CARDIOLOGY Flashcards

Question

renal artery stenosis TX

Answer 1

Start 1stline ACE inhib/ARB 2ndline CCB Percutaneous renal artery angioplasty for recurrence/refractory/PE *Reduce hypercholesterolemia with Statins *Diuretics **NOT** recommended ## Footnote * ACEI is considered in unilateral cases. In bilateral cases, ACEIs can accelerate kidney failure by preferential vasodilation of the efferent arteriole

Answer 2

Episodic headache, sweating/diaphoresis, palpitations/paroxysmal tachycardia

Answer 3

**BEST = 24hr urinary metanephrines and catecholamine levels** or Plasma metanephrines

Answer 4

First give **Alpha blockers** to control HTN *Next give **BB** to control tachycardia. (never give BB first as unopposed alpha-adrenergic stimulation will lead to refractory HTN) refractory= *Surgical resection

Answer 5

HTN, unexplained hypokalemia, metabolic alkalosis ## Footnote Mild hypernatremia *Hypomagnesemia ***Inc Plasma aldosterone, Dec Renin level and Inc aldosterone/renin ratio**

Answer 6

Retrosternal chest discomfort (pain or tightness) that lasts **10 minutes **or less and subsides promptly with rest. it occurs when myocardial oxygen demand exceeds supply, which is usually restricted by athero ## Footnote most common are shortness of breath, nausea, and diaphoresis

Answer 7

ST segment changes on exercise stress test with **ECG monitoring*** **Troponin** -They are unlikely to be elevated in patients with intermittent and relatively brief angina episodes. However, they may be useful when the anginal episode is more prolonged and for prognostication

Answer 8

Prinzmetal’s (variant) angina **mimics** angina pectoris but is caused by vasospasm of coronary vessels. It classically effects **young** **women** at rest in the **early** **morning** and is associated with ST-segment elevation in the **absence** of **cardiac** **enzyme** **elevation**. **The typical patient is a female smoker**

Answer 9

These episodes tend to self-resolve; however, cardiac-selective c**alcium channel blockers such as verapamil or diltiazem** CARDIAC SELECTIVE NIFEDIPINE

Answer 10

**Glyceryl trinitrate** | Before taking glyceryl trinitrate, they should sit down, to avoid orthos ## Footnote Glyceryl trinitrate spray 400 micrograms sublingually, repeat every 5 minutes if pain persists, up to a total of 3 doses if tolerated angina, treatmentORGlyceryl trinitrate tablet 300 to 600 micrograms sublingually, repeat every 5 minutes if pain persists, up to a total of 3 doses if tolerated.

Answer 11

**Rest + nitrate *Aspirinif no CI *call ambulance if pain doesn’t subside in 10 min**

Answer 12

Combo of 2 antianginal drugs 1. ***Short-acting glyceryl trinitrate **can be taken **before** **exercise** that is likely to provoke angina 2. ***Beta blockers**(atenolol, metoprolol tartare) enhance exercise tolerance by reducing myocardial oxygen demand. In LV dysfunction use these BB instead **Carvedilol**, **bisoprolol**, **nebivolol** or **metoprolol** **succinate** 3. **Nondihydropyridine CCB** (diltiazem, verapamil) reduce heart rate and can be used as an alternative if beta-blocker therapy is contraindicatedor not tolerated **Do not use BB and diltiazem/Verapamil** NOT = severe bradycardia and heart failure!!! . *Avoidusing diltiazem or verapamil for patients with left ventricular dysfunction **(LVEF <40%)** 4. dihydropyridine calcium channel blocker(amlodipine, modified-release nifedipine) can be added to a beta blocker if angina persists 5. **Long-acting nitrate **(transdermal glyceryl trinitrate, modified-release isosorbide mononitrate) can be added either to a beta blocker, or to a nondihydropyridinecalcium channel blocker (diltiazem, verapamil) 6. **Nicorandilis** an option for patients with refractory angina despite optimal therapy with the preceding drugs. Add to beta-blocker, diltiazem or verapamil therapy ## Footnote atenolol 25 mg orally, daily, increasing if required up to 100 mg daily OR metoprolol tartrate 25 mg orally, twice daily, increasing if required up to 100 mg twice daily

Answer 13

crushing or heavy central chest pain that may radiate to the arms, neck, back and jaw. **Left arm pain is common,** but **bilateral** or **right** **arm** pain are more **specific**. An acute coronary syndrome may be associated with shortness of breath, nausea and sweating

Answer 14

*burning pain, pain that increases with respiration, sharp pain (patients sometimes say ‘sharp’ when they mean ‘severe’ pain) *upper abdominal pain. *Pain may also be absent (‘silent’ acute myocardial infarction). In particular, consider an acute coronary syndrome in patients with ***diabetes*** and older patients who have no pain but do have associated symptoms (egshortness of breath, nausea, sweating), or poorly controlled diabetes.

