Cardiovascular 2011

Scope 1. Anatomy and Physiology, PE 2. Lab and Diagnostic Procedures 3. Disorders Anatomy of heart Anatomy Key Points! 1. Layers 2. Chambers 3. Valves 4. Conduction 5. Blood Supply 6. Circulatory System 7. Accessory Structures Layers Epicardium Myocardium Endocardium Pericardial membrane Chambers RA : LA RV : LV RA & LA (interatrial septum) RV & LV (interventricular septum) Valves RA & RV (tRicuspid) LA & LV (mitraL) AV valves RV & Pulmonary Artery (PuLmonic) LV & Aorta (AoRtic) Semilunar valves Location of valves Conduction Who regulates the conduction system? Who is the main generator?

SA-bachmanns bundle and internodal tract (anterior, middle, posterior) AV-bundle of his R & L bundle purkinje fiber purkinje network Blood Supply Circulatory System - Pulmonary Circuit - Systemic Circuit Accessory Structures Pericardium Mediastinum Thoracic Cavity 1. Layers 2. Chambers 3. Valves 4. Conduction 5. Blood Supply 6. Circulatory System 7. Accessory Structures TERMINOLOGIES CARDIAC OUTPUT: HR x SV STROKE VOLUME: amount of blood ejected by LV BLOOD PRESSURE: pressure of blood against walls of main arteries, systole, diastole, COxPVR PULSE: waves w/n artery upon contraction by the LV, HR PULSE DEFICIT: (apical pulse difference from radial pulse), a. fib. PULSE PRESSURE: (difference b/n sytolic and diastolic pressure), IICP Its all about the LEFT ventricle PRELOAD is the initial stretching of the heart prior to contraction AFTERLOAD "load" that the heart must eject blood against EJECTION FRACTION EDV = 120 ml (amt of blood in the LV before contraction) SV = 70 ml (amt of blood ejected in the LV per contraction) ESV = 50 ml (amt of blood in the LV after contraction) Ef = 58% =SV/EDV =70/120

=58% ASSESSMENT Chest pain Cyanosis Pallor Edema Fatigue Palpitations 1. Chest Pain Most common Related to activity Not related to activity Related to movement Related to breathing 2. Dyspnea Labored breathing Dyspnea on exertion Orthopnea Sudden or acute dyspnea 3. Cyanosis Bluish discoloration of the skin and mucous membrane O2 sat. is below 94% 4. Fatigue Indications? 5. Palpitations Awareness of rapid or irregular heart beat Autonomic Nervous System and Adrenal 6. Syncope Transient loss of consciousness Due to decreased cerebral tissue perfusion 7. Edema Causes? Bilateral Unilateral Grading Glands response (stress) Murmur Pericardial friction rub Gallop Syncope Dyspnea Arrhythmia

 Generalized 8. Skin Color, temperature, hair growth, nails, capillary refill, clubbing or spooning of fingers evaluation. 9. Cardiac rate and rhythm Tachycardia Bradycardia Heart block Arrhythmias Sinus arrest S1 S2 closure of AV valves (lub) closure of SL valves (dup)

S3 & S4 diastolic filling sound S3 is heard after S2, if present S4 is heard prior to S1, if present suspect noncompliant ventricles although this is common among elderly* Murmurs turbulence of blood flow, if positive watchout FVE, this is normal until 1 year old suspect CHF

Gallop (drumming), a metal drum beat typically using a double kick pedal Pericardial Friction Rub squeking sound suspect pericardial effusion and pericarditis if this is heard

Muffled Heart Sound Deadening sound, if this is positive rule out Cardiac Tamponade and other similar problem lik Effusion Cardiovascular Skills Procedures Laboratory Telemetry Wired com Dx and Lab Tests Cardiac enzymes Serum analysis CARDIAC CATH 1. Angiography (via Artery) 2. CVC (via Vein)

3. Swan- Ganz Catheter (via Vein) MUGA: technetium 99, thallium 201 EKG Pacemaker Pericardiocentesis PTCA IABP ACLS Lab results Serum Analysis INVASIVE Partial Thromboplastin Time (Activated) 1. 20 45 sec 2. will increase from Heparin administration Prothrombin Time 1. 9.5 12 sec 2. will increase from Warfarin administration 3. will decrease from vit K and hemostan INR 1. 3.5 sec 2. will increase from Warfarin administration BLEEDING TIME 1. 5-15 min (Ivy Method) 2. Will increase in FIBRINOLYTICS/THROMBOLYTICS administration Serum Electrolytes and Lipid Level Potassium 3.55.0 meq/L (to detect origin of cardiac dysrhythmias) Sodium 135145 meq/L (to evaluate fluid and elec and acid base balance) Serum Electrolytes and Lipid Level Calcium

4.55.5 meq/L (to diagnose cardiac dysrhythmias, neuromuscular, skeletal and endocrine disorders, blood clotting deficiencies (C Factor IV) Magnesium 1.52.6 meq/L (to detect cause of cardiac dysrhythmias, electrolyte status, neuromuscular and renal function)

