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PCCN Review Part 1 (of 2)
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PCCN Review Part 1 (of 2)

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PCCN Review

PCCN Review

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  • As plaque develops and the coronary arteries become increasingly narrower, collateral branches form to help supply those areas of heart muscle. MI’s with no collateral circulation tend to suffer more severe infarctions and more hemodynamic compromise. Edema and color changes (within the heart) are evident 6 hours after an MI. LV function is altered immediately in ischemic states as well as in infarctions. Wall thickness decreases 8 to 10 days later due to a natural physiological cleanup and/or necrotic tissue removal. Scar tissue and tissue remodeling occur later and may lead to cardiac failure. Transmural MI involves full thickness of the myocardium whereas subendocardial MI (non-Q wave) involves partial thickness.
  • Cardiac Enzymes: Troponin The troponin level rises within 4-6 hours after an AMI, peaks in 24 hours, and returns to baseline within 7-10 days. CK or CPK MB-CK is the cardiac specific isoenzyme MB-CK is normally less then 5% of the CK The CK level rises within 4-8 hours, peaks in 8-58 hours (with an average of 24 hours), and returns to baseline within 3-4 days. LDH LDH 1 is the cardiac specific isoenzyme When LDH 1 > LDH 2 , an AMI is probably occurring The LDH level rises within 24-48 hours, peaks within 3-6 days, and returns to baseline within 8-14 days. False positives enzyme levels may be seen in conditions that involve muscle injury (trauma, disease, vigorous exercise or rhabdomyolysis)
  • Coronary Circulation: RCA Supplies the SA node, AV node, bundle of his, posterior papillary muscles, inferior wall of the left ventricle, and the posterior third of the septum The RCA supplies most of the blood supply to the inferior wall of the left ventricle for most people A person is said to be right dominant when the RCA supplies most of the blood supply to the inferior wall (of the left ventricle) IWMI usually due to RCA occlusion Watch for problems associated with the SA node (tachycardia, bradycardia, sick sinus or sinus arrest), the AV node (AV blocks), the right ventricle (RV involvement), and the posterior papillary muscles (MR or papillary muscle rupture). LAD (branches off left main artery) Supplies the anterior wall of the left ventricle, some of the lateral wall, and most of the intra-ventricular septum (including it’s conduction system) AWMI usually due to LAD occlusion Watch for problems involving large areas of the anterior left ventricle (cardiogenic shock) and problems involving the septum (blocks and VSD). Circumflex (branches off left main artery) Supplies the lateral and posterior walls of the left ventricle A small percentage of people have a short RCA and the circumflex artery then wraps around and supplies most of the inferior wall A person is said to be left dominant when the circumflex artery supplies most of the blood supply to the inferior wall (of the left ventricle) Lateral and/or posterior wall MI usually due to circumflex occlusion
  • Two or more leads of a group: IWMI Leads II, III and aVF view the inferior wall (of the left ventricle) Reciprocal changes are seen in leads I, and aVL AWMI Leads V 1 -V 4 view the anterior-septal wall (left ventricle) Reciprocal changes are seen in leads II, III, and AVF Lateral wall MI Leads I, aVL, V 5 and V 6 view the lateral wall (left ventricle) Reciprocal changes are seen in leads II, III, and aVF Posterior wall MI Posterior MI’s are difficult to detect on a 12 lead EKG because no leads are placed directly over the posterior Changes are reflected on the opposite walls (Instead of ST elevations, you will see ST depression. Instead of Q waves, you will see tall R waves. Instead of T wave inversions, you will see upright T waves) Reciprocal changes may be seen in leads V 1 and V 2 Right Ventricle Leads V 6 R - V 3 R view the RV
  • Two or more leads of a group: IWMI Leads II, III and aVF view the inferior wall (of the left ventricle) Reciprocal changes are seen in leads I, and aVL AWMI Leads V 1 -V 4 view the anterior-septal wall (left ventricle) Reciprocal changes are seen in leads II, III, and AVF Lateral wall MI Leads I, aVL, V 5 and V 6 view the lateral wall (left ventricle) Reciprocal changes are seen in leads II, III, and aVF Posterior wall MI Posterior MI’s are difficult to detect on a 12 lead EKG because no leads are placed directly over the posterior Changes are reflected on the opposite walls (Instead of ST elevations, you will see ST depression. Instead of Q waves, you will see tall R waves. Instead of T wave inversions, you will see upright T waves) Reciprocal changes may be seen in leads V 1 and V 2 Right Ventricle Leads V 6 R - V 3 R view the RV
  • NTG Dilates coronary arteries Decreases preload (decreases afterload some) MSO 4 Morphine is the analgesic of choice with AMI because it also reduces preload and decreases myocardial oxygen demand. Morphine decreases anxiety, restlessness, and autonomic nervous system activity. Aspirin Inhibits platelet aggregation Heparin Prevents further extension of existing thrombi and/or new clot formation (blocks conversion of prothrombin to thrombin and fibrinogen to fibrin) Beta Blockers Slow heart rate and lower BP Encourages electrical stability Improves mortality ACE Inhibitors Reduce afterload (vasodilatation) Reduces work of heart Decreases remolding effects GP IIb IIIa Inhibitors (anti-thrombolytics) Integrilin Reopro Thrombolytics Given up to 12 hours from the onset of an AMI Contraindicated in patients with active bleeding, BP>200/120, major surgery within 2 weeks, CPR >10 min, recent head trauma, suspected aortic dissection, pregnancy, CVA within 1 year, history of a hemorrhagic CVA, of major illnesses or cancers Anti-Lipidemics HDH is associated with  risk LDH is associated with  risk Look at the HDL : LDL ratio
  • Increased incidence of sudden death or blood clots
  • Increased incidence of sudden death or blood clots
  • Generalized Treatment of Cardiomyopathy: Treat Symptoms Monitor For Signs of Worsening Heart Failure Daily Weights Prone To Digoxin Toxicity Due To  Renal Perfusion  Monitor Digoxin Levels Give Positive Inotropic Drugs (Except With Hypertropic Cardiomyopathy) Give Vasodilators (Except With Hypertropic Cardiomyopathy) Reduce Preload & Afterload Diuretics Calcium Channel Blockers As Indicated Beta Blockers As Indicated IABP Vasodilators As Indicated Fluid Restriction Give O2 With Exacerbations & As Needed Give Antidysrhythmic Agents As Needed Restrict Sodium Decrease Activity, Plan Activities & Rest Consider Heart Transplant Educate Patient & Family Give Emotional Support
  • AFib TREATMENT O2 and monitor. Slow rate when necessary. ECG Attempt to convert with medications if relatively new rhythm and hemodynamically stable. Prepare for synchronized cardioversion if hemodynamically unstable. Chronic atrial fibrillation usually treated with coumadin, ASA, etc.
