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Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
Anatomy, physiology & patophysiology of the cardiovascular
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Anatomy, physiology & patophysiology of the cardiovascular

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  • 1. Anatomy, Physiology & Patophysiology of the Cardiovascular System: Anesthesia Approach Prof. Karen Haddock MSN, CRNA
  • 2. Comprises and The• Heart four chambers, side,iseach divided into a right and left with an atrium and a ventricle. • The left ventricle generate greater pressures than the right ventricle, and so has a much thicker and more muscular wall. • Four valves ensure that blood flows only one way: – tricuspid and mitral valves - from atria to ventricle – pulmonary and aortic valves - to the arterial circulations • The myocardium consists of muscle cells which can contract spontaneously, also pacemaker and conducting cells, which have a specialized function.
  • 3. Coronary Circulation • Right coronary arterysupplies the right atrium, right ventricle, inferior wall left ventricle, SA node (60% of individuals), AV node (8590% of individuals) EKG: lead II, III y AVF • Left coronary arterysupplies left atrium, interventricular septum, the left ventricle (septal, anterior & lateral walls), SA node (40% of individuals) EKG: lead V3 yV5
  • 4. • Circumflex artery (CX)supplies lateral wall. EKG: lead I y AVL • Left anterior descending (LAD) - supplies septum and anterior wall EKG: Lead V5
  • 5. 1. left coronary artery (left main artery) 2. circumflex artery 3. obtuse marginal branch of the circumflex artery 4. atrioventricular groove branch of the circumflex artery 5. anterior interventricular artery (left anterior descending artery -
  • 6. The Coronary Circulation • Myocardial blood supply is from the right and left coronary arteries. • Venous drainage is mostly via the coronary sinus into the right atrium, but a small proportion of blood flows directly into the ventricles through the Thebesian veins, delivering unoxygenated blood to the systemic circulation. • Oxygen extraction by the tissues is dependent on consumption and delivery. • Myocardial oxygen consumption is higher than in skeletal muscle (65% of arterial oxygen is extracted as compared to 25%).
  • 7. • The sympathetic nerves – The SA node is an increase in heart rate. – The effect on the muscle is an increase in rise of pressure within the ventricle, thus increasing stroke volume. Α1, β1 & β2
  • 8. Effect of sympathetic stimulation on the heart: • Increased sympathetic stimulation > release of norepinephrine at SA node > decreased permeability of SA node cell membranes to potassium > membrane potential becomes less negative (closer to threshold) > more action potentials (and more contractions) per minute.
  • 9. • The vagus provides the parasympathetic The effect of the vagus at the SA node is the opposite of the sympathetic nerves, it decreases the heart rate. acetilcoline (MU 2)
  • 10. Effect of parasympathetic stimulation on the heart • Increased parasympathetic stimulation > release of acetylcholine at the SA node > increased permeability of SA node cell membranes to potassium > 'hyperpolarized' membrane > fewer action potentials (and, therefore, fewer contractions) per minute.
  • 11. • Depolarization is due to the inward diffusion of calcium (not sodium as in nerve cell membranes). • Depolarization begins when: – the slow calcium channels open (4), – then concludes (quickly) when the fast calcium channels open (0). – Repolarization is due to the outward diffusion of potassium (3).
  • 12. Cardiac Cycle • The first stage is diastole, which diastole represents ventricular filling and a brief period just prior to filling at which time the ventricles are relaxing. • The second stage is systole, which systole represents the time of contraction and ejection of blood from the ventricles.
  • 13. • P wave = caused by atrial depolarization • QRS complex = caused by ventricular depolarization • T wave = caused by ventricular repolarization
  • 14. Determinants of Ventricular Performance • Cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV): CO = HR x SV • Stroke volume is determined by three main factors: preload, afterload and contractility. • Preload is the ventricular volume at the end of diastole.
  • 15. Starling's law of the heart. • The relationship between ventricular end-diastolic volume and stroke volume is known as Starling's law of the heart. • An increase in preload (end-diastolic volume) increases stroke volume.