Answer 15

**Rest** **angina**, which is usually more than 20 minutes in duration *New onset angina that markedly limits physical activity *Increasing angina that is more frequent, longer in duration, or occurs with less exertion than previous angina ## Footnote Acute coronary syndromes result from unstable atherosclerotic plaques or endothelial disruption, with associated transient or permanent thrombotic occlusion of the coronary arteries, leading to myocardial infarction and ischaemia

Answer 16

****1. **ST elevation myocardial infarction (STEMI)**—a medical emergency *According to guidelines, to diagnose Acute STEMI. Patient should have chest pain/discomfort suggestive of AMI in the presence of ST elevation **more than 1mm** in two contagious leads , or a newly developed LBBB. 2. **Non–ST elevation acute coronary syndrome (NSTEACS**)—the initial description for patients without ST elevation. Subsequent investigation divides NSTEACS into: ** A)** Non–ST elevation myocardial infarction (NSTEMI)—patients with MI as determined by elevated cardiac **biomarkers** ** B)**Unstable angina—patients **without** elevated cardiac biomarkers. It signals impending infarction. ***NSTEACS can progress to STEMI; ongoing monitoring is essential***

Answer 17

Type 1 spontaneous MI -atherothrombotic coronary occlusion Type 2 MI -is secondary to ischaemic imbalance *tachyarrhythmias, bradyarrhythmias, anaemia, respiratory failure and hypotension*

Answer 18

1. ECG -12 leads **WITHIN 10 MIN of arrival to ER** normal does not rule out IM 2. **TROPONINE** ********Repeat Troponin levels after every 3-4hrs

Answer 19

A) Percutaneous coronary intervention or B)fibrinolytic therapy. ## Footnote Consider all patients with a STEMI for admission to a **coronary care unit** for monitoring and expert acute care Started within the **12** **hours** preceding presentation

Answer 20

Dual antiplatelet therapy for STEMI - 1) with aspirin 2) P2Y12 inhibitor (clopidogrel, prasugrel, ticagrelor) ## Footnote For a patient **receiving** **fibrinolytic** therapy, give with aspirin **CLOPIDOGREL**!

Answer 21

PCI is available within 90 minutes of first medical contact, **PCI** is **preferred** over fibrinolytic therapy. 2.If PCI cannot be delivered promptly, **fibrinolytic** **therapy** should be given **within 30 minutes** of the patient arriving at the hospital. .3 PCI is not available, and fibrinolytic therapy is not an option for them, then** promptly transfer them to a centrewhere PCI is available**. ## Footnote In some healthcare services, paramedics can give fibrinolytic therapy before the patient reaches hospital

Answer 22

**Psuedoaneurysmat** the site of insertion is a complication of PCI. It is a haematoma with communication to the artery (iliac/femoral/peroneal) that appears as a **pulsatile** **painful** **mass** in groin. It is treated by U**SG guided thrombin injection** away from the neck of sac

Answer 23

Adjuvant drug therapy:* dual antiplatelet therapy—aspirin + P2Y12 inhibitor *periprocedural anticoagulation:—UFH, **enoxaparin** or bivalirudin. ****glycoprotein IIb/IIIa inhibitor may also be indicated.

Answer 24

Alteplase OR Reteplase OR Tenecteplase Aboriginal Australians have high prevalence of IgG anti-streptokinase Ab, making Streptokinase inappropriate for thrombolytic therapy 1) should also be given a **parenteral** **anticoagulant** (enoxaparin or UFH). **Bleeding** can occur following treatment with a fibrinolytic drug and a parenteral anticoagulant. 2) .**Significant** **arrhythmias** including ventricular fibrillation can occur after reperfusion with fibrinolytic therapy.

Answer 25

1. *any prior **intracranial** **haemorrhage***known structural cerebral vascular lesion (egAV malformation) 2. *known **malignant** **intracranial** **neoplasm** (primary or metastatic) 3. ***ischaemic stroke** within 3 months, except acute ischaemic stroke within 4.5 hours 4. *suspected aortic dissection 5. ***active** **bleeding** or bleeding diathesis (excluding menses) 6. *significant closed head or facial trauma within 3 months

Answer 26

antiplatelet therapy and consider treatment with parenteral anticoagulant therapy, beta-blocker therapy, glycoprotein IIb/IIIa inhibitors and invasive management. *Fibrinolytic therapy is NOT used to treat NSTEACS ## Footnote Clinical trials have demonstrated the benefit of early invasive management for NSTEACS -coronary angiography and revascularisation[iestenting or bypass surgery]). *very high risk—recommended within 2 hours of admission*high risk—recommended within 24 hours of admission*intermediate risk—recommended within 72 hours of admission

Answer 27

antiplatelet therapy, a **statin**, *a **beta** **blocker** *an **ACEI**. *~Oral anticoagulation may be needed for patients with complications associated with myocardial infarction, such as mural thrombus or atrial fibrillation. ***Dual antiplatelet therapy*Aspirin (75-150 mg) + a P2Y12 inhibitor**[clopidogrel, prasugrel, ticagrelor]) *For patients who have had a coronary stent inserted, dual antiplatelet therapy is** usually recommended for 12 months after an ACS**.*Dual antiplatelet therapy for less than 12 months may be appropriate for patients at high risk of bleeding, and longer than 12 months may be appropriate for selected patients at high risk of recurrent ischaemicevents.*When stopping dual antiplatelet therapy, stop the P2Y12 inhibitor and continue aspirin indefinitely.*If aspirin is contraindicated, consider indefinite therapy with a P2Y12 inhibitor alone.