  • AFL TREATMENT O2 and monitor. ECG Attempt to convert with medications if relatively new rhythm and hemodynamically stable (beta-blockers, calcium channel blockers, digoxin). Prepare for synchronized cardioversion if hemodynamically unstable.
  • WAP TREATMENT O2 and monitor ECG
  • SVT TREATMENT O2 and monitor. ECG May attempt vagal maneuvers. May require beta-blockers, calcium channel blockers, etc. Prepare for synchronized cardioversion if hemodynamically unstable.
  • VT TREATMENT Immediate defibrillation or cardioversion. CPR and ACLS
  • Torsades TREATMENT MgSO4 Immediate defibrillation. CPR and ACLS.
  • Pulmonary (LVF) and/or systemic (RVF) congestion is present. The weakened LV doesn’t empty properly and backs up toward the pulmonary vasculature. The increased pressures allow fluid to leak back into the pulmonary interstitial spaces and into the alveolus. Back pressure form the RV to the systemic venous system leads to increased venous pressures with engorgement of the liver and spleen and third-spacing of fluid into interstitial spaces, causing peripheral edema and ascites.
  • Cardiogenic Pulmonary Edema = Elevated PAP, Elevated PAWP Non-cardiogenic Pulmonary Edema = Elevated PAP, Normal PAWP
  • Class I: Patient with cardiac disease without resulting limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations, dyspnea or angina.   Class II: Patient with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest but ordinary physical activity results in fatigue, palpitations, dyspnea or angina. Class III: Patient with cardiac disease resulting in marked limitations of physical activity. They are comfortable at rest but, less than ordinary activity causes fatigue, palpitations, dyspnea or angina. Class IV: Patient with cardiac disease resulting in inability to do any physical activity without discomfort. Symptoms of cardiac insufficiency or angina are increased when any activity is attempted.  
  • Improve Oxygenation O 2 Intubation PEEP Diuretics Decrease Myocardial Oxygen Consumption Bedrest (HOB elevated) Physical comfort (temperature control) Emotional control (keep informed, sedative prn) Gradually increase activity as tolerated, rest between activities Decrease Preload Diuretics (usually loop diuretics such as furosemide) High fowler’s position (legs dependent) Venous vasodilator (NTG, MSO 4 ) Sodium and fluid restriction Increase Contractility Cardiac glycosides (digoxin) Positive Inotropics (dopamine, dobutamine) Decrease Afterload Ace Inhibitors (captopril, enalapril) Nitroprusside (if hypertensive) Calcium channel blockers Dobutamine, Primacor Pulmonary vasodilators (aminophylline) IABP Prevent Valsalva Maneuvers Stool softeners Exhaling when turning Manage Dysrhythmias Atrial: Digoxin may be used to decrease ventricular rate by increasing refractoriness of the AV node. Ventricular: Lidocaine or amiodarone if necessary (procainamide and bretlium may significantly decrease contractility) Beta Blockers Used for mild CHF Protects heart form excessive catecholamines Cor Pulmonale (RVF) O 2 Therapy Pulmonary Vasodilators RVF Due to Pulmonary Embolus O 2 Therapy Anticoagulants Thrombolytics (if significant RVF or hypoxia)
  • Hypovolemic Shock Inadequate perfusion to the tissues due to insufficient intravascular volume.   Cardiogenic Shock Inadequate perfusion to the tissues due to heart failure.   Distributive Shock (Anaphylactic, Septic, and Spinal Shock) Inadequate perfusion to the tissues due to maldistribution of blood flow out of the intravascular space causing insufficient intravascular volume.   Obstructive Shock Inadequate perfusion to the tissues due to obstruction of blood flow. Causes: Pulmonary Embolus Tamponade Tension Pneumothorax Aortic Aneurysm
  • Self destructive form of shock High mortality rate (75-100%) Occurs in 10% of AMI’s Usually means loss of at least 40% LV function Ventricular gallop = S3
  • Histamines cause massive vasodilatation
  • Causes of Obstructive Shock: Pulmonary Embolus Tamponade Tension Pneumothorax Aortic Aneurysm
  • 1)  CO Positive Inotropes   2)  Preload & Afterload Diuretics Vasodilators IABP Positioning   3)  Myocardial Demand Bedrest O 2
  • Causes of Obstructive Shock: Pulmonary Embolus Tamponade Tension Pneumothorax Aortic Aneurysm            
  •          
  •          
  • Somatostatin Somatostatin is classified as an inhibitory hormone, whose main actions are to: Inhibit the release of growth hormone (GH) Inhibit the release of thyroid-stimulating hormone (TSH) Suppress the release of gastrointestinal hormones Gastrin Cholecystokinin (CCK) Secretin Motilin Vasoactive intestinal peptide (VIP) Gastric inhibitory polypeptide (GIP) Enteroglucagon (GIP) Lowers the rate of gastric emptying, and reduces smooth muscle contractions and blood flow within the intestine. Suppress the release of pancreatic hormones Inhibit the release of insulin Inhibit the release of glucagon Suppress the exocrine secretory action of pancreas. Somatostatin opposes the effects of Growth Hormone-Releasing Hormone (GHRH)
  • Transcript

    • 1. PCCN REVIEW PART 1 “Never let what you cannot do interfere with what you can do” - John Wooden - Sherry L. Knowles, RN, CCRN, CRNI
    • 2. PCCN REVIEW PART 1 TOPICS Acute Coronary Syndromes  ARDS Acute Myocardial Infarction  Chronic Lung Disease Heart Blocks  Drowning Heart Failure  Pneumonia Cardiac Alterations  Pneumothorax Aortic Aneurysms  Pulmonary Embolism Cardiomyopathy  Respiratory Failure Shock States  Gastrointestinal Alterations Peripheral Vascular Disease  GI Bleeding Respiratory Alterations  Pancreatitis
