Cardiovascular

Skills Procedures Laboratory Telemetry Wired com

Dx and Lab Tests

Cardiac enzymes Serum analysis CARDIAC CATH
1.

2. 3.

Angiography (MUGA: technetium 99, thallium 201) CVC SWAN-GANZ

EKG Pacemaker Pericardiocentesis PTCA

Lab results

Serum Analysis INVASIVE

Partial Thromboplastin Time (Activated)
1. 2.

20 45 sec will increase from Heparin administration 9.5 12 sec will increase from Warfarin administration will decrease from vit K and hemostan

Prothrombin Time
1. 2.

3.

INR

Serum Analysis INVASIVE

Serum Electrolytes and Lipid Level Potassium 3.55.3 meq/L (to detect origin of cardiac dysrhythmias) Sodium 135145 meq/L (to evaluate fluid and elec and acid base balance)

Serum Analysis INVASIVE

Serum Electrolytes and Lipid Level Calcium 4.55.5 meq/L (to diagnose cardiac dysrhythmias, neuromuscular, skeletal and endocrine disorders, blood clotting deficiencies (Factor IV) Magnesium 1.52.5 meq/L (to detect cause of cardiac dysrhythmias, electrolyte status, neuromuscular and renal function)

Possible ECG results: Flattening of T wave = hypokalemia Depression of ST segment = hypokalemia U wave = hypokalemia

Possible ECG results: Lengthened QT interval = hypocalcemia (torsades de pointes) Prolonged QT interval = hypermagnesemia

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 AST or SGOT CK-MB 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 Troponin I is usually utilized for MI Elevates within 3-4 hours, peaks in 4-24 hours and persists for 7 days to 3 weeks! Normal value for Troponin I is less than 0.6 ng/mL REMEMBER to AVOID IM injections before obtaining blood sample! Early and late diagnosis can be made!

Cardiac Enzyme Studies INVASIVE 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 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 is 0-7 U/L CK-BB CK-MM TOTAL CK = found in nervous tissues = found in muscle = detects post 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 heart, LDH3 = lungs = liver and skeletal muscle LDH4 and LDH5 = appear primarily in the RBC and kidneys

After 710 days LDH level returns to normal

Cardiac Enzyme Studies INVASIVE

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.

WBC count = 510T/cu mm (leukocytosis may result within 2 hours MI) Erythrocyte Sedimentation Rate ESR A rise usually follows after MI Blood glucose level Hyperglycemia may lead to coronary artery disease

Cardiac Enzyme Studies INVASIVE

Myoglobin 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

Cardiac Enzyme Studies INVASIVE

Troponin AST or SGOT CK-MB LDH Myoglobin Hydroxybutyric dehydrogenase

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

ECG
6 Electrodes V1 V2 V3 V4 = 4th ICS sternal border, right = 4th ICS sternal border, left = halfway between V2 and V4 = MCL (midclavicular line) 5th ICS, left

V5 = AAL (anterior axillary line) halfway between V4 and V6 V6 = MAL (midaxillary line) level with V4, left

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Travel of an impulse From the right shoulder across the chest to the left lower rib cage.

Placement of Four (4) Lead Wires

Lead 1 RA right arm Lead 2 LA left arm Lead 3 RL right leg Lead 4 LL left leg

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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

12 lead EKG

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Impulse Transmission
Travel of an impulse From the right shoulder across the chest to the left lower rib cage.
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Impulse Transmission
How are waveforms produced? Electrical impulses are generated by the: SA to AV to HIS BUNDLE to PURKINJE
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SA Node (60-100 bpm) Bachmanns Bundle Internodal Pathways Anterior Middle (wenckebachs) Posterior (thorels) DEPOLARIZATION OF ATRIA AV Node (30-60 bpm) His Bundle Right and Left bundle Purkinje fibers DEPOLARIZATION OF VENTRICLES

P-WAVE Depolarization of Atria Q-WAVE Purkinjes fibers R-WAVE Depolarization of ventricles S-WAVE Completion of ventricular depolarization

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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

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0.04sec/small square 0.20sec/big square 300/150/100/75/6 0/50 R-R wave (big square) 25 small boxes in 1 big box