Serum Analysis INVASIVE Total Cholesterol 120330 mg/dl (measures circulating free cholesterol, assess risk for Coronary Artery Disease CAD) Triglycerides 10190 mg/dl (screen hyperlipidemia, risk for CAD) Cardiac Enzyme Studies INVASIVE Troponin CK-MB AST or SGOT LDH Myoglobin Hydroxybutyric dehydrogenase Cardiac Enzyme Studies INVASIVE Troponin Reflects Catabolism of Normal Tissue First enzyme that will increase in MI Troponin I and T Elevates within 3-4 hours, peaks in 4-24 hours and persists for 7 days to 3 weeks! Normal value: less than 0.6 ng/mL REMEMBER to AVOID IM injections before obtaining blood sample! Early and late diagnosis can be made! Creatinine kinase CK CK-MB = most specific enzyme

Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 days Normal value: 0-7 U/L CK-BB CK-MM TOTAL CK = = = found in nervous tissues found in muscle detects post MI

Aspartate aminotransferase AST or SGOT Can be found in many cells like liver, pancreas, heart kidneys and skeletal muscle (not a good indicator of MI) Cardiac Enzyme Studies INVASIVE Lactic Dehydrogenase LDH Elevates in MI in 24 hours, peaks in 48-72 hours Normally LDH2 is greater than LDH1 MI- LDH1 greater than LDH2 (flipped LDH pattern)

Normal value is 70-200 IU/L LDH1 and LDH2 LDH3 LDH4 and LDH5 = appear primarily in the heart, = lungs = liver and skeletal muscle RBC and kidneys

After 710 days LDH level returns to normal Not specific, obsolete! Hydroxybutyric Dehydrogenase HBD 114 to 290u/ml. Ratio of LDH to HBD--1.2 to 1.6:1 Myocardial infarction Peaks in 72 hours and remain elevated for 2 weeks. Myoglobin Normal: 30-90 ng/ml Rises within 1-3 hours Peaks in 4-12 hours Returns to normal in a day Not used alone Muscular and RENAL disease can have elevated myoglobin Troponin AST or SGOT CK-MB LDH Hydroxybutyric dehydrogenase Myoglobin

WBC count = 510T/cu mm (leukocytosis may result within 2 hours MI) Erythrocyte Sedimentation Rate ESR Male: 1 - 13 mm/hr Female: 1 - 20 mm/hr A rise usually follows after MI Blood glucose level Tested after fasting: 70 - 110 mg/dL Hyperglycemia may lead to coronary artery disease It may affect 50% of MI patient

ECG EKG/ECG NON-INVASIVE Electrocardiogram - graphic record produced by electrocardiograph Electrocardiograph - device used for recording the electrical activity of the heart Electrocardiography - study of records of electric activity generated by the heart muscle Placement of 4 lead wires and 6 electrodes? 6 Electrodes V1 =R V2 =Y V3 =G V4 =BL V5 =BR V6 =V 4th ICS sternal border, right 4th ICS sternal border, left halfway between V2 and V4 MCL (midclavicular line) 5th ICS, left AAL (anterior axillary line) halfway MAL (midaxillary line) level with V4, left between V4 and V6

12 LEAD EKG AVR AVL lateral wall LEAD I lateral wall LEAD II inferior wall AVF inferior wall LEAD III inferior wall 6 CHEST LEADS V1 V4 = anterior wall V5 V6 = lateral wall Impulse Transmission Travel of an impulse From the right shoulder across the chest to the left lower rib cage. How are waveforms produced? Electrical impulses are generated by the: SA to AV to HIS BUNDLE to PURKINJE P-WAVE Depolarization of Atria Q-WAVE Purkinjes fibers

R-WAVE Depolarization of ventricles S-WAVE Completion of ventricular depolarization T-WAVE Complete repolarization of ventricles PR INTERVAL (whole P wave) 0.12 - 0.20 sec QRS DURATION Depolarization of Ventricles, 0.05 - 0.10 sec ST SEGMENT Early repolarization of the ventricles Heart Rate Computation Strip = NSR x 10 (constant) R-R interval = Big square = 300 (constant) / no. of big squares Small square = 1500 (constant) / no. of small squares NSR (normal sinus rhythm) Sinus Tachycardia and Sinus Bradycardia (considered normal rhythm) Arrhythmias (abnormal rhythm) Sinus Tachycardia Sinus Bradycardia Observe Regular pattern Irregular pattern Interval Height Length Elevation Depression Bizarre, awkward Elevation of ST segment = MI Peaked or inverted T wave = MI Prolonged P-R interval = 1st degree Heart Block 0.12 - 0.20 sec Widened QRS complex = delayed conduction to purkinje fiber No QRS-2nd degree Heart Block

