Cardiovascular Flashcards

Question 1

Q

What is the ECG?

Answer

A

Electrocardiography - A representation of the electrical events of the cardiac cycle

Question 2

Q

What can ECG identify?

Answer

A

Arrhythmias
Myocardial ischaemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (i.e. hyperkalemia or hypokalemia)
Drug toxicity (i.e. digoxin and drugs which prolong the QT interval)

Question 3

Q

What is the SA node? + what is the normal heart rate?

Answer

A

the dominant pacemaker with an intrinsic rate of 60-100 bpm

(NORMAL HEART RATE) - the fastest depolarising tissue

Question 4

Q

what is the AV node?

Answer

A

back-up pacemaker with an intrinsic rate of 40-60 bpm

Question 5

Q

Ventricular cells?

Answer

A

back-up pacemaker with an intrinsic rate of 20-45 bpm

Question 6

Q

Impulse conduction pathway?

Answer

A

Sinoatrial node → AV node → Bundle of His → Bundle branches →
Purkinje fibres

Question 7

Q

P wave

Answer

A

atrial depolarisation - seen in every lead apart from aVR

Question 8

Q

PR interval

Answer

A

time taken for atria to depolarise and electrical activation to get
through AV node

Question 9

Q

QRS complex

Answer

A

ventricular depolarisation, still called QRS even if Q and/or S
are missing depending on what lead you are looking at

Question 10

Q

ST segment

Answer

A

interval between depolarisation & repolarisation

Question 11

Q

T wave

Answer

A

ventricular repolarisation

Question 12

Q

Tachycardia

Answer

A

increased heart rate

Question 13

Q

Bradycardia

Answer

A

decreased heart rate

Question 14

Q

Dextrocardia

Answer

A

heart on right side of chest instead of left

Question 15

Q

Acute anterolateral myocardial infarction

Answer

A

ST segments are raised in

anterior (V3 - V4) and lateral (V5-V6) leads

Question 16

Q

Acute inferior MI

Answer

A

ST segments are raised in inferior (II, III, aVF) leads

Question 17

Q

Atrial repolarisation?

Answer

A

usually not evident on an ECG since it occurs at

the same time as the QRS complex so is hidden

Question 18

Q

On a 25mm/sec ECG

Answer

A

- Horizontally:
• One small box = 0.04s/40ms
• One large box = 0.20s
- Vertically:
• One large box = 0.5mV

Question 19

Q

Left ventricle

Answer

A

palpated in the 5th left intercostal space and mid-clavicular
line, responsible for the apex beat

Question 20

Q

Stroke volume

Answer

A

The volume of blood ejected from each ventricle during systole

Question 21

Q

Cardiac output

Answer

A

The volume of blood each ventricle pumps as a function of time
(liters per minute):
• Cardiac output (L/min) = Stroke volume (L) x Heart rate (BPM)

Question 22

Q

Total peripheral resistance

Answer

A

The total resistance to flow in systemic blood
vessels from beginning of aorta to vena cava - arterioles provide the most
resistance

Question 23

Q

Preload

Answer

A

the volume of blood in the left ventricle which stretches the cardiac
myocytes before left ventricular contraction - how much blood is in the
ventricles before it pumps (end-diastolic volume). When veins dilate it results in
a decrease in preload (since by dilating veins the venous return decreases).

Question 24

Q

Afterload

Answer

A

the pressure the left ventricle must overcome to eject blood during
contraction - dilate arteries = decrease in afterload

Question 25

Q

Contractility

Answer

A

force of contraction and the change in fibre length - how hard
the heart pumps. When muscle contracts myofibrils stay the same length but
the sarcomere shortens - force of heart contraction that is independent of
sarcomere length

Question 26

Q

Elasticity

Answer

A

myocardial ability to recover normal shape after systolic stress

Question 27

Q

Diastolic dispensibilty

Answer

A

the pressure required to fill the ventricle to the same

diastolic volume

Question 28

Q

Compliance

Answer

A

how easily the heart chamber expands when filled with blood

volume

Question 29

Q

Starlings law

Answer

A

Force of contrition is proportional to the end diastolic length of
cardiac muscle fibre - the more ventricle fills the harder it contracts

Question 30

Q

At rest the cardiac muscle

Answer

A

not at optimal length. Below optimal length means

the force of contraction is decreased - inefficient

Question 31

Q

↑ venous return

Answer

A

= ↑ end diastolic volume = ↑ preload = ↑ sarcomere
stretch = ↑ force of contraction thus = ↑ stroke volume and force of
contractions

Question 32

Q

Standing

Answer

A

decreases venous return due to gravity thus, cardiac output decreases, which causes a drop in blood pressure, stimulating baroreceptors to increase blood pressure

Question 33

Q

HEART SOUNDS:

- S1

Answer

A

mitral and tricuspid valve closure

Question 34

Q

S2

Answer

A

aortic and pulmonary valve closure

Question 35

Q

S3

Answer

A

in early diastole during rapid ventricular filling, normal in children and pregnant women, associated with mitral regurgitation and heart failure

Question 36

Q

S4

Answer

A

‘Gallop’, in late diastole, produced by blood being forced into a stiff
hypertrophic ventricle - associated with left ventricular hypertrophy

Question 37

Q

commonly develop atherosclerosis

Answer

A

Circumflex, Left anterior descending (LAD) and right coronary arteries

Question 38

Q

Risk factors for atherosclerosis:

Answer

A

Age - increases with age
Tobacco smoking - leads to endothelium erosion
High serum cholesterol
Obesity - since more pericardial fat and thus increase in inflammation
Diabetes - hyperglycaemia damages endothelium
Hypertension
Family history

Question 39

Q

Distribution of atherosclerosis plaques:

Answer

A

Found within peripheral and coronary arteries

- Focal distribution along the artery length

Question 40

Q

Structure of an atherosclerotic plaque:

Answer

A

- A complex lesion consisting of:
• Lipid
• Necrotic core
• Connective tissue
• Fibrous “cap”
- Eventually the plaque will either occlude the vessel lumen resulting in a
restriction of blood flow (ANGINA), or it may rupture (thrombus formation
and subsequent death)

Question 41

Q

Atherosclerosis formation: 1

Answer

A

Initiated by an injury to the endothelial cells which leads to endothelial dysfunction
Once initiated, chemoattractants (chemicals that attract leukocytes) are
released from endothelium to attract leukocytes which then accumulate and
migrate into the vessel wall
Chemoattractants are released from site of injury and a concentration-
gradient is produced
Inflammatory cytokines found in plaques:
• IL-1 - KEY ONE
• IL-6
• IFN - gamma
Fatty streaks:
• Earliest lesion of atherosclerosis
• Appear at a very early age (less than 10)
• Consist of aggregations of lipid-laden macrophages and T lymphocytes
within the intimal layer of the vessel wall

Question 42

Q

Atherosclerosis formation: 2

Answer

A

Intermediate lesions:
• Composed of layers of:
Lipid laden macrophages (foam cells - macrophages that have
taken up lots of lipids)
Vascular smooth muscle cells
T lymphocytes
• There is adhesion and aggregation of platelets to the vessel wall
(aspirin inhibits platelet aggregation)
Fibrous plaques/advanced lesions:
• Impede blood flow
• Prone to rupture
• Covered by dense fibrous cap made of extracellular matrix proteins
including collagen (strength) and elastin (flexibility) laid down by smooth
muscle cells that overly lipid core and necrotic debris
• May be calcified
• Contains:
Smooth muscle cells
Macrophages and foam cells (lipid laden macrophages)
T lymphocytes
Red cells
• Plaque is filled with fibrin

Question 43

Q

Atherosclerosis formation: - Plaque rupture:

Answer

A

Plaque rupture:
• Plaque is constantly growing and receding
• The fibrous cap needs to be resorbed and redeposited in order to be
maintained
• If balance shifts e.g. in favour of inflammatory conditions (increased
enzyme activity) then the cap becomes weak and the plaque ruptures
• Basement membrane, collagen and necrotic tissue exposure as well as
haemorrhage of vessel within the plaque
• Thrombus (clot) formation and subsequent vessel occlusion

Question 44

Q

Angina

Answer

A

is chest pain or discomfort as a result of reversible myocardial ischaemia
This usually implies narrowing of one or more of the coronary arteries
Tends to be exacerbated by exertion and relieved by rest

Question 45

Q

• Types:

- Stable angina:

Answer

A

• Induced by effort and relieved by rest

Question 46

Q

• Types:

- Unstable (crescendo) angina:

Answer

A

• Angina of recent onset (less than 24hrs) or
• Deterioration in previously stable angina, with symptoms frequently
occurring at rest
• Angina of increasing frequency or severity, occurs on minimal
exertion or even at rest - form of acute coronary syndrome

Question 47

Q

• Types:

- Prinzmetal’s angina:

Answer

A

• Caused by coronary artery spasm (rare)

Question 48

Q

• Epidemiology:

Answer

A

Myocardial ischaemia resulting in angina occurs when there is a mismatch
between blood supply and metabolic demand - this can occur due to:
• Atheroma/stenosis of coronary arteries thereby impairing blood flow -
most common cause
• Valvular disease
• Aortic stenosis
• Arrhythmia
• Anaemia - thus less O2 can be transported
Ischaemic metabolites including adenosine, stimulate nerve endings and
produce pain
More common in men

Question 49

Q

Risk factors for angina

Answer

A

Smoking
Sedentary lifestyle
Obesity
Hypertension
Diabetes mellitus
Family history
Genetics
Age
Hypercholesterolaemia

Question 50

Q

Pathophysiology:

That of atherosclerosis develops

Answer

A

narrowing of coronary arteries that results

in ischaemia and thus pain i.e. angina

Question 51

Q

Angina - Initiation:

Answer

A

• Endothelial dysfunction and injury around sites of sheer and damage with subsequent lipid accumulation at sites of impaired endothelial
barrier
• Local cellular proliferation and incorporation of oxidise lipoproteins occurs
• Mural thrombi on surface and subsequent healing and repeat of cycle

Question 52

Q

Angina - Adaption:

Answer

A

• As plaque progresses to 50% of vascular lumen size the vessel can no
longer compensate by re-modelling and becomes narrowed
• This drives variable cell turnover within the plaque with new matrix
surfaces and degradation of matrix
• May progress to unstable plaque

Question 53

Q

Angina - Clinical stage:

Answer

A

• The plaque continues to encroach upon the lumen and runs the risk of
haemorrhage or exposure of tissue HLA-DR antigens which might
stimulate T cell accumulation
• This drives an inflammatory reaction against part of the plaque contents
• Complications develop including ulceration, fissuring, calcification and
aneurysm change

Question 54

Q

Angina - - Pathological stages:

Answer

A

• Fatty streak:
- These show macrophages filled with abundant lipid (foam cells)
- Also smooth muscle cells with fat
• Intimal cell mass:
- These are collections of muscle cells and connective tissue
without lipid - “cushions”
• The atheromatous plaque:
- Characterised by distorted endothelial surface containing
lymphocytes, macrophages, smooth muscle cells and a variably
complete endothelial surface
- There is local necrotic and fatty matter with scattered lipid rich
macrophages
- Evidence of local haemorrhage may be seen with iron deposition
and calcification
- Complicated plaques are those which show calcification and mural
thrombus - making them vulnerable to rupture
• Complications of plaque rupture:
- Acute occlusion due to thrombus
- Chronic narrowing of vessel lumen with healing of the local
thrombus
- Aneurysm change
- Embolism of thrombus +/- plaque lipid content

Question 55

Q

• Clinical presentation Angina:

Answer

A

Central chest tightness or heaviness
Provoked by exertion, especially after meal or in the cold windy weather or by
anger or excitement
Relieved by rest or GTN spray
Pain may radiate to one or both arms, the neck, jaw or teeth
May be dyspnoea, nausea, sweatiness and faintness
Scoring:
• 1. Have, central, tight, radiation to arms, jaw & neck
• 2. Precipitated by exertion
• 3. Relieved by rest or spray GTN
• 3/3 = Typical angina
• 2/3 = Atypical pain
• 1/3 = Non-anginal pain

Question 56

Q

• Differential diagnosis Angina:

Answer

A

Pericarditis/myocarditis
Pulmonary embolism
Chest infection
Dissection of the aorta
GORD

Question 57

Q

• Diagnosis Angina: - 12 lead ECG:

Answer

A

Often normal
May show ST depression
Flat or inverted T waves
Look for signs of past MI

Question 58

Q

• Diagnosis Angina: - Treadmill test/Exercise ECG:

Answer

A

• Put ECG on patient, then make them run on treadmill uphill - trying to
induce ischaemia
• Monitor how long patient is able to exercise for
• If you see ST segment depression then this is a sign of late-stage
ischaemia
• Many patients unsuitable e.g. can’t walk, very unfit, young females and
bundle branch block

Question 59

Q

• Diagnosis Angina:- CT Scan Calcium scoring:

Answer

A

• CT the heart and if there is atherosclerosis in the arteries then the
calcium will light up white - if there is significant calcium then this would
indicate angina

Question 60

Q

• Diagnosis Angina:- SPECT/myoview:

Answer

A

• Radio-labelled tracer injected into patient
• Its taken up by the coronary arteries where there is good blood supply -
this will light up
• Where there is little blood supply these areas will not light up
• If there is no light after exercise then this is indicative of myocardial ischaemia

Question 61

Q

• Diagnosis Angina:- Cardiac catheterisation

Question 62

Q

Treatment Angina: - Modify risk factors:

Answer

A

Stop smoking
Encourage exercise
Weight loss

Question 63

Q

• Treatment angina : - Treat underlying conditions

Question 64

Q

• Treatment angina : - Pharmacological: • Aspirin:

Answer

A

Antiplatelet effect (inhibits platelet aggregation) in coronary arteries
thereby avoiding platelet thrombosis
To reduce events
E.g. salicylate
COX inhibitor - reduces prostaglandin synthesis including
thromboxane A2 resulting in reduced platelet aggregation
Side effects - gastric ulceration

Answer 63

A

HMG-CoA reductase inhibitors - reduces cholesterol produced by
liver
Reduce events and LDL-cholesterol
Anti-atherosclerotic

Answer 64

A

Reduce force of contraction of heart
E.g. Bisoprolol and atenolol
Act on B1 receptors in the heart as part of the adrenergic
sympathetic pathway
B1 activation → Gs → cAMP to ATP → contraction
Reduces:
• Heart rate (negatively chronotropic)
• Left ventricle contractility (negatively inotropic)
• Cardiac output
Side effects; tiredness, nightmares, bradycardia, erectile
dysfunction and cold hands and feet
DO NOT GIVE in asthma, heart failure/heart block, hypotension and bradyarrhythmias

Answer 65

A

Nitrate that is a venodilator
Dilates systemic veins thereby reducing venous return to right
heart
Reduces preload
Thus reduces work of heart and O2 demand
Also dilates coronary arteries
Side effect: profuse headache immediately after use

Answer 66

A

Primary arterodilators
Dilates systemic arteries resulting in BP drop
Thus reduces afterload on the heart
Thus less energy required to produce same cardiac output
Thus less work on heart and O2 demand
E.g. verapamil

