Rapibloc Training - Cardiology Basics PDF

RAPIBLOC TRAINING CARDIOLOGY BASICS © AOP Health 1 Agenda PART 1  CARDIOVASCULAR SYSTEM PART 2  ARRHYTHMIA PART 3  SEPTIC SHOCK © AOP Health 2 CARDIOVASCULAR SYSTEM  Anatomy of the heart and vascul...

RAPIBLOC TRAINING CARDIOLOGY BASICS © AOP Health 1 Agenda PART 1  CARDIOVASCULAR SYSTEM PART 2  ARRHYTHMIA PART 3  SEPTIC SHOCK © AOP Health 2 CARDIOVASCULAR SYSTEM  Anatomy of the heart and vascular system  Cardiac cycle  Cardiac output  Blood pressure  Hemodynamic regulation © AOP Health 3 ARRHYTHMIA  Conduction of the heart  Arrhythmia mechanism  Different type of arrhythmia  Physiopathology of AF  AF in Critical Care © AOP Health 4 SEPTIC SHOCK  Definition of Septic Shock  Physiopathology of Shock  Organ dysfonction  Septic shock management  Vasopressors in septic shock © AOP Health 5 CARDIOVASCULAR SYSTEM  Anatomy of the heart and vascular system  Cardiac cycle  Cardiac output  Blood pressure  Hemodynamic regulation © AOP Health 6 Chambers of the heart: right and left heart  The heart is composed of four chambers – two atria and two ventricles Aorta Superior vena cava Pulmonary artery Left atrium Mitral valve Aortic valve Right atrium Left ventricle Pulmonary valve Interior vena cava Tricuspid valve Right Descending aorta The right heart is thinner as ventricle compared to left heart © AOP Health 7 Blood flow through the systemic and pulmonary circulations Pulmonary Pulmonary arteries Pulmonary veins circuit Lung Lung O2 O2 Pulmonary circulation Systemic circulation CO2 CO2 Right atrium Left atrium Systemic circuit Right ventricle Left ventricle Venae cava Aorta In systemic capillary beds O2 leaves the blood and CO2 enters COO22 O22 CO Oxygenated blood Cells in tissues throughout the body Deoxygenated blood © AOP Health 8  Arteries*: vessels that come out from heart  Aorta carotid  The largest artery in the body Arch of the aorta  Carries oxygenated blood out of the left ventricle of the heart Ascending aorta  Arteries Thoracic aorta  Carry blood at high pressure from the heart to the tissues  Arterioles Abdominal aorta  Smaller arteries  Major function is to control blood Mesenteric arteries pressure by constricting or dilating © AOP Health *notes: arteries usually carries oxygenated blood except pulmonary artery that goes to the lungs. 9  Veins*: vessels that come back to the heart Venules Thinnest veins in the body Internal Receive blood from capillaries and pass it on to veins jugular Veins vein Move blood towards the venae cavae and right atrium Subclavian of the heart Superior vein vena cava Carry blood at lower pressure than arteries Most contain semi-lunar valves to prevent back-flow of Right atrium blood Contraction of skeletal muscle aids the flow of blood Venae cavae Renal The superior and inferior venae cavae return blood to Inferior vena vena cava the heart Gonadal vena *notes: large veins (e.g. subclavian, femoral) can be used to insert central catheters and infuse drugs © AOP Health 10  Arteries and Veins: main differences Arteries Veins Carry blood away from Carry blood toward the the heart heart Thicker walls Thinner walls Smaller lumen Larger lumen Higher blood pressure Lower blood pressure No valves Valves © AOP Health 11  Capillaries  Capillaries are present in all tissues  Oxygen, carbon dioxide, nutrients (e.g. glucose) and waste products diffuse across their thin walls  Gas exchange occurs in the capillary beds within the tissues:  Release of oxygen  Uptake of carbon dioxide  The reverse exchange occurs in the pulmonary capillaries of the lungs  Release of carbon dioxide  Uptake of oxygen © AOP Health 12  Lung - alveolar circulation and gaz exchange The pulmonary circulation carries blood to and from the lungs Left pulmonary vein Right pulmonary vein 13 Right pulmonary artery Pulmonary trunk Left pulmonary artery Circulation pulmonaire © AOP Health 13 Heart - Vessels of coronary circulation  The heart is supplied with oxygen and nutrients by the coronary arteries Right main Left main coronary artery coronary artery Left circumflex artery Left anterior descending artery Capillary density of heart is enormous! Heart: 3000 capil/mm2 ( Ø 18µm) Skeletal muscle: 400 capil/mm2 (Ø 50µm) © AOP Health 14  Heart and Coronary perfusion Cardiac cycle and coronary flow: O2 supply to the myocardium In healthy subject, volume myocardium perfusion remains stable (and may be increased) even though diastolic perfusion time is reduced (tachycardia) thanks to an increase in diameter of coronaries associated with tachycardia. (relaxation due to beta2) 15 In coronary or hypertensive or cardiac insufficient patients, , volume myocardium perfusion decreases due to reduction of diastolic perfusion time (tachycardia), poor relaxation of ventricle during diastole or spam and/or obstruction of coronaries, during tachycardia Note: coronary flow occurs during diastole (Left Ventricle) © AOP Health 15  Heart and Coronary perfusion Mechanism of Acute Coronary Syndrome Myocardial Infarction Occlusion : ST Elevated (ECG ) Non Occlusive: ST NON- Elevated (ECG ) ACS and Myocardial infarction are explored by angiography and mechanical reperfusion is frequently performed © AOP Health Thygesen et aL; Circulation. 