    • 3. PCCN REVIEW PART 1 OBJECTIVES1. Understand the different types of acute coronary syndromes.2. Identify basic coronary circulation and how it relates to different types of myocardial infarctions.3. Anticipate potential complications associated with an AMI.4. Identify the standard treatment of an AMI.5. Distinguish between various AV blocks.6. Recognize the signs & symptoms of heart failure.7. Identify the treatment of heart failure.8. Recognize the general definition and classifications of aortic aneurysms.9. Understand the different types of aortic dissections.10. Recognize the signs & symptoms of cardiomyopathy.11. Differentiate between the different types of cardiomyopathy.12. Identify the treatment for the different types of cardiomyopathy.
    • 4. PCCN REVIEW PART 1 OBJECTIVES13. Understand the different stages of shock.14. Differentiate between different types of shock.15. Distinguish between arterial and venous peripheral vascular disease.16. Identify the various treatments for peripheral vascular disease.17. Define respiratory failure.18. Identify the various treatments for acute respiratory failure.19. Recognize the signs & symptoms and causes of various respiratory alterations.20. Identify the standard treatment for various respiratory alterations.21. Explain the common causes of gastrointestinal bleeding.22. Describe the most commonly seen treatments for GI bleeding.23. Describe the signs & symptoms of acute pancreatitis and available treatments.
    • 5. Cardiovascular Conditions  Acute Coronary  Cardiomyopathy Syndromes  Acute MI  Heart Blocks  Aortic Aneurysms  Heart Failure  Cardiac Alterations  Shock States
    • 6. Acute Coronary Syndrome DEFINITIONS – Term used to cover a group of symptoms compatible with acute myocardial ischemia – Acute myocardial ischemia is insufficient blood supply to the heart muscle usually resulting from coronary artery disease
    • 7. Acute Myocardial Infarction DEFINITION – Infarction occurs due to mechanical obstruction of a coronary artery (or branch) caused by a thrombus, plaque rupture, coronary spasm and/or dissection. – STEMI vs. NSTEMI (non-STEMI)
    • 8. Acute Myocardial Infarction SIGNS & SYMPTOMS – Complains Vary  May include crushing chest pain (which may or may not radiate), back, neck, jaw, teeth and/or epigastric pain, SOB, nausea/vomiting and dizziness – ST elevations on ECG – Elevated cardiac enzymes
    • 9. Acute Myocardial Infarction SIGNS & SYMPTOMS ↑ PAWP, ↓ CO, ↑ SVR, dysrhythmias, S4, cardiac failure, cardiogenic shock – Diaphoresis, pallor, referred pains – Diabetics and women often present abnormal symptoms
    • 10. Coronary Circulation
    • 11. 12 Lead ECGI AVR V1V4II AVL V2 V5III AVF V3 V6IIV
    • 12. Acute Myocardial Infarction ST ELEVATIONS – Anterior Wall MI  Leads V1-V4  Reciprocal changes in leads II, III, and aVF  Area supplied by the LAD – Inferior Wall MI  Leads II, III and aVF  Reciprocal changes in leads I, and aVL  Area usually supplied by the RCA
    • 13. Acute Myocardial Infarction ST ELEVATIONS – Lateral Wall MI  I, aVL, V5 and V6  Area supplied by the Circumflex artery – Posterior Wall MI  Reflected on the opposite walls  Opposite deflections
    • 14. Coronary Arteries
    • 15. Anterior Wall MI
    • 16. Inferior Wall MI
    • 17. Acute Myocardial Infarction COMPLICATIONS – Dysrhythmias, heart failure, pericarditis, ventricular aneurysms, ventricular thrombus, VSD, mitral regurgitation, papillary muscle (or chordae tendineae) rupture, pericardial effusions, pericarditis
    • 18. Acute Myocardial Infarction NURSING INTERVENTIONS – O2 – Bedrest – Serial ECG’s – Serial cardiac enzymes – Keep pain free (NTG. MSO4) – MONA (Morphine, O2, Nitroglycerin, Aspirin), Heparin, beta-blockers, and ace inhibitors. May also include thrombolytics or Gp2b3a inhibitors – PCI, PTCA, IABP, CABG
    • 19. Acute Myocardial Infarction TREATMENT – Time Is Heart Muscle – Prompt ECG – Goals: Relieve pain, limit the size of the infarction and to prevent complications (primarily lethal dysrhythmias)
    • 20. Acute Myocardial Infarction TREATMENT – MONA (Morphine, O2, Nitroglycerin, Aspirin), Heparin, beta-blockers, and ace inhibitors. May also include thrombolytics or Gp2b3a inhibitors – Cardiac Catheterization (with angioplasty, atherectomy and/or stent) – IABP, CABG, education
    • 21. Balloon Angioplasty
    • 22. Vascular Stent Deployment
    • 23. Atherectomy
    • 24. Acute Myocardial Infarction SPECIFIC TREATMENTS – Inferior Wall (IWMI)  Fluids (with RV infarct)  Inotropics  Afterload reducing medications – Anterior Wall (AWMI)  Diuretics  Inotropics  Afterload reducing medications
    • 25. Aortic Aneurysms DEFINITION – A bulge or ballooning of the aorta  When the walls of the aneurysm include all three layers of the artery, they are called true aneurysms  When the wall of the aneurysm include only the outer layer, it is called a pseudo-aneurysm – May be thoracic or abdominal
    • 26. Aortic Aneurysms CAUSES  Atherosclerosis  Marfan syndrome  Hypertension  Crack cocaine usage  Smoking  Trauma
    • 27. Aortic Aneurysms Rupture  An aortic aneurysm, depending on its size, may rupture, causing life-threatening internal bleeding  The risk of an aneurysm rupturing increases as the aneurysm gets larger  The risk of rupture also depends on the location of the aneurysm  Each year, approximately 15,000 Americans die of a ruptured aortic aneurysm.
