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Phase 2a > My cardiovascular > Flashcards

My cardiovascular Flashcards

1
Q

Name the main cardiac conditions within iscaemic heart disease

A

Angina
Myocardial infarction
Chronic congestive heart failure
Sudden death

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2
Q

Name the three main acute coronary syndromes

A

Acute myocardial infarction - STEMI and NSTEMI
Unstable angina
Tako-Tsubo cardiomyopathy

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3
Q

How does myocardial infarction occur?

A

Rupture or erosion of a coronary artery plaque, leading to thrombosis blockage
Ischaemia of cardiac myocytes - death

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4
Q

Symptoms of myocardial infarction

A
  • Crushing chest pain, radiating to the left arm
  • Sweating
  • Nausea
  • Vomiting
  • Dyspnoea (shortness of breath)
  • Fatigue
  • Palpitations
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5
Q

Risk factors for MI

A

Increasing age
Male
Family history of IHD (MI in 1st degree relative <60)
Smoking
Hypertension
Hyperlipidaemia
Diabetes mellitus
Obesity, sedentary lifestyle
Renal failure
Left ventricular systolic dysfunction

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6
Q

Differential diagnoses for MI

A

Stable and unstable angina
Pneumonia
Pneumothorax
Oesophageal spasm
GORD
Acute gastritis
Pancreatitis
Musculoskeletal chest pain

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7
Q

How is an MI managed in the ambulance?

A

Aspirin
Pain relief - GTN spray and diamorphine
Oxygen therapy if the patient is hypoxic

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8
Q

How is an MI managed in hospital?

A
  • Apirin
  • Antiplatelets
  • Nitrates
  • Beta blockers
  • Statins
  • Reperfusion therapy - PCI or CABG
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9
Q

Tests for MI

A

ECG: ST elevation if STEMI
Peaked T waves followed by T inversion, Q waves
Cardiac enzymes: Troponin T, Troponin I

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10
Q

Describe type I myocardial infarction

A

The most common
Spontaneous MI with ischaemia
Due to a primary coronary event, eg atherothrombosis

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11
Q

Describe type II myocardial infarction

A

Mismatch in oxygen demand and supply to the myocardium
Due to

  • anaemia
  • bleeding
  • drug abuse
  • aortic dissection
  • coronary artery dissection
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12
Q

What is type III MI?

A

Sudden cardiac death - electrical failure, heart stops beating

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13
Q

What is type IV MI?

A

MI due to PCI, during the procedure or due to stent thrombosis

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14
Q

What is type V MI?

A

Due to a CABG procedure

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15
Q

What is a Q-wave MI?

A

An MI which results in new pathological Q waves on an ECG. These Q waves are very wide and deep.

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16
Q

Describe a STEMI

A

ST-elevation myocardial infarction.
Due to complete occlusion of a major coronary artery previously affected by atherosclerosis.
This causes full-thickness damage to the heart muscle.
On ECG - tall T waves and ST elevation

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17
Q

Describe an NSTEMI

A

Non-ST-elevation myocardial infarction
Due to either complete occlusion of a minor coronary artery, or partial occlusion of a major coronary artery due to atherosclerosis.
Retrospective diagnosis made after troponin results.
Causes only partial thickness damage of heart muscle.
On ECG - ST depression and/ or T wave inversion

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18
Q

What is the difference between an NSTEMI and unstable angina?

A

In an NSEMI, there is an occluding thrombus which leads to myocardial thrombosis. Myocardial damage is shown by a rise in serum troponin.

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19
Q

What are the differences between a STEMI and NSTEMI?

A
  • STEMI has ST elevation, NSTEMI has ST depression
  • STEMI is complete occlusion of a major artery, NSTEMI is partial occlusion or occlusion of only a minor artery
  • STEMI causes full-thickness damage, NSTEMI only partial thickness damage
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20
Q

What are the similarities between STEMI and NSTEMI?

A
  • Occlusion of a coronary artery typically due to acute thrombosis on a atherosclerotic plaque
  • Can lead to pathological Q waves
  • Causes increased troponin levels
  • Same symptoms
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21
Q

What is angina?

A

Chest pain or discomfort accompanied by breathlessness as a result of reversible myocardial ischaemia

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22
Q

Why does angina occur?

