Ventricular Dysfunction In Critical Illness

743 views

Published on

Published in: Health & Medicine
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
743
On SlideShare
0
From Embeds
0
Number of Embeds
1
Actions
Shares
0
Downloads
25
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide

Ventricular Dysfunction In Critical Illness

  1. 1. Ventricular Dysfunction In Critical Illness 心臟內科 張哲明醫師
  2. 2. Assessment of CV Dysfunction • Cardiac pump function - the relationship of cardiac output to RA pressure (Pra). • Measurement of cardiac output - thermodilution technique (pul. a. catheter), nuclear medicine imaging, or Doppler echo. • Measurement of Pra - distension of the jugular veins, CVP. • Cardiac dysfunction - LV dysfunction, RV dysfunction, or external compression (cardiac tamponade)
  3. 3. Definition of Cardiac Function and Its Relation To Venous Return The cardiac function curve relates RA pressure (Pra) or EDP to cardiac output. As EDP increases CO increase, but at high EDP further increases cause less increase in CO.
  4. 4. When EDP = mean systemic pressure (Pms), there is no pressure gradient (Pms-Pra) driving the blood flow back to the heart so venous return is zero. As EDP (Pra) decreases the gradient from the veins to the heart to drive blood flow back to the heart increase
  5. 5. The intersection point defines the operating point of the circulation. The interrupted cardiac function curve illustrates decreased cardiac function, causing reduced cardiac output at a higher EDP.
  6. 6. Control of Ventricular Pumping Function • The ventricular pump function curve can be altered by changes in contractility, preload, afterload, heart rate and rhythm, and valvular function. • ESPVR - end systolic pressure-volume relationship; - ↑ contractility → ESPVR shifts to the left - ↓ contractility → ESPVR shifts to the right • Stroke volume = EDV - ESV • Cardiac output = HR x Stroke volume
  7. 7. 1. During diastole the ventricle fills along a diastolic pressure-volume relationship 2. At the onset of systole LV pressure ↑ with no change in volume 3. When LV pressure > aortic P., the AV opens and the LV ejects blood to an end-systolic pressure-volume point 4. The LV then relaxes isovolumically ∗ Emax - end-systolic pressure-volume relationship (ESPVR), a good index of ventricular contractility independent of changes in preload and afterload. VOLUME PRESSURE ESV EDV ∗ Emax ↑ Pressure afterload ↑ Diastolic filling
  8. 8. Measurement of Ventricular Function • Clinical examination - perfusion status, mean BP, pulse pressure, HR., distention of jugular v. (↑ RV filling p.), dependent pul. crackles (↑ LV filling p. ≥ 20mmHg), S3 gallop. • Rt heart catheter - a thermistor -tipped catheter with a distal port at the tip and a proximal port 30 cm from the tip, can accurately determine C.O. (thermodilution method). • Gated radionuclide ventriculography and echocardiography
  9. 9. Mechanism and Management of LV Dysfunction ∀ ↓ Contractility ∀ ↑ Diastolic stiffness : ↓ preload volume ∀ ↑ Afterload • Abnormal heart rate and rhythm • valvular dysfunction
  10. 10. Decreased LV Systolic Function • Table 115-1 Chronic Causes of Decreased Contractility (Dilated Cardiomyopathies) Coronary artery disease Idiopathic Inflammatory (viral, toxoplasmosis, Chaga’s disease) Alcoholic Postpartum Uremic Diabetic Nutritional deficiency (selenium deficiency) Metabolic disorder (Fabry’s disease, Gaucher’s disease) Toxic (adriamycin, cobalt)