Answer 28

at least 6 weeks (ideally 3 months) following angioplasty with BMS 12 months after DES,

Answer 29

**1stday:** V.Fibanytime within 24hrs and especially within 1hr and Heart failure ***2-4 days: ** *Arrythmia -**Most** **common** *Pericarditis -when occurring post MI, **Aspirinis** the treatment of choice and not **other NSAID** ***5-10 days:** *LV wall rupture (acute pericardial tamponade) *Papillary muscle rupture with severe MR ***Weeks to months**: ***Dressler’s syndrome occurs** 2 -10 weeks post MI -autoimmune process with fever, pericarditis, pleural effusion, leucocutosis, incESR. Rx of choice is **Aspirin** if the cause is post MI. *CHF, arrythmia, persistantST elevation, MR, thrombus formation

Answer 30

Ventricular tachicardia

Answer 31

Heart failure with reduced ejection fraction (HFrEF LVEF <50% Impaired ventricular contraction Heart failure with preserved ejection fraction (HFpEF) LVEF >50% impairment of left ventricular filling

Answer 32

Impairment of left ventricular filling with preserved systolic function inotropic agents such as calcium-channel blockers (verapamil or diltiazem) and beta blockers. If possible, avoid diuretics (except for congestion), digoxin, nitrates/vasodilators and nifedipine. Excessive diuresis from overzealous diuretic therapy can cause severe consequences for cardiac output. ACE inhibitors can be used with caution.

Answer 33

EXERTIONAL DYSPNEA earliest and most common symptom Prognosis of systolic HF can be predicted by **JVP and S3 sound**. Elevated JVP and presence of S3 indicates poor prognosis.

Answer 34

1.**CXR** - cardiomegalia, pulmonary vesels etc ECG not diagnostic but can help found out the cause. **DIAGNOSTIC** - **echocardiograma EF <50% and ventricular dilatation** ** **B-type Natriuretic peptide >400** **if the diagnosis is unclear and an echocardiogram cannot be arranged in a timely fashion, then measurement of plasma B-type natriuretic peptide (BNP) or N-terminal pro-BNP levels improves diagnostic accuracy. It is highly sensitive although less specific for active CHF)*

Answer 35

1. includes a combination of diuretic therapy (as need to treat volume overload), 2. an angiotensin system blocker (ACE inhibitor, or single agent ARB), 3. beta blocker

Answer 36

initial assessment of volume status. **1.If hypervolemic** -First step is volume reduction using loop diuretic such as furosemide, bumetanide or **torsemide**. It is also important to start patient with **ACEIs** (or ARBs IF ACEIS is not tolerated). **2.If euvolemic** -*an ACEI (or ARB) + a BB is the management of choice.*Aldosterone antagonist (Spironolactopne) is used in euvolemic pts who have GFR >30ml/min and serum K level of <5mmol/lit with close monitoring of potassium levels **3.When euvolemic after hypervolemic** -add a cardio selective BB ## Footnote *** BB should only be started in pts who do NOT have crackles and no more than minimal peripheral edema. ~ BB is contraindicated in volume overload **Digoxinis indicated with EF <35%. It should be added only after maximally tolerated dose of BB. It is also the initial management of pts with AF and decompensated HF **

Answer 37

Inc JVP *Inc weight *Dyspnea *Crackles *More than minimal peripheral edema *Elevated BNP *Hepatomegaly, ascites or anasarca in severe cases

Answer 38

s/s : dyspnea, **bibasal coarse crackles** investigation: CXR TX: **LMNOP** -**Lasix** -**IV furosemide i**s one of the the initial step. ***Morphine** -decreases sympathetic tone causes vasodilation and reduction of preload ***Nitrates**-GTN reduces preload ***Oxygen** -cannula, Hudson mask; CPAP, BiPAP for reducing venous return and preload ***Position**( upright)

Answer 39

Causes: *HTN *Aortic stenosis* HOCM *O/E: *S4 gallop, *Systolic murmur of MR*Systolic murmur radiating to axilla due to LVTO *Initial inv: *CXR -left atrial enlargement secondary to mitral regurgitation *ECG (signs of LVH) *Diagnostic inv : Echo-shows asymmetrical thickened septum, dynamic obstruction of blood flow, valvular lesions

Answer 40

*is a congenital form, inheritedas an **autosomal dominant train in 50% of HOCM pts.** *Significant cause **of sudden cardiac death in young people**, including athletes. ***Positive family history **for sudden death at young age. ***Sudden loss of consciousnessin a young person while on exertion is most likely due to arrhythmia or HOCM** - INITIAL= BETABLOCKERS CCB = DILTIAZEM / VERAPAMILO -> implantable defibrilator if there is syncope surgery severe cases-septoplastia ## Footnote AVOID DIGITALIS, DIURETICS, VASODILATORS, EXCERSICE!

