Cardiology Flashcards
Describe a bicuspid aortic value?
- Go undetected initally
- Lead to aortic stenosis/regurgitation
- Treatment = surgically with valve replacement
- Affects 1% of live births, usually associated with other developmental issues
Describe atrial septal defect?
2 types of hole
1. Primum: presentation is earlier, may involve AV valves and effects lower atrial septum
- secundum: may be asymptomatic until adulthood when heart compliance is reduced, higher atrial septum
LEFT TO RIGHT SHUNT
Describe ventricular septal defects?
Larger holes = more problems in infancy
Smaller = asymptomatic but increase IE risk
Large pan systolic murmur
Smaller hole = louder murmur
Medically treated as hole may close spontaneously then surgical repair before Eisenmengers
What is Eisenmengers Sydrome?
Shunt reversed due to development of pulmonary hypertension
Causes deoxygenated blood to go back around the body
Once PHTN is high enough for reversal only heart transplant is curative
Cyanosis, clubbing, HF, syncope ,high RBC
What is this a typical history of?
A 24-year-old gentleman comes to see you for a routine check-up. On auscultation of his back you notice a systolic murmur over his left shoulder blade. Further CV examination shows a radio-femoral delay with a weak femoral pulse bilaterally. The BP in his right arm is 130/85 but in the left arm is 100/67
Coarctation of the Aorta
Describe Coarctation of the aorta
Aorta is narrowed at the site of the ductus arteriosus
Associated with biscuspid aortic valve and turners syndrome
Severe - blocked aorta
Mild - Raised bp and systolic murmur
Radiofemoral delay BP in right arm>left arm
Both need repairing surgically or stent but risk of aortic aneurysm after repair
What is this a typical history of?
Mother comes to see you. Her two year old has been having episodes where he gets restless and cries for no reason, however as soon as he is allowed to squat down the crying stops. He is a bit underweight for his age and on examination you notice a bit of clubbing.
Tetralogy of Fallot
Describe tetralogy of fallot?
Most common cyanotic cardiac disorder (3-6 in 100,000) with the highest survival to adulthood
After closure of the ductus arteriosus infants will become progressively more cyanotic as there is less flow to the lungs,
RIGHT TO LEFT SHUNT
Chest xray may show boot shaped heart
Toddlers may squat and infants become cyanotic
What are the 4 features of a tetralogy of fallot?
- VSD
- Pulmonary stenosis
- RV hypertrophy
- Overriding aorta
Two main problems with IHD?
- Gradual narrowing of coronary arteries
2. Risk of plaque rupture within coronary arteries
What are the risk factors for IHD?
Modifiable: Smoking Obesity Exercise Diet Cocaine
Clinical:
HTN
Diabetes
Hyperlipidaemia
Non modifiable:
Age
Gender
Psychosocial:
High demand, low control jobs
What are the symptoms of IHD?
Typically central or left sided pain
May radiate to the jaw or left side of the arm
Often describe as heavy or constricting ‘elephant on my chest’
Investigation of ischaemic heart disease?
Cardiac enzymes
ECG
Treatment if IHD?
MONA Morphine Oxygen Nitrates Aspirin
Management of IHD?
Prevent worsening
Revascularise if there has been an MI
Treat pain
Anterior IHD:
Which leads?
Which coronary artery?
V1-V4
Left anterior descending
Inferior IHD:
Which leads?
Which coronary artery?
II, III, aVF
Right coronary
Lateral IHD:
Which leads?
Which coronary artery?
1, V5-V6
Left circumflex
What is this a typical history of?
A 68 year old gentleman presents with a 1 month history of tight-chestedness and dyspnoea when he walks his dog. This resolves itself once he sits down and has a break for 10 minutes. It sometimes radiates to his jaw, especially when he has been walking uphill.
Stable Angina
Risk factors for stable angina?
Age Smoking Family history Dibetes Meillitus Obesity Physical activity Stress
Symptoms of stable angina?
Chest pain brought on by exertion but rapidly resolves with rest and GTN
May radiate to arms, jaw, back and neck
May be exacerbated by emotion
May also get some dyspnoea, palpitations or syncope
Investigations for stable angina?
ECG - usually normal, may show ST depression and T wave inversion
Bloods - anaemia
CXR - check heart size
Angiogram - gold standard, shows luminal narrowing
Treatment for stable angina?