Pathological Q wave = MI Flattening of T wave = hypokalemia U wave = hypokalemia Depression of ST segment = hypokalemia Long QT interval = hypocalcemia (torsades de pointes) Atrial Arrhythmias: Premature Atrial Contraction (PAC) No mx Atrial Flutter Antiarrhythmic (Amiodarone and Flecainide) Digitalis Betablockers Antiplatelet and anticoagulant Atrial Fibrillation Digitalis Defibrillation PAC Atrial Flutter-sawtooth ATRIAL FIBRILLATION ECG Ventricular Arrhythmias: Premature Ventricular Contraction (PVCs) Xylocaine Ventricular Tachycardia (vtach) Cardioversion (synchronized) Ventricular Fibrillation (vfib) Defibrillation (unsynchronized) PVC VENTRICULAR TACHYCARDIA VENTRICULAR FIBRILLATION Different Arrhythmias STANDSTILL-asystole Atrioventricular or AV Block First Degree Second Degree Third Degree

Atrioventricular or AV Block First Degree AV block (prolonged P wave followed by QRS) Lengthened PR interval Over 0.20 sec Impulse travelling from atria to ventricles is delayed Caused by: enhanced vagal tone (athlete), increased refractory time of AV node (CCB, BB, Digoxin, cholinergic drugs) Not serious unless associated to MI Second Degree AV block Type I Wenckebachs PR interval gradually lengthens untill beats dropped Type II PR interval is constant and one or more beats are non conducting Due to: cardiomyopathy, MI, Lenegre or Levs Disease (idiopathic) Dropped Q waves May progress to complete heart block Pacemaker recommended Third Degree AV block (complete heart block) atria and ventricles are beating independently or P and QRS complex are present but unrelated Pacemaker is necessary 3rd DEGREE AV BLOCK EKG PATTERN (PACEMAKER) ARRHYTHMIA Drugs commonly given: Atropine: for symptomatic bradycardia Digoxin: atrial fib. Lidocaine : PVC Adenosine (Adenocard): PVC Cardioversion: v. tac, a. fib Defibrillate: v. fib EKG Ambulatory (Holter) NON-INVASIVE Patient is connected to battery operated EKG recorder 24-hour continuous monitoring Patient keeps a diary and record his activities When chest pain or palpitation occurs an event button must be pressed

Doctor will interpret and read all the recorded activity of the heart While wearing the device, avoid: Electric blankets High-voltage areas Magnets Metal detectors Stress Test EKG Exercise (Stress Test) NON-INVASIVE A non-invasive test that studies the heart during activity Treadmill testing is the most commonly used stress test Used to determine heart problems (MI, chest pain, arrhythmias) Pre-test: consent may be required, adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine

Post-test: instruct client to notify the physician if any chest pain, dizziness or shortness of breath . Instruct client to avoid taking a hot shower for 10-12 hours after the test Allows evaluation of heart activity during physical stress There is predetermined heart rate or until fatigue or chest pain develops Heart activity and blood pressure are monitored during the test. Cardiac Pacemakers INVASIVE

An electrical impulse generator that transmits rhythmic impulses when the heart is unable to do its normal conduction of impulse (SA Node and AV Node) It may be temporary or permanent and ER pacemaker Temporary Pacemakers Consist of wire connected to an external battery-operated pulse generator box Wire is threaded via the SVC into the atrium or ventricle, where it remains to initiate impulses Permanent pacemakers Smaller and the box is implanted under the skin (chest or abdomen) under surgery What to avoid? ER Pacemaker TCP - Transcutaneous pacing (also called external pacing) is a temporary means of pacing a patient's heart during a medical emergency. It is accomplished by delivering pulses of electric current through the patient's chest, which stimulates the heart to contract. 2D-ECHO NON-INVASIVE Measures the size of the heart,

Study motion and appearance of the valves and the function of the heart muscle. Ejection fraction Interpreted by a cardiologist ejection fraction (Ef) is the fraction of blood pumped out of a ventricle with each heart beat EDV = 120 ml SV = 70 ml ESV = 50 ml Ef = 58% =SV/EDV =70/120 =58% NUCLEAR MEDICINE (Medical Imaging) MUGA-Multi Gated Acquisition Scan Technetium 99m (necrotic tissues absorb the dye) Thallium 201 (normal myocardium absorbs the dye) very toxic! cardiac blood pool study used to calculate ejection fraction Prep: Standard preparation for an ECG is required. Post: The patient may resume normal activities immediately following the test. A normal MUGA scan should not demonstrate areas of akinesis (lack of movement) or hypokinesis (decreased movement) CARDIAC Catheterization (artery) CATHETERIZATION C. ANGIOGRAPHY PTCA IABP (stays for 2 weeks) (vein) CATHETERIZATION CVC SGC IABP CA, PTCA, IABP Prep NPO, Bv/s, Consent Anxiolytic

Local Anes Entry Femoral artery Warmth sensation (dye) Post Bleeding, A-leg straight CVC, Swan Ganz Prep NPO, Bv/s, Consent Anxiolytic Local Anes Entry antecubital fossa or Femoral vein (peripheral)or IJV, SV (central) Post Infection (indwelling cath) Air embolism Clot Central Venous Catheter-CVC Normal value is 2-6 mm Hg or 5-10 cm H20 (variable) 60% of blood volume is contained in the venous system CVP is the measurement of systemic venous pressure at the level of right atrium Can be inserted via jugular, subclavian or other large veins like the antecubital fossa Valuable in assessing fluid volume excess or deficit Catheter ends at the right atrium Reasons: Long term IV therapy TPN administration Chemotherapy administration Dialysis Blood sampling CVP monitoring CVC-Key points OPD case or ICU CVC can be used for months to year Sedative and local anesthesia prior to insertion

