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Phase 2 Med > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Ischaemic heart disease definition

A 
Inadequate blood supply caused by an imbalance between the supply and demand of oxygen (and other nutrients) to the heart tissue. 
Divided into three segments: 
1. Angina 
2. Acute coronary syndrome 
3. Myocardial infarction
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2
Q

Ischaemic heart disease aetiology

A

Restriction of blood flow to a region of myocardium may be caused by:

  • atheroma
  • thrombosis
  • spasm
  • embolus
  • coronary ostial stenosis

Decrease in supply of oxygenated blood to the myocardium:

  • anaemia
  • hypotension (decreased flow to heart)
  • hypoxemia

Increased demand of heart tissue:

  • hypertension
  • tachyarrhythmia
  • valvular heart disease
  • hyperthyroidism
  • hypertrophic cardiomyopathy

Myocardial ischaemia most commonly occurs due to obstructive coronary artery disease (CAD) in the form of coronary atherosclerosis

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3
Q

Ischaemic heart disease risk factors

A

Modifiable:

  • diabetes mellitus
  • hyperlipidemia
  • hypertension
  • kidney disease
  • obesity
  • physical inactivity
  • cigarette smoking
  • alcohol

Non-modifiable

  • age
  • family history (not relevant if occured over 55yrs old)
  • male (oestrogen in women is protective)

Environmental exacerbating factors:

  • cold weather
  • heavy meals
  • emotional stress
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4
Q

Ischaemic heart disease pathophysiology

A

look at myles’ table

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5
Q

Angina definition

A

A major symptom of stable IHD. Characterised by chest pain. Main types are stable and unstable.

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6
Q

Angina aetiology

A

Stable angina:
narrowing of the artery from a plaque - symptoms felt at >70% occlusion
Unstable angina:
likely due to the development of a thrombus from plaque rupture. Comes under the umbrella term of acute coronary syndromes

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7
Q

Angina risk factors

A

same as atherosclerosis

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8
Q

Angina signs and symptoms

A

Stable angina:

  • central chest pain on exertion
  • relieved by GTN spray
  • radiation of pain to neck, jaw and arm

Untable angina:

  • new onset pain without exertion
  • gets worse quickly
  • GTN spray does not relieve symptoms
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9
Q

Angina 1st line investigations

A

Stable:

  • resting ECG - often normal, may reveal ST-T changes (St depression and T wave inversion) suggestive of ischaemia or Q waves indicative or prior infarction
  • Lipid profile - usually raised LDLs

Unstable:

  • ECG - may be normal or have transient ST segment depression or T wave inversion
  • cardiac biomarkers - troponin not usually elevated as there is no acute myocardial damage
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10
Q

Angina gold standard investigations

A

Stable: perfusion MRI

  • less available but best option
  • CT coronary angiography not great at determining severity

Unstable: coronary angiography is the gold standard for assessing the presence and severity of CAD and allows for concurrent treatment with angioplasty and stenting if needed.

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11
Q

Angina differential diagnosis

A

Other anginas:

  • prinzmetal’s angina - coronary artery syndrome
  • microvascular angina - syndrome X - predominantly women, abnormal structure causing increased resistance
  • crescendo angina - artery becomes so narrow blood struggles to flow even at rest
  • unstable vs stable
Chest pain not related to myocardial ischaemic: 
- preicarditis/myocarditis 
- pulmonary embolism/pleurisy
- chest infection/pleurisy 
- dissection of the aorta 
- GORD, spasm or ulceration 
- musco-skeletal 
psychological
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12
Q

Angina management

A

Stable (prevent it becoming unstable):

  • education for lifestyle factors - smoking, weight, exercise, diet…
  • anti platelet therapy - aspirin and clopidogrel or other P2Y12 inhibitor
  • lipid-lowering therapy - primary options are statins - secondary are ezetimibe or alirocumab
  • beta blocker
  • sublingual GTN
  • antihypertensives - beta-blockers and ACE inhibitors or angiotensin-II receptor antagonists
  • blood sugar control (if needed)
  • percutaneous Coronary Intervention (PCI) (for more severe cases)

Unstable (for ongoing confirmed unstable angina):
- may have PCI
Antiplatelet therapy - aspirin + P2Y12 inhibitor, may consider GPIIb/IIIa antagonists
- statin +/- ezetimibe
- beta blocker
- ACE inhibitor
- lifestyle education

May also consider ca++ channel blockers for underlying HTN

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13
Q

Angina prognosis

A

Reasonably good
Very low death rate per annum considering age
- cardiovascular events (includes non-fatal MIS, hospital admissions etc) a bit higher
- reassure patients diagnoses with angina

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14
Q

Acute coronary syndrome (NSTEMI) definition

A

Non-ST elevation myocardial infarction.
Myocardial infarction occurs when cardiac myocytes die due to myocardial ischaemia. NSTEMIs are usually a retrospective diagnosis made after troponin results and sometimes other investigations (echocardiogram, cardio angiogram)

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15
Q

NSTEMI aetiology

A

NSTEMIs are usually a result of a transient or near-complete occlusion of a coronary artery or acute factor that deprives myocardium of oxygen. Different from a STEMI as there is not usually complete occlusion of the affected coronary artery

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16
Q

NSTEMI risk factors

A

see unstable angina

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17
Q

NSTEMI pathophysiology

A

common mechanism of all ACS is rupture or erosion of the fibrous cap of a coronary artery plaque. This leads to platelet aggregation, localised thrombosis, vasoconstriction and distal thrombus embolisation.

