CCP Fall 2013 - Week 4

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CCP Fall 2013 - Week 4
2013-11-15 22:49:25
Critical Care Paramedic

Cardiac and Hemodynamics, Parts I-IV
Show Answers:

  1. What are the 3 layers of the heart?
    • 1: Epicardium
    • 2: Myocardium
    • 3: Endocardium
  2. What is the epicardium?
    Thin outermost layer of the heart
  3. What is the myocardium
    Thick muscular middle layer of the heart
  4. What is the endocardium?
    Thin inner layer of the heart
  5. Describe cardiac muscle tissue properties
    • Striated
    • Intercalated cells allow 2 syncytiums
    • Inner & outer spiral, middle circular
  6. What are the 2 types of valves?
    • Atrioventricular
    • Semilunar
  7. Describe the operation of the AV valves
    • Open as a result of ⇩ ventricular pressures
    • Close as a result of ⇧ ventricular pressures
  8. Name the 4 cardiac valves
    • 1: Tricuspid
    • 2: Pulmonic
    • 3: Mitral
    • 4: Aortic
  9. What mnemonic illustrates the order of valves by blood flow?
    Toilet Paper My Ass:

    • Tricuspid
    • Pulmonic
    • Mitral
    • Aortic
  10. What are the 2 main coronary arteries?
    • Right Coronary Artery (RCA)
    • Left Coronary Artery (LCA)
  11. The LCA bifurcates into what 2 arteries?
    • Left Anterior Descending (LAD)
    • Left Circumflex (LCX)
  12. What does the LAD supply?
    • Left anterior wall
    • Left anterior ⅔rds of septum
  13. What does the LCX supply?
    Left lateral wall
  14. What does the RCA become?
    Posterior Descending Artery (PDA)
  15. What does the RCA supply?
    • SA Node
    • Right Ventricle (RV)
    • AV Node
    • Left Posterior Wall
    • Left Inferior Wall
  16. What is the major intra-atrial pathway?
    Bachmann's Bundle
  17. What coronary artery feeds the Left Anterior Fascicle & the RBB?
    The LAD. It feeds the anterior ⅔ of the septum, which is where the Left Anterior Fascicle & the RBB are found.
  18. What are the 2 types of infarctions?
    • Transmural
    • Non-transmural/Subendocardial
  19. What constitutes 'Unstable Angina'?
    Dx’d w/+ cardiac markers & - 12-lead Δs
  20. What constitutes NSTEMI?
    Dx’d w/+ cardiac markers & ST depression or dynamic T wave Δs
  21. What constitutes STEMI?
    Dx’d w/+ cardiac markers & identified STE pattern on 12-lead
  22. What is the 1st enzyme to elevate in an MI?
  23. What is the 1st cardiac specific enzyme to elevate in an MI?
  24. Describe the significance of Septal wall MI
    • LAD occlusion
    • Associated w/anterior MI
    • Associated w/RBBB & LAFHB
  25. Describe the significance of Anterior Wall MI
    • LAD occlusion
    • Associated w/septal MI
    • Anticipate papillary muscle involvement – mitral valve
  26. Describe the significance of Lateral Wall MI
    • LCx occlusion
    • May be associated w/anterior wall MI or anteroseptal wall MI [Left main occlusion]
  27. Describe the significance of Inferior Wall MI
    • RCA occlusion
    • Associated w/posterior wall MI & RVI
    • Look for AV nodal involvement w/high occlusion
  28. Describe the significance of Posterior Wall MI
    • RCA Occlusion
    • Associated w/Inferior Wall MI & RVI
    • Look for AV nodal involvement w/high occlusion
  29. Describe the etiology of flash edema
    • LAD occlusion leads to infarct/weakening of papillary muscles
    • Papillary muscle incompetency allows mitral valve incompetence/prolapse during ventricular systole
    • MVP results in Mitral Valve regurgitation
    • Mitral valve regurgitation results in flash edema
  30. Define "Q" wave
    The 1st negative deflection before a positive deflection
  31. What is the difference between a physiological Q wave & a pathological Q wave?
    Physiological Q waves are not due to disease process. Pathological Q waves represent scar tissue.