    • 28. Aortic Aneurysms CLASSIFICATIONS – Classified by shape, location along the aorta, and how they are formed – May be symmetrical in shape (fusiform) or a localized weakness of the arterial wall (saccular)
    • 29. Aortic Aneurysms
    • 30. Aortic Aneurysms SIGNS & SYMPTOMS – Often produces no symptoms – If an aortic aneurysm suddenly ruptures it presents with extreme abdominal or back pain, a pulsating mass in the abdomen, and a drastic drop in blood pressure – An increase in the size of an aneurysm means an increased in the risk of rupture
    • 31. Aortic Aneurysms THORACIC SIGNS & SYMPTOMS – Back, shoulder or neck pain – Cough, due to pressure placed on the trachea – Hoarseness – Strider, dyspnea – Difficulty swallowing – Swelling in the neck or arms
    • 32. Aortic Dissections DEFINITION – Tearing of the inner layer of the aortic wall, which allows blood to leak into the wall itself and causes the separation of the inner and outer layers – Usually associated with severe chest pain radiating to the back
    • 33. Aortic Dissections A. Dissection B. Whenever the beginning in the ascending aorta ascending aorta is not involved
    • 34. Aortic Dissections A. Dissection B. Whenever the beginning in the ascending aorta ascending aorta is not involved
    • 35. Aortic Dissections
    • 36. Aortic Dissections
    • 37. Aortic Aneurysms COMPLICATIONS  Rupture  Peripheral embolization  Infection  Spontaneous occlusion of aorta
    • 38. Aortic Aneurysms TREATMENT  Medical management – Controlled BP (within specific range)  Surgical repair  > 4.5 cm in Marfan patients or > 5 cm in non- Marfan patients will require surgical correction or endovascular stent placement
    • 39. Cardiomyopathy DEFINITION – Diseases of the heart muscle that cause deterioration of the function of the myocardium
    • 40. Cardiomyopathy CLASSIFICATIONS – Primary / Idiopathic (intrinsic)  Heart disease of unknown cause, although viral infection and autoimmunity are suspected causes – Secondary (extrinsic)  Heart disease as a result of other systemic diseases, such as autoimmune diseases, CAD, valvular disease, severe hypertension, or alcohol abuse
    • 41. Cardiomyopathy  Hypertropic Cardiomyopathy  Restrictive Cardiomyopathy  Dilated Cardiomyopathy
    • 42. Hypertropic Cardiomyopathy Bizarre hypertrophy of the septum – Previously called IHSS  Idiopathic Hypertropic Subaortic Stenosis – Known as HOCM  Hypertropic Obstructive Cardiomyopathy Positive inotropic drugs Should Not Be Used ↑ Contractility will ↑ outflow tract obstruction Nitroglycerin Should Not Be Used – Dilation Will Worsen The Problem
    • 43. Harley
    • 44. Hypertropic Cardiomyopathy  TREATMENT – Relax the ventricles  Beta Blockers  Calcium Channel Blockers – Slow the Heart Rate  Increase filling time – Use Negative Inotropes  Optimize diastolic filling – Do Not use NTG  Dilation will worsen the problem
    • 45. Restrictive Cardiomyopathy  Rigid Ventricular Wall – Due to endomyocardial fibrosis – Obstructs ventricular filling  Least common form
    • 46. Restrictive Cardiomyopathy  TREATMENT – Positive Inotropics – Diuretics – Low Sodium Diet
    • 47. Dilated Cardiomyopathy Grossly dilated ventricles without hypertrophy – Global left ventricular dysfunction – Leads to pooling of blood and embolic episodes – Leads to refractory heart failure – Leads to papillary muscle dysfunction secondary to LV dilation
    • 48. Dilated Cardiomyopathy TREATMENT – Positive Inotropes – Afterload Reducers – Anticoagulants with Atrial Fib
    • 49. Cardiomyopathies
    • 50. Cardiomyopathy GENERALIZED TREATMENT – Positive Inotropes  Except with Hypertropic Cardiomyopathy – Vasodilators  Except with Hypertropic Cardiomyopathy – Reduce Preload & Afterload – Diuretics – Beta Blockers – Calcium Channel Blockers – IABP – Vasodilators (as indicated) – Fluid Restriction – Daily weights, prn O2, planned activities, education, and emotional support – Consider Heart Transplant
    • 51. PCCN REVIEW PART 1 BREAK!