Answer 67

A

• To restore patent coronary artery and increase flow reserve
• Done when medication fails (most) or when high risk disease is
identified
• Percutaneuos Coronary Intervention (PCI):
- Dilating coronary atheromatous obstructions by inflating balloon
within it
- Insert balloon and stent, inflate balloon and remove it, stent
persists and keeps artery patent
- Expanding plaque = make artery bigger
- Pros; less invasive, convenient, short recovery & repeatable
- Cons; risk of stent thrombosis, not good for complex disease
• Coronary Artery Bypass Graft (CABG):
- Left Internal Mammary Artery (LIMA) used to bypass proximal
stenosis (narrowing) in Left Anterior Descending (LAD) coronary
artery
- Pros; good prognosis, deals with complex disease
- Cons; invasive, risk of stroke or bleeding, one time treatment and
need to stay in hospital - long recovery

Answer 68

A

Develop a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis
This causes full thickness damage of heart muscle
Can usually be diagnosed on ECG at presentation
Will produce a pathological Q wave some time after MI so also known as Q-wave infarction

Answer 69

A

• Angina of recent onset (less than 24hrs) or
• Cardiac chest pain with crescendo pattern
• Deterioration in previously stable angina, with symptoms frequently
occurring at rest
• Angina of increasing frequency or severity, occurs on minimal
exertion or even at rest - form of acute coronary syndrome

Answer 70

A

• Occurs by developing a complete occlusion of a MINOR or a partial
occlusion of a major coronary artery previously affected by
atherosclerosis
• Is a retrospective diagnosis made after troponin results and
sometimes other investigation results are available
• This causes partial thickness damage of heart muscle
• Also known as a Non-Q wave infarction will see ST depression and/
or T wave inversion

Answer 71

A

in a NSTEMI there is
occluding thrombus which leads to myocardial necrosis and a rise in
serum troponin or creatine kinase-MB (CK-MB)

Answer 72

A

occurs when cardiac myocytes die due to myocardial

ischaemia

Answer 73

A

Spontaneous MI with ischaemia due to a primary coronary event e.g. plaque erosion/rupture, fissuring or dissection

Answer 74

A

MI secondary to ischaemia due to increased O2 demand or
decreased supply such as in coronary spasm, coronary
embolism, anaemia, arrhythmias, hypertension or
hypotension

Answer 75

A

MI due to sudden cardiac death, related to PCI and related to CABG respectively

Answer 76

A

Age
Male
Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative
below 55
Smoking
Hypertension, diabetes mellitus, hyperlipidaemia
Obesity & sedentary lifestyle

Answer 77

A

Rupture or erosion of the fibrous cap of a coronary artery plaque
Leading to platelet aggregation and adhesion, localised thrombosis,
vasoconstriction and distal thrombus embolisation
The presence of a rich lipid pool within the plaque and a thin, fibrous cap is
associated with an increased risk of rupture
Thrombus formation and the vasoconstriction produced by platelet release
of serotonin and thromboxane A2 result in myocardial ischaemia due to
reduction of coronary blood flow
Fatty streak → Fibrotic plaque → Atherosclerotic plaque → Plaque rupture/
fissure and thrombosis → MI or Ischaemic stroke or Critical leg ischaemia
or Sudden CVS death
In unstable angina the plaque has a necrotic centre and ulcerated cap and
the thrombus results in PARTIAL OCCLUSION
In myocardial infarction the plaque also has a necrotic centre but the
thrombus results in TOTAL OCCLUSION

Answer 78

A

- Unstable angina:
• Chest pain; new onset, at rest with crescendo pattern
• Breathlessness
• Pleuritic pain
• Indigestion
- New onset angina
- Recent destabilisation of pre-existing angina with moderate or severe
limitations of daily activities
- Acute central chest pain, lasting more than 20 minutes, associated with:
• Sweating
• Nausea and vomiting
• Dyspnoea
• Fatigue
• Shortness of breath
• Palpitations
- May present without chest pain (silent infarct) e.g. in elderly or diabetics
- Distress and anxiety
- Pallor
- Increased pulse and reduced BP
- Reduced 4th heart sound
- May be signs of heart failure (increase in jugular venous pressure)
- Tachy/bradycardia
- Peripheral oedema

Answer 79

A

Angina
Pericarditis
Myocarditis
Aortic dissection
Pulmonary embolism
Oesophageal reflux/spasm

Answer 80

A

• Can be normal
• ST depression and T-wave inversion (this tends to occur hours/days
after) (NSTEMI) are highly suggestive of an ACS, particularly if
associated with anginal chest pain
• Can get hyperacute (tall) T waves
• With a STEMI, complete occlusion of a coronary vessel will result in a
persistent ST-elevation, hyperacute (tall) T waves or new left bundle
branch block pattern - may see pathological Q waves a few days after
MI (sign of previous MI)

Answer 81

A

• Troponin (T & I):
- T & I are the most sensitive and specific markers of myocardial
necrosis
- Serum levels increase within 3-12 hours from the onset of chest
pain and peak at 24-48 hours
- They then fall back to normal over 5-14 days
- Can act as prognostic indicator to determine mortality risk and
define which patients may benefit from aggressive medical therapy
and early coronary revascularisation
• CK-MB:
- CK-MB can be used as a marker for myocyte death - but has low
accuracy since it can be present in the serum of normal
individuals and in patients with significant skeletal muscle damage
- However it can be used to determine re-infarction as levels drop
back to normal after 36-72 hours
• Myoglobin:
- Becomes elevated very early in MI but the test has poor specificity
since myoglobin is present in skeletal muscle

Answer 82

A

• Look for cardiomegaly, pulmonary oedema or a widened mediastinum
(aortic rupture)

Answer 83

A

- Pain relief:
• GTN spray
• IV opioid
- Anti-emetic
- Oxygen:
• Aim for 94-98% saturation
• 88-92% for those with COPD

Answer 84

A

• Atheromatous plaque rupture results in platelets being exposed to ADP/ThromboxaneA2/ adrenaline/thrombin/collagen tissue factor
• This results in platelet activation/aggregation via IIb/IIIa glycoproteins binding to fibrinogen (enables platelets to adhere to each other = aggregation)
• Then thrombin (already present in surroundings) is able to enzymatically convert fibrinogen to fibrin (insoluble) resulting in the formation of a fibrin
mesh over platelet plug and the formation of a thrombotic clot
• Aspirin (oral):
- COX1-inhibitor = blocks formation of thromboxane A2 thus
prevents platelet aggregation
• P2Y12 inhibitors (oral):
- Inhibit ADP-dependant activation of IIb/IIIa glycoproteins thereby preventing amplification response of platelet aggregation
- Can be used if allergic to aspirin
- Can also be used alongside aspirin as a dual anti-platelet therapy
- E.g. Clopidogrel, Prasugrel & Ticagrelor
- Side effects: neutropenia (low neutrophils), thrombocytopenia (low platelets) and INCREASED RISK OF BLEEDING
- AVOID if CABG planned
• Glycoprotein IIb/IIIa antagonists (IV):
- Only IV available
- Used in combination with aspirin and oral P2Y12 inhibitors in patients with ACS undergoing Percutaneous Coronary Intervention (PCI)
- INCREASES RISK OF MAJOR BLEEDING
- E.g. Abciximab, Tirofiban and Eptifbatide

Answer 85

A

- Beta blockers (IV &amp; oral):
• E.g. Atenolol (IV then oral) or Metoprolol (IV then oral)
• Side effects: Avoid with asthma, heart failure, hypotension and
bradyarrhythmias
- Statins (oral):
• HMG-CoA reductase inhibitors
• E.g. Simvastatin, Pravastatin and Atorvastin
- ACE inhibitors (oral):
• E.g. Ramipril and Lisonopril
• Monitor renal function
- Coronary revascularisation:
• PCI
• CABG - high risk mortality in high risk groups e.g. recent MI
- Risk factor modification:
• Stop smoking
• Lose weight and exercise daily
• Healthy diet
• Treat hypertension &amp; diabetes
• Low fat diet with statins

Answer 86

A

• Necrosis of cardiac tissue (myocyte death) due to prolonged myocardial ischaemia due to COMPLETE occlusion of artery by thrombus

Answer 87

A

ST elevation MI (STEMI):
• Develop a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis
• This causes full thickness damage of heart muscle
• Usually diagnosed on ECG at presentation
• Tall T waves
• ST elevation and subsequent pathological Q wave
• May present as new left bundle branch block (LBBB) on ECG
• COMPLETE
Non ST elevation MI (NSTEMI) or Non-Q infarction:
• Occurs by developing a complete occlusion of a MINOR or a partial
occlusion of a major coronary artery previously affected by
atherosclerosis
• This causes partial thickness damage of heart muscle
• A RETROSPECTIVE diagnosis made after troponin results and
sometimes other investigation results are available
• ST depression/T wave inversion
• STEMI is the most common medical emergency

Answer 88

A

Age
Male
History of premature coronary heart disease
Premature menopause
Diabetes mellitus
Smoking
Hypertension
Hyperlipidaemia
Obesity and sedentary lifestyle
Diabetes mellitus
Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative
below 55

Answer 89

A

Rupture or erosion of vulnerable fibrous cap of coronary artery atheromatous plaque
This results in platelet aggregation, adhesion, local thrombosis, vasoconstriction and DISTAL THROMBUS EMBOLISATION resulting in PROLONGED COMPLETE ARTERIAL OCCLUSION resulting in myocardial
necrosis within 15-30 minutes in a STEMI (since major artery occluded fully)
STEMI:
• The sub-endocardial myocardium is initially affected but, continued ischaemia, the infarct zone extends through the sub-epicardial myocardium, producing a transmural Q wave MI
• Early reperfusion may salvage regions of the myocardium - reducing future mortality and morbidity

Answer 90

A

Any patient presenting with severe chest pain lasting more than 20 minutes
may be suffering from an MI
Chest pain:
• Severe central ongoing pain, lasting more than 20 minutes
• Pain may radiate to the left arm, jaw or neck
• Pain DOES NOT usually respond to sublingual GTN spray - opiate
analgesia is required
• Pain described as substernal pressure, squeezing, aching, burning or
even sharp pain
• Associated with; sweating, nausea, vomiting, dyspnoea, fatigue and/or
palpitations
Breathlessness
Fatigue
Distress and anxiety
Pale, clammy and marked sweating
Significant hypotension (low BP)
Bradycardia or tachycardia

Answer 91

A

Stable angina, unstable angina, NSTEMI, pneumonia, pneumothorax, oesophageal spasm, GORD, acute gastritis, pancreatitis and MSK chest pain

Answer 92

A

Diagnosed on presentation
ST elevation
Tall T waves
L bundle branch block (LBBB)
T wave inversion and pathological Q waves follow

Answer 93

A

Diagnosis is retrospective made after troponin results etc.
ST depression and T wave inversion

Answer 94

A

• Performed on admission to A & E
• Continuous monitoring required due to high likelihood of significant
cardiac arrhythmias

Answer 95

A

Anterior - ST elevation V1-3
Inferior - St elevation II, III, AVF
Lateral - I, AVF V5-6
Posterior - ST depression V1-3 Dominant R wave ST elevation V5-6
Subendocardial - any

Answer 96

A

After the first few minutes, the T waves
become tall, pointed and upright, and there is
ST segment elevation
After the first few hours, the T waves invert, the R-wave voltage decreases and Q waves develop
After a few days, the ST segment returns to normal
After weeks or months, the T wave may return to upright but the Q WAVE REMAINS

Answer 97

A

Troponin I or T increased
Myoglobin increased
Transthoracic echocardiography (TTE) may be helpful to confirm MI, as
wall-motion abnormalities are detected early in STEMI

Answer 98

A

Aspirin 300mg chewable
GTN (sublingual)
Morphine

Answer 99

A

IV morphine
Oxygen if their sats are below 95% or are breathless
Beta-blocker - Atenolol
P2Y12 inhibitor - Clopidogrel

Answer 100

A

• PCI:
- Presented to all patients who present with an acute STEMI who can be
transferred to a primary PCI centre WITHIN 120 MINUTES of first
medical contact
- If not possible then give patient fibrinolysis and then transfer to PCI
centre after infusion
• CABG

Answer 101

A

- Fibrinolysis - enhance the breakdown of occlusive thromboses by the
activation of plasminogen to form plasmin
- Risk factor modification:
• Stop smoking
• Lose weight and exercise daily
• Healthy diet
• Treat hypertension &amp; diabetes
• Low fat diet with statins
- Secondary prevention:
• Statins
• Aspirin long term
• Warfarin if large MI
• o blockers
• ACE inhibitors

Answer 102

A

• Sudden death - often within hours often due to ventricular fibrillation
• Arrhythmias - in the first few days due to electrical instability following infarction,
pump failure and excessive sympathetic stimulation
• Persistent pain - 12 hours-few days after due to progressive myocardial necrosis
• Heart failure:
- When cardiac output is insufficient to meet the bodies metabolic demands
- Due to ventricular dysfunction following muscle necrosis also resulting in
arrhythmias
• Mitral incompetence - can happen in the first few days or occur later. Due to
myocardial scarring preventing valve closure
• Pericarditis - due to transmural infarct resulting in inflammation of pericardium,
more common in STEMI
• Cardiac rupture:
- Early rupture - the result of shearing between mobile and immobile
myocardium
- Late rupture - due to weakening of wall following muscle necrosis and acute
inflammation
• Ventricular aneurysm - due to stretching of newly formed collagenous scar tissue

Answer 103

A

• The inability of the heart to deliver blood and thus O2 at a rate that is commensurate with the requirement of metabolising tissue of the body
• Is a syndrome and not a diagnosis on its own
• Can result from any structural or functional cardiac disorder that impairs the hearts ability to function and meet the demands of supplying sufficient oxygen
and nutrients to the metabolising body

Answer 104

A

65 and older
African descent
Men (due to lack of protective effect provided by oestrogen resulting in the early onset of IHD in men
Obesity
People who have had an MI

Answer 105

A

When the heart begins to fail, there are many systems involved that initiate physiological COMPENSATORY CHANGES that try to maintain cardiac output and peripheral perfusion in order to negate the effects of the heart failure
However as heart failure progresses, these mechanisms are overwhelmed
and become pathophysiological also known as DECOMPENSATION

Answer 106

A

Myocardial failure leads to a reduction of the volume of blood ejected with each heart beat, and an increase in the volume of blood remaining after systole
This increased diastolic (or preload - the volume of blood in the ventricle before contraction) volume stretches the myocardial fibres and, as Starling’s law of the heart says, myocardial contraction is restored since the stretching of myocardial fibres will increase its force of contraction
However, in heart failure, the failing myocardium actually doesn’t contract as much in response to increased preload meaning cardiac output cannot be maintained and may decrease

