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Acute cardiovascular disorders
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- 2. Presentation Topics • SuddenCardiac Arrest (SCA): Current Management Strategies • Shock: Identification, Stratification, & Treatment • Heart Failure: 1 Heart, 2 Pumps! • Cardiopulmonary Hemodynamics of Shock • Pericardial Tamponade: Identification & Treatment • Continuous Cardiovascular Pharmacology: Principles & Practice
- 3. Hard & Fast! •What have we learned? • 250,000 SCA outside the Hospital • 7.6% (?) ROSC-does not correlate with Survival-to-D/C, OR—Neuro Intact! • Compressions: Hard and Fast 100 to 120. UNINTERRUPTED! • 30:2 • Push first? Defib when? • Differences in Witnessed vs Unwitnessed CA
- 4. Limited Progress over30 Years! • Access to AED’s & Therapeutic Hypothermia • Selected populations • National Effort Focus: Delivery of HIGH-QUALITY CPR • Greatest Improvement/No Improvement: Northeast/Midwest • Biphasic/Double Sequential? • Role of Mechanical Compression • Studies reveal 7% increase in Survival-to-Hospital • 2 MINUTES! 5 Cycles! No Pulse Checks! • Anti-dysrhythmics? Timing remains unclear… • Vasopressors? • Timing is clear, efficacy unclear…
- 5. CRM • Crisis ResourceManagement • Leadership & Communication • Team Leader • ‘Closed-Loop’ • Team Members • Delegation of duties
- 6. Defibrillation • Biphasic • Limittime to defib • Quicker the better in witnessed OHCA! • Max energy level • Increased efficacy at lower energy levels • 120 to 200 joules • Different manufacturers deliver different biphasic shock
- 9. Double Sequential Defibrillation? •Perform after Vfib persists after 5 shocks • The change in vectors presumed to ‘set up’ for the next shock • Reduces Vfib/Vtach defib threshold • Access to Procainamide may be limited • Considered a ‘Hail Mary’ intervention for refractory/recurrent VF/VT
- 10. Double Sequential DefibPad Placement
- 11. VF/Pulseless VT • Epinephrine,after 2 minutes CPR, defib • Admin 1 mg every 3 to 5 minutes • ‘Some’ researchers ‘theorize’ high circulating levels of catecholamines may be harmful to patients who experience ROSC • Increased afterload/SVR can decrease Cardiac Output • ‘Some’ studies have raised doubts about efficacy of Epi • Perhaps lower doses/longer intervals
- 12. Refractory VF/VT • Anti-dysrhythmics? •Evidence suggests meds provide little survival benefit • Timing not specified in protocols • Evidence suggests administration after 2nd unsuccessful defib, in anticipation of 3rd shock • Amiodarone: 300mg IVP, followed by 150mg IVP (post-ROSC hypotension) • Lidocaine: 1 to 1.5mg IVP, followed by 0.5 to 0.75mg/kg every 5 to 10 minutes • Magnesium: 2gm IVP, followed by maintenance, consistent for polymorphic VT/Torsade de Pointes • Procanimide?
- 13. Asystole/PEA • Addressed together •Absence of mechanical cardiac contracture • Both non-perfusing rhythms depending upon EXCELLENT CPR! • Require Rapid Reversal of underlying causes • H’s & T’s • Hypoxia, hypercarbia, hyperkalemia, hypokalemia, hemothorax, hypoglycemia, hypotension, tension pneumo, toxins, tamponade, thrombosis, thromboembolism
- 14. H’s & T’s •H’s • Hypoxia • Hydrogen Ion (acidosis) • Hypothermia • Hyper/hypo-kalemia • Hypovolemia • Hypoglycemia • T’s • Toxins • Tamponade • Tension pnx • Thrombosis • Cardiac • PE
- 15. Bradycardia • ‘Generally’ notsymptomatic until HR < 50 BPM • Hypoxemia common cause • Signs & Symptoms = hypotension, altered LOC, dyspnea, chest pain • Atropine: 0.5mg IVP, 3 to 5 minutes up to 3mg • Myocardial Demand: use cautiously in cardiac ischemia/NSTEMI/STEMI • Ineffective in transplanted hearts • Ineffective in high-degree AV block (Mobitz II/3rd degree AVB) • TCP: do not delay • Chronotropic Infusions: Epinephrine & Norepinephrine • Role of Calcium in bradycardia/shock?
