Cardio Nursing.pdf

Lecture Notes on Cardiovascular System Prepared By: Mark Fredderick R Abejo R.N, MAN

MEDICAL AND SURGICAL NURSING

C ardiov ardi ovascula ascularr System Lecturer: Mark Lecturer: Mark Fredderick R. Abejo RN, MAN

Anatomy and Physiology of the Heart

Cardiovascular system consists of the heart, arteries, veins & capillaries. The major function are circulation of blood, delivery of O2 & other nutrients to the tissues of the body & removal of CO2 & other cellular products metabolism Heart      

Muscular pumping organ that propel blood into the arerial system & receive blood from the venous system of the body. Hollow muscular behind the sternum and between the lungs Located on the middle of mediastinum Resemble like a close fist Weighs approximately 300 – 300 – 400 400 grams Has heart wall has 3 layers  Endocardium – Endocardium – lines lines the inner chambers of the heart, valves, chordate tendinae and papillary muscles.  Myocardium – Myocardium – muscular muscular layer, middle layer, responsible for the major pumping action of the ventricles.  Epicardium – Epicardium – thin thin covering(mesothelium), covering(mesothelium), covers the outer surface of the heart

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Pericardium – Pericardium – invaginated invaginated sac  Visceral – Visceral – attached attached to the exterior of myocardium Parietal – Parietal – attached attached to the great vessels and  diaphragm

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Papillary Muscle Arise from the endocardial & myocardial surface of the ventricles & attach to the chordae tendinae

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Chordae Tendinae Attach to the tricuspid & mitral valves & prevent eversion during systole

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Separated into 2 pumps:  right heart – heart – pumps pumps blood through the lungs  left heart – heart – pumps pumps blood through the peripheral organs

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Chamber of the Heart Atria  2 chambers, function as receiving chambers, lies above the ventricles 

Medical and Surgical Nursing

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Upper Chamber (connecting or receiving) Right Atrium: receives systemic venous blood through the superior vena cava, inferior vena cava & coronary sinus Left Atrium: receives oxygenated blood returning to the heart from the lungs trough the pulmonary veins

Coronary Veins Coronary sinus – sinus – main main vein of the heart Great Cardiac vein – vein – main main tributary of the coronary sinus Oblique vein – vein – remnant remnant of SVC, small unsignificant

Heart Circulation

Ventricles  2 thick-walled chambers; major responsibility for forcing blood out of the heart; lie below the atria  Lower Chamber (contracting or pumping)  Right Ventricle: contracts & propels deoxygenated blood into pulmonary circulation circulation via the aorta during ventricular systole; Right atrium has decreased pressure which is 60 – 60 – 80 80 mmHg  Left Ventricle: propels blood into the systemic circulation via aortaduring ventricular systole; Left ventricle has increased pressure which is 120 – 120 – 180 180 mmHg in order to prop el blood to the systemic circulation 

Heart Valves Tricuspid  Pulmonic  Mitral  Aortic 

Cardiac Conduction System

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Properties of Heart Conduction System • Automaticity • Excitability • Conductivity • Contractility

Coronary artery – artery – 1 1st branch of aorta Right Coronary  SA nodal Branch – Branch – supplies supplies SA node  Right marginal Branch – Branch – supplies supplies the right border of the heart  AV nodal branch – branch – supplies supplies the AV node  Posterior interventricular interventricular artery – artery – supplies supplies both ventricles Left Coronary Circumflex branch – branch – supplies supplies SA node in 40 % of  people Left marginal – marginal – supplies supplies the left ventricle   Anterior interventricular branch aka Left anterior descending(LAD) – – supplies supplies both ventricles and interventricular septum  Lateral branch – branch – terminates terminates in ant surface of the heart

Structure of Heart Conduction System

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Nodal tissues SA Node( Sino-atrial, Keith and Flack)  Primary Pacemaker  Between SVC and RA  Vagal and symphatetic innervation  Sinus Rhythms

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The Normal Cardiac Cycle

AV Node( Atrioventricular , Kent and Tawara) At the right atrium 3 zones  AN Zone(atrionodal)  N Zone (nodal)  NH zone (nodal – (nodal – HIS) HIS)

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General Concepts Systole - period of chamber contraction Diastole - period of chamber relaxation Cardiac cycle - all events of systole and diastole during one heart flow cycle

Internodal and Interatrial Pathways Connects SA and AV Node Ant. Internodal(bachman) tract Middle Internodal(wenkebach) tract Posterior internodal(Thorel) tract

Events of Cardiac Cycle

1.