Answer 107

A

Outflow resistance (afterload) is the load or resistance against which the ventricle contracts
It is made up of:
• Pulmonary and systemic resistance
• Physical characteristics of the vessel walls
• The volume of blood that is ejected
When there is an increase in afterload there is a increase in end-diastolic volume and a decrease in stroke volume and thus a DECREASE in cardiac output
This results in a increase of end-diastolic volume and dilatation of the ventricle itself (the more the ventricle is dilated the harder it must work i.e. the more resistance there is to contract against) which then further exacerbates the problem of afterload

Answer 108

A

When baroreceptors (located in the arterial wall of the aorta, carotid and in the heart walls and major veins) detect a drop in arterial pressure or an increase in venous pressure (due to back flow of blood) they stimulate sympathetic activation
This increases the force of contraction (positively inotropic) of the heart (which increases stroke volume) as well as heart rate - both resulting in an increase in cardiac output
However in heart failure there is chronic sympathetic activation which results in the receptors being acted on by the sympathetic system to down regulate resulting in their being less receptor to act on meaning the effect of sympathetic activation is diminished and cardiac output stops increasing in response to sympathetic
activation

Answer 109

A

Reduced cardiac output leads to diminished renal perfusion,thereby activating the renin-angiotensin system whereby; angiotensinogen is converted to angiotensin I under the action of renin, angiotensin I is then converted to angiotensin II under the act
of angiotensin converting enzyme (ACE), angiotensin II then stimulates the release of aldosterone from the adrenal cortex above the kidneys
This results in increased Na+ reabsorption and thus water reabsorption as well as the release of ADH which stimulates water retention
This results in the increased volume of the blood which in turn increases blood pressure and thus venous pressure which in turn increases pre-load thereby increasing the stretching of the heart and thus force of contraction and thus stroke volume and thus
cardiac output
However, with increased force of contraction the cardiac myocytes require more energy and thus more blood however in heart failure (which is most commonly caused by ischaemic heart disease) there will be no increase in blood and thus the cardiac myocytes will die resulting in a decrease in force of contraction and thus a decrease in stroke volume and a decrease in cardiac output

Answer 110

A

Inability of the ventricle to contract normally resulting in a decrease in cardiac output
Caused by ischaemic heart disease, myocardial infarction and cardiomyopathy (disease of heart muscle thus impairing function)

Answer 111

A

• Inability of the ventricles to relax and fill fully thereby
decreasing stroke volume and decreasing cardiac output
• Caused by hypertrophy (due to chronic hypertension which results in increased blood pressure thereby increasing afterload so heart pumps against more resistance and thus cardiac myocytes grow bigger to compensate for this) of ventricles resulting in there being less space for blood to fill in and thus decreased cardiac output
• Also caused by aortic stenosis (the narrowing of the aortic valve) which also increases afterload and thus decreases cardiac output

Answer 112

A

• Often used exclusively to mean new onset or decompensation of chromic heart failure characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypotension

Answer 113

A

Develops slowly

* Venous congestion is common but arterial pressure is well maintained until very late

Answer 114

A

Three cardinal symptoms are; shortness of breath, fatigue & ankle swelling but these are non-specific!
Dyspnoea especially when lying flat (orthopnoea)
Cold peripheries
Raised jugular venous pressure (JVP)
Murmurs and displaced apex beat
Cyanosis
Hypotension
Peripheral or pulmonary oedema due to back flow resulting from the decreased cardiac output
Tachycardia
Third & fourth heart sounds
Ascites
Bi-basal crackles
Use New York Heart Association (NYHA) classification for the assessment of the severity of symptoms:
• Class I: No limitation (asymptomatic) - exercise = no fatigue, dyspnoea or palpitation
• Class II: Slight limitation (mild HF (heart failure)) - comfortable at rest, normal activity = fatigue, dyspnoea and palpitations
• Class III: Marked limitation (moderate HF) - comfortable at rest, gentle activity = fatigue, dyspnoea & palpitations
• Class IV: Inability to carry out any physical activity without discomfort (severe HF) - symptoms occur at rest

Answer 115

A

Blood tests:
• Brain natriuretic peptide (BNP):
Secreted by ventricles in response to increase myocardial wall
stress
Increased in patients with heart failure
Levels correlate with ventricular wall stress and the severity of
heart failure
• FBC, U&E’s and liver biochemistry
CXR:
• Alveolar oedema
• Cardiomegaly
• Dilated upper lobe vessels of lungs
• Effusions (pleural)
ECG:
• Shows underlying causes; ischaemia, left ventricular hypertrophy in
hypertension or arrhythmia
• If ECG and BNP normal then heart failure is unlikely
• If both abnormal then go to echocardiogram
Echocardiography:
• Assess cardiac chamber dimension
• Look for regional wall motion abnormalities, valvular disease and
cardiomyopathies
• Look for sign of MI

Answer 116

A

Lifestyle changes:
• Avoid large meals, lose weight, stop smoking, exercise, vaccination
Diuretics:
• Promote sodium and thus water loss thereby reducing ventricular filling pressure (preload) decreasing systemic and pulmonary congestion
• Generally provide symptomatic relief
• Loop diuretic - furosemide
• Thiazide diuretic - bendroflumethiazide (inhibit sodium reabsorption in
the distal convoluted tubule)
• Aldosterone antagonist (thereby inhibiting ADH release resulting in
water loss) - spirolactone & epelerone - note with these beware of renal
impairment and hyperkalaemia
ACE inhibitors:
• Ramipril, enalipril, captopril
• Side effects: cough (since inhibit ACE and thus the breakdown of
substance P and bradykinin which results in cough), hypotension,
hyperkalaemia and renal dysfunction
• If cough is a problem then can give angiotensin receptor blockers (not
as effective as ACE-inhibitors) e.g. canderstan or valsartan

Answer 117

A

- Beta-blockers:
• Bisoprolol, nebivolol, carvedilol
• Start at low dose and titrate upwards
• DO NOT GIVE TO ASTHMATICS
- Digoxin
- Inotropes
- Revascularisation:
• When some viable myocardium remains
• Illicit PCI stenting
- Surgery to repair:
• Mitral valve repair, aortic or mitral valve replacement
- Heart transplant in young people
- Cardiac resynchronisation - improve the coordination of the atria and
ventricles

Answer 118

A

• Mitral valve is on the left side and is also known as the tricuspid valve, it separates the left atrium from the left ventricle

Answer 119

A

Obstruction of left ventricle inflow that prevents proper filling during diastole
Mitral valve has 2 cusps

Answer 120

A

Normal mitral valve area is 4-6cm2, symptoms begin at areas less than 2cm2
Most common cause of mitral stenosis is rheumatic heart disease
secondary to rheumatic fever due to infection with group A beta-haemolytic
streptococcus e.g. Streptococcus Pyogenes
The condition is more common in men than women
Inflammation due to rheumatic fever leads to commissural fusion and a
reduction in mitral valve orifice area, causing the characteristic doming
pattern seen on echocardiography
Over many years, the condition progresses to valve thickening, cusp fusion,
calcium deposition, a severely narrowed (stenotic) valve orifice and
progressive immobility of the valve cusps
Prevalence and incidence is decreasing due to a reduction of rheumatic
heart disease
Other causes include:
• Infective endocarditis (3.3%)
• Mitral annular calcification (2.7%) - rarely leads to mitral stenosis if extensive, particularly in elderly patients and those with end-stage renal
disease

Answer 121

A

History of rheumatic fever

- Untreated streptococcus infections

Answer 122

A

Thickening and immobility of the valve leads to obstruction of blood flow
from the left atrium to the left ventricle
In order for sufficient cardiac output to be maintained, the left atrial pressure
increases and left atrial hypertrophy and dilatation occur
Consequently pulmonary venous, pulmonary arterial and right heart
pressures also increase
The increase in pulmonary capillary pressure is followed by the development
of pulmonary oedema - this is seen particularly when atrial fibrillation occurs,
due to the elevation of left atrial pressure and dilatation, with tachycardia
and loss of coordinated atrial contraction
This is partially countered by alveolar and capillary thickening and
pulmonary arterial vasoconstriction (reactive pulmonary hypertension)
Pulmonary hypertension leads to right ventricular hypertrophy, dilatation
and failure with subsequent tricuspid regurgitation

Answer 123

A

Usually there are no symptoms until the valve orifice is moderately stenosed
i.e. area is less than 2cm2
This usually doesn’t occur until several decades after the first attack of
rheumatic fever
Progressive dyspnoea - due to left atrial dilation resulting in pulmonary
congestion (reduced emptying), which is worse with; exercise, fever,
tachycardia and pregnancy
Haemoptysis - due to rupture of bronchial vessels due to the elevated
pulmonary pressure
Right heart failure - due to the development of pulmonary hypertension with
symptoms of weakness, fatigue and abdominal or lower limb swelling
Atrial fibrillation - due to left atrium dilation giving rise to palpitations
Systemic emboli - due to atrial fibrillation, most commonly in the cerebral vessels

Answer 124

A

Prominent “a” wave in jugular venous pulsations - due to pulmonary
hypertension and right ventricular hypertrophy
Mitral facies/malar flush - bilateral, cyanotic or dusky pink discolouration
over the upper cheeks - pinkish-purple patches on the cheeks due to
vasoconstriction in response to diminished cardiac output
Heart sounds:
• Diastolic murmur (heard when blood flows over a valve):
Low-pitched diastolic rumble most prominent at the apex
Heard best with patient lying on the left side in held expiration

• Loud opening S1 snap: heard at apex when leaflets are still mobile:
- Due to the abrupt halt in leaflet motion in early diastole, after a
rapid initial opening, due to fusion at the leaflet tips
- As the valve cusps become more immobile, the loud first heart
sound softens and the opening snap disappears
• The more severe the stenosis, the longer the diastolic murmur and the
closer the opening snap is to S2 (second heart sound)

Answer 125

A

- CXR:
• Left atrial enlargement
• Pulmonary oedema/congestion
• Occasionally calcified mitral valve
- ECG:
• Atrial fibrillation
• Left atrial enlargement
- Echocardiogram:
• GOLD STANDARD for diagnosis
• Assess mitral valve mobility, gradient and mitral valve area

Answer 126

A

Mitral stenosis is a mechanical problem and medical therapy does not
prevent progression
Beta-blockers e.g. Atenolol and digoxin which control heart rate and thus
prolong diastole for improved diastolic filling
Diuretics for fluid overload e.g. Furosemide
Percutaneous mitral balloon valvotomy:
• Catheter is inserted into the right atrium vie the femoral vein under local
anaesthesia
• The interatrial septum is then punctured and the catheter advanced into
the left atrium and across the mitral valve
• The balloon is inflated and puts pressure on valve thereby separating
the leaflets thereby increasing the size of the mitral valve opening thus
enabling more blood to flow from left atrium into left ventricle
Mitral valve replacement

Answer 127

A

• Backflow of blood from the left ventricle to the left atrium during systole
• Mild physiological mitral regurgitation (MR) is seen in 80% of normal
individuals

Answer 128

A

Occurs due to abnormalities of the valve
leaflets, chordae tendinae, papillary muscles or left ventricle
Most frequent cause is myxomatous degeneration (MVP) (weakening of the chordae tendinae) - resulting in a floppy mitral valve that prolapses (mitral valve prolapse)
Other causes include:
• Ischaemic mitral valve
• Rheumatic heart disease
• Infective endocarditis
• Papillary muscle dysfunction/rupture
• Dilated cardiomyopathy

Answer 129

A

Associated with females
Lower BMI
Advanced age
Renal dysfunction
Prior MI

Answer 130

A

Regurgitation into the left atrium produces left atrial dilatation but little
increase in left atrial pressure if the regurgitation is longstanding, since the
regurgitant flow is accommodated by the large left atrium
Pure volume overload due to leakage of blood into left atrium during systole
Compensatory mechanisms: Left arterial enlargement, left ventricle
hypertrophy (since left ventricle must put in same effort to pump less blood(due to regurgitation) so needs to pump harder to maintain cardiac output and
thus hypertrophy to increase stroke volume) and increases contractility:
• Progressive left atrial dilatation and right ventricular dysfunction due to
pulmonary hypertension
• Progressive left ventricular volume overload leads to dilatation and
progressive heart failure

Answer 131

A

Auscultation:
• Soft S1 and a pan systolic murmur at the apex radiating to the axilla
• Prominent third extra heart sound (S3) in congestive heart failure/left
atrium overload
• In chronic mitral regurgitation, the intensity of the murmur does not
correlate with the severity
Exertion dysponea i.e. exercise intolerant
Dysponea develop because of pulmonary venous hypertension that arises as
a direct result of the mitral regurgitation and secondarily as a consequence
of left ventricular failure
Fatigue and lethargy due to reduced cardiac output
Increased stroke volume is felt as a palpitation
Symptoms of right heart failure and eventually lead to congestive cardiac
failure
Heart failure may coincide with increased haemodynamic burden e.g in
pregnancy, infection or atrial fibrillation

Answer 132

A

Compensatory phase: 10-15 years
Once patients ejection fraction becomes less than 60% and/or becomes
symptomatic then mortality rises sharply
Severe mitral regurgitation has a 5%/year mortality rate

Answer 133

A

ECG:
• May show left atrial enlargement, atrial fibrillation and left ventricle
hypertrophy in severe MR
• But not diagnostic
CXR:
• Left atrial enlargement and central pulmonary artery enlargement
Echocardiogram:
• Estimation of left atrium and left ventricle size and function
• Also gives valve structure assessment
• Transoesophageal is very helpful

Answer 134

A

Medications:
• Vasodilators such as ACE-inhibitors e.g. Ramipril or Hydralazine
(smooth muscle relaxer)
• Heart rate control for atrial fibrillation with Beta blockers (Atenolol),
Calcium channel blockers and digoxin
• Anticoagulation in atrial fibrillation and flutter
• Diuretics for fluid overload e.g. Furosemide
Serial echocardiography:
• Mild: 2-3 years
• Moderate: 1-2 years
• Severe: 6-12 months

- Indications for surgery:
• Any symptoms at rest or exercise then initiate repair if feasible
• Asymptomatic:
- If ejection fraction is less than 60%
- If new onset atrial fibrillation

Answer 135

A

Aortic valve is located on the left side of the heart and separates the left
ventricle from the aorta
Aortic valve has 3 cusps
It is one of the two semilunar valves of the heart, the other being the
pulmonary valve

Answer 136

A

• Narrowing of the aortic valve resulting in obstruction to the left ventricular
stroke volume, leading to symptoms of chest pain, breathlessness, syncope
and fatigue

Answer 137

A

Normal aortic valve area is 3-4cm2
Symptoms occur when valve area is 1/4th of normal
Primarily a disease of ageing
Congenital is the second most common cause
The most common type of valvular disease in the western world

Answer 138

A

• Supravalvular (above valve) e.g congenital
fibrous diaphragm above the aortic valve
• Subvalvular (below valve) e.g congenital
condition in which a fibrous ridge or
diaphragm is situated immediately below
the aortic valve
• Valvular - most common