Answer 41

Bradyarrhythmias should only be treated if they are causing significant haemodynamiccompromise

Answer 42

**At**ropine is the most effective treatment. *If atropine is ineffective, consider **transcutaneous** or **temporary** **transvenous** **pacing**. *If pacing is delayed or not immediately available, consider using chronotropic drugs (egisoprenaline, adrenaline). *Use with caution because they can provoke serious ventricular arrhythmias. ***Adrenaline is preferred if systolic blood pressure is very low**(less than 80 mmHg) because isoprenaline may further reduce blood pressure ## Footnote dosis .Atropine 0.5 mg IV, repeat after 3-5 minif necessary, uptomax of 3 mg.Adrenaline (epinephrine) 2 to 10 micrograms/minute by intravenous infusionIsoprenaline2 to 10 micrograms/minute by intravenous infusion

Answer 43

eperfusion therapy with urgent PCI

Answer 44

block is usually at the **level of the AV nodeand **is transientand not haemodynamically significant. Atropine **may** be required ----------------------------------------- AV block is at the level of the **distal conducting tissues** in the ventricle and is likely to be permanent and associated with haemodynamiccompromise. **Emergency** **temporary** **pacing** is usually required

Answer 45

*None if asymptomatic *Atropinewill incHR *Pacemakerin severe

Answer 46

Regularly Long PR interval *PR interval > 200ms ( >5 small squares). Age related degeneration of AV Node -MCC No specific treatment is required. Is **symptomatic** use **Atropine**

Answer 47

longer, longer, longer, DROP, now you have a Wenckebach.” *Progressively longer PR intervaltill one blocked/missed beat. AV nodal blocking drugs (BB, CCB, Digoxin, amiodarone) *Increased vagal tone, Athletic training*Inferior MI *Myocarditis* S/S: Usually benign, asymptomatic, low risk of progression to 3rddegree heart block TX:Usually no Rx needed. Atropine if symptomatic. **Remove triggers*

Answer 48

Intermittent non-conducted P waves **without** **progressive** **prolongation** of the **PR interval** Anterior MI, *Fibrotic disease of conducting syste S/S: Likely to have haemodynamic compromise and progression to 3rddegree heart block *Tx: PACEMAKER (transcutaneous or transvenous) ** Tx MI*

Answer 49

Severe bradycardia due to absence of AV conduction *Complete AV dissociation, S/S: Syncope (if self-terminating) or sudden cardiac death (if prolonged)*Rx: PACEMAKER

Answer 50

Sinus node dysfunction (formerly called sick sinus syndrome) *Aka Tachycardia-bradycardia syndrome intrinsic causes: idiopathic degenerative fibrosis (most common extrinsic: meds Chronic sinus node dysfunction associated with symptoms is an indication for permanent pacing but rarely requires acute intervention. *It is a **leading reason for a cardiac pacemaker** (in Australia it accounts for approximately 46% of devices

Answer 51

This is usually benign *Anxiety or stress, Response to fear, pain, exercise. *Less often -thyrotoxicosis,anaemia, infection, pulmonary embolism. *S/S: palpitations, SOB, HR 100 -150 bpm

Answer 52

Presents with irregular ventricular rate of about 160–180 beats/minute in untreated patients with a normal AV node. **absence of distinct P waves**

Answer 53

ACUTE = PIRATES -Pulmonary disease -Ischemia -RHD Anemia Thyrotoxicosis Ethanol, electrolyte abn Sepsis chronic **HTN most common cause of AF** CHF

Answer 54

*Hyperthyroidism *Alcohol excess *Electrolyte abnormalities *Sepsis

Answer 55

## Footnote 5. Lastly, consider pacemaker insertion followed by atrioventricular (AV) node ablation. *Best used for patients who have failed treatment with pharmacologicagents or cannot tolerate them due to hypotension

Answer 56

it can be helpful in patients who remain symptomatic despite adequate rate control therapy. are physically active *have paroxysmal or persistent AF lasting short periods of time *do not have significant underlying cardiac structural changes

Answer 57

For both methods of cardioversion, assess the stroke risk. Use CHA2DS2-VASc score! Immediately start **anticoagulant** therapy with UFH or LMWH in men with a score of ≥ 1 or women with a score of ≥ 2whoare to undergo cardioversion FLECAINIDE SOTALOL (renal) AMIODORONE (liver - pulmonary fibrosis)

Answer 58

Higher risk of embolism in AF >48hrs because left atrial thrombi likely to form due to atrial stagnation: 1.those in whom cardioversionto sinus rhythm is being considered (regardless of the CHA2DS2-VASc score or method of cardioversion [electrical or pharmacologic]). 2.those who meet criteria for long-term anticoagulation (risk of embolization exceeds the risk of bleeding) I**n all pts with AF,** assessment should be done prevent systemic embolization even for the first AF episode.Use** CHA2DS2-VASc score** *Risk of bleeding is assessed through **HAS-BLED score** *In planned cardioversion, **anticoagulation should be started 3-4 weeks before to 4 weeks after**