    • 52. Conduction Defects STABLE VS UNSTABLE – Stable  Start with medications – Unstable  Shock (cardioversion or defibrillation)
    • 53. Normal Sinus RhythmHeart Rate 60 - 100 bpmRhythm RegularP Wave Before each QRS & identicalPR Interval (in seconds) 0.12 to 0.20QRS (in seconds) < 0.12
    • 54. Atrial Fibrillation AFib – Multifocal atrial impulses at rate 300-600/min – Irregular conduction to ventricles
    • 55. Atrial Flutter AFL – Atrial impulses at rate of 250-350/min – Regularly blocked impulses at the AV node – Saw tooth flutter waves
    • 56. Wandering Atrial Pacemaker WAP – Multiple ectopic foci in the atria – Three or more p wave morphologies – Rate < 100
    • 57. Supraventricular Tachycardia SVT – Supraventricular rhythm at rate 150-250 – P waves cannot be positively identified Atrial Tach = supraventricular rhythm with p wave morphology that is noticeably different from the sinus p wave
    • 58. Ventricular Tachycardia VT – Ventricular rate of 100-250/min – Wide QRS
    • 59. Torsades de Pointes Polymorphic VT – VT with alternating ventricular focus – Often associated with prolonged QT Rate < 100
    • 60. Heart Blocks (AV Blocks) Sinus Rhythm with First Degree AV Block Sinus Rhythm with Second Degree AV Block, Type 1 Sinus Rhythm with Second Degree AV Block, Type 2 Third Degree AV Block
    • 61. Heart Failure DEFINITION – A condition in which the heart cannot pump sufficient blood to meet the metabolic needs of the body – Pulmonary (LVF) and/or systemic (RVF) congestion is present.
    • 62. Heart Failure DEFINITION – Pulmonary Edema  Fluid in the alveolus that impairs gas exchange by altering the diffusion between alveolus and capillary  Acute left ventricular failure causes cardiogenic pulmonary edema  Non-cardiogenic pulmonary edema is a synonym for Adult Respiratory Distress Syndrome (ARDS)
    • 63. Heart Failure COMPENSATORY MECHANISMS – Sympaththetic nervous system stimulation  Tachycardia  Vasoconstriction and increased SVR – Renin-angiotensin-aldosterone system activation  Hypo perfusion to the kidneys (renin)  Vasoconstriction (angiotension)  Sodium and water retention (kidneys)  Ventricular dilation
    • 64. Heart Failure FUNCTIONAL CLASSIFICATIONS –(without noticeable limitations) Class I – Class II upon activity) (symptoms – Class III(severe symptoms upon activity) – Class IV(symptoms at rest)
    • 65. Heart Failure COMPLICATIONS – Hypotension – Dysrhythmias – Respiratory Failure – Progressive Deterioration – Acute Renal Failure – Fluid & Electrolyte Imbalances
    • 66. Heart Failure TREATMENT – Improve Oxygenation – Decrease Myocardial Oxygen Demand – Decrease Preload – Decrease Afterload – Increase Contractility – Manage Dysrhythmias – Educate!
    • 67. Shock States DEFINITION – Inadequate perfusion to the body tissues – Low blood pressure with impaired perfusion to the end organs – May result in multiple organ dysfunction
    • 68. Shock States TYPES OF SHOCK – Hypovolemic Shock – Cardiogenic Shock – Distributive Shock – Obstructive Shock
    • 69. Shock States SIGNS & SYMPTOMS The body attempts to compensate for shock: 1. Tachycardia  Attempts to deliver more blood to the tissues 2. Vasoconstriction  Attempts to maintain adequate BP in order to adequately perfuse the body tissues 3. Increased ADH Secretion  ADH makes the body hold onto water in an effort to maintain volume and thus enough blood pressure to perfuse the body tissues
    • 70. Shock States SIGNS & SYMPTOMS – Hypovolemic Shock:  Low BP, tachycardia, orthostatic hypotension, restlessness, confusion, agitation (or listless), thirst, pallor, cool, clammy skin, ↑resp. rate, ↓ UOP, ↓ CO, ↓ PAWP, ↓ CVP, ↑ SVR, ↑ lactate levels
    • 71. Shock States SIGNS & SYMPTOMS – Cardiogenic Shock:  Low BP, tachycardia, restlessness, confusion, agitation (or listless), thirst, pallor, cool, clammy skin, ↑ resp. rate, ↓ UOP, ↓ CO, ↑ PAWP (low with RVF), ↑ CVP, ↑ SVR, JVD, peripheral edema, ventricular gallop, dyspnea, pulmonary crackles, ↑ lactate levels
    • 72. Shock States SIGNS & SYMPTOMS – Anaphylactic Shock:  Low BP, tachycardia, orthostatic hypotension, restlessness, confusion, agitation (or listless), thirst, pallor, warm feeling, pruritus, hives, angioedema, bronchoconstriction, wheezing, laryngoedema, dyspnea, cool, clammy skin, ↓ UOP, ↓ CO, ↓ PAWP, ↓ CVP, ↓ SVR, ↑ lactate levels