Prime the tubings with NSS or heparin pre procedure Xray to determine correct placement Occlusive dressing (air embolism) Sterile and dry dressing (infection) Flushing a CVC Sterile procedure 2 syringes (10 ml NSS, 5 ml Heparin) 10 U of heparin in 1 cc of NSS (0.1H:0.9NSS) Swab injection cap with povidone iodine and alcohol Clamp catheter and remove cap Attach NSS syringe, release clamp, aspirate and observe for blood, if blood return is positive flush with NSS, REPEAT FOR HEPARIN Place new cap, TAPE ALL TUBING CONNECTIONS, attach tubing to clients clothing Record the procedure Cleaning the site of CVC Sterile procedure Inspect the site for drainage or sign of infection (SHIRP), INFILTRATE Inspect from catheter hub to skin Povidone iodine from site outward in circular motion Apply occlusive dressing Label the dressing with date and time of dressing change Measuring CVP Mark X indelible INK, PHLEBOSTATIC AXIS (MAL, 4th ICS, RIGHT SIDE)

3 way stopcock, fill the manometer with fluid, close the line of patient, open the manometer line, hold the manometer level of P. zero, watch for water fluctuation synchronized with respiration, take the reading at the end of expiration Open the line to the patient after closing the manometer line, secure manometer upright position when not in use Document Changing the central venous tubing Frequency depends on the institution (2x a week) Should be changed ASAP if it is found to be damaged or contaminated Set the new tubings and fill it completely with fluid Clamp the old tubings, disconnect from the CVC, connect new tubings

Put a TAG on tubing with next date to be changed Groshong Catheter The GROSHONG catheter is a narrow plastic-like hollow tube. It is tunneled under the skin and placed in one of the veins just under the collarbone. The catheter is placed just above the heart (see picture). The GROSHONG catheter has many uses. Drawing blood Chemotherapy IV fluids Blood transfusions IV nutrition SWAN-GANZ CATHETER INVASIVE Other name: pulmonary artery catheter CVP: 5-10 cm H20, 2-6 mm Hg RVP: 15-25 mm Hg/0-8 PAP: 15-25 mm Hg/8-15 PAWP: 6-12 mm Hg LAP: 6-12 mm Hg LVEDP: 5-12 mm Hg LVESP: 90-140 mm Hg CO: 4-8 L/min Procedure: same with CVC Multi lumen, 110 cm PERICARDIOCENTESIS INVASIVE PERICARDIOCENTESIS Blind procedure Removes fluid in the pericardial sac (50 mL syringe) Dx and therapeutic effects Supine, 60 degrees head elevation Watch out for complications (arrhythmias) Properly label the specimen and send to the lab

After the procedure watch out for complications (cardiac tamponade, increased venous pressure, distended neck veins, tachypne muffled (depressed) heart sound, friction rub (scratchy or grating sound), anxiety and chest pain.

Dx and Lab Tests Cardiac enzymes Serum analysis CARDIAC CATH 1. Angiography (via Artery) 2. PTCA (via Artery) 3. IABP (via Artery) 4. CVC (via Vein) 5. Swan- Ganz Catheter (via Vein) 2 D Echo MUGA: technetium 99, thallium 201 EKG Pacemaker Pericardiocentesis Cardiovascular Drugs NTG: Nitrostat Morphine: Diuretics: K sparer Digitalis: Lanoxin Dobu-dopa: diuresis/cardiotonic Cardio accelerator: Epi, A. SO4 Anti arrhythmic: Lidocaine Beta blockers: Propanolol, Inderal Calcium blockers: Nifedipine, Adalat ACE Inhibitor: Captopril, Lisinopril Anticoagulants: Hepa, Warfarin Antiplatelets: ASA, Persantin Fibrinolytics: t-PA, Urokinase, Streptokinase Hemostasis: Amicar, Hemostan, Vit K Cardiovascular Drugs Vasodilators Opiate Analgesic Morphine Sulfate Nursing Responsibilities Cardiovascular Drugs ACLS

Anti Anginal Nitroglycerin NTG Isosorbide Dinitrate (Isordil) and Isosorbide Mononitrate(Imdur, Ismo, Monoket) Can be given SL or IV (Isordil) and topical (Nitrobid) VIAGRA! Sildenafil Citrate, Revatio Tadalafil (Cialis) and Vardenafil (Levitra) Nursing Responsibilities. Cardiovascular Drugs Calcium Channel Blockers Nifidepine (Adalat, Procardia) Diltiazem (Cardizem) Decrease muscle tone, interferes contraction, decrease BP S.E. hypotension, bradycardia, diarrhea and rashes Cardiovascular Drugs Beta Blocking Agent Propranolol Decreases workload Blocks beta receptors and capable of decreasing HR S.E. hypotension, vomiting, nausea and depression Adrenergic Receptors Alpha receptors fxn: Vasoconstriction Decrease GI muscle motility Alpha1 receptor Vasoconstriction Alpha2 receptor Inhibition of insulin, induction of glycogen Decrease GI motility Adrenergic Receptors Beta1 receptor Increase HR, Ef, CO Beta2 receptor Bronchodilation Increase renin