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18
Q

NSTEMI key presentations

A

New onset of chest pain or chest pain at rest or a deterioration of preexisting angina.

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19
Q

NSTEMI signs and symptoms

A

Often retrosternal pain radiating to the left arm but may also radiate to the lower jaw, neck, both arms, back and epigastrium.
GTN trial: ongoing pain
Angiography should be considered if high risk

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20
Q

NSTEMI 1st line investigations

A

ECG:

  • ST depression
  • T wave inversion
  • Usually pretty normal so diagnosed by troponin
  • FBC
  • Troponin: high, >99th percentile of normal.
  • Elevated troponin is sign of infarction
  • U&Es
  • Glucose
  • Lipids
  • CXR - DDx
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21
Q

NSTEMI gold standard investigations

A

Urgent coronary angiography for diagnoses and treatment in patients at a high risk for progression to MI or death.

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22
Q

NSTEMI differential diagnosis

A 
Can be distinguished from unstable angina by troponin levels 
Aortic dissection 
PE 
Peptic ulcer 
Acute pericarditis 
Psychological 
Stable ischaemic heart disease
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23
Q

NSTEMI management

A

Acute presentation:

  • antiplatelet therapy
  • oxygen
  • GTN
  • beta-blocker
  • calcium channel blocker
  • assess need for PCI
  • heparin
  • GPIIa/IIb inhibitor
Intermediate management: 
M- morphine 
N- nitrates vasodilator 
A- aspirin stops the platelets sticking together 
C- clopidogrel AntiPlatelet drug
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24
Q

STEMI definition

A

Acute myocardial infarction is myocardial cell death occurring due to a prolonged mismatch between perfusion and demand. In the case of ST-elevation MI this is caused by complete atherothrombotic occlusion of a coronary artery.

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25
Q

STEMI aetiology

A

Usually occurs due to complete occlusion of a coronary artery:

  • rupture of an atherosclerotic plaque and a consequent arterial thrombosis is the major cause
  • coronary vasospasm without plaque rupture
  • drug abuse (emphetamines, cocaine)
  • dissection of the coronary artery related to defects of the vessel connective tissue
  • thoracic aortic dissection
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26
Q

STEMI pathophysiology

A

Causes full thickness heart damage

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27
Q

STEMI key presentations

A

Typically presents with central chest pain

  • classically retrosternal, crushing, heavy, severe and diffuse
  • may radiate to left arm, neck or jaw
  • might be described as ‘pressing or squeezing’
  • may have associated nausea, vomiting, dyspnoea
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28
Q

STEMI signs and symptoms

A

In elderly and diabetic patients the symptoms may be atypical and include dyspnea, fatigue, syncope or presyncope

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29
Q

STEMI 1st line investigations

A 
ECG 
- ST elevation, may be LBBB
- tall T waved 
- ' pathological Q waves' 
Cardiac troponin - elevated, consider with time context 
- glucose
- FBC
- U&Es, creatinine 
- CRP 
- Lipids
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30
Q

STEMI management

A

Immediate management on way to hospital (eg paramedics)
- MONA - morphine, oxygen, nitrates, aspirin

Immediate hospital management 
M- morphine 
N- nitrates vasodilator 
A- aspirin stops the platelets sticking together 
C- clopidogrel anti platelet drug

Investigations (eg coronary angiography) will confirm if surgery eg PCI needed

  • ST elevation of over 2mm in 2 counties chest leads of over 1mm in continuous limb leads
  • chest pain or other evidence of ischaemia
  • new or presumed left bundle branch block
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31
Q

STEMI monitoring

A

ECG may show ‘pathological Q waves’ (wide, deep or seen in leads V1-3)
Inverted T waves may appear in days after MI

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32
Q

STEMI complications

A
  • death
  • rupture of heart septum/papillary muscles
  • oedema (heart failure)
  • arrhythmias, sinus bradycardia - usually due to occlusion of the right coronary artery and caused by infarction of the AV node and conduction system
  • Dressler’s syndrome - post-infarction pericarditis
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33
Q

Heart failure (ischemic, valvular, myopathic, hypertensive, cor pulmonale) definition

A

Complex syndrome resulting from any structural or functional cardiac disorder that impairs the ability for the heart to function as a pump to support physiological circulation. This is not a disease rather a syndrome caused by any cardiac problem.