2018;138:e618–e651. DOI: 10.1161/CIR.0000000000000617 16 Innervation of the heart  The heart is innervated by the autonomic nervous system (ANS) Aorta Superior vena cava Pulmonary artery Left atrium Purkinje fibres Impulse conduction:  Sinoatrial (SA) node Right Left ventricle atrium  Internodal pathway Right Interventricular septum  Atrioventricular (AV) node ventricle  AV bundle (bundle of His)  Bundle branches Descending aorta Interior vena cava  Purkinje fibers © AOP Health 17  Cardiac Cycle and Electric Stimulation The cardiac conduction system Atrioventricular Atria node Bundle of Sinoatrial node His fibres (pacemaker) Bundle branches Purkinje fibres Ventricles Heart at rest AtrioVentrocular node, AV bundle and Sinus Atrium node fires Purkinje fibers fire ATRIUM CONTRACT VENTRICULE CONTRACT © AOP Health 19  Cardiac cycle : Diastole and Systole During (a) cardiac diastole, the heart muscle is relaxed and blood flows into the heart = Early phase of heart filling = Passing filling During (b) atrial systole, the atria contract, pushing blood into the ventricles. = late phase of heart filling = completion of heart filling = “atrial kick” # 25% of end-diastolic left ventricle volume During (c) atrial diastole, the ventricles contract (ventricular systole), forcing blood out of the heart. =Blood volume ejected = STROKE VOLUME © AOP Health 20  Cardiac stimulation and Electrocardiogram Lead (II) corresponds to ECG “standard” usually represented Electrical Cardiac stimulation can be registered with a six leads EKG , with applying leads on the body such as: V1 : 4th intercostal space (between ribs 4 and 5) just to the right of the sternum V2 : 4th intercostal space just to the left of the sternum V3 : Between leads V2 and V4 V4 : 5th intercostal space, (between ribs 5 and 6) in the mid- clavicular line. V5 : Horizontally even with V4, in the left anterior axillary line. V6 : Horizontally even with V4 and V5 in the mid-axillary line. Leads can also be positioned on the limbs to obtain a 12 lead ECG. © AOP Health 21  Cardiac cycle in relation with ECG P wave= atrial depolarization 22 QRS segment = fast impulse from His fibers to Purkinje fibers T wave corresponds to ventricle repolarization Note: atrial repolarisaton is masked by QRS © AOP Health 22  https://www.youtube.com/watch?v=IS9TD9fHFv0 © AOP Health 23  Cardiac cycle and pulse pressure Normal electrocardiogram (ECG) reflect regular beats (beat per minutes= bpm) producing cardiac output (liter of blood per minutes) resulting in pulsatile blood flow Systole is shorter than diastole  when heart rate increases, diastole time will be reduced Diastole Systole Diastole Systole Diastole Systole Diastole Systole R R R R T T T T P P P P ECG Q Q Q Q S S S S Blood flow is ejected at systole and blood pressure increases Blood pressure Volume of blood ejected at each contraction is STROKE VOLUME During diastole, heart is filled and pressure goes down « Lub » « Dub » ( S1 ) ( S2 ) First heart sound (S1) represents closure of the atrioventricular (mitral and tricuspid) valves as the ventricular pressures exceed atrial pressures at the beginning of systole © AOP Health The second heart sound (S2) represents closure of the semilunar (aortic and pulmonary) valves 24  Regulation of cardiac output Factors effecting Cardiac Output (CO) As seen on previous slide, the only way to fast increase cardiac output is to eject stroke volume more frequently. Due their own limitation, volume (preload) and contractility cannot be enhanced much and have a small contribution in CO increasing vs increase of HR. © AOP Health 25  Cardiac Ouput and Heart Rate Cardiac output – the volume of blood pumped from each ventricle per minute: CO = SV x HR cardiac output = stroke volume X heart rate (ml/minute) (ml/beat) (beats/min) a. Average heart rate = 70 bpm b.Average stroke volume = 70−80 ml/beat c. Average cardiac output = 5,5 l/minute TIP: 70 (b/min) X70 (ml) = 4900 (ml) # 5 L/min © AOP Health 26  Cardiac Ouput and Heart Rate Caridiac output is increasing as heart rate Decreasing Heart Rate increase until a certain point and then drop as is able to ventricule cannot no longer fill properly increase cardiac output What’s more, contraction strength that increase with heart rate (Bodwitch effect) with calcium accumulation, decreases beyond this point, by failing of relaxation. https://www.intechopen.com/chapters/53797 © AOP Health 27  Cardiac output and hemodynamic What makes the flow with a pump (heart)? Volume of blood being returned to the heart Pressure the heart (left ventricle) has (ventricles) at the end of diastole. The stretching to overcome to eject blood out of of the muscle fibers just before contraction the heart. 