Cardiovascular Flashcards

Acute Coronary Syndrome

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1
Q

ACS: Included conditions & Definitions

A

Acutely compromised myocardial perfusion

1: Unstable angina: ACS without cell death. Big sclerotic plaque but not yet dislodged
2. NSTEMI: Subendocardial cell death
3. STEMI: Transmural cell death

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2
Q

ACS: Risk factors

A

Non-modifiable:

  • sex: male
  • age: old
  • Hx: FMHx of ACS and other CVS. Hx of DM and previous ACS

Modifiable

  • Smoking
  • Central obesity
  • High LDL and low HDL
  • HTN
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3
Q

ACS: Investigations

A

Blood: Troponin (STEMI & NSTEMI)

ECG: NSTEMI (normal or abnormal), Angina (ST depression/ T wave inversion wtihtou

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4
Q

Coronary arteries: Route and areas of supply

A

LAD: follows Interventricular groove

  • Diagonal branch: lateral wall of LV
  • Septal branch: Anterior 2/3 of interventricular septum,
  • Terminal bifurcation: Inferior LV, apex of LV

LCx: follows Left AV groove
- Lateral & Posterior wall of LV

RCA: follows right AV groove

  • SAN, AVN & Right atrium
  • Posterior descending artery: inferior wall of LV, inferior 1/3 of interventricular septum (most common - otherwise ‘dominated’ by LCx)
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5
Q

Posterior MI: ECG interpretation

A

Changes seen in V1-V3

  • horizontal ST depression
  • Tall R waves
  • Dominant R wave (R/S > 1)
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6
Q

ACS: other causes of troponin rise

A

Troponin rises within 12hrs of myocardial injury, peaks at 24 hrs and remains elevated for 14 days

Cardiac causes

  • Myocarditis
  • Pericarditis

Other causes:

  • Pulmonary embolism
  • Sepsis
  • Renal failure
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7
Q

ACS: Other differentials

A

Aortic dissection: presents with chest pain and ST elevation

  • distinguished by abrupt onset, migration to back and tearing sensation
  • when ST elevation recorded, usually in inferior region (RCA) as dissection in left main stem is fatal

Acute pericarditis: Chest pain and ST elevation

  • Presentation: pain worsens on inspiration and relieves by sitting upright
  • ECG changes: Widespread ST elevation and saddle shaped
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8
Q

ACS: Causes

A

Atherosclerotic plaque

Non-athreroscleotic causes:

  • Embolus
  • Concentric ventricular hypertrophy: hypertropic cardiomyopathy, HTN, aortic stenosis
  • Aortic valve stenosis (decreased blood flow -> Coronary from aorta)
  • Vasculitis (eg. Kawasaki syndrome (high suspicious if paeds. ACS)
  • Vasospasm (cocaine abuse)
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9
Q

ACS - Immediate management

A

MONAC

Morphine (IV) - 10mg + Metoclopramide IV

Oxygen: if SpO2 outside 94-98%

Nitrates: Sublingual GTN 92 sprays), if not hypotensive (the PRN)

Aspirin: 300mg PO loading dose then 75mg OD

Clopidpgrel: 300-600mg loading dose then 75mg OD

Plus start: atorvastatin 80mg ON, beta-blocker (eg. bisoprolol 2.5mg OD), ACS-specific LMWH below.