HF definitions:

  • HF-REF (reduced ejection fraction) (left ventricular systolic impairment with LVEF <40%)
  • HF-PEF (preserved ejection fraction) (LVEF > 50%, with dilated LA > 34ml/m2)
  • HF-PH (pulmonary hypertension)
  • HF-valve (valve disease) (severe stenosis or regurgitation)
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34
Q

Heart failure epidemiology

A

It is common (up to 20% in over 75yo), it costs approx 2% of the NHS expenditure. It is also disabling diminishing quality of life (worse than RA and COPD patients).

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35
Q

Heart failure aetiology

A

Main causes:

  • ischaemic heart disease
  • cardiomyopathy
  • hypertension
  • valvular heart disease
  • cor pulmonale (linked to underlying respiratory issues)
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36
Q

Heart failure risk factors

A

age, male

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37
Q

Heart failure key presentations

A

Paroxysmal nocturnal dyspnea - very specific symptom - episodes of shortness of breath that occur during the night
Othopnea - patient can’t breathe when they lie flat
Cardinal signs - SOB, fatigue, ankle oedema

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38
Q

Heart failure signs and symptoms

A
  • SOB
  • Fatigue
  • ankle swelling and oedema
  • cold peripheries (inadequate perfusion)
  • displaced apex beat
  • raised JVP
  • added heart sounds and mumurs
  • ascites (fluid in abdominal cavity)
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39
Q

Heart failure 1st line investigations

A

NT-proBNP - will be significantly raised in heart failure
Transthoracic ECHO - needed if NT-proBNP raised ECG - unlikely to be normal. Use to identify aetiology such as MI or arrhythmia

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40
Q

Heart failure management

A
  • diuretics eg furosemide
  • mineralocorticoid receptor antagonist eg spironalactone
  • sacubitril-valsartan
  • cardiac resynchronization therapy
  • implantable defibrillator
  • left ventricular assist device
  • heart transplant
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41
Q

Hypertension definition

A

High blood pressure
Stage 1 - 140/90 and 135/85
Stage 2 - 160/100 and 150/95

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42
Q

Hypertension aetiology

A

Normally primary (unknown and due to lifestyle and age). Can be secondary eg Conn’s

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43
Q

Hypertension key presentations

A

usually asymptomatic

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44
Q

Hypertension signs and symptoms

A

ACE inhibitors: side effects: hypotension, dry cough, contraindicated in early pregnancy

ARB blocker: ‘sartans’ eg candesartan side effects: hypotension, hyperkalemia, contraindicated in pregnancy

CCBs: side effects: peripheral vasodilation; flushing, headache, oedema; negatively chronotropic (slowing of heart); bradycardia, AV block; constipation (gut calcium channels)

BBs: can be B1 selective (cardio selective) or non-selective. Side effects: contraindicated in asthma, fatigue, headache, bradycardia, cold peripheries

Diueritcs: side effects: hypovolaemic (mainly loop diuretics), hypotension, hypokalemia, hyponatremia, impaired glucose tolerance (mainly thiazides)

Alpha blockers
Renin inhibitors
Centrally acting drugs

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45
Q

Atrial fibrillation definition

A

A type of supraventricular tachyarrhythmia

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46
Q

Atrial fibrillation aetiology

A

Associated with all types of cardiac disease. Most commonly associated with HTN, CAD and MI. Mitral valve disease can also be a cause, as can hyperthyroidism.

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47
Q

Atrial fibrillation signs and symptoms

A

Common presentation:

  • presence of risk factors
  • palpitations
  • tachycardia
  • irregular pulse
  • chest pain
  • dizziness
  • SOB
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48
Q

Atrial fibrillation diagnosis

A 
ECG: 
Irregularly irregular QRS complexes 
Absence of P waves 
QRS usually < 120ms unless patient has other conducting problems 
ECHO if suspected valvular disease
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49
Q

Atrial fibrillation management

A

Hemodynamically unstable: immediate heparin and attempted cardio version with synchronised DC shock

Hemodynamically stable:

  • rate control - patient not in severe tachycardia but will still have Afib rhythm, BBs are first line; CCBs or Digoxin are second line
  • rhythm control - returns to sinus rhythm, given to patients with reversible causes, or new onset of Afib, achieved by cardioversion

Cardioversion - process of returning patient to normal sinus rhythm

  • electrical cardio version - controlled shock delivered
  • pharmacological cardio version - amiodarone
  • long term BBs for rate and rhythm control
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50
Q

Atrial fibrillation complications

A 
Risk of thrombosis in atria causing stroke 
Use of CHA2DS2-VASc score 
C - congestive heart failure 
H - HTN 
A - age 
D - diabetes 
S - stroke/TIA/thomboembolism
V - vascular disease
A - age 
S - sex category

If risk >1 offer anticoagulation therapy

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51
Q

Atrial flutter definition

A

Type of supraventricular tachycardia. Atrial rates are usually above 250bpm.

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52
Q

Atrial flutter aetiology

A

Due to finctional or structural abnormalities of the atria. Structural abnormalities include atrial dilation due to for example; scars from atrial surgery, prior atrial ablation sites and idiopathic fibrosis within the atrium. Can be precipitated by toxic and metabolic conditions.

