4th year · Cardiology

The P wave represents atrial depolarization.

The normal QRS complex lasts less than 80 ms (< 0.08 s).

DII, DIII and aVF explore the lower wall of the left ventricle.

The normal axis of the QRS is between -30° and +90°.

The Sokolow-Lyon criterion is the main ECG criterion for LVH.

The aortic focus is in the 2nd right intercostal space, sternal border.

The pathological Q wave: duration > 40 ms and amplitude > 25% of the R in ≥ 2 contiguous leads.

The normal PR interval is between 120 and 200 ms (0.12-0.20 s).

B3 is a proto-diastolic gallop suggestive of heart failure with volume overload.

Horizontal or descending ST depression suggests subendocardial ischemia.

The Holter ECG is indicated for the detection of paroxysmal rhythm disturbances.

Symptomatic severe aortic stenosis is an absolute contraindication to stress testing.

The Sokolow-Lyon criteria and the Cornell index are two criteria for LVH.

ETT, myocardial scintigraphy, and isotope ventriculography assess LVEF.

Systolic ejection murmur, B3 in an older adult, and diastolic murmur are pathological.

Rhythm (regular/irregular, frequency), P wave (present/morphology), PR, QRS (duration, axis, morphology), ST (high/low), T wave, corrected QT.

Dyspnea on exertion then at rest, orthopnea, paroxysmal nocturnal dyspnea, tachycardia, bilateral pulmonary crackles, B3 gallop.

Grade 1 hypertension corresponds to SBP 140-159 mmHg or DBP 90-99 mmHg.

Hypertension resistant to triple therapy including a diuretic points to a secondary cause.

Hypertensive encephalopathy (neurological symptoms) associated with severe hypertension constitutes a hypertensive emergency.

Left ventricular hypertrophy is a target organ damage of hypertension.

The overall cardiovascular risk includes blood pressure level, associated risk factors and target organ damage.

Primary hyperaldosteronism combines hypertension, spontaneous hypokalemia and metabolic alkalosis.

ACE inhibitors and ARBs II are contraindicated during pregnancy (fetal nephrotoxicity).

Hypertension accelerates atherosclerosis and promotes coronary insufficiency.

ABPM can detect white coat hypertension and masked hypertension.

Type 2 diabetes is a major independent cardiovascular risk factor.

Microalbuminuria is the early sign of hypertensive nephropathy.

The target organ damage sought is LVH, retinopathy and nephropathy.

Renal artery stenosis, pheochromocytoma and primary hyperaldosteronism are classic causes of secondary hypertension.

Hygiene-dietary measures include sodium restriction, physical activity and smoking cessation.

Emergency: Severe hypertension + acute target organ damage (encephalopathy, dissection, PAO, anuria, eclampsia). Simple push: high numbers without acute visceral damage.

Blood pressure level, smoking, diabetes, dyslipidemia, age, sex, familial ATCD, target organ damage, established cardiovascular diseases.

Stable angina is reproducible with exercise and resolves quickly with rest or trinitrin.

STEMI is defined by persistent ST elevation; the NSTEMI by its absence.

Coronary pain is typically constrictive retrosternal with radiation to the left arm.

The ECG evolution of STEMI: ST elevation → necrotic Q wave → negative T wave.

Type A aortic dissection can mimic STEMI and is a contraindication to thrombolysis.

Rupture of the free wall of the LV is the most lethal mechanical complication of early infarction.

NSTEMI is distinguished from unstable angina by an elevation of troponin (myocardial necrosis).

Active smoking is the most potent modifiable cardiovascular risk factor.

The V1-V4 territory corresponds to the area perfused by the IVA (anterior interventricular artery).

High sensitivity troponin I or T is the reference biomarker for MI.

Pericarditis gives diffuse, concave ST elevation, without mirror or Q wave.

The earliest possible reperfusion (primary angioplasty as a priority) is the fundamental principle of treatment of STEMI.

VF, complete BAV, and sustained VT are early electrical complications of MI.

Aortic dissection, massive pulmonary embolism and pneumothorax are emergencies to be eliminated.

Effort, stress and cold are classic triggers of angina.

Emergency 12-lead ECG, high sensitivity troponin, clinical assessment (pain characteristics, coronary FDR), elimination of differential diagnoses (dissection, PE, pneumothorax).

Transmural myocardial necrosis. Criteria: duration > 40 ms, amplitude > 25% of R, present in at least two contiguous leads.