28 Tubes must be not too narrow and/or Circuit must be pressure already too high = « traffic jam » « well filled » and Pump must be in « reservoir» good shape to compliant…. « push » © AOP Health 28  Cardiac Ouput and Heart Rate Why beta-blocker usually fail to maintain Cardiac Output while decreasing Heart rate? *CO = SV × HR Decrease with Beta-blockers SV maintained EDV Increase with HR Negative chronotropic effect decrease (Amount to eject) HR SV Inotropism Usually Decrease with (contractility) Beta-blockers CO DC BP = Blood pressure BP PA CO = Cardiac Output SVR = Systemic Vascular Resistance SVR RVS HR= Heart Rate SV = Stroke Volume © AOP Health * Calculated with normal Preload and constant SVR EDV = End Diastolic Volume 30  Cardiac Ouput and Heart Rate How could a beta-blocker succeed to maintain Cardiac Output while decreasing Heart rate? *CO = SV × HR Decrease with Increase with HR Beta-blockers decrease EDV Increase with HR Negative chronotropic effect decrease (Amount to eject) HR SV Inotropism No impact contraction no negative inotropism (contractility CO DC BP = Blood pressure BP PA CO = Cardiac Output SVR SVR = Systemic Vascular Resistance RVS HR= Heart Rate SV = Stroke Volume © AOP Health * Calculated with normal Preload and constant SVR EDV = End Diastolic Volume 31  Cardiac Ouput and Ejection Fraction ALTERED contraction HEALTHY NORMAL HEALTHY Ejected Volume = reduced Contraction REDUCED PRESERVED Ejection fraction Ejection fraction 40% Amount of Blood ejected from ventricule (ml) X 100 Ejection Fraction (%) ALTERED relaxation Total voilume of blood Filling Volume = reduced in ventricle (ml) Fraction éjectée HEALTHY NORMAL © AOP Health =50-60% 32  Cardiac Ouput and Ejection Fraction Ejection Fraction REDUCED Ejection fraction PRESERVED HEALTHY Ejection fraction =50-60% 40% TIP: CI (cardiac Index) REDUCED appears in RAPIBLOC SPC NORMAL REDUCED CARDIAC OUTPUT CARDIAC OUTPUT for cardiac dysfunction CARDIAC OUTPUT definition) Cardiac Index (CI) = Cardiac Output/ body surface CARDIOGENIC CI < 3 à 2,5 CI < 3 à 2,5 SHOCK normal # 3,5 L / min /m2. L/min/m2 L/min/m2 CI < 2,2 L/min/m2 © AOP Health 33  Cardiac Ouput and Blood Pressure BP 34 Higher systemic vascular resistance (< caliber or stiffer wall) Lower systemic vascular resistance (> caliber or relaxed wall) BP © AOP Health 34  Blood Pressure in Vascular System Pulmonary aretries Pulmonary veins Large veins Small veins Capillaries Capillaries Vena Cava Pressue in the lungs is much lower than in systemic circulation Large aretries Small aretries Lungs are COMPLIANT Aorta Right heart is weaker than left heart because LUNG Systemic Pulmonary AFTERLOAD is lower As blood flows further in vessels, blood pressure drops until reaching # « 0 » The normal value of Central venous pressure in healthy persons is very low, not exceeding 5 mm Hg © AOP Health 35 35  Blood Pressure and capillary flow MAP CVP (Mean Arterial Pressure) (Central Venous Pressure) microcirculation in capillaries can be monitored by different techniques Organ Perfusion Pressure # (MAP – CVP) Mottling Score ↓ density of capillaries ↑ heterogenicity of perfusion © AOP Health 36  Measuring the pumping action of the heart: Summary Parameter Equation Measurement Typical value method Pulse detection, 70 Heart rate – ascultation beats/minute Cardiac output CO = SV × HR Various methods 5 litres/minute 2.6-4.2 CO – cardiac output Cardiac index CI = CO / BSA – SV – stroke volume litres/minute HR – heart rate CI – cardiac index Angiogram, BSA – body surface area Stroke volume SV = EDV – ESV 70ml EDV – end diastolic volume echocardiogram ESV – end systolic volume © AOP Health 37 Measuring the pumping action of the heart: Summary continued Parameter Equation Measurement Typical value method Ejection fraction EF = SV / EDV Angiogram, 55-70% echocardiogram, MRI, CTscan Mean arterial MAP = CO × SVR 70-110mmHg pressure Pulse pressure PP = SBP – DBP Sphygmo 40mmHg manometer EF – ejection fraction SV – stroke volume EDV – end diastolic volume MRI – magnetic resonance imaging MAP – mean arterial pressure CT – computed tomography CO – cardiac output RNA – radionuclide angiocardiography SVR – systemic vascular resistance PP – pulse pressure © AOP Health SBP – systolic blood pressure 38 DBP – diastolic blood pressure  How hemodynamic is regulated? 3 main systems interplays to maintain hemodynamic homeostasis Hypotension Hypovolemia Baroreceptors Voloreceptors Aorte/ Carotides ventricles catecholamines 39 (adrenaline, Antidiuretic hormone noradrenaline) Vasopressin posthypophyse VASOCONSTRICTION VASOCONSTRICTION WATER REABSORPTION Autonomus Renin-angiotensine Baroreceptors Sympathic Adrenal gland Renal Afferent Arteriola Nervous system Aldosterone system VASOCONSTRICTION renin SODIUM REABSORPTION aldosterone angiotensine © AOP Health 39  How hemodynamic is regulated? The Autonomus Sympathic Nervous system The cardiovascular system is “equiped” with sensitive nerves which are connected to sensors which detect blood pression variation and send signal to brain stem where centres of cardiac control are located. Then the cardiac center sent back an appropriate response to Cardiovascular system via the Autonomic Nervous System © AOP Health 40  Autonomic innervation of vascular system Arteries and Veins have different type and density of receptors Vascular system is innervated by Beta and alpha adrenergic receptors are located on sympathetic nerves arteries while only alpha adrenergic receptors are The lower the artery caliber, the higher present on veins. nerves density. Note; beta2 receptors density is higher than alpha1 in coronary arteries to ensure relaxation during stress (effort) Blood No beta1 receptors Flow on vessels !!! Sympathetic ganglion Pressure flow (diameter) Caliber Elastic arteries