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53
Q

Atrial flutter signs and symptoms

A

Usually occurs as part of an acute disease process Identifying underlying (cardiac, respiratory, diabetes, hyperthyroidism).
Palpitations, dizziness, syncope

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54
Q

Atrial flutter diagnosis

A

ECG is diagnostic
- organised ‘sawtooth pattern’
- important factor is a regular beat
Murmers or rubs on auscultation suggest valvular disease, pericarditis, or congenital heart disease

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55
Q

Atrial flutter management

A
  • Beta-blockers

- Definitive treatment is catheter ablation

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56
Q

Atrioventricular block definition

A

Cardiac electrical disorder defined as impaired (delayed or absent) conduction from the atria to the ventricles.
Can be separated into degrees of severity:
- first degree - delay in conduction at AV node
- second degrees (types I & II) - not every atrial depolarisation is conducted to the ventricles
- third degree (complete) - not atrial impulses at all make it through to the ventricles. Ventricles respond by generating an escape rhythm. Atria and ventricles contract but at their own intrinsic rate

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57
Q

Atrioventricular block aetiology

A

Causes include fibrosis and calcification of the conduction system, CAD and medication such as AV-nodal blocking agents (ie BBs, CCBs, digitalis, adenosine), anti arrhythmic medications such as sodium-channel blockers. May be due to congenital defects or damage from surgery or other cardiac interventions.

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58
Q

Atrioventricular block presentation

A

Patients tend to be older males with underlying cardiovascular disease. May have acid-base disturbance or neuromuscular disease.
Usually bradycardia.
Blood pressure is often high with a wide pulse pressure.
Syncope may be present

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59
Q

Atrioventricular block diagnosis

A

ECG:

  • first degree showing fixed prolonged of the PR interval (PR interval > 0.2s)
  • second degree type I showing progressive prolongation of the PR interval with resumption of AV conduction with a PR interval that progressively prolongs with eventual loss of AV conduction for 1st beat
  • second degree type II showing occasional loss of AV conduction for 1 beat preceded and followed by fixed, unchanging PR intervals
  • third degree is complete, persistent loss of conduction from the atria to ventricles. Also called complete heart block, third-degree shows no consistent PR relationship. QRS are usually wide and bizarre shape.
60
Q

Atrioventricular block management

A

First-degree or type I second-degree block

  • if asymptomatic only monitoring is needed
  • if symptomatic: review meds to treat underlying cause, rarely a pacemaker is used

Type II second degree or third degree

  • discontinuation of AC node-blocking drugs
  • treat underlying cause (often heart disease such as ACS)
  • pacemaker if symptomatic
61
Q

Atrioventricular block complications

A

Second degree can progress to third. First degree does not usually progress

62
Q

Left and right bundle branch block (LBBB & RBBB) definition

A

Bundle branch block is a defect of the bundle branches or fascicles in the electrical conduction system of the heart.
In LBBB activation of the LV is delayed, causing the LV to contract later than the RV. Always pathological.
In RBBB activation of the RV is delayed and caused by spread from the myocardium of the LV rather than the normal conducting system.

63
Q

LBBB & RBBB aetiology

A

LBBB is ofetn associated with extensive left ventricular disease such as aortic stenosis and HTN.

RBBB often occurs as an isolated congenital anomaly or is associated with cardiac or pulmonary conditions.

64
Q

LBBB & RBBB presentation

A

Usually asymptomatic. RBBB causes wide but physiological splitting of the second heart sound. LBBB may cause reverse splitting of the second heart sound. BBB patients may complain of syncope due to intermittent complete heart block or ventricular tachyarrhythmia.

65
Q

LBBB & RBBB diagnosis

A 
ECG: 
Widened QRS (>0.12s) the shape of the QRS depends on if its LBBB or RBBB

LBBB: broad QRS with V1 showing ‘W’ appearance and V6 showing ‘M’ appearance R wave. Remeber WiLLiaM. May have ST depression in (leads I, AVL and V6, all of these are lateral leads)
Diagnostic criteria:
- QRS > 120ms
- Dominant S wave in V1
- broad monophasic R wave in lateral leads (I, aVL, V5-6)
- absence of Q waves in lateral leads
- prolonged R wave peak time

RBBB: classic is ‘M’ shape seen in V1 and ‘W’ shape in V6.
Remember ‘MaRRoW’
- broad QRS
- RSR pattern in V1-3 (‘M-shape’ QRS complex)
- wide, slurred S wave in lateral leads (I, aVL, V5-6)

66
Q

Tachycardia (sinus, supreventricular, ventricular) definition

A

Sinus tachycardia: heart rate > 100bpm in adults with sinus rhythm. Can be normal or pathological

Ventricular tachycardia: ectopic focus in ventricle which depolarises with high frequency: can be life threatening. Diastole not long enough for proper ventricular filling.

