Cardiovascular 2 Flashcards

Question

what is Takotsubo cardiomyopathy?

Answer 1

'Stress'-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure they will be ST elevation but normal coronary angiogram Transient, apical ballooning of the myocardium Treatment is supportive

Answer 2

- inflammation of the pericardium - new onset of inflammation lasting less than 4-6 weeks - it can be either fibrinous or effusive with a purulent, serous or haemorrhagic exudate

Answer 3

it is characterised by a triad of chest pain, pericardial friction rub and serial ECG changes - the chest pain is usually pleuritic - and often relieved by sitting forward - non productive cough - dyspnoea - flu like symptoms - tachypnoea - tachycardia

Answer 4

``` viral infections (Coxsackie) tuberculosis uraemia (causes 'fibrinous' pericarditis) trauma post-myocardial infarction, Dressler's syndrome connective tissue disease hypothyroidism malignancy idiopathic ```

Answer 5

ECG changes the changes in pericarditis are often global/widespread, as opposed to the 'territories' seen in ischaemic events 'saddle-shaped' ST elevation PR depression: most specific ECG marker for pericarditis transthoracic echo serum troponins, ESR, CRP, FBC, UREA pericardial fluid/blood culture

Answer 6

treat the underlying cause a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis if there is tamponade or symptomatic effusion - pericardiocentesis if it is purulent - pericardiocentesis and antibiotics - vancomycin and ceftriaxone

Answer 7

any cause of pericarditis but particularly TB

Answer 8

``` dyspnoea right heart failure: elevated JVP, ascites, oedema, hepatomegaly JVP shows prominent x and y descent pericardial knock - loud S3 Kussmaul's sign is positive ``` CXR - will show pericardial calcification

Answer 9

cardiac tamponade JVP - absent Y descent Pulsus paradoxus - present Kaussmaul's sign - rare ``` Constrictive pericarditis JVP - X + Y present pulsus paradoxus - absent Kussmaul's sign - present preicardial calcification on CXR ```

Answer 10

Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure.

Answer 11

Classical features - Beck's triad: hypotension raised JVP muffled heart sounds Other features: dyspnoea tachycardia an absent Y descent on the JVP - this is due to the limited right ventricular filling pulsus paradoxus - an abnormally large drop in BP during inspiration Kussmaul's sign - much debate about this ECG: electrical alternans

Answer 12

- ECG - low voltage, electrical alternans, electromechanical dissociation associated with end stage tamponade - Transthoracic echo - large pericardial effusion, chamber collapse and respiratory variation of ventricular filling - CXR - enlarged heart - FBC, ESR, cardiac enzymes

Answer 13

pericardiocentesis | or surgical drainage

Answer 14

NSAIDs plus PPI plus colchicine 2nd line corticosteroid 3rd line immunosupressant

Answer 15

defined as abnormal dilation of a blood vessel by more than 50% of its normal diameter

Answer 16

An abdominal aortic aneurysm (AAA) is defined as a dilatation of the abdominal aorta greater than 3cm they can be true or false aneurysm true - all 3 layers of the arterial wall are involved false - only a single layer of fibrous tissue forms the aneurysm wall *it is important to identify and manage early

Answer 17

The aetiology of abdominal aortic aneurysm is largely unknown. Possible causes include: - atherosclerosis - trauma - infection - connective tissue disease (e.g. Marfan’s disease, Ehler’s Danlos, Loey Dietz) - inflammatory disease (e.g. Takayasu’s aortitis). Risk factors for AAA include: - smoking, hypertension, hyperlipidaemia, family history, male gender, and increasing age. - Diabetes mellitus is a negative risk factor for AAA (the mechanism for this is still poorly understood).

Answer 18

Many abdominal aortic aneurysms are asymptomatic and are simply detected on incidental finding or screening. Symptomatic patients with an AAA can present with: - Abdominal pain - Back or loin pain - Distal embolisation producing limb ischaemia - Aortoenteric fistula On examination, a pulsatile mass can be felt in the abdomen (above the umbilical level), and rarely, signs of retroperitoneal haemorrhage may be evident. A patient with a ruptured AAA may present with pain (abdominal, back, or loin) and a degree of shock or syncope

Answer 19

In the UK, the national abdominal aortic aneurysm screening programme (NAAASP) offer an abdominal US scan for all men in their 65th year.

