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PHASE 2A (Mine) > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is atherosclerosis?

A

A combination of fatty deposits (plaque) in the artery walls and the hardening of the walls

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2
Q

Which blood vessels does atherosclerosis affect?

A

The medium and large arteries

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3
Q

What causes atherosclerosis?

A

Chronic inflammation and activation of the immune system in the artery wall.

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4
Q

What can atherosclerotic plaques cause?

A

Stiffening of artery walls–> leading to hypertension
Stenosis–> reduced blood flow (angina)
Plaque rupture–> may give off a thrombus that leads to ischeamia

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5
Q

What are the non-modifiable risk factors for athersclerosis?

A

Age
Family history
Male

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6
Q

What are the modifiable risk factors?

A 
Smoking
Alcohol consumption
Poor diet
Low exercise
Obesity
Poor sleep
Stress
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7
Q

What co-morbidities increase the risk of atherosclerosis?

A 
Diabetes
Hypertension
Chronic kidney disease
Inflammatory conditions
Atypical antipsychotic medication
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8
Q

What are the end results of atherosclerosis?

A 
Angina
MI
Transient ischaemic attacks
Stroke
Peripheral vascular disease
Mesenteric ischaemia
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9
Q

What is secondary prevention of cardiovascular disease?

A

Trying to prevent another attack in those who have had angina, MI, TIA, stroke or peripheral vascular disease

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10
Q

What algorithm calculates the percentage risk of a patient having cardiovascular disease in the next 10 years?

A

QRISK 3 score

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11
Q

What should happen if a patient has a >10% risk of stroke/ heart attack in the next 10 years according to their QRISK 3 score?

A

They should be offered a statin (e.g. atorvastatin 20mg)

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12
Q

Who other than those identified at risk should be offered a statin?

A

Patients with chronic kidney disease of Type 1 diabetes for >10 years

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13
Q

What are the 4 A’s of secondary cardiovascular disease prevention?

A

Aspirin
Atorvastatin (80mg)
Atenolol (or other beta-block)
ACE0 inhibitor

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14
Q

What are the main side effects of statins?

A

Myopathy
Type 2 diabetes
Heamorrhagic strokes

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15
Q

What is angina?

A

A narrowing of the coronary arteries, reducing blood flow to the myocardium

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16
Q

What are the main symptoms of angina?

A

Constricting chest pain
Radiating pain to jaw or arms
(usually worse during times of high demand e.g. exercise)

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17
Q

When is angina classed as ‘stable’?

A

When symptoms are always relieved by rest or GTN.

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18
Q

When is angina unstable?

A

When the symptoms come on randomly while at rest (ACUTE CORONARY SYNDROME)

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19
Q

What are the main investigations into angina?

A 
CT Coronary Angiography
Physical exam
ECG
FBC, U&E's
LFTs
Lipid profile
Thyroid function tests and HbA1C
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20
Q

What is CT coronary angiography?

A

Contrast is injected and CT images are taken in time with the heart beat to give a detailed view of the coronary arteries.

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21
Q

What are the four principles of management of angina?

A 
RAMP
Refer to cardiology
Advise them about diagnosis and management
Medical treatment
Procedural or surgical interventions
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22
Q

What are the three main aims to medical management of angina?

A

Immediate symptomatic relief
Long term symptomatic relief
Secondary prevention of cardiovascular disease

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23
Q

What is used for immediate symptomatic relief of stable angina?

A

GTN spray (take it then repeat after 5 minutes. If pain persists, call ambulance)

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24
Q

What does GTN spray do?

A

Causes vasodilation to help relieve symptoms of angina.

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25
Q

What is used for long term symptomatic relief of stable angina?

A

Beta blocker
Calcium channel blockers
(can be just one or both if needed)

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26
Q

What are the main procedural/ surgical interventions for treatment of angina?

A
  • Percutaneous coronary intervention with coronary angioplasty
  • Coronary artery bypass graft (CABG)
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27
Q

What is PCI?

A

Percutaneous coronary intervention with coronary angioplasty involves dilating the blood vessel with a balloon and/or inserting a stent.

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28
Q

What is CABG surgery?

A

Coronary artery bypass graft: A graft vein from the patients leg is taking and sewn onto the affected coronary artery to bypass the stenosis.

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29
Q

What is acute coronary syndrome?

A

Range of conditions associated with sudden, reduced blood flow to the heart.

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30
Q

What causes acute coronary syndrome?

A

The result of a thrombus from an atherosclerotic plaque blocking a coronary artery.

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31
Q

What is the main treatment of acute coronary syndrome?

A

Anti-platelet medications (e.g. aspirin, clopidogrel and ticagrelor)

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32
Q

Why are anti-platelets used in the treatment of acute coronary syndrome?

A

When a thrombus forms in a fast flowing artery, it is made up mostly of platelets.

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33
Q

What does the left coronary artery branch into?