67
Q

Tachycardia aetiology

A

Sinus tachycardia: hyperthyroidism, PE, fever, pain, anemia, hypovolemia, drugs

Ventricular tachycardia: cardiac scars, cardiomyopathies, drugs, long QT-syndrome

68
Q

Tachycardia presentation

A

Sinus tachycardia: palpitations, dizziness

Ventricular tachycardia: often asymptomatic: palpitations, hypotension, syncope, angina, cardiogenic shock

69
Q

Tachycardia diagnosis

A

Sinus tachycardia:
regular rhythm, normal P waves, narrow QRS, rate > 100bpm

Ventricular tachycardia: no visible P waves, wide abnormal QRS, QRS rapid but regular (120-200bpm), T waves can’t be seen

70
Q

Tachycardia management

A

Sinus tachycardia: beta-blockers if symptomatic

Ventricular tachycardia:

  • hemodynamically unstable with pulse - cardioversion
  • hemodynamically unstable without pulse - defibrillator
  • hemodynamically stable - antiarrhthmics (amiodarone)
  • long-term therapy - antiarrhythmics or ICD (implantable defibrillator)
71
Q

Ventricular fibrillation definition

A

It is a preterminal event seen in very damaged hearts. Most frequently encountered arrhythmia in adults who experience sudden death. Heart generated no cardiac output

72
Q

Ventricular fibrillation aetiology

A

Underlying cardiovascular disease; CAD, previous MI, myocarditis; congenital heart defects; electrophysiology disorders, ventricular tachycardia, WPW syndrome

73
Q

Ventricular fibrillation presentation

A

Chest pain, palpitations, SOB, dizziness syncope, eventually death

74
Q

Ventricular fibrillation diagnosis

A

ECG: sporadic (coarse vfib) for undulates (fine vfib), no true QRS complexes, no P waves, no T waves, wide irregular waves at a rapid rate

75
Q

Ventricular fibrillation management

A

immediate defibrillation and advance cardiac life support

76
Q

Sinus bradycardia defiinition

A

Heart rate <60bpm in adults with sinus rhythm. Normal in well trained athletes

77
Q

Sinus bradycardia aetiology

A

Can be healthy. Pathological cause: drugs (BBs, CCBs), hypothyroidism, hypothermia, raised ICP, acute ischaemia of SA following MI

78
Q

Sinus bradycardia presentation

A

syncope, fatigue, dizziness

79
Q

Sinus bradycardia diagnosis

A

ECG: regular rhythm, normal P waves, might see U waves, narrow QRS, rate > 60bpm

80
Q

Sinus bradycardia management

A

Persistent symptomatic - pacemaker

Acute symptomatic - atropine

81
Q

Ventricular ectopic definition

A

Ectopic beats are common, they’re extra beats which arise out of the normal sequence from either atria or ventricle. They can occur in runs in couplets/triplets or alternatively if in the pattern of ectopic-normal-ectopic-normal then its called bigeminy.

Origin of beat from ventricle - using slower myocyte-myocyte conduction

82
Q

Ventricular ectopic management

A

Symptomatic relief from reassurance/beta-blockers

83
Q

Ventricular ectopic complications

A

A high burden of VEB can cause heart failure

84
Q

Long QT syndrome definition

A

Genetic or acquired condition characterised by a prolonged QT interval. Associated with a high risk of sudden cardiac death due to ventricular tachyarrhythmia

85
Q

Long QT syndrome aetiology

A

Genetic long QT
Acquired
- drugs: quinidine, procainamide, sotalol, amiodarone, tricyclic antidepressants, methadone
- electrolyte imbalances: hypokalemia, hypomagnesaemia, hypocalcemia
- bradyarrhythmias
- CNS lesions

86
Q

Long QT syndrome presentation

A

Genetic long QT patients may have had episode triggered by a sudden event (exercise, startle)
May present with syncope or palpitations

87
Q

Long QT syndrome diagnosis

A

Medication history
Family history
U&Es
ECG (long QT interval) also look for signs of electrolyte imbalance

88
Q

Long QT syndrome management

A

Treat underlying cause
Acquired and genetic
- beta-blockers
- lifestyle modification - avoid extreme sports
May need an implantable cardioverter-defibrillator (ICD) in some cases

89
Q

Long QT syndrome complications

A

Ventricular tachycardia, cardiac arrest, sudden death

90
Q

Wolf-parkinson syndrome definition

A

Congenital condition characterised by intermittent tachycardias and signs of ventricular preexcitation. Ventricles depolarize before expected time. This is due to an accessory pathway (bundle of Kent) which connects the atria and ventricles, bypassing the AV node and leading to ventricular preexcitation.

91
Q

Wolf-parkinson sydrome aetiology

A

Associated with other cardiac structural abnormalities (most common is Ebstein’s abnormailuty) and a family history)

92
Q

Wolf-parkinson syndrome presentation

A

Acute presentations may be with acute arrhythmia and may present with palpitations, dizziness, SOB, chest pain and/or sudden cardiac death.
Specific symptom is paroxysmal tachycardia (abrupt onset and termination) can be brought on by exertion, caffeine, alcohol

93
Q

Wolf-parkinson syndrome diagnosis

A

ECG:

  • delta wave: slurred upstroke in the QRS, in WPW is associated with a short PR interval
  • board QRS
94
Q

Wolf-parkinson syndrome management

A

Vagal manoeuvre to increased AV nodal delay
- blow into a syringe (Valsalva)
- carotid sinus massage
Adenosine if that doesn’t work
Long term - radiofrequency ablation of accessory pathway

95
Q

Wolf-parkinson syndrome complications

A

Sudden cardiac death
WPW is dangerous in AF as there isn’t an upper limit to the ventricular contractions which would normally be mediated by AV nodal delay, therefore this can result in ventricular fibrillation and death.