Answer 139

A

3 main causes:
• Calcific aortic valvular disease (CAVD) - essentially calcification of the
aortic valve resulting in stenosis, most commonly seen in elderly
• Calcification of a congenital bicuspid aortic valve (BAV) (valve has 2
leaflets instead of 3 due to genetic disease - this is the most common
congenital heart disease) resulting in stenosis
• Rheumatic heart disease - rare now due to eradication

Answer 140

A

Congenital bicuspid aortic valve (BAV) predisposes to stenosis and
regurgitation - bicuspid valves are more likely to develop stenosis
Congenital BAV is predominant in males

Answer 141

A

Due to the narrowing there is obstructed left ventricular emptying and a pressure gradient develops between the left ventricle and the aorta resulting in an increased afterload
This results in increased left ventricular pressure and compensatory left
ventricular hypertrophy
In turn, this results in relative ischaemia of the left ventricular myocardium
(since hypertrophy results in increased blood demand), and consequent
angina, arrhythmias and left ventricular failure
The obstruction to left ventricular emptying is relatively more severe on
exercise - since exercise causes a many-fold increase in cardiac output,
however due to the severe narrowing of the aortic valve, the cardiac output
can hardly increase - thus, the blood pressure falls, coronary ischaemia
worsens, the myocardium fails and cardiac arrhythmias develop
When this compensatory mechanism is exhausted left ventricular function
decline rapidly

Answer 142

A

Think aortic stenosis in ANY elderly person with chest pain, exertional
dysponea or syncope (loss of consciousness due to lack of blood)
Classic triad:
• Syncope - usually exertional
• Angina (increases myocardial oxygen demand; with resulting demand/
supply mismatch)
• Heart failure (usually after 60)
• Dysponea on exertion due to heart failure
Sudden death
Slow rising carotid pulse (pulsus tardus) and decreased pulse amplitude
(pulsus parvus)
Heart sounds:
• Soft or absent second heart sound
• Prominent 4th (S4) heart sound due to left ventricular hypertrophy
• Ejection systolic murmur-crescendo-decrescendo character
• Loudness does NOT tell you anything about severity

Answer 143

A

Aortic regurgitation

- Subacute bacterial endocarditis

Answer 144

A

Echocardiogram:
• Two measurement obtained are:
Left ventricular size & function; left ventricular hypertrophy, dilation
and ejection fraction
Doppler derived gradient and valve area (AVA), allows for the
assessment of the pressure gradient across the valve during
systole
ECG:
• Left ventricular hypertrophy
• Left atrial delay
• Left ventricular ‘strain’ pattern due to ‘pressure overload’ - depressed
ST segments and T-wave inversion in leads orientated towards left
ventricle i.e. I, AVL, V5 & 6 when disease is severe
CXR:
• Left ventricular hypertrophy
• Calcified aortic valve

Answer 145

A

Rigorous dental hygiene/care due to the increased risk of infective
endocarditis (IE) in anyone with valvular heart disease - consider IE
prophylaxis in dental procedures
There is a limited role for medication due to the fact that aortic stenosis is a
mechanical problem
Vasodilators are contraindicated in severe aortic stenosis due to the fact that
they may trigger hypotension and thus syncope

Answer 146

A

Surgical aortic valve replacement is the definitive treatment:
• Indications:
Any SYMPTOMATIC patients with severe aortic stenosis (include
symptoms with exercise)
Any patient with decreasing ejection fraction
Any patent undergoing CABG with moderate or severe aortic
stenosis
An alternative for surgical replacement is percutaneous in what is known as
Transcutaneous Aortic Valve Implantation (TAVI):
• Minimally invasive
• Pass catheter up the aorta then inflate balloon across the narrowed
valve which will crack the calcification
• Then pass another catheter which leaves a stent with a valve = new
aortic valve

Answer 147

A

• Leakage of blood into the left ventricle from aorta during diastole due to
ineffective coaptation (bringing together) of the aortic cusps, of which there
are three

Answer 148

A

Can be associated with aortic stenosis
Main causes:
• Congenital bicuspid aortic valve (BAV) - chronic
• Rheumatic fever - chronic
• Infective endocarditis - acute

Answer 149

A

SLE
Marfan’s and Ehlers-Danlos syndrome - connective tissue disorders
Aortic dilatation
Infective endocarditis or aortic dissection

Answer 150

A

Aortic regurgitation is reflux of blood from the aorta through the aortic valve
into the left ventricle during diastole
If net cardiac output is to be maintained, the total volume of blood pumped
into the aorta must increase and, consequently, the left ventricular size must
enlarge resulting in left ventricle dilation and hypertrophy
Progressive dilation leads to heart failure
Furthermore due to the fact that the remaining blood in the root of the aorta
supplies the coronary arteries via the coronary sinus during diastole -
regurgitation causes diastolic blood pressure to fall and thus coronary
perfusion decreases
Also the large left ventricular size is mechanically less efficient, so that the
demand for oxygen is greater and cardiac ischaemia develops

Answer 151

A

In chronic regurgitation, patients remain asymptomatic for many years
before symptoms develop
Exertional dysponea
Palpitations
Angina
Syncope
Wide pulse pressure
Apex beat is displaced laterally
Heart sounds:
• Diastolic blowing murmur at the left sternal border
• Systolic ejection murmur; due to increased flow across the aortic valve
Collapsing water hammer pulse (bounding and forceful rapidly increasing and
subsequently collapsing)
Quincke’s sign - capillary pulsation in the nail beds
de Musset’s sign - head nodding with each heart beat
Pistol shot femoral - a sharp bang heard on auscultation
Asymptomatic until 4th or 5th decade

Answer 152

A

Heart failure
Infective endocarditis
Mitral regurgitation

Answer 153

A

Echocardiogram:
• Evaluation of the aortic valve and aortic root
• Measurement of left ventricle dimensions and function
• Cornerstone for decision making and follow up evaluation
CXR:
• Enlarged cardiac silhouette and aortic root enlargement
• Left ventricular enlargement
ECG:
• Signs of left ventricular hypertrophy due to ‘volume overload’ - tall R
waves and deeply inverted T waves in the left-sided chest leads, and
deep S waves in the right-sided leads

Answer 154

A

In general consider infective endocarditis prophylaxis
Vasodilators such as ACE-inhibitors such as Ramipril will improve stroke
volume and reduce regurgitation but only if patient is symptomatic or has
hypertension
Serial echocardiograms to monitor progression
Surgery for valve replacement:
• If symptoms are increasing, enlarging heart on CXR/ECHO, ECG
deterioration (T wave inversion in lateral leads)

Answer 155

A

• An infection of the endocardium or vascular endothelium of the heart
• Known as subacute bacterial endocarditis
• Infection occurs on the following:
- Valves with congenital or acquired defects (usually on the left side of
the heart). Right sided endocarditis is more common in IV drug addicts
- Normal valves with virulent organisms such as Streptococcus
pneumoniae or Staphylococcus aureus
- Prosthetic valves and pacemakers

Answer 156

A

More common in developing countries
Disease of:
• the elderly or those with prosthetic valves
• the young IV drug user
• the young with congenital heart disease
More common in males
Caused by:
• Staphylococcus aureus (IVDU, diabetes and surgery) - most common
cause
• Pseudomonas aeruginosa
• Streptococcus viridans (dental problems) - GRAM POSITIVE, alpha
haemolytic and optochin resistant (Strep. mutans, strep, sanguis, strep.
milleri & strep. oralis)

Answer 157

A

IV drug use
Poor dental hygiene
Skin and soft tissue infection
Dental treatment
IV cannula
Cardiac surgery
Pacemaker

Answer 158

A

Usually the consequence of two factors; the presence of organisms in the
bloodstream and abnormal cardiac endothelium that facilitates their
adherence and growth
Bacteraemia may arise for patient-specific reasons:
• Poor dental hygiene - bacteria in tooth plaque can cause gum disease
which results in bleeding and inflammation of gums meaning when
brushing/in dental procedure this bacteria can enter the bloodstream
and reach the heart
• IV drug use
• Soft tissue infections
It may also be associated with diagnostic or therapeutic procedures:
• Dental treatment
• Intravascular cannulae
• Cardiac surgery
• Permanent pacemakers

Answer 159

A

Damaged endocardium promotes platelet and fibrin deposition, which allows
organisms to adhere and grow, leading to an infected vegetation
Aortic and mitral valves are most commonly involved - IV drug users are
the exception since right-sided lesions are more common in them
Virulent organisms destroy the valve they are on resulting in regurgitation
and worsening heart failure

Answer 160

A

High clinical suspicion:
• New valve lesion/regurgitant murmur
• Embolic events of unknown origin
• Sepsis of unknown origin
• Haematuria, glomerulonephritis and suspected renal infarction
• Fever plus:
Prosthetic material inside the heart
Risk factor for infective endocarditis e.g. IV drug user
Newly developed ventricular arrhythmias or conduction
disturbances
Headache, fever, malaise, confusion, and night sweats - quite unspecific so
often misdiagnosed and missed
Also finger clubbing

Answer 161

A

If Staphylococcus aureus then will develop very quickly - high fever and feel
ill rapidly, with the other virulent ones you don’t feel as ill
Embolisation of vegetations e.g. stroke, pulmonary embolus, bone
infections, kidney dysfunction and myocardial infarction
Valve dysfunction result in in arrhythmia and heart failure
Endocarditis should be excluded in ANY patient with a heart murmur and
fever
Clinical manifestations:
• Splinter haemorrhages on nail beds of fingers
• Embolic skin lesions - black spots on skin (infarcts causes by bits of
infective vegetation blocking small capillaries)
• Osler nodes - tender nodules in the digits
• Janeway lesions - haemorrhages and nodules in the fingers
• Roth spots - retinal haemorrhages with white or clear centres seen on
fundoscopy
• Petechiae - small red/purple spots caused by bleeds in the skin

Answer 162

A

Use Dukes criteria
Blood cultures:
• 3 sets from different sites over 24 hours
• Take BEFORE ANTIBIOTICS STARTED
• Identifies in 75% of cases
Blood test:
• CRP & ESR raised
• Normochromic (normal concentration of haemoglobin), normocytic
(normal sized red blood cells) anaemia
• Neutrophilia
Urinalysis - look for haematuria

Answer 163

A

CXR - cardiomegaly
ECG - long PR interval at regular intervals
Echocardiogram:
• Two options:
Transthoracic echo (TTE) - safe, non invasive, no discomfort BUT
often poor images so low sensitivity but can identify vegetations
(if greater than 2mm) - however a negative TTE DOES NOT exclude
the diagnosis of infective endocarditis
Transoesophageal echo (TOE) - much more sensitive but very
uncomfortable, is useful for visualising mitral lesions and possible
development of aortic root abscess - BETTER AT DIAGNOSING,
ANSWER THIS IN EXAM!

Answer 164

A

Antibiotic treatment (which one is decided on organism ascertained from
cultures) for 4-6 weeks
If not staphylococcus then use penicillin ideally Benzylpenicillin &
Gentamycin (doesn’t work on own since cannot get through bacterial cell wall)
If staphylococcus then use Vancomycin & Rifampicin (if MRSA)
Treat complications e.g. arrhythmia, heart failure, heart block,
embolisation, stroke rehab and abscess drainage
Surgery - removing valve and replacing with prosthetic one:
• Operate if the infection cannot be cured with antibiotics i.e. returns after
treatment
• Operate to remove infected devices
• Operate to remove large vegetations before they embolise
In term of prevention recommend GOOD ORAL HEALTH and inform patients
of symptoms that may indicate infective endocarditis

Answer 165

A

• Group of diseases of the myocardium that affect the mechanical or electrical
function of the heart

Answer 166

A

All carry an arrhythmic risk
Can occur at younger ages
Restrictive cardiomyopathy is rare in childhood and has a poor outcome
once symptoms develop
In general they are inherited genetic conditions although there are some
acquired ones
4 types:
• Hypertrophic
• Dilated
• Restricted
• Arrythmogenic right ventricular

Answer 167

A

Family history of cardiomyopathy
High blood pressure
Obesity
Diabetes
Previous MI

Answer 168

A

Ventricular hypertrophy/thickening of the muscle

Answer 169

A

Quite common, second most common cardiomyopathy (behind dilated)
1/500 people have it
Autosomal dominant - familial
May present at any age
Most common cause of sudden cardiac death in the young
HCM refers to otherwise unexplained primary cardiac hypertrophy

Answer 170

A

• Caused by sarcomeric protein gene mutations e.g troponin T and B-
myosin

• All in the absence of hypertension and valvular disease
• The hypertrophic, non-compliant ventricles impair diastolic filling
resulting in reduced stroke volume and thus cardiac output
• Another issue with thick powerful heart is that there is a disarray of
cardiac myocytes so conduction is affected

Answer 171

A

Hypertrophy of myocardium, particularly the intraventricular septum
Sudden death may be the first manifestation
Chest pain, Angina, dysponea, dizziness, palpitations, syncope
Left ventricular outflow obstruction may be a feature
Cardiac arrhythmia
Ejection systolic murmur
Jerky carotid pulse

Answer 172

A

• ECG: is abnormal and shows signs of left ventricular hypertrophy with
progressive T wave inversion and deep Q waves
• Echocardiogram: shows ventricular hypertrophy and a small left
ventricle cavity
• Genetic analysis can confirm diagnosis since most cases are
autosomal dominant and familial

Answer 173

A

• Amiodarone - anti-arrythmatic medication, if at high risk of arrhythmia
then can place an implantable cardiac defibrillator
• Calcium channel blocker e.g. Verampil
• Beta-blocker e.g. Atenolol

Answer 174

A

Dilated left ventricle which contracts poorly/has thin muscle

Answer 175

A

• Most common cardiomyopathy
• Autosomal dominant - familial
• Can be caused by; ischaemia, alcohol, thyroid disorder or familial/
genetic

Answer 176

A

• Caused by cytoskeletal gene mutations
• Left ventricle or right ventricle or all 4 chamber dilatation and thus
dysfunction
• Theory is that poorly generated contractile force leads to progressive
dilatation of heart with some diffuse interstitial fibrosis

Answer 177

A

Shortness of breath at first and fatigue
Dysponea
Heart failure since can’t contract
Arrhythmias
Thromboembolism
Sudden death
Increased jugular venous pressure

Answer 178

A

CXR: cardiac enlargement
ECG: tachycardia, arrhythmia and non-specific T wave changes
Echo: shows dilated ventricles

Answer 179

A

• Heart failure and atrial fibrillation treated in conventional way

Answer 180

A

Rare condition

Answer 181

A

• Causes are; amyloidosis, idiopathic, sarcoidosis, end-myocardial
fibrosis

Answer 182

A

• There is normal or decreased volume of both ventricles with bi-atrial
enlargement, normal wall thickness, normal cardiac valves and
impaired ventricular filing
• Restrictive physiology
• Poor dilation of the heart restricts its the ability of the heart to take on
blood and pass it to the rest of the body
• Rigid myocardium restricts diastolic ventricular filling

Answer 183

A

• Similar to constructive pericarditis
• Dysponea, fatigue and embolic symptoms
• Elevated jugular venous pressure with diastolic collapse and elevation
of venous pressure with inspiration
• Hepatic enlargement, ascites and dependent oedema
• Third and fourth heart sounds