A

The circumflex and Left anterior descending (LAD)

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34
Q

What does the right coronary artery supply?

A

Right atrium and ventricle
Inferior aspect of left ventricle
Posterior septal area

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35
Q

What does the circumflex artery supply?

A

Left atrium

Posterior aspect of left ventricle

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36
Q

What does the LAD supply?

A

Anterior aspect of left ventricle

Anterior aspect of septum

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37
Q

What are the 3 types of acute coronary syndrome?

A
  1. Unstable angina
  2. ST elevation myocardial infarction (STEMI)
  3. Non-ST elevation myocardial infarction (NSTEMI)
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38
Q

How should a diagnosis of acute coronary syndrome be made?

A

If a patient comes in with potential symptoms, perform an ECG:

  • If there is ST elevation, it is a STEMI
  • If there is no ST elevation, perform troponin blood tests
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39
Q

What do troponin blood tests diagnose?

A
  • If there are raised troponin levels/ other ECG changes= NSTEMI
  • If troponin levels are normal and the ECG is normal= Unstable angina or other cause
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40
Q

What are the main symptoms of unstable angina?

A 
Central, constricting chest pain
Nausea/ vomiting
Sweating
Feeling of impending doom
Shortness of breath
Palpitations
Pain radiating to jaw/ arms
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41
Q

What ECG changes are seen in a STEMI?

A

ST segment elevation (in leads consistent with an area of ischaemia)
New left bundle branch block

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42
Q

What ECG changes are seen in an NSTEMI?

A

ST segment depression
Deep T wave inversion
Pathological Q waves

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43
Q

What are troponins?

A

Proteins found in cardiac muscle

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44
Q

What investigations would be done to diagnose acute coronary artery disease?

A

Same as stable angina + Chest X-ray, Echocardiogram, CT coronary angiogram

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45
Q

What is the treatment of an acute STEMI?

A 
Primary PCI (if available within 2 hours of presentation)
Thrombolysis (If PCI not available)
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46
Q

What does thrombolysis treatment involve?

A

Injecting a fibrinolytic medication that rapidly dissolves clots

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47
Q

Why is thrombolytic medication not the first choice?

A

Significant risk of bleeding

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48
Q

How is an acute NSTEMI treated?

A 
BATMAN:
Beta blockers
Aspirin
Ticagrelor (blood thinner)
Morphine
Anticoagulant (LMW Heparin)
Nitrates (GTN)
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49
Q

What is the difference between a STEMI and NSTEMI?

A

A STEMI (ST-elevation myocardial infarction) is caused by a sudden complete (100 percent) blockage of a coronary artery. A non-STEMI is usually caused by a severely narrowed artery but the artery is usually not completely blocked.

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50
Q

What is used to assess for PCI in NSTEMI?

A

GRACE score: gives a 6 month risk of death or repeat MRI. 5-10%= medium risk, >10%= High risk both of which would be considered

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51
Q

What are the complications of heart failure? (DREAD)

A 
Death
Rupture (of heart septum of papillary muscles)
Edema (Heart failure)
Arrhythmia/ aneurysm
Dressler's syndrome
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52
Q

What is Dressler’s syndrome?

A

Post-myocardial infarction sydrome: Pericarditis caused by an immune system response after damage to heart tissue or pericardium

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53
Q

When does Dressler’s syndrome usually occur?

A

Around 2-3 weeks after an MI

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54
Q

What are the presentations of Dressler’s syndrome?

A

Pleuritic chest pain
Low grade fever
Pericardial rub on auscultation
Can cause pericardial effusion or tamponade.

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55
Q

How can Dressler’s syndrome by diagnosed?

A

With ECG, echo and raised inflammatory markers

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56
Q

How is Dressler’s syndrome managed?

A 
With NSAIDS (aspirin/ ibuprofen) and in severe cases steroids
May need pericardiocentesis to remove fluid from around the heart.
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57
Q

What is the secondary prevention medical management of acute coronary syndrome?

A 
6 A's:
Asprin (75mg o.d)
Another antiplatelet (e.g. clopidogrel, ticagrelor)
Atorvastatin (80mg o.d)
ACE inhibitors
Atenolol (B blocker)
Aldosterone antagonist
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58
Q

What is acute left ventricular failure?

A

When the left ventricle is unable to move blood through the left side of the heart and into the body, causing a backlog of blood in the left atrium, pulmonary veins and lungs.

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59
Q

What are the main triggers of acute LVF?

A

Latrogenic (e.g. Lots of IV fluid in elderly patient with impaired LV function)
Sepsis
Myocardial infarction
Arrhythmias

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60
Q

What is the main presentation of acute LVF?

A

Rapid onset breathlessness (exacerbated by lying flat)

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61
Q

What type of respiratory failure does acute LVF cause?