Answer 20

<3 cm - normal - nor further action 3-4.4cm - small aneurysm - rescan every 12 months 4.5 - 5.4cm - medium aneurysm - rescan every 3months >5.5cm = large aneurysm - refer within 2 weeks to vascular surgery for probable intervention

Answer 21

USS | once USS confirmed diagnosis - CT scan with contrast is warranted when the threshold diameter of 5.5.cm

Answer 22

Any AAA less than 5.5cm can be monitored via Duplex USS, as surgery prior to this diameter provides no survival benefit either for open repair or endovascular repair 3. 0 – 4.4cm: yearly ultrasound 4. 5 – 5.4cm: 3-monthly ultrasound A patient with a small (3cm-5.5cm) AAA* has a 3% per year risk of cardiovascular mortality, hence cardiovascular risk factors should be reduced as appropriate: Smoking cessation (reduces rate of expansion and risk of rupture) Improve blood pressure control Commence statin and aspirin therapy Weight loss and increased exercise surgical intervention - considered when greater than 5.5.cm or if it is increasing >1cm per year or if it is symptomatic in a patient who is otherwise fit Open repair involves a midline laparotomy or long transverse incision, exposing the aorta, and clamping the aorta proximally and the iliac arteries distally, before the segment is then removed and replaced with a prosthetic graft Endovascular repair involves introducing a graft via the femoral arteries and fixing the stent across the aneurysm

Answer 23

endovascular leak, whereby an incomplete seal forms around the aneurysm resulting in blood leaking around the graft. Endoleaks are often asymptomatic hence regular surveillance (usually ultrasound unless a complication is noted) is needed. If left untreated, the aneurysm can expand and subsequently rupture. As such, any aneurysm expansion following EVAR warrants investigation for endoleak.

Answer 24

In the UK, any AAA >6.5cm requires notification to the DVLA and disqualifies from driving until repaired.

Answer 25

- rupture - retroperitoneal leak - embolisation - aortoduodenal fistula

Answer 26

abdo pain back pain syncope vomiting on examination they will be haemodynamically compromised with a pulsitle abdominal mass and tendernes Around 50% patients present with the ‘classic triad’ of ruptured AAA (flank or back pain, hypotension, and a pulsatile abdominal mass).

Answer 27

any suspected AAA warant high flow oxygen, IV access (2 large bore cannulas) and urgent bloods taken with cross match for minimum 6 units aim to keep BP<100mmHg - termed permissive hypotension to prevet excessive blood loss send to surgery for repair.

Answer 28

Thoracic aortic aneurysms develop due to degradation of the tunica media, the layer of the artery which provides tensile strength and elasticity to the wall. As a result, the artery loses structural integrity and dilates, and as the diameter increases, the wall tension rises and further increases the diameter in a vicious cycle. The main causes of thoracic aneurysm are: Connective tissue diseases (e.g. Marfan’s syndrome or Ehlers-Danlos syndrome) Bicuspid aortic valve Other causes include trauma, aortic dissection, aortic arteritis (e.g. Takayasu Arteritis), and tertiary syphilis

Answer 29

A thoracic aortic aneurysm can involve the ascending aorta or aortic root (60%), aortic arch (10%), descending aorta (40%), or thoracoabdominal aorta (10%) segments

Answer 30

``` fam history hypertension atherosclerosis smoking high BMI male gender advancing age ```

Answer 31

typically asymptomatic In those that are symptomatic, the most common presenting complaint is pain, with the location of the pain potentially localising the aneurysm: ascending aorta - anterior chest pain aortic arch - neck pain descending aorta - pain between the scapula Other symptoms of thoracic aneurysms include: - Back pain – secondary to spinal compression by descending or thoracoabdominal aneurysm - Hoarse voice – from damage to the left recurrent laryngeal nerve in arch aneurysms - Distended neck veins – from SVC compression - Symptoms of heart failure – from involvement of the aortic valve - Dyspnoea or cough – secondary to tracheal or bronchial compression

Answer 32

Thoracic aneurysms are diagnosed through imaging They can be seen on plain film CXR however not sensitive enough to make a definitive diagnosis CT scan with contrast transoesophageal echo

Answer 33

they are at increased CV risk so statin and antiplatelet control BP stop smoking Surgical management is dependent on the location of the aneurysm > Ascending Aorta Treated when the diameter >5.5cm, the affected region of the aorta is excised and replaced with a dacron graft. If the aortic root is involved, a Bentall procedure is often performed, using a graft that also contains a prosthetic aortic valve > Aortic Arch Once the aneurysm is over 5.5cm surgery should be considered; the affected aorta is replaced with a multi-limbed graft, allowing for the branching of the great vessels (these procedures have a high risk of cerebral ischaemia from embolisation) > Descending Aorta Intervention is indicated when the diameter exceeds 6.0cm. These can be repaired open or with endovascular techniques, yet endovascular techniques have been shown to produce fewer postoperative complications and to have a lower mortality

Answer 34

The wall of an artery consists of the tunica intima (innermost layer), tunica media (middle layer), and tunica adventitia (outermost layer). An aortic dissection is a tear in the intimal layer of the aortic wall, causing blood to flow between and splitting apart the tunica intima and media. Aortic dissections from the initial intimal tear can progress distally, proximally, or in both directions from the point of origin. Anterograde dissections propagate towards the iliac arteries and retrograde dissections propagate towards the aortic valve (at the root of the aorta). Retrograde dissections can result in prolapse of the aortic valve, bleeding into the pericardium, and cardiac tamponade

Answer 35

Stanford classification type A - ascending aorta, 2/3 of cases type B - descending aorta, distal to left subclavian origin, 1/3 of cases 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

Answer 36