Answer 59

**NOAC**-indicated in non-valvular AF only. Do not use in pts with renal impairement. ***Warfarin**-In the special case of **‘valvular AF’** (defined as the presence of a mechanical heart valve or moderate-to-severe mitral stenosis),warfarin therapy is the only effective recommended treatment option, and the NOACs should not be used.It is also used in non-valvular AF. ***Heparinis used with warfarin** initially till the INR levels fall within 2-3 and then warfarin only

Answer 60

Immediate electrical cardioversion synchronized with sedation (emergency)

Answer 61

**Rate control is the preferred initial treatment** (if thrombus cannot be excluded or ptnot on anticoag) **Defer acute cardioversion unless** left atrial thrombus has been excluded, or the patient has had therapeutic anticoagulation for the previous 3 weeks. ***Transoesophagealechocardiography (TOE)** may be considered to exclude left atrial thrombus and allow early cardioversion. For these patients, anticoagulant therapy should be started at the time of cardioversion and continued for a minimum of 4 weeks after cardioversion ## Footnote 1.- beta 2.block Channels C

Answer 62

**Narrow complex tachycardia ** *Regular atrial activity at ~300 bpm **ventricular rate 125-150** *Loss of the isoelectric baseline *“Saw-tooth” pattern of inverted flutter waves in leads II, III, aVF **Atrial flutter commonly reverts with a low-energy direct current (DC) shock** treatmen similar to AF (insensive to antiarrhythmic drug therapy ## Footnote difference to atrial fibrilation by the irregular rhythm

Answer 63

Sudden-onset regular rapid palpitations will signify episodes of SVT . **HT 150-200** younger patients like athletes, STABLE - **1 first LINE vagal manoeuvres **(valsava , cold stimulus face, carotid massage (avoid in older pts and those with vascular disease) - - 2n LINE if vagal doesnt work - **ADENOSINE IV** - VERAPAMILO IV - METROPROLOL IV (**no in asthma)** -3 LINE **CARDIOVERSION** **UNSTABLE** Cardioversion !

Answer 64

WPW syndrome **Short PR interval** -coz of preexcitedVentricular tissue ***Delta wave** -V stimulation for a longer period of tim Tx stable - vagal meassures, antiarrythmics unstable - DC cardioversion

Answer 65

**ECG: rate 150-250 bpm** S/S: Palp, SOB, angina, syncope, lightheadedness Tx stable - vagal meassures, antiarrythmics unstable - DC cardioversion

Answer 66

Hypoxia, electrolyte imbalance, hyperthyroidism Inv: *ECG-early wide QRS( >440 msec, ~ 11 small boxes), not preceded by a P wave Rx:*Treat underlying cause *If symptomatic: 1stline is BB (atenolol, metoprolol), 2ndline Verapamil or flecainide if AUSENCE OF HEART DISEASE OR SIGNIFICANT RISK FACTORS **REASURANCE**

Answer 67

**VT is 3 or more ventricular ectopic beats at a rate of > 130 beats/min** ustained VT is if it lasts > 30 seconds Monomorphic (MC) -regular, wide (≥120 milliseconds) QRS complex tachycardia with uniform and stable QRS morphology Polymorphic -multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration

Answer 68

Etiology:*MCC is CAD, MI ECG: 3 or more VEB, Wide QRS complexes

Answer 69

Sustained VT Rx 1.-**UNSTABLE** check for pulse A) PULSLESS VT: is a shockable rhythm. So CPR + **Defibrillation (unsynchronous cardioversion)** B) WITH PULSE: Non-shockable rhythm. So Synchronized Cardioversion 2.-**STABLE***antiarrhythmic drug therapy **-Amiodarone is 1stline** ------------------------------ NON Sustained VT Rx **1stline**: **BB-Atenolol, metoprolol** ***2ndline**: **Verapamil** or **flecainide** may be a suitable alternative if beta blockers are contraindicated or not tolerated, provided the patient has no evidence of left ventricular dysfunction. Also avoid flecainide if the patient has coronary disease. ***3rdline**: If symptoms persist or there is suspicion of a cardiomyopathy secondary to the nonsustained ventricular tachycardia consider **amiodarone** ***4thline**: Consider **catheter** **ablation** for a patient with significant symptoms not controlled by drug therapy, or if there is suspicion of cardiomyopath ## Footnote IN CHILDREN WITH **WIDE** QRS ASYMPTOMATIC OR STABLE ( SUSTAINED OR NOT if has symptoms) = **ADENOSINA ** Porque en ninos un QRS ancho > 0,09 sec = puede ser SVT with aberrancy, en adultos es mas del ventriculo.