alpha1 stimulation Adrenal gland triggers Innervation vasoconstriction Adrenalin Mucle arteries noradrenalin noradrenalin and arterioles beta2 stimulation triggers vasorelaxation capillaries No nerves !!! © AOP Health 41 Cardiac Output, organ perfusion and autonomic regulation Cardiac output is adapted to organ perfusion needs © AOP Health driven by physical activity and stress Autonomic nervous system 42 Autonomic nervous system: Sympathetic nervous system Catecholamines and stress Heart is principally equipped with bêta-1 receptors which contribute to heart contraction and cardiac stimulation Lungs have bêta-2 receptors involved in bronchial relaxation Coronary arteries have principally bêta-2 receptors and are relaxed in response to sympathetic stimulation to allow adapted myocardium perfusion β1 contracte β2 relaxe Stress (catecholamines) increase cardiac output and increase Oxygen supply same stress message, different organ response © AOP Health 43 Regulating autonomic nervous system with drugs Beta-blockers acts by inhibiting catecholamine effect on beta-adrenergic receptors Noradrenaline Sympathic Noradrenaline Sympathic nerve nerve Bêta Blocker Bêta1 receptor Bêta2 récepteur Bêta1 receptor Bêta2 receptor When not inhibited, catecholamines (noradrenaline) Non selective beta-blockers bind to both to beta-1 released by sympathetic nerves bind to beta-1 and beta-2 and beta-2 receptors of target cells, competing and receptors of target cells. inhibiting with noradrenaline, leading to decrease With same stress message, different response depending of of heart rate and contraction, but also organs needs and contribution to hemodynamic and bronchoconstriction of bronchioles. oxuygen supply, leads to increase in heart rate and © AOP Health contractility, and bronchodilation of bronchioles in lungs 44 Regulating autonomic nervous system with drugs Selective Beta-blockers acts by inhibiting catecholamine effect on beta1-adrenergic receptors Noradrenaline Sympathic Noradrenaline Sympathic nerve nerve Bêta Bêta blocker Blocker Bêta1 receptor Bêta2 receptor Bêta1 receptor Bêta2 receptor Coronary Arteries : Arteries remain relaxed Selective beta-blockers bind ONLY to beta-1 receptors of target cells, competing and inhibiting with noradrenaline, leading to decrease of heart arte and contraction, without © AOP Health bronchoconstriction of bronchioles and also with maintaing coronary perfusion 45 Regulating autonomic nervous system with drugs Excessive continuous stimulation by catecholamine triggers desensitization of beta-adrenergic receptors Lower density on surface membrane and/or Small dose of beta-blocker can restore sensitivity uncoupling with Gs protein © AOP Health De Lucia et al. Front. Pharmacol., 10 August 2018 Sec. Cardiovascular and Smooth Muscle Pharmacology 46 Volume 9 - 2018 | https://doi.org/10.3389/fphar.2018.00904 Interaction between the renal and cardiovascular systems: the renin-angiotensin-aldosterone system Angiotensinogen Renin Angiotensin I Angiotensin- converting enzyme (ACE) Angiotensin II Arteriole constriction Aldosterone BP increases Increased sodium and water reabsorption Renin release is stimulated by internal baroreceptors in renin-secreting cells of the juxtaglomerular apparatus due to a reduction in the afferent arteriole pressure. © AOP Health Catecholamine additional stimulates renin secretion by juxtaglomerular apparatus 47 Vasopressin: osmoregulation blood pressure regulation In addition to Sympathetic System and Renin-Angiotensin-Aldosterone System, vasopressin plays an important role in maintaining blood pressure. Relations between plasma osmolality and blood volume © AOP Health and AVP concentration in blood 48 Vasopressin: multiple roles in blood pressure and organ homeostasis ACTH release => Cortisol : stimulation of V1b receptor + Insuline release : stimulation stimulation of V1b receptor + Platelet agregation : stimulation of V1a receptor + Release of coagulation factors stimulation of V2 receptor + in endothelium Vasoconstriction: stimulation Water reabsorption: of V1a receptor + stimulation of V2 receptor + => aquaporine © AOP Health 49 Demiselle et al. Ann Intensive Care 2020 Jan 22;10(1):9. doi: 10.1186/s13613-020-0628-2. CARDIOVASCULAR SYSTEM: Summary  Heart is a pump that provide cardiac output and blood flow to warrant organ perfusion and oxygenation.  Heart, vessels, lungs have different receptors to provide adapted response to same stress message (e.g. catecholamine stress)  Heart Rate, Cardiac Output and Blood pressure are related.  