Cardio conditions Flashcards

Question

2 complications of atrial fibrillation

Answer 1

Ischemic stroke Heart failure

Answer 2

A supraventricular tachycardia with atrial rates 250-300bpm. PATHOLOGY (Fast atrial ectopic firing) Re-entrant rhythm with Abnormal signals typically arise from the tricuspid annulus SYMPTOMS - Palpitations - Fatigue - Dyspnoea INVESTIGATIONS 1st line + GS - ECG Saw toothed pattern (F wave?), often with a 2:1 block (2 P waves for 1 QRS) - atrial rate at about 300bpm TREATMENTS Acutely unstable (Shock, syncope, MI) --> Synchronised DC cardioversion Stable - 1st line - rate control BB - Bisoprolol + DOAC depending on CHADSVASC score (Permanent - Radiofrequency ablation)

Answer 3

Sinus tachycardia - Normal P wave, QRS complex and T wave Supraventricular tachycardia (AVNRT, AVRT, atrial tachycardia) - (in AVNRT - QRS followed immediately by T waves (with P waves buried - P wave and QRS occurs at same time) Atrial fibrillation - Absent P waves, irregularly irregular ventricular rhythm Atrial flutter - Saw toothed pattern with mostly 2:1 conduction

Answer 4

A supraventricular tachycardia caused by electrical signals re entering the atria AVRT - Re entry through an accessory pathway called the BUNDLE OF KENT - A pre excitation syndrome - which allows for electric signals to prematurely enter the ventricles (leading to delta waves in the QRS complex) SYMPTOMS - Palpitation - Dizziness - Dyspnoea INVESTIGATIONS 1st and GS - ECG - Short PR interval - Delta waves (in QRS complex) - slurred upstroke - Wide QRS TREATMENT 1st line - Vagal maneuvers - Carotid massage - Valsalva maneuver 2nd line - IV adenosine CI asthma give CCB - verapamil Definite - last resort - Radiofrequency ablation of bundle of Kent.

Answer 5

Paroxysmal supraventricular tachycardia due to the presence of a re-entry circuit within the AV node MOST COMMON SVT ECG - Absent P waves as p wave is buried within QRS complex, T waves immediately after QRS TREATMENT 1st line - Vagal maneuvers - Carotid massage - Valsalva maneuver 2nd line - IV adenosine Definite - last resort - Radiofrequency ablation

Answer 6

Ventricular tachycardia - Wide QRS + regular rhythm --> IV amiodarone Polymorphic ventricular tachycardia (e.g. Torsades de pointes) - Wide QRS + irregular rhythm --> IV magnesium Atrial fibrillation with BBB --> Treated like normal A fib. Unstable - Synchronised DC cardioversion Stable - BB + DOAC if needed (CHADSVASC) Supraventricular tachycardia with BBB (treated like SVT) 1st line - Vagal maneuvers - Carotid massage - Valsalva maneuver 2nd line - IV adenosine Definite - last resort - Radiofrequency ablation of bundle of Kent.

Answer 7

Caused by electrolyte imbalance (Hypokalemia, hypocalcemia, drugs - amiodarone, SSRIs, Romano Ward syndrome - Autosomal dominant) Takes the heart longer than usual to recharge between beats QT interval >440 milliseconds

Answer 8

A form of polymorphic ventricular tachycardia. Recurrent contractions of the ventricles (before proper repolarisation) leading to faster contractions than the atria. Treat with correcting the underlying cause e.g. Electrolyte imbalance otherwise --> MAGNESIUM INFUSION

Answer 9

RF - Obesity, physical inactivity, alcohol, black ethnicity, diabetes PATHOLOGY Primary/essential hypertension - Idiopathic (90% of cases) Secondary causes: ROPED Renal disease Obesity Pregnancy induced Endocrine (Phaechromocytoma, conns, cushings) Drugs -- NSAIDS RAAS + SNS increase in activity Hypertension can lead to atherosclerosis and end organ damage. SYMPTOMS Mostly asymptomatic Pulsatile headaches Fever In malignant hypertension (phaeochromocytoma) - Blurred vision - Heart failure - Renal failure INVESTIGATIONS If BP in hospital >140/90 mmHg, do Ambulatory blood pressure monitoring to confirm diagnosis (135/85 mmHg throughout the day) Assess for end organ damage - Fundoscopy - Papilloedema - Urinalysis + eGFR - Kidney function - Echo - LVH TREATMENT If <55 YO or T2DM (Not a black African) 1) Ace inhibitor NO MATTER WHAT AGE/ETHNICITY, if patient has T2DM give Ace-Inhibitor If >55 YO or Black African 1) CCB 2) Ace inhibitor + CCB 3) Ace inhibitor + CCB + Thiazide