Answer 70

Hypocalcemia, hypokalemia, hypomagnesemia

Answer 71

**Antiarrhythmic**-Sotalol, amiodarone, flacainamide ***Antipsychotics**-haloperidol, chlorpromazine ***SSRI**, TCA ***Antihistamine** ***Antifungal** -ketoconazole, fluconazole ***Abx** -Azithro, erythro *Antimalarial -chloroquine *Domperidone *Opiate -methadone *Other -arsenic, droperidol

Answer 72

Chaotic irregular deflections of varying amplitude *No identifiable P waves, QRS complexes, or T waves *Rate 150 to 500 per minute

Answer 73

S/S frequently self limiting Treatment involves **immediately stopping any drug suspected of causing TdP, and correcting electrolyte abnormalities.** *Drug-induced TdPand to control underlying bradycardia: **IV Magnesium Sulphate **or IV Isoprenaline or temporary transvenous pacing *Congenital QT prolongation: Metoprolol, propranolol. Consider implantable cardioverter defibrillator. *If TdPhas an underlying bradycardia: Use Atropine

Answer 74

*ACLS protocol *Immediate electrical cardioversion

Answer 75

Aortic Stenosis, Pulmonary Stenosis *Mitral Regurgitation, Tricuspid regurgitation *Mitral valve prolapse

Answer 76

Aortic Regurgitation, Pulmonary regurgitation *Mitral stenosis, Tricuspid stenosis

Answer 77

Ejection systolic murmur, that **radiates to the carotids**. in elderly to the **apex** **most comon dyspnea** syncope dx: ECHO TTE TX: Aortic valve replacementespif aortic area <0.7 cm2 *Furosemide for symptomatic relief initially *Metoprolol for angina

Answer 78

Chronic –Calcified aortic sclerosis, dilatation of ascending aorta from HTN, Connective tissue disorder (Marfan’s syndrome Acute –Aortic dissection, infective endocarditis, RF, chest injury -Increased pulse pressure –high SBP due to incstroke volume and low DBP ***Corrigan**’s pulse (bounding carotid pulse), Water hammer pulse (radial and ulnar artery)–rapid systolic rise and rapid diastolic collapse *De **Musset**’s sign –head bobbing synchronous with heartbeat ***Decrescendo early-Diastolic blowing murmur at the lower left sternal borde** ***Systolic flow murmur at Aortic area/Apex** –due to inc blood flow across aortic valve ***Austin-Flint murmur** low pitched mid-diastolicrumble at apex –due to a functional MS -severe AR dx - echo tx Vasodilators/ACEI, Aortic valve replacement

Answer 79

reumatic fever

Answer 80

Opening Snap ->Mid-diastolic murmurat Mitral area (rapid filling phase) tx BB/diuretics/ Antiarrhythmics and anticoagulants as AF is common *Percutaneous balloon valvuloplasty –in favorable valve morphology *Mitral valve replacement

Answer 81

Etiology - *Primary: affecting mitral leaflets (**MVP**, ruptured chordae tendineae, calcific degeneration) *Secondary ischemic: Reversible ischemia or **papillary muscle infarction (AMI)** *Secondary non-ischemic: RF, Papillary muscle apical displacement (LVH) *Signs –**Holosystolic/Pansystolic murmur** (flat, no change in intensity) in Mitral area, radiating to axilla *Diag–Echo, Angiography (assess severity) *Tx –*Vasodilators (ACEI/ARB)/Antiarrhythmics as AF is common*Valve repair vs replacement ## Footnote papilary muscle disfuction vs infarction (EF %< 50 rupture)

Answer 82

Primary –Sporadic, familial (AD, XR) *Secondary –Connective tissue disorders, cong. disorder **signs** **Mid-systolic non-ejection click followed by Systolic Murmer**

Answer 83

Dilatation greater than 1.5 times the expected diameter of all three layers of the aortic wall An infrarenal aorta 3 cm in diameter or more OR having increase >50% from baselineis considered aneurysmal Advancing Age -rarely seen <50 *M > F *Family history of aortic dissection or thoracic aortic aneurysm –20% risk of AAA *Atherosclerosis–eg: Smoking, HTN, hypercholesterolemia *Other vascular aneurysm *Prior aortic dissection *Marfan’s, vascular Ehlers-Danlos, Turner, or other connective tissue disease. *Known aortic valve disease (eg, bicuspid aortic valve, aortic valve replacement, or aortic stenosis). Usually **asymptomatic**, incidental finding *AAA -Epigastric pain radiating to back *Thromboembolism* Signs: Pulsatile abdominal mass, abdominal bruit **Dx: USG (bedside –FAST)** *CT abdwith contrast & MRI*in elective settings, if diagnosis uncertain and ptis stable*CT angiogram

Answer 84

Classic triad’–* Pain -severe tearing abdominal pain radiating to the back *Hypotension/circulatory compromise *Pulsatile mass in abdomen *Inv: ***USG/FAST** ***CT –Crescent sign***acute haematoma within the thrombus or wall *sign of impending rupture or contained rupture *Mx: Immediate FAST USG -> DRSABC -> emergency surgery ## Footnote retroperitoneal savable / peritoneo muertisimo

Answer 85

Haematoma that forms as a result of leaking hole in an artery. Haematoma MUST communicate to the arteryto consider it pseudoaneurysm. Haematoma forms outside the wall and is contained by the fibromuscular tissue **femoral** Trauma, iatrogenic injury(at the anastomotic site of sx) or infection Asymptomatic pulsating mass, **Painful pulsating mass** with associated hematoma +/-bruit Doppler Duplex USG TX **USG guided thrombin injection away from the neck of sac **-Femoral/Iliac/peroneal *Angiographic interventionretrograde approach –for acute vessel occlusion due to distal emboli