A

Type 1 respiratory failure–> low oxygen without an increase in CO2 in the blood

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62
Q

What are the main symptoms of acute LVF?

A

Shortness of breath
Looking/ feeling unwell
Cough

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63
Q

What signs would be found on examination of acute LVF?

A 
Increased respiratory rate
Reduced oxygen saturations
Tachycardia
3rd heart sound
Bilateral basal crackles
(Hypotension in severe cases)
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64
Q

What would be found if the patient has right sided heart failure as well as LVF?

A

Raised jugular venous pressure (caused by a backlog)

Peripheral oedema

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65
Q

What investigations would be done to look into LVF?

A

ECG
ABG
Chest X ray
Bloods: Routine, kidney function, BNP and troponin

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66
Q

What is the BNP blood test?

A

B-type Natriuretic peptide (BNP)= hormone released from the heart ventricles when the myocardium is stretched beyond the normal range. A high results can indicate that the heart is overloaded.

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67
Q

What is the action of BNP?

A

Relax the smooth muscle in blood vessels, reducing systemic vascular resistance.
Also acts as a diuretic on the kidneys to reduce the circulating blood volume.

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68
Q

What are causes of raised BNP other than heart failure?

A 
Tachycardia
Sepsis
Pulmonary embolism
Renal impairment
COPD
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69
Q

What is the main measure of left ventricular function and what is a normal result?

A

Ejection fraction >50%

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70
Q

What is cardiomegaly (on a CXR)?

A

Cardiothoracic ratio > 0.5–> When the diameter of the widest part of the heart is more than half the diameter of the widest part of the lung fields

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71
Q

What things might be seen on a chest Xray that would indicate LVF?

A

Cardiomegaly
Upper lobe venous diversion

If fluid is leaking:
Bilateral pleural effusions
Fluid in interlobar fissures

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72
Q

What is upper lobe venous diversion?

A

Usually the lower lobe veins contain more blood and the upper lobe veins remain relatively small.
When there is such a back-pressure that the upper lobe veins fill with blood and become engorged, it becomes visible as increased prominence and diameter of upper lobe vessels on a chest X-ray.

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73
Q

What is the management of acute LVF?

A

Pour SOD:

Pour away (stop) IV fluids
Sit up
Oxygen
Diuretics

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74
Q

What does the backlog of blood in the LA, pulmonary veins and lungs cause?

A

Fluid leakage and they are unable to reabsorb fluid from surrounding tissues:
Pulmonary oedema

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75
Q

What is pulmonary oedema?

A

When the lung tissues and alveoli become full of interstitial fluid

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76
Q

What does pulmonary oedema cause?

A

Interferes with normal gas exchange, causing shortness of breath and oxygen desaturation

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77
Q

Why are diuretics given in LVF treatment?

A

They reduce the circulating volume and means the heart is less overloaded, allowing it to pump more effectively.

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78
Q

What is chronic heart failure?

A

Ongoing inability of the heart to pump enough blood through the body to ensure a sufficient supply of oxygen

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79
Q

What is systolic heart failure?

A

Impaired left ventricular contraction

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80
Q

What is diastolic heart failure?

A

Impaired left ventricular contraction

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81
Q

What is the cause of chronic heart failure?

A

Impaired left ventricular failure (either systolic or diastolic) resulting in a chronic back-pressure of blood trying to flow into/through the left side of the heart.

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82
Q

What are the key presentations of chronic heart failure?

A 
Breathlessness (worsened by exertion)
Cough (may produce  frothy white/ pink sputum)
Orthopnoea
Paroxysmal nocturnal dyspnoea
Peripheral oedema (swollen ankles)
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83
Q

What is orthopnoea?

A

The sensation of shortness of breath when lying flat, which is relieved by sitting or standing

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84
Q

What is Paroxysmal Nocturnal Dyspnoea (PND)?

A

Sudden waking at night with a sever attack of shortness of breath or cough

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85
Q

How is chronic heart failure diagnosed?

A

Clinical presentation
BNP blood test
Echocardiogram
ECG

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86
Q

What are the main causes of chronic heart disease?

A

Ischaemic heart disease
Valvular heart disease (e.g. aortic stenosis)
Hypertension
Arrhythmias (e.g. atrial fibrillation)

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87
Q

What is the first line medical treatment in chronic heart failure?

A 
ABAL:
ACE inhibitor
Beta blocker
Aldosterone antagonist (when symptoms not controlled by first two)
Loop diuretics
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88
Q

What can be used instead of an ACE inhibitor is they are not tolerated?

A

Angiotensin Receptor Blocker (ARB)

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89
Q

What is Cor pulmonale?

A

Right sided heart failure caused by respiratory disease

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90
Q

What causes Cor pulmonale?

A

The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries.

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91
Q

Where does back pressure of blood occur in Cor pulmonale?

A

Right atrium
Vena cava
Systemic venous system

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92
Q

What are the main causes of Cor pulmonale? (most common?)