Answer 10

Development of a blood clot in a major deep vein in the leg, thigh, pelvis or abdomen RF - Major surgery, bedridden for 3 days or more, active cancer, increased age, plaster immobilisation PATHOLOGY Mostly caused by Virchow's triad: venous stasis, hypercoagulability, Endothelial damage SYMPTOMS - Unilateral calf swelling with veins that are warm and oedematous - May be red

Answer 11

Phlegmasia cerulea Dolens --> Significant pain, cyanosis and swellling INVESTIGATIONS If Wells Score is 1 or less (Unlikely DVT) --> Do a D-dimer test - If its normal - DVT excluded - If its elevated do a venous duplex ultrasound - where a reduced or absent spontaneous flow CONFIRMS the diagnosis If Wells score is 2 or more (likely DVT) --> Do a venous duplex ultrasound (Diagnostic) TREATMENT 1st line - DOAC (Apixaban, rivaroxaban) LMWH if CI (renal impairment) Non pharmacological treatment - Physical activity - mobilisation, walking exercises - Compression stockings

Answer 12

Life threatening condition resulting from a dislodged thrombi occluding pulmonary vasculature RF - Age, hormone replacement therapy (estrogen increases risk of thrombus formation) PATHOLOGY - Complication of DVT - Thrombus trapped in pulmonary vasculature --> increases pulmonary vascular resistance --> can cause Cor pulmonale where RVH is caused by increase strain on the RV to overcome pulmonary vascular resistance --> eventual RV failure SYMPTOMS - Sudden onset pleuritic chest pain - Dyspnoea (with possible haemoptysis) - Evidence of DVT (swollen calf, immobilisation) (increased JVP) INVESTIGATIONS 1st line If Wells score >4 (likely PE) --> CT pulmonary angiogram (diagnostic) If Wells score <4 (unlikely PE) --> D-dimer test : - If raised --> CTPA - If not raised --> Not PE ECG - Sinus tachycardia + S1Q3T3 (also sign of cor pulmonale) T wave inversion of anterior and inferior leads + new RBBB Chest X-ray - normal TREATMENT Non massive PE (usually this) 1st line DOAC - Apixaban LMWH if CI (renal impairment) mit Massive PE Thrombolytics e.g. alteplase, streptokinase

Answer 13

Range of syndromes caused by obstruction of vessels of the lower extremity RF - Smoking, diabetes, hypertension, obesity, ageing PATHOLOGY Mostly caused by thrombus from an atherosclerotic plaque Increasing stages of severity (Fontaine classification) - Asymptomatic - Intermittent claudication (divided into pain free walking >/< 200m. - Ischemic rest pain - Chronic limb ischemia - Ulceration or gangrene Intermittent claudication (least severe) --> inadequate blood flow on exertion leading to crampy pain Critical/chronic limb ischaemia (most severe) --> results in SYMPTOMATIC reduced blood supply to the limbs --> caused by atherosclerosis --> ischemic rest pain SYMPTOMS Generally - Intermittent claudication - Ischemic rest pain (pulseless on palpation of extremities or bruits - pulsatile regions) --> may develop to Acute limb ischaemia in which cause 6 P symptoms. Skin changes on the leg - cooler + ulcerations INVESTIGATIONS First line - Ankle brachial pressure index. (ratio of BP) <0.9 = intermittent claudication <0.5 = Chronic limb ischemia Buerger's test - elevate leg at 45 degree angle for 1-2 minutes, if there is pallor, test is positive TREATMENT Intermittent claudication - Graded exercise therapy - RF modification - Stop smoking, balanced diet, increase physical activity - Pharmacological: Atorvastatin, clopidogrel Chronic limb ischaemia - Revascularisation surgery PCI - if small Bypass surgery - if bigger

Answer 14

A complication of peripheral vascular disease (main difference with CLI is that onset is sudden) There is a sudden decrease in limb perfusion threatening the viability of the limb --> Rapid onset ischemia due to occlusion of arterial supply (by thrombus/embolus) SYMPTOMS Pain Pallor Paraesthesia Paralysis Perishingly cold Pulselessness TREATMENT If non viable limb (Sign of tissue loss, nerve damage or significant sensory loss) --> Amputate If limb is viable on assessment --> Urgent revascularisation within 4-6 hours (Endovascular thrombolysis/thrombectomy, bypass surgery)