    • 73. Shock States SIGNS & SYMPTOMS – Obstructive Shock:  Low BP, tachycardia, restlessness, confusion, agitation (or listless), pallor, cool, clammy skin, ↓ UOP, ↓ CO  Symptoms related to cause
    • 74. Shock States SIGNS & SYMPTOMS – Septic Shock:  Early Stage (Hyper-dynamic, Warm Phase) – Normal BP, tachycardia, confusion, agitation (or listless), ↑ resp. rate, ↑ temp, normal color, normal or ↑ UOP, ↓ CO, normal PAWP, ↑ CO, ↓ SVR, ↑
    • 75. Shock States SIGNS & SYMPTOMS – Septic Shock:  Late Stage (Hypo-dynamic, Cold Phase) – Low BP, tachycardia, orthostatic hypotension, restlessness, confusion, agitation (or listless), thirst, pallor, cool, clammy skin, ↓ UOP, ↓ CO, ↓ PAWP, ↓ CVP, ↑ SVR, ↑ lactate levels
    • 76. Shock States TREATMENTS – Hypovolemic Shock:  Volume (IVF, Blood) – Cardiogenic Shock:  ↑ CO  ↓ Preload & Afterload  ↓ Myocardial Demand
    • 77. Shock States TREATMENTS – Anaphylactic Shock:  Epinephrine  IVF  Vasoconstrictors  Support/Maintain Airway – Obstructive Shock:  Treat the Cause
    • 78. Shock States TREATMENTS – Septic Shock:  IVF (150cc/hr or wide open)  Treat Cause (pan culture, antibiotics)  Vasoconstrictors in warm phase  Treat temp (if needed)
    • 79. Vascular DiseaseAorto/Iliac Disease: Pre & Post PTA/Stent
    • 80. Peripheral Vascular DiseaseSYMPTOMS ARTERIAL VENOUSPAIN Upon walking While standingPAIN RELIEF On resting, standing or Elevation of extremities dependent position of lower limbsEDEMA None Present, edematousPULSES Decreased or absent May be difficult to palpateINTEGUMENT Hair loss Brownish pigmentation Skin shiny May be cyanotic whenCHANGES Nail thickening extremities are dependent Pallor when elevated Red when dependent Ulcers located on toes, lateral Ulcers located on ankles,ULCERS areas or site of trauma medial or pre-tibial areas Gangrene possibleSKIN TEMPERATURE Cool Normal or warmSEXUAL ISSUES Impotency Not present Sexual dysfunction
    • 81. Peripheral Vascular Disease TREATMENTS – Medical  Are they taking ASA, Coumadin, Ticlid, Plavix, Oral Contraceptives, Hormones? – Invasive  PTA, atherectomy, stents – Surgical  Grafts
    • 82. Peripheral Vascular Disease Bypass Grafts
    • 83. PCCN REVIEW PART 1 BREAK!
    • 84. Respiratory Alterations  ARDS  Chronic Lung Disease  Drowning  Pneumonia  Pneumothorax  Pulmonary  Respiratory Embolism Failure
    • 85. ARDS DEFINITIONS – Severe respiratory failure associated with pulmonary infiltrates (similar to infant hyaline membrane disease) – Pulmonary edema in the absence of fluid overload or depressed LV function (Non-cardiogenic pulmonary edema) – Originates from a number of insults involving damage to the alveolar-capillary membrane
    • 86. Acute Respiratory Distress Syndrome
    • 87. ARDS PATHOPHYSIOLOGY – Inflammatory mediators are released causing extensive structural damage – Increased permeability of pulmonary microvasculature causes leakage of proteinaceous fluid across the alveolar– capillary membrane – Also causes damage to the surfactant-producing type II cells
    • 88. ARDS CXR CHARACTERISTICS – Normal size heart – No pleural effusion – Ground Glass appearance – Often normal early in the disease but may rapidly progress to complete whiteout
    • 89. ARDS
    • 90. ARDS SIGNS & SYMPTOMS – Symptoms develop 24 to 48 hours of injury  Sudden progressive disorder  Pulmonary edema  Severe dyspnea  Hypoxemia REFRACTORY to O2  Decreased lung compliance  Diffuse pulmonary infiltrates – Symptoms may be minimal compared to CXR – Rales may be heard
    • 91. ARDS RISK FACTORS Common Risk Other Risk Factors Factors Sepsis Smoke inhalation Acute Pancreatitis Massive Inhaled toxins DIC Trauma Burns Head Injury Shock Near Drowning ↑ ICP Multiple DKA Fat Emboli Transfusions Pregnancy Blood Products Pneumonia Eclampsia Heart/Lung Bypass Aspiration Amniotic Fluid Embolus Tumor Lysis Infection Drugs Pulmonary Contusion Narcotics
    • 92. ARDS TREATMENT – Respiratory Support – PEEP, CPAP
    • 93. Chronic Lung Disease COPD – Presents with hyper-inflated lung fields  Due to chronic air trapping  May be barrel chested – May lead to cor pulmonale (right-sided heart failure)  Due to chronic high pulmonary pressures – Often hypercarbic (high pCO2)  Often dependent upon hypoxic drive
    • 94. Chronic Lung Disease COPD TREATMENT – Avoid overuse of oxygen (except in emergencies) – Bronchodilators – Steroids – Hydration – Education  Pursed Lip Breathing  Leaning Upright