Lifestyle - eat less move more stop smoking
Medical - control hypertension and diabetes
Symptomatic relief - nitrates e.g. GTN spray
Drugs - B blockers, statin, aspirin, ACEi, ivabradine
PTCA - stenting or ballooning the narrowing, risk of restenosis or thrombosis, less invasive
CABG - good prognosis but longer recovery
What is unstable angina?
Acute coronary syndrome that is defined by the absence of biochemical evidence of myocardial damage
Aetiology of unstable angina?
- brought on by trivial provocation or for no apparent reason
- may have crescendo pattern
- 50% of patients with unstable angina will get an infarction within 30 days if it is left untreated
Symptoms of unstable angina?
Chest pain or pressure
Pain radiating anywhere in upper body
Sweating
Dyspnoea
Nausea
Vomiting
Dizziness or sudden weakness
Investigation of unstable angina?
FBC = anaemia aggravates it
Cardiac enzymes = excluded infarction as troponin normal
ECG = when in pain shows ST depression
Coronary anigography
Treatment of unstable angina
Similar to stable but more direct
Use antiplatelet agents and anticoagulants to break up clots and prevent new ones
Add in nitrates, BB and CCBs
CABG and PCTA are both viable options once the lesion has been identified as may develop into a full STEMI
What is a myocardial infarction?
Plaque rupture leads to a clot forming which then occludes one of the coronary arteries causing myocardial death and inflammation
Symptoms of myocardial infarction?
Acute central chest pain radiating to jaw and shoulder lasting >20mins
Nausea
SoB
Palpitations
(Some are silent > DM+ old)
Signs of MI?
Clammy and pale
4th heart sound
Pansystolic mumur
May later develop peripheral oedema
Acute management of STEMI?
Do a 12 lead ECG, give O2 if sats <94%
Establish IV for bloods and enzymes
Brief histor, BP, JVP, murmurs, signs of CCF
Aspirin 300mg PO
Morphine 5-10mg IV and an anti ememtic
(MONA and refer for PCI or thrombolysis if not CI)
What is the subsequent management of an MI?
Aspirin - 75mg OD reduces the risk of repeat by 29%
Beta blocker - long term risk reduces risk by 25% ( CI = verapamil)
ACEi
Statin
Address modifiable risk factors!!
What advice would you give post MI?
Return to work after 2 months, encourage exercise and no air travel for 2 months
Diet high in oily fish, fruit and veg, low in saturated fats
Exercise: regular daily exercise
What is this a typical history of?
A 67-year-old man comes to see you complaining of cramping pain in his left calf when he gets back from walking uphill to the shops. On examination you notice both his legs are cold and hairless, with an increased capillary refill time in the left but not the right.
Peripheral arterial disease
Symptoms of peripheral arterial disease?
Cramping in calves, thighs and buttocks that is relived with rest
(signs are the 6 Ps)
What are the 6 Ps of limp ischaemia?
- Pain
- Pallor
- Pulselessness
- Parethesis
- Paralysis
- Perishing cold
What are the signs of limb ischaemia?
Absent pulses
Punched out ulcers
Postural colour change (Buergers test)
Explain buergers test?
- Patient supine, elevate legs to 45 degrees for 1-2 mins, observe colour, pallor indicated ischaemia
(occurs when peripheral arterial pressure is inadequate to overcome gravity)
- Sit patient up, hang legs over side of bed at 90 degrees, as gravity aids blood flow
Blue first as deoxygenated blood passes through ischaemic tissue
Then red due to reactive hyperaemia from post hypoxic vasodilation
What investigations are carried out for peripheral limb ischaemia?
Exclude DM, arteritis, anaemia, renal disease
ABPI - normal is 1-1.2, PAD is 0.5 to 0.9
Colour duplex USS - quick and non invasive, can show vessels and blood flow within them
MR/CT angiography - identify stenosis and quality of vessels
Blood tests - raised CK MM shows muscle damage
What is the management of peripheral limb ischemia?
Risk factor modification - quit smoking, treat HTN, lower chloesterol, improve DM
Medications - antiplatelet - clopidogrel is first line
Excercise programs - reduce claudication by improving blood flow
PTA or surgery if severely stenosed
What is this a typical history of?
Despite your advice, the gentleman from earlier comes in a few weeks later complaining of left foot pain at rest which is relieved by hanging it out of the side of the bed at night.