Answer 15

Inflammation of the pericardium characterised by a triad of chest pain, pericardial friction rub and serial electrocardiogram changes RF - male, transmural MI, cardiac surgery PATHOLOGY Causes: - idiopathic Main cause - VIRAL INFECTIONS - coxsackie viruses, EBV, adenovirus - TB (bacterial), - Autoimmune - SLE, Sjorgen's - Dressler syndrome - when pericarditis develops post MI Due to causes mentioned, the inflamed pericardial layers rub against each other and exacerbate further inflammation SYMPTOMS - Sharp, pleuritic chest pain that may radiate to the trapezius ridges or left shoulder - Pain is worse on inspiration and a supine position and is relived on leaning forward - Pericardial friction rub on ausculation INVESTIGATIONS FBC - ESR elevated, leukocytosis GS - ECG - Localised PR depression + Global Saddle shaped ST elevation TREATMENT NSAIDS + colchicine

Answer 16

Due to pericardial layers rubbing against each other, it can lead to PERICARDIAL EFFUSION (Inflammation leads to increased vascular permeability) Pericardial cavity fills with fluid, creating an inward pressure on the heart, making it difficult to expand during diastole. This can in turn lead to CARDIAC TAMPONADE When pericardial effusion is large enough to raise intrapericardial pressure --> It can squeeze the heart, reducing filling during diastole --> reducing CO --> Leading to Shock and DEATH Cardiac tamponade will present with PULSUS PARADOXUS (a fall in BP >10mmHg on inspiration) SYMPTOMS of cardiac tamponade BECK's Triad - Hypotension - Increased Jugular venous pressure - Muffled S1+S2 heart sounds + Pulsus paradoxus INVESTIGATIONS 1st line - ECG Chest X-ray - Big heart GS - Transoesophageal echocardiogram Treat pericardial effusion with NSAIDS + colchicine Treat cardiac tamponade with URGENT PERICARDIOCENTESIS

Answer 17

1st Degree - Slow conduction through AV node - PR interval is prolonged (>200ms) 2nd degree MOBITZ 1 (WENCKEBACH) - Progressively longer PR interval till a non conducted P wave/QRS drop (AV node completely fails) MOBITZ 2 (HAY) - Intermittent non conducted P wave - Constant PR interval (higher risk of progression to 3rd degree AV block) 3rd degree - No association between atria and ventricles - P waves not correlated with QRS complex (more P waves than QRS)

Answer 18

1st degree - Drugs (e.g. BB, CCB, Digoxin) 2nd degree - Drugs (above), inferior MI, rheumatic fever 3rd degree - Acute MI, structural heart disease

Answer 19

1st degree Sx - Usually asymptomatic Tx - Asymptomatic so no treatment (Mobitz 1 also no treatment unless very symptomatic then give PACEMAKER) 2nd and 3rd degree Sx - Syncope, fatigue, hypertension, chest pain, dyspnoea MOBITZ 2 Tx--> Pacemaker 3rd degree Tx --> IV atropine and pacemaker

Answer 20

An infection involving the endocardial surface of the heart, including valvular structure and chordae tendinae. RF - Presence of artificial prosthetic valves, IV drug abusers, rheumatic HD PATHOLOGY Bacteria can be introduced endogenously (bacteria within body enters bloodstream) or exogenously (bacteria introduced by contaminated objects) --> Leads to vegetations forming on heart valves. (Bacteria adhere to platelet deposition) Main bacteria: 1) S.aureus (MC) - IVDU, prosthetic valves 2) S.viridans - alpha haemolytic strep associated with poor dental hygiene 3) Pseudomonas aeruginosa - contaminated water (Enteroccocus) SYMPTOMS - Fever - Malaise - Sweating - Headache - Osler nodes - finger nodules - Janeway lesions - painful marks on palms - Splinter haemorrhages - on fingernails - Roth spots - Retinal haemorrhage INVESTIGATIONS 1st line - 3 sets of blood cultures at 3 different sites over 24 hours FBC Urinalysis GS - Transoesophageal echocardiogram DIAGNOSIS MADE WITH MODIFIED DUKES CRITERIA (2 major, 1 major 3 minor, 5 minor) TREATMENT S.viridans (S.bovis) - Benzylpenicillin (Pen G) + Gentamicin S.aureus - Flucloxacillin Enterococci --> Amoxicillin + Gentamicin