Reperfusion therapy (/ Thrombolysis)

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10
Q

ACS additional management (after MONAC)

A

Atorvastatin 80mg ON
beta-blocker (eg. atenolol 50mg PO TDS) in absence of HF or BP < 80
ACS-specific LMWH

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11
Q

ACS: Repurfusion therapy (+ indications)

A

PCI (gold-standard): Any ACS - STEMI, NSTEMI, Unstable angina

indications:

  • Evidence of myocardial ischaemia
  • Onset within 12 hrs or symptoms persist for up to 24hrs
  • ST elevation of > 0.1 mV (1mm) on at least 2 limb leads or > 0.2mV (2mm) on 2 contiguous leads
  • New LBBB
  • True posterior MI

Thrombolysis: STEMI with ST-elevation in 2 contiguous leads
- >1mm in limb leads or >2mm in chest leads or new LBBB

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12
Q

ACS - Contraindications to reperfusion therapy

A

PCI: significant co-morbidities (relative contraindication)

Thrombolysis: active internal bleeding, bleeding. disorder, aortic dissection, stoke or surgery/trauma <2 weeks

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13
Q

ACS - Investigations

A

Bloods - FBC, U&E LFTs, CRP & glucose Troponin, BNP, Magnesium, phosphate and lipids

Imaging: Chest X-ray & ECG

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14
Q

NSTEMI - high risk patients and management

A

High risk: Raised troponin/ persistent pain/ ST depression/ diabetic

Management for high risk: PCI on semi-elective basis (depends on TIMI/GRACE score)

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15
Q

Aneurysm: Pathology

A

Abnormal dilation in blood vessels: 1.5x larger than normal vessel dieter ( >3.0cm in aortic & thoracic)

Occurs in areas of high blood pressure: aorta, femoral, iliac, popliteal and cerebral arteries.
Uncommon: veins - pressure on blood vessel walls increase with diameter of vessel lumen (LaPlace’s law)

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16
Q

Aneurysm: Life threatening locations

A

Abdominal Aortic Aneurysm (AAA): diameter > 3cm or >50% larger than normal

Thoracic AA: less common AAA

Cerebral aneurysm: particularly threatening in Circle of Willis

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17
Q

AAA: Main causes

A
Atherosclerosis
Infection
Trauma
Arteritis
Cystic medial necrosis
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18
Q

Aneurysm: True vs Pseudoaneurysm

A

True Aneurysm: all layers of vessel wall dilate

  • Fusiform: symmetrical wall dilation
  • Saccular (berry): asymmetrical ballooning of vessel due to increased BP on one side of vessel wall

Pseudo-aneurysms: small hole in blood vessel wall -> blood leaks out, pools; resembles true aneurysm.

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19
Q

Aneurysm: Causes

A

Ischaemia:

  • Ischaemia of arteries with vasa vasorum: hyaline arterioscelersis leads to decreased smooth muscle in tunica media
  • Ischaemia of arteries without vasa vasorum: plaque form atherosclerosis blocks blood vessel walls from receiving O2

Infection:

  • Tertiary syphilis
  • Mycotic aneurysm

Genetic
- Connective tissue disorders: Marfan’s syndrome, EDS

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20
Q

Aneurysm: Risk factors

A

Non-modifiable:

  • Advancing age
  • Sex: male
  • Race: white, EU descent
  • PMHx: Connective tissue syndrome (Marfan’s & EDS), cystic medial degeneration, syphilis, bicuspid aortic valve

Modifiable:

  • Lifestyle: smoking
  • Diet: hyperlipidemia, HTN
21
Q

Aneurysm: Complications

A

High mortality rate,
Rupture: internal exsanguination; increased ICP (if cerebral aneurysm),
Compression to surrounding structure: SVC syndrome, aortic insufficiency,
Thrombosis/ emboli: stagnant blood in extra lumen space,

22
Q

Aneurysm: Signs & Symptoms

A

Asymptomatic until rupture: severe pain in specific location (abdomen, chest, lower back & groin), pulsating mass, hypotension, syncope

23
Q

AAA: Sign & symptoms

A

On rupture: pain in abdomen/back, pulsating sensation in abdomen (expansile mass), low BP, syncope
Intermittent/ continuous radiating pain (groin, iliac fossa.& back)

Large aneurysm felt by pushing on abdomen

24
Q

Aneurysm: Diagnosis

A

Gold-standard (if patient stable): Abdomen CT before surgery

US: confirms presence, location, size, monitors growth

CTA scan: CT + injecting contrast dye shows blood flow; used for surgery

Other diagnostics: ECG (rules out MI)