Cardiovascular system is regulated by several system including autonomic nervous system, renin-angiotensin-aldosterone and vasopressin © AOP Health 50 ARRHYTHMIA  Conduction of the heart  Arrhythmia mechanism  Different type of arrhythmia  Physiopathology of AF  AF in Critical Care © AOP Health 51  Heart conduction Sinus node is « naturally » unstable and depolarise spontaneously It is the pacemaker responsible for automaticity of the heart AV node role is to naturally « slow down conduction » to allow for ventricle filling completion and optimize preload before ventricular rapid stimulation triggering contraction and blood ejection. Normal electrical heart conduction : Sinus Node SN (cardiac pacemaker) trigger action potential → signal propagate through atrium and triggers its contraction → signal reach AV node and is slowed down→ AV node conduct signal towards bundle of His along interventricular septum towards Purkinje fibres in myocardium → convey signal throughout ventricles → ventricles contract ( electromechanical coupling). © AOP Health 52  Diastolic Depolarisation and Heart Rate The cells of SINUS NODE are naturally “unstable” and depolarize REGULARLY and SPONTANEAOUSLY Thanks to FUNNY CHANNELS that is regulated by autonomous system. These cells are called : pacemaker cells HCN Hyperpolarisation-activated Cyclic-Nucleotid = FUNNY CHANNELS if https://link.springer.com/chapter/10.1007/978-3-030-75326-9_1 http://www.vnsanalyse.de/files/userdata/bilder/hf_modulation_1_650.png © AOP Health 53 53  Diastolic Depolarisation and Heart Rate Impact of autonomic nervous system on heart rate at sinus node (pacemaker cells) Sympathetic nervous system: positively chronotropic Parasympathetic nervous system: negatively chronotropic (beta1-Gs-cAMP – Funny channels open) (m2-Gi-cAMP decreases – Funny channels closed) Heart Rate is increased Heart Rate is reduced Potential [mV] Sympathetic nervous system: positively Activation of chronotropic Activation of Rest Sympathetic Vagus Nerve Nervous System 0.5 Time [s] © AOP Health 54 54  Systolic Depolarisation and Heart contraction Cardiac action potential (contractile cells) 55 Contractile Myocardium cells are depolarizing quickly thanks to Na entry, then Ca entry and K going out of the cell Calcium entry is key to trigger internal cell Ca reserve movement out of sarcoplasmic reticulum to participate to the contraction. Antiarrhythmic drugs can interfere with this Ca turn over and/or alter refractory period, this is why AA often decrease cardiac contraction © AOP Health Mechanisms of Cardiac Arrhythmias L. Gaztan˜aga et al. / Rev Esp Cardiol. 2012;65(2):174–185 55 Heart Conduction: different speed of depolarisation Contractile Myocardium cells are able to propagate electric signals They depolarize quickly Contractile Myocardium cells are also transforming the electrical signal into mechanical contraction © AOP Health = ElectroMechanical Coupling 56 From heart conduction to heart contraction Effects and roles of catecholamines on heart function Excitation, conduction, contraction, relaxation Catecholamines role is to facilitate increase heart function in order to increase cardiac output. With accelerating heart rate By increasing automaticity * = positive chronotropic effect By lowering excitability threshold = positive bathmotropic effect By increasing speed of conduction** = positive dromotropic effect 57 and also easing « pumping efficacy » By increasing strength of contraction = positive inotropic effect By increasing speed of relaxation*** = positive lusitropic effect However, Some of the effects on heart conduction system, when in excess and/or prolonged period can contribute to trigger arrhythmia, especially in patients at risk or in combination with other triggers. * At sinus node level ***Sequential phenomenum following contraction: Catecholamines ease calcium **increase speed of conductuion of AV node recapture by sarcoplasmic reticulum, which increase relaxation of myocardium and Reduce refractory time period allow for optimizing ventricle filling before the next contraction © AOP Health Gillies M, Bellomo R, Doolan L, et al. Bench-to-bedside review: Inotropic drug therapy after adult cardiac surgery -- a systematic literature review. Crit Care. 2005;9(3):266-79. 57  Heart Conduction: mechanism of drugs Rate control agents (BB and CCB) acts on nodes tissues (slow depolarizing cells) Antiarrhytmic agents act on high speed depolarizing cells (bundle of His Purkinje fibres and contractile myocardium) by blocking Na channels or K channels  Note: historically, beta-blockers and calcium blockers are listed in Vaugham-Williams classification of antiarrhythmic agents while there are rather rate control agents not interfering with Na or K channels © AOP Health 58 Heart Conduction: mechanism of arrhythmia Disorder Mechanism Types of arrhythmias Disorders of impulse generation Abnormal automaticity Suppression or acceleration of Phase 4 of Sinus tachycardia the action potential Sinus bradycardia Triggered activity Torsades de pointes Early afterdepolarizations (EADs) Possibly idiopathic and acquired long QT syndromes and associated ventricular arrhythmias Delayed afterdepolarizations (DADs) Digitalis-induced arrhythmias Reperfusion VT Disorders of impulse conduction Unidirectional block with reentry Reentry Atrial fibrillation Atrial flutter Other SVTs Ventricular tachycardia Unidirectional block or bidirectional Blocked impulse conduction Bradyarrhythmias block without reentry Abnormal automaticity can be caused by altered rate of spontaneous depolarization Its can also be caused by autonomic nervous activity, hypokalemia, ischemia © AOP Health 59 Electrocardiogram abnormalities Examples of ECG abnormalities related to pathologies that may involve beta-blockers or antiarrhythmic agents ECG ECG features in acute coronary syndrome Myocardial Inéfarction Acute Coronary Syndrome Normal ST Segment ACS