cardiovascular 2011 108

7/27/2019 Cardiovascular 2011 108

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Cardiovascular 2011

Scope

1. Anatomy and Physiology, PE2. Lab and Diagnostic Procedures3. Disorders

Anatomy of heart

Anatomy Key Points!

1. Layers2. Chambers3. Valves4. Conduction5. Blood Supply6. Circulatory System7. 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?


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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. Layers2. Chambers3. Valves4. Conduction5. Blood Supply6. Circulatory System7. 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


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=58%

ASSESSMENT

Chest pain Murmur

Cyanosis Pericardial friction rub

Pallor Gallop

Edema Syncope

Fatigue Dyspnea

Palpitations Arrhythmia

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 Glands response (stress)

6. Syncope

Transient loss of consciousness Due to decreased cerebral tissue perfusion

7. Edema

Causes? Bilateral Unilateral Grading


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Generalized8. 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 closure of AV valves (lub) S2 closure of SL valves (dup) 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*

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

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)


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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 sec2. will increase from Heparin administration

Prothrombin Time

1. 9.5 12 sec2. will increase from Warfarin administration3. will decrease from vit K and hemostan

INR

1. 3.5 sec2. 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 (

Factor IV)

Magnesium

1.52.6 meq/L (to detect cause of cardiac dysrhythmias, electrolyte status, neuromuscular and renal function)


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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


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 = found in nervous tissues

CK-MM = found in muscle

TOTAL CK = 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)


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)


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Normal value is 70-200 IU/L

LDH1 and LDH2 = appear primarily in the heart, RBC and kidneys

LDH3 = lungs

LDH4 and LDH5 = liver and skeletal muscle

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


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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 4th ICS sternal border, right

V2 =Y 4th ICS sternal border, left

V3 =G halfway between V2 and V4

V4 =BL MCL (midclavicular line) 5th ICS, left

V5 =BR AAL (anterior axillary line) halfway between V4 and V6

V6 =V MAL (midaxillary line) level with V4, left

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

V5V6 = 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


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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


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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


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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


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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

EKGExercise (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 impuls

(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,


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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


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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


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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


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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, tachypn

muffled (depressed) heart sound, friction rub (scratchy or grating sound), anxiety and chest pain.


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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

ACLSPacemaker

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


Vasodilators

Opiate Analgesic Morphine Sulfate

Nursing Responsibilities



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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.


Calcium Channel Blockers

Nifidepine (Adalat, Procardia) Diltiazem (Cardizem)

Decrease muscle tone, interferes contraction, decrease BP

S.E. hypotension, bradycardia, diarrhea and rashes


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


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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



Dopamine diuresis effect

Increase Na excretion (kidney)

Vasodilators

Norepinephrine effect

Dobutamine

Increase CO

More potent on contraction


Diuretics

1. Spironolactone (Aldactone) K sparer2. Furosemide (Lasix) K waster3. Nursing Responsibilities

Anti hypertensive

1. ACE inhibitors Captopril (Capoten)Cardiovascular Drugs

Cardioaccelerator

1. Norepinephrine (Levophed) powerful vasoconstrictor2. Epinephrine increase conduction, contractility and automaticity3. Atropine S04-to treat symptomatic bradycardia


Anti dysrhythmic drug

1. Lidocaine (Xylocaine) for PVC2. Atropine for Mobitz type I3. Isoproterenol (Isuprel) for sinus

bradycardia

4. Quinidine for atrial fib


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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.


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 activator4. Antidote Amino Caproic Acid5. Nursing Responsibilities


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



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)


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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: LARGEHypertrophic: THICK

Restrictive: STIFF

Hyperlipidemia

Elevated serum total cholesterol

Elevated low density lipoprotein

HDL: good C.


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LDL: bad C.

Elevated triglycerides and cholesterol

Cause

Dx:


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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 SBPmm Hg DBPmm Hg

Normal < 120 and < 80

Prehypertension 120-139 or 80-90

Hypertension, Stage 1 140-159 or 90-99

Hypertension, Stage 2 160 or 100

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


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?


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Angina

1. Incomplete block2. Less 15 minutes (pain)3. Relieved by NTG4. ST and T wave changes5. Attack is precipitated by activity6. Not life threatening

MI

1. Complete block2. Over 15 minutes (pain)3. Not relieved by NTG4. ST segment depression and T wave inversion5. Attack is not precipitated by activity6. Life threatening*

Types of Angina

1. Stableactivity = pain, relieved by rest2. Unstableactivity = pain, relieved by NTG3. Pre infarction pain at rest, relieved by NTG4. Prinzmetal (variant) pain at rest with vasospasm , relieved by NTG5. 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 test2. Coronary angiography3. MUGA: MULTI GATED ACQUISITION SCAN

(Nuclear Medicine)

Thallium 201 Imaging (normal)

Technetium-99 Imaging (necrotic)

1. Cardiac enzymes: increasedTroponin-T or I

CK MB


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LDH1 higher than LDH2

(flipped LDH)

AST

1. ECG2. WBC, ESR and Myoglobin*

Possible ECG results:




Nursing Diagnosis

1. Pain related to an imbalance in oxygen supply and demand2. Anxiety related to chest pain, fear of death and threatening environment3. Decreased cardiac output related to impaired contraction of the heart4. Altered tissue perfusion (myocardial) related to coronary stenosis5. Activity intolerance related to insufficient oxygenation6. Risk for injury (bleeding) related to dissolution of clots7. Ineffective individual coping related to threats to self esteem*

MI management:

1. CBR without BP2. Oxygen therapy3. Pain control4. Morphine or Meperidine5. Vasodilator (NTG)6. Anxiolytic (Benzodiazepine)7. IV access line8. Cardiac monitor9. Central venous access line10.Cardiac enzymes evaluation11.ACLS*

Other drugs for MI:

Pharmacologic Therapy1. Thrombolytic Agents

1. TPA tissue plasminogen activator2. Streptokinase (streptase)3. Urokinase


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2. Anticoagulant1. Heparin2. Warfarin3. ASA (antiplatelets)

3. Beta adrenergic blocking agents1. Propranolol

4. Antidysrhythmic1. Lidocaine (Xylocaine)

5. Calcium Channel Blockers1. 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 pumpfunction, 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?


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Heart and lungs?

Vascular?

Kidneys?

Liver?

Skin?

GIT?

Treatment:

1. Increase CO2. Cardiovascular drugs and mechanical equipment utilization3. Cardiovascular Drugs:

IV Dopamine (vasopressor)

IV Dobutamine (diuretic effects)

IV Epinephrine (vasoconstrictor)

IV Nitroprusside (vasodilator)

4.Mechanical:

IABP intra aortic balloon pump (improve coronary perfusion)

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


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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


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Excavation of the skin surface produced by sloughing of inflammatory necrotic tissue

Varicose Veins

Dilatation and elongation ofsaphenous 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 blanchingof 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 for2-5 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

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

TAO

Smoking Artery S/sx:Intermittent claudication LOSS OF SENSATION Doppler UTZ test (speed)


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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 block2. Less 15 minutes (pain)3. Relieved by NTG4. ST and T wave changes5. Attack is precipitated by activity6. Not life threatening

MI

1. Complete block2. Over 15 minutes (pain)3. Not relieved by NTG4. ST segment depression and T wave inversion5. Attack is not precipitated by activity6. Life threatening*

Types of Angina

1. Stableactivity = pain, relieved by rest2. Unstableactivity = pain, relieved by NTG


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3. Pre infarction pain at rest, relieved by NTG4. Prinzmetal (variant) pain at rest with vasospasm , relieved by NTG5. Intractable continued pain not relieved by NTG

Angina and MI

Dx:1. Pain and NTG test2. Coronary angiography3. MUGA: MULTI GATED ACQUISITION SCAN

(Nuclear Medicine)

Thallium 201 Imaging (normal)

Technetium-99 Imaging (necrotic)

1. Cardiac enzymes: increasedTroponin-T or I

CK MB

LDH1 higher than LDH2

(flipped LDH)

AST

1. ECG2. WBC, ESR and Myoglobin*

Nursing Diagnosis

1. Pain related to an imbalance in oxygen supply and demand2. Anxiety related to chest pain, fear of death and threatening environment3. Decreased cardiac output related to impaired contraction of the heart4. Altered tissue perfusion (myocardial) related to coronary stenosis5. Activity intolerance related to insufficient oxygenation6. Risk for injury (bleeding) related to dissolution of clots7. Ineffective individual coping related to threats to self esteem*

MI management:

1. CBR without BP2. Oxygen therapy3. Pain control4. Morphine or Meperidine5. Vasodilator (NTG)6. Anxiolytic (Benzodiazepine)7. IV access line8. Cardiac monitor


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9. Central venous access line10.Cardiac enzymes evaluation11.ACLS*

Possible ECG results:




Other drugs for MI:

Pharmacologic Therapy1. Thrombolytic Agents

1. TPA tissue plasminogen activator2. Streptokinase (streptase)3. Urokinase

2. Anticoagulant1. Heparin2. Warfarin3. ASA (antiplatelets)

3. Beta adrenergic blocking agents1. Propranolol

4. Antidysrhythmic1. Lidocaine (Xylocaine)

5. Calcium Channel Blockers1. 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


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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 CO2. Cardiovascular drugs and mechanical equipment utilization3. Cardiovascular Drugs:

IV Dopamine (vasopressor)

IV Dobutamine (diuretic effects)

IV Epinephrine (vasoconstrictor)

IV Nitroprusside (vasodilator)

4.Mechanical:

IABP intra aortic balloon pump (improve coronary perfusion)

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


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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

Venous stasis Vein Homans sign duplex test Venogram Embolism Fibrinolytics and anticoagulant Dipyridamole (Persantin) to prevent occlusion

TAO

Smoking Artery Intermittent claudication Doppler test Arteriogram Gangrene 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


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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 SBPmm Hg DBPmm Hg

Normal < 120 and < 80

Prehypertension 120-139 or 80-90

Hypertension, Stage 1 140-159 or 90-99

Hypertension, Stage 2 160 or 100

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: Captopril (Capoten)5. Renin Inhibitor: Aliskiren (Tekturna)*

Aneurysm


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


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reaction within the aneurysm )

Stent

Thank you!

Believe iN urself

Believe in iNurse

cardiovascular 2011 108

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