CVS Flashcards

Question

What is AF?

Answer 1

An SVT characterised by uncoordinated atrial activity, manifesting as fibrillatory F waves, loss of p waves and irregular QRS complexes on an ECG.

Answer 2

HTN, DM, old age, hyperthyroid, thryotoxicosis, alcohol toxicity, large consumption caffeine, HF, valvular disease, hypoxic pulmonary conditions,

Answer 3

Palpitations, dyspnoea, dizziness | Irregularly irregular pulse, JVP, rales (hf)

Answer 4

``` ECG - F waves, loss P waves, iregireg QRS TTE/TOE - valvular disease CXR - pulmonary precipitants TFTs - hyperthyroid Cardiac biomarkers - check in case MI U+Es - LOW K+ OR HIGH K+ or low mg2+ ``` Stress test possible

Answer 5

Less than 48 hours = can dc cardiovert ``` If unsure / over: Haemostable 1. Rate slowing - Bblockers and CCBs (diltiazem + verapamil) + a/c for 3-4 weeks with warf or DABIGATRAN then electrical or pharm cardioversion. UNSTABLE 1. DC cardioversion + a/cs ```

Answer 6

MI STOKE HF

Answer 7

Cardiac electrical abnormality characterised by impaired (absent or delayed) conduction between the atria and ventricles.

Answer 8

Age, DM, Valvular disease, ACS, HF, antiarrythmics eg Bblockers CCBs, Increased vagal tone, IE

Answer 9

1deg 2degT1 = block at AVN | 2degt2 3deg = block at purkinje fibres

Answer 10

1 deg - fixed prolonged PR 2 deg T1 - PR gradually lengthens before dropped beat 2 deg T2 - fixed Prolonged PR then dropped beat 3 deg - no relation between P and QRS (a + V contraction)

Answer 11

Bradycardia - <40bpm | Syncope, dyspnoea, ACS risk, fatigue, FHx

Answer 12

``` ECG - see changes Cardiac biomarkers - potential ACS U+Es - low k+/ca2+ may be causing (pH too) Reversal of meds - see effect CXR - cardiomegaly / HF TTE assessment of valvular function ```

Answer 13

1deg/2deg1 asymptomatic = observe - regular ECGs and symptom education symptomatic = PPM/ICD/Cardioversion 2deg2/3deg = PPM/ICD/Cardioversion

Answer 14

Asymptomatic 2deg2/3deg = bad Asymptomatic = T2 Once on PPM = outlook is very good - few complications

Answer 15

Pre-excitation syndrome that results from accessory pathways, that run across the Tcuspid or MV annulus, connecting the ipsilateral ventricles.

Answer 16

EBSTEINS ANOMALY = the only strong RF | HCM, VSD, ASD, AF, MVP

Answer 17

Palpitations, dizziness, syncope, SOB, chest pain, SUDDEN CARDIAC DEATH

Answer 18

ECG - presence of q waves signifies bidirectional AP, intermittent pre-excitation Treadmill exercise - preexcitation disappears or intermittent Electrophysiological studies - locates the accessory pathway Echo - underlying disease

Answer 19

Includes a range of arterial syndromes that result from obstruction caused by atherosclerosis. (Less commonly arterial entrapment/embolsation)

Answer 20

Atherosclerotic RFs - smoking, dyslipidaemia, inactivity, low LDL, DM, hx CAD, DM, HTN

Answer 21

Symptoms - claudication in one leg, worse on standing/exercise, usually 1 leg, thigh/buttocks pain, relief on rest, ED, May be asymptomatic Signs - dec pulse, absent pulse, dry skin, loss of hair, haemosiderin deposition, thickened toe nails, underperfused, cold, poor healing, ulcers, muscle atrophy, dec sensation POSITIVE BUERGERS TEST

Answer 22

``` ABI < 90 (ratio of BPs) TBI < 0.6 Doppler - segmental increases in pulse pressure moving up the leg/ down moving down Segmental BP exam MRI/CT angiography ```

Answer 23

Formation of a blood clot in the deep veins of the leg, thigh, pelvis or abdomen that results in impaired blood flow and concomitant swelling and pain.

Answer 24

Stasis - immobility, recent surgery, anaesthesia, Obesity, long haul flights Coag - 5aLeiden, antithrombin def, protein c/s def, COCs, tamoxifen Injury - RTA FHx

Answer 25

Pain, swelling, redness, decreased ability to walk potentially Signs - >3cm swelling between legs, Pain on palpation, Pain on dorsiflexion

Answer 26

``` Scoring used to assess likelihood of DVT - 2+ = likely Score 1 for: (7total) Active cancer Recent surgery 3 day stay Immobile >3cm diameter Swelling of entire leg Prev DVT Localised pain ```

Answer 27

Roughly 3 months anticoagulation at target INR if warfarin Warfarin - target INR Dabigatran 150mg OD Rivaroxaban - 15 mg OD 1 week - inc to 20mg OD Extended thromboprophylaxis if unprovoked.

Answer 28

A heterogenous group of disease of the myocardium associated with mechanical or electrical abnormalities which usually exhibit inappropriate dilation or hypertrophy. Due to a variety of causes often genetic.

Answer 29

Pathological dilation of the myocardium with associated LV dysfunction in the absence of CAD. 30% familial, other causes include DM, Hyperthyroid, acromegaly

Answer 30

Cardiomyopathy with a restrictive physiology but normal wall thickness, associated with N/dec says/dec dias function

Answer 31

Cardiomyopathy that displays hypertrophy without dilatation. FHx sudden cardiac death SCD RFs - prev MI, sustained tachy, hypertrophy >30mm, unexplained syncope

Answer 32

Non specific. Palpation of apex beat stron and sustained can signify LVH Syncope Potential murmurs/bibasal fluids/oedema/JVP

Answer 33

ECG - may point to an aetiology FBC - TFTs - troponins - BNP - CKMB - U+Es CxR Echo - differentiates between dilated/restrictive/hypertrophy (Perform cardiac catheterisation if echo inconclusive) Cardiac MRI Latter three = used to exclude constrictive pericarditis

Answer 34

Inflammation of the pericardium that can be fibrous or effusive (haem/serous/purulent) associated with decreased diastolic filling. Constrictive pericarditis impedes normal diastolic filling and can be a medium to late complication of acute pericarditis. Pericarditis is the most common disease of the pericardium encountered in clinical practice. Symptoms include sharp, severe retrosternal chest pain worse with inspiration and a supine position. The classic physical finding is a pericardial friction rub. A low-grade fever is often present. Diagnostic signs include diffuse electrocardiographic ST elevations and at least a small pericardial effusion on echocardiography; blood tests generally suggest systemic inflammation. Treatment is directed at any underlying systemic disorder. Idiopathic or viral pericarditis responds to non-steroidal anti-inflammatory drugs and colchicine. Complications include chronic recurrent pericarditis, cardiac tamponade, and constrictive pericarditis.

Answer 35

``` STRONG Male 20s-40s, Viral - coxsackie, Parvo 19, VCZ, HIV, EBV, CMV, MUMPS, Rubella Bacterial - TB systemic - RhA, SLE Transmural MI Neoplasm Cardiac surgery Uraemia / dialysis 20-50s in general ``` WEAK Pericardial injury Mediastinal radiation

Answer 36

Chest pain - sharp, constant, relief on leaning forward, no ass with exercise Pericardial rub - 33% Fever, myalgia, RSHF

Answer 37

ECG - concave ST elevation globally, PR depression WCC ^ / CRP and ESR mild elevation / troponin raised mildly Pericardial fluid aspiration and culture Urea - if greater that 21.4 (but less than 60 which signifies CKD/RF) then ureamic associated is the cause. Echo - visualisation of effusion/ddxruleout MRI - """" Biopsy possible

Answer 38

Infection involving the endocardial surface of the valves, chordinae tendinae, sites of septal defects or the mural endocardium.

Answer 39

Strep Vivians = most common Others - S aureus (acute), enterococcus, actinobacillus, fungi Also HACEK organisms - haemophilia, actino, cardiobactum, echenella and kigella

Answer 40

IVDU (r sided), artificial valves, Hx endocarditis, congenital HD, septal defects, MVP, degenerative valvular disease, HCM,

Answer 41

Fever/chills, chest pain, night sweat, fatigue, malaise, weakness (think microemboli), SOB, headache Janeway lesions, ostlers nodes, roth spots, NEW MURMER, meningeal signs, cutaneous infarcts, back pain/chest pain, splinter haemorrhages

Answer 42

``` FBC - WCC + possible anaemia + ESR U+E - possible raised urea Echo - definitive gold standard - visualisation of vegetation/valve disease Blood cultures - bacteraemia/fungaemia ECG - prolonged PR Cardiac MRI possible ```

Answer 43

``` Supportive + aspirin + blood cultures Empirical rx = for strep as most abundant cause Strep = Benzylpenicillin + gentamicin Staph = Vanco Hacek/Enterococci - Ampicillin + gent ALL IV Fungal = consult a specialist ```

Answer 44

``` Pericardiocentesis to stop tamponade IV gentamicin 3mg/kg/day PPI NSAID Restrict exercise until normalisation ``` IF IDIOPATHIC/VIRAL - USE COLCHIDINE 0.5mg orally Recurrent tamponade = pericardectomy

Answer 45

A complication of necrosis characterised by the decay of body tissue. Two types - infections vs ischaemic

Answer 46

Infective - DM, IVDU, HIV, immunosuppression, trauma, malnutrition Ischaemic - thrombosis, prev thrombosis, smoking, atherosclerosis, renal disease, malignancy, trauma

Answer 47

Crepitus if c perf gas gangrene Oedema, erythema, ecchymosis, purpura, black Escher round outside, low grade fever and chills, pain, dec pulses in affected limbs

