25 September 2017 เอกราช อร ยะช ยพาณ ชย Heart Failure and Transplant Cardiology aekarach.a@chula.ac.th Presentation at 1
Agenda Physiology of the heart Pathophysiology of shock Pathophysiology of heart failure http://fullpulse.weebly.com/conversation 1. What is the heart? 2. What is the function of the heart? 2
To pump the blood Cardiac output (CO) The amount of blood that the heart pump in 1 minute (L/min) Normal = 6 L/min Heart rate (bpm) Stroke volume (ml/beat) 3
What regulate stroke volume What regulate stroke volume Preload Afterload Contractility 4
What is the preload? 1 Preload 2 3 4 5
Frank-Startling Mechanism SV Preload Preload A load (force/tension) that stretch the muscle before the initiation of contraction Myocardial cell length LV end diastolic volume --- LV size Pressure that streactch the heart End diastolic pressure --- LVEDP Atrial pressure 6
What is the afterload? Afterload 1 2 3 4 7
Afterload SV If channel inhibitor - Ivabradine Afterload Afterload in Clinical A load (resistant) that the heart has to contract against o Vascular resistant o Systolic blood pressure o Vaso-constriction o etc. 8
What is the contractility? Contractility An intrinsic property of the myocyte at a giving load 9
Cardiac output CO = SV x HR preload contractility afterload 10
What is shock? N Engl J Med 2013; 369:1726-1734 What is shock? The clinical syndrome characterize by an inadequate global tissue perfusion. Usually have hypotension (MAP < 60 mmhg) Initiate by various causes Lead to a vicious cycle of damages, due to Cellular dysfunction functional and structural change. Multiple organ failure and death. Adapt from harrison principles of internal medicine 18th edition 11
HYPOTENSION SHOCK Hypoperfusion: Lead to a vicious cycle of damages Cellular ATP depletion Aerobic to anaerobic Abnormal membrane function Cell dysfunction, swelling, death Inflammatory response Hematologic response Multiorgan involments Renal failure Acute kidney injury Liver failure Ischemic hepatitis, shock liver Respiratory distress or failure Cardiac depression DIC 12
S&S symptoms of hypoperfusion mental status Tachycardia BP urine cold skin Cr Lactic acid etc 13
Initiate by various causes NEJM 2013 Type of shock initiation and compensatory mechanism Type of Shock Preload CO Afterload Cause Hypovolemic shock Cardiogenic shock Distributive shock Other type of shocks: Hypoadrenal, neurogenic, obstructive 14
Type of shock initiation and compensatory mechanism Type of Shock Preload CO Afterload Cause Hypovolemic shock Cardiogenic shock High preload: JVP, (+) ascites, edema, (+) crepitations Low preload: dry mucosa, low JVP, skin turgor, orthostatic hypotension Distributive shock Other type of shocks: Hypoadrenal, neurogenic, obstructive Type of shock initiation and compensatory mechanism Type of Shock Preload CO Afterload Cause Hypovolemic shock Cardiogenic shock High afterload: cold skin, pale, SVR Low preload: warm skin, SVR Distributive shock Other type of shocks: Hypoadrenal, neurogenic, obstructive 15
Type of shock initiation and compensatory mechanism Type of Shock Preload CO Afterload Cause Hypovolemic shock Cardiogenic shock Distributive shock Other type of shocks: Hypoadrenal, neurogenic, obstructive Type of shock initiation and compensatory mechanism Type of Shock Preload CO Afterload Cause Hypovolemic shock Cardiogenic shock Distributive shock Blood or fluid loss (internal, external) Acute MI, acute HF Arrhythmia, cardiac tamponade pulmonary emboli Septic, anaphylaxis, inflammation, toxin Other type of shocks: Hypoadrenal, neurogenic, obstructive 16