``` hypertension Atherosclerotic disease Male gender Connective tissue disorders (typically Marfan’s syndrome or Ehler’s-Danlos syndrome) Biscuspid aortic valve ``` As a general rule, younger cases often have associated connective tissue disorders, whilst older patients are more likely to have underlying hypertension or atherosclerosis.

Answer 37

``` tearing chest pain radiates through the back tachycardia hypotension - secondary to hypovolaemia from blood loss into the dissection or cardiogenic from severe aortic regurgitation or pericardial tamponade new aortic regurgitation murmur ``` other features may result from the involvement of specific arteries. For example: coronary arteries → angina spinal arteries → paraplegia distal aorta → limb ischaemia the majority of patients have no or non-specific ECG changes. In a minority of patients, ST-segment elevation may be seen in the inferior leads

Answer 38

MI PE pericarditis MSK back pain

Answer 39

``` baseline bloods (FBC, U&E, LFTs, troponin, coagulation) with a crossmatch of at least 4 units ABG to aid initial assessment ECG to exclude any cardiac pathology CT angiogram tranoesophageal echo ```

Answer 40

Start high flow oxygen and gain IV access (x2 large bore cannulas); fluid resuscitation should be done cautiously. In the setting of a rupture, then the target pressure should be sufficient for cerebral perfusion only. In the setting of an uncomplicated dissection then the target systolic pressure should be kept below 110mmHg systolic Stanford type A: carry high mortality - surgery is needed (usually removal of ascending aorta with replacement with synthetic graft) BP should be controlled whilst awaiting intervention - target systolic 11-120mmHG) Stanford type B: best managed medically - management of hypertension with IV BB - labetalol (or CCB as 2nd line). Acutely endovascular repair not recommenced due to risk of retrograde dissection. surgical intervention in Type B dissections is only warranted in the presence of certain complications, such as rupture, renal, visceral or limb ischaemia, refectory pain, or uncontrollable hypertension.

Answer 41

``` aortic rupture aortic regurgitation myocardial ischaemia cardiac tamponade stroke or paraplegia secondary to cerebral artery or spinal artery involvement ```

Answer 42

hypertension is defined as a blood pressure above 140/90 in clinic or 135/85 with ambulatory or home readings

Answer 43

essential hypertension = 95% of hypertension secondary causes of hypertension ROPE: R – Renal disease. This is the most common cause of secondary hypertension. If the blood pressure is very high or does not respond to treatment consider renal artery stenosis. O – Obesity P – Pregnancy induced hypertension / pre-eclampsia E – Endocrine. Most endocrine conditions can cause hypertension but primarily consider hyperaldosteronism (“Conns syndrome”) as this may represent 2.5% of new hypertension. A simple test for this is a renin:aldosterone ratio blood test. drugs - steroid, MAOIs, COCP, NSAIDs, leflunomide

Answer 44

``` Ischaemic heart disease Cerebrovascular accident (i.e. stroke or haemorrhage) Hypertensive retinopathy Hypertensive nephropathy Heart failure ```

Answer 45

stage 1: Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg stage 2: Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg stage 3, severe: Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

Answer 46

Patients with a clinic blood pressure between 140/90 mmHg and 180/120 mmHg should have 24 hour ambulatory blood pressure or home readings to confirm the diagnosis. Having your blood pressure taken by a doctor or nurse often results in a higher reading. This is commonly called “white coat syndrome”. The white coat effect is defined as more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.