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

R-R INTERVAL

0.04sec/small square 0.20sec/big square 300/150/100/75/60/50 R-R wave 25 small boxes for 1 big box

ECG
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

Possible ECG results: Elevation of ST segment = MI Peaked or inverted T wave = MI Pathological Q wave = MI Prolonged P-R interval = 1st degree heart block Widened QRS complex = delayed conduction to purkinje fiber

Possible ECG results: Flattening of T wave = hypokalemia Depression of ST segment = hypokalemia U wave = hypokalemia Long QT interval = hypocalcemia (torsades de pointes) Prolonged QT interval = hypermagnesemia*

ECG
Atrial Arrhythmias: Premature Atrial Contraction (PAC) Atrial Flutter Atrial Fibrillation

PAC

Atrial Flutter-sawtooth

ATRIAL FIBRILLATION

ECG
Ventricular Arrhythmias: Premature Ventricular Contraction (PVCs) Ventricular Tachycardia (vtach) Ventricular Fibrillation (vfib)

PVC

PVC

VENTRICULAR TACHYCARDIA

VENTRICULAR FIBRILLATION

STANDSTILL-asytole
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Atrioventricular or AV Block First Degree Second Degree Third Degree

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Atrioventricular or AV Block First Degree AV block (prolonged P wave followed by QRS)

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Atrioventricular or AV Block Second Degree AV block Type I Wenckebachs PR interval gradually lengthens then drops Type II PR interval is constant and one or more beats are non conduction or dropped

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Click to edit Master text styles Second level Third level Fourth level Third Degree AV block Fifth level (complete heart block) atria

Atrioventricular or AV Block

and ventricles are beating independently or P wave have no relationship to the QRS complex . Pacemaker is necessary

AV BLOCK

AV BLOCK
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3rd DEGREE AV BLOCK

EKG PATTERN (PACEMAKER)

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ARRHYTHMIA
Drugs commonly given: Atropine = for symptomatic bradycardia Digoxin = a-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

Stress Test

EKG Exercise (Stress Test) NON-INVASIVE

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.

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 CAD, Chest pain causes and dysrhythmias in exercise

EKG Exercise (Stress Test) NON-INVASIVE

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

Cardiac Pacemakers INVASIVE

An electrical impulse generator that transmits rhythmic impulses when the heart is unable to do its normal conduction of impulses (SA Node and AV Node) It may be temporary or permanent

Cardiac Pacemakers INVASIVE

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

Cardiac Pacemakers INVASIVE

Permanent pacemakers Smaller and the box is implanted under the skin (chest or abdomen) under surgery

Cardiac Pacemakers INVASIVE

Electrical impulses seen on ECG Generated by the pacemaker cause a straight and upright deflection (pacer spike) on the EKG baseline A spike precedes every QRS complex stimulated by the pacemaker

2D-ECHO NON-INVASIVE
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Echocardiography NON-INVASIVE
Special transducer is moved over the precordium to find an area where bone and lung tissues are absent (acoustic window) It picks up echoes or reflections of sound waves directed from the Doppler probe and converts them to electrical impulses to waveforms on an oscilloscope (graphic presentation) or videotape

2D ECHO NON-INVASIVE
Transducer that rapidly sweeps an ultrasonic (very high sound) beam (primary radiation emitted by X-ray tube) Producing a fan-shaped view of a heart section Intra-cardiac structures can be evaluated

CARDIAC Catheterization
LEFT SIDE CATHETERIZATION C. ANGIOGRAPHY
MUGA-Multi Gated Acquisition Scan Thallium 209, Technetium 99

PTCA IABP RIGHT SIDE CATHETERIZATION

Central Line Broviac and Hickman line

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IABP INVASIVE
Intra-Aortic Balloon Pump Insertion of a catheter up to the aortic arch (0.5- 2 cm below) Balloon is inflated during diastole (DN dicrotic notch) and must be deflated before systole With this blood is forced back to the coronary arteries thereby increasing blood flow Done every 3-4 beats

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Central Venous Catheter

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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.A. 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

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Estimating CVP

SWAN-GANZ CATHETER INVASIVE

Other name: pulmonary artery catheter Records: CVP, RVP, LVP, PAP/PAWP and CO Procedure: same with CVC Multi lumen, 110 cm
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SGC