A 
COPD= most common: low oxygen levels cause pulmonary hypertension
Pulmonary embolism
Interstitial lung disease 
Cystic fibrosis
Primary pulmonary hypertension
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93
Q

What is primary pulmonary hypertension?

A

A rare lung disorder in which the blood vessels in the lungs narrow and the pressure in the pulmonary artery rises far above normal levels

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94
Q

How does interstitial lung disease cause right sided heart failure?

A

ILD= Group of diseases that cause scarring (fibrosis) of the lungs. The scarring causes stiffness in the lungs which makes it difficult to breathe and get oxygen to the bloodstream. In people who have pulmonary hypertension, changes in the small blood vessels inside the lungs can lead to increased blood pressure in the right side of the heart.

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95
Q

What are the main presentations of cor pulmonare?

A 
Early= usually asymptomatic.
Shortness of breath
Peripheral oedema
Syncope
Chest pain
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96
Q

What are some signs of cor pulmonale?

A 
Hypoxia
Cyanosis
Raised JVP
Peripheral oedema
Third heart sound
Murmers
Hepatomegaly
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97
Q

How is Cor pulmonare treated?

A

Treating symptoms and underlying cause.

Long term oxygen therapy is often used.

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98
Q

How is a diagnosis of hypertension made?

A

Clinic blood pressure taken. If between 140/90 and 180/20 should have ambulatory or home reading to confirm.

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99
Q

What is ambulatory blood pressure monitoring?

A

Blood pressure is tested automatically every 30 minutes over a 24-hour period using a cuff attached to a portable device worn on your waist.

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100
Q

What is essential hypertension?

A

Primary hypertension: developed on its own with no secondary cause

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101
Q

What percentage of hypertension cases are primary?

A

95%

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3
4
5
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102
Q

What are the secondary causes of hypertension?

A 
ROPE:
Renal disease
Obesity
Pregnancy (pre-eclampsia)
Endocrine conditions
How well did you know this?
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2
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4
5
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103
Q

What is the most common endocrine causes of hypertension?

A

Hyperaldosteronism (Conn’s syndome)

104
Q

What are the main complications of hypertension?

A 
Ischaemic heart disease
Cerebrovascular accident (stroke/ haemorrhage)
Hypertensive retinopathy
Hypertensive nephropathy
Heart failure
105
Q

What is stage 1 hypertension?

A

> 140/90 in clinic

>135/85 with ambulatory or home readings

106
Q

What is stage 2 hypertension?

A

Clinic: >160/100

Ambulatory/ Home: >150/95

107
Q

What is stage 3 hypertension?

A

> 180/120

108
Q

What other tests should those with newly diagnosed hypertension undergo to look for end-organ damage?

A

Kidney damage: Urine albumin:creatinine ratio + dipstick.
Bloods for HbA1c, renal function and lipids
Fundus examination for hypertensive retinopathy
ECG for cardiac abnormalities

109
Q

What medications are used to treat hypertension?

A 
A-Ace inhibitor
B- Beta blocker
C- Calcium channel blocker
D- Thiazide-like diuretic
ARB- Angiotensin II receptor blocker
110
Q

When are angiotensin receptor blockers used in place of an ACE inhibitor?

A

If the person does not tolerate ACE inhibitors (due to cough) or the patient is black, African or Afro-Caribbean descent

111
Q

What is the initial management of stage 1 hypertension?

A

Investigation for possible causes/ end organ damage

Advise on lifestyle changes

112
Q

Which hypertension patients is medical management offered to?

A

All patients with Stage 2 hypertension
All patients under 80 with stage 1 as well as a Q-risk score of >10%, or an associated condition (diabetes, renal disease, cardiovascular disease or end organ damage)

113
Q

What is step 1 of medical management in normal patients and in those >55 or black?

A

> 55/ non-black= Ace inhibitor

>55/ Black= Calcium channel blocker

114
Q

What is step 2 in medical management in hypertentsion?

A

Ace inhibitor + calcium channel blocker

** OR A+D, C+D
If black, use ARB instea d of A

115
Q

What is step 3 in the medical management of hypertension?

A

A+ B + C

Ace inhibitor, Beta blocker and calcium channel blocker

116
Q

What additional things can be added for step 4 of medical management of hypertension?

A

If potassium< 4.5: Potassium sparing diuretic (Spironolactone)
If posassuim> 4.5: Alpha blocker or beta blocker

117
Q

Why is important to monitor U+E’s regularly when using ACE inhibitors and diuretics?

A

ACE inhibitors and diuretics can cause hyperkalaemia and other electrolyte disturbances

118
Q

What are the hypertension treatment targets?

A

< 80 years= <140/90

>80 years= <150/90

119
Q

What is the first heart sound and what causes it?

A

S1
Caused by the closing of the atrioventricular valves (tricuspid and mitral) at the start of the systolic contraction of the ventricles

120
Q

What is the second heart sound and what causes it?