Answer 21

Modified Dukes Criteria 2 major 1 major + 3 minor 5 minor Major - Blood culture positive for organisms typical of IE in at least 2 samples - Evidence of IE on TOE MINOR - Predisposing factors - Prosthetic heart valves, IVDU - Fever - Vascular phenomenon - Janeway lesion, septic emboli - Immunologic phenomenon - Osler node, roth spots - Blood culture positive - but not an organism constant with IE.

Answer 22

Right - Marrow Causes: Lung pathology - esp PE (COPD), IHD, congenital heart disease M in V1 W in V6 (Double R waves in V1, prolonged S wave in V6) Left - William Causes: MC - IHD, valve disorders W in V1 M in V6 (Deep S in V1, Prolonged R in V6)

Answer 23

Hypertrophic cardiomyopathy

Answer 24

Autosomal dominant genetic disease of sarcomere proteins (Troponin T/I) that results in myocyte hypertrophy and septal thickening. --> You have a thick, non compliant heart - reduced ability to expans--> Impaired diastolic filling --> decreased CO SYMPTOMS - Syncope - Dyspnoea - Chest pain --> May present with sudden cardiac death INVESTIGATIONS 1st line - ECG --> Abnormal (LVH) GS - Transeosophageal echocardiogram Genetic testing (mutations in Troponin T and I) TREATMENT BB, CCB, amiodarone

Answer 25

Most common cardiomyopathy Autosomal dominant mutation of the cytoskeleton gene --> Results in thinning and stretching of cardiac walls leading to dilation and dysfunction --> reduced CO SYMPTOMS Dyspnoea Heart failure Atrial fibrillation INVESTIGATIONS ECG GS - TOE TREATMENT Treat underlying condition - e.g. Heart failure, atrial fibrillation

Answer 26

Caused by granulomatous disease e.g. Amyloidosis, sarcoidosis Leads to a Rigid, Fibrotic myocardium that is stiff --> impaired ventricular filling --> decreased CO INVESTIGATIONS ECG GS - ECHO TREATMENT - No curative treatment - Heart transplant

Answer 27

1) Distributive - Failure of vasoregulation (vasodilation/constriction) e.g Sepsis, anaphylaxis 2) Cardiogenic - Pump dysfunction e.g. Post MI 3) Hypovolemic - Loss of intravascular volume e.g. GI bleed, trauma (generally haemorrhagic causes) (Obstructive - Barriers to cardiac flow e.g. PE) Take note for treatment ABCDE Hypovolemic - Oxygen, IV fluids Septic - Broad spec antibiotics Cardiogenic - IV fluids, diuretic Anaphylactic - IM adrenaline

Answer 28

Autoimmune disease that occurs usually post strep pyogenes infection. (Pharyngitis) 50% lead to rheumatic heart disease PATHOLOGY M protein from S.pyogenes has regions sharing similarities with cardiac tissue (Molecular mimicry) --> When the immune system produces antibodies against the M protein, antibodies can cross react with cardiac myosin and other cardiac proteins --> auto-antibody mediated destruction (MOSTLY AFFECTS MITRAL VALVE) SYMPTOMS - New murmur (mitral stenosis) - Sydenham's chorea (jerky uncoordinated movement) - Arthritis - Erythema nodosum - painful patches of darker skin INVESTIGATIONS 1st line - Chest X-ray --> Cardiomegaly (because of over working heart) - signs of mitral stenosis GS - TOE - shows valvular damage DIAGNOSE WITH JONES CRITERIA Recent S.pyogenes infection + 2 major or 1 major 2 minor Major - Polyarthritis, carditis, sydenham's chorea, erythema nodosum, new murmur Minor - fever, arthralgia, elevated ESR/CRP TREATMENT 1st line - IV benzylpenicillin then phenoxypenicillin for 10 days Haloperidol for sydenham's chorea

Answer 29

Right heart failure - Increased JVP - Hepatomegaly - Peripheral oedema (pedal oedema) - Ascites Left heart failure - Paroxysmal nocturnal dyspnoea - Orthopnea - Pulmonary oedema (bibasal crepitation) (nocturia, cold fingers)

Cardio conditions Flashcards

(54 cards)