Answer 184

A

CXR, ECHO & ECG are abnormal but non-specific

* Cardiac catheterisation helps to diagnose restrictive cardiomyopathy

Answer 185

A

No specific treatment with poor prognosis
Patients die within a year
Can consider cardiac transplantation

Answer 186

A

• Progressive genetic cardiomyopathy characterised by progressive fatty
and fibrous replacement of ventricular myocardium
• Cause is unknown
• Familial form is usually autosomal dominant with incomplete penetrance
but can be recessive

Answer 187

A

Desmosome (normally hold cardiac cells together) gene mutation
Right ventricle replaced by fat and fibrous tissue
Muscle dies and replaced by fat as part of inflammatory process

Answer 188

A

Cardiac cells are held less together thus conduction issues
ARRHYTHMIA is most common feature
Syncope
In late stages may be signs of right heart failure

Answer 189

A

• ECG usually normal but may show T wave inversion
• ECHO may also be normal but in advanced disease may show right
ventricular dilation
• Genetic testing is the gold standard

Answer 190

A

• Beta-blockers e.g. Atenolol for patients with non-life-threatening
arrhythmias
• Amiodarone for symptomatic arrhythmias
• Occasionally cardiac transplant indicated i.e. in cardiac failure or devastating arrhythmia

Answer 191

A

• 1% of all live births have some form of cardiac defect - common
• Vary from minor to incompatible with life ex-utero
• There is an overall male predominance
• Although some individual lesions such as atrial septal defect and persistence
ductus arteriosus occur more commonly in females
• Usually due to misplaced structures or the arrest of the progression of normal
structure development

Answer 192

A

One child with defect increases the chance of the second child having
another defect
Maternal prenatal rubella infection - persistent ductus arteriosus and
pulmonary valvular and arterial stenosis
Maternal alcohol misuse - septal defects
Single genes associated e.g. Trisomy 21 (Down’s - septal, mitral and
tricuspid valve defects)
Drugs e.g. Thalidomide, Amphetamines and Lithium
Diabetes of mother
Genetic abnormalities e.g. the familial form of arterial spatial defect and congenital heart block

Answer 193

A

Congenital heart disease should be recognised as early as possible since
the response is usually better the earlier treatment is initiated
Central cyanosis:
• Occurs because of right-left shunting of blood or because of complete
mixing of systemic and pulmonary blood flow resulting in poorly
oxygenated blood entering the systemic circulation
• Skin will go blueish
• Seen in Tetralogy of Fallot and Tricuspid atresia
Clubbing of the fingers - associated with prolonged cyanosis

Answer 194

A

Pulmonary hypertension:
• Results from large left-to-right shunts
• The persistently raised pulmonary flow leads to the development of
increased pulmonary artery vascular resistance and consequent
pulmonary hypertension
• This resistance is due to the thickening of the vascular walls of the
pulmonary arteries in response to the higher pressure
• This resistance causes right ventricular pressure to increase and causes
the REVERSAL OF SHUNT to right-to-left resulting in the patient going
blue i.e. cyanosis
• Known as Eisenmenger’s reaction and known as Eisenmenger’s
complex specifically in relation to a ventricular-septal defect
• The development of pulmonary hypertension significantly worsens the
prognosis

Answer 195

A

Growth retardation - common in children with cyanotic heart disease
Syncope:
• Common when severe right or left ventricular outflow tract obstruction
is present
• Exertional syncope is associated with keeping central cyanosis and may
occur in Fallot’s tetralogy
Adolescents and adults with congenital heart disease present with specific
common problems related to the longstanding structural nature of these
conditions:
• Endocarditis - especially in small ventricular septal defects or bicuspid aortic valve
• Calcification and stenosis of congenitally deformed valves e.g. bicuspid aortic valve
• Atrial and ventricular arrhythmias
• Sudden cardiac death
• Right heart failure
• End-stage heart failure

Answer 196

A

• Most common form of congenital heart disease, occurring in 1-2% of live
births
• More common in males than females
• Normal aortic valve has 3 cusps (looks like Mercedes sign)
• Bicuspid only has 2 cusps
• These can work well at birth and go undetected but can be severely stenotic
in infancy or childhood
• Degenerate quicker than normal valves
• Become regurgitant earlier than normal valves
• Are associated with coarctation and dilation of the ascending aorta
• May eventually develop aortic stenosis (requiring valve replacement) with to
without aortic regurgitation thereby predisposing to infective endocarditis
• Intense exercise may accelerate complications so do yearly
echocardiograms on affected athletes

Answer 197

A

• Often first diagnosed in adulthood and represents
one third of congenital heart disease
• More common in women than men
• Abnormal connection between the two atria
• A probe can be passed through the layers of the
foramen ovale (called the primum and secundum)
so is sometimes known as “Probe patent foramen
ovale”
• Slightly higher pressure in the left atrium than the
right atrium
• Shunt is left-to-right
• Thus NOT blue i.e. acyanotic
• Increased flow into the right heart and lungs
• If left untreated develop right heart overload and dilatation - the right
ventricle is compliant and easily dilates to accommodate the increased
pulmonary flow however this can result in:
- Right ventricular hypertrophy
- Pulmonary hypertension - Eisenmenger’s reaction
- Increased risk of infective endocarditis

Answer 198

A

Dysponea
Exercise intolerance
May develop atrial arrhythmias from right atrial dilatation
Pulmonary flow murmur
Fixed split second heart sound (delayed closure of the pulmonary
valve because more blood has to get out)
CXR:
• Large pulmonary arteries
• Large heart
ECG:
• Right bundle branch block (RBBB) due to right ventricle dilatation
Echocardiogram:
• Hypertrophy and dilation of right side of heart and pulmonary
arteries

Answer 199

A

Surgical closure

- Percutaneous (key hole technique)

Answer 200

A

Abnormal connection between the two ventricles
Many close spontaneously during childhood
Common - 20% of all congenital heart defects
Higher pressure in left ventricle than right ventricle
Thus left-to-right shunt
Thus does NOT go blue i.e. acyanotic
Increased blood flow through the lung

Answer 201

A

- Large defects:
• The large volumes of blood flowing through the pulmonary
vasculature lead to pulmonary hypertension and eventual
Eisenmenger’s complex, when right ventricular pressure becomes
higher than the left, as a result blood starts to shunt right-to-left
resulting in cyanosis
• Small breathless skinny baby
• Increased respiratory rate
• Tachycardia
• CXR:
- Big heart
• Murmur varies in intensity
- Small defects:
• Large systolic murmur
• Thrill (buzzing sensation)
• Well grown
• Normal heart rate
• Normal heart size

Answer 202

A

Medical initially since many will spontaneously close
Surgical closure
If small then no intervention is required
Prophylactic antibiotics
If moderately sized lesion; furosemide, ACE inhibitor e.g. ramipril and digoxin may suffice

Answer 203

A

• Associated with Downs syndrome
• Basically a hole in the very centre of the heart
• Involves; the ventricular septum, the atrial septum,
the mitral and tricuspid valves
• Can be complete or partial
• Instead of two separate atrio-ventricular valves
there is JUST ONE big malformed one which
usually leaks

Answer 204

A

Complete defect:
• Breathlessness as neonate
• Poor weight gain and feeding
• Torrential pulmonary flow which can result in Eisenmenger’s
resulting in cyanosis over time
Partial defect:
• Can present in late adulthood
• Presents similar to ventricular/atrial septal defect e.g. dysponea,
tachycardia, excecrsicse intolerance etc.

Answer 205

A

Pulmonary artery banding if large defect in infancy - band reduces
blood flow to lungs thereby reducing pulmonary hypertension and
Eisenmenger’s syndrome
Surgical repair is challenging
A partial defect may be left alone if there is no right heart dilatation

Answer 206

A

• Affects girls more than boys
• Ductus arteriosus is a persistent communication
between the proximal left pulmonary artery and the
descending aorta
• In foetal life pulmonary vascular resistance is high
(since bronchioles are filled with fluid and vessels are
vasoconstricted due to lack of O2) and the right heart
pressure exceeds that of left - consequently flow is
from right to left atrium through foramen ovale, and
from pulmonary artery to aorta via ductus
arteriosus
• Normally, the ductus arteriosus closes within a few
hours of birth in response to decreased pulmonary
resistance; however in some cases e.g. in
premature babies and in cases with maternal
rubella, the ductus persists
• If it remains open then there is an abnormal left-to-
right shunt (from aorta to pulmonary artery) and
eventually means that the lung circulation is
overloaded with pulmonary hypertension (leading
to Eisenmenger syndrome) and right side cardiac
failure (due to right ventricular hypertrophy in
response to increased afterload) subsequently
• Also increases risk of infective endocarditis

Answer 207

A

Continuous ‘machinery’ murmus
Bounding pulse
If large then large heart and breathlessness
Eisenmenger’s syndrome with differential cyanosis that is clubbed and
blue toes BUT pink and not clubber fingers
Tachycardia
CXR:
• With large shunt the aorta and pulmonary arterial system may be
prominent
ECG:
• May demonstrate left atrial abnormality and left ventricular
hypertrophy
Echocardiogram:
• May show dilated left atrium and left ventricle

Answer 208

A

Can be closed surgically or percutaneously
Low risk of complications
Venous approach may require an AV loop
Indometacin (prostaglandin inhibitor) can be given to stimulate duct
closure

Answer 209

A

• More common in men than women
• A narrowing of the aorta at, or just distal to, the
insertion of the ductus arteriosus (distal to the origin of
the left subclavian artery)
• The net result is a narrowing of the aorta just after the
arch, with excessive blood flow being diverted through
the carotid and subclavian vessels into systemic
vascular shunts to supply the rest of the body, thus stronger perfusion to upper body compared to lower
• Associated with Turner syndrome, berry aneurysms and patent ductus arteriosus
• Resultant decreased renal perfusion leads to systemic hypertension that
persists even after surgical correction

Answer 210

A

Often asymptomatic for many years
Right arm hypertension
Bruits (buzzes) over the scapulae and back from collateral vessels
Murmur
Headaches and nose bleeds (due to hypertension)
Hypertension in the upper limbs
Discrepant blood pressure in the upper and lower body (will notice
radial pulse BEFORE femoral pulse)
Long term problems:
• Hypertension:
Early coronary artery disease
Early strokes
Sub-arachnoid haemorrhage
CXR:
• Dilated aorta indented at the site of the coarctation
ECG:
• Left ventricular hypertrophy
CT:
• Can accurately demonstrate the coarctation and quantify flow

Answer 211

A

Surgery
Balloon dilatation (preferred for re-coarctation) and stenting
Risk of aneurysm formation at the site of repair

Answer 212

A

• Most common form of cyanotic congenital
heart disease
• Consists of:
- A large, maligned Ventricular Septal
Defect (VSD)
- An overriding aorta
- Right ventricular outflow obstruction
e.g. due to pulmonary stenosis
- Right ventricular hypertrophy
• The stenosis of the right ventricle outflow leads to the right ventricle being at
a higher pressure than the left
• Thus blue blood passes from the right ventricle to the left ventricle
• The patients are BLUE i.e CYANOTIC

Answer 213

A

Central cyanosis
Low birthweight and growth
Dysponea on exertion
Delayed puberty
Systolic ejection murmurs
CXR:
• Boot shaped heart

Answer 214

A

Full surgical treatment during first two years of life due to the
progressive cardiac debility and cerebral thrombosis risk
Often get pulmonary valve regurgitation in adulthood and require redo
surgery

Answer 215

A

• Narrowing of the outflow of the right ventricle
• Can be; valvar, sub valvar or supra valvar
• Severe:
- Right ventricular failure as neonate
- Collapse
- Poor pulmonary blood flow
- Right ventricular hypertrophy
- Tricuspid regurgitation
• Moderate/mild:
- Well tolerated for many years
- Right ventricular hypertrophy

Answer 216

A

Balloon valvoplasty - place catheter with balloon through femoral vein
then inflate balloon at stenosis to crush it but this can result in
regurgitation
Open valvotomy
Shunt - to bypass the blockage

Answer 217

A

• Involves the aorta coming off the right ventricle and the pulmonary trunk
coming off the left ventricle
• Two closed circulations result
• More common in men and associated with diabetes
• Survival is only possible if there is communication between the two circuits
and virtually all have some form of atrial septal defect with blood mixing
• Treatment:
- Atrial switch operation with good results

Answer 218

A

Heart points to the right side of chest instead of to the left
Associated with severe cardiovascular abnormalities

Answer 219

A

• The pericardium acts as a protective covering for
the heart
• It consists of an outer fibrous pericardial sac and
an inner serous pericardium
• The inner serous pericardium is made up of:
- Inner visceral epicardium - single cell layer
that’s adherent to the epicardium (myocytes), that lines the heart and
great vessels, and its reflection
- Outer parietal pericardium - mainly collagen and elastin fibres, with no cells, that lines the fibrous sac
- In between the layers is around 50ml of serous fluid that acts as a lubricant to allow the two surfaces to move over each other easily
• Great vessels lie in the pericardium, if the proximal segment (ascending) of the
aorta is ruptured then it will bleed in into the pericardial space and result in a
cardiac tamponade

Answer 220

A

• Left atrium is mainly outside the pericardium
• It promotes cardiac efficiency by limiting dilation, maintaining ventricular
compliance and distributing hydrostatic forces
• Aids atrial filling by creating a closed chamber, reduces external friction
and acts as a barrier against infection and extension of malignancy
• Anatomically fixes the heart to the sternum, diaphragm and costal cartilages
• The pericardium is similar to an elastic band - initially stretchy but becomes
stiff at higher tension, thus at low tension the pericardium has a small reserve
volume
• If this volume is exceeded the pressure is translated to the cardiac chambers
and thus puts pressure on the heart
• Small amount of volume added to this space has dramatic effects on filling
e.g a cardiac tamponade
• Pressure in the pericardium is very low
• In a chronic pericardial effusion, the pericardium adapts slowly by laying
down elastin & collagen and becomes more elastic so there is a much slower
tamponade (thus there is no collapse of the right atrium) since the pressure
equalises - but the entrance of fluid making up the effusion must be slow

Answer 221

A

• Acute inflammation of the pericardium; with or without effusion

Answer 222

A

Majority are idiopathic and most commonly seen in the young, previously
healthy patient
Occurs in men more than women
Occurs in adults more than children
Causes:
• Infectious:
Viral (common):
• Enteroviruses e.g. coxsackieviruses & echoviruses
• Adenoviruses
Bacterial:
• Mycobacterium tuberculosis (other bacteria are rare)
Fungal (very rare):
• Histoplasma spp. - most likely to be seen in
immunocompromised patient
• Non-infectious:
Autoimmune (common):
• Sjorgrens syndrome
• Rheumatoid arthritis
• SLE
Neoplastic; secondary metastatic tumours (common, above all is
lung or breast cancer)
Dressler’s syndrome - post cardiac injury syndromes
Traumatic & iatrogenic:
• Early onset (rare):
Direct injury - penetrating thoracic injury or
oesophageal perforation
Indirect injury - non-penetrating thoracic injury or
radiation
• Delayed onset (common):
Pericardial injury syndromes (common)
Iatrogenic trauma e.g. coronary percutaneous
intervention or pacemaker lead insertion