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PERICARDIOCENTESIS INVASIVE

PERICARDIOCENTESIS INVASIVE
Blind Procedure Removes fluid that has accumulated in the pericardial sac to relieve cardiac tamponade and obtain fluid for analysis 50 ml syringe is inserted through the chest wall into the pericardial sac (needle insertion site is prepared as any sterile procedure Supine in bed, 60 degrees head elevation, arms supported with pillow

PERICARDIOCENTESIS INVASIVE
Monitor EKG during the procedure for the ff: PVC and ST elevation = needle contacted the ventricle Elevated P wave and PAC = needle contacted the atrium Large erratic QRS = needle contacted the myocardium Monitor 5-15 minutes, note character of aspirated fluids and blood (blood clot = needle punctured the chamber)

PERICARDIOCENTESIS INVASIVE
Properly label the specimen and send to the lab After the procedure watch out for complications (cardiac tamponade, increased venous pressure, distended neck veins, tachypnea, muffled (depressed) heart sound, friction rub (scratchy or grating sound), anxiety and chest pain.

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Cardiovascular Drugs
Anti Anginal Opiate Analgesic Morphine Sulfate cardiac workload and BP, improve LOC and sedative effect Vasodilators Nitroglycerin NTG Relax smooth muscle, dec. BP and alleviate headache Increase blood vessel diameter and improves blood flow S.E. hypotension, dizziness and flushing Can be given SL or IV (Isordil) and topical (Nitrobid)

Cardiovascular Drugs
Calcium Channel Blockers Nifidepine (Procardia) Diazepam (Cardizem) Decrease muscle tone, interferes contraction, decrease BP S.E. hypotension, bradycardia, diarrhea and rashes

Beta Blocking Agent Propranolol Decrease workload Blocks beta receptors and capable of decreasing HR S.E. hypotension, vomiting, nausea and depression

Cardiovascular Drugs

Digitalis, Digoxin Positive Inotropic (Increases contraction of the heart) Increase emptying capacity of the heart Negative chronotropic (Decreases HR) AV node

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 Furosemide (Lasix) K waster

2.

Cardiovascular Drugs
Cardioaccelerator
1.

Norepinephrine (Levophed) powerful vasoconstrictor Epinephrine increase conduction, contractility and automaticity

2.

Anti dysrhythmic drug

1. 2. 3.

Lidocaine (Xylocaine) for PVC Atropine for Mobitz type I Isoproterenol (Isuprel) for sinus bradycardia Quinidine for atrial fib

4.

Cardiovascular Drugs
Thrombolytic/Fibrinoly tic Agent
1.

Streptokinase lyses the clot (20T IU IV bolus or 4T IU/min drip) Urokinase avtivates plasminogen to plasmin

2.

Cardiovascular Drugs
Blood thinner 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

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)

Cardiovascular 09
Sonny M. Moreno, RN, MAN, USRN

Scope
Anatomy and Physiology Assessment Diagnostic and Lab Disorders

Anatomy Key Points!

1. 2. 3. 4. 5. 6. 7.

Layers Chambers Valves Conduction Blood Supply Circulatory System Accessory Structures

Anatomy Key Points!

1.

Layers

Epicardium Myocardium Endocardium Pericardial membrane

Anatomy Key Points!

2. Chambers RA RV LA LV RA & LA (interatrial septum) RV & LV (interventricular septum)

Anatomy Key Points!

3. Valves RA & RV (tRicuspid)

LA & LV (mitraL)

AV valves RV & Pulmonary Artery (Pulmonic)

LV & Aorta (Aortic)

Location of valves

Anatomy Key Points!

4. 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

Anatomy Key Points!

5. Blood Supply

Anatomy Key Points!

6. Circulatory System - Pulmonary Circuit - Systemic Circuit

Anatomy Key Points!

7. Accessory Structures Pericardium Mediastinum Thoracic Cavity

Anatomy Key Points!

1. 2. 3. 4. 5. 6. 7.