25
Q

Aneurysm: Treatment

A

Medication: BP control

Conservative: Screening & Surveillance

Surgery:
- Indications: Diameter >5cm, 0.5cm growth in 6 mths, individual symptomatic

Repair methods: Surgical clipping, Endovascular coiling, Endovascular stenting (can be used to avoid major surgery)

26
Q

Aortic Dissection: Pathology

A

Tearing/ widening of artery’s internal layer, followed by blood entering vessel wall, causing pain -> typically affects aorta

tear forms in tunica intima of aorta -> high BP flows between tunica intima/ media -> layer separation -> false lumen -> dilate aorta

Most aneurysm develop in first 10 cm of aorta

Can present acutely/ chronically

27
Q

Aortic Dissection: Stanford classification

A
Stanford A (70%) : Involves ascending aorta (+/- aortic arch +/- descending)
-> consider urgent cardiothoracic advice and consider surgery

Stanford B (30%): No ascending aorta involvement

28
Q

Aortic Dissection: Causes

A

Weakness of aortic wall

  • Chronic HTN
  • blood vessel co-arctation
  • Aneurysm
  • Connective tissue disorder
29
Q

Aortic Dissection: Risk Factors

A

Non-modifiable

  • PMHx: Cystic medial necrosis (congenital condition leading to weakened walls), vasculitis, trauma, Turner’s syndrome
  • Previous open heart surgery
  • FMHx - aortic dissection

Modifiable:

  • Pregnancy
  • Cocaine use
30
Q

Aortic Dissection: Sign & Symptoms

A

Chest pain: Sudden (+/- radiating to the back)
Associated symptoms: N&V, diaphoresis

Signs: Unequal arm pulses and BP, or acute limb ischaemia
Diastolic decrescendo murmur: Type A dissection leading to aortic regurgitation
Neurological deficits

31
Q

Aortic Dissection: Complications

A

Moves proximally:
Aortic valve incontinence
Inferior MI
Cardiac Arrest

Carotid artery: hemiplegia
Anterior spinal artery: paraplegia
renal arteries: anuria

32
Q

Aortic Dissection: Associated Heart Murmur and why?

A

Diastolic decrescendo murmur: Type A dissection leading to aortic regurgitation

33
Q

Aortic Dissection: Diagnosis

A

Chest X-ray: widening of mediastinum (inadequate for diagnosis)

Transoesophageal Echocardiogram (TOE): Best for unstable patient. High sensitivity for identifying dissection, complications like AR, cardiac tamponade, involvement of coronary arteries

CT-Angio: For stable patients. High sensitivity for identifying dissection, can provide anatomic information useful in planning surgical repair; visualise/ locate dissection

ECG: rule out alternative diagnostic possibilities eg. MI

34
Q

Aortic Dissection: Management (Type A & Type B)

A

Type A:
Consider surgery: medical emergency, surgical repair indicated

Type B: 
Medication: lower BP & HR
  first line: beta-blockers
  second: CCB 
  Pain rangement for acute     dissection

Surgical repair indicated when acute, complications arise, medication ineffective

35
Q

PAD: Definition

A

Narrowing/ occlusion of peripheral arteries, affecting blood supple to lower limbs

36
Q

PAD: Conditions included

A

Chronic Limb Ischaemia:

  1. Intermittent claudication: when diminished circulation leads to pain in the lower limb on walking or exercise that is relieved by rest
  2. Critical Limb ischaemia:when circulation is so severely impaired that there is an imminent risk of limb loss
  3. Chronic Limb-threatening ischaemia: describes clinical patterns with threatened limb viability related to several factors.