96
Q

Aortic dissction definition

A

A condition where separation has occured in the aortic wall intima, causing blood flow into a new false channel composed of the inner and outer layers of the media.
Dissection most commonly occurs with a discrete intimal tear, but can occur without one.

97
Q

Aortic dissection risk factors

A

Most common in men over 50ys. Hypertension, smoking and raised cholesterol are significant risk factors.
Previous cardiac surgery and pre-existing aortic and valve disease are also risk factors.
Congenital risk factors include Markfan’s, Ehlers-Danlos syndrome and congenital bicuspid aortic valve.

98
Q

Aortic dissection presentation

A

Acute severe chest pain - severe tearing or ripping chest pain. May change location with time as the dissection extends. Pain is abrupt in onset and maximal at time of onset (unlike with MIs where pain is progressive)

Left/right blood pressure differential - hallmark of aortic dissection. Pulse differences in the lower limbs may also be evident.

Diastolic murmur - crescendo pattern, indicating aortic incompetence. Common in proximal dissections.

Pulse deficit.

99
Q

Aortic dissection diagnosis

A

ECG - look for evidence of myocardial ischaemia. ST depression may occur in acute dissection.

CT angiography - order if diagnosis is suspected. Look for intimal flap.

Transesophageal ECHO

Cardiac enzymes - usually negative, rule out MI

100
Q

Aortic dissection management

A

Only definitive treatment is surgical

101
Q

Aortic dissection complications

A

Pericardial tamponade

Aortic incompetence

102
Q

Abdominal aortic aneurysm definition

A

Permanent pathological dilation of the aorta. More than 90% originate below the renal arteries. Highest prevalence in male smokers.

103
Q

Abdominal aortic aneurym presentation

A

Patients with AAA are usually asymptomatic and they are usually an incidental finding on screening.
May have a palpable pulsatile abdominal mass, abdominal, back or groin pain.

Ruptured AAA: hypotension, pain in the abdomen, back or loin. May present with syncope, shock or collapse.

104
Q

Abdominal aortic aneurysm diagnosis

A

Abdominal ultrasound - very good test, shows abdominal aortic dilation
Take usual blood and U&Es: may show anaemia if ruptured

105
Q

Abdominal aortic aneurysm management

A

If small asymptomatic: surveillance and cardiovascular risk management

Large, symptomatic, ruptured: surgical repair

106
Q

Abdominal aortic aneurysm complications

A

Abdominal compartment syndrome
Illeus, intestinal obstruction and ischemic colitis
AKI (acute kidney injury)

107
Q

Peripheral arterial disease (claudication and critical ichaemia) definition

A

A range of arterial syndromes usually caused by atherosclerotic obstruction of the lower-extremity arteries

108
Q

Peripheral arterial disease epidemiology

A

More common in men

109
Q

Peripheral arterial disease aetiology

A

Most commonly athersclerosis

110
Q

Peripheral arterial disease risk factors

A

Smoking, diabetes, HTN, hypercholesterolemia

111
Q

Peripheral arterial disease pathophysiology

A

See IHD for atherosclerosis pathology

112
Q

Peripheral arterial disease signs and symptoms

A

Symptoms:

  • ‘severe cramp’ on exercise which resolves when they stop walking. Often worse going uphill but never at rest. This is called intermittent claudication. Claudication refers to pain in the thigh, calf or buttocks when walking.
  • severe unremitting pain occurs with critical lower limb ichaemia. There may also be ulceration and gangrene
  • erectile dysfunction

Signs:

  • lower limbs are cold with dry skin and lack of hair
  • pulses may be diminished or absent

‘6 Ps’: pulseless, pain, pallor, paraesthesia, paralysis, perishingly cold

113
Q

Peripheral arterial disease 1st line investigations

A

Toe-brachial index

Segmental pressure examination

114
Q

Peripheral arterial disease gold standard investigations

A

Doppler ultrasound

115
Q

Peripheral arterial disease management

A

Acute limb ischaemia is a medical emergency. Will need revascularization or amputation if severe.
Anti-platelet therapy (all levels of severity) and anticoagulation (if severe)

116
Q

Peripheral arterial disease complications

A

Critical limb ischaemia

117
Q

Pericarditis definition

A

Inflammation of the pericardium. Can either be ‘dry’ (fibrinous) or effusive (liquid).
The pericardial sac has a small reserve volume and if exceeded this pressure is transferred onto the cardiac chambers causing cardiac tamponade.