Answer 223

A

Pericardium becomes acutely inflamed, with pericardial vascularisation and
infiltration with polymorphonuclear leukocytes
A fibrinous reaction frequently results in exudate and adhesions within the
pericardial sac, and a serous or haemorrhagic effusion may develop

Answer 224

A

Chest pain:
• Severe
• Sharp & pleuritic (without constricting crushing character of ischaemic
pain)
• Rapid onset
• Worse on inspiration or lying flat - relieved by sitting forward
• Left anterior chest or epigastrium

• Radiates to arm, more specifically the trapezius ridge (has co-
innervation with the phrenic nerve) - whereas a STEMI would be arms,

jaw & teeth

Dysponea
Cough
Hiccups - due to phrenic involvement
Pericardial friction rub present on auscultation
Fever and lymphocytosis (increase in lymphocytes) if due to virus or bacteria
Tachycardia

Answer 225

A

Angina
MI - most important to rule out
Pleuritic pain
Pulmonary infarction
Pneumonia, GI reflux, peritonitis & aortic dissection

Answer 226

A

ECG:
• Is diagnostic
• Widespread concave-upwards - SADDLE SHAPED ST ELEVATION (arrowed)
• Diffuse ST segment elevation - present in
all leads (must exclude STEMI which would have ST segment elevation but will be limited to the infarcted area e.g. anterior or inferior)
• PR depression
CXR:
• May demonstrate cardiomegaly in cases of effusion - if found then
confirm with echocardiography
• Often normal in idiopathic
• Pneumonia is common with bacterial pericarditis
FBC:
• Slight increase in white cell count
• Anti Neutrophil Antibody in young females - SLE
• Troponin - elevated suggests myopericarditis
ESR/CRP:
• High ESR is indicative of autoimmune

Answer 227

A

Restrict physical activity until resolution of symptoms and see improvement
in ECG and CRP
NSAID e.g Ibuprofen for two weeks or Aspirin for two weeks
Colchicine for 3 weeks however is limited by nausea and diarrhoea but does
reduce recurrence

Answer 228

A

About 20% of cases of acute pericarditis go on to develop idiopathic relapsing pericarditis
This may occur within 6 weeks during weaning off NSAIDs or intermittently i.e. recurs more than 6 weeks after the initial presentation
The first line treatment is oral NSAIDs e.g. Ibuprofen
Colchicine has been proven to be more effective than Aspirin alone
In resistant cases, oral corticosteroids e.g. Prednisolone may be effective, and in some patients, pericardiectomy (removal of part/most of the pericardium) may be appropriate

Answer 229

A

• A pericardial effusion is a collection of fluid within the potential space of the
serous pericardial sac
• It commonly accompanies an episode of acute pericarditis
• When a large volume collects in this space, ventricular filling is
compromised, leading to the embarrassment of the circulation - this is a
CARDIAC TAMPONADE

Answer 230

A

- Symptoms of a pericardial effusion commonly reflect the underlying
pericarditis
- Soft &amp; distant heart sounds
- Apex beat obscured
- Raised jugular venous pressure
- Dysponea

Answer 231

A

High pulse but low blood pressure
High jugular venous pressure
Muffled 1st & 2nd heart sounds
Kussmaul’s sign - rise in jugular venous pressure and increased neck vein
distension during inspiration
Pulsus paradoxus - an exaggeration in the normal variation in pulse
pressure seen with inspiration, such that there is a drop in systolic blood
pressure
Reduced cardiac output

Answer 232

A

- CXR:
• Large globular heart
- ECG:
• Low-voltage QRS complexes
• Sinus tachycardia
- Echocardiogram:
• Most useful for demonstrating effusion
• Echo-free zone surrounding heart

Answer 233

A

- CXR:
• Big globular heart
- Beck’s triad:
• Falling blood pressure
• Rising jugular venous pressure
• Muffled heart sounds
- ECG:
• Low voltage QRS
- Echocardiogram:
• IS DIAGNOSTIC
• Echo-free zone around heart
• Late diastolic collapse of RIGHT ATRIUM (remember most of L atrium is
outside pericardium)
• Early diastolic collapse of right ventricle

Answer 234

A

Underlying cause should be sought and treated if possible
Most pericardial effusions resolve spontaneously
Pericardial effusions may re-accumulate most often due to malignancy - this
may require a pericardial fenestration (a window in the pericardium is created
to allow the slow release of fluid into the surrounding tissues)

Answer 235

A

See expert help!
Require URGENT DRAINAGE via a PERICARDIOCENTESIS which will drain
the fluid to relieve the pressure on the heart
Send fluid for culture, Ziehl-Nielsen stain and for cytology

Answer 236

A

Certain causes of pericarditis such as tuberculosis, bacterial infection and rheumatic heart disease result in the pericardium becoming thick, fibrous
and calcified
Cause is often unknown and can actually occur after any pericarditis

Answer 237

A

In many cases, these pericardial changes do not cause any symptoms
If, however, the pericardium becomes so inelastic as to interfere with the
diastolic filling of the heart, CONSTRICTIVE PERICARDITIS is said to have developed
As these changes are chronic, allowing the body time to compensate, this
condition is not as immediately life-threatening as cardiac tamponade, in
which the circulation is more acutely embarrassed
Constrictive pericarditis should be distinguished from RESTRICTIVE
CARDIOMYOPATHY:
• These conditions are very similar in their presentation, but the former is
treatable!
In the later stages of constrictive pericarditis, the sub-endocardial layers of
myocardium may undergo fibrosis, atrophy and calcification

Answer 238

A

Kussmaul’s sign - rise in jugular venous pressure and increased neck vein
distension during inspiration
Pulsus paradoxus - an exaggeration in the normal variation in pulse
pressure seen with inspiration, such that there is a drop in systolic blood
pressure
Diffuse heart sounds
Ascites
Oedema
Right heart failure signs
Atrial dilatation

Answer 239

A

CXR:
• Small heart with/without pericardial calcification
ECG:
• Low-voltage QRS
Echocardiography:
• Thickened, calcified pericardium
• Small ventricular cavities with normal wall thickness

Answer 240

A

Complete resection of the pericardium - risky with high complication rate

Answer 241

A

• Hypertension is a major cause of premature vascular disease, leading to
cerebrovascular events, ischaemic heart disease and peripheral vascular
disease
• Mortality rises with increasing blood pressure

Answer 242

A

Often symptomless so screening is vital
Major risk factor for CVD
Remain under diagnosed, under treated and poorly controlled in the UK
Prevalence is in those older than 35
More common in men
Less than 140/90mmHg = Normotensive
Hypertension values:
• Stage 1 hypertension:
More than or equal to 140/90mmHg clinic BP
Daytime average Ambulatory blood pressure monitoring (ABPM -
24hr BP monitor) or Home blood pressure monitoring (HBPM);
greater than or equal to 135/85mmHg
• Stage 2 hypertension:
More than or equal to 160/100mmHg clinic BP
Daytime average ABPM or HBPM greater than or equal to
150/95mmHg
• Severe hypertension:
Clinic systolic BP greater than or equal to 180mmHg and/or
diastolic BP greater than or equal to 110mmHg
Start immediate anti-hypertensive drug treatment!

Answer 243

A

The commonest cause of cardiac failure and a major risk factor for atherosclerosis and cerebral haemorrhage
Hypertension can be classified according to whether the cause is unknown
‘essential (primary or idiopathic) hypertension’ or is known ‘secondary hypertension’
Most cases are classified as essential
Essential hypertension:
• Primary cause unknown
• Accounts for the majority of cases
• Multifactorial involving:
Genetic susceptibility
Excessive sympathetic nervous system activity
Abnormalities of Na+/K+ membrane transport
High salt intake
Abnormalities in renin-angiotensin-aldosterone system
• Drug therapy:
Prescription drugs associated with hypertension include:
• Corticosteroids e.g. Prednisolone
• Cyclosporin
• Erythropoietin
• Some types of the contraceptive pill
Alcohol, amphetamines, ecstasy and cocaine are also causes of
hypertension

Answer 244

A

Secondary hypertension:
• Commonly caused by renal disease or pregnancy
• Other potential underlying conditions include; endocrine causes, coarctation of the aorta and drug therapy
• Renal disease & hypertension:
Kidney disease can be both the cause and result of hypertension
CHRONIC KIDNEY DISEASE is the MOST COMMON CAUSE of secondary hypertension
Diabetes is the most common cause of chronic kidney disease
The vascular changes induced by hypertension (the acceleration of atherosclerosis and endothelial cell dysfunction resulting in the promotion of pheochromocytoma vasoconstriction) may cause or exacerbate renal disease
Chronic glomerulonephritis is another potential cause although less common now
• Coarctation of the aorta:
Systemic hypertension is once of the commonest features in coarctation
Raised blood pressure will be detected in either arm, but NOT in the legs
The femoral pulse is often delayed relative to the radial
Undetected or untreated patients die from cardiac failure, hypertensive cerebral haemorrhage or dissecting aneurysm

Answer 245

A

• Endocrine causes:
- Cushing’s syndrome:
• Hypersecretion of corticosteroids (which enhance
adrenalines resulting in a vasoconstrictive effect) is
associated with systemic hypertension
- Conn’s syndrome:
• Adrenal tumour that secretes ALDOSTERONE (resulting in Na+ retention and thus water retention thereby increasing blood volume and pressure) can cause hypertension
- Phaemochromocytoma:
• Adrenal tumour that secretes CATECHOLAMINES (resulting in
the stimulation of alpha-adrenergic receptors resulting in vasoconstriction, increased cardiac contractility as well as the stimulation of beta-adrenergic receptors resulting in an increase in heart rate and contractility) can cause
hypertension
- Note these tumours are rare

Answer 246

A

Age - risk increases as you age
Race - hypertension is more common in blacks
Family history - hypertension runs in families
Overweight and obese
Little exercise
Smoking
Too much salt in diet
Alcohol
Diabetes
Stress

Answer 247

A

Vascular changes:
• Hypertension accelerates atherosclerosis
• Also causes the thickening of the media of muscular arteries
• It is the smaller arteries and arterioles that are especially affected in
hypertension
• The resulting endothelial cell dysfunction is associated with impaired nitric oxide-mediated vasodilatation and enhanced secretion of vasoconstrictors including endothelins and prostaglandins
Heart:
• Hypertension is a major risk factor for ischaemic heart disease
Nervous system:
• Intracerebral haemorrhage is a frequent cause of death in hypertension
Kidneys:
• Hypertension can be the cause or result of renal disease
• Kidney size is often reduced and small vessels show intimal thickening
and medial hypertrophy and the numbers of sclerotic glomeruli are
increased

Answer 248

A

Malignant hypertension:
• Characteristic features are a markedly raised diastolic blood pressure,
usually over 120mmHg and progressive renal disease
• Quite rare
• Renal vascular changes are prominent and there is usually evidence of
acute haemorrhage and papilloedema (optic disc swelling caused by
increase intercranial pressure)
• Can occur in previously fit individuals, often black males in their 30s-40s
• Consequences:
Cardiac failure with left ventricular hypertrophy and dilatation
Blurred vision due to papilloedema and retinal haemorrhages
Haematuria and renal failure due to fibrinoid necrosis of glomeruli
Severe headache and cerebral haemorrhage

Answer 249

A

Usually asymptomatic (except malignant hypertension)

- Found on screening

Answer 250

A

Look for end-organ damage e.g. left ventricular hypertrophy, retinopathy
and proteinuria - indicates severity and duration of hypertension and
associated with a poorer prognosis
Urinalysis:
• For protein, albumin:creatine ratio and haematuria
Blood tests:
• Serum creatinine
• eGFR
• Glucose (to assess diabetes risk)
Fundoscopy/Opthalmoscopy:
• Looking for retinal haemorrhage or papilloedema
ECG:
• To detect left ventricular hypertrophy
Echocardiography:
• To further detect left ventricular hypertrophy
24 hour ambulatory blood pressure monitoring

Answer 251

A

Treatment GOAL is 140/90mmHg
Change diet:
• High consumption of vegetable and fruits and low-fat diet
Regular physical exercise
Reduce alcohol intake
Reduce salt intake
Lose weight
Stop smoking
ACD pathway:
• A - ACE-inhibitor e.g. Ramipril or Enalapril, or Angiotensin receptor
blocker (ARB) (use if ACEi is contraindicated e.g. due to cough) e.g.
Candesartan or Losartan
• C - Calcium channel blocker (CCB) e.g. Nifedipine or Amlodipine
• D - Diuretics e.g. Bendroflumethiazide (thiazide, distal tube - less
potent) or Furosemide (loop diuretic, loop of henle - more potent)
• NOTE: Beta-blocker e.g. Bisoprolol or Metoprolol (B1 selective) are
NOT the FIRST LINE TREATMENT FOR HYPERTENSION but consider in
young people especially if they are intolerant of ACEi/ARB
• Less than 55 yrs old:
Ramipril/Candesartan
- Nifedipine
- Bendroflumethiazide
- Furosemide
  • Older than 55 yrs/black/African-Caribbean origin:
Ramipril/Candesartan + Nifedipine
- Bendroflumethiazide
- Furosemide
  • If higher dose not tolerated then consider beta-blocker

Answer 252

A

• An abnormality of the cardiac rhythm is called a cardiac arrhythmia
• Arrhythmias may cause:
- Sudden death
- Syncope
- Heart failure
- Chest pain
- Dizziness
- Palpitations
- No symptoms at all
• There are two main types of arrhythmia:
- Bradycardia:
• Heart rate is slow (less than 60bpm during the day and less than 50bpm
at night)
• Usually asymptomatic unless the rate is very slow
• Normal in athletes owing to increased vagal tone and thus
parasympathetic activity
- Tachycardia:
• Heart rate is fast (more than 100bpm)
• More symptomatic when the arrhythmia is fast and sustained
• Subdivided into:
- Supraventricular tachycardias - arise from the atrium or the AV
junction
- Ventricular tachycardias - arise from the ventricles

Answer 253

A

SAN → Action potential → Muscle cells of atria →
Depolarisation of the AVN → Slow →
Interventricular septum → Bundle of His → Right
and left bundle branches → Free walls of both
ventricles → Purkinje cells → Ventricular myocardial
cells
Sinoatrial node (SAN) is found at the junction
between the superior vena cava (SVC) and right
atrium
The action potential travels through gap junctions to get to the muscle cells
The AVN is found in the lower interatrial septum
The slow spread of the action potential between the AVN and ventricles is to allow for the complete contraction of the atria before the ventricles are excited