A

S2

Closing of the semilunar valves (pulmonary and aortic) once the systolic contraction is complete

121
Q

What is the third heart sound in younger/ healthy people?

A

Rapid ventricular filling causing the chordae tendineae to pull their full length and twang (like a guitar string)

122
Q

how long after the second is the third heart sound heard?

A

S3= 0.1 seconds after second

123
Q

What can the third heart sound indicate in older people?

A

Can indicate heart failure as the ventricles and chordae are stiff and weak so reach their limit much faster than normal

124
Q

What is the fourth heart sound and when is it heard?

A

S4 is heard directly before S1. It is always abnormal and rare. Caused by turbulent flow from the atria contracting against a non-compliant (stiff/ hypertrophic) ventricle.

125
Q

What does mitral stenosis do to the myocardium?

A

Causes left atrial hypertrophy

126
Q

What does aortic stenosis do the myocardium?

A

Causes left ventricular hypertrophy

127
Q

What does mitral regurgitation do to the myocardium?

A

Causes left atrial dilation

128
Q

What does aortic regurgitation do to the myocardium?

A

Causes left ventricular dilation

129
Q

What is valvular stenosis?

A

Narrowing/ hardening of a valve, making it harder for blood to get through

130
Q

What causes mitral stenosis?

A

Rheumatic heart disease

Infective endocarditis

131
Q

What is mitral regurgitation and what does it cause?

A

An incompetent mitral valve that allows blood to leak back through during systolic contraction of the left ventricle. Results in congestive cardiac failure.

132
Q

What are the causes of mitral regurgitation?

A 
Idiopathic weakening of the valve with age
Ischeamic heart disease
Infective endocarditis
Rheumatic heart disease
Connective tissue disorders
133
Q

What is the most common valvular disease?

A

Aortic stenosis

134
Q

What are the causes of aortic stenosis?

A

Idiopathic age related calcification

Rheumatic heart disease

135
Q

What is atrial fibrillation?

A

When the contraction of the atria is uncoordinated, rapid and irregular

136
Q

What causes atrial fibrillation?

A

Disorganised electrical activity that overrides the normal, organised activity from the SA node.

137
Q

What will an ECG show in atrial fibrillation?

A

Absent p waves
Narrow QRS complex tachycardia
Irregular ventricular rhythm

138
Q

What does atrial fibrillation cause

A 
Irregular ventricle contraction
Tachycardia
Heart failure
Risk of stroke
Emboli that can cause ischaemic stroke
139
Q

What are the key presentations of atrial fibrillation?

A 
Often asymptomatic
Palpitations
Shortness of breath
Syncope
Symptoms of associated conditions (stroke, sepsis e.t.c.)
140
Q

What are the two differential diagnoses for an irregularly irregular pulse and how are they differentiated?

A

Atrial fibrillation
Ventricular ectopics
Differentiated by ECG

141
Q

What are the most common causes of atrial fibrillation?

A 
SMITH;
Sepsis
Mitral valve pathology
Ischemic heart disease
Thyrotoxicosis
Hypertension
142
Q

What are the 2 main principles when treating AF?

A

Rate/ rhythm control

Anticoagulation to prevent stroke

143
Q

Why is heart rate control the first line when treating atrial fibrillation?

A

In AF, the ventricles have to fill up by suction and gravity. Therefore, the heart rate needs to be controlled to give the ventricles more time to fill with blood and increase cardiac output.

144
Q

How can heart rate be controlled?

A

Beta blockers
Calcium channel blocker
Digoxin

145
Q

When is rhythm control the preferred treatment option for AF?

A

If there is a reversible cause
If it is new onset <48 hrs
If it is causing heart failure
If they remain symptomatic after rate control

146
Q

How can rhythm be returned to normal sinus rhythm?

A

A single cardioversion event or long term medical rhythm control

147
Q

What is cardioversion?

A 
Electrical= Electric shocks sent to the heart through electrodes placed on your chest to restore normal rhythm.
Pharmacological= Medicines used to return the heart to normal rhythm
148
Q

What are arrhythmias?

A

Abnormal heart rhythms that result from an interruption to the normal electrical signals that coordinate the contraction of the heart muscle.

149
Q

What are the four possible rhythms seen in a pulseless unresponsive patient?

A

Ventricular tachycardia
Ventricular fibrillation
Pulseless electrical activity
Asystole

150
Q

What are shockable rhythms?

A

Means defibrillation may be effective:
Ventricular tachycardia
Ventricular fibrillation

151
Q

What are non-shockable rhythms?

A

Defibrillation will not be effective:
Pulseless electrical activity
Asystole (flatline)

152
Q

What causes atrial flutter?

A

A re-entrant rhythm in an atrium: where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway.

153
Q

What is atrial flutter?