  32. Describe the criteria to diagnose a pathological Q wave
    • 1: 0.04 s [40 ms] [1 small box] in width OR
    • 2: 1/3 the total amplitude in height
  33. What mnemonic describes the anatomical lead groups?
    • I See All Leads
    • Inferior
    • Septal
    • Anterior
    • Lateral
  34. What are the Inferior leads?
    II, III, aVF
  35. What are the Septal leads?
    V1, V2
  36. What are the Anterior leads?
    V3, V4
  37. What are the Lateral leads?
    I, aVL, V5, V6
  38. What vessel is occluded when you have an Inferior MI?
  39. What vessel is occluded when you have a Septal MI?
  40. What vessel is occluded when you have an Anterior MI?
  41. What vessel is occluded when you have a Lateral MI?
  42. What is the J Point?
    The juncture between the end of the QRS complex & the beginning of the T wave [the beginning of the S-T segment]
  43. What does the J Point represent?
    The end of ventricular depolarization & the beginning of ventricular repolarization
  44. How does pericarditis present on EKG?
    • abnormalities in multiple, seemingly unrelated leads
    • J point notching
  45. Describe the clinical presentation of pericarditis
    • Sharp pain
    • Pain is positional
    • Pain is reproducible with pressure
    • Pt wants to lean forward
    • Deep inspiration provokes
  46. Describe stable angina
    Onset w/physical exertion or emotional stress. Pain lasts 1-5 min & is relieved by rest. Predictable
  47. Describe unstable angina
    Stable angina that has changed in frequency, quality, duration or intensity. Pain lasts longer than 10 minutes despite rest & NTG therapy.
  48. Describe variant angina
    Spontaneous episodes of CP frequently noted at rest or on early rising (associated w/circadian pattern) & relieved by NTG
  49. Describe silent angina
    Objective evidence of ischemia in asymptomatic patients, typically positive 12 lead Δs or elevated enzymes.
  50. Describe mixed angina
    Combination of stable & variant angina
  51. Describe the use of nitrates in the treatment of AMI/USA
    • Improve coronary blood flow through vascular smooth muscle relaxation.
    • Venous pooling ⇩ pre-load & LVEDPs [Left Ventricular End Diastolic Pressures].
    • NTG dosage 5-200 mcg/min.
  52. What is the maximum dose for IV NTG?
    • No maximum dose had been determined.
    • Although 200 mcg/min is commonly cited, you should interpret this as, 'If 200 mcg/min isn't working, I need a different drug.'
  53. What reflexive response can be expected upon administering nitroprusside?
    • Tachycardia
    • Controlled w/β blockade
  54. Describe the use of morphine in the treatment of AMI/USA
    • Opioid that ⇩pre-load as well as ⇩ sympathetic tone causing a ⇩ in HR & ⇩ O2 demand.
    • Common dosage is 2-4 mg q 5-15 min.
  55. What is the formula for calculating coronary perfusion pressure?
    • CorPP = DBP - PCWP
    • Coronary Perfusion Pressure = Diastolic Blood Pressure - Pulmonary Capillary Wedge Pressure
  56. What is a desirable CorPP?
    > 50
  57. How do β-blockers ⇩ HR & MRO2 demand?
    ⇩ HR & contractility as well as ⇧ diastolic filling time. Indications for use only in the post-acute phase.
  58. metoprolol drug card
    • Lopressor®
    • 5 mg 
    • Repeat q10min
    • Max 15 mg
  59. How is carvedilol (Coreg®) effective @ ⇩ HR & myocardial O2 demand (MRO2)?
    α/β blocker w/antioxidant properties
  60. How are Ca+ Channel Blockers useful in the treatment of AMI/USA?
    Ca+ Channel Blockers produce dilation of the coronary arteries & collateral vessels along w/the cost of a ⇩ in myocardial contractility & conduction
  61. Describe hydralazine (Apresoline®) administration in the treatment of AMI/USA
    5-20 mg over 10 min
  62. What are the Glycoprotein IIb/IIIa inhibitors used for clot prevention & lysis in the treatment & management of AMI/USA?