Layers Chambers Valves Conduction Blood Supply Circulatory System 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 PULSE waves w/n artery upon contraction by the LV, HR PULSE DEFICIT- (apical pulse difference from radial pulse) PULSE PRESSURE (difference b/n sytolic and diastolic pressure)

ASSESSMENT
Chest pain Cyanosis Fatigue Syncope Arrhythmia Gallop Dyspnea Pallor Palpitations Edema Murmur Pericardial friction rub

ASSESSMENT
1. l.

Chest Pain Most common Related to activity Not related to activity Related to movement Related to breathing

l.

l.

l.

l.

ASSESSMENT
2. Dyspnea
l l l l

Labored breathing Dyspnea on exertion Orthopnea Sudden or acute dyspnea

ASSESSMENT
3. Cyanosis
l

Bluish discoloration of the skin and mucous membrane Sat O2 is below 94% Indications?

4. Fatigue
l

ASSESSMENT
5. Palpitations l Awareness of rapid or irregular heart beat l Autonomic Nervous System and Adrenal Glands response (stress) 6. Syncope l Transient loss of

ASSESSMENT
7. Edema
l l l l l

Causes? Bilateral Unilateral Grading Generalized

ASSESSMENT
8. Skin
l

Color, temperature, hair growth, nails, capillary refill, clubbing or spooning of fingers evaluation.

ASSESSMENT
9. Cardiac rate and rhythm
l l l l l

Tachycardia Bradycardia Heart block Arrhythmias Sinus arrest

ASSESSMENT
l l l l

S1 closure of AV valves (lub) S-VC S2 closure of SL valves (dup) D-VR S3 & S4 diastolic filling sound S3 is heard after S2, if present suspect CHF S4 is heard prior to S1, if present suspect non- compliant ventricles although this is common among elderly*

ASSESSMENT
l

Murmurs turbulence of blood flow, if positive watchout FVE, this is normal until 1 year old 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 like Effusion

Definition of terms Hyperlipidemia

Group of metabolic disorders that lead to: Elevated serum total cholesterol (hypercholesterolemia ) Elevated low density lipoprotein

Atherosclerosis fats accumulation Arteriosclerosis hardening of arteries due to aging

Coronary Artery Disease Accumulation of fatty deposits in the innermost layer of the coronary arteries Atheroma or plaque can lead to narrowing of the lumen decreasing coronary blood flow and

Angina Diminished O2 supply to the myocardium Myocardial Infarction Absent of O2 supply to the myocardium

Cardiogenic Shock Occurs when the heart muscle loses its contractile power Extensive damage to left ventricle due to MI may lead to shock

Infective Endocarditis Infection of the inner lining due to direct invasion of bacteria May lead to deformity of valve leaflets

Rheumatic Endocarditis Valvular problem Valvular insufficiencyvalve leakage causing regurgitation Valvular stenosisnarrowing causing the heart to exert more effort to eject blood

Myocarditis Inflammation of the myocardium Pericarditis Pericardial effusion-fluid in the pericardial cavity Constrictive pericarditis-thickening of the pericardium compressing the heart

Cardiomyopathy Idiopathic 3 Groups

Dilated Hypertrophic Restrictive

Heart Failure or Congestive Heart Failure Hearts inability to pump blood Acute Pulmonary Edema

Cardiac Dysrhythmias Disturbances in regular rate/rhythm due to changes in electrical automaticity or conduction

Phlebitis Inflammation in the wall of a vein Phlebothrombosis Formation of thrombi in the vein Deep Vein

Chronic Venous Insufficiency Chronic occlusion of the vein or destruction of valves leading to venous stasis. Stasis Ulcers Excavation of the skin surface produced by sloughing of inflammatory necrotic tissue

Arteriosclerosis
Loss of elasticity and hardening of vessel wall

Atherosclerosis
Common type of arteriosclerosis, manifested by formation of atheromas

Inflammation of arterial wall followed by thrombosis Also affects adjacent veins and nerves

Thromboangitis Obliterans or Buergers Disease

Aneurysm
Distension of an artery due to weakening of arterial wall High pressure in the lumen due to plaque deposits

Acute Arterial Occlusion

Sudden interruption of blood supply lead to gangrene formation

Raynauds Phenomenon or Vasospastic Disorder

Unusual sensitivity to cold or emotional stress Intermittent vasoconstriction leads to coldness, pain, pallor of fingertips, toes, tip of the nose