A

Uninterrupted atrial contraction due to the electrical signal recirculating

154
Q

How quickly do the atria contract in atrial flutter?

A

300bpm

155
Q

How often do the ventricles contract in atrial fibrillation and why?

A

150bpm–> Every second lap due to the long refractory period to the AV node.

156
Q

What does the ECG of atrial flutter look like?

A

‘Sawtooth appearance’ with P wave after P wave

157
Q

How is atrial flutter treated?

A

Rate/ rhythm control with beta blockers/ cardioversion
Treat underlying condition
Radiofrequency ablation of re-entrant rhythm
Anticoagulation

158
Q

What are the associated/ underlying conditions of atrial flutter?

A

Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis

159
Q

What causes supraventricular tachycardias (SVT)?

A

Electrical signal re-entering the atria from the ventricles and reaching the AV node, triggering another ventricular contraction.

160
Q

What does supraventricular tachycardia cause? (ECG)

A

Fast narrow complex tachycardia (QRS <0.12)

QRS complex followed immediately by a T wave.

161
Q

What is paroxysmal SVT?

A

Where SVT reoccurs and remits in the same patient over time

162
Q

What are the 3 main types of SVT?

A

Atrioventricular nodal re-entrant tachycardia
Atrioventricular re-entrant tachycardia
Atrial tachycardia

163
Q

What is atrioventricular nodal re-entrant tachycardia?

A

When the signal reentry point is back through the AV node

164
Q

What is atrioventricular re-entrant tachycardia?

A

When the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome)

165
Q

What is atrial tachycardia?

A

When an abnormal electrical signal originates in the atria somewhere other than the SA node.

166
Q

What is the stepwise acute management of stable patients with SVT?

A 
Valsalva manoeuvre
Carotid sinus massage
Adenosine
Verapamil (Calcium channel blocker(
Direct current cardioversion
**All with continuous ECG monitoring
167
Q

What is adenosines action?

A

Slows cardiac conduction through the AV node–> Interrupts the AV node/ accessory pathway during SVT and resets it back to sinus rhythm.

168
Q

What is Wolff-Parkinson White syndrome?

A

When there is an extra electrical pathway connecting the atria and ventricles (bundle of Kent)

169
Q

What is the treatment for Wolff-Parkinson White syndrome?

A

Radiofrequency ablation of the accessory pathway

170
Q

What does the ECG look like in Wolff-Parkinson White syndrome?

A

Short PR interval
Wide QRS complex
Delta wave

171
Q

What does a prolonged QT interval on an ECG indicate?

A

Prolonged repolarisation of the muscle cells in the heart after contraction.

172
Q

What can prolonged repolarisation result in in the myocardium?

A

Random spontaneous depolarisation of myoctyes prior to repolarisation (afterdepolarisations), which spread through the ventricle and cause a ventricular contraction prior to proper repolarisation.

173
Q

What is Torsades de pointes?

A

Polymorphic ventricular tachycardia caused by afterdepolarisations continuing to stimulate ventricular contractions without proper repolarisation.

174
Q

What does Torsades de pointes look like on an ECG?

A

Like normal ventricular tachycardia with a QRS that twists around the base.

175
Q

What are the causes of a prolonged QT?

A
  • Long QT syndrome (inherited)
  • Medications
  • Electrolyte disturbance
176
Q

What are ventricular ectopics?

A

Premature ventricular beats caused by random electrical discharges from outside the atria. (relatively common)

177
Q

How do ventricular ectopics present and what does it look like on ECG?

A

Present with random, brief palpitations

Appear on ECG as induvidual random, abnormal broad QRS complexes

178
Q

What is Bigemy?

A

Where ventricular ectopics occur so frequently that they appear after every sinus beat.

179
Q

What is first degree heart block?

A

When there is delayed atrioventricular conduction through the AV node, but each atrial impulse leads to a ventricular contraction

180
Q

What does first degree heart block look like on ECG?

A

PR interval> 0.2 seconds

181
Q

What is second degree heart block?

A

Where some of the atrial impulses do not make it through the AV node to the ventricles.

182
Q

What are the different types of second degree heart block?

A

Mobitz type 1 (Wenckeback’s phenomenon)
Mobitz type 2
2:1 block

183
Q

What is Mobitz type 1 (Wenckebach’s phenomenon)?

A

Cycle where the atrial impulses become gradually weaker until they do not pass through the AV node. After the failed stimulation of a ventricular contraction, the atrial impulse returns to being stonrg.

184
Q

How does Mobitz type 1 appear on ECG?

A

Increasing PR interval until the P wave no longer conducts to ventricles, causing absent QRS complex which then returns to normal.

185
Q

What is Mobitz type 2?

A

Intermitted failure or interruption of AV conduction.

186
Q

How does Mobitz type 2 appear on ECG?

