling’s forces?

A

Starling forces are the physical forces that determine the movement of fluid between capillaries and tissue fluid.

36
Q

what are the three starling’s forces?

A

hydrostatic pressure.
oncotic pressure.
permeability characteristics and area of the endothelium.

37
Q

what is hydrostatic pressure?

A

– force exerted by the fluid within the capillary walls, which tends to push fluid out of the capillaries and into the surrounding tissue.

38
Q

what is oncotic pressure?

A

opposite to hydrostatic pressure. The pressure is created by the concentration of proteins, such as albumin, within the plasma. Tends to pull fluid back into the capillaries from surrounding tissues.

39
Q

what is oedema?

A

> abnormal accumulation of fluid in the interstitial spaces of tissues.

40
Q

what can happen if hydrostatic pressure within the capillaries increases or oncotic pressure outside the capillaries increases?

A

fluid may be forced out of the capillaries and into surrounding tissues. This can occur in conditions such as heart failure. Similarly, liver disease can cause a decrease in the production of albumin, leading to a decrease in oncotic pressure and fluid accumulation in the abdomen, a condition known as ascites.

41
Q

what can happen if oncotic pressure within the capillaries increases or hydrostatic pressure outside the capillaries increases?

A

fluid may be pulled out of the tissues and into the capillaries. This can occur in conditions such as malnutrition and kidney disease where there is a decrease in the production of albumin or an increase in capillary permeability, leading to a decrease in oncotic pressure and fluid accumulation in the tissues.

42
Q

what the pathophysiology of pulmonary oedema?

A
  • Left ventricular failure:
    o Increased left atrial pressure > passive retrograde flow to pulmonary veins, capillaries, and arteries.
    o Increased pulmonary vascular pressure.
    o Increased pulmonary blood volume.
    o Increased PC > increased filtration and pulmonary oedema.
  • In lungs:
    o Perivascular and interstitial transudate.
    o Progressive oedematous widening of alveolar septa.
    o Accumulation of oedema fluid in alveolar spaces.
43
Q

whats the pathophysiology of peripheral oedema?

A
  • Right heart failure – cannot empty RV in systole.
  • Blood retained in systemic veins > increased pressure in capillaries > increased filtration > peripheral oedema.
    o Also secondary portal venous congestion via the liver.
  • Congestive cardiac failure:
    o Right and left ventricles both fail.
    o Pulmonary oedema and peripheral oedema at the same time.
    o All about hydrostatic pressure.
44
Q

what is heart failure?

A
  • Heart failure is a clinical syndrome comprising of dyspnoea, fatigue or fluid retention due to cardiac dysfunction, either at rest or on exertion, with accompanying neurohormonal activation.
45
Q

what are the risk factors of heart failure?

A

Increasing age
hypertension
coronary heart disease
obesity
diabetes
MI
hyperlipidaemia
cardiomyopathy
valvular disease

46
Q

what are the different types of heart failure?

A

left ventricular systolic dysfunction (LVSD)
left ventricular diastolic (or relaxation) heart failure

47
Q

what causes LSVD?

A

decreased pumping function of the heart, which results in fluid backup in the lungs and heart failure.

48
Q

what causes left ventricular diastolic heart failure?

A

 Involves a thickened and stiff heart muscle.
 As a result, the heart does not fill with blood properly.
 This results in fluid backup in the lungs and heart failure.

49
Q

describe the final result of heart failure

A
  • A failing heart that cannot pump out sufficient blood to supply the needs of the body.
  • Progressive retention of salt and water which results in peripheral and pulmonary oedema.
  • Progressive vasoconstriction, myocyte death and fibrosis.
50
Q

what is the prognosis of heart failure?

A
  • HF has high morbidity and mortality.
  • One-year survival rate is just over 60%.
51
Q

what are the clinical symptoms of heart failure?

A

o Breathlessness.
o Fatigue.
o Oedema.
o Reduced exercise capacity.

52
Q

what are the clinical signs of heart failure?

A

o Oedema.
o Tachycardia.
o Raised JVP.
o Chest crepitations or effusions.
o 3rd heart sound.
o Displaced or abnormal apex beat.

53
Q

discuss the grading of heart failure

A
  • Degree of LV impairment or valvular dysfunction etc.
  • NYHA class i.e., the severity of symptoms.
  • Degree of elevation of BNP.
54
Q

what are the relevant investigations of heart failure?

A
    1. Symptoms and signs of heart failure (rest or exercise) and
    1. Objective evidence of cardiac dysfunction and (in doubtful cases)
    1. Response to therapy (diuretics).
55
Q

how is objective evidence of cardiac dysfunction obtained?