  • 16. Determinants of Ventricular Performance • Afterload is the resistance to ventricular ejection. This is caused by the resistance to flow in the systemic circulation and is the systemic vascular resistance. – Is affected mainly by: • ventricular volume (size) • arterial vasomotor tone (arterial resistance) • ventricular wall thickness – Afterload is increased by: • increase in ventricular volume • increase in arterial vasomotor tone • decrease in ventricular wall thickness – Afterload is decreased by the opposite changes
  • 17. Determinants of Ventricular Performance • Contractility describes the ability of the myocardium to contract in the absence of any changes in preload or afterload. • In the sympathetic nervous system, Beta-adrenergic receptors are stimulated by noradrenaline released from nerve endings, and contractility increases. • A similar effect is seen with circulating adrenaline and drugs such as ephedrine, digoxin and calcium. • Contractility is reduced by acidosis, myocardial ischemia, and the use of beta-blocking and anti-arrhythmic agents.
  • 18. Hemodynamics Monitoring Values and Equations 1. Systemic Vascular Resistance (SVR) = [(MAP-PAWP)/CO]x80 → SVR=1170 dynes/sec/cm-5 (range 700-1200). 2. MAP=mean arterial pressure=1/3(SBP-DBP)+DBP or MAP (1) SBP+ (2) DBP / 3 3. CO (cardiac output)= SV x HR → 5 - 6L/m 4. SV (Stroke Volume)= CO/HR 4. PAWP or PCWP=pulmonary artery wedge pressure. PCWP 5. Cardiac Index (CI)=CO/BSA → CI=2.5-3.5 L/min/m2 (CI) 6. BSA=body surface area. BSA
  • 19. Swan-Ganz Catheter pressures • RA - 0-8 mmHg • RV -15-30/2-8 mmHg • PA – – Systolic 20-30 mmHg, Diastolic 8-12 mmHg, Mean 25 mmHg • PAWP or PCWP6-12 mmHg (measured at end-expiration)
  • 20. Cardiovascular Disorders: Anesthesia Management
  • 21. Heart failure • Is the inability of the heart to supply adequate blood flow and therefore oxygen delivery to peripheral tissues and organs. Under perfusion of organs leads to reduced exercise capacity, fatigue, and shortness of breath. • It can also lead to organ dysfunction (e.g., renal failure) in some patients.
  • 22. Path physiology of Heart Failure • Systolic heart failure occurs when the heart is unable to pump a sufficient amount of blood to meet the body's metabolic requirements. • Clinical manifestations usually reflect the effects of the low cardiac output on tissues (eg, fatigue, oxygen debt, acidosis), the damming up of blood behind the failing ventricle (systemic or pulmonary venous congestion), or both. • The left ventricle is most commonly involved, often with secondary involvement of the right ventricle. Isolated right ventricular.
  • 23. Path physiology of Heart Failure • Diastolic dysfunction can also cause symptoms of heart failure as a result of atrial hypertension. • Common causes include hypertension, coronary artery disease, hypertrophic cardiomyopathy, and pericardial disease. • Although diastolic dysfunction can cardiac output is reduced in most forms of heart failure. Inadequate oxygen delivery to tissues is reflected.
  • 24. Anesthesia Management in presence of CHF • • • • Not deshydration or fluids overload Ketamine, Etomidate & Opioids Isoflurane in low MAC Positive Pressure ventilation may decrease pulmonary congestion • Invasive monitoring • Regional anesthesia is acceptable
  • 25. Hypertension • Essential hypertension accounts for 80-95% of cases and may be associated with an abnormal baseline elevation of cardiac output, systemic vascular resistance (SVR), or both. • The chronic increase in cardiac afterload results in concentric LVH and altered diastolic function. • Hypertension also alters cerebral autoregulation in the range of mean blood pressures of 110180 mm Hg.
  • 26. Hypertension • In the perioperative period, poorly controlled hypertension is associated with an increased incidence of ischemia, left ventricular dysfunction, arrhythmia, and stroke. • The goal should be a systolic blood pressure less than 140 mm Hg and a diastolic blood pressure lower than 90 mm Hg before proceeding with elective surgery.