with ST elevated segment ACS WITHOUT ST elevated segment Long QT Class I or III antiarrhytrhmic agents are syndrome contra-indicated in case of prolonged QT Congenital Septic shock cardioac damage or injury or can be associated with long QT and worst Acquired prolonged QT prognosis Normal QT Intervalle © AOP Health 60 ECG abnormalities: STEMI and Non-STEMI In STEMI, Electric impulse is stopped by large heart wall (transmural) necrosed o stunned myocardium while in non-STEMI, electric impulse can still continue in par the heart, with ischemia principally affecting small extremities of coronary vessels at endocardium level, which are the first to suffer from lower coronary pressure or flo © AOP Health 61 Heart Conduction: mechanism of arrhythmia 63 Heart rate ≥ 100 bpm originating from sinus node Atrial fibrillation (AF) is the most frequent type of supraventricular and associated with regular rhythm. Frequency of tachyarrhythmia observed in critical care or emergency settings. beating (rate of beating) alone is affected and AF is characterized by disorganized atrial activation and irregular impulse accelerated. © AOP Health triggering irregular response. 63 Heart Conduction: mechanism of arrhythmia Different type of supraventricular tachycardia Junctionnal tachycardia There are other existing type of supraventricular tachyarrhythmia which ca,n be also observed in critical care or emergency settings, but are much less frequent. (5 to 10% of SVT) They can be encountered and diagnosed early in paediatrics as some of their mechanism stems from heart conduction malformation and abnormalities. Vagal manoeuver or adenosine injection are first line management, rate control agents are usually second or 3rd line treatment option. © AOP Health 64  Atrial Flutter A supraventricular tachyarrhythmia usually caused by a single macroreentrant rhythm within the atria that is classically characterized on ECG by the sawtooth appearance of P waves, also known as “flutter waves”, with narrow QRS complexes. The risk factors for atrial flutter are similar to those of Afib. In atrial flutter, the atrial rate is slower than in Afib and the ventricular rhythm is usually regular. Treatment is similar to that of Afib, consisting of anticoagulation and strategies to control heart rate and rhythm. Atrial flutter frequently degenerates into atrial fibrillation. Type of tachyarrhythmia Causes and mechanisms Main ECG findings Flutter atrial Macroreentrant rhythms Regular rhythm within the atria Rate: atrial 250–350 ventricular < 200 66 P waves ECG Flutter atrial Occur before every QRS complex Sawtooth appearance of regular P waves (flutter waves) especially in leads II, III and aVF Narrow QRS complex Normal ECG 1. The rhythm may be regularly irregular if atrial flutter occurs with a variable AV block occurring in a fixed pattern (2:1 or 4:1), and irregularly 2. irregular with a variable block occurring in a non-fixed pattern. 3.  The exact ventricular rate depends on the ratio of atrioventricular conduction (e.g., 1:1 or 2:1 conduction). https://www.mayoclinic.org/diseases-conditions/atrial-flutter/symptoms-causes/syc-20352586 © AOP Health 66  Atrial Fibrillation Atrial fibrillation (Afib) is a commonly seen type of supraventricular tachyarrhythmia that is characterized by uncoordinated atrial activation resulting in an irregular ventricular response. Individuals with Afib are typically asymptomatic. However, when symptoms do occur, these usually include palpitations, lightheadedness, and shortness of breath. Physical examination typically reveals an irregularly irregular pulse. Ineffective atrial emptying as a result of Afib can lead to stagnation of blood and clot formation in the atria, which in turn increases the risk of stroke and other thromboembolic complications. The diagnosis is confirmed by an ECG showing indiscernible P waves and a narrow QRS complex with irregular QRS intervals.. Causes and Type of tachyarrhythmia 67 Main ECG findings mechanisms Atrial Fibrillation Multiple mechanisms Rhythm: irregularly irregular atrial Fibrillation ECG which are not completely Rate: atrial 350–450 bpm; understood ventricular < 200 bpm (valvular cardiopathy, coronary P-waves are indiscernible disease, hyperthyroïdism, Narrow QRS complex Normal ECG electrolyte disorders) © AOP Health 67  Physiopathology of Atrial Fibrillation Hemodynamic and cardiovascular impacts Structural ou electro-physiologic abnormalities of atrial tissues are associated with : Excessive Heart Rate Loss of effective atrial contraction (atrial kick) Irregular and reduced ventricle filling time Reduction of cardiac output from 15t to 20%. Blood stagnation in atrium and risk of clotting and thrombosis * * Stagnation time is directly related to the risk of thrombus formation :  generally >48h Recovery of sinusal rhythm and recovery of atrial contraction allows for thrombus to be expelled into circulation :  CNS embolism (stroke) or in other arteries vessels (rarely pulmonary embolism as thrombus mainly forms in left atrium) © AOP Health 68  Physiopathology of Atrial Fibrillation Hemodynamic and cardiovascular impacts Heart Rate(bpm) Mean Arterial Pressure (mmHg) Rythme sinusal Before AF AF 160 100 140 132 80 77 75 120 73 105 