    • 95. Near Drowning Salt Water – Causes body fluids to shift into lungs  Osmosis: From low to high concentration  Results in hemoconcentration & hypovolemia – Results in acute pulmonary edema Fresh Water – Fluids shift into body tissues  Results in hemodilution & hypervolemia  Can result in gross edema – Damaged alveoli fill with proteinaceous fluid  May lead to pulmonary edema
    • 96. Pneumonia Lung infection (bacterial, viral, or fungal) – Most commonly caused by Streptococcus pneumoniae Symptoms include fever, pleuretic chest pain, productive cough, and tachypnea – Often presents bronchial breath sounds over the lung area Treatment involves giving the right antibiotic
    • 97. Pneumothorax  DEFINITIONS – Simple pneumothorax  Results from buildup of air or pressure in the pleural space – Spontaneous pneumothorax  May be due to blebs that rupture  The 2 key risk factors are increased chest length and cigarette smoking – Tension pneumothorax  Involves a buildup of air in the pleural space due to one-way movement of air  Progressively worsens  Requires immediate intervention
    • 98. Pneumothorax
    • 99. Tension Pneumothorax
    • 100. Pneumothorax  CAUSES – Barotrauma – Injury – Blebs
    • 101. Pneumothorax  SIGNS & SYMPTOMS – Standard Pneumothorax  Sharp "pleuritic" chest pain, worse on breathing  Sudden shortness of breath  Dry, hacking cough (may occur due to irritation of the diaphragm)  May cause mediastinal shift – Tension pneumothorax  Signs of standard pneumothorax with signs of cardiovascular collapse  Immediately life threatening  May cause mediastinal shift
    • 102. Pneumothorax  TREATMENT  Spontaneous pneumothorax – Depends on symptoms & size of pneumothorax – Provide respiratory support – May need chest tube or needle decompression  Some resolve without intervention  Tension pneumothorax – Requires immediate intervention – May cause cardiovascular collapse – May need chest tube or needle decompression  2nd intercostal space
    • 103. Pneumothorax  TREATMENT – Pleurodesis  Chemical or surgical adhesion of the lung to the chest wall  Used for multiple collapsed lungs or persistent collapse
    • 104. Flail Chest
    • 105. Pulmonary Embolism Definition – Arterial embolus that obstructs blood flow to the lung Signs & Symptoms – Symptoms include sudden dyspnea, cough, chest pain, hemoptysis and sinus tachycardia – Blood gas shows low pO2 & low pCO2 – May present positive Homan’s Sign – May present loud S2
    • 106. Pulmonary Embolism Diagnostic Tests – CXR – VQ Scan – Spiral CT – Pulmonary arteriogram – Venous ultrasound of the lower extremities – ABG with low pO2 & low pCO2 – D-Dimer
    • 107. Pulmonary Embolism  Treatment – Requires immediate intervention – Provide respiratory support – Treat pain & comfort – Usually includes intravenous heparin  Heparin reduces risk of secondary thrombus formation while clot is reabsorbed – May require embolectomy – May require thrombolysis – May need umbrella filter – May need long term anticoagulants
    • 108. Respiratory Failure DEFINITIONS – Failure to maintain adequate gas exchange – Inadequate blood oxygenation or CO2 removal – PaO2 < 50 mmHg and/or PaCO2 > 50 mmHg and/or pH < 7.35 on Room Air
    • 109. Respiratory Failure TYPE I Hypoxemia without hypercapnia TYPE II Hypoxemia with hypercapnia
    • 110. Respiratory Failure CAUSES – V/Q Mismatching – Intrapulmonary Shunting – Alveolar Hypoventilation
    • 111. Respiratory Failure V/Q MISMATCHING – COPD – Interstitial Lung Disease – Pulmonary Embolism
    • 112. Respiratory Failure PULMONARY SHUNTING – AV fistulas/malformations – Alveolar collapse (atelectasis) – Alveolar consolidation (pneumonia) – Excessive mucus accumulation
    • 113. Respiratory Failure SIGNS & SYMPTOMS – Restlessness / Agitation – Confusion / ↓ LOC – Tachycardia / Dysrhythmias – Tachypnea / Dyspnea – Cool, clammy, pale skin
    • 114. Respiratory Failure ARTERIAL BLOOD GASES – pH 7.30 / pO2 45 / pCO2 80 – pH 7.30 / pO2 55 / pCO2 65 – pH 7.32 / pO2 50 / pCO2 50 – pH 7.55 / pO2 65 / pCO2 22
    • 115. Respiratory Failure TREATMENT – Ensure Adequate Ventilation ↑ FiO2  Ineffective with shunting  Prolonged O2 > 40% causes O2 toxicity  Must use caution with CO2 retainers – Chronic hypercapnia causes CO2 retainers to use hypoxic drive – Too much O2 can depress respirations
    • 116. PCCN REVIEW PART 1 BREAK!