118
Q

Pericarditis epidemiology

A

It fluctuates with seasonal viral trends and is higher in young, previously healthy patients
Autoimmune (Sjorens, rhematoid arthritis)
Uraemic (irritation of pericardium due to toxins)
Malignant (commonly carcinoma of the bronchus, breast or Hodgkin’s lymphoma)

119
Q

Pericarditis risk factors

A

men

120
Q

Pericarditis key presentations

A

Classical sign is pericardial friction rub (sounds like crunching snow).

May be signs of effusion
- pulsus paradoxus, abnormal decrease in stroke volume, systolic bp and pulse wave amplitude during inspiration

Beck’s triad (clinical presentation of cardiac tamponade): hypotension, elevated JVP and quiet heart sounds

121
Q

Pericarditis signs and symptoms

A

Sharp central chest pain, pleuritic-exacerbated by movement, deep respiration or lying down.

Often relieved by sitting forwards
May be referred to neck and shoulders

Other: dyspnoea, cough, hiccups, fever

122
Q

Pericarditis 1st line investiations

A

ECG

  • relatively subtle difference to a STEMI
  • diffuse ST segment elevation, concave ST segment
  • no reciprocal ST depression (except in AVR and V1)
  • saddle shaped
  • PR depression
  • mechanism is due to epicardial inflammation

Troponin

  • not particularly specific or sensitive
  • mildly elevated
  • elevation may suggest myopericarditis

Bloods

  • ESR and CRP may be elevated
  • white count may be high

CXR
- normally normal unless pericardial effusion is very large, may help is lung problem thought to be related

Echocardiogram
- useful in pericardial effusion

123
Q

Pericarditis differential diagnosis

A

Main are angina and pleurisy

124
Q

Pericarditis monitoring

A

Non-purulent (non-pus related)

  • NSAIDS
  • colchicine
125
Q

Pericarditis complications

A

Pericardial effusion and cardiac tamponade

126
Q

Valve disease - aortic stenosis, mitral regurgitation, other valves stenosis/regurgitation definition

A

Four main diseases:

  • aortic stenosis - narrowing of the root of aorta
  • mitral regurgitation - backflow of blood from LV to LA during systole
  • aortic regurgitation - leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps
  • mitral stenosis - obstruction of LV inflow that prevents proper filling during diastole. Very uncommon in the western world
127
Q

Valve disease aetiology

A

Aortic stenosis: three types: supravalvular, subvalvular and valvular. Most are valvular

Mitral valve regurgitation: myxomatous degeneration, IHD, rheumatic heart disease, infective endocarditis, chorade tendinae rupture

Aortic regurgitation: bicuspid valves (most common - less effective than tiscuspid), rheumatic heart disease and infective endocarditis

Mitral valve stenosis: almost always rheumatic heart disease, infective endocarditis, mitral annular calcification

128
Q

Valve disease pathophysiology

A

Aortic stenosis: pressure gradient between LV and aorta increasing the after load. LV function initially maintained compensatory pressure hypertrophy. When compensatory mechanisms exhausted, LV function declines.

Mitral regurgitation: pure volume overload. Compensatory mechanism: LA enlargement, LVH and increased contractility. Progressive LA dilatation and RV dysfunction due to pulmonary hypertension. Progressive LV volume overload leads to dilation and progressive heart failure.

Aortic regurgitation: combined pressure AND volume overload. Compensatory mechanisms: LV dilation. Progressive dilation leads to heart failure.

129
Q

Valve disease key presentations

A

AS:

  • syncope: (exertional) 15%
  • angina: (increased myocardial oxygen demand) 35%
  • dyspnoea: on exertion due to heart failure (systolic and diastolic) 50%
  • sudden death: 2%

MR:

  • auscultation: pansystolic mumur at the apex radiating tp axilla. S3 (CHF/LA overload). Displaced hyperdynamic apex beat (hypertrophy)
  • exertion dyspnea
  • heart failure

AR:

  • wide pulse pressure
  • hyperdynamic and displaced apical impulse
  • ascultation: diastolic blowing murmur (increased flow across the aortic valve)
  • progressive symptoms: orthopnea, paroxysmal nocturnal dyspnea, palpitations

MS:

  • ‘A’ wave in JVP
  • signs of right-sided HF
  • lous opening S1 snap
130
Q

Valve disease signs and symptoms

A

AS: slow rising carotid pulse (pulsus tardus) and decrease pulse amplitude (pulsus parvus). Heart sounds - soft or absent, S4 gallop due to LVH, ejection systolic murmur - crescendo-decrescendo character

131
Q

Valve disease 1st line investigations

A

AS: echocardiography: look for LVH, dilatation and ejection fraction

MR: ECG (LA enlargement, AF, LV hypertrophy), CXR (LA enlargement, central pulmonary enlargement), ECHO (LA and LV size and valve structure assessment)

AR: CXR (enlarged cardiac silhouette and aortic root enlargement), ECHO (evaluation of AV and aortic root, LV size and function)

MS: ECG, CXR, ECHO is gold standard

132
Q

Valve disease management

A

AS: dental hygiene (avoiding infective endocarditis), medical role limited, vasodilators contraindicated, surgical replacement is definitive treatment

MR: IE prophylaxis, vasodilator (ACEi), rate control for AF (B-blockers, CCD, digoxin), anticoagulation in AF and flutter, diuretics for fluid overload, serial ECHOs, surgery

AR: IE prophylaxis, vasodilators (ACEi if symptomatic or HTN), serial ECHOs, surgery

MS: mechanical problem like AS so medical therapy does not prevent progression. B blockers, CCBs, digoxin, diuretics, surgery

133
Q

Shock (haemorrhagic, anaphylactic, septic, cardiogenic, neurogenic) definition

A

Shock: a state of reduced end-organ oxygenation caused by an imbalance between tissue oxygen delivery and demand resulting in an oxygen debt.