A

Due to narrowing of one or more of the coronary arteries.
Imbalance between the heart’s oxygen demand and supply, usually from an increase in demand accompanied by a limitation of supply.

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23
Q

What causes impaired blood flow (and so angina)?

A
  • Proximal arterial stenosis
  • Increased distal resistance
  • Reduced oxygen-carrying capacity eg anaemia
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24
Q

How much occlusion is needed to cause angina?

A

70% occluion of the blood vessel

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25
Q

Where does angina pain radiate?

A
  • One or both arms
  • The neck
  • The jaw
  • The teeth
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26
Q

What are other symptoms of angina?

A
  • Dyspnoea (laboured breathing)
  • Nausea
  • Sweatiness
  • Faintness
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27
Q

What actually causes the sensation of pain in angina?

A

Ischaemic metabolites including adenosine stimulate nerve endings and produce pain.

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28
Q

Types of angina

A
  • Stable angina
  • Unstable angina
  • Microvascular angina
  • Prinzmetal’s angina
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29
Q

Describe stable angina

A

Comes during exercise, and is relieved by rest

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30
Q

Describe Prinzmetal’s angina

A

Caused by coronary artery spasm
Rare

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31
Q

Describe microvascular angina

A

Due to narrowing only in small arteries

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32
Q

Describe unstable angina

A

Angina of recent onset (less than 24 hours) or deterioration in previously stable angina
Cardiac chest pain at rest, following a crescendo pattern of worsening

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33
Q

How is unstable angina diagnosed?

A

Diagnosed with troponin test, will have no significant rise

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34
Q

Predisposing factors for angina

A
  • Age
  • Cigarette smoking
  • Family history - cardiovascular events under around 65 in parents, siblings
  • Diabetes mellitus
  • Hyperlipidemia
  • Hypertension
  • Obesity
  • Physical inactivity (sedentary)
  • Stress
  • Male sex
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35
Q

Reasons for imperfect blood supply to the heart

A
  • Anaemia
  • Atherosclerosis
  • Thrombosis
  • Thromboemboli
  • Artery spasm
  • Hypoxemia
  • Polycythemia (high rbc count)
  • Hypothermia
  • Hypovolaemia
  • Hypervolaemia
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36
Q

Causes of increased heart demand

A
  • Hypertension
  • Tachyarrhythmia
  • Valvular heart disease
  • Hyperthyroidism
  • Hypertrophic cardiomyopathy
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37
Q

Environmental factors which can exacerbate angina

A
  • Cold weather
  • Heavy meals
  • Emotional stress
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38
Q

Differential diagnoses for angina

A
  • Pericarditis/ myocarditis
  • Pulmonary embolism
  • Chest infection
  • Dissection of the aorta
  • Gastro-oesophageal
  • Musculoskeletal
  • Psychological
39
Q

Testing for angina

A

ECG - often normal, may have some ST depression, and flat or inverted T waves
CT coronary angiography - uses a contrast dye given by IV to identify narrowing or blockages
Myoview scan - radio-labelled tracer is injected, and the light and dark shows well and poorly perfused myocardium

40
Q

Non-medical treatment for angina

A

Reassurance - MI is still unlikely
Advice for emergency: ring 999
Lifestyle changes:

  • Stop smoking
  • Weight loss
  • Exercise
  • Diet
41
Q

Medication for angina

A
  • Beta blockers
  • Glyceryl trinitrate (GTN) spray
  • Calcium channel blockers
  • Statins
  • Antiplatelets
  • ACE inhibitors
42
Q

Describe beta blockers

A
  • First-line antianginal
  • Negatively chronotropic (decrease HR) and negatively ionotropic (decrease contractility)
  • Act on beta 1 receptors in the heart as part of the adrenergic sympathetic pathway
43
Q

Side effects of beta blockers

A
  • Tiredness
  • Bradycardia - dizziness
  • Erectile dysfunction
  • Cold hands and feet
44
Q

Contraindications for beta blockers

A
  • Severe athsma: binds to beta 2 receptors
  • Hypotension
  • Bradyarrhythmias
45
Q

Describe GTN spray

A
  • Dilates coronary arteries to reduce blood pressure
  • Dilates veins to reduce preload
  • Thus reduces work of the heart and the oxygen demand
46
Q