Hypertension
CNS factor Renin-angiotensin/aldosterone system factor ECF volume Increased cardiac output plus increased peripheral resistance factor

Cardiovascular Disorders

What is CAD?
fatty deposits in the inner layer of coronary arteries. Risk Factors? Modifiable Non modifiable*

Comparison?
MI Angina 1. Incomplete block 1. Complete block 2. Less 15 minutes 2. Over 15 minutes (pain) (pain) 3. Relieved by NTG 3. Not relieved by NTG 4. ST and T wave 4. ST segment changes depression and 5. Attack is T wave inversion precipitated by 5. Attack is not activity precipitated by 6. Not life

Types of Angina
1. 2. 3. 4.

Stable activity = pain, relieved by rest Unstable activity = pain, relieved by NTG Pre infarction pain at rest, relieved by NTG Prinzmetal (variant) pain at rest with vasospasm , relieved by NTG Intractable continued pain not relieved by NTG

5.

Angina and MI Dx: 1. Pain and NTG test 2. Coronary angiography Thallium 201 Imaging (normal)

Nursing Diagnosis
1.

2.

3.

4.

Pain related to an imbalance in oxygen supply and demand Anxiety related to chest pain, fear of death and threatening environment Decreased cardiac output related to impaired contraction of the heart Altered tissue perfusion (myocardial) related to coronary stenosis

MI management:
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

M-O-N-A CBR without BP Oxygen therapy Pain control Morphine or Meperidine Vasodilator (NTG) Anxiolytic (Benzodiazepine) IV access line Cardiac monitor Central venous access line Cardiac enzymes evaluation ACLS*

Possible ECG results: Elevation of ST segment = MI Peaked or inverted T wave = MI Pathological Q wave = MI

Other drug for MI:

1.

Pharmacologic Therapy Thrombolytic Agents

1. 2. 3.

2.

Anticoagulant
Heparin Warfarin ASA

TPA tissue plasminogen activator Streptokinase (streptase) Urokinase

1. 2. 3.

3. 4. 5.

Beta adrenergic blocking agents Antidysrhythmic

Diltiazem* Propranolol

1.

1.

Calcium Channel Blockers

Lidocaine (Xylocaine)

1.

MI surgical Surgical interventions: revascularization:

PTCA Percutaneous Transluminal Coronary Angioplasty CABG coronary artery bypass graft*

CHF
Causes? Right side and left side failure? Dx? 2DECHO, PMI, s/sx Drugs?*

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.

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

Comparison
DVT Venous stasis Vein Homans sign duplex test Venogram Embolism Fibrinolytics and anticoagulant Dipyridamole (Persantin) to prevent TAO Smoking Artery Intermittent claudication Doppler test Arteriogram Gangrene Fibrinolytics and anticoagulant Dipyridamole (Persantin) to

Phlebitis: inflammation

Other vascular diseases:

Chronic venous insufficiency: valve defects Raynauds phenomenon: spasmW-poolingBrewarmingR Arteriosclerosis:

HPN
Cause: Primary and secondary Risk factors: MRF or NMRF Dx: BP readings, identification of RF s/sx: asymptomatic (silent killer) Mx: non pharmacologic first Cx: CHF, aneurysm, Kidney Failure, CVA etc*

NEW Classifications:
Gold standard = 115/75 Prehypertension = 120-139/80-89 Stage I Stage II Stage III = 140-159/90-99 = 160-179/100-109 = 180 / 110*

1. 2.
1. 2. 3. 4. 5.

Anti hypertensive drugs:(Lasix) Diuretics: Furosemide

Adrenergic Inhibitor
Peripheral Agent: Reserpine (Serpasil) Central Alpha-Agonist: Methyldopa (Aldomet) Alpha-Blockers: Prazosin HCl (Minipress) Beta-Blockers: Propranolol HCl (Inderal) Direct Vasodilators: Hydralazine (Apresoline)

3.

4.

5.

Calcium Antagonist: Diltiazem HCl (Cardizem) Angiotensin-Converting Enzyme Inhibitor: Captopril (Capoten) Renin Inhibitor: Aliskiren (Tekturna)*

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