Acute limb ischaemia: sudden decrease in limb perfusion that threatens limb viability. Symptoms develop <2 weeks

37
Q

Chronic. limb ischaemia: Causes

A

Most common cause: arteriosclerosis

Less common causes: Inflammatory disorders (vasculitis), non-inflammatory arteriopathies (eg. fibromuscular dysplasia).

Chromic limb-threatening ischaemia: thromboembolism, Buerger’s disease trauma, dissection, physiological entrapment syndromes

38
Q

Acute limb ischaemia: Causes

A

Ruptured artherosclerotic plaque
In-situ thrombus (60%), emboli (30%),
Other: graft, angioplasty occlusions or trauma.

39
Q

PAD: risk factors

A

Strongest risk factors: Smoking & DM

Non-modifiable

  • advancing age
  • PMHx: CKD, known atherosclerotic disease elsewhere (eg. coronary, carotid, abdominal aorta)
  • Hyperhomocysteinemia
40
Q

PAD: prognosis

A

Critical limb ischaemia at 1 year

  • Alive with 2 limbs - 50%
  • Amputation - 25%
  • All cause mortality - 30%

5yr all cause mortality - 30-40%

41
Q

PAD/Chronic limb ischaemia: Presentation

A

Chief feature: intermittent claudication (to limp)

Limb pain: cramping pain in calf (femoral disease), thigh or buttock (iliac disease). Worsen with exertion/ elevation and relieved by rest.

Sign: Absent LL pulses, cold, pallor, atrophic skin, arterial ulcers (often painful), postural dependent colour change (Buerger’s angle 15 and Cap. refill of >15s = severe ischaemia)

42
Q

Critical limb ischaemia: Cardinal feature

A

Ulceration/ gangrene and foot pain at rest (burning pain at night relieved by handing legs over side of bed)

43
Q

Acute Limb ischaemia: Presentation

A

Sign: 6 P’s

Onset of fixed mottling -> irreversibility of disease

44
Q

Acute limb ischaemia: Thrombus vs Embolus (causes)

A

Thrombus: PVD and gradual onset (hours)

Embolus: Risk factors, multiple sites and sudden onset (min/secs)

Causes of embolus: Arterial thrombus, infective (fungal, vegetation), metastatic, iatrogenic and other

45
Q

PAD: Investigations

A

Bedside: FBC (anaemia, polycythaemia), ESR & CRP (arteritis), U&Es (renal disease), lipids (hyperlipidaemia), ECG (cardiac ischaemia)

Imaging: Arterial USS duplex (1st line). MRI/CT angiography for extent and location of stenoses and quality of distal vessel.

Special tests: ABPI - normal = 1-1.2; PAD = 0.5-0.9; critical limb ischaemia <0.5 pr ankle systolic pressure <50mmHg.

46
Q

PAD: Management

A

Conservative: Exercise, Smoking cessation

Medical: risk factor modification (HTN & lipids, antiplatelet eg. clopidogrel), Vasodilation

Surgical: Endovascular & Open

47
Q

Acute Limb Ischaemia: Management

A

Embolic: Embolectomy (Fogarty catheter), surgical reconstruction

Thrombotic: Thrombolysis (eg. t-PA), Thrombectomy or surgical reconstruction

Post-operative: anti-coagulate with heparin after procedure and look for source of emboli. Be aware of post-op repercussion injury and subsequent compartment syndrome

48
Q

Acute Limb ischaemia: Potential surgical complications and considerations

A

Post-operative: anti-coagulate with heparin after procedure and look for source of emboli. Be aware of post-op repercussion injury and subsequent compartment syndrome

49
Q

Limb Claudication: Management

A

PAD Intervention indications:

  • Failure of conservative treatment
  • PAD is severely affecting patient’s life
  • becoming limb threatening

Percutaneous Transluminal Angioplasty (PTA): if disease limited to single arterial segment.

Surgical reconstruction (with bypass graft): If atheromatous disease is extensive but distal run-off is good.

Amputation <3% of patients with claudication