Digitalis, Digoxin Positive Inotropic (Increases contraction of the heart) Increase emptying capacity of the heart Negative chronotropic (Decreases HR) AV node control Increase CO (improves stroke volume) T.L. 0.8 to 2.0 ng/mL Antidote Digibind Nursing Responsibilities Cardiovascular Drugs Dopamine diuresis effect Increase Na excretion (kidney) Vasodilators Norepinephrine effect Dobutamine Increase CO More potent on contraction Cardiovascular Drugs Diuretics 1. Spironolactone (Aldactone) K sparer 2. Furosemide (Lasix) K waster 3. Nursing Responsibilities Anti hypertensive 1. ACE inhibitors Captopril (Capoten) Cardiovascular Drugs Cardioaccelerator 1. Norepinephrine (Levophed) powerful vasoconstrictor 2. Epinephrine increase conduction, contractility and automaticity 3. Atropine S04-to treat symptomatic bradycardia Cardiovascular Drugs Anti dysrhythmic drug 1. Lidocaine (Xylocaine) for PVC 2. Atropine for Mobitz type I 3. Isoproterenol (Isuprel) for sinus bradycardia 4. Quinidine for atrial fib

Lidocaine Lidocaine's concentration for anesthetic use depends on the degree of the site. If it is use for lacerated wound, a concentration of 2 percent is used (a bottle with yellow label). for dental and wound debridement , a concentration of 1 percent is used (a bottle with white label). Lidocaine as an anti-dysrythmnic drug, 1 bolus (50 mg/IV) or 1mg/kg/dose is used. Lidocaine for IV administration is dispense in concentrated and dilute formulation. The concentrated formulation must be diluted with 5 percent dextrose in water. Cardiovascular Drugs Thrombolytic/Fibrinolytic Agent 1. Streptokinase lyses the clot (20T IU IV bolus or 4T IU/min drip) 2. Urokinase activates plasminogen to plasmin (intracoronary) 3. TPA tissue plasminogen activator 4. Antidote Amino Caproic Acid 5. Nursing Responsibilities Cardiovascular Drugs Anticoagulant Heparin prevent formation of new clot (4-8T IU/30 min) Check APTT Antidote Protamine Sulfate Warfarin (Coumadine) decrease viscosity of blood (PO) home meds Dont give to pregnant Check PT or INR Antidote Vitamin K Nursing Responsibilities Cardiovascular Drugs Stop bleeding Hemostan 1 ampule q 8 hours (500mg/amp in 5 mL) Vitamin K Phytomenadione 1 ampule q 6 hours (20mg/amp in 2 mL)

Aminocaproic acid (Amicar) THANK YOU Cardiovascular Disorders Infective Endocarditis Infection of the inner lining due to direct invasion of bacteria (dental carries, surgeries etc.) May lead to deformity of valve leaflets(stenosis) Commissurotomy- separates the thickened, adherent leaves of a stenosed mitral valve. Valvular problems: Valvular insufficiencyvalve leakage causing regurgitation Valvular stenosisnarrowing causing the heart to exert more effort to eject blood Mitral Valve Prolapse MVP Nonclassic type, 2-5 mm displacement Classic type, over 5 mm displacement Due to: Marfan Syndrome (chordae tendinae heart strings) At risk: infection, clot, arrhythmias Take: BB, ASA, prophylactic Abx MVP Myocarditis Inflammation of the myocardium Cardiac Tamponade Pericarditis Pericardial effusion-fluid in the pericardial cavity Constrictive pericarditis-thickening of the pericardium compressing the heart Cardiomyopathy Idiopathic 3 Groups Dilated: LARGE Hypertrophic: THICK Restrictive: STIFF Hyperlipidemia Elevated serum total cholesterol Elevated low density lipoprotein HDL: good C.

LDL: bad C. Elevated triglycerides and cholesterol Cause Dx: <200 mg/dl (no dse.) S/sx: Cx: Mx: Cardiovascular Drugs Statin: Lipitor NTG: Nitrostat Morphine: Diuretics: K sparer Digitalis: Lanoxin Dobu-dopa: diuresis/cardiotonic Cardio accelerator: Epi, A. SO4 Anti arrhythmic: Lidocaine Beta blockers: Propranolol, Inderal Calcium blockers: Nifedipine, Adalat ACE Inhibitor: Captopril, Lisinopril Anticoagulants: Hepa, Warfarin Antiplatelets: ASA Fibrinolytics: t-PA, Urokinase, Streptokinase Hemostasis: Amicar, Hemostan, Vit K Lidocaine's concentration for anesthetic use depends on the degree of the site. if it is use for lacerated wound, a concentration of 2 percent is used (a bottle with yellow label). for dental and wound debridement , a concentration of 1 percent is used (a bottle with white label). Lidocaine ... as an anti-dysrythmnic drug, 1 bolus (50 mg/IV) or 1mg/kg/dose is used. Lidocaine for IV administration is dispense in concentrated and dilute formulation. the concentrated formulation must be diluted with 5 percent dextrose in water. Hypertension CNS factor Renin-angiotensin/aldosterone system factor ECF volume