Answer 48

``` FBC - WCC ESR up Blood culture - possibly positive Doppler - if suspect ischaemic Plain X-ray - see gas if c perf CT chest - if malignancy expected Surgical exploration / biopsy ```

Answer 49

Backflow of blood across the mitral valve due to aberrations of the MV apparatus due to mechanical, infections, degenerative, traumatic or congenital causes.

Answer 50

Acute - RhF, papillary muscle rupture/dysfunction, IE, myocarditis Chronic - degenerative valve disease, MVP, mitral annular enlargement

Answer 51

Dyspnoea on exertion, lower limb oedema, orthopnoea, PNdyspnoea, palpitations, fatigue, sweating Signs = PAN SYSTOLIC MURMER, soft s1, s3 heart sound, displaced apex, pulmonary closure louder than aortic

Answer 52

TTEcho/cardiac MRI/TOE - visualisation of the structural/blood flow abnormalities Colour flow doppler - flow abnormalities ECG - underlying arrhythmias/precipitating causes

Answer 53

The pathological narrowing of the mitral valve orifice, predominantly due to (95%) Rheumatic fever, which results in fusion of the valve commissures and thickening of the leaflet.

Answer 54

RhF = 95% Hx Step infections untreated, Female SLE AMYLOID

Answer 55

Symptoms - dyspnoea, PND, orthopnoea, flushed cheeks, hoarseness, ascites, haemoptysis Signs - Mid diastolic murmer, loud s1, opening snap, possible AF (causes AF), JVP.

Answer 56

ECG - concomitant AF, RVH, right atrial enlargement TTE - visualisation of hockey stick shape CxR - if suspect RV failure - double right border, Kelley B lines Dynamic exercise testing - pressure increase with testing

Answer 57

Inflammation of the myocardium in the absence of acute or chronic ischaemia associated with CAD.

Answer 58

Recent infection, HIV, smallpox vaccine, SLE, sarcoidosis, scleroderma, cocaine, catecholamines, digoxin, thiazides and lithium

Answer 59

KEY ONE = viral syndrome common 2-3 weeks prior to symptoms onset, associated with fever, myalgia, resp symptoms and gastroenteritis Signs - rales, s3 gallop, pericardial rub, s3/s4 summation gallop, lymphadenopathy, JVP Symptoms - chest pain, dyspnoea, orthopnoea, fatigue, palpitations, tachycardia, peripheral hypoperfusion.

Answer 60

People often suspect MI - angriography and ECG say otherwise ECG - non spec st and t wave abnormalities Troponin - increased, CK CKMB inc but not as much Cardiac MRI shows areas of inflammation Echo - LV abnormalities Cxr - pulmonary infiltrates Endomyocardial biopsy = definitive but invasive Coronary angiography - N

Answer 61

Life threatening subcutaneous soft tissue infection that may spread to fascia but not into underlying muscle. T1 = polymicrobial more common T2 = 1

Answer 62

IVDU, immunosuppression, chronic skin breakages, recent trauma/surgery, chronic illness, VCZ

Answer 63

Anaesthesia over site/ severe pain over site Warmth over site N+V, tachypnoea, tachycardia, fever, palpitations Crepitus, Bullae, vesicles Grey discolouration of skin

Answer 64

``` FBC - WCC up with inc left shift ESR up, CK up ABG - possible acidosis / hypoxia BP - hypotension U+E possible dec Na+ MRI - extent of inflammation and soft tissue destruction/oedema along fascial plane ``` Surgical exploration

Answer 65

ACUTE Ruptured: ABC- Resus Urgent surgical repair - endovascular aneurysm repair (EVAR) is preferred, open also option Symptomatic In patients with symptomatic aortic aneurysm, surgical repair is indicated regardless of diameter Low dose aspirin Perioperative ABx ONGOING Incidental = surveillance <5.5cm Early open surgery for the treatment of smaller AAAs does not reduce all-cause or AAA-specific mortality. >5.5cm Repair of aneurysms ≥5.5 cm offers a survival advantage Endovascular aneurysm repair (EVAR) should be considered in patients who are unfit for open surgery EVAR is equivalent to open repair in terms of overall survival, although the rate of secondary interventions is higher for EVAR. ALL: CVS risk reduction - smoking cessation, BP control, statins, exercise. Postoperative surveillance can detect major endoleaks and aneurysm sac expansion. Risk of endoleak following endovascular aneurysm repair (EVAR) is 24% Five types of endoleak.

Answer 66

``` Abdominal compartment syndrome Ileus, IO, ischaemic colitis AKI Post-implantation syndrome Amputation due to limb ischaemia Spinal cord ischaemia Impaired sexual function Anastamotic pseudo-aneurysm Aortic neck dilation Graft infection Ureteric obstruction Functional gastric outlet obstruction Graft limb occlusion Endoleak Distal embolisation ```

Answer 67

Five-year survival rates after intact aneurysm repair average 60% to 75%. Those undergoing endovascular aneurysm repair (EVAR) are more likely to have a delayed complication and require re-intervention. The natural course involves slow and steady growth with ultimate progression to rupture. Most patients with rupture will not survive to reach the operating theatre. Given the morbidity and mortality associated with surgical intervention, repair is typically deferred until the theoretical risk of rupture exceeds the estimated risk of operative mortality. The majority of patients undergoing open repair remain without significant graft-related complications during the remainder of their lives (0.4% to 2.3% incidence of late graft-related complications).

Answer 68

AD The pain of aortic dissection usually manifests as acute, tearing chest and back pain (Stanford Type A) or tearing back pain (Stanford Type B). It may also migrate through the thorax or abdomen. Symptoms of stroke or visceral or acute limb ischaemia may be present. It may also migrate through the thorax or abdomen. Symptoms of stroke or visceral or acute limb ischemia may be present. Patients may be haemodynamically stable or in hypovolaemic shock. Occasionally, depressed mental status or neurological changes, limb pain, paraesthesias or weakness, paraplegia, or syncope are presenting symptoms. Infrequently (less than 10%), patients present atypically without pain.[4] There may be signs of heart failure, pericardial tamponade, or a left pleural effusion. Younger patients can present with a recent history of heavy lifting or cocaine use. Patients with connective-tissue disorders such as Marfan syndrome often present in their 30s, most often due to aortic root enlargement. Patients with Marfan syndrome with a normal diameter aorta may also be at risk

Answer 69

Haemodynamically unstable: ABCDE +/- Norad +/- dobutamine CONFIRMED Beta-blockade - labetalol, esmolol, metoprolol Analgesia - opioid - morphine sulfate 2-5mg iv every 5-30mins Diltiazem / nitroprusside TYPE A (or B with complications) - Open surgery (preferred) or EV-stent-graft repair TYPE B Endovascular stent-graft repair preferred - thoracic endovascular aortic repair (TEVAR) AGGRESSIVE BP MANAGEMENT POST SURGERY No patient is considered cured. Blood pressure control is continued after discharge from hospital. Beta-blockers and ACE inhibitors are usually required, with additional antihypertensives such as diuretics or calcium-channel blockers used if necessary.

Answer 70

ACUTE Inotropes - dopamine, dobutamine Vasodilators - nitroprusside AVReplacement Ongoing Mild-moderate chronic AR Asymptomatic with normal LV funciton - Patients with normal left ventricular function (ejection fraction >50%) do not require treatment and can be reassured. The outcome in these patients with no therapy is excellent. Symptomatic-or LV dysfunction - MILD - Medical therapy and surgery are not recommended, as an alternative cause is likely. Patient should be investigated for alternative causes for the symptoms of left ventricular dysfunction: for example, hypertension, CAD, or a cardiomyopathy. IF POSITIVE EXERCISE TEST Vasodilator Rx - nifedipine / hydralazine IF DECOMPENSATED but SURGICAL CANDIDATE - Patients with normal left ventricular (LV) function but an end-diastolic diameter >70 mm or an end-systolic diameter >50 mm have decompensated disease. TAVI OR OPEN REPAIR DEOCMPENSATED - not a surgical candidate Vasodilator /ACEi / TAVI

Answer 71

``` Operative mortality - 4% risk of death with AVR CHF Arrythmias IE Sudden death MI ```

Answer 72

Mortality is low (<0.4 % per year) in this group and therefore aortic valve replacement is not required, but patients do need to be monitored closely for developing symptoms or LV dysfunction. These patients are at risk of progressing to symptoms and/or LV dysfunction at the rate of 5% per year with a mortality of 0.2% per year In patients with more severe LV dilation (end-systolic diameter >50 mm or end-diastolic diameter >70 mm), there is an even higher risk of developing LV dysfunction (19%) or symptoms (10%). The outcome and prognosis of patients depends on the magnitude of LV function and symptoms. The 5-year survival in patients with normal LV function has been reported as 96% whereas that in patients with reduced LV function is 62%.

Answer 73

Open surgery requires placement of a prosthetic graft. The vascular surgeon accesses the affected portion of the aortic artery through an incision in your abdomen. Most patients stay in the hospital 4–10 days. Recovery time may be up to 3 months. Endovascular aneurysm repair (EVAR) is a less invasive treatment. Two small groin incisions are made. Guided by X-ray imaging, the vascular surgeon introduces a tiny device into the artery. The device is used to reinforce the artery wall and exclude the aneurysm. Most patients stay in the hospital 1–3 days. Recovery time is shorter than with open surgery.

Answer 74

AAAs are grouped into 3 sizes: small AAA – 3cm to 4.4cm across medium AAA – 4.5cm to 5.4cm across large AAA – 5.5cm or more across Scans are done: - every year if you have a small AAA - every 3 months if you have a medium AAA

Answer 75

Risks of endovascular surgery include: the graft leaking or slipping out of position – you'll have regular scans to check for this, and may need another operation to fix any problems a wound infection or infection of the graft heavy bleeding from your groin a blood clot, heart attack or stroke Risks of open surgery include: The risk of complications is generally higher than with endovascular surgery, and the hospital stay and recovery time is often longer. Around 95 to 97% of people make a full recovery. a wound infection or infection of the graft a blood clot heavy bleeding from your groin a heart attack or stroke erectile dysfunction or ejaculation problems in men The risk of graft problems is lower than with endovascular surgery. The graft will usually work well for the rest of your life and you will not normally need regular scans to check it.

Answer 76

``` Pericardial tamponade Aortic incompetence MI Anuerysm degeneration/rupture Regional ischaemia Left arm ischaemia / subclavian steal syndrome Endoleak ```

Answer 77

Syncope at presentation is usually associated with worse outcomes. A deadly triad of hypotension/shock (not syncope), lack of chest or back pain (presumably related to delay in diagnosis), and branch vessel involvement is also described. Left untreated, the natural history of proximal acute aortic dissection is of false channel rupture with fatal exsanguination in 50% to 60% of patients within 24 hours. Late degeneration of the dissected aorta into a false lumen aneurysm occurs in 30% to 50% of patients. Following treatment, patients remain at risk for further aneurysmal degeneration of remaining diseased aorta. The 10-year survival after surgery of ascending aortic dissection is 52%. Freedom from re-operation at both 5 and 10 years ranges from 59% to 95%. The 5-year survival after thoracic endovascular aortic repair (TEVAR) for acute type B aortic dissection is 81% Longer term outcomes after TEVAR for the treatment of either acute or chronic type B aortic dissection are currently unknown.

Answer 78

ALS and haemodynamic support LABETALOL - Intravenous beta blockade is essential to reduce the continued pulsatile force (dP/dt) on the already-thinned walls of the false channel. Analgesia = morphine sulfate Vasodilators - diltiazem CCB or nitroprusside SURGICAL REPAIR: Type A - open or EVAR Type B - EVAR ONGOING - AntiHTN

Answer 79

Acute AR is a surgical emergency Haemodynamic support with inotropic agents (dopamine and dobutamine) and vasodilators may be necessary for stabilisation before surgery. Aortic valve replacement or repair should be performed as soon as possible. Aortic valve repair is possible in selected patients but is only performed in specialist centres. Prosthetic valve patients are at high risk for thromboembolism and need antithrombotic therapy. The risk of bleeding must be weighed against the benefit of anticoagulation. ONGOING MILD-MOD CHRONIC Asymptomatic + normal LV function (EF>50%) -> reassurance Symptomatic or left ventricular dysfunction -> Medical therapy and surgery are not recommended, as an alternative cause is likely. Patient should be investigated for alternative causes for the symptoms of left ventricular dysfunction: for example, hypertension, CAD, or a cardiomyopathy. SEVERE CHRONIC Compensated -> reassure Exercise test positive -> vasodilator therapy with nifedipine or hydralazine Decompensated surgical candidate -> AVR or TAVI Decompensated but NOT surgical candidate -> ACEi or nifedipine or hydralazine

Answer 80