Bilateral crackles at the lung bases indicate pulmonary edema of the left IC.

Jugular turgor indicates central venous hypertension specific to the right IC.

Crepitants, jugular turgor and the context of heart disease point towards cardiogenic PAO.

Cardiogenic shock presents with elevated pulmonary capillary wedge pressure (overload); hypovolemic shock low pressure (deficit).

Orthopnea is increased dyspnea in recumbency, relieved by sitting or standing.

Neurohormonal activation (sympathetic + RAAS) is the primary compensatory mechanism of HF.

NYHA class III corresponds to dyspnea for moderate efforts with notable limitation of activity.

HFpEF: LVEF ≥ 50% with clinical signs of HF and relaxation disorder (diastolic dysfunction).

BNP and NT-proBNP are the reference biomarkers for HF.

Septic shock is vasodilatory (low SVR); cardiogenic shock is vasoconstrictive (high SVR).

Pinkish foamy sputum with cyanosis and drawing indicates a serious, life-threatening PAO.

PE, PAH, and chronic cor pulmonale are causes of right-sided HF.

Beta-blockers, ACE inhibitors and MRAs have a demonstrated prognostic benefit in rHFp.

Refractory desaturation, respiratory exhaustion and cardiogenic shock are serious criteria.

Cardiogenic shock: tissue hypoperfusion due to heart pump failure. SBP < 90 mmHg, signs of hypoperfusion, high filling CI (PCP ≥ 18 mmHg), low cardiac index (< 2.2 L/min/m²). Differences with hypovolemic shock (low pressure, signs of dehydration) and septic shock (vasodilation, low SVR, fever/infectious focus).

Left HF: dyspnea, orthopnea, pulmonary crackles, B3 gallop, tachycardia, pink sputum. Right IC: jugular turgor, hepatomegaly, hepatojugular reflux, sloping edema, ascites.

RM gives a diastolic roll with presystolic strengthening at the apex.

MI: holosystolic murmur. RM: diastolic rolling.

Symptomatic tight RAo manifests as exertional angina, exertional syncope and dyspnea.

The IAO gives a decreasing holodiastolic murmur to the left border of the sternum.

Carditis is a major Jones criterion for RAA.

The diagnosis of IE is certain with 2 major criteria, or 1 major + 3 minor, or 5 minor according to Duke.

Viridans streptococci (oral) are the most common germs of native valve IE.

A cerebral embolism in a febrile patient with valvular disease should suggest an IE with emboligenic vegetation.

Severe chronic IAO gives a bounding (Corrigan) pulse with widened pulse pressure.

AAR results from an autoimmune cross-reaction between streptococcal antigens and cardiac tissues.

Wearers of mechanical prostheses risk thrombosis or embolism due to insufficient anticoagulation.

Typical blood cultures and echocardiographic data are the major criteria at Duke.

AF, PAH and congestive HF are common complications of mitral valve disease.

Migratory arthritis, Sydenham's chorea and erythema marginatum are manifestations of AAR.

Duke criteria: repeated blood cultures (before antibiotic therapy) + echocardiography (ETT then TEE if negative or inconclusive). Front door search.

RAA → fibrosis and progressive calcification of the mitral valves → transmitral gradient → post-capillary PAH → right IC. Complications: AF (OG dilatation), systemic embolism, hemoptysis, endocarditis.

AF is characterized by anarchic atrial activity 'f' and an irregular RR interval.

Flutter: regular sawtooth F waves at ~300/min. AF: irregular anarchic atrial activity.

The BAV Mobitz II: fixed PR then sudden blocking of a P wave without prior lengthening.

The junctional escape rate in the complete BAV is 40-60/min.

The BBGC: QRS ≥ 120 ms, R wide and hooked in V5-V6, QS in V1.

Vagal maneuvers (Valsalva, carotid massage) can reduce junctional tachycardia.

The concordance of the precordial QRS indicates ventricular tachycardia.

Rhythmic syncope occurs suddenly without a prodrome, often traumatic, during exercise or at rest.

AF puts you at risk of ischemic stroke through left atrial (auricular) thrombus embolism.

1st degree BAV: PR > 200 ms constant without QRS block.

ESV: Wide and bizarre QRS, premature, without P wave, followed by a compensatory pause.

Complete BAV and symptomatic Mobitz II BAV are classic indications for permanent pacemaker.

Hyperthyroidism, mitral valve disease, and acute pericarditis can trigger AF.