  11. 11. Table 115-2 Acute Reversible Contributors to Decreased Contractility Ischemia Hypoxia Respiratory acidosis Metabolic acidosis Hypocalcemia Hypophosphatemia Possibly other electrolyte abnormalities (Mg++ , K+ ) Exogenous substances (alcohol, β-blockers, calcium channel blockers, antiarrhythmics) Endogenous substances (endotoxin, histamine, tumor necrosis factor, interleukin-1, platelet activating factor) Hypo- and hyperthermia
  12. 12. Acute Causes • Myocardial ischemia - O2 demand > supply; ↑ O2 demand : ↑ HR, contractility, afterload, preload, and basal metabolic rate. • Myocardial hypoxia - sepsis, anemia, etc. ↑ ↑ hypoxic → anaerobic metabolism → lactic acid ↑ → ↓ contractility (vicious cycle) (occurred when SaO2 ≤ 75%); Tx.- keep SaO2 > 90% and normal Hct. • Myocardial acidosis - resp. and metab. acidosis • Resp. acidosis → intracell. acidosis → ↓ the effect of intracell. Ca. on the contractile proteins → ↓ contractility (can be countered by β agonists)
  13. 13. • Metab. acidosis - less effect on ↓ LV contractility, organic acids not easily cross into the intracell. compartment. • Ionized hypocalcemia - septic shock, blood transfusion (citric acid), lactic acid → extracell. ionized Ca → ↓ flux and ↓ contractility. • Side effects of common drugs - ethanol, β-blockers, Ca blockers, and antiarrhythmics
  14. 14. Management • Identify and correct acute reversible causes - coronary vasodilation, blood transfusion, O2, iv calcium, bicarbonate, correct electrolyte abnormality. • Managing the depressed heart - optimizing of ventr. filling p., ↓ afterload, IABP etc. • Inotropic or vasoactive agents - 1. Dobutamine- acts mainly on β1-receptors - ↑ contractility, peripheral vasodilation - 2-15 µg/kg
  15. 15. • 2. Dopamine- 0.5-5 µg/kg/min, dopaminergic effect, ↑ renal blood flow - 5-10 µg/kg/min, β agonist effect - > 10 µg/kg/min, α agonist effect (↑ arterial resistance) • 3. Amrinone, milrinone- phosphodiesterase inhibitors - ↑ intracell. Ca. → ↑ contractility. - ↓ afterload, 0.75 mg/kg bolus then 5-10 µg/kg/min infusion ∀ ↑ contractility vs ↑ myocardial O2 demand
  16. 16. Table 115-3 Effect of Direct-Acting Vasodilators Drug Route Dosage Onset Duration Large a. Arterioles Veins of Effect Nipride IV 25-400 µg/min immediate - + +++ +++ Nitroglycerin IV 10-200 µg/min immediate - ++ + +++ Isodil P.O 20-60 mg 30 min 4-6h ++ + +++ Hydralazine P.O 50-100mg 30 min 6-12h 0 +++ ± Hydralazine IV or IM 5-40 mg 15 min 4-8h 0 +++ ± Minoxidil P.O 10-30 mg 30 min 8-12h 0 +++ 0 Diazoxide IV bolus 100-300 mg immediate 4-12h 0 +++ ± Nifedipine P.O 10-20 mg 20-30min 2-4h +++ +++ ± S.L 10-20 mg 15min 2-4h +++ +++ ±
  17. 17. Increased Diastolic Stiffness • Increased diastolic stiffness reduces SV because ↓ EDV (depressed systolic function reduces SV because ↑ ESV) • much more difficult to treat • Dx is suggested by finding depressed ventr. pump function unresponsive to fluid loading, inotropic agents, and afterload reduction.
  18. 18. Chronic Causes • Nondilated cardiomyopathies - HCM, concentric LVH, HCVD and restrictive myocardial disease (amyloidosis, hemochromatosis, sarcoidosis, endomyocardial fibrosis etc.) • Disease of the pericardium - constriction and effusion, and other processes which ↑ intrathoracic pressure.
  19. 19. Acute Causes • Regional or global ischemia - delayed systolic relaxation → ↑ diastolic stiffness ∀ ↑ intrathoracic or intrapericardial pressure - positive- pressure mechanical ventilation, pericardial effusion • Hypovolemic shock and septic shock • Hypothermia (BT < 35o C) • Management - treat underline disorder.
  20. 20. Abnormal Heart Rate and Rhythm • Normally HR and contractile states are matched to venous return and afterload to maximize the efficiency of the CV system. • Excessively high or low HR may limit C.O. • Afib, AF, VT, VF, PSVT, MAT (pul. dz) • Management included correcting potential contributing abnormalities.