``` Operative mortality - There is a 4% risk of death with AVR, and the risk increases to 6.8% if performed along with CABG CHF Arrhythmias Infective Endocarditis Sudden death Myocardial Ischaemia ```

Answer 81

Mortality is low (<0.4 % per year) in this group and therefore aortic valve replacement is not required, but patients do need to be monitored closely for developing symptoms or LV dysfunction. These patients are at risk of progressing to symptoms and/or LV dysfunction at the rate of 5% per year with a mortality of 0.2% per year. In patients with more severe LV dilation (end-systolic diameter >50 mm or end-diastolic diameter >70 mm), there is an even higher risk of developing LV dysfunction (19%) or symptoms (10%). The 5-year survival in patients with normal LV function has been reported as 96% whereas that in patients with reduced LV function is 62%

Answer 82

Acute rheumatic fever is an autoimmune disease that may occur following group A streptococcal throat infection. It can affect multiple systems, including the joints, heart, brain, and skin. Only the effects on the heart can lead to permanent illness; chronic changes to the heart valves are referred to as chronic rheumatic heart disease. Without long-term penicillin secondary prophylaxis, acute rheumatic fever can recur, leading to cumulative damage to the cardiac valvular tissue. Acute rheumatic fever continues to cause a large burden of mortality and morbidity in developing countries. It is less common in developed countries but continues to be seen in indigenous communities and during outbreaks. No single test can diagnose acute rheumatic fever. Diagnosis is clinical and relies on the Jones criteria. The 5 major manifestations of acute rheumatic fever are carditis, arthritis, chorea, erythema marginatum, and subcutaneous nodules, of which the most common are carditis and arthritis. The Jones criteria were revised in 2015 to include separate criteria for low-risk and moderate- to high-risk populations. While all other manifestations of acute rheumatic fever resolve without sequelae, carditis can lead to chronic rheumatic heart disease. No treatment has been shown to alter the progression of acute rheumatic fever to chronic rheumatic heart disease. Secondary prophylaxis can improve the prognosis of established rheumatic valvular disease.

Answer 83

Primary episodes of acute rheumatic fever occur mainly in children aged 5 to 14 years and are rare in people over 30 years old. More than 2.4 million children have rheumatic heart disease worldwide; 94% of these are in developing countries. Worldwide there are over 330,000 new cases of acute rheumatic fever each year Recurrent episodes remain relatively common in adolescents and young adults but uncommon in those over 35 years old.

Answer 84

STRONG ``` Poverty Overcrowded living Fix D8/17B antigen positivity HLA DRB1, DQA1, and DQB1 haplotypes Genetic susceptibility ```

Answer 85

Carditis Arthritis Fever Subcut nodules Erythema marginatum = the 5 ``` Fever Joint pain - asymmetrical Recent group A streptococcal pharyngitis. Chest pain / SOB / palpitations / heart rub / murmur / CHF -> carditis Swollen joints Choreiform Pronator, spooning, milkmaids sign Subcutaenous nodules Pregnancy or OCP ```

Answer 86

ESR - H CRP - H WBC - H Blood cultures - -ve ECG - prolonged PR interval is a minor criterion of acute rheumatic fever Echo-cardiogram - may reveal morphological changes to the mitral and/or aortic valves; severity of regurgitation (mitral, aortic, and tricuspid); pericardial effusion if pericarditis present CXR - may demonstrate chamber enlargement and congestive cardiac failure Throat culture - growth of beta-haemolytic group A streptococci RAT for GAS - beta-haemolytic group A streptococci Anti-strep serology - above normal range (region dependent)

Answer 87

``` ABx - BenPen / erythromycin NSAIDs for arthritis HF - add diuretic + ACEi + corticosteroids With AF - amiodarone / digoxin Severe chorea - carbamezepine ``` If needed emergency valvular surgery - ie rupture of leaflet

Answer 88

Left untreated, acute rheumatic fever usually resolves within 12 weeks. With treatment, the symptoms of acute rheumatic fever usually resolve within several weeks, but cardiac inflammation lasts weeks to months. Around 30% to 50% of all patients with rheumatic fever will develop chronic rheumatic heart disease, and this risk increases to more than 70% if the initial attack is severe or if there has been at least one recurrence. Therefore, secondary prophylaxis to prevent recurrent attacks is very important, particularly as 75% of recurrences occur within 2 years of the first attack and more than 90% occur within the first 5 years.

Answer 89

Rheumatic heart disease

Answer 90

Focal atrial tachycardia (focal AT) is characterised as a rapid regular rhythm arising from a discrete area within the atria. It occurs in a wide range of clinical conditions, including catecholamine excess, digoxin toxicity, paediatric congenital heart disease, and cardiomyopathy. Focal AT is a regular tachycardia and is often confused with other regular supraventricular tachycardias, specifically re-entry tachycardias, sinus tachycardia, and atrial flutter. It may be difficult to diagnose by ECG alone. The diagnosis of focal AT is usually based on ECG, clinical history, and response to interventions such as vagal manoeuvres and adenosine. Occurs in the settings of coronary artery disease, congestive heart failure, cardiac surgery, catecholamine ingestion, digoxin toxicity, and alcohol dependency. Symptoms and signs include palpitations, fatigue, pre-syncope/syncope, chest pain. ECG shows a regular atrial tachycardia with P-wave morphology different from that in sinus tachycardia. Treatment consists of a trial of adenosine, withdrawal of the causative agent, or treatment of the underlying cause. For sustained tachycardias, cardiology consultation, class Ia/Ic or III anti-arrhythmic agents, and ablative therapy are appropriate. Complications include haemodynamic instability and congestive heart failure.

Answer 91

Focal atrial tachycardia is a relatively uncommon arrhythmia that occurs in all age groups and represents approximately 3% to 17% of the patients referred for supraventricular tachycardia ablation. There is no particular pattern in relation to sex or ancestry. Of the supraventricular tachycardias observed in children, atrial tachycardia accounts for 10% to 23% in children with normal hearts. Prevalence is higher among children with congenital heart disease or a history of cardiac surgery.

Answer 92

STRONG Substance misuse - alcohol, cocaine, amphetamines Digoxin toxicity Previous cardiac surgery WEAK Coronary artery disease Exacerbation of chronic lung disease

Answer 93

COMMON Hx cardiac disease Medications Palpitations Fatigue, weakness UNCOMMON ``` Chest pain SOB cough N+V Lightheadedness, syncope Rales Oedema ```

Answer 94

ECG - regular tachycardia that does not vary in rate; P waves may have an unusual axis, such as being inverted in the inferior leads Digoxin levels - may precipitate Theophylline levels - elevated if toxicity CXR - cardiomeg Electrolytes - hypokalaemia Toxicology screen Adenosine trial - NO response or transient slowing of ventricular rate TSH - suppressed if hyperthyroid CONSIDER Echo 24hr holter Electrophysiology study

Answer 95

IF UNDIFFERENTIATED -> adenosine. Transient slowing of the ventricular response rate with sustained atrial activity indicates flutter or focal AT. Lack of response to adenosine suggests either sinus tachycardia or focal AT, and strongly suggests that the rhythm is not re-entrant supraventricular tachycardia or atrial flutter. IF haemostable -> 1. BB or CCB, esmolol or diltiazem 2. Amiodarone 3. Flecainide / DC cardio version / cardio consult IF haemounstable -> DC cardioversion IF DIGOXIN EXCESS -> digoxin immune Fab Sustained or recurrent -> catheter ablation

Answer 96

Prognosis depends on the ability to control the arrhythmia. This is further influenced by the patient's age, underlying cause of the arrhythmia, tolerance of adverse effects of the chosen treatment, and comorbidities. Eventually, the rhythm is controlled in nearly all patients, but some may go through a period of trial and error, ultimately needing ablative therapy. This treatment may have to be repeated.

Answer 97

CHF Resistance to therapy Cardiomyopathy

Answer 98

Tamponade or effusion -> Pericardiocentesis Purulent -> Pericardiocentesis + ABx eg Vancomycin. + NSAID + PPI + Exercise restriction 2nd line = pericardectomy Pericardectomy is necessary in the presence of dense adhesions or loculations, persistent bacteraemia, recurrent tamponade, or progression to constrictive physiology. Non-purulent: 1st: NSAID + PPI + Colchicine + exercise restriction +/- anti-viral 2nd: Corticosteroids IF 2ndary to cause eg Underlying causes include tuberculosis (a common cause in the developing world), secondary immune processes (e.g., rheumatic fever, post-cardiotomy syndrome, post-MI syndrome), metabolic disorders (e.g., uraemia, myxoedema), radiotherapy, cardiac surgery, percutaneous cardiac interventions, systemic autoimmune disorders (e.g., rheumatoid arthritis, systemic sclerosis, reactive arthritis, familial Mediterranean fever, systemic vasculitides, inflammatory bowel disease), bacterial/fungal/parasitic infections, trauma, certain drugs, and neoplasms. Rx the causes Recurrent Disease may benefit from immunosuppressants

Answer 99

Pericardial effusion +/- tamponade | Chronic constrictive pericarditis

Answer 100

Major prognostic factors: Evidence of a large pericardial effusion (i.e., diastolic echo-free space >20 mm) High fever (i.e., >38°C [>100.4°F]) Sub-acute course (i.e., symptoms over several days without a clear-cut acute onset) Failure to respond within 7 days to a non-steroidal anti-inflammatory drug (NSAID). Minor prognostic factors: Pericarditis associated with myocarditis (myopericarditis) Immunosuppression Trauma Oral anticoagulant therapy.

Answer 101

A monophasic, biphasic, or triphasic pericardial friction rub is pathognomonic of acute pericarditis with virtually 100% specificity. However, the rub can come and go over hours so the sensitivity is based upon the frequency of cardiac auscultation. In a significant pericardial effusion, there can be signs of cardiac tamponade such as tachycardia, tachypnoea, pulsus paradoxus, and Beck's triad (hypotension, jugular venous distention, and distant heart sounds). The presence of high, spiking fevers indicates an infectious aetiology. A prodrome of myalgias and malaise may be reported, particularly in young adults

Answer 102

Occurs when one or more strands of myocardial fibres capable of conducting electrical impulses (known as accessory pathways [APs] or bypass tracts) connect the atrium to the ipsilateral ventricle across the mitral or tricuspid annulus. Conduction from the atrium reaches the adjacent ventricle earlier via the AP, and a part of the ventricle is pre-excited. The term 'Wolff-Parkinson-White (WPW) syndrome' is restricted to symptomatic patients with a typical ECG abnormality, whereas the term 'WPW pattern' signifies an asymptomatic patient with typical ECG abnormalities. Myocardial fibres extending from the atrium to the ipsilateral ventricle across the mitral or tricuspid annulus (accessory pathway) pre-excite the ventricle. WPW syndrome is restricted to symptomatic patients with a typical ECG abnormality; WPW pattern signifies an asymptomatic patient with typical ECG abnormalities. Patients often present with atrioventricular re-entrant tachycardia, less commonly atrial fibrillation, and, rarely, sudden cardiac death. Asymptomatic patients can either be monitored or screened to determine whether they have a 'high-risk' accessory pathway, in which case catheter ablation is typically performed. Screening to determine whether a patient has a high-risk accessory pathway is recommended for patients who have high-risk occupations, such as school bus drivers or pilots, and also for competitive athletes. Symptomatic patients usually undergo catheter ablation as first-line therapy. Pharmacological therapy can be considered for patients in whom catheter ablation fails and also for patients who prefer a non-invasive approach. Catheter ablation is highly effective with low risk and can be used either as initial therapy or for patients experiencing side effects or arrhythmia recurrences despite medical treatment.

Answer 103

The exact prevalence of ventricular pre-excitation is difficult to estimate because most patients are asymptomatic. The prevalence of WPW-pattern ECG in the general population is 0.1% to 0.3% The male-to-female ratio is 2:1.

Answer 104

STRONG Ebsteins anomaly WEAK ``` Hypertrophic cardiomyopathy Mitral valve prolapse Atrial septal defect Ventricular septal defect TOGA Coarctation of Aorta Dextrocardia Coronary sinus diverticular R+L aneurysms Cardiac rhabdomyomas Marfans syndrome Friedreichs ataxia FHx ```

Answer 105

COMMON ``` AVRT Dizziness SOB Chest pain AF AFlut ``` UNCOMMON SCD Syncope/pre-syncope Tachycardia

Answer 106

12-lead ECG - When an individual is in normal sinus rhythm, the ECG characteristics of WPW are a short PR interval (less than 120 milliseconds in duration), widened QRS complex (greater than 120 milliseconds in duration) with slurred upstroke of the QRS complex, and secondary repolarization changes (reflected in ST segment-T wave changes). Consider Echo - associated structural HD ie ebsteins, hypertrophic cardiomyopathy

Answer 107

Unstable: DC cardioversion Stable tachycardia: Carotid sinus massage or valsalva IV adenosine or AVN blockade or antiarrythmics - EG CCB, BB, amiodarone/flec Adenosine is preferred because of its ultra-short half life (<18 seconds). It can be used a second time if there is no response. It should be given in the veins closer to the heart. AV nodal blocking drugs (diltiazem, verapamil, metoprolol) can be used when there is no response or a recurrence after carotid sinus massage and adenosine. Anti-arrhythmic drugs (procainamide, ibutilide, amiodarone, flecainide) can be used when there is no response or a recurrence after carotid sinus massage, adenosine, and AV nodal blocking drugs. 3rd line - rapid atrial pacing 4th - DC cardioversion ONGOING ASYMPTOMATIC 1. Risk stratification and modification + Catheter ablation - Asymptomatic patients in specialised jobs with particular safety issues (e.g., airline pilot, school bus driver) can be considered for catheter ablation. Catheter ablation is also performed in asymptomatic patients who are found to have a 'high-risk' accessory pathway at the time of electrophysiology testing, showing high-risk antegrade conduction characteristics. SYMPTOMATIC: 1. Catheter ablation 2. Anti-arrhythmics Class I anti-arrhythmic agents (fleicanide or propafenone) are suitable for patients with no additional cardiac disease but cannot be used in people with coronary artery disease or structural heart disease. In patients with coronary artery disease or structural heart disease, class III anti-arrhythmic agents (sotalol, amiodarone, or dofetilide) may be used. QT interval must be determined prior to starting therapy with dofetilide as it is contraindicated if QTc is >440 msec (>500 msec in patients with ventricular conduction abnormalities).

Answer 108

SCD Catheter ablation complications: The common minor complications are related to the vascular access, catheter manipulation, transseptal atrial puncture for left-sided accessory pathway ablation, application of radiofrequency energy, and left-sided ablation: bleeding from vascular sites, haematomas, deep venous thrombosis, arteriovenous fistula, pseudoaneurysm at the arterial access sites, pneumothorax, infection.

Answer 109

Symptomatic patients with WPW syndrome should undergo catheter ablation as a first-line therapy. Catheter ablation has a high efficacy and low risk and can be used either as initial therapy or for patients experiencing side effects or arrhythmia recurrence during drug therapy. Patient preference is always an important consideration in these scenarios. Subjects with WPW pattern (asymptomatic patients), except for those with specialised jobs, should not be treated but can be monitored for symptoms.

Answer 110

WPW Asymptomatic people are diagnosed during routine screening ECGs.

Answer 111

Syncope is a syndrome characterised by a relatively sudden, temporary, and self-terminating loss of consciousness, associated with the inability to maintain postural tone, with rapid and spontaneous recovery. The transient loss of consciousness with syncope is the result of a temporary inadequacy of cerebral nutrient flow, most often triggered by a fall in systemic arterial pressure below the minimum needed to sustain cerebral blood flow. Neurally mediated reflex syncope (NMRS) refers to a group of related conditions or scenarios in which symptomatic hypotension occurs as a result of neural reflex vasodilation and/or bradycardia. Vasovagal syncope (VS) refers to a particular type of NMRS also known as the common faint. Neurally mediated reflex syncope (NMRS) refers to a group of related conditions or scenarios in which symptomatic hypotension occurs as a result of neural reflex vasodilation and/or bradycardia. Vasovagal syncope (VS) refers to a particular type of NMRS also known as the common faint. VS has many manifestations and is generally considered to encompass faints triggered by emotional upset, fear, and pain, as well as those occurring in less well-defined circumstances. Patient education is the foundation of treatment for most NMRS syndromes, including VS. Patients must be informed that, although reflex faints are almost never life-threatening, they tend to recur (often in clusters), and injury can result if preventive measures are not taken seriously. Strategies for reducing syncope recurrences in the long term comprise 1) physical techniques to improve orthostatic tolerance, 2) pharmacological interventions to prevent depletion of intravascular volume and/or enhance arterial and venous tone, 3) cardiac pacing to avert bradycardia.

Answer 112

Syncope is estimated to account for approximately 1% of accident and emergency department visits in Europe. Prevalence of syncope varies in the population: 15% of children (<18 years); 25% of a military population aged 17 to 26 years; 16% and 19%, respectively, in men and women aged 40 to 59 years; and up to 23% in a nursing home population aged >70 years.

Answer 113

Syncope has many possible causes, and these causes are commonly grouped in 3 main groups: neurally-mediated reflex syncopal syndromes, orthostatic, or cardiovascular. NMRS syndromes include vasovagal faint (common faint), carotid sinus syncope, situational faint, and glossopharyngeal and trigeminal neuralgia. These neurally mediated reflex faints, especially the vasovagal faint, are the most common causes of syncope overall and are particularly prevalent in people without evidence of underlying heart disease or vascular disease. In susceptible people, vasovagal syncope may be triggered by prolonged periods of upright posture; relative dehydration; excessively warm, closed-in environments; or extreme emotions. Common places for these events are churches, restaurants, and long queues. Transient insufficiency of global cerebral nutrient flow is the common thread underlying the mechanism of all forms of syncope.

Answer 114

STRONG Hx syncope Hx MI, arythmies, HF, cardiomyopathy Severe AS ``` WEAK Prolonged standing Emotional stress Dehydration Hypovolaemia Previous episode N+V Hx of severe pain ```

Answer 115