    • eptifibatide (Integrilin®)
    • abciximab (ReoPro®)
    • tirofiban (Aggrestat®)
  63. How does Heparin/LMWH work to stop the buildup of a current clot?
    • Inactivates thrombin & factors IX, X, XI, & XII
    • Prevents the conversion of fibrinogen I to fibrin
  64. How do fibrinolytics work to break down a current clot?
    • Work by various mechanisms to activate plasminogen to plasmin
    • Result is fibrin degradation (“thrombolysis”)
    • Accelerates the breakdown of the clot from the inside out
  65. How do fibrinolytics work to break down a current clot?
    • Work by various mechanisms to activate plasminogen to plasmin
    • Result is fibrin degradation (“thrombolysis”)
    • Accelerates the breakdown of the clot from the inside out
  66. What is the indication for the use of thrombolytics in a cardiac patient?
    New onset STEMI
  67. What re the complications from the use of thrombolytics?
    • Bleeding… Everywhere… Anywhere
    • Reperfusion dysrhythmias common
  68. What are the relative contraindications for the use of thrombolytics?
    • HTN
    • Recent trauma
    • Pg
  69. What are the absolute contraindications for the use of thrombolytics?
    • Active internal bleeding
    • Suspected aortic dissection
    • Known intracranial neoplasm
    • Previous hemorrhagic stroke at any time
    • Any stroke w/in last year
  70. Discuss the process for treating AMI & USA using angioplasty
    • Treat angina
    • Inhibit clotting
    • Post-procedure watch for re-occlusion
    • Maintain sheath
    • Vessel patency
    • Sheath removal
  71. What is PTCA?
    Percutaneous Transluminal Coronary  Angioplasty
  72. Potential complications of PTCA?
    • (Primary) Stagnant Hypoxia in extremity cannulated
    • Hemorrhage
    • Iatrogenic coronary artery injury
  73. What are the complications of pacing?
    • Over sensing: Pacer "sees" more 'R' waves than there are (usually confuses prominent 'T' waves for 'R' waves) ∴ demand pacer will be mislead into not firing or not firing @ a fast enough rate
    • Failure to sense: Pacer doesn't sense legitimate 'R' waves ∴ pacer reads a false low rate & proceeds to pace (asynchronously)
    •   Potentially most lethal complication d/t R-on-T
    • Failure to capture: Paced beats do not produce a paced QRS or pulse
    • Myocardial penetration/perforation leading to Cardiac tamponade
  74. What are the issues with dilated cardiomyopathies?
    • Related to tension: the most critical factor in myocardial oxygen requirements
    •   ⇧ Tension = ⇧ MRO2 & the inverse holds true
    •   Directly related to diameter of container, inversely proportional to wall thickness
    • 2° volume overload, not pressure
    • Weakened walls & contractile dysfunction
    •   Stretched beyond the limits of Starling’s law
  75. Describe the management of dilated cardiomyopathies
    • Cardiac glycosides [digitalis]
    • Inotropes [dobutamine, dopamine]
    • Diuretics [lasix]
  76. Describe how digitalis functions
    • Takes 24°-72° to take effect
    • Poisons the Na+/K+ pump,
    • heart holds on to Na+
    • Anteporter required to kick Na+ out
    • Na+ goes out, Ca+ comes in
    • Ca⇧ output of the cell⇨ ⇧ inotropic effect
  77. Describe the issues with hypertrophic cardiomyopathies
    • 2° to pressure overload, not volume
    • Sacrifice of ventricular volume for ⇧ muscle mass
    • Builds muscle towards the inside, reducing volume available for blood
  78. Describe the treatment of hypertrophic cardiomyopathies
    • Do not allow them to get pre-load deficient
    • Need longer fill time, lots of pre-load
    • β-blockers
    • Ca+ Channel blockers
    • amiodarone (Cordarone®)