Main side effect of GTN spray

A

Causes headache, as blood vessels around the brain dilate

47
Q

Describe calcium channel blockers

A
  • Cause dilation of the systemic arteries, resulting in a drop in blood pressure
  • Reduces afterload (pressure needed to eject blood from the ventricles) on the heart
  • Thus less energy is required to produce the same cardiac output
48
Q

Describe statins

A
  • Inhibits the enzyme which causes synthesis of cholesterol by the liver
  • Lowers low-density lipoprotein by 50%
  • Anti-atherosclerotic
49
Q

Describe antiplatelets

A
  • Inhibits cyclo-oxygenase and prostaglandins
  • Reduces platelet aggregation in coronary arteries, thereby avoiding platelet thrombosis
50
Q

Main side effect of antiplatelets

A

Cause gastric ulceration

51
Q

Describe ACE inhibitors

A

Reduce blood pressure through the renin-angiotensin-aldosterone system

52
Q

Types of surgical intervention for angina

A

Percutaneous coronary intervention (PCI)
Coronary artery bypass graft (CABG)

53
Q

When is surgical intervention used?

A
  • If the drugs are not effective enough
  • When a high risk disease is identified

Revascularisation restores the coronary artery to become patent and increase its flow reserve

54
Q

Describe PCI

A

Dilating coronary atheromatous obstructions by inflating a balloon and stent within it
The balloon is removed, leaving the stent and patent artery

55
Q

Pros of PCI

A
  • Non-invasive
  • Convienient
  • Short recovery
  • Repeatable
56
Q

Cons of PCI

A
  • Risk of stent thrombosis
  • Not good for complex disease
57
Q

Describe CABG

A
  • Vein removed from saphenous vein to connect aorta and right atrium
  • Internal mammary artery swung round to connect to the left atrium to bypasss stenosis in the LAD
58
Q

Pros of CABG

A
  • Good prognosis
  • Deals with complex disease
59
Q

Cons of CABG

A
  • Invasive
  • Risk of stroke or bleeding
  • Need to stay in hospital
  • Long recovery
60
Q

Tako-Tsubo cardiomyopathy

A
  • Stress-induced cardiomyopathy
  • May look like MI
  • Causes transient (short-time) left ventricular systolic dysfunction, ballooning of the left ventricular apex during systole
  • Recovers over a few days or weeks
  • Limited or no permanent damage
61
Q

How are acute coronary syndromes managed?

A
  1. Diagnosis: history, ECG, troponin, coronary angiography
  2. Pain relief: opiates, nitrates
  3. Check no active/ recent life threatening bleeding/ anaemia
  4. If ST elevation, arrange PCI
  5. Cardiac monitoring for anaemia
  6. Antithrombolytic therapy
62
Q

Define congenital heart disease

A

Faulty embryonic developmentof the heart - misplaced structures or arrest of the progression of normal structure development

63
Q

Describe tetralogy of fallot

A
  • Ventricular septal defect
  • Pulmonary stenosis
  • Hypertrophy of the right ventricle
  • Overriding aorta
64
Q

When does surgery for tetralogy of fallot take place?

A

First before the age of two years
Often again in adult life, for pumonary valve regurgitation

65
Q

Describe ventricular septal defects (VSD)

A
  • Abnormal connection between the two ventricles.
  • Blood flows from high pressure left ventricle to low pressure right ventricle, increasing blood flow through the lungs.
  • May close spontaneously during childhood
66
Q

Signs of large ventricular septal defect

A
  • Breathless
  • Poor feeding
  • Small, skinny baby
  • Increased respiratory rate
  • Tachycardia
  • Big heart on chest x ray
  • Murmur
  • May lead to Eisenmenger’s syndrome
67
Q

Signs of a small septal defect

A
  • Loud systolic murmur due to high force through a small hole
  • Asymptomatic
  • Well grown
  • Normal heart rate and size
  • Risk of endocarditis
68
Q

What is Eisenmenger’s syndrome?