``` COMMON Low risk for adverse outcomes Hx recurrent faints Provocative factor Nausea Lightheadedness Pallor Diaphoresis Diminished vision/hearing Physical injury Fatigue after episode Palpitations Bradycardia Absence FHx of SCD ``` UNCOMMON Neuralgia

Answer 116

12-lead ECG - rules out AV block, bradycardia, asystole, long QT, bundle branch block Serum haemoglobin - normal; low in anaemia Plasma BG - normal; low in hypoglycaemia Serum B-HCG - Obtained to rule out differential diagnosis of syncope caused by pregnancy. Cardiac enzymes - Obtained to rule out myocardial infarction if there is clinical suspicion. D-Dimer - normal; elevated in pulmonary embolism Serum cortisol - Obtained to rule out differential diagnosis of syncope caused by adrenal insufficency. Urea + creatinine - Obtained to rule out differential diagnosis of syncope caused by dehydration.

Answer 117

VASOVAGAL 1. Patient education Patients need to recognise and respond to warning symptoms; such understanding not only reduces injury risk but also may ultimately enhance treatment compliance. Patients should be educated on the avoidance of triggers such as prolonged standing, warm environments, and coping with dental and medical settings. Patients susceptible to recurrent vasovagal faints should learn techniques for both aborting attacks and reducing susceptibility to future episodes (e.g., physical manoeuvres, hydration with electrolyte-rich fluids). These patients should also be taught the value and possible risks of increased salt intake. Physical Counter pressure Manoeuvres measures such as squatting, arm tensing, leg crossing, and leg crossing with tensing of the lower body muscles have proved useful. 2. Volume expansion with conventional measures Conventional approaches include increased dietary salt and electrolyte-rich sports drinks. The primary safety concern is initiation of hypertension. Fortunately, this is rare in younger patients, but it is a concern in older patients. Contraindications to increased salt and fluid intake include history of hypertension, renal disease, heart failure, or cardiac dysfunction. 3. Fludrocortisone 4. Mirodrine SITUATIONAL FAINT - Education re-triggers CAROTID SINUS SYNDROME 1. Education Patients with carotid sinus syndrome should avoid wearing tight collars or neckties. Scientific data are lacking for the role of physical techniques, volume expansion, fludrocortisone, and midodrine in patients with dominant vasodepressor or mixed carotid sinus syncope but may have been used in selected cases. 2. Cardiac pacing Cardiac pacing may play a role in the treatment of carotid sinus syndrome with documented bradycadia to prevent bradycardia-induced faint. However, patients may remain symptomatic because of persistent vasodepressor response.

Answer 118

Recurrences are common but often occur in clusters. Most therapies have not been studied adequately to ascertain effectiveness for preventing subsequent events. However, data for physical manoeuvre intervention and for the drug midodrine tend to support benefit. In the long term, the mortality risk is very low, but injury is a concern due to recurrent falls, especially in older people.

Answer 119

Injuries + fractures | Extradural or cerebral haemorrage due to trauma

Answer 120

Vasovagal syncope

Answer 121

The history suggested the possibility of carotid sinus syndrome (CSS). In the laboratory, carotid sinus massage was undertaken while the patient was in the upright posture on a tilt table. The massage induced 10 seconds of asystole with near loss of consciousness. A dual-chamber pacemaker was implanted on the basis of a presumptive diagnosis of CSS; there was no recurrence of syncope during the next year. This patient has had no further faints but occasionally becomes dizzy when turning his head abruptly (CSS).

Answer 122

The history suggested the possibility of carotid sinus syndrome (CSS). In the laboratory, carotid sinus massage was undertaken while the patient was in the upright posture on a tilt table. The massage induced 10 seconds of asystole with near loss of consciousness. A dual-chamber pacemaker was implanted on the basis of a presumptive diagnosis of CSS; there was no recurrence of syncope during the next year. This patient has had no further faints but occasionally becomes dizzy when turning his head abruptly (CSS).