The BBDC: QRS ≥ 120 ms, RSR' in V1, wide and deep S wave in DI and V6.

BAV 1°: PR > 200 ms stable, benign. BAV 2° Mobitz I: progressive PR lengthening + blocked QRS, often benign vagal. BAV 2° Mobitz II: sudden blockage without lengthening, risk of progression to complete BAV. BAV 3°: complete AV dissociation, slow, serious escape rhythm.

Three axes: rate control, rhythm control (cardioversion), thromboembolic prevention (anticoagulation according to CHA2DS2-VASc score). Treatment of the underlying cause.

Venous Doppler ultrasound is the gold standard for the diagnosis of DVT.

The S1Q3T3 appearance is classically associated with severe pulmonary embolism.

Sudden dyspnea, tachycardia, sign of DVP, cyanosis and right ECG deviation point to a massive PE.

Negative D-dimer allows exclusion of VTE in a patient with low clinical probability.

AVK inhibit the hepatic synthesis of vitamin K-dependent factors (II, VII, IX, X).

The red, warm, edematous limb with positive Homans sign indicates DVT.

Intracranial hematoma is the most serious hemorrhagic complication of anticoagulants.

Aspirin irreversibly inhibits platelet COX-1, reducing thromboxane A2 synthesis.

After coronary stenting for ACS, dual antiplatelet aggregation is indicated.

Virchow's triad: venous stasis, endothelial injury and hypercoagulability.

LMWHs have predictable subcutaneous bioavailability and preferentially inhibit factor Xa.

Immobilization, neoplasia, and thrombophilia are FDRs of VTE.

Recent intracranial hemorrhage, severe thrombocytopenia and recent surgery with high hemorrhagic risk are contraindications to anticoagulants.

Clinical probability (Wells score), D-dimer if low probability, CT angiography if positive or intermediate/high probability. Severity: hemodynamics, echocardiography (RV dysfunction), troponin, BNP.

Balance thrombotic benefit vs hemorrhagic risk. Biological monitoring adapted to the type (INR for AVK, anti-Xa for LMWH). Adaptation to renal and hepatic functions. Duration according to the indication (short term for provoked PE, long term if AF or recurrence).

Intermittent claudication: exertional muscular pain relieved by stopping, linked to exertional ischemia.

Acute limb ischemia: pallor, coldness, intense pain, lost pulse, paresthesias/paralysis.

Aortic dissection causes immediate maximal tearing pain, migrating to the back and abdomen.

Stanford A: damage to the ascending aorta. Stanford B: limited to the descending aorta.

An ABI < 0.9 indicates PAD.

An AAA is defined by an aortic diameter > 30 mm (or > 50% of the overlying segment).

Thrombolysis can aggravate aortic dissection by promoting intraparietal hemorrhage.

Leriche-Fontaine stage IV corresponds to trophic disorders (ulcers, gangrene).

Cardiac embolism is the main cause of acute limb ischemia.

Arterial ischemia: pale, cold limb, absent pulse. DVT: warm, erythematous, edematous limb, preserved pulse.

Type A dissection can result in tamponade, acute IAO, and coronary occlusion.

Smoking, diabetes and dyslipidemia are the main risk factors for PAD.

Clinical: migrating tearing pain, blood pressure asymmetry. Urgent assessment: ECG (eliminate IDM), chest x-ray (mediastinal widening), reference thoraco-abdomino-pelvic angioscan. Don't forget to eliminate a PE.

Deprivation of blood supply exposes one to irreversible muscle necrosis in less than 6 hours. Beyond that, amputation is inevitable. Restoration of flow must be as rapid as possible (surgical or endovascular revascularization).

Pericardial friction is the pathognomonic auscultatory sign of acute pericarditis.

PR depression is a specific ECG sign of acute pericarditis.

Beck's triad: hypotension, jugular turgor, muffled heart sounds.

Myocarditis manifests as chest pain and elevation of troponin after a viral infectious episode in young adults.

PAH is defined by an average PAP > 20 mmHg at right catheterization at rest.

COPD is the most common cause of chronic cor pulmonale.

Dilated cardiomyopathy: dilated LV, collapsed LVEF. HCM: hypertrophic LV with preserved or supernormal LVEF.

Tamponade: compression by acute effusion. Constriction: thickened and rigid pericardium chronically limiting filling.

Primary PAH: RV dilatation, normal LV. Left IC: LV dilation, LVEF lowered.