A

o Echocardiography.
o Radionucleotide ventriculography
o MRI
o Left ventriculography.
o Potential screening tests:
 12 lead ECG, LVSD very unlikely if ECG normal.
 BNP (brain (B-type) natriuretic peptide).

56
Q

delete

A

delete

57
Q

what are the causes of LVSD?

A

o Ischaemic heart disease (usually MI).
o Dilated cardiomyopathy > means LVSD not due to IHD or secondary to another lesion i.e., valves/VSD.
o Severe aortic valve disease or mitral regurgitation.

58
Q

left ventricular ejection fraction (LEVF)

A
  • Can be hard to determine from an echocardiogram.
  • Much easier to determine by a MUGA scan.
    o Normal 55-70%.
    o Mild 40-55%.
    o Moderate 30-40%.
    o Severe <30%.
59
Q

discuss the strengths of diuretic therapy in the treatment of heart failure

A

o The mainstay of treatment for patients with salt and water retention is to reduce symptoms of tiredness, and fatigue and improve exercise capacity.
o The loop diuretics induce profound diuresis by inhibiting the Na-K-Cl transporter in the loop of Henle.
o Work at very low glomerular filtration rates.
o Prevent the absorption of 20% of filtered sodium and water.

60
Q

discuss the weaknesses of diuretic therapy in HF

A

o Adverse drug reactions such as dehydration, hypotension, hypokalemia, hyponatremia, gout, impaired glucose tolerance, and diabetes.
o Drug-drug interactions with furosemide:
 Aminoglycosides > aural and renal toxicity.
 Lithium > renal toxicity.
 NSAIDs > renal toxicity.
 Antihypertensives > profound hypotension.
 Vancomycin > renal toxicity.

61
Q

discuss the strengths of ACEi’s in the treatment of HF

A

o Reduce preload and after load on the heart.
o In CHF patients significantly reduce morbidity and mortality.

62
Q

discuss the weaknesses of ACEi’s in the treatment of HF

A

o Adverse drug reactions:
 Cough.
 Angioedema.
 Renal impairment.
 Renal failure.
 Hyperkalaemia.
o Drug-drug interactions:
 NSAIDs > acute renal failure.
 Potassium supplements > hyperkalaemia.
 Potassium sparing diuretics > hyperkalaemia.

63
Q

discuss the use of mineralocorticoid receptor blockers in the treatment of heart failure

A

o E.g., spironolactone and eplerenone.
o Block receptors that bind aldosterone and other steroid hormones (e.g., corticosteroids, androgens) receptors.
o Recommended in all symptomatic patients to reduce mortality and HF hospitalization.
o Proven to reduce mortality when used in combo with ACEis.

64
Q

discuss the use of beta blockers in the treatment of heart failure

A

o E.g., carvedilol and bisoprolol.
o Block the actions of the sympathetic system/
o Have been demonstrated to reduce morbidity and mortality in mild/moderate and severe heart failure by 30%.
o Should only be used when a patient has been stabilized.

65
Q

when is digoxin commonly used?

A

Digoxin is a commonly used medication for patients in AF who are also in heart failure or are hypotensive.

66
Q

how does digoxin work?

A

It inhibits the Na+/K+ ATPase ion pump in the myocardium and also has parasympathetic effects on the AV node. It is therefore negatively chronotropic and positively ionotropic (i.e. slows heart rate but increases contractility).

67
Q

digoxin toxicity features

A

Nausea/vomiting
Diarrhoea
Blurred vision
Yellow/green discolouration of vision
Haloes in vision
Confusion
Fatigue
Palpitations
Syncope

68
Q

definition of torsades de pointes

A

Torsades de pointes (TDP) is a form of polymorphic VT that can occur in patients with a long QT interval. It can degenerate into VF, and it can cause significant haemodynamic compromise and death.

69
Q

what are the ECG features of WPW syndrome?

A

Delta waves (slurred upstroke in the QRS)
Short PR interval (<120ms)
Broad QRS
If a re-entrant circuit has developed the ECG will show a narrow complex tachycardia

70
Q

how does bundle branch block show up on an ECG?

A

lengthened QRS complex

71
Q

is congestive heart failure caused by failure of both ventricles?

A

yes

72
Q

what will low serum protein levels cause?

A

Low protein levels in serum, for example low albumin levels, will cause a low capillary oncotic pressure. There will therefore be poor fluid retention/re-absorption, leading to oedema.

73
Q

what is a shockable rhythm?

A

Shockable rhythms include ventricular fibrillation and pulseless ventricular tachycardia.

74
Q

what is Beck’s triad of cardiac tamponade?

A

hypotension
muffled heart sounds
raised JVP

Cardiovascular Block (5 decks)

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