    •   K+ channel blocker
  79. Describe Restrictive Cardiomyopathies
    • 2° ischemia
    • Tissue fibrosis w/⇩ dynamics
  80. Describe the management of restrictive cardiomyopathies
    • Diuretics
    • Anticoagulation
    • Cardiac glycoside
  81. Identify the 2 classes of valvular disease
    • Stenosis
    • Regurgitant
  82. Which 2 valves are most commonly afflicted by disease?
    Mitral & Aortic
  83. Which 2 valves are least commonly afflicted by disease?
    Tricuspid & Pulmonic
  84. What is the 1° cause of multi-valvular disease?
    Rheumatic Fever
  85. Describe the effect Rheumatic Fever has on the heart valves
    • Autoimmune disorder triggered by Streptococcus
    • Bulbous lesions develop on leaflet/cusp edges
    • Scarring & Fusions develop
    • Stenosis & Regurgitation follow
  86. Where do you listen for aortic valve sounds?
    2nd intercostal just right of the sternal margin
  87. Where do you listen for pulmonic valve sounds?
    2nd intercostal just left of the sternal margin
  88. Where do you listen for mitral valve sounds?
    5th intercostal mid-clavicular
  89. Where do you listen for tricuspid valve sounds?
    4th intercostal just left of the sternal margin
  90. Describe normal valve sounds
    lub dub ... lub dub
  91. Describe the sound of a systolic murmur
    lub murmur dub ... lub murmur dub
  92. Describe the sound of a diastolic murmur
    lub dub murmur ... lub dub murmur
  93. Describe a VSD murmur
    • Ventriculoseptal defect
    • Systolic murmur predominantly
    • Lub murmur dub
    • Loud murmur = small defect; Quiet murmur = large
    • Auscultated primarily over the apices of the heart
  94. What is IHSS?
    Idiopathic Hypertrophic Subaortic Stenosis
  95. What is the 1° complication associated w/IHSS?
    • Aortic Stenosis
    • Auscultated @ the 2nd intercostal space just right of the sternal margin during SYSTOLE
  96. Define Aortic Dissection
    An intimal tear in the aorta
  97. Describe a Type I Aortic Dissection
    • (Begins @ the aortic valve) Occurs in the ascending aorta & extends distally beyond the aortic arch
    •   Commonly causes an MI
    •   Least likely to be operable
  98. Describe a Type II Aortic Dissection
    • Process is limited to the ascending aorta
    •   Jet erosions
    •   Marfan’s Syndrome
  99. Describe a Type III Aortic Dissection
    • Dissection distal to the origin of the LSC artery & extends distally to the abdominal aorta
    •   Most survivable
  100. How does Aortic Dissection present on X-Ray?
    • Widened mediastinum
    • w/Diffuse infiltrates
  101. Describe the field management of aortic dissection
    • ⇩ SBP to 100-110 mmHg w/vasodilators
    •   Nipride – Start minimally & gradually ⇧ to effect
    • β-blockers to ⇩ HR & ⇩ EF
    • Pain relief – Be aggressive
  102. What are the complications of aortic dissection?
    • Occlusion of carotid arteries
    • Occlusion of coronary arteries
    • HTN
  103. What is the goal in the management of HTN crisis?
    To lower their BP to the patient's normal level within 30-60 minutes.
  104. What is the value of arterial monitoring?
    More accurate & second to second
  105. What is the value of CVP (Central Venous Pressure) monitoring?
    • Primarily hydration status
    • Right heart function
  106. What is the value of PA (Pulmonary Artery) [Swan-Ganz catheter] monitoring?
    • Pulmonary pressures
    • Isolates left heart
  107. How long is a Swan-Ganz line?
    100 cm
  108. Which port should be monitored?
  109. What type fluid can be run through a fluid filled monitoring system?
    LR & NS
  110. Do fluid filled monitoring systems need to be heparinized?
    • No but they can be
    • Long term use of heparinized fluid filled monitoring system tends can alter coags