A
  • High pressure pulmonary blood flow leads to damage to delicate pulmonary vasculature
  • Resistance to blood flow through the lungs increases, the right ventricle pressure increases - the shunt direction reverses.
  • The patient becomes blue in the lips and hands.
69
Q

Describe atrial septal defects (ASD)

A
  • Abnormal connection between the two atria.
  • Shunt is left to right, increasing flow into right heart and the lungs.
  • Common, often the patient will present in adulthood.
70
Q

Effects of large atrial septal defect

A
  • Significant increased flow through the right heart and lungs in childhood
  • Right heart dilatation
  • Shortness of breath on exertion
  • Increased chest infections
71
Q

Effects of small atrial septal defect

A
  • Small increase in flow
  • No right heart dilatation
  • No symptoms
  • Leave alone
  • Increases in size with age
72
Q

Heart sounds and x-ray of small atrial septal defect

A
  • Heart sounds: pulmonary flow murmur, split second heart sound (due to delayed closure of pulmonary valve due to increased right heart blood flow)
  • X ray: big pulmonary arteries and big heart
73
Q

Describe atrio-ventricular septal defect

A
  • Hole in the very centre of the heart, involving the ventricular septum, the atrial septum, the mitral valve, and tricuspid valve.
  • Instead of two separate atrioventrcular valves there is one large malformed one
  • Often seen in down syndrome patients
74
Q

Complete atrio-ventricular septal defect signs

A
  • Breathless neonate
  • Poor weight gain
  • Poor feeding
  • Extremely high pulmonary blood flow
75
Q

Partial atrio-ventricular septal defect signs

A
  • Can present in late adulthood
  • Presents like a small VSD
76
Q

How are atrio-ventricular septal defects treated?

A
  • Complete defect: Needs repair or pulmonary artery band in infancy - repair is surgically challenging
  • Partial defect: May be left alone if there is no right heart dilatation
77
Q

Describe a patent ductus arteriosus

A

Failure of the ductus arteriosus (between pulmonary artery and aorta) to close during the first breath.
High pressure, high blood flow into the pulmonary vasculature.

78
Q

Signs of a large patent ductus arteriosus

A
  • Continuous ‘machinery’ murmur
  • Big heart
  • Breathless, poor feeding, failure to thrive
  • Eisenmenger’s syndome
79
Q

Signs of a small patent ductus arteriosus

A
  • Usually asymptomatic
  • Murmur found incidentally
  • Endocarditis risk
80
Q

How is a patent ductus arteriosus treated?

A

Surgically or percutaneously

81
Q

Describe coarctation of the aorta

A

Narrowing of the aorta at the site of insertion of the ductus arteriosus

82
Q

Severe coarctation of the aorta symptoms

A
  • Complete or almost complete obstruction of aortic flow
  • Collapse with heart failure
  • Needs urgent repair
83
Q

Mild coarctation of the aorta symptoms

A
  • Presents with hypertension
  • Incidental murmur finding
  • Should be repaired to prevent long-term problems
84
Q

Signs of coarctation of the aorta

A

Right arm hypertension
Bruit (buzzing) over the scapulae and back from collateral vessels
Murmur

85
Q

How is coarctation of the aorta repaired?

A

Surgical or percutaneous repair.

86
Q

Long-term complications of coarctation of the aorta

A
  • Hypertension
  • Early coronary artery disease
  • Early strokes
  • Subarachnoid haemorrhage
  • Re-coarctation requiring repeat intervention
  • Aneurysm formation at the site of repair
87
Q

Describe bicuspid aortic valves

A

Can have only two flaps, or two of the flaps are fused.

88
Q

Effects of bicuspid aortic valves

A
  • Can be severely stenotic in infancy or childhood
  • Degenerate quicker than normal valves.
  • Become regurgitant earlier than normal valves
89
Q

Describe pulmonary stenosis

A

Narrowing of the outflow of the right ventricle

90
Q

Effects of severe pulmonary stenosis

A
  • Right ventricular failure as a neonate
  • Collapse
  • Poor pulmonary blood flow
  • Right ventricle hypertrophy
  • Tricuspid regurgutation
91
Q

Mild pulmonary stenosis effects

A
  • Well-tolerated for many years
  • Right ventricular hypertrophy
92
Q

Treatment of pulmonary stenosis

A
  • Balloon valvuloplasty (balloon opens it up)
  • Open valvotomy
  • Open trans-annular patch to enlarge
  • Shunt to bypass the blockage
93
Q

Describe univentricular hearts

A
  • Singular ventricle
  • Number of congenital heart defects which result in the lack of two fully developed ventricles.
94
Q

Surgical treatment for univentricular hearts

A

Fontan circulation: passive connection of vena cava to the pulmonary artery. This surgery has long-term complications and risks.

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