66 99 60 80 40 40 20 0 0 Seeman, 2015 Klein, 2016 Seeman, 2015 Klein, 2016 Introduction or need to increase vasopressors: 41% © AOP Health Seeman et al AIC, 2015 & Klein et al AJRCCM 2017 69  Atrial Fibrillation: risk factors © AOP Health 70  Risk factors and triggers for AF in critical care Bedford et al. https://doi.org/10.1016/j.iccn.2021.103114 © AOP Health 71  Types of Atrial Fibrillation Most common after surgery (especially cardiac surgery) due to sympathetic overstimulation and inflammation (80% of AF cases in ICU) Kirchhof et al. Europace (2007) 9, 1006–1023 © AOP Health 72 Time course and management of of Atrial Fibrillation © AOP Health 73 Time course and management of of Atrial Fibrillation © AOP Health 74  Atrial Fibrillation Incidence in Intensive Care ICU Population Subset settings Incidence of new-onset Reference atrial fibrillation Surgical ICU General non-thoracic Surgery 5-10% Pulmonary surgery Rozencwajg 2016 10-23% Imperatori 2012 Esophagectomy 16-22% Schizas 2019 Cardiac surgery 10-65% Medical ICU General ICU 5-21% Carrera et al. 2016 Gupta et al. Septic shock 11 – 46% Meierhenrich 2010 Liu 2016 Cardiac ICU, Coronary Care Myocardial infaction 4- 10% Almendro-Delia 2013 Unit 6-21% Braga 2013 Schmitt et al. 2009 Acute Heart Failure 16% Arrigo 2017 Percutaneous Valve 17,5% [6 - 20%] Sanino 2016 replacement Chopard 2015, © AOP Health Maan 2015 75  Risk factors and triggers for Postoperative Atrial fibrillation * Increase of Hypothermia * surgery Pain sympathetic hypoglycemia stimulation Anemia* Hypoxia hypovolemia Thoracicic non-Thoracic Beta-blockers Hypotension * surgery surgery withdrawal * 76 *Identify and treat causes of sympathetic stimulation et de myocardium Local Systemic correct factors that can damage Inflammation Inflammation contribute to trigger arrhythmia directly Postoperative Hypokaliemia * Atrial Fibrillation Hypomagnesemia * Hypervolemia Chelazzi C, Villa G, De Gaudio AR. Postoperative atrial fibrillation. ISRN (International Scholarly Research Notices) Cardiol. 2011;2011:203179. doi: 10.5402/2011/203179. Boriani G, et al. Europace. 2019 Jan 1;21(1):7-8. doi: 10.1093/europace/euy110. © AOP Health 76  Impact of Postoperative Atrial fibrillation on patient outcome Mortalité toute cause pour les cohortes de pontage seul, avec FAPO (POAF) versus sans FAPO (No-POAF). Un taux de mortalité hospitalière plus élevé chez les patients souffrant de FA de novo en postopératoire comparé aux patients ne présentant pas de FA a été observé dans 8 études, dont sept démontrant une différence significative. POAF (Post Operative Atrial Fibrillation) = FAPO Postoperative Atrial fibrillation after cardiac surgery is associated with higher hospital mortality Alex Chau Y-L. et al. The impact of post-operative atrial fibrillation on outcomes in coronary artery bypass graft and combined procedures. J Geriatr Cardiol 2021; 18(5): 319–326 © AOP Health 77 77  Impact of Postoperative Atrial fibrillation on patient outcome 8,0% 7,0% 6,0% 5,0% 4,0% 3,0% 2,0% 1,0% 0,0% Ahlsson 2010 Attaran 2009 Bramer 2010 Girerd 2012 Mariscalco 2009 Saxena 2012 Villareal 2004 POAF No POAF Taux de mortalité rapporté chez les patients présentant une fibrillation atriale. Histogramme rouge = avec Fibrillation Atriale; Histogramme Blanc = sans Fibrillation Atriale Postoperative Atrial fibrillation after cardiac surgery is associated with higher hospital mortality Phan K, Ha HSK, Phan S, Medi C, Thomas SP, Yan TD. New-onset atrial fibrillation following coronary bypass surgery predicts long-term mortality: a systematic review and meta-analysis. Eur J Cardiothorac Surg 2015;48:817–24. © AOP Health 78 78  Risk factors and triggers for new onset Atrial fibrillation in Critical Care Patient admitted in Critical Care setting can have already altered atria conduction system or normal atria, however critical care conditions will contribute to extend injury/remodelling or create injury © AOP Health 80  Risk factors and triggers for AF in critical care Inflammation, Infection, Trauma, Ischemia, along with hypovolemia or electrolyte inbalance are part of many triggers common in postoperative setting and intensive care setting. Excessive adrenergic stress is also a frequent trigger contributing to develop NOAF. © AOP Health 81  Atrial fibrillation in Critical Care Impact on patient outcome AF No AF NOAF is associated with higher hospital mortality Yoshida T, Fujii T, Uchino S, Takinami M. Epidemiology, prevention, and treatment of new-onset atrial fibrillation in critically ill: a systematic review. J Intensive Care. 2015 Apr 23;3(1):19. doi: 10.1186/s40560-015-0085-4. © AOP Health 82 82  Atrial fibrillation in Critical Care Impact on patient outcome The prospective FROG-ICU cohort confirms relations between NOAF and patient outcome NOAF is an independent factor of mortality Arrigo M et al. New-onset atrial fibrillation in critically ill patients and its association with mortality: A report from the FROG-ICU study International Journal of Cardiology 266 (2018) 95–99 © AOP Health 83 83  Atrial fibrillation in Critical Care Impact of return to sinus rhythm on patient outcome Failure to restore sinus rhythm in septic patients with NOAF seems to be associated to higher risk of hospital mortality as compared to patients with conversion bask to sinus rhythm. Liu et al. Prognostic impact of restored sinus rhythm in patients with sepsis and new- © AOP Health 84 onset atrial fibrillation Critical Care (2016) 20:373  Management of New Onset AF in Critical Care Identify and correct triggers first, Then rate control to imoprve hemodynamic conditions. If hemodynamic does not improves, rhythm control can be implemented. © AOP Health Walkey AJ, Hogarth DK, Lip GYH. Optimizing atrial fibrillation management: from ICU and beyond. Chest. 