Increased cardiac output plus increased peripheral resistance factor Based on the Seventh Report of The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), 2003 Gold Standard: 115/75 CATEGORY Normal Prehypertension SBPmm Hg < 120 and 120-139 or 140-159 or 160 or 80-90 90-99 100 DBPmm Hg < 80

Hypertension, Stage 1 Hypertension, Stage 2

The Joint National Committee (JNC 7), 2003 Aneurysm Distension of an artery due to weakening of arterial wall Cause: hereditary, HPN Cerebral A. Ant. Comm. Art. Internal carotid Art. Aorta Dissecting Aneurysm A.A.A. Mx: Drugs? Surgical clipping Endovascular coiling (coils initiate a clotting or thrombotic reaction within the aneurysm ) Stent Aneurysm Distension of an artery due to weakening of arterial wall High pressure in the lumen due to plaque deposits Arteriosclerosis Loss of elasticity and hardening of vessel wall: aging Atherosclerosis Loss of elasticity and hardening of vessel wall: atheromas Coronary Artery Disease Accumulation of fatty deposits in the innermost layer of the coronary arteries Comparison?

Angina 1. Incomplete block 2. Less 15 minutes (pain) 3. Relieved by NTG 4. ST and T wave changes 5. Attack is precipitated by activity 6. Not life threatening

MI 1. Complete block 2. Over 15 minutes (pain) 3. Not relieved by NTG 4. ST segment depression and T wave inversion 5. Attack is not precipitated by activity 6. Life threatening* Types of Angina 1. Stable activity = pain, relieved by rest 2. Unstable activity = pain, relieved by NTG 3. Pre infarction pain at rest, relieved by NTG 4. Prinzmetal (variant) pain at rest with vasospasm , relieved by NTG 5. Intractable continued pain not relieved by NTG Refractory angina pectoris, defined as angina refractory to maximal medical therapy and standard coronary revascularization procedures Angina pectoris that occurs with increasing frequency, intensity, or duration. crescendo angina Angina and MI Dx:

1. Pain and NTG test 2. Coronary angiography 3. MUGA: MULTI GATED ACQUISITION SCAN (Nuclear Medicine) Thallium 201 Imaging (normal) Technetium-99 Imaging (necrotic) 1. Cardiac enzymes: increased Troponin-T or I CK MB

LDH1 higher than LDH2 (flipped LDH) AST 1. ECG 2. WBC, ESR and Myoglobin* Possible ECG results: Elevation of ST segment = MI Peaked or inverted T wave = MI Pathological Q wave = MI Nursing Diagnosis 1. Pain related to an imbalance in oxygen supply and demand 2. Anxiety related to chest pain, fear of death and threatening environment 3. Decreased cardiac output related to impaired contraction of the heart 4. Altered tissue perfusion (myocardial) related to coronary stenosis 5. Activity intolerance related to insufficient oxygenation 6. Risk for injury (bleeding) related to dissolution of clots 7. Ineffective individual coping related to threats to self esteem* MI management: 1. CBR without BP 2. Oxygen therapy 3. Pain control 4. Morphine or Meperidine 5. Vasodilator (NTG) 6. Anxiolytic (Benzodiazepine) 7. IV access line 8. Cardiac monitor 9. Central venous access line 10. Cardiac enzymes evaluation 11. ACLS* Other drugs for MI: Pharmacologic Therapy

1. Thrombolytic Agents 1. TPA tissue plasminogen activator 2. Streptokinase (streptase) 3. Urokinase

2. Anticoagulant 1. Heparin 2. Warfarin 3. ASA (antiplatelets) 3. Beta adrenergic blocking agents 1. Propranolol 4. Antidysrhythmic 1. Lidocaine (Xylocaine) 5. Calcium Channel Blockers 1. Diltiazem* MI surgical interventions: PTCA Percutaneous Transluminal Coronary Angioplasty IABP Intraaortic Balloon Pump CABG coronary artery bypass graft Triple Saphenous Vein, LIMA and RITA* Cardiovascular Left Ventricular Assist Device placement (LVAD) It is used while waiting for heart transplant or if heart transplant is contraindicated. CHF Cause: Dx: 2DECHO, PMI, s/sx S/sx: Right side and left side failure? Mx: CHF Nursing Considerations: 1. The goal of treatment is to improve pump function, rest the heart and reverse the compensatory mechanism of the heart. 2. Observe complete bed rest and reduce myocardial oxygen demand. 3. Employ FVE management and prevent the complications to occur. 4. Give Diuretics and Digoxin (T.L. 0.5-2.0 ng/ml) as ordered and watch-out the adverse effects. Cardiac Arrest Heart stops beating or contraction is ineffective Watch-out for tissue perfusion manifestations: Brain?