  • 27. Hypertension • In any patient with stage 3 hypertension (ie, >180/110 mm Hg), blood pressure should be well controlled prior to surgery. • Intravenous esmolol, hidralazine, labetalol, nitroprusside, or nitroglycerin may be used for acute episodes of intraoperative hypertension, whereas calcium channel blockers or angiotensin-converting enzyme (ACE) inhibitors may be used in less acute situations.
  • 28. Hypertension General Anesthesia • • • Intravenous Agent : all except Ketamine. Volatile anesthetics are secure. Neuromuscular Blocking Agent: all except pancuronium. • Narcotics: secure Narcotics Regional anesthesia is acceptable.
  • 29. Ischemic Heart Disease • Otherwise known as Coronary Artery Disease, is a condition that affects the supply of blood to the heart. The blood vessels are narrowed or blocked due to the deposition of cholesterol plaques on their walls. • This reduces the supply of oxygen and nutrients to the heart musculature, which is essential for proper functioning of the heart.
  • 30. Angina pectoris • The myocardial ischemia of unstable angina, like all tissue ischemia, results from excessive demand or inadequate supply of oxygen, glucose, and free fatty acids. • Stable Angina -is chest pain or discomfort that typically occurs with activity or stress. • Instable Angina- chest pain happens unexpectedly after light activity or occurs at rest.
  • 31. Myocardial Infarction • The pathogenesis can include: – Occlusive intracoronary thrombus – Vasospasm – Emboli • Complications can include: • Arrhythmias and conduction defects, with possible "sudden death" • Extension of infarction, or re-infarction • Congestive heart failure (pulmonary edema) • Cardiogenic shock • Pericarditis • Mural thrombosis, with possible embolization • Myocardial wall rupture, with possible tamponade • Papillary muscle rupture, with possible valvular insufficiency • Ventricular aneurysm formation
  • 32. Anesthesia Management in Patient with MI • Goal: Avoid the activation of Sympathetic nervous system all the time. • Preoperative preparation – Sedation – Antihypertensive drugs
  • 33. Anesthesia Management in Patient with MI • Intraoperative management Avoid increase the heart rate (>110beats/min) & systemic pressure more than 20%. Invasive monitoring ( arterial line & PA cath if required) Lead II & V Short duration on direct laryngoscopy (<15 sec.)
  • 34. Anesthesia Management in Patient with MI • Intraoperative management In patients with normal left ventricular functionvolatile anesthetics with or without nitrous oxide (Forane is the best) In patients with severely impaired left ventricular functionthe use of short-acting opioids (fentanyl, 50-100 /Lg/kg IV, or equivalent doses of other opioids) Etomidate is the best
  • 35. • Drugs Intended to Attenuate the Systemic Blood Pressure and/or Heart Rate Response to Tracheal Intubation Laryngotracheal lidocaine • Lidocaine 1.5 mg/kg IV 90 seconds before beginning direct laryngoscopy • Nitroprusside 1-2 /Lg/kg IV 15 seconds before beginning direct laryngoscopy • Esmolol 100-300 /Lg/kg/min IV before and during direct laryngoscopy • Fentanyl 1-3 /Lg/kg IV 90-120 seconds before beginning direct laryngoscopy • Nitroglycerin 0.25-1.00 /Lg/kg/min IV to decrease the pressor response (no evidence that the incidence of intraoperative myocardial ischemia is decreased)
  • 36. Cardiac Tamponade • Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. • Cardiac tamponade is a medical emergency.
  • 37. Clinical Manifestations of Cardiac Tamponade • Increased central venous pressure • Activation of the sympathetic nervous system (tachycardia and vasoconstriction) • Equalization of right and left atrial pressures and right ventricular end-diastolic pressures at about 20 mmHg (exception may be accumulation of blood and clots over the right ventricle, as may follow cardiac surgery) • Paradoxical pulse (decrease> 10 mmHg in systolic blood pressure during inspiration) • Hypotension (low cardiac output)
  • 38. Cardiac Tamponade
  • 39. Anesthesia management in Cardiac Tamponade • Treatment – Removal of fluid (pericardiocentesis) – Temporizing measures are designed to maintain stroke volume until definitive surgical treatment of cardiac tamponade. – Intravenous infusion of colloid or crystalloid solutions – Catecholamines – Correction of metabolic acidosis
  • 40. Anesthesia Management in Cardiac Tamponade • Pericardiocentesis performed with local anesthesia is often preferred for the initial management of patients who are hypotensive owing to low cardiac output produced by cardiac tamponade. • The goal is to maintain cardiac output. Ketamine is useful for induction and maintenance of anesthesia, as it increases myocardial contractility, systemic vascular resistance, and heart rate. • Continuous intravenous infusions of catecholamines, such as isoproterenol, dopamine, or dobutamine, may be isoproterenol dopamine useful for maintaining cardiac output until the cardiac tamponade can be relieved by surgical drainage.
