CCRN/ 2-Day CCRN Certification Prep Course. Complete Study Guide.

CCRN/ 2-Day CCRN Certification Prep Course. Complete Study Guide. Norepinephrine (Levophed)  Alpha (vascular) and Beta (heart) stimulant  Increase in heart rate, BP and contractility ◦ Dose ranges from 1-20 mcg/min intravenously  Titrated to blood pressure effect 49 Dopamine (Intropin)  Strong Alpha and Beta stimulant  Clinical effect varies with dose ◦ Minimal vasopressor effect occurs at 1 to 5 mcg/kg/min ◦ Improvement in contractility at 5 to 10 mcg/kg/min ◦ Vasopressor response usually at 10-20 mcg/kg/min  Titrated to blood pressure effect. 50 Epinephrine  Stronger beta than alpha stimulant *Increases oxygen demand by increasing HR  Increases in heart rate, SV/SI, CO/CI, SVR and BP ◦ Dose starts at 1 mcg/min intravenously ◦ Titrated to effect  If using in shock, doses above 4 mcg/min give predominantly alpha (vasoconstriction) effect 51 Phenylephrine (Neosynephrine)  Strong alpha stimulant with beta (heart rate) stimulating effect present only at high doses  Increases in BP is normally seen with its use ◦ Dose is 10-100 mcg/min intravenously 52 Vasopressin Dose: 0.01-0.05 units/min  Consider using it in any patient with refractory distributive (low SVR) shock.  Caution: Can cause coronary artery vasoconstriction! 53 Increased Afterload  High systemic vascular resistance (SVR) – clamped down  Increased CVP and PAWP (wedge pressure)  Reduced cardiac output  Increased BP (usually the cause)  Patients with poor LV function can have a high afterload with a normal or low BP 54 9 Treatment goal in High Afterload = Improve left ventricular performance by reducing resistance to ventricular ejection Increased Afterload Cont… Treatment of increased Afterload ◦Vasodilators (Nipride and Nitroglycerin) ◦ Ace Inhibitors (ACE’s and ARB’s) ◦ Calcium Channel Blocking agents (Cardizem) Vasodilators - Nipride  Powerful direct arterial dilator (has mild venous dilator effects) ◦ Rapid onset and offset of action ◦ Dose range is 10-400 mcg/min or 0.5-10 mcg/kg/min ◦ Used for short periods (24-48 hrs) due to thiocyanate (cyanide) - byproduct  Signs of cyanide/thiocyanate toxicity: ◦ unexplained confusion or depressed level of consciousness ◦ tachycardia ◦ metabolic acidosis 57 Nitrogylcerin  Systemic & pulmonary vasodilator ◦ Decreases preload ◦ Decreases afterload  Indicated for:  Chest pain, CHF, BP Control  Adverse Effects:  Hypotension  Headache  Nitrate tolerance develops over time 58 ACE inhibitors  Reduce afterload by preventing the production of angiotensin II, which is a potent vasoconstrictor  Indirectly increases SV/SI and CO/CI by decreasing afterload ◦ Reduces preload/afterload by producing arterial and venous dilation ◦ Decreases aldosterone secretion causing diuresis and decreased preload 59 Common Ace Inhibitors Captopril (Capoten) Lisinopril (Zestril, Prinivil) Enalapril (Vasotec) Actopril (Captopril) Fosinopril (Monopril) Quinapril (Accupril) Ramipril (Altace)  Most common side effect? 10 Angiotensin Receptor Blockers (ARB’s) Angiotensin II antagonists = deter vasoconstriction ◦ Candesartan (Atacand) ◦ Irbesartan (Avapro) ◦ Losartan (Cozaar) ◦ Telmisartan (Micardis, Kinzal) ◦ Valsartan (Diovan) 61 Calcium Channel Blockers  Calcium channel blockers reduce afterload by lowering intracellular calcium which inhibits vascular smooth muscle contraction = vasodilation  CCBs negatively affect contractility to varying degrees and some may cause bradycardia and heart block. * With CCB’s watch for: Heart failure Bradycardia and heart block 62 Cardizem (Diltiazem)  Cardizem - Bolus 0.25 mg/kg IV over 2 min. A second dose of 0.35 mg/kg IV may be given over 2 minutes. ◦Continuous infusion may be started following an initial bolus at 5 mg/hr. ◦ Increase in 5 mg/hr increments to 15 mg/hr as needed. 