Heart and lungs? Vascular? Kidneys? Liver? Skin? GIT? Treatment: 1. Increase CO 2. Cardiovascular drugs and mechanical equipment 3. Cardiovascular Drugs: IV Dopamine (vasopressor) IV Dobutamine (diuretic effects) IV Epinephrine (vasoconstrictor) IV Nitroprusside (vasodilator) 4.Mechanical: IABP intra aortic balloon pump (improve coronary Defibrilator (arrhythmias can be stopped) Cardiac monitor (to detect arrhythmias)* Cardiac Dysrhythmias Disturbances in regular rate/rhythm due to changes in electrical automaticity or conduction Ventricular Arrhythmias: Premature Ventricular Contraction (PVCs) Xylocaine Ventricular Tachycardia (vtach) Cardioversion (synchronized) Ventricular Fibrillation (vfib) Defibrillation (unsynchronized) Atrial Arrhythmias: Premature Atrial Contraction (PAC) No mx Atrial Flutter Antiarrhythmic (Amiodarone and Flecainide) Digitalis Betablockers Antiplatelet and anticoagulant perfusion) utilization

Atrial Fibrillation Digitalis Defibrillation Cardiogenic Shock Occurs when the heart muscle loses its contractile power Extensive damage to left ventricle due to MI may lead to shock CARDIAC ARREST! Types: CHDans Stages: early, late, end stage or decompensatory BV, CO, CB, TP: brain, heart, kidneys, lungs ER situation!!! Mx: Position: Modified Trendelenburg, v.s. monitoring O2 therapy (high flow) IV line, BT, Cut Down (CVP) ETT, Mechanical Ventilator Drugs: Cardiotonics (Dopamine, digitalis) Epinephrine, Antihistamine, Steroids, Bronchodilators Ranitidine, Antibiotics* Vascular Diseases Atherosclerosis Arteriosclerosis HPN, CAD, Stroke, Retinopathy etc PVD DVT, CVI, Varicosities, Thrombophlebitis TAO or Buergers Disease Raynauds Phenomenon RP Raynauds Phenomenon or Vasospastic Disorder PVD Deep Vein Thrombosis Thrombosis of deep veins Phlebothrombosis Formation of thrombi in the vein Thrombophlebitis Inflammation in the wall of a vein Stasis Ulcers

Excavation of the skin surface produced by sloughing of inflammatory necrotic tissue Varicose Veins Dilatation and elongation of saphenous veins Chronic Venous Insufficiency destruction of valves PACK YEARS For example: a patient who has smoked 15 cigarettes a day for 40 years has a : (15x40)/20 = 30 pack year smoking history. Buerger-Allen exercises - A series of exercises administered to patients with peripheral vascular disease. These exercises are repeated 6-7 times at each sitting and done several times a day. 1. Support legs in an elevated position at 60-90 degrees for 30-180 seconds, or until you produce blanching of the extremity. The patient is instructed to actively dorsiflex and plantarflex the ankle throughout the procedure. 2. Allow feet to dangle over the edge of the bed for 2-5 minutes or as long as it takes to produce hyperemia, then add one minute. The total time should not exceed 5 minutes. 3. Place legs in a horizontal position for 3-5 minutes. Tandaan!!! DVT TAO Smoking Artery S/sx:Intermittent claudication LOSS OF SENSATION Doppler UTZ test (speed) Venous stasis Vein S/sx:Homans sign POOLING Duplex UTZ test (sounds to image) Venogram Thrombectomy Embolism Fibrinolytics and anticoagulant Dipyridamole (Persantin) ANTIPLATELET: to prevent occlusion

Arteriogram Endarterectomy Gangrene Fibrinolytics and anticoagulant

Dipyridamole (Persantin) ANTIPLATELET: to prevent occlusion * Cardiovascular Disorders What is CAD? Fatty deposits in the inner layer of coronary arteries. Cause: Risk Factors? Modifiable Non modifiable Dx: S/sx: Dx: Mx: Comparison? Angina 1. Incomplete block 2. Less 15 minutes (pain) 3. Relieved by NTG 4. ST and T wave changes 5. Attack is precipitated by activity 6. Not life threatening

MI 1. Complete block 2. Over 15 minutes (pain) 3. Not relieved by NTG 4. ST segment depression and T wave inversion 5. Attack is not precipitated by activity 6. Life threatening* Types of Angina 1. Stable activity = pain, relieved by rest 2. Unstable activity = pain, relieved by NTG

3. Pre infarction pain at rest, relieved by NTG 4. Prinzmetal (variant) pain at rest with vasospasm , relieved by NTG 5. Intractable continued pain not relieved by NTG Angina and MI Dx:

1. Pain and NTG test 2. Coronary angiography 3. MUGA: MULTI GATED ACQUISITION SCAN (Nuclear Medicine) Thallium 201 Imaging (normal) Technetium-99 Imaging (necrotic) 1. Cardiac enzymes: increased Troponin-T or I CK MB LDH1 higher than LDH2 (flipped LDH) AST 1. ECG 2. WBC, ESR and Myoglobin* Nursing Diagnosis 1. Pain related to an imbalance in oxygen supply and demand 2. Anxiety related to chest pain, fear of death and threatening environment 3. Decreased cardiac output related to impaired contraction of the heart 4. Altered tissue perfusion (myocardial) related to coronary stenosis 5. Activity intolerance related to insufficient oxygenation 6. Risk for injury (bleeding) related to dissolution of clots 7. Ineffective individual coping related to threats to self esteem* MI management: 1. CBR without BP 2. Oxygen therapy 3. Pain control 4. Morphine or Meperidine 5. Vasodilator (NTG) 6. Anxiolytic (Benzodiazepine) 7. IV access line 8. Cardiac monitor