Cardiac MRI with non-systematized late enhancement confirms myocarditis.

Neoplasia, renal failure and hypothyroidism can cause profuse pericardial effusion.

Jugular turgor, hepatomegaly and edema indicate right heart failure in PAH.

At least 2 of the 4 criteria: pericardial chest pain (pleuritic, relieved leaning forward), pericardial rub, concave diffuse ST elevation with PR depression, new pericardial effusion. ECG: diffuse elevation without territory, concave, without Q wave, with PR depression.

Chronic hypoxia → hypoxic pulmonary vasoconstriction → PAH → RV pressure overload → hypertrophy then RV dilatation → right HF.

CIA is a congenital heart disease with left-right shunt (initial non-cyanogenic).

The L-R shunt leads to pulmonary overload → PAH → reversal of the R-L shunt (Eisenmenger syndrome).

The innocent murmur is systolic, soft, short, grade 1-2/6, modified by position and breathing.

Increased cardiac output and heart rate in pregnancy worsen the MR gradient and may trigger PAO.

Mechanical prostheses expose you to the risk of thrombosis or embolism if anticoagulation is insufficient.

Pulmonary stenosis + CIV causes a D-G shunt with passage of non-oxygenated blood into the greater circulation.

The bioprosthesis does not require long-term anticoagulation (after the initial period).

Childbirth and the immediate postpartum period represent the maximum hemodynamic risk for the cardiopath.

Multiple blood cultures before any antibiotic therapy are the first diagnostic step.

Severe PAH and Eisenmenger syndrome constitute almost absolute contraindications to pregnancy.

Tetralogy of Fallot and transposition of the great vessels are cyanogenic heart diseases.

Monitoring echocardiography, blood pressure and signs of decompensation is a priority in pregnant women with heart disease.

Thrombosis, endocarditis and degeneration (for bioprostheses) are the specific risks of valve prostheses.

L-R shunt: oxygenated blood to the pulmonary circuit → pulmonary overload → PAH, without initial cyanosis. D-G ​​shunt: non-oxygenated blood to the general circulation → central cyanosis.

Mechanical prostheses are thrombogenic. Anticoagulation (AVK) prevents intraprosthetic thrombosis and embolisms. Underdosing exposes you to thrombosis; an overdose exposes you to hemorrhage. The INR must remain within the therapeutic target.

Loop diuretics inhibit the Na-K-2Cl cotransporter in the ascending loop of Henle.

Severe asthma or COPD with bronchospasm are absolute contraindications for non-selective beta-blockers.

Chronic dry cough is the most common side effect of ACE inhibitors.

ACE inhibitors/ARBs II reduce aldosterone production, reducing renal elimination of potassium → hyperkalemia.

Digitalis inhibits Na+/K+-ATPase, leading to an increase in intracellular calcium and a positive inotropic effect.

Beta blockers are class II in the Vaughan Williams classification.

The thyroid should be monitored under amiodarone, which can cause hypothyroidism or hyperthyroidism.

Loop diuretics: increased distal flow → K+ secretion. Savers: aldosterone blockade → K+ retention.

Thrombolytics activate plasminogen to plasmin, which lyses the fibrinous thrombus.

IEC: inhibit ACE → bradykinin ↑ → cough. ARA II: block AT1 without accumulation of bradykinin → no cough.

Beta-blockers have a demonstrated prognostic benefit in rHF, post-MI and for rate control in AF.

Antiaggregant: inhibits platelets. Anticoagulant: acts on the coagulation cascade (plasma factors).

The reference triple therapy for HFrEF: IEC (or RNAi), beta-blocker and ARM.

Hyperkalemia, IR in case of bilateral stenosis and contraindication in pregnancy are common to ACE inhibitors and ARB II.

Digoxin is indicated for rate control of AF and symptomatic HF with reduced EF.

Class III (K+ blocker). Multi-channel (Na+, K+, Ca²+, beta blocker). Very long half-life (40-55 days). Adverse effects: thyroid (hypo- or hyperthyroidism), lung (pneumonitis), liver (hepatotoxicity), skin (photosensitization, blue-gray coloring), eyes (corneal deposits), contraindicated pregnancy.

Blocking beta-adrenergic receptors: negative chronotropic effect (bradycardia), negative inotropic, negative dromotropic, hypotensive. Indications: HF with stable reduced EF, post-MI, hypertension, stable angina, AF (rate control), supraventricular tachycardias, prevention of sudden death.