Treatment Reverse the cause(s) In a timely fashion Support and prevent further end organ damage Restore perfusion, reverse the physiology ICU: Fluid resuscitation: Crystalloid > colloid, Cardiogenic shock Circulatory support: Inotrope, vasopressor medications, Devices Ventilation support: O2 support, Mechanical Ventilator/ Endotracheal tube Invasive monitor: Arterial line, PA catheter (Swan-Ganz), Foley cath Epinephrine Action Usual dose C 1 A 2 Note 1 1 2 0.01-0.1mcg/kg/min 1 mg iv bolus q 3 mins Norepinephrine 1 1 2 0.01-3 mcg/kg/min Low dose = more. (like dobutamine) High dose = more. (like norepi) Use: ACLS, anaphylaxis, S/E: splanchnic vasoconstrict. Potent vasoconstriction. Moderate CO. HR effect (reflex bradycardia from increased MAP. Use: Septic shock. Dopamine Low Moderate High DA 1 1 2 DA 1 1 2 DA 0.5-2 mcg/kg/min 2-10 mcg/kg/min 10-20 mcg/kg/min Precursor to norepi but less, more effect. Dose-dependent effects. Dose is varied pt to pt. Use: Septic shock, 2 nd -line alternative to norepinephrine. Dobutamine 1 2 ( 1) 2-20 mcg/kg/min Milrinone PDE inh 0.375 0.75 mcg/kg/min Isoproterenol 1 2 2-10 mcg/min Phenylephrine 1 0.5-10 mcg/kg/min 0 Not a vasopressor. Inotrope with a vasodilation. The net effect = CO + SVR, may not BP. Use: HF, cardiogenic. Similar to dobutamine more vasodilator, PA Use: HF, cardiogenic. Prominent chronotropic. Prominent vasodilation. Use: Bradycardia Pure vasoconstriction. May decrease SV. Vasopressin V 1 0.04 unit/min 0 Pure vasoconstriction. Use: 2 nd -line in refractory vasodilatory shock.. S/E: coronary, mesenteric ischemia, skin necrosis. Na and pulm vasoconstriction 17
Sample A 55 yo M with hx of HTN, DM presents with crushing substernal CP, diaphoresis, hypotension, tachycardia and cool, clammy extremities An 81 yo F from a nursing home presents to the ED with altered mental status. She is febrile to 39.4, hypotensive with a widened pulse pressure, tachycardic, with warm extremities A 68 yo M with hx of HTN and DM presents to the ER with abrupt onset of diffuse abdominal pain with radiation to his low back. The pt is hypotensive, tachycardic, afebrile, with cool but dry skin Cause of Hypovolemic Shock Non-hemorrhagic Vomiting Diarrhea Neglect, environmental (dehydration) Bowel obstruction, pancreatitis Burns Hemorrhagic GI bleed Trauma Massive hemoptysis AAA rupture Ectopic pregnancy, post-partum bleeding 18
Cause of Septic shock Most common type of shock Hypoperfusion + infection + 2 SIRS (systemic inflammatory response syndrome) criteria S&S of hypoperfusion Temp > 38 or < 36 C HR > 90 RR > 20 WBC > 12,000 or < 4,000 Plus the presumed existence of infection Cause of cardiogenic shock 19
Pathophysiology Cardiac dysfunction Vicious cycle relaxation contraction SV, CO Coronary flow LVEDD, PCWP ischemia preload afterload Systemic hypopurfusion Hypoxia ischemia Pulmonary edema 20
Heart failure Definition of HF 1. A syndrome caused by cardiac abnormality 2. Leads to circulatory abnormalities and neurohormonal abnormality 3. Resulting in typical symptoms of Congestion Poor perfusion a. Common pathway from any cardiac injury b. Progressive, remodeling c. Vicious cycle from maladaptation 1 LVEDP dysfunction 2 Circulatory Abnormalities Neurohormonal abn. 3 Typical symptoms Dyspnea fatigue swelling 21
Cause of HF Circulation. 2013;128:e240-e327. Pathophysiology Remodeling 22
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J Am Coll Cardiol 2009;54:375 85. The result of Adverse remodeling 24
Stage of HF Classification of HF Chronicity Acute Chronic Stage A, B, C, D EF ref (< 40%) pef ( 50%) mref (40-50) Hemodynamic profile Wet - Dry Cold - warm NYHA fn class I, II, III, IV Etiology Ischemic cause Non-ischemic cause involvement LV RV Both phenotype Dilated Hypertrophic Restrictive Endo / myo / epi Backward / Forward failure Low / High output Systolic / diastolic failure 25
S&S of HF Non-specific Dyspnea from increased breathing drive Reduction in exercise capacity (NYHA II-IV) Orthopnea, PND Wt gain, leg swollen, fatigue, early satiety, N/V, confusion Apical shift, S3, S4, JVP, (+) HJR, crepitations, ascites, edema Treatment Treat the cause Self-care weight monitor, salt intake Diuretics to control volume status 26
Treatment: Chronic Chronic Betablocker ACE / ARB Aldosterone blocker - spironolactone Angiotensin receptor, neprilysin inhibitor(arni) - Valsartan/sacubitril Other meds: Ivabradine, HDZ, ISDN, dignoxin CRT - Cardiac resynchronize therapy (special pacemaker) ICD - Implantable cardioverter Defibrillator Acute Aggressive diuresis, vasodilator, inotrope End-staged HF Heart transplant, mechanical circulatory support, palliative care Circ Heart Fail.2008;1:63-71 27
Thank you Aekarach.a@chula.ac.th 28