Critical Limb ischemia
Describe critical limb ischemia?
May be due to a thrombosis, emboli, graft occlusion or trauma
Deep duskiness of limb + sudden deterioration shows arterial occlusion NOT gout or cellulitis
If not revascularised in 4-6 hours then limb loss
Surgical emobolectomy or local thrombolysis
Ulcers more likely on limbs with poor blood supply, healing takes longer due to poor perfusion of lumb and therefore hampers the healing process
What is this typical of?
34 year old male presents to GP with chest pain. What do you want to know? – S = central, retrosternal – O = 3 days ago – C = sharp – R = left shoulder – A = SOB, cough, hiccups – T = constant – E = made worse on inspiration, relieved by leaning forwards – S = 7/10
Pericarditis
What is the most common cause of pericarditis?
Viral infections = Coxsackie B
Other viral infections include EBV and mumps
What are the other causes of pericarditis?
Bacterial = pneumonia, rheumatic fever, TB, strep, staph
Post MI = Dresslers sydrome
Autoimmune
What is the management of pericarditis?
Treat the cause
NSAIDS
Corticosteroids for symptomatic relief
Manage complications
What is cardiac failure?
A clinical sydrome rather than one specific disease - a symptomatic condition where breathlessness, fluid retention and fatigue are associated with a cardiac abnormality that reduces cardiac output
A state where the heart is unable to satisfy the needs of the metabolising tissues
What are the causes of heart failure?
Ischaemic heart disease (most common)
Cardiomyopathy
Hypertension
Describe systolic heart failure?
Failure to contract
EF = <40%
IHD, MI, CM
Describe diastolic heart failure?
Inability to relax and fill
EF>50%
Constructive pericarditis, cardiac tamponade, hypertension
Describe the pathophysiology of heart failure?
One the heart begins to fail, compensatory changes begin to occur
As the HF progresses, these compensatory changes become overwhelmed and pathological
What compensatory changes occur in heart failure?
Sympathetic stimulation = increases afterload by causing peripheral vasoconstriction
RAAS = increases salt and water retention, increases the afterload and preload (increased volume and vasocontriction)
Cardiac changes = Ventricular dilation, myocyte hypertrophy
Describe the mechanism of heart failure?
- Increased preload
(failure of heart means more blood is left in the ventricles after systole = increased preload)
Stretching of myocardium maintaining CO
- Increased afterload
- Salt and water retention
(reduced cardiac output leading to decreased renal perfusion activating RAAS) - Myocardial remodelling
(in response to ischaemia myocyte damage etc. Hypertrophy, loss of myocytes and increased interstitial fibrosis)
What are the symptoms of left sided cardiac failure?
- exertional dyspnoea
- fatigue
- PND
- Nocturnal cough - pink frothy sputum
What are the signs of left sided cardiac failure?
- Cardiomegaly
- 3rd and 4th heart sounds
- Crepitations in the lung bases
- Weight loss
- Reduced BP
- Tachycardia
- Cool periphery
- Heart murmur
What are the symptoms of right sided heart failure?
- Peripheral oedema
- Ascites
- Nausea
- Anorexia
What are the signs of right sided heart failure?
- Raised JVP
- Hepatomegaly
- Pitting oedema
- Ascites
What investigations would you carry out for heart failure?
Bloods = B type Natiuretic peptide: FBC, LFTs, U=E, BNP. TFTs
Cardiac enzymes = Creatinine Kinase, Troponin i, troponin T
CXR
ECHO
What is the treatment for acute heart failure?
100% oxygen Nitrates - GTN spray IV opiates - diamorphine IV furosemide - reduce fluid overload Consider inotropic drug
What is the treatment for chronic heart failure?
ABCD
A. ACE inhibitors - Ramipril B. Beta blockers - Atenolol C. CCB and other vasodilators - amlodipine, hydralazine D. Diuretics + digoxin - Spironolactone = aldosterone antagonist Furosemide = loop diuretic
What is the management of heart failure?
Lifestyle = education, obesity control, diet, smoking cessation, cardiac rehab
Symptomatic = Loop diuretics - furosemide
Disease altering = ACEi BB Aldosterone agonists Digoxin
What is atrial fibrillation?
Most common arrhythmia - 5-10% of patients are >65
Atrial activity is chaotic and mechanically ineffective
What causes atrial fibrillation?