- 16. Bradycardia… • Consider Causes! •Toxicity • Supra-therapeutic doses of Beta-Blockers, Calcium Channel Blockers, & Digoxin • CCB’s: can be ‘tricky’ to treat OD. Some are stronger vasodilators, while others affect cardiac contractility/conduction • 2 Types of CCB’s: dihydropyridines & nondihydropyridines • Digoxin: cardiac glycosides, slow conduction but increase contractility (A-fib, HF, & LV dysfunction)
- 17. Tachycardia • ‘Generally’ notsymptomatic until HR > 150 BPM • No treatment for Sinus Tachycardia: focus on cause, Anemia, Shock, Fever… • Approach similar to Bradycardia: assess stability, signs & symptoms of decreased Cardiac Output (CO) • Unstable = immediate synchronized cardioversion! • Stable = Adenosine: 6mg IVP, 12mg IVP X2
- 18. Dysrhythmia Management • SystematicApproach to ECG Interpretation • 5 Questions • Regular or Irregular? • Stable, Unstable? • Too Fast, Too Slow? • Complex Narrow or Wide? • Is there a P wave for every QRS?
- 19. Narrow complex tachycardia •Most commonly caused by reentry mechanism within conduction system • QRS typically narrow, < 0.12: May be > 0.12 if aberrancy or BBB present • Vagal maneuvers may interrupt the reentry circuit through the AV node • Valsalva, carotid massage: converts up to 25% of SVT to Sinus Rhythm • Valsalva, with supine repositioning and passive leg raise converts even more
- 20. Regular narrow complex •Adenosine • Administer into large, proximal vein • Followed by 20mL flush • Raise the extremity • Repeat second/third time • Warn/prepare the patient: flushing, dyspnea, chest discomfort. Continuous ECG monitoring • Larger doses (18mg) for pts on Theophylline/Caffeine • Smaller doses (3mg) for pts on Tegretol. Transplanted hearts, central line
- 21. Conversion failure • Considerother etiologies for the rhythm • Atrial Flutter or Non-reentry SVT • Administer CCB or BB: Cardizem/Verapamil or Metoprolol/Labetalol
- 22. Irregular narrow complex •Most common rhythms: Afib, Multifocal Atrial Tach (MAT), & Sinus Tachycardia with frequent, premature atrial beats
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- 26. Pericardial Tamponade • Pericardialsac normally has ‘small’ amount of fluid • Sac can hold up to 2 liters of fluid if effusion is chronic • Can take less < 50 ml of blood/fluid to cause an acute tamponade • Fluid or blood accumulates between visceral & parietal pericardium • Causes myocardial constriction, resulting in decreased Cardiac Output • Can lead to Obstructive Shock, decreased ventricular filling, & right atrial collapse • If left untreated can lead to PEA • May occur from Blunt or Penetrating injuries (less common) • Acute Pericarditis (EKG changes?) • ESRD/Neoplasm
- 28. Beck’s Triad • Hypotension •Muffled/distant Heart Sounds • Jugular Venous Distention • Decreased CO/Hypotension • CO = HR x SV • Patient may exhibit Pulsus Paradoxus • Pulse intensity Decreases with inspiration • Decrease in Systolic BP of 10 mm Hg during inspiration Removal of as little of 5 to 10 ml’s of blood/fluid can result in an increase of SV to 25% to 50%!
- 29. Other Signs oftamponade • Low voltage QRS • Electrical alterans • Enlarged cardiac silhouette • Equalization of right-heart & left-heart filling pressures • CVP & PCWP • Ultrasound • Fluid in pericarial sac • Collapse of right artria & right ventricle • Dilated vena cava
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- 36. Pericarditis…Myocarditis…ECG Changes • NormalSTE vs STEMI vs Dynamic Early Repolarization vs ‘itis’ • Diffuse ST Segment Elevation • PR Segment Depression • Prominent J-waves in Precordial Leads • Precordial Leads High ST/T Ratio (V5, V6)—favors pericarditis over repol • R-wave Amplitude is High
- 40. Measuring JVD • JVDMeasurement • Pt placed at 45 degrees/semi-fowler’s position • Have pt turn head to left shoulder • Look for a jugular pulse, not confusing it with carotid pulse • Measured from the Angle of Louis • Add 5 cm to measure b/c the right atrium is approx. 5 cm below chest wall • Normal Central Venous Pressure/CVP 2 to 5 cm of water
- 41. Clinical Scenario • 42yr old male patient arrives POV to the ED • Physical examination reveals multiple stab wounds to left & right chest • Attack occurred approx. 1 hour prior. No pmhx, no meds, no allergies • Patient is diaphoretic, but speaking in clear, full sentences • Lung sounds were diminished on left, left chest tube placed/returned 1200cc blood • FAST exam was negative for blood/fluid • BP 90/50 • JVD at 14 cm • Most likely cause of hypotension/decreased CO?