9. Central venous access line 10. Cardiac enzymes evaluation 11. ACLS* Possible ECG results: Elevation of ST segment = MI Peaked or inverted T wave = MI Pathological Q wave = MI Other drugs for MI: Pharmacologic Therapy

1. Thrombolytic Agents 1. TPA tissue plasminogen activator 2. Streptokinase (streptase) 3. Urokinase 2. Anticoagulant 1. Heparin 2. Warfarin 3. ASA (antiplatelets) 3. Beta adrenergic blocking agents 1. Propranolol 4. Antidysrhythmic 1. Lidocaine (Xylocaine) 5. Calcium Channel Blockers 1. Diltiazem* MI surgical interventions: PTCA Percutaneous Transluminal Coronary Angioplasty IABP Intraaortic Balloon Pump CABG coronary artery bypass graft Triple Saphenous Vein, LIMA and RITA* CHF Cause: Dx: 2DECHO, PMI, s/sx S/sx: Right side and left side failure? Mx: CHF

Nursing Considerations: 1. The goal of treatment is to improve pump function and reverse the compensatory mechanism of the heart. 2. Observe complete bed rest and reduce myocardial oxygen demand. 3. Employ FVE management and prevent the complications to occur. 4. Give Diuretics and Digoxin (T.L. 0.5-2.0 ng/ml) as ordered and watch-out the adverse effects. Cardiac Arrest Heart stops beating or contraction is ineffective Watch-out for tissue perfusion manifestations: Brain? Heart and lungs? Vascular? Kidneys? Liver? Skin? GIT? Cardiac Arrest Treatment: 1. Increase CO 2. Cardiovascular drugs and mechanical equipment 3. Cardiovascular Drugs: IV Dopamine (vasopressor) IV Dobutamine (diuretic effects) IV Epinephrine (vasoconstrictor) IV Nitroprusside (vasodilator) 4.Mechanical: IABP intra aortic balloon pump (improve coronary Defibrilator (arrhythmias can be stopped) Cardiac monitor (to detect arrhythmias)* Cardiogenic Shock! Types: CHDans Stages: early, late, end stage or decompensatory BV, CO, CB, TP: brain, heart, kidneys, lungs ER situation!!! Mx: Position: Modified Trendelenburg, v.s. monitoring perfusion) utilization

O2 therapy (high flow) IV line, BT, Cut Down (CVP) ETT, Mechanical Ventilator Drugs: Cardiotonics (Dopamine, digitalis) Epinephrine, Antihistamine, Steroids, Bronchodilators Ranitidine, Antibiotics* Comparison DVT TAO Smoking Artery Intermittent claudication Doppler test Arteriogram Gangrene Fibrinolytics and anticoagulant Dipyridamole (Persantin) to prevent occlusion * Venous stasis Vein Homans sign duplex test Venogram Embolism Fibrinolytics and anticoagulant Dipyridamole (Persantin) to prevent occlusion

Other vascular diseases: Phlebitis: inflammation Chronic venous insufficiency: valve defects Raynauds phenomenon: spasmW-poolingB-rewarmingR Arteriosclerosis: aging Atherosclerosis: fats* HPN Cause: Primary and secondary Risk factors: MRF or NMRF

Dx: BP readings, identification of RF s/sx: asymptomatic (silent killer) Cx: CHF, aneurysm, Kidney Failure, CVA etc Mx: non pharmacologic first Gold Standard: 115/75

CATEGORY Normal Prehypertension

SBPmm Hg < 120 and 120-139 or 140-159 or 160 or

DBPmm Hg < 80 80-90 90-99 100

Hypertension, Stage 1 Hypertension, Stage 2 Anti hypertensive drugs:

1. Diuretics: Furosemide (Lasix) 2. Adrenergic Inhibitor 1. Peripheral Agent: Reserpine (Serpasil) 2. Central Alpha-Agonist: Methyldopa (Aldomet) 3. Alpha-Blockers: Prazosin HCl (Minipress) 4. Beta-Blockers: Propranolol HCl (Inderal) 5. Direct Vasodilators: Hydralazine (Apresoline) 3. Calcium Antagonist: Diltiazem HCl (Cardizem) 4. Angiotensin-Converting Enzyme Inhibitor: 5. Renin Inhibitor: Aliskiren (Tekturna)* Aneurysm Distension of an artery due to weakening of arterial wall Cause: hereditary, HPN Cerebral A. Ant. Comm. Art. Internal carotid Art. Aorta Dissecting Aneurysm A.A.A. Mx: Drugs? Surgical clipping Endovascular coiling (coils initiate a clotting or thrombotic Captopril (Capoten)

reaction within the aneurysm ) Stent

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