Answer 86

Symptoms: **chest pain anteriorly (ascending aorta)**; r**adiating to back(descending aorta**) Typically, Hypertensive with compensatory tachycardia. ***Asymmetric** pulses and BP measurements *Murmur of AR –if aortic valve involved *STEMI *If hypotensive –consider pericardial tamponade, DX Transesophageal echo -1stchoice –provides details of artery, pericardial effusion, AR, MI

Answer 87

Ascending aortic dissection–are surgical emergencies *Descending aortic dissection –emergencies that can be often treated medically *Meds: Monitor and manage BP and HR –Start B Blockers before starting vasodilators **Morphine -> B Blockers -> Arrange TEE (or CT angioif TEE not available) -> Surg/Med** *Absolute CONTRAINDICATION! -Aspirin, clopidogrel, anticoagulants, and Thrombolytics

Answer 88

risk factors: smoking hx CVD HTN diabetes

Answer 89

**Aortoiliac disease: ** *Affects Common Iliac artery, External iliac artery *Pain in buttocks, especially when walking up the stairs *Decreased femoral pulses ***Male impotence -Leriche’s syndrome** ***Femoropopliteal disease: ** *Affects most commonly superficial femoral artery *Pain in calf *Decreased pulses below the femoral artery Subtotal occlusion of Rt CIASFA stenosis

Answer 90

***1stline Duplex USG-assess flow, stenosis >75% is clinically significant** ***2ndline CT angiography –done before intervention/operative planning**. *Digital Subtraction angiography, MRA **TREATMENT:** SM –Avoid smoking, eat healthy, exercisecan develop collateral circulation*Meds –Anti HTN, lipid-lowering agents, glycemiccontrol *Cilostazol (phosphodiesterase III inhibitor)–good for intermittent claudication pain *Antiplatelet (aspirin, clopidogrel) –especially after surgery *Surgical intervention -endovascular angioplasty or stenting, peripheral bypass or endarterectomy

Answer 91

Tx: *Supportive *NSAIDS for pain *compression stockings for edema

Answer 92

Commonest site: Common femoral artery 6 P’s of Acute Ischemia: *PAIN –sever and sudden *PALLOR ***PARALYSIS**(light touch, weakness)–Most reliable indicator for immediate SURGERY *PULSE DEFICIT *PARASTHESIA *POIKILOTHERMIA –least reliable reversible within 4hrs of symptoms with intervention. *Diagnosis: Usually enough by history and physical examination ***1stline investigation is CT angiography** -Done before interventions, as it can give a lot of info + . ***Antithrombotic: IV Unfractionated** Heparin (UFH)5000 IU then 1250 IU/h should be started with confirmed diagnosis (absent pulse). **Start before diagnostic procedures. Do NOT wait**. Then chkAPTT (1.5-2.5 times abv pt’sbaseline)every 6hrs till 65-100 sec + Hx, PE = IV UFH = CT angio=>Surgery => DAPT/Antithrombotic Surgical Mx: *Emergency revascularisation -open thromboembolectomy, endarterectomy, bypass surgery, patch angioplasty, or intraoperative thrombolysis *Paralysis/Paraesthesia: **Definite Mx is Embolectomyunder 4hrs (after UFH)** ## Footnote After Surgery: *Patients who underwent angioplasty or stentingare typically placed on dual-antiplatelet therapywith **aspirin** (81 or 325 mg) + **clopidogrel** (75 mg)* Patients with **underlying thromboembolic** disease are typically **anticoagulated** with **warfarin** or a **NOAC**

Answer 93

HIPERCALCEMIA CONGENITAL QT SYNDROME DIGOXINA

Answer 94

TALL T WAVES P FLAT WAVES SHORT QT (QRS LOOKS WIDE AND BIZARRE) ## Footnote AMLODIPINO AMIODORONA

Answer 95

first **ATROPINE to stablize the patient** once stable requieres the placement of a Pacemaker. 1. atropina , transcutaneos pacing and transvenous pacing 2. pacemaker unstable=atropina no cardioversion no defibrilation

Answer 96

**william**

Answer 97

**marrow ** RSR' v1-3

Answer 98

extreme right axis deviation S1 Q3 T3 (s en I pronunciada, q en 3 y t negativa )

Answer 99

VENTRICULAR FIBRILATION

Answer 100

>=4 = DVT likely

Answer 101

**Pleuritic Chest pain**: Aggravated by cough and deep inspiration, worse with lying flat, relieved by sitting up. **Shortness Of Breath**

Answer 102

Fist: Chest pain-ECG (S1Q3T3) Diagnostic Second: SOB-CXR---> Rule out pulmonary pathology Pregnancy (Doppler USD of legs)

Answer 103

Wells Score: - Low: D dimer - High: CTPA (Gold standard) V/Q (Pregnancy or ♀< 45 yo)

Answer 104

Clinical symptoms of DVT (leg swelling, pain with palpation) 3 Another diagnosis less likely than pulmonary embolism 3 Heart rate >100 1.5 Immobilization (≥3 days) or surgery in the previous four weeks 1.5 Previous DVT/PE 1.5 Hemoptysis 1 Malignancy 1