  21. 21. Mechanism and Management of RV Dysfunction • RV pump function also depends on contractility, afterload, preload, HR, and valve function. • RV, a thin-walled pump, not suited as a high pressure generator.
  22. 22. Decreased RV Systolic Function • Many causes reduce the LV contractility also decrease contractility of the RV. • RV ischemia in the absence of CAD is very important during critical illness (↑ RV p. → ↑ RV intramural p. → ↓ gradient for RV coronary blood flow → RV ischemia)
  23. 23. Disorder of RV Preload, Afterload, Rhythm, and Valves • Pra is heavily influenced by intraabdominal, intrathoracic, and intrapericardial pressure; a poor indicator of RV preload. • RV also depends on normal rate and rhythm to attain optimum function. • RV valvular dz is less common and less important than LV valvular dz. • Endocarditis (tricuspid valve) is common in critically ill pts (preexisting valve dz or medical instrumentation) • The afterload of the RV is the pulmonary a. pressure.
  24. 24. Table 115-4 Causes of Elevated RV Afterload Chronic Chronic hypoventilation Recurrent pulmonary embolism Primary pulmonary hypertension Associated with connective tissue diseases Chronically elevated LA pressure (MS, LV failure) Acute Pulmonary embolus Hypoxic pulmonary vasoconstriction Acidemic pulmonary vasoconstriction ARDS Sepsis Acute elevation in LA pressure Positive-pressure mechanical ventilation
  25. 25. Ventricular Interaction • Combined pump dysfunction of RV and LV is more common than isolated RV or LV pump dysfunction.
  26. 26. Acute on Chronic Heart Failure • CHF - poor prognosis with a survival rate of only 50% after 5 years. • Mortality is highest during the first 2 years with worsened functional status, often related to episodes of acute decompensation. • NYHA class III or IV - survival rate ≅ 50 % after 1 yr and 30 % after 2 yrs.
  27. 27. Table 115-5 Common Precipitating Factors of Acute on Chronic Heart Failure Poor compliance with medications Dietary indiscretion (salt load, alcohol) Infection Fever High environmental temperature Effect of a new medication (β-blockers, calcium channel blockers, antiarrhythmics, NSAID) Arrhythmia (typicallly, new atrial fibrillation) Ischemia or infarction Valve dysfunction (endocarditis, papillary m. dysfunction) Pulmonary embolism Surgical abdominal event (cholecystitis, pancreatitis, bowel infarct) Worsening of another disease (DM, hepatitis, hyperthyroidism, hypothyroidism)
  28. 28. Clinical Features • Often anxious, tachycardiac, and tachypneic with hypoperfused extremities and possibly cyanosis. • Jugular veins distended and hepatojugular reflux • Apical impulse lateral to the midclavicular line or > 10 cm from the midsternal line • Apical diameter > 3cm indicates LV enlargement • S3 or summation gallop • Crackles (+) in dependent lung fields, dependent edema • Wheezing, hepatomegaly (may be pulsatile esp. TR) • CXR - upper zone redistribution of vasculature, perivascular and peribrochial cuffing, perihilar filling and pleural effusion, azygos vein enlarge.
  29. 29. Management • Treat intravascular overload and improve gas exchange - diuresis, O2, 450 supine bed rest • Morphine - ↓ venous tone, ↓ LV filling p. ↓ anxious, ↓ O2 demand • Nitrates - venodilators, ↓ LV filling p., mild a. vasodilators (↓ afterload), coronary vasodilators • Rotating tourniquets or phlebolomy (100-150mL blood) • Nitroprusside • Afterload reducing agents - ACEI • Positive inotropic agents - dobutamine, dopamine, phosphodiesterase inhibitor. • IABP - cardiogenic shock
  30. 30. Thanks For Your Attention

×