Block 2: AAA, aortic dissection, heart failure Flashcards
GRACE score
- Predicts 6 month mortality and risk of future adverse cardiovascular event
- Considers age, heart rate, blood pressure, Cardiac (Killip class), renal function (serum creatinine), cardiac arrest on presentation, ECG findings, troponin levels
- Determines whether patients has coronary angiography or conservative management
When should patients with NSTEMI/unstable angina have coronary angiography
- Immediate <2 hours: patient who are clinically unstable (e.g. hypotensive), acute heart failure, refractory chest pain, mechanical complications
- Early invasive <24 hours: established NSTEMI diagnosis with elevated troponin. Dynamic ST-T wave change. GRACE score >140
- Within 72 hours: patients with a GRACE score > 3% i.e. those at immediate, high or highest risk. GRACE score >109 and <150, T2DM, CKD, LVEF <40%, early post infarct angina
- Coronary angiography should also be considered for patients is ischaemia is subsequently experienced after admission
PCI for NSTEMI/unstable angina
- Unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not
- Further antiplatelet (‘dual antiplatelet therapy’, i.e. aspirin + another drug) prior to PCI
- if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor
- if taking an oral anticoagulant: clopidogrel
Medical management for NSTEMI/unstable angina
- further antiplatelet (‘dual antiplatelet therapy’, i.e. aspirin + another drug)
- if the patient is not at a high-risk of bleeding: ticagrelor
- if the patient is at a high-risk of bleeding: clopidogrel
Complications for ACS 1
- Cardiac arrest: due to patients developing ventricular fibrillation, most common cause of death after MI
- Cardiogenic shock: id myocardium is damaged and the ejection fraction decreases. May require ionotropic support and/or an intra-aortic balloon pump
- Chronic heart failure: ventricular myocardium may become dysfunctional leading to heart failure. Treatment is Furosemide, ace inhibitors and beta blockers
- Tachyarrhythmias: ventricular fibrillation or ventricular tachycardia
- Bradyarrhythmia’s: atrioventricular block is more common after inferior myocardial infarctions
Complications of ACS 2
- Pericarditis: tends to occur 48 hours after a transmural MI. Dresslers syndrome occurs 2-6 weeks post MI, symptoms of fever, pleuritic pain, pericardial effusion and a raised ESR. Treated with NSAID’s
- Left ventricular aneurysm: due to ischaemic changes weakening the myocardium, associated with persistent ST elevation and left ventricular failure
- Left ventricular free wall rupture: occurs 1-2 weeks after. Present withacute heart failuresecondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.
- Ventricular septal defect: occurs in the first week with acute heart failure with a pan-systolic murmur
- Acute mitral regurgitation: more common in an infero-posterior infarction, may be due to ischaemia or rupture of the papillary muscle. Early to mid systolic murmur heard, treated with vasodilator therapy
ACS: poor prognostic factors
- age
- development (or history) of heart failure
- peripheral vascular disease
- reduced systolic blood pressure
- Killip class= stratifies risk post myocardial infarction
- initial serum creatinine concentration
- elevated initial cardiac markers
- cardiac arrest on admission
- ST segment deviation
Abdominal aortic aneurysm: overview
- Failure of elastic proteins in the extracellular matrix
- Dilation of all layers of the arterial wall
- Diameter of the abdominal aorta >3cm is an AAA, greater than 5cm there’s significant risk of rupture and its life threatening
- Process: loss of intima and elastic fibres from media. Associated with proteolytic activity and lymphocytic infiltration
- Risk factors: smoking, hypertension, syphilis, connective tissue disorders like Ehlers Danlos type 1 and Marfans syndrome.
AAA: risk factors
- Male: 75% are male, risk of rupture is higher in woman with AAA and occur at smaller diameter
- Age: men >50 and women >70with risk factors are offered screening
- Smoking
- COPD: especially in older woman
- Hypertension
- Existing vascular disease: peripheral vascular disease, coronary heart disease or cerebrovascular disease
- Family history
- note: diabetes offers no further risk
AAA: pathophysiology
Lipid accumulation in the wall of the abdominal aorta causes inflammation and activation of matrix metalloprotease enzymes from inflammatory cells which damage the aortic wall.
AAA: clinical features of rupture
- Pain: back or loin, some describe as abdominal pain which radiates to the back
- May have notice pulsatile mass in abdomen before rupture (palpable, tender, pulsatile and expansile)
- Cardiovascular failure: haemorrhage can cause tachycardia and hypotension (shock) resistant to volume rescusitation
- Distal ischaemia: if there is a haematoma within the aneurysm it can embolise after rupture and cause distal arterial occlusion leading to lower limb ischaemia, rarely presenting complaint
- Death: 1/3 of patients die at rupture
AAA: investigations
- Abdominal ultrasound to assess aortic diameter- first line
- CT angiogram- gold standard
- Bloods: FBC, U&E, Coagulation screen, Cross match (for surgery)
AAA: open surgical repair
- Must have good baseline health, also dangerous for patients with significant cardiac disease
- Cross clamp the aorta and place a sutured synthetic graft to bridge the diseased area of the aorta
- Suitable for any aneurysm
AAA: Endovascular aneurysm repair (EVAR)
- A wire is passed through the aneurysm sac and a stent graft is inserted to occlude the aneurysm
- Requires only small incisions to access the femoral arteries so can be done if frail, more suitable for cardiac disease
- Cant be done for AAA’s involving the renal artery
- Not suitable in renal impairment due to contrast
AAA: palliative care
- A ruptured AAA without treatment is terminal. Done if too frail for any procedure
- Sometimes subsequent shock means interventions arent an option
- Midazolam for agitation, haloperidol for nausea and morphine for pain. Can use a syringe driver
AAA: complications
- Acute limb ischaemia: either by embolus of clot or injury to vessels in surgery
- Lower bowel ischaemia: if the marginal artery supply to the left colon is inadequate after damage to the inferior mesenteric
- Abdominal compartment syndrome: more common in open surgery
- Graft infection: in either surgery can cause catastrophic bleeding
- From transfusion: coagulopathy, electrolyte disturbance and lung injury
Complications of surgery AAA
Complications from open surgery: abdominal wound dehiscence, a large laparotomy wound can cause incisional hernias later on in life
Complications from endovascular repair: Haematomas or pseudo-aneurysm can occur in the site of access to the femoral arteries. Can have leakage of blood around the stent graft into the aneurysm sac, increasing the aneurysm around the graft. Surveillance for it means CT angiograms for the rest of your life after endovascular treatment for an AAA.
Screening for AAA
- A single abdominal ultrasound for males aged 65
- Aorta width 3-4.4cm= small aneurysm= Rescan every 12 months
- Aorta width 4.5-5.4 = Medium aneurysm = Rescan every 3 months
- ≥5.5cm = Large aneurysm = refer to vascular surgery for probable intervention
AAA: further management
- Low rupture risk: asymptomatic, aortic diameter <5.5cm: have ongoing US surveilance and optimise cardiovascular risk factors i.e. stop smoking
- High rupture risk: Symptomatic, aortic diameter ≥5.5cm or rapidly enlarging (>1cm/year): Treat with elective (EVAR) or open repair. In EVAR a stent is inserted via the femoral artery to prevent blood collecting in the aneurysm
Repair of AAA is indicated
- Aneurysm > 5.5 cm
- Rapid expansion > 0.5 cm/ 6 months
- Evidence of AAA tenderness
- Rupture
Acute aortic syndrome
- Acute dissection (90%)
- Intra-mural haematoma
- Penetrating atherosclerotic ulcer