Answer 123

Aortic stenosis (AS) represents obstruction of blood flow across the aortic valve due to pathological narrowing. It is a progressive disease that presents after a long subclinical period with symptoms of decreased exercise capacity, exertional chest pain (angina), syncope, and heart failure. Obstruction of blood flow across the aortic valve due to aortic calcification. Presentation includes shortness of breath with exertion, angina, or syncope. Characteristic murmur is systolic, mid-to-late peaking with a crescendo-decrescendo pattern, and radiates to the carotids. Doppler echo is essential to the diagnosis and will show a pressure gradient across the stenotic aortic valve. Surgical aortic valve replacement was the only effective therapy for aortic stenosis for over 50 years. However, with the advent of transcatheter valve therapies, patients and physicians have more options. Following valve replacement, patients are subject to the complications of prosthetic valves.

Answer 124

AS is the most common valvular disease in the US and Europe and is the second most frequent cause for cardiac surgery. It is largely a disease of older people, and patients typically present in the seventh or eighth decade of life. Although the prevalence of AS is only 0.2% in adults aged 50 to 59 years, estimates increase to 1.3% in patients aged 60 to 69 years, and up to 9.8% in patients aged 80 to 89 years. Overall, AS is present in 2.6% of adults older than 75 years of age. It is preceded by aortic sclerosis (defined as aortic valve thickening without flow limitation), often suspected by the presence of an early-peaking, systolic ejection murmur, and confirmed by echocardiography. Nearly 25% of people ≥65 years have aortic sclerosis, and nearly 17% of people with aortic sclerosis will progress to AS in their lifetime. The average time from diagnosis of aortic sclerosis to the development of moderate and severe AS is 6 and 8 years, respectively. Patients with bicuspid valves and AS present two decades earlier on average than patients with trileaflet valves.

Answer 125

Calcification of normal trileaflet valves is the most common cause of AS in adults and accounts for as many as 80% of cases in the US and Europe. Several risk factors have been associated with aortic sclerosis including smoking, hypertension, diabetes, LDL-cholesterol, and elevated C-reactive protein. Retrospective studies have shown that high LDL-cholesterol levels and smoking are associated with progression to AS, but causality has not been confirmed. Congenitally bicuspid valves account for the majority of the remainder of cases. Patients with coarctation of the aorta and Turner's syndrome have a higher incidence of bicuspid valves. Rheumatic heart disease has historically been an important cause of AS, but due to improvements in treatment, it is now uncommon in industrialised countries. Rheumatic heart disease remains prevalent in developing nations. Other circumstances including connective tissue diseases, radiotherapy, and hyperlipoproteinaemia syndromes can cause AS, but these are unusual consequences of rare conditions. Chronic kidney disease is associated with abnormal calcium homeostasis, and it has been shown that AS progresses faster in patients with this condition.

Answer 126

``` STRONG Age >60 Bicuspid AV Rheumatic HD CKD ``` WEAK Radiotherapy High LDL Hyperlipoproteinaemia

Answer 127

Dyspnoea Chest pain Syncope Ejection systolic murmur - A systolic murmur ≥3/6 is present with a crescendo-decrescendo pattern that peaks in mid-systole and radiates to the carotid. The murmur is loudest at the right upper sternal border. S2 diminished - With progression of AS, the aortic component of the second heart sound becomes soft or absent due to decreased mobility of the aortic valve leaflets. Aortic valve closure is delayed and often coincides with pulmonic valve closure, producing a single second heart sound. UNCOMMON Carotid parvus et tarsus - The carotid upstroke is frequently delayed and diminished in severe AS (parvus et tardus). Paradoxical split S2 - With more severe stenosis, aortic valve closure may become so delayed that it follows pulmonic valve closure during expiration, producing the paradoxically split S2. Gallavardins phenomenon - A musical-quality, holosytolic murmur is present at the apex of the heart that occurs in older patients with calcific AS, which may mimic mitral regurgitation. Bleeding - Some patients may develop an acquired von Willebrand deficiency that predisposes to bleeding and is caused by turbulent flow across the stenotic valve.

Answer 128

TTE including doppler - elevated aortic pressure gradient; measurement of valve area and left ventricular ejection function ECG - may demonstrate left ventricular hypertrophy and absent Q waves, AV block, hemiblock, or bundle branch block CONSIDER Cardiac MRI / catheterisation - elevated aortic pressure gradient ECG stress testing - if asymptomatic Dobutamine stress echo

Answer 129

CLINICALLY UNSTABLE Medical therapy OR Transcatheter aortic valve replacement (TAVR) or balloon valvuloplasty. SURGICAL CANDIDATE 1. AVR or TAVR + Long term anticoagulation if mechanical + IE prophylaxis before dental procedures: Antibiotic prophylaxis for the prevention of infective endocarditis should be considered in patients with prosthetic cardiac valves, including transcatheter-implanted prostheses and homografts, before dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa.[ MEDICAL Rx There is no medical treatment that has been shown to improve survival in patients with aortic stenosis. Medical therapy should thus target comorbid conditions such as CAD, hyperlipidaemia, hypertension, and heart failure. AS patients with heart failure symptoms are frequently treated with vasodilators such as ACE inhibitors and diuretics, though caution is required to avoid complications such as hypotension and syncope. NON SURGICAL CANDIDATE Balloon valvuloplasty A reasonable palliative option for patients who are highly symptomatic yet too high-risk to undergo operative repair, and where transcatheter aortic valve replacement is not available or contraindicated. A percutaneous procedure, done in the cardiac catheterisation laboratory, in which a balloon is forcefully inflated across the aortic valve to relieve stenosis. Re-stenosis rates are high at 6 months, and there is no confirmed improvement in mortality. Patients do have symptomatic relief, and there is some evidence that serial dilations may improve survival. May occasionally be used as a bridge to more definitive therapy (e.g., aortic valve replacement surgery) if this is deemed to be possible at a later date.

Answer 130

For those patients with mild or moderate stenosis, the aortic valve area decreases on average by 0.1 cm^2/year and the mean gradient increases by 7 mmHg annually. It is recommended that patients with moderate AS have an echocardiogram every 1 to 2 years, and those with mild AS have one every 3 to 5 years. The onset of symptoms is a significant milestone and portends a poor prognosis, with an average survival of only 2 to 3 years without surgery. Between 8% and 34% of symptomatic patients die suddenly. Patients who survive surgery have near-normal life expectancy, with relative survival at 5, 10, and 15 years of 99%, 85%, and 82%, respectively.

Answer 131

``` Acute congestive HF SCD IE Thrombosis due to mechanical valve Re-stenosis Valve dehiscence - Suspected when patients develop new signs of heart failure or have a diastolic murmur of aortic regurgitation. ```

Answer 132

Other presentations AS is a progressive disease that presents after a long subclinical period with symptoms of chest pain, syncope, and heart failure. While the most common complaint is dyspnoea with exertion, patients also frequently note syncope or chest pain that may be identical to that caused by CAD. Many cases of AS are diagnosed during the subclinical phase while a murmur noted on physical examination is being investigated. Even with severe AS, patients may be truly asymptomatic. A careful history is important to determine if the patient has altered his or her habits in response to slowly worsening stenosis.

Answer 133

Nec Fasc: Surgical debridement + ICU + Empirical BS-ABx +/- irrigations Tailor ABx to sensitivities The addition of IVIG may also be considered for treatment of streptococcal toxic shock syndrome, although data on efficacy are conflicting GAS GANGRENE Surgical debridement + Empirical BS-ABx Hyperbaric Oxgen therapy ISCHAEMIC GANGRNE IV heparin bolus + infusion Surgical revascularisation / amputation The absence of rest pain, sensory loss, and muscle weakness helps differentiate a viable limb from a threatened limb. Phlegmasia cerulea dolens, a rare condition in which there is total or near-total obstruction of venous drainage from a limb, may be treated by intravenous thrombolytic therapy to help prevent the onset and progression of venous gangrene.

Answer 134

``` Sepsis Shock Acute renal failure Haemolysis Loss of Limb DIC ```

Answer 135

Mortality from necrotising fasciitis properly treated with surgery plus antibiotics has been estimated to be between 10% and 40% Before the availability of antibiotics, gas gangrene was usually fatal. However, with aggressive antibiotic therapy and aggressive surgical therapy this is no longer the case In patients with critical leg ischaemia, 50% to 60% will undergo some form of surgical or endovascular procedure (although in some specialist units the figure may be nearer 90%). Primary amputation rates range from 10% to 40%. Mortality rate in these patients with standard therapy is around 20% at 1 year, and between 40% and 70% at 5 years. However, 95% of patients who present with ischaemic gangrene, and 80% of those presenting with rest pain, are dead within 10 years.

Answer 136

gangrene In patients with conditions such as post-surgical infection, gunshot or knife wounds, or diabetes, the early signs and symptoms of infection may not be apparent or may be misinterpreted. For example, in patients with diabetes, pain may be reduced or absent due to neuropathy at the site of infection. In surgical patients, people with traumatic injuries, and postnatal patients, pain may be assumed to be part of the normal convalescence rather than due to acute infection. Delay in diagnosis may allow the disease to progress to later stages before treatment is initiated.[5] In immunocompromised patients, atypical organisms may be involved in the formation of gangrene. For instance, mucormycotic gangrenous cellulitis may occur in patients with diabetes mellitus or patients receiving immunosuppressive therapy. Spores of Rhizopus species may contaminate occlusive dressings. Apophysomyces elegans may infect patients with Pseudomonas bacteraemia or with thermal burns.[1] Patients with chronic renal disease have extensive calcification of the small arteries of subcutaneous tissue and marked elevation of calcium-phosphate product (calciphylaxis), which can contribute to the development of gangrene by reducing blood supply to the tissues.[12]

Answer 137

gangrene In patients with conditions such as post-surgical infection, gunshot or knife wounds, or diabetes, the early signs and symptoms of infection may not be apparent or may be misinterpreted. For example, in patients with diabetes, pain may be reduced or absent due to neuropathy at the site of infection. In surgical patients, people with traumatic injuries, and postnatal patients, pain may be assumed to be part of the normal convalescence rather than due to acute infection. Delay in diagnosis may allow the disease to progress to later stages before treatment is initiated.[5] In immunocompromised patients, atypical organisms may be involved in the formation of gangrene. For instance, mucormycotic gangrenous cellulitis may occur in patients with diabetes mellitus or patients receiving immunosuppressive therapy. Spores of Rhizopus species may contaminate occlusive dressings. Apophysomyces elegans may infect patients with Pseudomonas bacteraemia or with thermal burns.[1] Patients with chronic renal disease have extensive calcification of the small arteries of subcutaneous tissue and marked elevation of calcium-phosphate product (calciphylaxis), which can contribute to the development of gangrene by reducing blood supply to the tissues.[12]

Answer 138

Although the exact incidence and prevalence of MR is unknown it has been suggested that the prevalence probably exceeds 5,000,000 worldwide

Answer 139

Acute MR: Emergency surgery + preoperative diuretics Severe acute MR associated with hypotension is an indication for intra-aortic balloon counterpulsation. The intra-aortic balloon pump consists of a cylindrical balloon that sits in the aorta and actively deflates in systole, increasing forward blood flow by reducing afterload, and actively inflates in diastole, increasing blood flow to the coronary arteries. The balloon is inflated with helium by a computer-controlled, ECG-linked mechanism. Left ventricular ejection fraction >60% and/or left ventricular end-systolic diameter <45 mm: 1. ACEi + BB Left ventricular ejection fraction 30% or more ``` Valvuloplasty OR Annuloplasty OR Mechanical valve + anticoag OR Bioprosthesis ``` ``` + Medical: There is no specific accepted medical treatment for chronic management of MR. The treatment of choice is surgery for patients with chronic MR and New York Heart Association class II, III, and IV symptoms. All such patients should be treated with ACE inhibitors, beta-blockers, and diuretics. ```

Answer 140

There is a 1% per-year risk of reoperation after mitral valve repair or replacement. The risk of mortality is lower with mitral valve repair than with replacement. MR may remain asymptomatic for many years. Progression of mitral valve disease is variable and depends on progression of lesions or mitral annulus size. Severe MR also has a variable prognosis, but most experts agree that left ventricular (LV) dysfunction will occur within 6 to 10 years. For flail posterior mitral leaflet at 10 years, 90% of the patients are dead or require MV operation.

Answer 141