Answer 254

A

The normal cardiac pacemaker is the sinoatrial node and it depolarises
spontaneously
The rate of SAN discharge is modulated by the autonomic nervous system
Normally, the parasympathetic system predominates, resulting in slowing of
the spontaneous discharge rate
A reduction of PARASYMPATHETIC TONE or an increase in SYMPATHETIC
STIMULATION leads to TACHYCARDIA
Conversely, increased PARASYMPATHETIC TONE or decreased
SYMPATHETIC STIMULATION produces BRADYCARDIA
The sinus rate in women is slightly faster than in men
Normal sinus rhythm is characterised by P waves that are upright in leads I &
II of the ECG, but inverted in the cavity leads AVR & V1

Answer 255

A

Fluctuations of autonomic tone result in changes of the sinus discharge rate
During inspiration:
• Parasympathetic tone falls and the heart rate quickens
During expiration:
• Parasympathetic tone increases and so heart rate falls
This variation is normal especially in children and young adults

Answer 256

A

• A chaotic irregular atrial rhythm at 300-600bpm; the AV node responds
intermittently, hence an irregular ventricular rate

Answer 257

A

Most common sustained cardiac arrhythmia
Males more than females
Around 5-15% of patients over age of 75
Can either be paroxysmal (self terminating) or persistent (continues without
intervention)
Clinical classification:
• Acute: onset within the previous 48 hours
• Paroxysmal: stops spontaneously within 7 days
• Recurrent: two or more episodes
• Persistent: continuos for more than 7 days and not self terminating
• Permanent

Answer 258

A

• Idiopathic (5-10%)
• Any condition that results in raised atrial pressure, increased atrial
muscle mass, atrial fibrosis, or inflammation and infiltration of the
atrium may cause atrial fibrillation
• Hypertension (most common in developed world)
• Heart failure (most common in developed world)
• Coronary artery disease
• Valvular heart disease; especially mitral stenosis
• Cardiac surgery (1/3rd of patients after surgery)
• Cardiomyopathy (rare cause)
• Rheumatic heart disease
• Acute excess alcohol intoxication

Answer 259

A

Older than 60
Diabetes
High blood pressure
Coronary artery disease
Prior MI
Structural heart disease (valve problems or congenital defects)

Answer 260

A

Atrial fibrillation (AF) is maintained by continuous, rapid (300-600/min) activation of the atria by multiple meandering re-entry wavelets
These are often driven by rapidly depolarising automatic foci, located predominantly within the pulmonary veins
The atria respond electrically at this rate but there is NO COORDINATED MECHANICAL ACTION and only a proportion of the impulses are conducted
to the ventricles i.e. there is no unified atrial contraction instead there is atrial spasm
The ventricular response depends on the rate and regularity of atrial activity, particularly at the entry to the AV node, and the balance between sympathetic and parasympathetic tone
Cardiac output DROPS by 10-20% as the ventricles are not primed reliably by the atria
NOTE: people with atrial fibrillation are at a higher risk of thromboembolic events e.g. stroke due to the fact that when the atria are spasming and some parts are not contracting it causes the blood to POOL in these parts and thus remain still and when blood remains still and DOESN’T MOVE and thus begins to CLOT forming a THROMBUS that could easily turn into an EMBOLI
and result in a stroker - thus why people with atrial fibrillation are given some
sort of blood thinner e.g. Warfarin

Answer 261

A

Symptoms are highly variable
May be asymptomatic
Palpitations
Dyspnoea and or chest pains following the onset of atrial fibrillation
Fatigue
NO P WAVES on ECG
Rapid & irregular QRS rhythm
Apical pulse rate is greater than the radial rate
1st heart sound is of variable intensity

Answer 262

A

Atrial flutter

- Supraventricular tachyarrhythmias

Answer 263

A

ECG:
• ABSENT P WAVES
• IRREGULAR & RAPID QRS COMPLEX

Answer 264

A

Acute management:
• When AF is due to an acute precipitating event, such as alcohol toxicity,
chest infection or hyperthyroidism - the provoking cause should be
treated
• Cardioversion:
Conversion to sinus rhythm achieved electrically by DC shock e.g. defibrillator - NOTE: give low molecular weight heparin e.g. Enoxaparin or Dalteparin to minimise the risk of thromboembolism associated with cardioversion
If this fails then achieved medically by IV infusion or anti-arrhythmic drug such as flecainide or amiodarone
• Ventricular rate control:
Achieved by drugs that block AV node:
• Calcium channel blocker e.g. Verapamil
• Beta-blocker e.g. Bisoprolol
• Digoxin
• Anti-arrhythmic e.g. Amiodarone

Answer 265

A

Long term & stable patient management:
• Two strategies; which to choose should be decided based on individual patient needs
• Rate control:
AV nodal slowing agents plus oral anticoagulation
Beta-blocker e.g. Bisoprolol
Calcium channel blocker e.g. Verapamil or Diltiazem
If above fails then try Digoxin and then consider Amiodarone
• Rhythm control:
Advocated for younger, symptomatic and physically active patients
Cardioversion to sinus rhythm and use Beta-blockers e.g. Bisoprolol to suppress arrhythmia
Can use pharmacological cardioversion e.g. Flecainide if no structural heart defect or use IV Amiodarone instead if there is structural heart disease
Appropriate anti-coagulation e.g. Warfarin due to
thromboembolism risk with cardioversion

Answer 266

A

Use the CHA2DS2-VASc score to calculate stroke risk and thus need for
anticoagulation:
• Congestive heart failure (1 point)
• Hypertension (1 point)
• A2ge greater or equal to 75 (2 points)
• Diabetes mellitus (1 point)
• S2troke/TIA/thromboembolism (2 points)
• Vascular disease (aorta, coronary or peripheral arteries) (1 point)
• Age 65-74 (1 point)
• Scex Category: female (1 point)
• If score is 1 then it merits consideration of anticoagulation and or aspirin
• If score is 2 and above then oral anticoagulation is required

Answer 267

A

• Atrial flutter is usually an ORGANISED atrial rhythm with an atrial rate
typically between 250-350bpm

Answer 268

A

- Often associated with atrial fibrillation and frequently require a similar initial
therapeutic approach
- Either paroxysmal or persistent
- Much less common than atrial flutter
- More common in men
- Prevalence increases with age
- Causes:
• Idiopathic (30%)
• Coronary heart disease
• Obesity
• Hypertension
• Heart failure
• COPD
• Pericarditis
• Acute excess alcohol intoxication

Answer 269

A

Atrial fibrillation

Answer 270

A

Palpitations
Breathlessness
Chest pain
Dizziness
Syncope
Fatigue

Answer 271

A

Atrial fibrillation

- Supraventricular tachyarrthymias

Answer 272

A

- ECG:
• Definitive diagnosis
• Regular sawtooth-like atrial flutter
waves (F waves) between QRS
complexes due to continuous
atrial depolarisation
• Note if F waves are not visible then they may be able to be unmasked by by slowing atrioventricular conduction by carotid sinus massage or IV adenosine (AV nodal blocker)

Answer 273

A

Electrical cardioversion but anticoagulate before e.g low molecular weight
heparin e.g. Enoxaparin or Dalteparin if acute i.e. atrial flutter started less
than 48 hours ago
Catheter ablation - creating a conduction block to try an restore rhythm and
block offending re-entrant wave
IV Amiodarone to restore sinus rhythm and use a beta-blocker e.g.
Bisoprolol to suppress further arrhythmias

Answer 274

A

• Can occur at any level in the conducting system
• Block in either the AV node or the His bundle results in AV BLOCK
• Whereas block lower in the conduction system produces BUNDLE BRANCH
BLOCK

Answer 275

A

• First-degree AV block:
- This is simple prolongation of the PR interval to greater than 0.22 seconds
- Every atrial depolarisation is followed by conduction to the ventricles but
with delay
- Causes:
• Hypokalaemia
• Myocarditis
• Inferior MI
• Atrioventricular node (AVN) blocking drugs e.g. beta blockers
(Bisoprolol), calcium channel blockers (Verapamil) and Digoxin
- ASYMPTOMATIC so no treatment!

Answer 276

A

• Second-degree AV block:
- Occurs when some P waves conduct and other do not
- Acute MI may produce second degree heart block
- Mobitz I block:
• Also known as the Wenckebach block phenomenon
• A progressive PR interval prolongation until beat is ‘dropped’ and P
wave fails to conduct i.e. excitation completely fails to pass through the
AVN/bundle of His
• The PR interval before the blocked P wave is much longer than the PR
interval after the blocked P wave
• Causes:
- Atrioventricular node (AVN) blocking drugs e.g. beta blockers
(Bisoprolol), calcium channel blockers (Verapamil) and Digoxin
- Inferior MI
• Results in light headiness, dizziness and syncope
• Does not require a pacemaker unless its poorly tolerated
- Mobitz II block:
• PR interval is constant and QRS interval is dropped
• Failure of conduction through the His-Purkinje system
• Causes:
- Anterior MI
- Mitral valve surgery
- SLE and Lyme disease
- Rheumatic fever
• Results in shortness of breath, postural hypotension and chest pain
• High risk of developing sudden complete AV block and a pacemaker
should be inserted

Answer 277

A

• Third degree - COMPLETE AV BLOCK:
- Complete heart block occurs when all atrial activity fails to conduct to the
ventricles
- Ventricular contractions are sustained by spontaneous escape rhythm
which originates below the block
- P waves are COMPLETELY INDEPENDENT of QRS complex
- Causes:
• Structural heart disease e.g. transposition of great vessels
• Ischaemic heart disease e.g. acute MI
• Hypertension
• Endocarditis or Lyme disease
- Narrow-complex escape rhythm:
• QRS complex less than 0.12 seconds
• Implies block originates in the His bundle and thus the region of block lies
more proximally in the AV node
• Recent-onset, narrow-complex AV block that has transient causes may
responses to IV atropine
• Chronic narrow-complex AV block requires permanent pacemaker if it is symptomatic
- Broad-complex escape rhythm - B = BELOW His:
• QRS complex is greater than 0.12 seconds
• Implies block originates BELOW the bundle of His and thus the region of block lies more distally in the His-Purkinje system
• Dizziness and blackouts often occur
• Permanent pacemaker implantation is recommended

Answer 278

A

Depends on aetiology
One option is permanent pacemaker
IV atropine

Answer 279

A

• Usually asymptomatic
• The His bundle gives rise to the right and left bundle branches
• The left branch subdivides into the anterior and posterior divisions of the left
bundle
• Bundle branch conduction delay results in the slight widening of the QRS
complex (up to 0.11 seconds) - this is incomplete bundle branch block
• Complete block of a bundle branch:
- This is associated with a wider QRS complex (larger than 0.12 seconds)
- The shape of the QRS depends on whether the right or the left bundle is
blocked

Answer 280

A

Right bundle branch block (RBBB):
• Causes; Pulmonary embolism, Ischaemic heart disease & Atrial/
Ventricular septal defect
• Right bundle no longer conducts, meaning that the two ventricles do
not get impulses at the same time, and instead spread from left to right
• Produces the late activation of the right ventricle
• Seen as deep S wave in leads I & V6 and as a tall late R wave in lead V1
• On ECG:- Looks like maRRow
maRRow - Right bundle branch block
MarroW:
• M - QRS looks like an M in lead V1
• W - QRS looks like W in V5 & V6
• Causes wide physiological splitting of the SECOND HEART SOUND

Answer 281

A

Left bundle branch block (LBBB):
• Causes; Ischaemic heart disease and aortic valve disease
• Produces the late activation of the left ventricle
• Seen as deep S wave in lead V1 and a tall late R wave in leads I & V6
• Since the left bundle branch conduction is normally responsible for the
initial ventricular activation, left bundle branch block also produce
abnormal Q waves
• On ECG:
Looks like wiLLiam
wiLLiam - Left bundle branch block
WilliaM:
• W - QRS looks like a W in leads V1 & V2
• M - QRS looks like an M in leads V4-V6
• Causes reverse splitting of the SECOND HEART SOUND

Answer 282

A

• Defined as heart rate greater than 100bpm
• Causes:
- Anaemia
- Anxiety
- Exercise
- Pain
- Heart failure
- Pulmonary embolism
• Treated by treating causes
• If necessary then beta-blockers can be used e.g. Bisoprolol

Answer 283

A

• Arise from the atria or atrioventricular junction
• NOTE: TACHYARRHYTHMIA & TACHYCARDIA can be used INTERCHANGEABLY
• ATRIOVENTRICULAR JUNCTIONAL TACHYCARDIAS:
- AV nodal re-entrant tachycardia (AVNRT) and AV re-entrant tachycardia
(AVRT) are usually referred to as paroxysmal supraventricular tachycardias
(SVTs)
- They are often seen in young patients with no or little structural heart
disease
- First presentation is commonly between ages 12-30
- In these tachycardias the AV node is an essential component

Answer 284

A

More common in women than men
Strikes suddenly without obvious provocation but there are some risk factors
An attack may stop spontaneously or may continue indefinitely until medical
intervention

Answer 285

A

Exertion
Emotional stress
Coffee
Tea
Alcohol

Answer 286

A

There are two pathways within the AV node in AVNRT:
• One has a short effective refractory period (the window of time where cells cannot be excited again after they have already been excited) and SLOW conduction
• One has a longer effective refractory period and FAST conduction
In sinus rhythm, the atrial impulse that depolarises the ventricles usually conducts through the fast pathway
If the atrial impulse occurs early e.g. atrial premature beat when the fast pathway is still refractory then the slow pathway takes over in propagating the atrial impulses to the ventricles
By the time the impulse has been propagated to the ventricles the FAST PATHWAY has finished its refractory period and is once again able to
transmit impulses
Thus the same impulse that was carried by the SLOW PATHWAY can be transmitted to the ventricles but ALSO travel back UP the FAST PATHWAY which by that time would be out of its refractory period
Then by that time the SLOW PATHWAY would have recovered from its
refractory period (since its very short) so the signal will be able to go back
down the SLOW PATHWAY again
This sets up a RE-ENTRANT LOOP at the AV NODE hence why its AVNRT and the loop sends signals through the AV node at a MUCH FASTER RATE than a
normal pacemaker would so you see TACHYARRHYTHMIA! with a heart rate of 100-250 bpm
It then travels back through the fast pathway, which has already recovered its excitability, thereby initiating the slow-fast AVNRT in which the atria contract
SLOWLY in one cycle and then FAST in the next

Answer 287

A

Rapid regular palpitations with abrupt onset and sudden termination
Chest pain and breathlessness
Neck pulsations - prominent jugular venous pulsations due to atrial
contractions against closed AV valves
Polyuria (due to the realise of atrial natriuretic peptide in response to
increased atrial pressures during the tachycardia)

Answer 288

A

ECG:
• Sometimes the QRS complexes will show typical bundle branch block
• P waves are either not visible or are seen immediately before (normal) or
after the QRS complex due to simultaneous atrial and ventricular
activation

Answer 289

A

Large circuit involving the AV node, the His bundle, the ventricle and an
abnormal connection of myocardial fibres from the ventricle back to the
atrium
This ‘abnormal connection’ is called the accessory pathway or bypass tract
and results from an incomplete separation of the atria and the ventricles
during fetal development
Thus there are two circuits; the normal AV circuit and this accessory circuit
which both transmit impulses from the atria to the ventricles
Note: with the accessory circuit impulse can travel from atria to ventricle
(anterograde) or from ventricle back to atria (retrograde)

Answer 290

A

Atrial activation occurs after ventricular activation
Patients are prone to atrial fibrillations and sometime ventricular fibrillation
Good example of AVRT is in WOLFF-PARKINSON-WHITE (WPW)
SYNDROME - a aberrant pathway syndrome:
• Where there is normal AV conduction but also an accessory pathway
• So when the SAN depolarises the impulse can travel to the AVN via the
atria as well as to the accessory pathway
• If the accessory pathway conducts from the atrium to the ventricle
during sinus rhythm, the electrical impulse can conduct QUICKLY over
this abnormal connection to depolarise part of the ventricles ABNORMALLY this is known as pre-
excitation

Answer 291

A

• Pre-excitation is reflected on an ECG like this:
- Short PR interval
- Wide QRS complex that begins as a slurred part known as a delta
wave
• This pre-excitation is not the thing that results in the AVRT and will not
result in a tachyarrhythmia
• However, if you had a premature beat coming from the SAN; the signal will
travel to the AVN and it the accessory pathway is in a refractory period
i.e. it CANNOT TRANSMIT THE SIGNAL
• Then the impulse will travel down via the AVN, down the interventricular
septum through the bundle of His through the left and right bundle
branches and into the free walls of both ventricles via the Purkinje cells
until it meets the ACCESSORY PATHWAY
• At this point the accessory pathway will be out of its refractory period
and will thus be able to conduct the impulse BACK into the atria
• Once back in the atria the impulse can then travel back to the AVN thereby setting up a RE-ENTRY CIRCUIT and the signal will just go around and around resulting in the TACHYARRHYTHMIA!