Answer 47

> Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage > Bloods for HbA1c, renal function and lipids > Fundus examination for hypertensive retinopathy > ECG for cardiac abnormalities

Answer 48

admit for specialist assessment if: - signs of retinal haemorrhage or papilloedema (accelerated hypertension) or - life-threatening symptoms such as new-onset confusion, chest pain, signs of heart failure, or acute kidney injury NICE also recommend referral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis) if none of the above then arrange urgent investigations for end-organ damage (e.g. bloods, urine ACR, ECG) - if target organ damage is identified, consider starting antihypertensive drug treatment immediately, without waiting for the results of ABPM or HBPM. - if no target organ damage is identified, repeat clinic blood pressure measurement within 7 days

Answer 49

at least 2 measurements per hour during the person's usual waking hours (for example, between 08:00 and 22:00) use the average value of at least 14 measurements

Answer 50

for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated BP should be recorded twice daily, ideally in the morning and evening BP should be recorded for at least 4 days, ideally for 7 days discard the measurements taken on the first day and use the average value of all the remaining measurements

Answer 51

lifestyle advice: reduce salt intake, reduce caffeine intake, stop smoking, reduce alcohol intake, exercise, weight loss. *for patients less than 40 consider specialist referral to exclude secondary causes. treat stage one hypertension if <80 and any of the following apply; target organ damage, established CV disease, renal disease, diabetes or 10 year CV risk >10%. stage 2 hypertension - offer drug treatment regardless of age Step 1 treatment - patients < 55-years-old or a background of type 2 diabetes mellitus: (ACE-i or ARB): (A) - patients >= 55-years-old or of black African or African–Caribbean origin: CCB (C) Step 2 treatment if already taking an ACE-i or ARB add a CCB or a thiazide-like Diuretic if already taking a CCB add an ACE-i or ARB (A + C) or (A + D) ``` Step 3 treatment add a third drug to make, i.e.: if already taking an (A + C) then add a D if already (A + D) then add a C (A + C + D) ``` Step 4 treatment NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice first, check for: - confirm elevated clinic BP with ABPM or HBPM - assess for postural hypotension. - discuss adherence if potassium < 4.5 mmol/l add low-dose spironolactone if potassium > 4.5 mmol/l add an alpha- or beta-blocker * ARB can be used instead of ACEi where they are not tolerated because of cough * ACE inhibitors have reduced efficacy in patients of black African or African–Caribbean origin are therefore not used first-line * for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor

Answer 52

<80 years <140/<90 | >80 years <150/<90

Answer 53

Cushing's syndrome Conn's syndrome (primary hyperaldosteronism) Liddle's syndrome 11-beta hydroxylase deficiency

Answer 54

When dealing with heart failure not responding to ACE-inhibitor, beta-blocker and aldosterone antagonist therapy, a widened QRS complex favours cardiac resynchronisation therapy

Answer 55

it is used as a 3rd line management for heart failure | criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%

Answer 56

Warfarin acts on the extrinsic pathway, whilst heparin acts on the intrinsic pathway. Thus, warfarin efficacy is monitored using the INR – which utilises the prothrombin time. Heparin is measured using the aPPT *in a warfarin overdose you would expect the PT and APTT to be prolonged.

Answer 57

a chronic condition due to atherosclerosis of arteries in the limbs. The level of arterial occlusion present is proportional to the symptoms. The pathogenesis and risk factors are the same as for coronary artery disease (CAD) It can present as an emergency as acute limb ischaemia

Answer 58

``` > Hypertension > Dyslipidaemia - High LDL and low LDL levels > Diabetes > Obesity > FHx of arterial disease - Significant if a first degree > relative had MI before the age of 55 > Smoking > Age > Male gender ```

Answer 59

``` angina ACS TIA Stokes PVD chronic mesenteric ischaemia ```

Answer 60

Critical Limb Ischaemia is the end stage of peripheral arterial disease, where there is inadequate supply of blood to a limb to allow it to function normally at rest.

Answer 61

Intermittent Chlaudication is the symptom of having ischaemia in a limb during exertion that is relieved by rest. It is typically a crampy, achy pain in the calf muscles associated with muscle fatigue when walking beyond a certain intensity.

Answer 62

The main differential is “spinal claudication” caused by impingement of the caudal equina by a spinal stenosis. This also classically causes pain in the back of the legs on exertion.