``` AF Pulmonary hypertension Post-op stroke Prosthesis stenosis LV dysfunction -> CHF Recurrent MR Prosthesis dysfunction Post op endocarditis ```

Answer 142

``` STRONG Mitral valve prolapse Rheumatic HD Infective endocarditis Hx cardiac trauma Hx MI Hx IHD Hx CHD LV dysfunction Hypertrophic cardiomyopathy Anorectic / dopaminergic drugs ```

Answer 143

CHRONIC MR Acute MR is serious and rare. It may occur in the setting of acute MI and leads to high left atrial pressure and pulmonary oedema secondary to reduced left atrial compliance. It usually presents as a sudden and marked increase in CHF symptoms, with weakness, fatigue, dyspnoea, and sometimes respiratory failure and shock. It is usually associated with peripheral vasoconstriction, pallor, and diaphoresis. Occasionally no murmur is heard, because the lack of left atrial compliance leads to equalisation of pressures between the left atrium and ventricle midway through systole. Chronic MR is associated with a laterally displaced apical impulse (with left ventricular dilation), diminished S1, with or without S3, with or without right ventricular heave, and palpable P2 (if pulmonary hypertension has developed).

Answer 144

MR Acute MR is serious and rare. It may occur in the setting of acute MI and leads to high left atrial pressure and pulmonary oedema secondary to reduced left atrial compliance. It usually presents as a sudden and marked increase in CHF symptoms, with weakness, fatigue, dyspnoea, and sometimes respiratory failure and shock. It is usually associated with peripheral vasoconstriction, pallor, and diaphoresis. Occasionally no murmur is heard, because the lack of left atrial compliance leads to equalisation of pressures between the left atrium and ventricle midway through systole. Chronic MR is associated with a laterally displaced apical impulse (with left ventricular dilation), diminished S1, with or without S3, with or without right ventricular heave, and palpable P2 (if pulmonary hypertension has developed).

Answer 145

Mitral stenosis is a narrowing of the mitral valve orifice, usually caused by rheumatic valvulitis producing fusion of the valve commissures and thickening of the valve leaflets. Fusion of the leaflet commissures reducing orifice area. Usually occurs as a consequence of rheumatic fever. Causes decreased filling of the left ventricle, while simultaneously increasing left atrial pressure, producing the syndrome of heart failure. As disease progresses, pulmonary hypertension and right heart failure occur. Mild disease can be treated symptomatically with diuretics. Moderate to severe disease requires mechanical correction of the valve obstruction by valvotomy, valve repair, or valve replacement.

Answer 146

Most cases of mitral stenosis are caused by rheumatic fever. While rheumatic fever is now very rare in developed nations, it remains epidemic in much of the world. In the US rheumatic fever occurs in about 2 per 100,000 people, whereas in the developing world the attack rate may be 50 times that. Although the attack rate of rheumatic fever for both sexes is similar, it is primarily women who develop mitral stenosis, with a frequency of about 3 times that of men.

Answer 147

Rheumatic fever leading to rheumatic heart disease is the cause of mitral stenosis in more than 95% of cases. Rarer causes of mitral stenosis include congenital deformity of the valve, the carcinoid syndrome, use of ergot and/or serotogenic drugs such as fenfluramine, SLE, mitral annular calcification due to ageing, and amyloidosis. It is thought that some M antigens are held in common by the heart and some strains of group A streptococci.

Answer 148

STRONG Strep infection Female WEAK Ergot medications - methysergide or ergotamine Serotogenic meds SLE Amyloidosis Bronchial carcinoid syndrome - Carcinoid syndrome typically causes right heart valve disease (tricuspid and pulmonary valve) unless bronchial carcinoid is present, in which case left heart lesions may occur.[

Answer 149

``` COMMON RFs Hx RhF Dyspnoea Orthopnoea Opening snap Diastolic murmur Loud P2 Neck vein distension. ``` ``` UNCOMMON Paroxysmal nocturnal dyspnoea Haemopytsis Hoarseness Peripheral oedema Ascites ``` COMMON 40-50yo Loud S1 UNCOMMON AF pulse Flushed cheeks

Answer 150

ECG - This non-specific test is performed at baseline and again if there is a change in the patient's rhythm. May show - atrial fibrillation; left atrial enlargement; right ventricular hypertrophy CXR - may show double right heart border indicating an enlarged left atrium; prominent pulmonary artery; Kerley B lines TTE - When the typical findings of mitral stenosis are discovered on physical examination, an echocardiogram is the definitive test to confirm the diagnosis and to quantitate the severity of the disease. - > hockey stick-shaped mitral deformity

Answer 151

IN GENERAL Asymptomatic -> No therapy Severe -> 1. Loop diuretic +/- Balloon valvotomy OR open valve commissurotomy OR valve replacement Mechanical relief from valve obstruction is often the only effective remedy for severe symptoms and for pulmonary hypertension. Percutaneous balloon valvotomy is the treatment of choice when valve anatomy is suitable for this procedure. Each of the following is graded on a severity score of 1 to 4: valve mobility, calcification, leaflet thickening, and sub-valvular apparatus distortion. Thus a minimum score of 4 and a maximum of 16 are possible. Valves with a score of less than 9 are usually considered optimal for balloon valvotomy. In patients with higher valve scores, surgery to perform open valve commissurotomy or valve replacement is undertaken.

Answer 152

With recognition of the proper use of anticoagulants and of the proper timing of mechanical intervention, prognosis is excellent. In one study, the 12-year survival was 82%. However, for patients with advanced symptoms and/or pulmonary hypertension treated medically the average survival is about 3 years

Answer 153

AF Stroke Warfarin induced haemorrhage IE

Answer 154

mitral stenosis Other presentations May present with atrial fibrillation, heart failure, or systemic embolism.

Answer 155

mitral stenosis Other presentations May present with atrial fibrillation, heart failure, or systemic embolism.

Answer 156

If AI cause -> require steroids LV dysfunction -> ARB or ACEi (Improve cardiac output and haemodynamics by arterial vasodilatation) +/- BBs +/- oral vasodilators +/- Over-diuresis can cause acute renal failure. Volume status should be monitored. Diuretic therapy may also precipitate hypokalaemia or hypomagnesaemia +/- Aldosterone antagonists Refractory cardiogenic shock: adult patients - intra-aortic balloon pump / left ventricular assist device

Answer 157

Patients who present with fulminant myocarditis surprisingly tend to have better outcomes than those who present with a clinically milder acute myocarditis. An 11-year study of patients presenting with myocarditis showed a 93% survival free of heart transplantation in patients with fulminant myocarditis as opposed to 45% in patients who presented with acute myocarditis. Despite modest improvement in mortality with immunosuppressive therapy, patients with giant cell myocarditis have the worst outcomes with a median survival of 5.5 months from the onset of heart failure symptoms. Patients presenting with chest pain and ECG changes similar to those seen in ST-segment elevation myocardial infarction have almost uniform recovery without any residual cardiac dysfunction