A

Missing QRS complexes–> usually a ratio of P waves to QRS complexes (e.g. 3:1 block)

187
Q

What is a 2:1 heart block?

A

When there are 2 P waves for each QRS complex: every second P wave is not strong enough to stimulate a QRS complex. (Can be caused by either Mobitz)

188
Q

What is third degree heart block?

A

Complete heart block: no relationship between P waves and QRS complexes/

189
Q

What is heart block?

A

AV node blocks causing electrical signals from the atria to not correctly conduct to the ventricles

190
Q

How is tachycardia treated in unstable patients?

A

Up to 3 synchornised shocks

Amiodarone infusion

191
Q

What is the first line treatment for unstable bradycardias?

A

Atropine

192
Q

What are the main indications for a pacemaker?

A 
Symptomatic bradycardias
Mobitz type 2 AV heart block
Third degree heart block
Severe heart failure
Hypertrophic obstructive cardiomyopathy
193
Q

What is the dominant pacemaker and what is its intrinsic rate?

A

SA node: 60-100bpm

194
Q

What is the backup pacemaker and what is its intrinsic rate?

A

AV node: 40-60bpm

195
Q

What other heart cells have an intrinsic rate and what is it?

A

Ventricular cells: 20-45 bpm

196
Q

What is the P wave on an ECG?

A

Atrial depolarisation

197
Q

What is the PR interval on ECG?

A

Time for atria to repolarise and signal to get through AV node

198
Q

What is the QRS complex?

A

Ventricular depolarisation

199
Q

What is the ST segment?

A

Interval between depolarisation and repolarisation

200
Q

What is the T wave?

A

Ventricular repolarisation

201
Q

How much time does one small square indicate on ECG?

A

0.04s

202
Q

How much time does one large square indicate on ECG paper?

A

0.2 s

203
Q

What does one large box on an ECG indicate vertically?

A

0.5mV

204
Q

What is stroke volume?

A

The volume of blood ejected from each ventricle during systole

205
Q

What is cardiac output?

A

The volume of blood pumped out in a minute:

Stroke volume X heart rate

206
Q

What is total peripheral resistance and what vessels provide the most?

A

The resistance that must be overcome to push blood through the circulatory system and create flow: arterioles provide the most resistance

207
Q

What is preload?

A

The initial stretching of the cardiac myocytes prior to contraction, related to ventricular filling.

208
Q

What is afterload?

A

The pressure the left ventricle must overcome to eject blood during contraction.

209
Q

What is contractility?

A

The force of contraction and change in fibre length

210
Q

What is Starling’s law?

A

The force of contraction is proportional to the end-diastolic length of cardiac muscle fibre: The more the ventricles fill, the harder they contract

211
Q

What is the structure of an atherosclerotic plaque?

A

Lipid
Necrotic core
Connective tissue
Fibrous cap

212
Q

Outline the steps in atherosclerosis formation

A
  1. Endothelial dysfunction
  2. Entrance of LDL’s followed by WBC into tunica intima
  3. Macrophages + LDL’s= foam cells which release cytokines and IGF-1, causing smooth muscle cell migration/ proliferation
  4. Foam cell death, releasing lipid contents, growing the plaque and pro-inflammatory cytokines
  5. T cells enter plaque and release interferon- gamma which increases inflammation and activates more endothelial cells
213
Q

What inflammatory cytokines are found in plaques?

A

IL-1
IL-6
IFN-gamma

214
Q

What is the first sign of atherosclerosis without magnification?

A

Fatty streak

215
Q

What is a fatty streak?

A

Lipid containing foam cells in the arterial wall just beneath the endothelium (intimal layer)

216
Q

What are the different stages of atherosclerosis?

A
  1. Fatty streak
  2. Intermediate lesion
  3. Fibrous plaque/ advanced lesion
  4. Plaque rupture
217
Q

When do fatty streaks first appear?

A

Early age- as early as 10

218
Q

What are intermediate lesions?

A

Composed of foam cells, smooth muscle cells and T-lymphocytes. Also involves adhesion and aggregation of platelets to the vessel wall.

219
Q

What are fibrous plaques?

A

Impede blood flow and are prone to rupture. Contain smooth muscle cells, macrophages, foam cells, T lymphocytes and red cells covered by dense fibrous cap.

220
Q

What happens when an atherosclerotic plaque ruptures?

A

Thrombus formation: coagulation occurs to stop the contents spilling out.

221
Q

What are they symptoms of atherosclerosis of the coronary arteries?

A 
Vomiting
Anxiety
ANgina
Coughing
Syncope
MI
Heart failure
222
Q

What are they symptoms of atherosclerosis of the carotid arteries?

A 
Weakness
Dyspnea
Headache
Facial numbness
Paralysis
223
Q

What are they symptoms of atherosclerosis of the peripheral vessels?

A

(depends where)
Hair loss
Erectile dysfunction
Weakness of associated area

224
Q

What are they symptoms of atherosclerosis of the renal arteries?