  • 41. Mitral Stenosis • The clinical manifestations of mitral stenosis are caused by the mechanical obstruction that impairs ventricular filling through the narrowed mitral orifice. • This obstruction results in the development of a pressure gradient across the valve in diastole and causes an elevation in left atrial and pulmonary venous pressure. • Avoid atrial fibrillation & tachycardia. The gradient tachycardia (and left atrial pressure) can be elevated by an increase in cardiac output, a decrease in diastolic filling time (which occurs with faster heart rates), or the development of atrial fibrillation.
  • 42. Mitral Stenosis • The characteristic findings of mitral stenosis on auscultation are an accentuated first heart sound (diastolic), an opening snap, and a mid-diastolic rumble, which is best heard at the cardiac apex. • Reduced cardiac output from the restricted filling of the left ventricle. • Mitral stenosis is usually secondary to rheumatic disease. • Most patients are female
  • 43. Anesthetic Management in Mitral Stenosis • The goals of anesthetic management are to maintain cardiac output through the tight mitral valve while avoiding pulmonary congestion. • Patients already in atrial fibrillation should have the rate controlled aggressively. aggressively • The pulmonary vasculature is sensitive to hypoxemia or hypercarbia so meticulous attention should be paid to these values. While epidural and spinal anesthesia can be safely performed in patients with MS,
  • 44. Mitral regurgitation • Is leakage of blood from the left ventricle into the left atrium during systole. • The characteristic finding in a patient with mitral regurgitation is a blowing systolic murmur that is heard best at the cardiac apex. • The pathophysiology of MR is volume overload of the LV, similar to AR.
  • 45. Mitral Valve Replacement
  • 46. Anesthesia Management in Mitral Regurgitation • Cardiac output is best when the heart is full and reasonably fast, and the blood pressure is lownormal. • Bradycardia is associated with an increase in ventricular size; avoid. • The need for a low “afterload” as determined by blood pressure is explained avoidance of myocardial depression within reason should be a goal. • Patients with MR often require inotropic assistance to accomplish these hemodynamic goals in the face of general anesthesia.
  • 47. Aortic Stenosis • The gradual process of narrowing of the aortic orifice leads to concentric left ventricular. • Hypertrophy and a reduction in left ventricular compliance – the myocardium become thick, the enddiastolic pressure (LVEDP) rises, but there is no dilatation. Concentric hypertrophy.
  • 48. Aortic Stenosis • The gradual process of narrowing of the aortic orifice leads to concentric left ventricular hypertrophy and a reduction in left ventricular compliance – the myocardium becomes thick, the end-diastolic
  • 49. Anesthesia Management • Invasive monitoring with an arterial catheter is probably indicated for most procedures; the use of a pulmonary artery catheter (PAC) or transesophageal echo (TEE). • Hypotension and dysrhythmias must be treated early and aggressively. aggressively • Conversely, hypertension should be treated very cautiously. • The anesthetic was planned accordingly, in some cases including spinal or epidural
  • 50. Aortic Regurgitation • The commonest causes of AR in the adult are rheumatic fever, bacterial endocarditits, trauma, and aortic dissection. • Congenital diseases such as Marfan syndrome. • The pathophysiology of AR is volume overload of the left ventricle, with dilatation and eccentric hypertrophy rather than the concentric hypertrophy
  • 51. The Anesthetic Management in Aortic Regurgitation • Maintaining an adequate preload to assure filling of the hypertrophied, dilated LV (maintaining cardiac output). • High-normal heart rate to reduce the proportion of time spent in diastole. • Low-normal systemic blood pressure to encourage forward rather than regurgitant flow (decrease afterload) afterload

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