Answer 63

Pain in the calves on walking, relieved by rest - This pain is also known as claudication - The pain can occur anywhere along the leg, and down into the foot - Many patients do NOT present with classic claudication – often because they are not doing enough activity to induce the symptoms – particularly if they have another comorbidity that limits their activity. Pain may also occur when legs are raised (e.g. in bed), and abate when legs are lowered (e.g. by sitting)

Answer 64

``` Associated with occlusion in the distal aorta or proximal common iliac artery A clinical triad: - Thigh / buttock claudication - Absent femoral pulses - Male impotence ```

Answer 65

Elevating the leg may cause it to go pale and cold, as well as causing pain.- Beuger’s angle <20’ – the leg will go pale and cold upon raising it 20’ off the couch. Increased vascular filling time – Upon lowering, the leg may become hot and red as reperfusion occurs. Perfusion time tends to be reduced (>15s) Oedema is not usually present There may be evidence of poor skin health due to poor perfusion, such as ulcers, dry scaly skin, cool peripheries and reduced capillary refill time Check the pulse in the foot (posterior tibial and dorsals pedis) Palpable pulses indicate low likelihood of peripheral vascular disease Absent pulses represent an increased chance of peripheral vascular disease If you are unable to locate a pulse by hand, you can use a doppler probe to assess if significant blood flow is present in the artery

Answer 66

``` ankle-brachial index - ABI arterial doppler angiography - CT or RI bloods - ESR and CRP to exclude arteritis, platelets and clotting ECG - to exclude cardiac involvement ```

Answer 67

ABPI is a measure of the ratio of the blood pressure in the ankle vs the arm. Using only systolic values, divide the ankle pressure by the brachial pressure A normal value is >1 A value of <0.9 is pathological for limb ischaemia (PVD). The lower the number, the greater the degree of PVD >0.9 is normal 0.6 – 0.9 is mild disease - claudication 0.3 – 0.6 is moderate to severe disease - rest pain <0.3 is severe disease to critical ischaemic

Answer 68

- ‘Punched out’ ischaemic ulcers – usually on the toes and heels, rarely higher up the limb. These tend to occur after a localised traumatic event. They are often painful, but diabetic and alcoholic patients may not have pain. - Gangrene – often black necrotic gangrenous tissue surrounds the punched out ulcer lesions. Infection of this areas can occur (wet gangrene). - Reduced / absent peripheral pulses – start distally, and work your way up until you find the pulse - Skin atrophy – in chronic disease - Hair loss – in chronic disease - Cyanosis - Excessive sweating – due to overactivity of the sympathetic nerves - Erectile Dysfunction – Leriche syndrome – the result of distal aortic disease. Other features of the syndrome

Answer 69

Burning pain at night, due to elevation (which reduces limb perfusion), and is relieved by hanging the legs over the side of the bed

Answer 70

anti-platelet therapy - aspirin or clopidogrel exercise risk factor modification statin if it is lifestyle limiting add symptomatic relief - cilostazol or naftidrofuryl if severe it can be treated by: angioplasty stenting bypass surgery

Answer 71

sudden decrease in limb perfusion that threatens the viability of the limb can be caused by: Embolisation whereby a thrombus from a proximal source travels distally to occlude the artery (most common) The original thrombus source may be as a result of AF, post-MI mural-thrombus, abdominal aortic aneurysm, or prosthetic heart valves Thrombosis in situ whereby an atheroma plaque in the artery ruptures and a thrombus forms on the plaque’s cap (presenting as acute or acute-on-chronic) Trauma (less common), including compartment syndrome

Answer 72

``` 6 P's Pain Pallor Pulselessness Paresthesia perishingly cold paralysis ``` usually a sudden onset of the above symptoms

Answer 73

critical chronic limb ischaemia acute DVT spinal cord/peripheral nerve compression

Answer 74

routine bloods - including serum lactate to assess the level of ischaemia thrombophilia screen if less than 50 without known risk factors group and save ECG doppler USS of both limbs CT angiography

Answer 75

acute limb = sudden onset from blockage critical chronic limb = long term from PVD

Answer 76

Acute limb ischaemia is a surgical emergency. Complete arterial occlusion will lead to irreversible tissue damage within 6 hours. High flow oxygen get adequate IV access Heparin - bolus then infusion ASAP also give anti-platelet - aspirin if the limb is viable intra-arterial thrombolysis - urokinase and endovascular revascularisation if it is an embolic cause - embolectomy via a fogarty catheter - local intra-arterial thrombolysis - bypass surgery if thrombotic cause - local intra-arterial thrombolysis - angioplasty - bypass surgery if the limb is not viable - amputation

Answer 77

assess for revascularisation | aspirin

Answer 78

death An important complication of acute limb ischaemia is reperfusion injury; sudden increase in capillary permeability can result in: Compartment syndrome Release of substances from the damaged muscle cells, such as: - K+ ions causing hyperkalaemia - H+ ions causing acidosis - Myoglobin, resulting in significant AKI It is imperative that patients at risk of compartment syndrome are closely monitored and rapidly treated. Electrolyte imbalance due to reperfusion injury requires close monitoring and potentially haemofiltration.

Cardiovascular 2 Flashcards

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