- 42. Pericardiocentesis • Cardiac monitoring •Hemodynamic monitoring • EKG • Ultrasound • Code Cart • 20 ml syringe • 3 way stopcock • 18 ga spinal needle • Wire with alligator clips
- 43. Procedure • Immediate sub-xiphoidapproach • Insert needle with catheter in place, removing the needle once placement is verified via ultrasound • Attach stopcock to catheter and advance towards left shoulder while aspirating continuously • Monitor with ultrasound and EKG • IF U/S not available, utilized wire with alligator clip, attach to a precordial lead. • If the need is to far, ST segment elevation will be noted on EKG tracing. Withdraw until it disappears. Aspirate blood/fluid. • Alternative: PARASTERNAL APPROACH (5 ICS, LSB)
- 44. COMPLICATIONS: -Aspiration of ventricularblood -Laceration of coronary arteries/veins, epicardium/myocardium -Puncture of peritoneum, esophagus -Cardiac dysrhythmia -Pneumothorax
- 45. Aftercare • X-ray torule out pleural effusion, PXT • Continue to monitor for repeat accumulations in pericardial sac • Monitor for cardiac dysrhythmias, tamponade, hypotension, etc
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- 47. Heart Failure: 1Heart, 2 Pumps • Clinical syndrome of decreased cardiac function • One or both ventricles are unable to maintain adequate CO • Typically refers to LV • Can be bi-ventricular, systolic/diastolic • Systole: Ejection of blood from the ventricle • Diastole: Relaxation of the ventricle, ventricular filling
- 48. To be ‘Preserved,’or not to be…that is the ?
- 49. Heart Failure • SystolicDysfunction: Weak ventricle, difficulty pumping blood forward • Diastolic Dysfunction Not enough filling time to maintain stroke volume, myocardial coronary arteries
- 55. Defined • Sustained hypotensionof SBP < 90 mm Hg lasting > 30 minutes with evidence of tissue hypoperfusion, despite adequate LV filling pressures • Insufficient tissue perfusion = oliguria, cool extremities, altered LOC
- 56. Mortality/Morbidity • Most commoninitiating event in Cardiogenic Shock in AMI, producing marked decrease in contractility (reduced EF/CO) • Prevalence 8.6% of pts with STEMI • Leading COD in AMI • Overall in-hosp mortality 57% • Outcomes significantly improve with rapid revascularization
- 57. Normal Cardiac Cycle •Opening/closing of atrio- ventricular & semi-lunar valves • When pressure increases & exceeds, valves open • Ventricular Filling occurs • 2 phases:Systole/Diastole • Isovolumic Contraction • Ultimately: Pressure to Volume & Volume to Compliance affect Cardiac Output
- 58. Compensatory Mechanisms • IncreasedHR & Contractility • Arterial constriction • Venoconstriction • Retention of salt & water • Increased blood glucose & lipids • Release of inflammatory mediators
- 59. RAAS • Renin-Angiotension-Aldosterone System •Compensation for decreased cardiac output • Sustained/prolonged compensation results in excessive fluid/CHF
- 61. Dysfunction • Left-sided HeartFailure/Systolic Dysfunction: LV function, decreased ability to pump blood forward • Ejection fraction < 60%, normal >65% • Left-sided Heart Failure/Diastolic Dysfunction: Normal EF • Compensation: • Left atrium & pulmonary venous pressure increase, pulmonary congestion & edema result • Increased pressure in the pulmonary system leads to right heart failure, systemic congestion, & edema develops
- 62. Treatment & Management •Vasopressors • Dopamine, Norepinephrine • Dobutamine, PDE Inhibitors • Nitrates • NTG/NTP • Preload/Afterload reduction – ‘coronary steal’ • IABP/LVAD • Augment diastolic filling • Bridge to heart transplant
- 63. Caveats • Reductions inafterload will increase CO • High doses of systemic vasoconstrictors will produce increased afterload/SVR, paradoxically compromising CO further • In pts with refractory shock on high levels of vasopressors, decrease dosages incrementally to increase CO & SBP
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- 65. Shock…The Rude Unhingingof the Machinery of Life… • Definition • Inadequate tissue perfusion/oxygenation • Multiple Forms • Hypovolemic • Distributive • Obstructive • 3 Stages • Compensatory • Decompensated • Irreversible
- 66. Overview • Widespread cellulardysfunction d/t anaerobic metabolism resulting from Inadequate Tissue Perfusion • Mitrochondrial energy stores depleted • Cell membrane compromised • MODS • ATLS: “Abnormality in circulatory system resulting in inadequate organ perfusion and tissue oxygenation.”
- 67. Shock • Inadequate tissueoxygenation & perfusion… • Types & Subtypes: • Hypovolemic • Distributive • Obstructive • Hypovolemic • Hemorrhagic • Pressure Problem! • Distributive • Septic • Anaphylatic • Neurogenic • Pipes Problem! • Obstructive • Tamponade • Cardiogenic • Tension pnx • Pump Problem!
- 68. Caveats! • Look foran identifiable cause…treatment depends on dx • Tachycardia is the earliest measurable circulatory sign of shock! • PEARL: Any pt that is diaphoretic & tachycardic is presumed to be in shock until proven otherwise
- 69. Serum Lactate? • Normal< 2 mmol; <5 mmol poor prognosis • What’s the latest on lactate levels? • Relationship between serum lactate levels and epinephrine…
- 70. General Principles toShock Management • Intravascular volume deficits should be initially tx with isotonic fluids before administering vasopressors • Hypotensive CHF pts commonly treated as Volume Overloaded, while actually they are in a state of Fluid Volume Deficit – 3rd spacing (decreased colloid & protein pressure) • Vasopressors in hemorrhagic shock pts may worsen tissue ischemia • Decreased CO with normal/increased BP = Dobutamine. Low CO with hypotension = Dopamine • MAP of at least 60 to 65 mm Hg. MAP < 60 mm Hg for at least 40 min predisposes pts to pre-renal failure
- 71. Management • Rapidly identify! •Treat specifically! • Treat aggressively!
- 72. Any patient diaphoretic& tachycardic is in shock until proven otherwise!
- 73. Fix the Cause! •Hypovolemic • Fluid resuscitation/IVF/Blood Products/SURGERY! • Septic • Early & Late: Pink & Warm versus Pale & Cool • Blood Cx’s/Broad-spectrum ABX/IVF/Pressors • Neurogenic • IVF/Pressors • Anaphylatic • Epinephrine/Steroids • Obstructive • Pericardiocentesis/Needle Thoracostomy • Cardiogenic • Meds/PCI/Revascularization/LVAD/Balloon Pump/Transplant
- 74. Hypovolemic Shock &Trendelenburg • “It is axiomatic that hypotension r/t fluid volume deficit be treated with IVF, NOT BODY CHANGES!” • Trendelenburg Position does not augment Cardiac Output when increased greater than 20 to 30% • It can, decrease CO by increasing intrathoracic pressure, thereby compressing organs and collapsing the Right Atrium, preventing ventricular fill
- 75. Dangers of CompensatedShock? • Value of Vital Signs? • BP? • HR? • RR? • Skin? • Mentation? • Urine output?
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- 82. Vasoactive Medications • Indications/Contraindications •Classes/Effects • Hemodynamic profile • Titration
- 83. General Principles ofUse • One drug, many receptors! • Alpha-1 • Beta-1, beta-2 • Not a definitive treatment! • Supports MAP & tissue & end- organ perfusion • Dose-responsive curve • Dopamine, example… • Direct versus Reflex Actions • Example,bradycardia associated with pure alpha-adrenergic receptor agonists • Do not “micromanage” every BP • Causes lability in vital signs • Medications specifically with short half-like, e.g., Sodium Nitroprusside
- 84. Vasopressor Caveats • Fluidresuscitate with 2 liters of Isotonic IVF prior to starting pressors • Increased afterload/SVR will decrease cardiac output/compromise perfusion • Beta-1 agonists can potentiate cardiac dysrhythmias, tachycardia & worsen myocardial ischemia, etc • Sometimes ‘less is more…’ • Best if infused via large, antecubital veins/CVC not necessary
- 85. • Cardiac output •4-8 lpm • HR x SV = CO • SV • Preload • Afterload • Contractility • Viscosity
- 91. Vasopressors • Epinephrine/Adrenalin • Norepinephrine/Levophed© “Levophed,Leave ‘em Dead” • Neosynephrine/Phenylephrine© • Dopamine/Intropin • Dobutamine • Phosphodiesterase Inhibitors • Systemic vasodilator • Increased end-organ perfusion • Decreased afterload/SVR • Decreased arterial pressure • may cause hypotension when initiating infusion • Cardiopulmonary • + chronotropic/+dromotropic • + inotropic/ contractility • Decreased preload
- 92. Vasopressors • Epinephrine • 2-20mcg/min • Effect on serum lactate levels? • 8mg in 250 ml’s • Beta-1 agonist • Mixed alpha-beta • More beta than alpha • Norepinephrine • 2-20 mcg/min • 8 mg in 250 ml’s • Mixed alpha-beta • More alpha than beta • Phenylephrine • Large therapeutic window • 10 -200 mcg/min • Reserved for late shock • Reflex bradycardia • 100 mg in 250 ml’s • Pure alpha-agonist
- 93. Vasodilators: Mediated vianitric oxide • Nitroglycerin • 2-200 mcg/min • Use low-absorption IV tubing • Reflex tachycardia! • Sodium Nitroprusside (Nipride©) • 0.2 -10 mcg/kg/min • Coronary Steal Phenom • Protect from light! • 10 mcg/kg/min MAX dose..10 minute limit!! • Breaks down to cyanide! (thiosulfate) • Dilates • Veins • Arteries • Cardiac Output • Augments stroke volume • Decreases afterload • Ventricular Filling Pressures • Preload • CVP (right heart) • PCWP (left heart)
- 94. Vasoactive Management inHeart Failure • Concomitant Strategies • Utilizing a vasopressor + vasodilator = anytime afterload is decreased, cardiac output will increase - Preserved Ejection Fraction - Dobutamine Gtt + Nipride Gtt - Sounds counterintuitive
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Editor's Notes
- #4 Limited scientific evidence d/t high mortality of SCA. Mostly retrospective or anectdotal. Compressions of 100-119 resulted in only 35% inadequate quality. Over 120 ineffective compressions. Witnessed SCA defib first. If > 4 to 5 minutes, or unwitnessed, 2 minutes of CPR. Lesser energy with biphasic 150 to 200, 360 monophasic. 30:2, in the past we over-ventilated pts, reducing venous return, decreased cardiac output, decreased cerebral perfusion. Intubated patients receive no more than 6 to 10 breaths per minute, 600 ml tidal volume. Lower minute ventilations. Supraglottic airway until ROSC is achieved. All studies proved significant rates of neurologic function w
- #6 CRM utilized in aviation industry. Team Leader refrains from performing procedures, unless necessary, leadership turned over until done. (Portable Radio Example)
- #7 In witnessed arrest, perform defib ASAP! Decreased time to defib results in improved rates of successful conversion to a perfusing rhythm and patient survival.
- #12 Premature Epi results in decreased ROSC/no improvement in survival. Excessive vasoconstriction can result in significant afterload thus reducing cardiac output.
- #13 Pick one! Prodysrhythmic.
- #16 Transplanted hearts lack vagal innervation. May be useful in narrow-complex 3rd AVB. Might buy you a few minutes. Block is at level of Node or Bundle of HIS.
- #17 Massive med doses above may not be easily reversed with Atropine or TCP: May required transvenous pacing & expert cardiology consultation. Use of Dig has decreased substantially, however, the rate of toxicity has remained stable. In 2011, 132 patient toxicities, 27 died. Chance of toxicity increases in hypokalemia.
- #18 Cardiac monitors reset to unsynchronized defib after every cardioversion, thus must hit ‘Sync’ button EVERYTIME! Sedate, if appropriate.
- #29 Most patients will exhibit at least 1 of these symptoms, rarely all three, and mostly prior to cardiac arrest.
- #35 ‘Hour Glass’ appearance
- #41 Jugular pulse is normally non-pulsatile and consists of 2 beats per cardiac cycle, carotid 1 beat per cycle. If not palpable, push the abdominojugular reflex, or hepatojugular reflex.
- #43 Relative contraindications: aortic dissection, bleeding disorder, myocardial rupture. A traumatic pericardial effusion may require resuscitative thoracotomy.
- #44 Blind Approach associated with increased complications.