Heart failure, hypertension, thyrotoxicosis
Any condition causing raised arterial pressure
Describe the pathophysiology of atrial fibrillation?
Atrial activiation 300-600min
Only a proportion of these impulses are conducted to the ventricles (due to the refractory period of the AVN)
HR = 120-180
Symptoms of atrial fibrillation?
Asymptomatic Palpitations Fatigue Heart failure 5x risk of stroke, embolism due to thrombus formed in the atrium
What is used for rate control in atrial fibrillation?
Beta blockers (atenolol)
CCB (verapamil, diltiazem)
Digoxin
What is used for rhythm control in atrial fibrillation?
Electrical DC cardioversion
Amiodarone = anti arrhythmia medication
Anticoagulation with warfarin - target INR - 2-3
What does Atrial fibrillation look like on an ECG?
Irregularly irregular
F waves
No clear P waves
ORS is rapid and irregular
What is atrial flutter?
Often associated with AF
Atrial rate = 300bpm
Ventricular rate = 150bpm
ECG = sawtooth flutter waves (F waves)
Rx = radiofrequency catheter ablation
What is AV nodal re entry tachycardia?
Commonest type of SVT
There is a ‘ring’ of conducting pathways in theAV node of which the limbs have different conducting times and refractory periods
This allows a re-entry circuit and impulse to produce a circus movement tachycardia
On ECG = p waves are either not visible, or seen immediately before QRS complex
QRS is a normal shape because the ventricles are activated normally, down the bundle of His
What is AV reciprocating tachycardia?
Accessory pathway connecting the atria and the ventricles - capable of antegrade or retrograde conduction (in some cases both)
What is Wolf Parkinson White syndrome?
- Best known type of AVRT
- There is an accessory pathway (bundle of Kent) between the atria and the ventricles
- ECG = shows evidence of the pathway, if path allows some of the atrial depolarisation to pass quickly before it goes through the AVN
- Early depolarisation of part of the ventricle = shortened PR interval and a slurred start to the QRS (delta wave) and the QRS is narrow
- Patients are also prone to atrial and occasionally ventricular fibrillation
What is sinus bradycardia?
<60bpm
Extrinsic causes of bradycarida?
Treat the underlying cause!
- Drug therapy
- Hypothyroidism
- Hypothermia
- Raised inter cranial pressure
Intrinsic causes of bradycardia?
Treat with atropine or temporary pacing in acute causes
- Acute ischaemia
- Infarction of the SAN
- Sick sinus sydrome
What is sick sinus syndrome?
Bradycardia caused by the intermittent failure of the SAN depolarisation due to the failure of the sinus node to propogate to the atria (sinoatrial block)
If symptomatic - permanent pacemaker insertion
Where can the heart be blocked?
- Block in the AVN or bundle of His
2. Block in the lower conduction system
Describe first degree heart block?
If R is far from P then you have FIRST DEGREE
Delayed AV conduction = PR interval prolonged >0.2s
Asymptomatic = no treatment
Caused by
- Acute ischemia
- Hypokalemia
Describe second degree heart block? (I)
Longer, longer, longer DROP then you have a WENCKEBACH
- Progressive PR interval prolongation, until a P wave fails to conduct and a QRS is dropped, then cycle repeats itself
- Lightheadedness, dizziness, syncope
Describe second degree heart block? (II)
If some Ps don’t get through then you have a MOBITZ TYPE II
- Same PR interval but QRS is dropped
- Chest pain, SOB, postural hypotension
What is the difference between mobitz type I and type II?
In Mobitz type I the PR interval progressively lengthens until an impulse is blocked
In Mobitz type II the PR interval is prolonged but constant with an occasional impulse being blocked
Describe third degree heart block?
WiLLiM MaRRoW
- Causes = all atrial activity fails to conduct to the ventricles
- ECG = P waves and QRS are independent - ventricular contractions are sustained by spontaneous escape rhythm
- Rx = IV atropine (acute) or permanent pacemaker insertion
What would a right bundle branch block look like?
MaRRoW
M in V1
W in V6
Cause = PE, IHD, ASD and VSD
What would a left bundle branch block look like?
WiLLiaM
W in V1
M in V6
What can cause heart block>
Coronary artery disease
Cardiomyopathy
Fibrosis in the conducting tissues
What is hypertension?