  111. Do fluid filled monitoring systems need to be pressurized?
    Use, must use pressure bag set @ 300
  112. Define transduce
    Convert mechanical energy into electrical energy
  113. What are steps of pressure monitoring setup?
    • Purge & flush line
    • Pressurize fluid to 300 mmHg
    • Transducer should be even with the phlebostatic axis
    • Attach all tubing & remove air
    • Zero
    • Perform fast flush test
  114. Where is the phlebostatic axis?
    Even with the 4th intercostal space, mid-axillary line
  115. How is proper damping in a fast flush test shown?
    2-5 peaks/bounces
  116. What are the 2 most common sites for arterial line placement?
    • Radial Artery [Typically best choice]
    • Femoral Artery
  117. What are arterial lines used for?
    • Monitor
    •   Real time pressure
    • Draws
    •   ABGs
    •   Labs
  118. What are arterial lines NOT used for?
    • Medication administration
    • Fluid resuscitation
  119. Slurring of the dicrotic notch indicates what?
    Aortic stenosis
  120. What does an anacrotic notch indicate?
    Aortic stenosis
  121. How do the kidneys notice reduced renal blood flow?
    Reduced Na+
  122. How do the kidneys respond to reduced Na+?
    Releases Renin
  123. What does Renin do?
    Converts Angiotensinogen to Angiotensin I
  124. What happens to Angiotensin I
    Converted to Angiotensin II by Angiotensin Converting Enzyme (ACE) (Found in the pulmonary epithelium)
  125. What does Angiotensin II do?
    • Causes vasoconstriction
    • Causes the release of Aldosterone
  126. What effect does Aldosterone have on the body?
    • Renal Na+/K+ pump shoved into high gear
    • Aquaporin channels open allowing the kidneys to retain water
  127. What causes the release of Atrial Natriuretic Peptide (ANP)?
    Stretching of the Atria 2° to ⇧ volume
  128. How do the ventricles respond to ⇧ volume/stretching?
    Releases Brain Natriuretic Compound (BNP), the test for CHF
  129. What is the focus of CHF management?
    • Relieving immediate failure
    • Preventing further myocardial damage
  130. What is the CHF lab marker?
    BNP level
  131. What is the goal of CHF therapy?
    • Decrease preload
    • Decrease afterload
    • Decrease rate
    • Inhibit RAA system
    • Improve contractility
  132. How do you differentiate CHF from cardiogenic shock?
    CHF is not typically hypotensive while cardiogenic shock is
  133. What drugs are used to treat CHF?
    • dopamine (Intropin®)
    • dobutamine (Dobutrex®)
    • amrinone (Inocor®)
    • milrinone (Primacor®)
    • sodium nitroprusside (Nitropress®)
  134. What is normal CVP?
    2-6 mmHg
  135. What can a low CVP indicate?
    • Hypovolemia
    • Vasodilation
    • Negative pressure ventilation
  136. What can a high CVP indicate?
    • Hypervolemia
    • RV failure / RVI
    • Cardiac tamponade
    • Positive pressure ventilation
    • Pulmonary hypertension
    • PE
    • Pulmonic stenosis
    • Tricuspid stenosis & regurgitation
  137. What is a normal RVP systolic?
    Normal systolic 15-25 mmHg
  138. What is a normal RVP diastolic?
    Normal diastolic 0-5 mmHg
  139. What is normal Pulmonary Artery Systolic (PAS) Pressure?
    15-25 mmHg
  140. What is normal Pulmonary Artery Diastolic (PAD) pressure?
    8-15 mmHg
  141. What can cause low Pulmonary Artery Pressures (PAPs)?
    • Dehydration
    • RV failure or RVI
    • Pulmonic stenosis
  142. What can cause high Pulmonary Artery Pressures?
    • Fluid overload
    • Mitral stenosis or regurgitation
    • Left ventricular failure
    • High PVR & SVR
    • AV communications
    • Pulmonary HTN
    • HPVR
  143. What is normal PCWP?
    8-12 mmHg
  144. What are the 2 causes of inadvertent wedge in PA catheter waveform?
    • Migration
    • Balloon inflation
  145. How do you correct inadvertent wedge in PA Catheter waveform?
    • Verify balloon fully deflated
    • Have pt cough forcefully or roll to side and
    • back
    • Withdraw catheter until waveform returns to PA waveform
  146. What causes inadvertent RV waveform in PA Catheter waveform?
    PA catheter tip is whipping around in ventricle
  147. How do you correct inadvertent RV waveform in PA Catheter waveform?
    Verify balloon deflated & withdraw catheter until CVP waveform visible