Answer 292

A

Palpitations
Severe dizziness
Dysponea
Syncope

Answer 293

A

ECG:
• Short PR interval
• Wide QRS complex that begins as a slurred part known as a DELTA
WAVE
• Both hallmarks of Wolff-Parkinson-White (WPW) syndrome

Answer 294

A

Patients presenting with haemodynamic instability (hypotension &
pulmonary oedema) require emergency cardioversion
If stable then vagal manoeuvres:
• Breath-holding
• Carotid massage
• Valsalva manoeuvre - abrupt voluntary increase in intra-abdominal and
intrathoracic pressure by straining - several seconds after the release of the
strain, the resulting intense vagal effect may terminate the AVNRT or
AVRT
If manoeuvres unsuccessful then IV adenosine - causes complete heart
block for a fraction of a second and is highly effective at terminating AVNRT
and AVRT
Surgery:
• Catheter ablation of the accessory pathway in AVRT
• Modification of the slow pathway in AVNRT

Answer 295

A

Umbrella term encompassing:
- Ventricular ectopics
- Ventricular tachycardia
- Sustained ventricular tachycardia
- Ventricular fibrillation
- Some of these condition are cardiac channelopathies - these are congenital
disorders that are caused by mutations that affect the function of cardiac ion
channels and hence the electrical activity of the heart, these include:
• Long QT syndrome

Answer 296

A

• Premature ventricular contraction

Answer 297

A

These are the most common POST-MI arrhythmia

- Can also occur in healthy patients

Answer 298

A

Patient complains of extra beats, missed beats or heavy beats
If the ectopics are frequent then left ventricular dysfunction may develop
These premature beats have a broad (greater than 0.12 seconds) and bizarre
QRS complex because they arise from an abnormal (ectopic) site in the
ventricular myocardium
Following a premature beat, there is usually a complete compensatory pause
because the AV node or ventricle is refractory (i.e. cannot accept new
impulses) to the next sinus impulse - resulting in missed beat
Can provoke VENTRICULAR FIBRILLATION - potentially fatal

Answer 299

A

May be uncomfortable especially when frequent
Pulse is irregular owing to the premature beats
Usually are asymptomatic
Can feel faint or dizzy

Answer 300

A

ECG:

• Widened QRS complex - greater than 0.12 seconds

Answer 301

A

Reassure patient

- Give beta-blockers e.g. Bisoprolol if symptomatic

Answer 302

A

• Pulse of more than 100bpm with at leat 3 irregular heart beats in a row
• Commonly found in patients with structurally normal hearts (known as idiopathic
ventricular tachycardia), in these cases it is usually a benign condition with an
excellent long-term prognosis
• Occasionally it is pathological and known as Gallavardin’s tachycardia and if
untreated may lead to cardiomyopathy
• Essentially there is rapid ventricular beating so much so that they is inadequate
blood filling of ventricles since they are filled in between beats and thus id beating
faster there is less time to fill and thus less blood fills
• Results in decreased cardiac output and thus a decrease in the amount of
oxygenated blood that is circulated around the body

Answer 303

A

Breathlessness (lack of lung perfusion)
Chest pain (lack of heart perfusion)
Palpitations
Light headed or dizzy (lack of brain perfusion)

Answer 304

A

Treatment of symptoms is usually with beta-blockers e.g. Bisoprolol

Answer 305

A

• Ventricular tachycardia for longer than 30 seconds

Answer 306

A

Dizziness (pre-syncope)
Syncope
Hypotension
Cardiac arrest
Pulse rate between 120-220 bpm

Answer 307

A

Rapid ventricular rhythm

- Broad & abnormal QRS complex (greater than 0.14 seconds)

Answer 308

A

Haemodynamically unstable (e.g. hypotensive or pulmonary oedema):
• Emergency electrical cardioversion
Stable:
• IV beta-blocker e.g. Esmolol
• IV Amiodarone
Prevented by the use of beta-blockers and implantable cardiac defibrillator

Answer 309

A

• Involves very rapid and irregular ventricular activation with NO MECHANICAL
EFFECT i.e NO CARDIAC OUTPUT
• Patient is pulseless and becomes unconscious and respiration ceases (CARDIAC
ARREST)
• ECG shows shapeless, rapid oscillations and there is no hint of organised
complexes
• Usually caused by a ventricular ectopic beat
• Only effective treatment is ELECTRICAL DEFIBRILLATION
• Survivors are at increased risk of sudden death so long term, implantable
cardioverter-defibrillators are the first-line therapy

Answer 310

A

• Describes an ECG where the ventricular repolarisation - QT interval is greatly prolonged

Answer 311

A

Congenital:
• Jervell-Lange-Nielsen syndrome (autosomal recessive) - mutation in
cardiac potassium and sodium-channel genes
• Romano-Ward syndrome (autosomal dominant)
Acquired:
• Hypokalaemia
• Hypocalcaemia
• Drugs; Amiodarone and Tricyclic antidepressants e.g. Amitriptyline
• Bradycardia
• Acute MI
• Diabetes

Answer 312

A

Syncope
Palpitations
Due to polymorphic ventricular tachycardia that usually terminate
spontaneously but may degenerate to ventricular fibrillation

Answer 313

A

Syncope
Palpitations
Due to polymorphic ventricular tachycardia that usually terminate
spontaneously but may degenerate to ventricular fibrillation

Answer 314

A

• ECG shows prolonged QT interval

Answer 315

A

Treat underlying cause
If acquired long QT then give IV isoprenaline (contraindicated for congenital
long QT)

Answer 316

A

• Classified as true and false
• An aneurysm is defined if there is a permanent dilatation of the artery to TWICE
the normal diameter
• Normal diameter of aorta is around 2cm - this increases with age

Answer 317

A

Abnormal dilatations that involve all layers of the arterial wall
Arteries most frequently involved are:
• Abdominal aorta (most common)
• Iliac, popliteal and femoral arteries
• Thoracic aorta

Answer 318

A

Also known as pseudoaneurysm
Involves the collection of blood in the OUTER LAYER ONLY (ADVENTITIA)
which communicates with the lumen e.g after trauma from a femoral artery
puncture

Answer 319

A

Aortic aneurysms are classified as ABDOMINAL or THORACIC

Answer 320

A

Most commonly occur BELOW the renal arteries (infra-renal)
Incidence increases with age
AAA’s are present in 5% of the population above 60
More common in men than women
Abdominal aneurysm is classified as an aortic diameter EXCEEDING 3cm
Causes & Risk factors:
• Most have no specific identifiable causes
• Severe atherosclerotic damage
• Family history
• Tobacco smoking
• Male
• Increasing age
• Hypertension
• COPD
• Trauma
• Hyperlipidaemia

Answer 321

A

Degradation of the elastic lamellae resulting in leukocyte infiltrate causing
enhanced proteolysis and smooth muscle cell loss
The dilatation affects ALL THREE LAYERS of the vascular tunic
If it doesn’t then it is a pseudoaneurysm

Answer 322

A

• Often asymptomatic and only picked up via a routing abdominal
examination or plain X-ray
• Pain in abdomen, back, loin or groin
• Pulsatile abdominal swelling (less pronounced)

Answer 323

A

• Rupture is more likely if there is; increased BP, female, smoker, strong
family history
• Intermittent or continuous abdominal pain (radiates to the back, iliac
fossa’s or groin)
• Pulsatile abdominal swelling (more pronounced)
• Collapse
• Hypotension
• Tachycardia
• Profound anaemia
• Sudden death

Answer 324

A

GI bleed
Ischaemic bowel
MSK pain
Perforated GI ulcer
Pyelonephritis
Appendicitis

Answer 325

A

Abdominal ultrasound - can assess aorta to degree of 3mm

- CT and or MRI angiography scans

Answer 326

A

Small aneurysms below 5.5cm are generally just monitored
Treat underlying causes
Modify risk factors e.g. smoking and diet
Smoking cessation
Vigorous BP control
Lowering of lipid in blood
Surgery:
• Patients tend to do better if aneurysm is symptomatic, larger than 5.5cm
and expanding yearly
• Open surgical repair
• Endovascular repair - stent inserted via femoral or iliac arteries

Answer 327

A

Normal size of the mid-descending thoracic aorta is 26-28mm
The ascending, arch or descending thoracic aorta may become aneurysmal
Ascending thoraco-abdominal aneurysms occur most commonly in patients
with Marfan syndrome or hypertension
Descending or arch TAAs occur secondary to atherosclerosis and are now
rarely due to syphilis
Causes:
• STRONG GENETIC LINK - in some families it appears to be an
autosomal dominant trait
• Certain connective tissue disorders:
Marfan’s syndrome
Ehlers-danlos syndrome
Loeys-dietz syndrome
• Mycotic aneurysm is endocarditis
• Aortic dissection in some cases
• Weight lifting, cocaine and amphetamine use - perhaps due to the large
rise in BP when undertaking these activities

Answer 328

A

Hypertension
Increasing age
Smoking
Bicuspid or unicuspid aortic valves
Atherosclerosis
COPD
Renal failure
Previous aortic aneurysm repair

Answer 329

A

Involves inflammation, proteolysis and reduced survival of the smooth muscle cells in the aortic wall
Once the aorta reaches a crucial diameter (around 6cm in the ascending and 7cm in the descending) it loses all distensibility so that a rise in BP to around 200mmHg can exceed the arterial wall strength and may trigger dissection or rupture

Answer 330

A

Most TAA’s are asymptomatic
May be diagnosed incidentally e.g. on routing CXR or cardiological
investigation or if complicated by dissection, rupture or other complications
Pain in chest, neck, upper back, mid-back or epigastrium
Aortic regurgitation
Fever if there is infective cause
Symptoms due to compression of local structures
Acute pain
Collapse, shock and sudden death
Cardiac tamponade
Haemoptysis

Answer 331

A

Thoracic back pain
Arterial ischaemia
Collapse
MI

Answer 332

A

CT or MRI used for assessment of TAA
Aortography may be helpful for assessing the position of the key branches in relation to the aneurysm
Transoesophageal echocardiography can be useful for identifying aortic dissection
Ultrasound

Answer 333

A

Immediate urgent surgery is required for ruptured TAA
Symptomatic TAA’s merit surgery regardless of size
Regular monitoring by CT or MRI every 6 months
Rigorous BP control using beta-blockers e.g. Bisoprolol
Smoking cessation
Treat underlying cause

Answer 334

A

Aortic dissection begins with a tear in the intima (inner wall)
Blood then penetrates the diseased medial layer and flows between the layers of the aorta, forcing the layers apart resulting in dissection
A medical emergency that can lead to death
The most common emergency affecting the aorta
Affects men more than females
Most common between the ages of 50-70 and is rare below 40
Very rare in children
Can be classified according to the timing of diagnosis from the origin of symptoms:
• Acute - less than 2 weeks
• Subacute - 2-8 weeks
• Chronic - more than 8 weeks

Answer 335

A

Inherited
Degenerative
Atherosclerotic
Inflammatory
Trauma e.g. shearing stresses in a road traffic accident (RTA)

Answer 336

A

Aortic dissection begins with a tear in the intimal lining of the aorta
The tear allows a column of blood under pressure to enter the aortic wall,
forming a haemotoma which separates the intima from the adventitia and creates a false lumen
The false lumen extends for a variable distance in either direction; anterograde (towards bifurcations) and retrograde (towards the aortic root)
The most common sites for the intimal tears are:
• Within 2-3cm of the aortic valve
• Distal to the left subclavian artery in the descending aorta

Answer 337

A

Sudden onset of severe and central chest pain that radiates to the back and down the arms - mimics a MI
Pain is often describes as tearing in nature and may be migratory
Hypertension
Pain is maximal from the time of onset, unlike in MI where the pain gains in intensity
Patients may be shocked and may have neurological symptoms secondary to loss of blood supply to the spinal cord
May develop aortic regurgitation, coronary ischaemia and cardiac tamponade
Distal extension may produce acute kidney failure, acute lower limb ischaemia or visceral ischaemia
Peripheral pulses may be absent

Answer 338

A

Acute coronary syndrome, MI, Aortic regurgitation without dissection, MSK
pain, pericarditis, cholecystitis, atherosclerotic embolism

Answer 339

A

CXR:
• Widened mediastinum
Urgent CT scan, Transoesophageal echocardiography or MRI will CONFIRM
DIAGNSOS

Answer 340

A

At least 50% are hypertensive and may require urgent antihypertensive medication to reduce blood pressure to less than 120mmHg - give IV beta-blockers e.g. IV metoprolol or vasodilators e.g. IV GTN
Adequate analgesia e.g. morphine
Surgery to replace aortic arch
Endovascular intervention with stents
Patients require long term follow-up with CT or MRI

Answer 341

A

- Essentially its the partial blockage of leg
or peripheral vessels by an
atherosclerotic plaque and or resulting
thrombus resulting in insufficient
perfusion of the lower limb resulting in
LOWER LIMB ISCHAEMIA
- Commonly caused by atherosclerosis and usually affects the aorta-iliac and
infra-inguinal arteries
- More common in men than women

Answer 342

A

Smoking
Diabetes
Hypercholesterolaemia
Hypertension
Physical inactivity
Obesity

Answer 343

A

ALWAYS due to ATHEROSCLEROSIS of the arteries distal to the aortic arch
Atherosclerosis can result in many complications:
Symptoms of Ischaemia:
• Normal oxygen pressures in different activities: