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
Aortic dissection: definition
The separation of the aortic wall layers resulting in a fake lumen. Occurs due to an intimal tear allowing blood to enter and dissect through the media layer. Can cause rupture of the outer layer of the aortic wall which is life threatening due to blood loss
Risk factors for aortic dissection
Hypertension, connective tissue disorders i.e. Marfan syndrome, catheterisation or cardiac surgery, male
Presentation of aortic dissection
- sudden onset severe chest pain radiating to the back, syncope or neurological deficits
- Can cause Myocardial infarction, bowel ischaemia
- Most dont have features of haemodynamic compromise
Aortic dissection: imaging and overview of the two types
Imaging: CT angiography, MRI and Transesophageal echocardiography (TEE)
Overview of two types: Type A requires emergent surgical intervention due to increased risk of complications like pericardial tamponade, myocardial ischemia, and aortic regurgitation. Type B dissections are primarily managed medically with strict blood pressure control unless exhibiting signs of malperfusion syndromes or impending rupture.
Aortic dissection: risk factors
- Hypertension, atherosclerosis
- Connective tissue disorders: Marfan syndrome, Ehlers-Danlos,Loey-Dietz and Turner
- Inflammatory conditions: Takayasu arteritis and GCA
- Iatrogenic: cardiac surgery or catheterisation
- Blunt chest trauma
- Pregnancy
- Bicuspid aortic valve
Aortic dissection: Stanford classification
- type A - ascending aorta, 2/3 of cases
- type B - descending aorta, distal to left subclavian origin, 1/3 of cases (back pain)
Aortic dissection: DeBakey classification
- type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
- type II - originates in and is confined to the ascending aorta
- type III - originates in descending aorta, rarely extends proximally but will extend distally
Aortic dissection: investigations
- Chest x-ray: widened mediastinum
- Gold standard: CT angiography of the chest, abdomen and pelvis= suitable for stable patients and planning surgery, see a false lumen
- Transoesophageal echocardiography: more suitable for unstable patients
Aortic dissection: treatment
- Type A: immediate surgical management but blood pressure should be controlled to a systolic of 100-120 whilst awaiting intervention
- Type B: conservative management, bed rest, reduce blood pressure IV labetelol to prevent progression. Thoracic Endovascular Aortic Aneurysm Repair (TEVAR) may be considered for complicated cases.
- Opiate analgesia, beta blockers are commonly given
Aortic dissection: complications
- Backward tear: aortic incompetence/regurgitation. MI- inferior pattern often seen due to right coronary involvement
- Complications of forward tear: unequal arm pulses and BP, stroke, renal failure
Heart failure: definition and ejection fraction
Definition
- The cause of the heart to fail to pump effectively
- Reduced or preserved ejection fractions
- Left or right sided heart failure
Ejection fraction: the ability of the left ventricle to pump blood out of the body during systole
Heart failure with reduced ejection fraction
- Left ventricular systolic dysfunction (LVSD) describes poor systolic function and can lead to the clinical syndrome of heart failure., systolic heart failure
- Ejection fraction is <40%
- Causes: Ischaemic heart disease, muscle damage after an MI, dilated cardiomyopathy and hypertension
- Causes cardiomegaly but weaker muscles
- Orthopnoea is a specific symptom
Heart failure with preserved ejection fraction
- Failure of ventricles to fill properly, diastolic heart failure
- Causes: hypertension, ischaemic heart disease and diabetes, hypertrophic cardiomyopathy, amylosis and sarcoidosis
- Inward growth of ventricle wall reducing volume of ventricles- heart looks the same
- Ankle oedema and raised JVP are specific symptoms
Left and right sided heart failure
- Left sides: Congestion in the lungs, causing pulmonary oedema. The patient may experience dyspnoea, orthopnoea, paroxysmal noctural dyspnoea, cough or cardiac wheeze.
- Right sided: Congestion in the body, causing oedema and raised venous pressure. The fluid is affected by gravity, so will collect in the ankles for a mobile patient, or the sacrum in someone lying flat. Right sided failure can be due to increased resistence in the left ventricle (i.e. left-sided heart failure) or in the lungs (i.e. pulmonary hypertension, causing cor pulmonale)
- Heart failure activates the RAAS system increasing preload and afterload, worsening heart failure
Blood tests: Heart failure
Bloods for heart failure: FBC, U/E, LFT, Gamma GT, Thyroid function, Pro-BNP.
A Pro-BNP >400 is suggestive of heart failure
Heart failure classification: New York Heart Association (NYHA)
- Class I: no symptoms, no limitations
- Class II: mild symptoms, slight limitations of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
- Class III: moderate symptoms. Marked limitations of physical activity, comfortable at rest but less than ordinary activity results in symptoms
- Class IV: severe symptoms. unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
Heart failure: features
- dyspnoea
- cough: may be worse at night and associated with pink/frothy sputum
- orthopnoea, paroxysmal nocturnal dyspnoea
- wheeze (‘cardiac wheeze’)
- weight loss (‘cardiac cachexia’): occurs in up to 15% of patients. Remember this may be hidden by weight gained secondary to oedema
- bibasal crackles on examination
- ankle oedema
Heart failure: interpreting pro-BNP
- if levels are ‘high’ (>2000) arrange specialist assessment (including transthoracic echocardiography) within 2 weeks
- if levels are ‘raised’ (>400) arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks
Management of heart failure
- first-line= ACE-inhibitor and a beta-blocker (ARB if ACEi not tolerated). Generally, one drug should be started at a time. If symptoms persist offen an MRA (Mineralocorticoid receptor antagonist) i.e. Spironolactone
- second-line treatment is either an aldosterone antagonist, angiotensin II receptor blocker or a hydralazine in combination with a nitrate
- if symptoms persist cardiac resynchronisation therapy or digoxin should be considered. An alternative is ivabradine. The criteria for ivabradine include that the patient is already on suitable therapy (ACE-inhibitor, beta-blocker + aldosterone antagonist), has a heart rate > 75/min and a left ventricular fraction < 35%
- diuretics (Furosemide) should be given for fluid overload- symptoms
- sacubitril-valsartan is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs. Initiate after ACEi or ARB wash out period
ACEi + BB + MRA + SGLT2
Heart failure investigations and CXR
Chest x-ray, ecg (no one finding but is often abnormal)
Chest x-ray: heart failure:
- A - alveolar edema (bat wing opacities)
- B - Kerley B lines
- C - cardiomegaly
- D - dilated upper lobe vessels
- E - pleural effusion
Heart failure: lifestyle management
- Salt reduction, exercise
- Stop smoking, reduce alcohol
- Annual flu and pneumococcal vaccine
- Tracking weight: sudden weight gain can be oedema
- NHS website for patient education
Heart failure: Progression
Periods of relative stability and progressive decline where they may not achieve previous levels of functioning. Sudden cardiac death, can be an arrhythmia or MI. An implantable cardioverter defibrilator (ICD) can reduce this risk. Recognising end stage helps support palliation.
Medication for heart failure: MLE
- First line: ACE inhibitor e.g. lisinopril and a beta blocker e.g. bisoprolol
- If ACE inhibitor is not tolerated (often due to a cough) then an angiotensin II receptor blocker (ARB) e.g. candesartan is used instead
- A mineralocorticoid receptor antagonist (MRA or aldosterone receptor antagonist) e.g. spironolactone or eplerenone is added if symptoms are not fully controlled.
- Sacubitril/valsartan e.g. entresto is an angiotensin receptor-neprilysin inhibitor (ARNI). It is used to replace the ACE inhibitor if the patient still has symptoms and a reduced ejection fraction.
- Furosemide is used for symptom control but doesn’t impact mortality
Treatment for heart failure with preserved ejection fraction
- No evidence that heart failure treatment is effective in preserved ejection fraction.
- Focus on symptomatic relief and treating comorbidities
- Furosemide for oedema
Heart failure: implantable cardiac defibrilator
- Implanted under the skin with leads going to the heart
- Can detect potentially fatal rhythms and deliver electric pacing or shock defibrillation
- Will treat shockable cardiac arrhythmias
- Recommended for people who have an LVSD with an ejection fraction for <35%
- Not appropriate for severe disease or co-morbidities
- ICD can be deactivated if deemed inappropriate
Heart failure: Cardiac Resynchronisation therapy (CRT)
- When there is poor ventricle co-ordination: QRS of >150ms and a LBBB
- Delivers electrical impulses to co-ordinate the ventricles and improve heart output
- Can be implanted with defibrilator
- CRT-D: CRT with a defibrillator
- CRT-P: CRT with pacing only (no defibrillator function)
Heart failure: Heart transplantation
In end stage heart failure, rarely available/appropriate. Often done in cardiomyopathy. Must be able to undergo invasive cardiac surgery and strong immunosuppression. Contraindications: cancer, CKD, pulmonary hypertension. A left ventricle assist device (LVAD) is used to keep a patient alive prior to transplant, this physically pumps the blood from the heart.
Signs of decompensated heart failure
- Bi-basal coarse crackles
- Raised JVP
- Peripheral oedema
- Wheeze, S3 heart sound and ascites
- Poor perfusion: cool peripheries, prolonged CRT, low urine output
Triggers for acute heart failure
- Acute coronary syndrome (e.g. myocardial infarction)
- Tachyarrhythmia (e.g. atrial fibrillation)
Pulmonary embolism - Severe hypertension
- Infection
- Drugs e.g. NSAIDs, steroids
- Renal insufficiency
- Not taking usual medication or following
Stable angina: definition and examinations
Definition: insufficient blood flow to the heart muscles from narrowing of a coronary artery
Examinations:
- clinical examination: anaemia, valve disease
- Baseline investigation: ECG
- Anatomical test: CT coronary angiogram, Invasive angiogram
-Functional test: stress echo, Perfusion scan, Stress cardiac MRI
Stable angina treatment
-GTN spray
- Statin according to QRISK 3 score
- An antianginal agent
- Asprin
Indications for PCI in NSTEMI/unstable angina
Consider coronary angiography (with follow‑on PCI if indicated) within 72 hours of first admission for people with unstable angina or NSTEMI who have an intermediate or higher risk of adverse cardiovascular events (predicted 6‑month mortality above 3.0%) and no contraindications to angiography
-if ischaemia is subsequently experienced