63 Contractility  Defined as the force of ventricular contraction or the strength of the ventricular muscle  Contractility enhancers are positive inotropic agents that are used to increase the inotropic state of the heart via stimulation of the beta-1 receptors. ◦ Dopamine ◦ Dobutamine ◦ Digoxin ◦ Milrinone 64 Dopamine  Immediate pre-cursor of norepinephrine  Acts on Alpha & Beta receptors  Effects are dose dependent: ◦ 0.5-2 mcg/kg/min = dopaminergic ◦ 5-10 mcg/kg/min = inotropic ◦ 10-20 mcg/kg/min = vasoconstriction  Adverse effects ◦ Tachycardia ◦ Vasoconstriction 65 Dobutamine  Synthetic catecholamine  Directly stimulates Beta1 & Beta2 receptors  Increases myocardial contractility  Decreases afterload ◦ Side Effects:  Increases HR  Arrhythmogenic – PVC’s, V-tach  Can cause hypotension  Tolerance due to down regulation of beta receptors 66 11 Digoxin  Cardiac glycoside  Increases intracellular calcium levels  Strengthens myocardial contractility (positive inotropic)  Slows AV node conduction  Measure levels to prevent toxicity  Increased risk of toxicity with hypokalemia or renal insufficiency  Normal Therapeutic Range: 0.8-2.0 ng/ml  Potentially toxic levels: 2.0 ng/ml 67 Digoxin  Signs of Toxicity ◦ Arrhythmias  PVCs most common  1st, 2nd, 3rd degree AV blocks ◦ Yellow/green colors (halos) in visual fields ◦ N/V/D/Anorexia ◦ Palpitations/Syncope  Treatment: Digibind IV or magnesium IV (if patient unstable) 68 Milrinone  Phosphodiasterase inhibitor  Inhibits the degradation of intracellular AMP, increasing intracellular calcium  Positive inotrope  Decreases afterload (inodilator)  Loading dose of 0.05 mg/kg intravenously over 10 minutes followed by a 0.375-0.75 mg/kg/min continuous infusion  To prevent hypotension, avoid loading dose 69 Spectrum of Coronary Ischemia  Asymptomatic state  Stable angina pectoris ◦ Worsened with exertion ◦ Relieved by rest & sublingual nitroglycerin  Unstable angina (acute coronary syndrome) ◦ Unpredictable ◦ Not relieved by rest or sublingual nitroglycerin 70 Acute Coronary Syndrome (ACS) Prinzmetal’s (Variant) Angina: ◦ Results from unpredictable coronary artery vasospasm ◦ Treatment: calcium channel blockers  Acute Myocardial Infarction (AMI) ◦ STEMI ◦ NSTEMI 71 Who is at Risk for ACS/AMI?  Family history of premature coronary artery disease (CAD)  Hyperlipidemia  Hypertension  Cigarette smoking  Diabetes mellitus  Obesity  Increased age 60 72 12 Classic Signs & Symptoms  Chest pressure or pain ◦ Radiates to jaw +/- left arm  Not relieved by rest or sublingual nitroglycerin  Shortness of breath  Diaphoretic, pallor, anxiety  Nausea +/- vomiting 73 Atypical Signs/Symptoms  Fatigue  Palpitations & dizziness caused by ischemia induced arrhythmias  Acute CHF  Pulmonary edema  Silent myocardial ischemia ◦ Asymptomatic  Sudden cardiac arrest – 20% of population this first sign of CAD 74 Who is at Risk for Atypical Presentation? Women Diabetics Elderly 75 Ischemia Occurs When Oxygen Demand Oxygen Supply 76 Altered Supply & Demand • Vasospasms • Decreased Coronary Artery Perfusion • Decreased Blood O2 Decreased Supply 77 • Stenosis or Thrombus • Increased HR • Increased Contractility • Increased LV Wall Tension Increased Demand 78 Plaque ruptures Platelets adhere Clot forms Ischemia 13 Pathophysiology  Location, degree, & duration of blockage dictates whether the patient has ACS or AMI & its severity. 79 Unstable Angina (ACS)  Thrombus PARTIALLY occludes vessel  Can progress to subendocardial MI (aka: NSTEMI) due to distal microthrombi that cause myocyte necrosis 80 ST Depression vs. ST Elevation 81 Transmural MI (STEMI)  Decreased flow through a coronary artery.  Leads to myocardial ischemia.  Damage extends through the myocardial layers = STEMI 82 Acute Myocardial Infarction 83 Treatment MONA Oxygen  Nitro Aspirin Morphine 14