Answer 158

``` AF Ventricular tachyarrythmias DCM SCD MOF ```

Answer 159

Other presentations The clinical manifestation of myocarditis is highly variable and ranges from asymptomatic ECG abnormalities to cardiogenic shock.[11][12] When cardiac involvement manifests clinically, it typically occurs 7 to 10 days after a systemic illness. Chest pain occurs in 35% of patients and may be typical, atypical, or positional in nature.[4] Occasionally, patients present with ischaemic-sounding chest pain and ST-segment elevations on ECG that mimic acute coronary syndrome. Left ventricular dysfunction tends to be global instead of regional, and coronary angiography is normal.[13] Rarely, patients with myocarditis present with sudden cardiac death, usually due to ventricular arrhythmias.

Answer 160

Other presentations The clinical manifestation of myocarditis is highly variable and ranges from asymptomatic ECG abnormalities to cardiogenic shock.[11][12] When cardiac involvement manifests clinically, it typically occurs 7 to 10 days after a systemic illness. Chest pain occurs in 35% of patients and may be typical, atypical, or positional in nature.[4] Occasionally, patients present with ischaemic-sounding chest pain and ST-segment elevations on ECG that mimic acute coronary syndrome. Left ventricular dysfunction tends to be global instead of regional, and coronary angiography is normal.[13] Rarely, patients with myocarditis present with sudden cardiac death, usually due to ventricular arrhythmias.

Answer 161

Peripheral arterial disease (PAD) includes a range of arterial syndromes that are caused by atherosclerotic obstruction of the lower-extremity arteries. The most common cause is atherosclerosis. Most patients are asymptomatic. Patients require aggressive risk factor control. Long-term patency of lower-extremity revascularisation should be monitored with a surveillance programme. First line of therapy for patient with lifestyle-limiting claudication is a supervised 12-week exercise programme and medication. Revascularisation should be considered if these therapies fail. Death from a cardiac cause has a relative risk of 3 to 6 in patients with peripheral vascular disease.

Answer 162

The prevalence of PAD increases with age, beginning after 40 years of age. PAD, as defined by abnormal ankle brachial index of <0.90, was prevalent in 1.0% among a 40- to 49-year-old population. In the age group of 50 to 59 years the prevalence was around 3.0% to 5.0%, in the age group of 60 to 69 years it was around 5.0%, and in those over the age of 80 years it was >20.0% (and even >25.0% in men). A US study found black people to have a higher prevalence of PAD, even after accounting for other risk factors, and Asian people have a lower prevalence compared with white people. In high-income countries, the prevalence of PAD is equal between women and men.

Answer 163

PAD is most commonly caused by atherosclerosis. Rarer causes of claudication are aortic coarctation, arterial fibrodysplasia, arterial tumour, arterial dissection, arterial embolism, thrombosis, vasospasm, and trauma. Other rare causes are Takayasu's arteritis, temporal arteritis, thoracic outlet obstruction, and Buerger's disease. Adventitial cystic disease, occluded limb aneurysms, popliteal artery entrapment, iliac endofibrosis, ergot toxicity, radiation fibrosis, and retroperitoneal fibrosis can also cause PAD. These can usually be distinguished based on clinical history and examination.

Answer 164

STRONG ``` Smoking DM HTN Hyperlipidaemia Age >40 Hx CAD or CeVD Reduced exercise ``` WEAK ``` Elevated CRP Hyperhomocysteinaemia Vasculitis Arterial fibrodysplasia Trauma ```

Answer 165

COMMON ASYMPTOMATIC Intermittent claudication Relief with rest Diminished pulse UNCOMMON SO Severe pain with numbness, weakness, pallor +reduced temp = CRITICAL LIMB ISCHAEMIA The classic 6 signs of acute limb ischaemia are: pain, paralysis, paraesthesias, pulselessness, perishingly cold, and pallor. OTHER ``` ED Pain worse in one leg Pain at rest Gangrene Non-healing ulcer Atrophy Dependent rubor Pallor with leg elevation Loss of hair on foot Thickened toe nails Shiny/scaly skin Pale Nerve loss ```

Answer 166

ABI - ABI ≤0.90 Sensitivity of 95% and specificity of 100%. May not be accurate in patients with non-compressible arteries (e.g., patients with long-standing diabetes mellitus, or renal patients on dialysis). Patients with either severely stenotic or totally occluded arteries may also have normal ABI if there is abundant collateral system present. TBI <0.6 [TOE] The TBI should be used to establish the diagnosis of PAD in patients in whom lower extremity PAD is clinically suspected, but in whom the ABI test is not reliable due to non-compressible vessels (usually patients with long-standing diabetes, advanced age, or renal patients on dialysis). Segmental pressure Duplex USS Pulse volume recording Continuous wave doppler

Answer 167

ACUTE LIMB ISCHAEMIA 1. Urgent assessment for revascularisation or amputation Non-viable limb: these patients will have signs of tissue loss, nerve damage, and sensory loss and will require amputation. Viable limb: these patients will have no significant tissue loss, nerve damage, or significant sensory loss. Patients should have arterial anatomy defined and undergo revascularisation. + anti-platelet + analgesia + anticoagulation with hep IF VIABLE ->. endovascular or surgical revascularisation or intra-arterial thrombolysis IF NOT -> Amputation NON-LIFE LIMITING CLAUDICATION 1. Antiplatelet therapy 2. Exercise 3. RF modification LIFE LIMITING CLAUDICATION 1. Antiplatelet therapy 2. Exercise 3. RF modification 4. Symptom relief - pentoxifylline, cilostazol, or naftidrofuryl. 5. Revascularisation Endovascular revascularisation treatment may include either percutaneous transluminal balloon angioplasty (PTA) or bypass surgery. CRITICAL CHRONIC LIMB ISCHAEMIA SAME BUT: Patients with critical limb ischaemia who are unsuitable for revascularisation will be those unable to walk before the episode of critical limb ischaemia, and who have a limited life expectancy. AMPUTATION

Answer 168

A more rapid deterioration in ABI carries a worse prognosis for all-cause mortality and cardiovascular disease mortality, independent of baseline ABI and potential confounding variables. At 1 year, 25% of patients with critical limb ischaemia will have died and 30% will have undergone amputation. At 5 years, more than 60% of patients with critical limb ischaemia will have died.

Answer 169

Leg/foot ulcers Gangrene Permanent limb weakness/numbness Permanent limb pain

Answer 170

peripheral arterial disease Other presentations Patients with a previously diagnosed history of PAD can also present with sudden onset of leg numbness and paralysis. Non-healing leg or foot ulcers may also be the first presentation of PAD.

Answer 171

Idiopathic pulmonary arterial hypertension (IPAH) is a disease of the small pulmonary arteries characterised by vascular proliferation and remodelling. It results in a progressive increase in pulmonary vascular resistance (PVR) and, ultimately, right ventricular failure and death. It is defined by a mean pulmonary arterial pressure ≥25 mmHg at rest with pulmonary capillary wedge pressure ≤15 mmHg and PVR >3 Woods units, without a known cause. A rare, frequently fatal disease, most commonly seen in women, that is best managed in centres with expertise in pulmonary hypertension. Presenting symptoms and signs are non-specific and include dyspnoea on exertion, fatigue, and a loud pulmonary component of the second heart sound. Diagnosis of exclusion. Transthoracic Doppler echocardiography and right heart catheterisation can diagnose pulmonary hypertension. Laboratory tests and imaging studies can rule out known causes of pulmonary hypertension. General supportive therapy includes oral anticoagulants, diuretics, supplemental oxygen, and digoxin. Targeted treatment options include parenteral, inhaled, and oral prostanoids, oral endothelin receptor antagonists, oral phosphodiesterase type-5 inhibitors, the soluble guanylate cyclase stimulator riociguat, and the selective prostacyclin IP receptor agonist selexipag. Prognosis is not good, as most patients eventually develop right ventricular failure.

Answer 172

Estimated prevalence of 15.0 cases per million adult inhabitants and incidence of 2.4 cases per million adult inhabitants per year

Answer 173

Mutations in the gene encoding bone morphogenetic protein receptor type 2 (BMPR2), a member of the transforming growth factor-beta (TGF-beta) superfamily, are responsible for familial cases of pulmonary arterial hypertension. These mutations lead to changes in intracellular signalling pathways that result in proliferative and anti-apoptotic effects in the pulmonary vasculature. Other predisposing genetic factors include mutations and variants in the genes; ACVRL1 (encoding activin receptor-like kinase 1, a type 1 receptor for TGF-beta family proteins); ENG (encoding endoglin, a glycoprotein); SMAD9 (encoding a SMAD family protein, which transduces signals from TGF-beta family members); CAV1 (encoding caveolin 1 protein); and KCNK3 gene (encoding a potassium channel) The main vascular changes are vasoconstriction, smooth-muscle cell and endothelial-cell proliferation, and thrombosis.

Answer 174

Idiopathic pulmonary arterial hypertension

Answer 175

``` STRONG FHx Female BMPR2 mutation Appetite suppressants ``` WEAK Drugs+toxins

Answer 176

``` COMMON Age 20-50 Female Dyspnoea Loud P2 (93%) TR murmur (40%) Fatigue Peripheral oedema Cyanosis ``` ``` UNCOMMON Syncope Stimulant use Chest pain Near syncope Early diastolic murmur in P area (PR) Jugular vein distension ```

Answer 177

CXR - attenuated peripheral vascular markings ('pruning'), enlarged pulmonary artery shadows, and opacification of the retrosternal space on the lateral view ECG - RVH, right axis deviation, right atrial enlargement TT-doppler - assess TR GOLD RH catheterisation - mean pulmonary arterial pressure >25 mmHg at rest or >30 mmHg with exercise, with pulmonary capillary wedge pressure ≤15 mmHg and pulmonary vascular resistance (PVR) >3 Wood units ANA - Low titre ANA can be seen in up to 40% of patients PFTs - normal or mild reductions in lung volumes; mild reduction in diffusion capacity Nocturnal oximetry - >10% of sleep time with oxygen saturation by pulse oximetry <90% V/Q - normal or low probability 6 min walk - absolute value of distance, percent of predicted distance, oxygen saturation by pulse oximetry, heart rate, and Borg dyspnoea scale BNP + NT-PRO-BNP - elevated (>99 nanograms/L or >99 picograms/mL) FBC - N LFTs - N TFTs - N (hyperT can cause secondary) HIV - N (can cause secondary)

Answer 178

There are 3 reasons to perform acute vasoreactivity testing in a patient diagnosed with PAH. The first is to identify the small subset of patients who may exhibit a favorable long-term response to CCB therapy. The second is to provide prognostic information. The third is for the purposes of research. +ve response = trial of CCB (everything else same thereafter) Endothelin receptor antagonist OR phosphodiesterase inhibitor OR Riociguat (Soluble guanylate cyclase stimulator) OR selexipag (Selective prostacyclin IP receptor agonists) LIFESTYLE CHANGES - low level exercise Anticoagulation - warfarin (IPAH patients have in situ microscopic thrombosis in the pulmonary vasculature and prothrombotic abnormalities) Diuretic Supplemental O2 Digoxin Prostanoids Atrial septostomy or lung transplantation

Answer 179

Estimated median survival in IPAH, without specific therapies, is 2.8 years, with 1-year, 3-year, and 5-year survival rates of 68%, 48%, and 34%, respectively Associated with worse prognosis: syncope; male sex; older age; renal insufficiency; New York Heart Association (NYHA) functional class IV; short 6-minute walk distance (6MWD) (variable cut-offs in different studies, approximately <300 to 440 metres); echocardiography showing pericardial effusion and/or tricuspid annular plane systolic excursion <1.5 cm; elevated B-type natriuretic peptide (BNP) levels (>180 nanograms/L or >180 picograms/mL); and invasive haemodynamics showing right atrial pressure >15 mmHg and/or cardiac index ≤2 L/minute/m².

Answer 180

RVF Supraventicular tachyarythmies Rx related headaches Central venous catheter related infections

Answer 181

Ventricular fibrillation (VF) is a life-threatening cardiac arrhythmia in which the coordinated contraction of the ventricular myocardium is replaced by high-frequency, disorganized excitation, resulting in [the effective] failure of the heart to pump blood. VF is the most commonly identified arrhythmia in cardiac arrest patients. In the prehospital setting, 65%-85% of patients in cardiac arrest have VF identified as the initial rhythm by emergency services personnel.

Answer 182

In the prehospital setting, 65%-85% of patients in cardiac arrest have VF identified as the initial rhythm by emergency services personnel VF is often the first expression of coronary artery disease (CAD) and is responsible for approximately 50% of deaths from CAD. VF often occurs within the first hour after the onset of an acute myocardial infarction (MI) or acute coronary syndrome (ACS). Survivors of a major cardiovascular event have an increased risk for VF in the first 6-24 months after the event. Up to 30% of survivors of cardiac arrest may experience recurrent VF in the first year afterward. Of the approximately 300,000 cases of SCD that occur each year in the United States, up to one third are attributed to VF.

Answer 183

``` CAD HCM LQTS WPW BRUGADA SYNDROME AS Congenital disease ``` An estimated 3%-9% of cases of VT and VF occur in the absence of myocardial ischemia. Up to 1% of patients with out-of-hospital cardiac arrest have idiopathic VF with no discernable structural heart disease. Risk factors that relate to coronary artery disease (CAD) and to subsequent myocardial infarction (MI) and ischemic cardiomyopathy are also important and include a family history of premature CAD, smoking, dyslipidemia, hypertension, diabetes, obesity, and a sedentary lifestyle.

Answer 184

Coronary artery disease (CAD) is the single most common etiologic factor predisposing patients to ventricular fibrillation (VF). In survivors of cardiac arrest, CAD with over 75% stenosis is observed in 40%-86% of patients, depending on the age and sex of the population studied. In postmortem studies of people who have died from VF, extensive atherosclerosis is the most common pathologic finding.