Raised blood pressure
Can have primary (95%) or secondary origin
Secondary origins e.g. CKD, Conn’s syndrome, pregnancy
If someone is over 55 OR of Black African-Carribean origin what would be the first line of treatment in hypertension?
CCB
calcium channel blocker
If someone is under 55, and not Black African-Carribean origin OR had type 2 diabetes what would be the first line of treatment?
ACEi or ARB
What would the second line of treatment for hypertension be?
First line (ACEi OR ARB / CCB) \+ add either CCB if on A or A/ add A or A if on CCB OR add a thiazide like diuretic
What would third line of treatment be for hypertenison?
ACEi or ARB + CCB + thiazide like diuretic
What would be fourth line of treatment for hypertension?
ACEi or ARB + CCB + thiazide like diuretic
+
Low dose spironolactone
Alpha or beta blocker
What lifestyle changes for HTN?
- Stop smoking
- Low fat diet
- Reduce alcohol and salt
- Increase exercise + reduce weight if obese
Describe aortic stenosis?
Symptoms occur when valve area is 1/4 of the normal (normal = 3-4cm2)
Types = supravalvular, subvalvular, valvular
Aetiology: congenital bicuspid valve, degenerative calcification, rheumatic disease
How does aortic stenosis present?
Syncope
Angina
Dyspnoea
Heart failure
Old person who is SAD AS
What are the physical signs of aortic stenosis?
Pulsus pardus an pulsus tardus
Heart sounds - soft or absent, S4 gallop due to LVH
Ejection systolic murmur - crescendo - decrescendo character
What investigations would you carry out for aortic stenosis?
Echocardiography - diagnostic
ECG
CXR - LVH calcified aortic valve
Management of aortic stenosis
General = dental care/hygiene - IE prophylaxis in dental procedures
Surgical = valve replacement, if not medically fit for surgery - transcatheter aortic valve replacement
What is mitral regurgitation?
Backflow of blood from the LV to the LA during systole
Describe the pathophysiology of mitral regurgitation?
Exertion dyspnoea
Palpitations
Fatigue
What are the signs of mitral regurgitation?
Pansystolic murmur at the apex radiating to the axilla
Soft S1
Displaced hyperdynamic apex
Investigations for mitral regurgitations?
Echocardiogram
CXR - englarged LA and LV
ECG
Management of mitral regurgitation?
Vasodilator - ACEi e.g. hydralazine
Rate control for AF - BB, CCB, digoxin
Anticoagulation for AF and Flutter
Diuretics to control symptoms
Surgery for deteriorating symptoms - aim to replace the valve
Describe aortic regurgitation?
Leakage of blood into the left ventricle during diastole due to ineffective coaptation or aortic cusps
Aetiology - RF, IE, bicuspid aortic valves
Pathophysiology of aortic regurgitation?
Combined pressure and volume overload = left ventricle dilation and LVH
What is the presentation of aortic regurgitation?
- Exertional dyspnoea
- Orthopnoea
- Paroxysmal nocturnal dyspnoea
Signs of of aortic regurgitation?
- Collapsing water hammer pulse
- Wide pulse pressure
- Displaced hyperdynamic apex beat
- Early diastolic murmur
What are the notable eponyms of aortic regurgitation?
Corrigans signs De Mussets sign Durioziez's sign Austin flint murmur Traube's sign
Investigation of aortic regurgitation?
Echocardiogram
ECG
CXR - cardiomegaly
Management of aortic regurgitation?
Medical - vasodilators, ACEi only if symptomatic or HTN
Surgical - Replace valve before LV dysfunction
Describe mitral stenosis?
Obstruction of the left ventricle inflow that prevents proper filling during diastole
Causes = Rheumatic, IE, mitral annular calcification, congential
Presentation of mitral stenosis?
Dyspnoea, fatigue, palpitations, chest pain
Signs of mitral stenosis?
Malar flush on cheeks Low volume pulse Tapping, non displaced apex beat Rumbling, mid diastolic murmur Loud opening S1
Investigations for mitral stenosis?
Echocardiogram
CXR - LA enlargement
ECG - AF and LA englargement
Management of mitral stenosis
If in AF, rate contril
Anticoagulate with warfarin
Diuretics
Percutaneous mitral ballon valvotomy
What is shock?