A

Reduction in appetite
Hand/ feet swelling
Increase in BP (due to increased renin release)

225
Q

How does smoking promote the development of atherosclerosis?

A

Free radicals, nicotie and carbon monoxide are absorbed into the blood stream and damage endothelial cells.

226
Q

How does hypertension promote the development of atherosclerosis?

A

When blood vessels bifurcate, there is strong pressure on the fork causing sheering forces on the endothelial cells. This is exacerbated by high blood pressure.

227
Q

How does poorly controlled diabetes promote the development of atherosclerosis?

A

Prolonged hyperglycaemia damages blood vessels and also increases chances of many other risk factors such as obesity.

228
Q

How does increasing age promote the development of atherosclerosis?

A

You get microdamages all throughout life which slowly build up to form atherosclerosis.

229
Q

How is angina diagnosed? (1st line/ gold standard)

A

(Clinical examination)+
ECG
CT coronary angiography

230
Q

What drugs can be given to help angina?

A 
GTN spray
Aspirin
Statins
Betablockers
Calcium channel blockers
231
Q

How does aspirin help in heart disease?

A

It is an antiplatelet, reducing the blood’s ability to clot and therefore reducing the risk of thrombus

232
Q

How do statins help in heart disease?

A

Lower cholesterol, decreasing the fatty deposit formation (atherosclerosis) in arteries.

233
Q

How do beta blockers help in heart disease?

A

Block the effects of adrenaline, causing the heart to beat more slowly and with less force, lowering blood pressure.

234
Q

Why are calcium channel blockers given in angina?

A

Prevent calcium from entering the heart and artery cells, meaning they contract less strongly, reducing blood pressure.

235
Q

What are the two main ways of revascularising an atherosclerotic artery?

A

PCI

CABG

236
Q

What is PCI?

A

Percutaneous coronary intervention–> Dilating coronary atheromatous obstructions by inserting a stent and inflating a balloon.

237
Q

What is a CABG?

A

Coronary artery bypass graft: When the left internal mammary artery is used to bypass stenosis in the left anterior descending artery.

238
Q

What are the main types of ischaemic heart disease?

A

angina
acute coronary syndrome
myocardial infarction

239
Q

What diseases does acute coronary syndrome include?

A

STEMI
NSTEMI
Unstable angina

240
Q

What is a STEMI and when does it occur?

A

ST-elevation MI:

Caused by a complete occlusion of a major coronary artery.

241
Q

What does a STEMI cause?

A

Necrosis of the heart muscle supplied by the occluded coronary artery.

242
Q

Why does ST elevation occur in a STEMI?

A

ST= between ventricular depolarisation and repolarisation. Segment elevation occurs because when the ventricle is at rest and therefore repolarised, the depolarised ischeamic region generates electrical currents that are traveling away from the recording electrode

243
Q

What is an NSTEMI and what causes it?

A

Non-ST elevation myocardial infarction. Caused by COMPLETE occlusion of a MINOR artery or PARTIAL occlusion of a MAJOR coronary artery.

244
Q

How is an NSTEMI diagnosed?

A

Retrospective diagnosis made after troponin results

245
Q

What is unstable angina?

A

Angina of recent onset (<24 hours), cardiac pain with a crescendo pattern, or deterioration of previously stable angina where symptoms occur at rest/ increasing frequency or severity

246
Q

What is the differene between unstable angina and NSTEMI?

A

In NSTEMI, there is an occluding thrombus which causes myocardial necrosis (and a rise in serum troponin/ CK-MB)

247
Q

What is type 1 MI?

A

Traditional MI due to an acute coronary event

248
Q

What is a type 2 MI?

A

Ischaemia secondary to increased demand or reduced supply of oxygen.(e.g. anaemia, tachycardia, hypotension)

249
Q

What is a type 3 MI?

A

Sudden cardiac death/ cardiac arrset suggestive of ischaemia

250
Q

What are type 4/5 MI’s?

A

MI associated with PCI and CABG

251
Q

What is plericardial effusion?

A

Build up of fluid/bood in the potential space of the pericardial sac.

252
Q

What is cardiac tamponae?

A

When pericardial effusion causes extreme pressure on the heart, prevent it from pumping effectively.

253
Q

What classifies as Bradycardia?

A

Heart rate < 60bpm

<50bpm at night

254
Q

What classifies as tachycardia?

A

Heart rate >100bpm.

255
Q

What is CHA2DS2-VASc?

A

A tool for assessing whether a patient with atrial fibrillation should be started on anticoagulation. >1 then offer anticoagulation

256
Q

What does CHA2DS2-VASc stand for?

A 
Congestive heart failure
Hypertension
A2--> Age> 75
Diabetes
S2--> Stroke or TIA
Vascular disease
Age 65-74
Sex

PHASE 2A (Mine) (15 decks)

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