Answer 185

Patients at risk for VF may have prodromes of chest pain, fatigue, palpitations, and other nonspecific complaints, but many are asymptomatic. Up to 45% of persons who have VF have been noted to visit their physician in the 4 weeks before death, although in up to 75% of these patients, the complaints were not related to the cardiovascular system. A history of left ventricular (LV) dysfunction (LV ejection fraction [LVEF] < 30%-35%) is the single greatest risk factor for sudden death from VF. Risk factors that relate to coronary artery disease (CAD) and to subsequent myocardial infarction (MI) and ischemic cardiomyopathy are also important and include a family history of premature CAD, smoking, dyslipidemia, hypertension, diabetes, obesity, and a sedentary lifestyle. Specific considerations include the following: CAD Previous cardiac arrest Syncope or near-syncope Prior MI, especially within 6 months LVEF less than 30%-35% History of frequent ventricular ectopy (>10 premature ventricular contractions [PVCs] per hour or nonsustained ventricular tachycardia [VT]) Drop in systolic blood pressure or ventricular ectopy upon stress testing, particularly when associated with acute myocardial ischemia Dilated cardiomyopathy (DCM) from any cause (but most commonly ischemic or idiopathic) Hypertrophic cardiomyopathy (HCM), obstructive or nonobstructive Use of inotropic medications, particularly in patients with decompensated heart failure or acute myocardial ischemia Valvular heart disease (severe uncorrected aortic or mitral stenosis or regurgitation; valve replacement within 6 months) Myocarditis

Answer 186

Only an ECG can diagnose VF -> the following investigations relate to cause only Echo - valvular disease Coronary angiography - CAD Cardiac enzymes - MI Electrophysiologic (EP) studies (EPS) are usually performed after ischemic and structural heart disease has been diagnosed and addressed as best as it can be. These studies are generally not indicated for the subset of patients in whom ventricular fibrillation (VF) occurred within the first 24-48 hours of an acute myocardial infarction (MI), unless the patient had previous VF events. In all other patients with VF, however, consider EPS for diagnostic and therapeutic guidance. EPS have been used to distinguish patients with inducible ventricular tachycardia (VT)/VF from those with no inducible sustained ventricular arrhythmias. The presence of inducible sustained VT or VF, at baseline or when the patient is on antiarrhythmic medications, confers a higher risk for sudden death.

Answer 187

Defibrillation success rates decrease about 5%-10% for each minute after the onset of VF. In strictly monitored settings where defibrillation was performed most promptly, success rates of 85% have been reported. Consider placement of an advanced airway (continuous chest compressions can be given after an advanced airway is in place) Consider waveform capnography Obtain intravenous (IV) or intraosseous (IO) access Consider administering vasopressors and antiarrhythmics Correct reversible causes Vasopressors (epinephrine or vasopressin) are given per the asystole/pulseless electrical activity (PEA) advanced cardiac life support (ACLS) algorithm: Epinephrine 1 mg IV/IO, repeat every 3-5 minutes, or Vasopressin (1-time dose), 40 U IV/IO, to replace the first or second dose of epinephrine. Antiarrhythmic agents can be given before or after the shock. Amiodarone is given as 300 mg IV/IO once (then, consider an additional 150 mg IV/IO, once). Alternatively, lidocaine is given in a first dose of 1-1.5 mg/kg IV/IO, followed by 0.5-0.75 mg/kg IV/IO, for a maximum of three (3) doses or 3 mg/kg. If torsade de pointes is present, consider administering magnesium sulfate, loading dose 1-2 g IV/IO. ``` Treat the following underlying provocative abnormalities, if present: Myocardial infarction Hypovolemia Hemorrhagic shock Anoxia/hypoxia Pneumothorax/hemothorax Hypercalcemia Drug overdose (eg, narcotic, tricyclic antidepressant, cocaine, barbiturate) Carbon monoxide poisoning Hyperkalemia ``` Radiofrequency Ablation Radiofrequency ablation (RFA) is indicated for prevention of ventricular fibrillation (VF) in patients with the following: Atrioventricular (AV) bypass tracts Bundle-branch block ventricular tachycardia (VT) Right ventricular outflow tract (RVOT) tachycardia Idiopathic left ventricular (LV) tachycardia Idiopathic VF [34] Rare forms of automatic focal VT (however, these almost never cause VF) Scar-related VT due to ischemic or nonischemic myopathy Survivors of ventricular fibrillation (VF) that does not have a clear and readily reversible cause should undergo placement with an implantable cardioverter-defibrillator (ICD).

Answer 188

The chances of survival from an index ventricular fibrillation (VF) event depend on bystander cardiopulmonary resuscitation (CPR), rapid availability or arrival of personnel and apparatus for defibrillation and advanced life support, and transport to a hospital. Although patients with nontraumatic cardiac arrest are more likely to be successfully resuscitated from VF than from any other arrhythmia, success is highly time dependent. The probability of success generally declines at a rate of 2%-10% per minute.

Answer 189

Venous leg ulcers are estimated to affect around 1 in 500 people in the UK, although they become much more common with age. It's estimated around 1 in 50 people over the age of 80 has one.

Answer 190

Signs and symptoms of venous ulcers include: Moderate pain, which improves on elevation (unlike arterial ulcers which worsen with elevation) Irregular, sloping edges Associated oedema, due to increased hydrostatic pressure, which contributes to 'atrophie blanche' 'Atrophie blanche', localised loss of skin pigmentation due to death of erythrocytes and scarring Lipodermatosclerosis, a hardening of the skin which can lead to an "inverted champagne bottle" appearance to the leg Associated superficial varicose veins or "ankle flare", a collection of small, dark, engorged superficial veins[6]

Answer 191

Clinical The National Institute for Health and Care Excellence (NICE) recommends referral to a vascular service for anyone with a leg ulcer that has not healed within 2 weeks or anyone with a healed leg ulcer.

Answer 192

Most venous leg ulcers heal within 3 to 4 months if they're treated by a healthcare professional trained in compression therapy for leg ulcers. But some ulcers may take longer to heal, and a very small number never heal. Treatment usually involves: cleaning and dressing the wound using compression, such as bandages or stockings, to improve the flow of blood in the legs Antibiotics may also be used if the ulcer becomes infected, but they do not help ulcers heal. There are several ways to help prevent developing a venous leg ulcer in people at risk. These include: ``` wearing compression stockings losing weight if you're overweight exercising regularly elevating your leg when possible stopping smoking if you smoke ``` Pentoxifylline is a useful add on treatment to compression stockings and may also help by itself.[28] It works by reducing platelet aggregation and thrombus formation. Gastrointestinal disturbances were reported as a potential adverse effect.[28] Sulodexide, which reduces the formation of blood clots and reduces inflammation, may improve the healing of venous ulcers when taken in conjunction with proper local wound care.[29] Further research is necessary to determine potential adverse effects, the effectiveness, and the dosing protocol for sulodexide treatment. An oral dose of aspirin is being investigated as a potential treatment option for people with venous ulcers. A 2016 Cochrane systematic review concluded that further research is necessary before this treatment option can be confirmed to be safe and effective.[30]

Answer 193

Venous ulcers are costly to treat, and there is a significant chance that they will recur after healing;[2][7] one study found that up to 48% of venous ulcers had recurred by the fifth year after healing.[7] However treatment with local anaesthetic endovenous techniques suggests a reduction of this high recurrence rate is possible.[36] Without proper care, the ulcer may get infected leading to cellulitis or gangrene and eventually may need amputation of the part of limb in future. Some topical drugs used to treat venous ulcer may cause venous eczema.[39]

Answer 194

Venous ulcers are costly to treat, and there is a significant chance that they will recur after healing;[2][7] one study found that up to 48% of venous ulcers had recurred by the fifth year after healing.[7] However treatment with local anaesthetic endovenous techniques suggests a reduction of this high recurrence rate is possible.[36] Without proper care, the ulcer may get infected leading to cellulitis or gangrene and eventually may need amputation of the part of limb in future. Some topical drugs used to treat venous ulcer may cause venous eczema.[39]

Answer 195

Most often endothelial dysfunction is causative factor in diabetic microangiopathy and macroangiopathy When pressure is placed on the skin, the skin is damaged and is unable to be repaired due to the lack of blood perfusing the tissue. The wound has a characteristic deep, punched out look, often extending down to the tendons. The wounds are very painful.[ DM

Answer 196

DM PAD RFs Cardiac RFs

Answer 197

Arterial insufficiency ulcers (also known as Ischemic ulcers or Ischemic wounds) are mostly located on the lateral surface of the ankle or the distal digits. The ulcer has punched-out appearance. It is intensely painful. It has gray or yellow fibrotic base and undermining skin margins. Sx of PAD Pulses are not palpable. Associated skin changes may be observed, such as thin shiny skin and absence of hair. They are most common on distal ends of limbs. A special type of ischemic ulcer developing in duodenum after severe burns is called Curling's ulcer.

Answer 198

The lesion can be easily identified clinically. Arterial doppler and pulse volume recordings are performed for baseline assessment of blood flow. Radiographs may be necessary to rule out osteomyelitis.

Answer 199

The affected region can sometimes be revascularized via vascular bypass or angioplasty. If infection is present, appropriate antibiotics are prescribed. When proper blood flow is established, debridement is performed. If the wound is plantar (on walking surface of foot), patient is advised to give rest to foot to avoid enlargement of the ulcer. Proper glycemic control in diabetics is important. Smoking should be avoided to aid wound healing.

Answer 200

Osteomyelitis Sepsis Septic arthritis

Answer 201

Osteomyelitis Sepsis Septic arthritis

Answer 202

Tricuspid insufficiency (TI), more commonly called tricuspid regurgitation (TR), is a type of valvular heart disease in which the tricuspid valve of the heart, located between the right atrium and right ventricle, does not close completely when the right ventricle contracts (systole). TR allows the blood to flow backwards from the right ventricle to the right atrium, which increases the volume and pressure of the blood both in the right atrium and the right ventricle,[1] which may increase central venous volume and pressure if the backward flow is sufficiently severe.

Answer 203

RV dilation IE Inferior MI Cor pulmonale ``` Primary causes Rheumatic Myxomatous Ebstein anomaly Endomyocardial fibrosis Endocarditis Traumatic (blunt chest injury) Secondary causes Left ventricular systolic dysfunction Mitral valve stenosis or regurgitation Chronic lung disease Pulmonary thromboembolism Myocardial disease Right ventricular ischemia and infraction Left to right shunt Carcinoid heart disease ```

Answer 204

The symptoms of TR depend on its severity. Severe TR causes right-sided heart failure, with the development of ascites and peripheral edema A pansystolic heart murmur may be heard on auscultation of the chest. The murmur is usually of low frequency and best heard on the lower left sternal border. It increases with inspiration, and decreases with expiration: this is known as Carvallo's sign. However, the murmur may be inaudible due to the relatively low pressures in the right side of the heart. A third heart sound may also be present, also heard at the lower sternal border, and increasing in intensity with inspiration. With severe TR, there may be an enlarged liver detected on palpation of the right upper quadrant of the abdomen; the liver may be pulsatile on palpation and even on inspection.

Answer 205

The diagnosis of TR may be suspected if the typical murmur of TR is heard. Severe TR may be suspected if right ventricular enlargement is seen on chest x-ray, and other causes of this enlargement are ruled out. Definitive diagnosis is made by echocardiogram, which is capable of measuring both the presence and the severity of the TR, as well as right ventricular dimensions and systolic pressures.

Answer 206

Generally, medical rather than surgical treatment of TR is recommended if the cause is right ventricular dilatation or left-sided heart failure. Tricuspid valve replacement using either a mechanical prosthesis or a bioprosthesis may be indicated. (Mechanical prostheses may cause thrombo‐embolic phenomena, bioprostheses may have a degeneration problem)

Answer 207

The prognosis of TR is less favorable for males than females. Survival rates are proportional to TR severity; but even mild TR reduces survival compared to those with no TR. If the TR is due to left heart failure or pulmonary hypertension, prognosis is usually dictated by these conditions, not the TR

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