134
Q

Shock aetiology

A

Hypovolaemic:

  • haemorrhagic: due to blood loss
  • fluid depletion: diarrhoea, vomiting, burns

Cardiogenic: results from heart pump dysfunction causing a decrease in cardiac output in the setting of increase preload

Septic: infection with any organism - acute vasodilation from inflammatory cytokines

Anaphylactic: type-I IgE mediated hypersensitivity, release of histamine

Neurogenic: spinal cord injury, epidural or spinal anaesthesia

135
Q

Shock pathophysiology

A

Whatever the aetiology, shock is characterised by release of cytokines and other inflammatory mediators that cause a systemic inflammatory response syndrome mediated by tissue hypoxia. This causes alterations in flow at the level of the microcirculation that casually be reversed by intravascular volume resuscitation and as appropriate vasopressor and inotropic support.

136
Q

Shock key presentation

A

Systemic inflammatory response syndrome (SIRS):
- temp > 38C or <36C
- tachycardia > 90bpm
- RR >/= 20 breaths per min or PaCO2 < 4.3kPa
WBC > 12x10^9/L or 4x10^9/L

137
Q

Shock management

A

ABC - Airways, Breathing, Circulation
Investigation and treatment - depend on the cause
IN septic chock, take blood cultures before antibiotics

138
Q

Structural heart defects definition

A

Can be thought of as acyanotic or acyanotic

Cyanotic: shunt blood from right to left (deoxygenated blood gets into the oxygenated circulation). Main ones begin with T, generally more worrying:

  • tetralogy of fallot
  • truncus arteriosus
  • TGA

Acyanotic: shunt firm left to right. If the condition is severe such as a big VSD the shunt can reverse and become cyanotic. This is Eisenmenger’s syndrome.

  • VSD - Ventricular Septal Defect: hole in the septum between the ventricles. Usually close by themselves in early childhood
  • AVSD - Atrioventricular septal defect: usually close by themselves in early childhood, start to cause a problem if they cause a left to right shunt.
  • ASD - atrial septal defect: a hole in the septum between the atria. Less common, usually close by themselves
  • patent ductus arteriosus
  • valve disorders - eg aortic stenosis
139
Q

Structural heart defects aetiology

A 
Male dominance 
Genetics
Maternal drinking 
- drinking 
- rubella 
- lithium or thalidomide use
140
Q

Structural heart defects signs and symptoms

A 
Stunted growth in childhood 
Failure to thirve 
Finger clubbing 
Syncope 
Central cyanosis 
Pulmonary hypertensive (due to Eisenmenger's)
141
Q

Structural heart defects gold standard investigations

A

Diagnosis is ECHO for all

142
Q

Structural heart defects management

A

Treatment for all is surgical, may not require treatment

143
Q

Cardiomyopathy definition

A

A group of diseases affecting the heart muscle without coronary artery disease, hypertension, valvular or congenital heart disease

  • dilated cardiomyopathy: most common form. Left or both ventricles are dilated with impaired contraction
  • hypertrophic cardiomyopathy: second most common
  • restrictive cardiomyopathy: rare
144
Q

Cardiomyopathy epidemiology

A

Can occur at younger ages

145
Q

Cardiomyopathy aetiology

A

Dilated: ischaemia, alcohol, thyroid disorders, genetic
Hypertrophic: genetic - autosomal dominant, 50% sporadic
Restirctive: amyloidosis, idiopathic, sarcoidosis, end-myocardial fibrosis

146
Q

Cardiomyopathy signs and symptoms

A

Dilated: SOB. fatigue, dyspnea, heart failure, arrhythmia, thromboembolism, increase JVP, sudden death
Hypertrophic: sudden death may be first symptom, chest pain/angina, dyspnoea, dizziness, palpitations syncope, ejection-systolic murmur, jerky carotid pulse
Restrictive: dyspnoea, fatigue, embolic symptoms, increased JVP, diastolic collapse, hepatic enlargement, ascites, oedema, 3rd and 4th heart sounds

147
Q

Cardiomyopathy investigations

A

Dilated:

  • CXR: cardiac enlargement
  • ECG: tachycardia, arrhythmia, T-wave changes
  • ECHO: dilated ventricles

Hypertrophic:

  • ECG: T wave inversion, deep Q waves
  • genetic analysis

Restrictive:
- cardiac catheterisation diagnostic

Phase 2 Med (9 decks)

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