Circulatory failure resulting in inadequate organ perfusion
Low BP - systolic <90mmHg
What are the different types of shock?
- SEPTIC: infection with any organism - acute vasodilation from inflammatory cytokines
2, ANAPHYLATIC: Type-I mediated hypersensitivity, release of histamine
- NEUROGENIC: Spinal cord injury, epidural or spinal anaesthesia
- HYPOVOLAEMIC: Bleeding, trauma, rupture, AA, GI bleed
Define SIRS?
Systemic Inflammatory Response Sydrome (SIRS) is defined as
Temp >38 degrees or <36 degrees
Tachycardia >90bpm
Respiratory rate >/= 20 breaths per minute OR PACO2 <4.3kPA
WBC >12 x 10^9
Describe the sepsis continuum?
SIRS
Sepsis = SIRS + presumed or confirmed infectious process
Severe sepsis = sepsis with end organ failure
Septic shock refractory hypotension
Management of septic shock?
ABC = airways, breathing, circulation
Investigations and treatment - depend on the cause
Note: in septic shock, take blood cultures before antibiotics
What is dilated cardiomyopathy?
Dilated cardiomyopathy is a progressive disease of the heart muscle that is characterised by ventricular chamber enlargement
Third most common cause of heart failure and most frequent reason for heart transplantation
Symptoms and signs of dilated cardiomyopathy?
Fatigue
Dyspnoea on exertion
Orthopnoea, paroxysmal nocturnal cough
increasing oedema/weight
S3 gallop Tachycardia Tachypnoea Irregular BP Balloon shape heart on chest Xray
Pathology of dilated cardiomyopathy?
Enlarged, heavy, dilated heart, possible cardiac weight of up to 900g
Histology shows variable atrophy and hypertrophy
Increased interstitial tissue
Occasional inflammatory cells
Investigations for dilated cardiomyopathy?
- Complete blood count
- B-type natriuretic peptide assay
- Chest radiography
- Echocardiography
- Cardiac magnetic resonance imaging (MRI)
- Electrocardiography (ECG)
What is restrictive cardiomyopathy?
Poor dilation of the heart restricts the eventual ability of the heart to take on blood and pass it on to the rest of the body
Describe a heart with restrictive cardiomyopathy?
Firm enlarged heavy heart with diffuse infiltration of the protein into the myocytes bloody vessels and valves
ECG would be low voltage
Describe hypertrophic cardiomyopathy?
Many mutations recognised involving B myosin, myosin binding protein C, troponin T, titin
Some mutations are associated with clinical feature=
B myosin: cardiac hypotrophy and dysrhythmia
Troponin T: sudden death
What is the pathophysiology of aortic dissection?
Tear in the tunica intima of the wall of the aorta
What are the associations / risk factors with aortic dissection?
- Hypertension: most important risk factor
- Trauma
- Collagens (marfans syndrome)
- Turners and Noonans syndrome
- Pregnancy
- Syphillis
What are the features of aortic dissection??
- Chest pain, typically severe, radiated through to the back and tearing in nature
- Aortic regurgitation
- Hypertension
- Other features may result from the involvement of specific arteries e.g. coronary arteries
- Majority of patients have no or non specific ECG changes, in a minority of patients ST segment elevation may be seen in inferior leads
What investigations would be carried out for an aortic dissection?
History and physical examination
Imaging studies - chest radiography is first line, CT is the definitive test
Electrocardiography
Full blood count, serum chemistry, cardiac markers
What management for aortic dissection?
Surgical treatment - area of the aorta with intimal tear is resected and replaced
Medical treatment - antihypertensives and narcotics
Who is screened for AAA?
Men over 65
Which groups suffer with aortic aneurisms?
Those who suffer with standard arterial disease
Those with connective tissue disorders e.g. Marfan’s
Symptoms of AAA?
Pulsing sensation in the stomach like a heart beat
Stomach pain that does not go away
Lower back pain that does not go away
What are the symptoms of a burst AAA?
Sudden, severe pain in the tummy or lower back
Dizziness
Sweaty, pale and clammy skin
A fast heartbeak
SoB
Syncope
Investigations for AAA?
Screening
CT of the abdomen
Ultrasound of the abdomen
What is the management of AAA?
Surgery:
- Symptomatic aneurysms (80% annual mortality if untreated)
- Increases size about 5.5.cm
- Rupture (100% mortality without surgery)