2015 Oct;148(4):859-864. 85  AF and Other Acute conditions in CCU/CICU STEMI/ ACS Include AF section Acute Coronary Syndrome(ischemia) AF Other SVT HF  Acute Heart Failure Troubles du rythme Acute Cardiac Dysfunction Tachyarythmies Include AF section  VT J-LAND © AOP Health Nagai et al. 86  Atrial Fibrillation and Acute Heart Failure AF and AHF are often associated in a vicious circle © AOP Health 87 Regulating autonomic nervous system with drugs Excessive continuous stimulation by catecholamine triggers desensitization of beta-adrenergic receptors and calcium cytosol overload Desensitization of beta-adrenergic receptors is both affecting coupling with Gs protein (transudction of intracellular signal) and also receptor density on cell surface. https://doi.org/10.1038/ s41569-020-0394-8 observed observed mortality mortality Calcium is quickly in and Because of Prolonged and out of sarcoplasmic excessive Adrenergic stimulation, reticulum and contribute Calcium is remains in cytosol ending up in Ca overload due to efficiently to contraction poor recapture in sarcoplasmic and relaxation even if reticulum by SERCA and leakage heart arte increase of Ryanodin De Lucia et al. Front. Pharmacol., 10 August 2018 Sec. Cardiovascular and Smooth Muscle Pharmacology Dridi et al. Nature Review cardiology https://doi.org/10.1038/s41569-020-0394-8 © AOP Health 89 Volume 9 - 2018 | https://doi.org/10.3389/fphar.2018.00904  Heart Failure severity and classification NYHA class Conséquence of Heart Failure: poor cardiac output, poor organ perfusion  incapacity to adjust cardiac output to organ needs = reduced muscle activity = reduced mobilisation. Inadequate O2 supply = Shortness of Breath © AOP Health 90  Heart Failure And Ejection Fraction © AOP Health 91  Heart Failure and symptoms in acute setting From Acute Heart Failure to Cardiogenic Shock observed mortality © AOP Health 92  Acute Heart decompensation and AF Left Ventrocular Ejection fraction potentially alredy altered before the episode of decompensation and further decrease during the episode. Causes of decompensation of the heart failure can be myocardial infarction or coronary syndrome (50%), infection (14%), hypertensive crisis (11%), non compliance with HF treatment (8%) and also Tachyarrhythmia such as AF (16%) Episodes of cardiac decompensation due to rapid AF Evolution of Cardiac insufficiency RAPID AF = Tachyarrhythmia LVEF%  Rapid HR + loss of « atrial kick » Hypoperfusion   adrenergic response Lower diastolic ventricular Decrease of Ejection Fraction of left ventricle filling *  EDV  SV=  Cardiac Output ++  Oxygenation   ATP  Cardiac Output (CO) Cardiac adaptation\maladaptation Peripheral maladaptation  Force of Contraction Acute episode of HF  Relaxation* Coronary Hypoperfusion Arrigo et al. Precipitating factors and 90-day outcome of acute heart failure: a report  Diastole duration +  CO from the intercontinental GREAT registry European Journal of Heart Failure (2017) 19, 201–208 *ventricular relaxing requires energy (ATP) © AOP Health 94 © AOP Health 95 Acute Heart decompensation and AF While AF was 16% of cause in Arrigo cohort, in Chioncel cohort, AF is 30% of the cause, similar to Myocardial Ischemia © AOP Health Chioncel et al. American Journal of Therapeutics 25, e475–e486 (2018) 96  Fibrillation Atriale en Réanimation Conséquences cliniques en postopératoire La FA préexistante et la FAPO sont associées à risque de réhospitalisation pour insuffisance cardiaque plus élévé comparé à une absence de FAPO Goyal P, Kim M, Krishnan U, Mccullough SA, Cheung JW, Kim LK, Pandey A, Borlaug BA, Horn EM, Safford MM, Kamel H. Post-operative atrial fibrillation and risk of heart failure hospitalization. Eur Heart©J.AOP 2022 Aug 14;43(31):2971-2980. doi: 10.1093/eurheartj/ehac285 Health 97 Acute HF : Progonosis in relation with cause of Acute HF Precipitating factors of AHF were identified in 8784 patients (55%), while in 7044 patients (45%) no specific precipitant could be identified. ACS was the most common cause (52%), followed by AF (n=1228, 16%), infection (n=1104, 14%), uncontrolled hypertension (n=831, 11%), and non-compliance with HF treatment (n=597, 8%). Cardiogenic shock was more frequent in patients with ACS (13%) compared with patients with infection (6%) and non-compliance (5%) (P 2 mmol/L in the absence of hypovolemia, associated with in-hospital mortality > 40% 2016 SEPSIS—3 Singer et al. Singer, M.; Deutschman, C.S.; Seymour, C.W.; Shankar-Hari, M.; Annane, D.; Bauer, M.; Bellomo, R.; Bernard, G.R.; Chiche, J.-D.; Coopersmith, C.M.; et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016, 315, 801–810. © AOP Health 110 Septic Shock epidemiology Sepsis inciden