    • 117. Gastrointestinal Alterations  GI Bleed  Pancreatitis
    • 118. Gastrointestinal Bleeding CAUSES – UGI Bleeding  Includes the esophagus, stomach, duodenum – Peptic Ulcer Disease (PUD), or Esophageal Varices – ASA, NSAID’s, Anticoagulants, Alcohol – H. Pylori – LGI Bleeding  Includes the jejunum, ileum, colon, rectum – Colorectal cancer, Polyps, Hemorrhoids, IBD
    • 119. Gastrointestinal Bleeding
    • 120. Gastrointestinal Bleeding Hematemesis – vomiting of blood (or coffee ground material) (indicates bleeding above the duodenum ) Melena – passage of black tarry stools > 50ml (indicates degradation of blood in the bowel) Hematochezia – passage of red blood (rectal bleeding) Occult Bleeding – bleeding that is not apparent to the patient and results from small amounts of blood Obscure Bleeding – occult or obvious but source not identified
    • 121. Gastrointestinal Bleeding Hematemesis – always UGI source Melana – indicates blood has been in GI tract for extended periods – Mostly UGI – Small bowel – Rt colon (if bleeding relatively slow) Hematochezia – Mostly colon – Massive UGI bleeding (not enough time for degradation)
    • 122. Gastrointestinal Bleeding TREATMENT – Find the underlying cause – Fluid volume replacement – Endoscopy or colonoscopy – Medical and /or surgical therapy  Somatostatin  IV or intra-arterial vasopressin  Sclerotherpay  Angiography with embolization  Electrocoagulation  Band ligation  Balloon tamponade (Sengstaken-Blackmore tube)
    • 123. The Pancreas The Pancreas secretes digestive enzymes, bicarbonate, water, and some electrolytes into the duodenum via the pancreatic duct – Lipase, Amylase, Trypsin The Pancreas also produces and secretes insulin
    • 124. Pancreatitis DEFINITION – An autodigestive process resulting from premature activation of pancreatic enzymes
    • 125. Pancreatitis PATHOSHYSIOLOGY • Inactive pancreatic enzymes are activated outside of the duodenum • The swelling pancreas causes fluids to shift into the retro peritoneum and bowel • Fluid shifts can cause severe hypovolemia and hypotension • Inflammation cause commotion around pancreas
    • 126. Pancreatitis MANY CAUSES – Alcoholism – Hypercalcemia – Biliary Disease – Peptic Ulcer Disease – Gallstones – Cystic Fibrosis – Infections – Vascular Disease – Hyperparathyroidism – Multiple Drugs – Hypertriglyceridemia – Much Much More
    • 127. Pancreatitis SIGNS & SYMPTOMS – Abdominal Pain – Hematemesis – Nausea & Vomiting – Grey Turner’s Sign – Abdominal Distention – Cullen’s Sign – Jaundice – Elevated Amylase, – Malnutrition Lipase, LDH, AST, WBC’s BUN, and Glucose
    • 128. Pancreatitis COMPLICATIONS – Hypocalcemia – Pleural Effusion (left) – Hypotension – Pulmonary Infiltrates – Acute Tubular Necrosis – Hypoxemia – DIC – Atelectasis – Obstructive Jaundice – ARDS – Erosive Gastritis – Pericardial Effusion – Paralytic Ileus – Mediastinal Abscess – Pseudocyst or Abscess – Hyperglycemia – Bowel Infarction – Internal Bleeding – Hypertriglyceridemia – Fat Necrosis – Encephalopathy
    • 129. Pancreatitis TREATMENT – Stabilization – Monitor For Complications  Correct Fluid And – Monitor Blood Sugar Electrolyte Status – Respiratory Support – Drug Therapies – Control Pain  Somatostatin,  Demerol Anticholinergics – NG Tube – Watch For Signs Of  NPO Infection – TPN – Pray  Restricted Diet
    • 130. Pancreatitis FULMINATING PANCREATITIS • Overwhelming form • Necrotizing form • Extreme symptoms • Seen with ESRF patients • May lead to ARDS & DIC
    • 131. Pancreatitis FULMINATING PANCREATITIS • Signs & Symptoms  Tachycardia & low BP (may be the only sign)  Pulmonary & cerebral insufficiency  Acute diabetic ketosis or oliguria  Hemorrhagic pancreatitis may appear
    • 132. PCCN REVIEW THE END PART 1
    • 133. PCCN REVIEW PART 1 THANK YOU
    • 134. Resources Aehlert, B. (2007). RAPID ACLS (2nd Edition). Mosby, Inc., an affiliate of Elsevier Inc. pgs. 67-84, 131-142. American Heart Association. (2005). Guidelines 2005 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Available at: www.americanheart.org. www.americanheart.org. Anderson, L. (July 2001). Abdominal Aortic Aneurysm, Journal of Cardiovascular Nursing:15(4):1–14, July 2001. Chulay, M., Burns S. M. (2006). AACN Essentials of Critical Care Nursing. McGraw-Hill Companies, Inc., Chapter 23. Finkelmeier, B., Marolda, D. Aortic Dissection, Journal of Cardiovascular Nursing: 15(4):15–24. Hughes E. (2004). Understanding the care of patients with acute pancreatitis. Nurs Standard: (18) pgs 45-54. Irwin, R. S.; Rippe, J. M. (January 2003). Intensive Care Medicine. Lippincott Williams & Wilkins, Philadelphia: pgs. 35-548. Sole, M. L., Hartshorn, J., & Lamborne, M. L. (2001). Introduction to Critical Care Nursing (3rd ed). Philadelphia: W. B. Saunders/Elsevier. Thelan, L. A., Urden, L. D., Lough, M. E. (2006). Critical care: Diagnosis and Treatment for repair of abdominal aortic aneurysm. St. Louis, Mo.: Mosby/Elsevier. pg 145-188. Urden, L., Lough, M. E. & Stacy, K. L. (2005). Thelans Critical Care Nursing: Diagnosis and Management (5th ed). St. Louis, Mo.: Mosby/Elsevier. Woods, S., Motzer, S. U. (2004). Cardiac Nursing (4th ed): Philadelphia: Lippincott Williams & Wilkins. Wung, S., Aouizerat, B. E. (Nov/Dec 2004). Aortic Aneurysms. Journal of Cardiovascular Nursing. Lippincott Williams & Wilkins, Inc.:19(6):409-416, 34(2). Wynne J, Braunwald E. (2004). The Cardiomyopathies in Braunwalds Heart Disease: A Textbook of Cardiovascular Medicine (7th Edition). Philadelphia: W.B. Saunders, vol. 2, pps. 1659–1696, 1751–1803. Zimmerman & Sole. (2001). Critical Care Nursing (3rd Edition). WB Saunders., pgs. 41-80, 176-180, 242-266.

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