Answer 105

Wells criteria High >6.0 Moderate 2.0 to 6.0 Low <2.0 Modified Wells criteria PE likely >4.0 PE unlikely ≤4.0

Answer 106

1. Aged <50 years 2. Pulse <100 bpm 3. SaO ≥95% 4. No haemoptysis 5. No oestrogen use 6. No surgery or trauma requiring hospitalisation within 4 weeks 7. No prior venous thromboembolism 8. No unilateral leg swelling RESULT: IF ALL YES RULE OUT PE

Answer 107

ABCD/Oxygen/Morphine Stable: - LMWH. - Renal disease --> Unfractionated Unstable: Thrombolysis

Answer 108

Sudden-onset of SOB with tachypnea Diaphoresis and cyanosis Productive cough: pink or white frothy sputum Crackles and Wheezes (Kettle boiling) * Hypotension: Cardiogenic shock

Answer 109

1. Acute Mitral and Aortic Regurgitation 2. LV Systolic Dysfunction: anterolateral MI 3. AF with rapid ventricular response

Answer 110

1. CXR 2. ECG 3. Troponin 4. FBE 5. TTE

Answer 111

Arterial/Venous Blood Gases to assess the severity of hypoxemia.

Answer 112

1. O2 2. IV line 3. NGT spray or SL / IV is preferred to Morphine (BP > 100) 4. Furosemide IV 5. Morphine IV (chest pain) 6. CPAP APO + AF = BB APO + AF + CHF = Digoxin inf

Answer 113

1. Staphiloccocus Aureus 2. Streptococci 3. Enterococci (at least 90% faecalis)

Answer 114

 Artificial heart valves.  Congenital heart defects.  A history of endocarditis.  Damaged heart valves: rheumatic fever  History of intravenous (IV) illegal drug use.  Immunocompromised patient.

Answer 115

Modify Duke's criteria: DEFINITIVE Infectious Endocarditis: 2 Major Criteria OR 1 Major + 3 Minor Criteria OR 5 Minor Criteria POSSIBLE Infectious Endocarditis: 1 Major Criteria + 1 Minor criteria 3 Minor Criteria In POSSIBLE Management: Repeat TTE + TOE

Answer 116

TWO MAJOR CRITERIA 1. Positive blood cultures for infective endocarditis: Typical microorganisms for infective endocarditis: Coxiella burnetii, Viridans streptococci, Streptococcus bovis, and HACEK group OR Community-acquired Staphylococcus aureus or enterococci in the absence of a primary focus. NOTE: 2 blood cultures drawn 12 hours apart or all of 3 or most of 4 or more separate blood cultures, with the first and last drawn at least one hour apart OR Single blood culture positive for Coxiella Burnetii or IgG titre > 1:800 ----------------------------------------------------- 2. Evidence of endocardial involvement: Positive echocardiogram for infective endocarditis OR Cardiac Vegetation OR Cardiac Abscess OR New partial dehiscence of prosthetic valve OR New valvular regurgitation

Answer 117

FIVE MINOR CRITERIA 1. Predisposing heart condition or intravenous drug user 2. Fever: 38°C 3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions 4. Immunologic phenomena: Glomerulonephritis Osler nodes Roth spots Rheumatoid factor (+) 5. Microbiologic evidence: positive blood culture but not meeting major criterion as noted previously or echocardiography findings consistent with infective endocarditis but not meeting major criteria as noted previously

Answer 118

1. Blood culture: Diagnostic 2. FBE: leucocytosis with neutrophilia and anemia. 3. ECG: Cardiac monitoring 4. CXR: Signs suggestive of heart failure. NOTE: 2 blood cultures drawn 12 hours apart or all of 3 or most of 4 or more separate blood cultures, with the first and last drawn at least one hour apart

Answer 119

Transesophageal echo (TOE) BUT: - If HACEK: CT angio - If arrhythmias: ECG - If spread: CT/MRI (brain, thorax, and abdomen)

Answer 120

Slow-growing, fastidious gram-negative organisms 1. Haemophilus species: Aggregatibacter aphrophilus, H. Paraphrophilus. 2. Aggregatibacter actinomycetemcomitans 5. Cardiobacterium hominins 4. Eikenella corrodens 5. Kingella kingae

Answer 121

Large vegetation Perivalvular abscess Multiple emboli Secondary septic events

Answer 122

Benzylpenicillin + Gentamicin + Flucloxacillin IV

Answer 123

Methicillin-susceptible: Flucloxacillin x 6 weeks Methicillin-resistant (MRSA): Vancomycin IV x 6 weeks ATB treatment is usually at least 2 weeks IV and oral until completing 4-6 weeks

Answer 124

UNCOMPLICATED: Benzylpenicillin + Genta IV x 2 weeks OR Benzylpenicillin IV x 4 weeks OR Ceftriaxone IV x 4 weeks COMPLICATED: Add gentamicin IV x 2 weeks ATB treatment is usually at least 2 weeks IV and oral until completing 4-6 weeks

Answer 125

Benzylpenicillin x 6 weeks Complicated: Add gentamicin IV ATB treatment is usually at least 2 weeks IV and oral until completing 4-6 weeks