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Bundle of His/ Purkinje Fibers Provides for ventricular conduction system Fastest conduction among cardiac tissues Right bundle Left Bundle

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Cardiac Action Potential 

Depolarization: electrical activation of a cell caused by the influx of sodium into the cell while potassium exits the cell

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Repolarization: return of the cell to the resting state caused by re-entry of potassium into the cell while sodium exits

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Refractory periods: Effective refractory period: phase in which cells are incapable of depolarizing Relative refractory period: phase in which cells require a stronger-than-normal stimulus to depolarize

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b.

Atrioventricular node (AV node) - impulses impulses pass from SA via gap junctions in about 40 ms.; impulses are delayed about 100 ms to allow completion of the contraction of both atria; located just above tricuspid valve (between right atrium & ventricle)

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Atrioventricular bundle (bundle of His) - in the interATRIAL septum (connects L and R atria)

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L and R bundle of His branches - within the interVENTRICULAR septum (between L and R ventricles)

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Purkinje fibers - within the lateral walls of both the L and R ventricles; since left ventricle much larger, Purkinjes more elaborate here; Purkinje fibers innervate “papillary muscles” before ventricle walls so AV can valves prevent backflow


ventricles relax, ventricular pressure becomes LOW semilunar valves close, aorta & pulmonary trunk backflow

TOTAL CARDIAC CYCLE TIME = 0.8 second second (normal 70 beats/minute) atrial systole (contraction) = ventricular systole (contraction) = quiescent period (relaxation) =

0.1 second 0.3 second 0.4 second

Cardiac Output - Blood Pumping of the Heart

General Concepts • Stroke volume: the amount of b lood ejected with each heartbeat • Cardiac output: amount of blood pumped by the ventricle in liters per minute • Preload: degree of stretch of the cardiac muscle fibers at the end of diastole • Contractility: ability of the cardiac muscle to shorten in response to an electrical impulse • Afterload: the resistance to ejection of blood from the ventricle • Ejection fraction: the percent of end-d iastolic volume ejected with each heartbeat

(from SA through complete heart contraction = 220 ms = 0.22 s) Sinoatrial node (SA node) "the pacemaker" - has the fastest autorhythmic rate (70-80 per minute), and sets the pace for the entire heart; heart; this rhythm is called the sinus rhythm; located in right atrial wall, just inferior to the superior vena cava

filled ventricles begin to contract, AV valves CLOSE contraction of closed ventricles increases pressure ventricular ejection phase - blood forced out semilunar valves open, blood -> aorta & pulmonary trunk

isovolumetric relaxation: early ventricular diastole 

(right atrium) sinoatrial node (SA) (right AV valve) atrioventricular node (AV) atrioventricular bundle (bundle of His) right & left bundle of His branches Purkinje fibers of ventricular walls

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the AV valves are open pressure: LOW in in chambers; HIGH in aorta/pulmonary trunk aortic/pulmonary semilunar valves CLOSED blood flows from vena cavas/pulmonary cavas/pulmonary vein INTO atria blood flows through AV valves INTO INTO ventricles (70%)

ventricular systole: blood ejected from heart 

Anatomical Anatomical Sequence of Excitation of the Heart   

mid-to-late ventricular diastole: ventricles filled

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hypernatremia - HIGH Na+ concentration; can block Na+ transport & muscle contraction

General Variables of Cardiac Output

1. Cardiac Output (CO) - blood amount pumped per minute CO (ml/min) (ml/min) = HR (beats/min) (beats/min) X SV (ml/beat) (ml/beat)  Normal CO = 75 beats/min X 70 ml/beat  = 5.25 L/min

3. Other Factors Effecting Heart Rate (HR) normal heart rate - fetus 140 - 160 beats/minute female 72 - 80 beats/minute male 64 - 72 beats/minute

2. Heart Rate (HR) - cardiac cycles per minute  Normal range is 60-100 beats per minute Tachycardia is greater than 100 bpm  Bradycardia is less than 60 bpm  Sympathetic system INCREASES HR  Parasympathetic system (Vagus) DECREASES HR 

1. 2. 3. 4.

3. Blood pressure - Cardiac output X peripheral resistance Control is neural (central and peripheral) and  hormonal  Baroreceptors in the carotid and aorta  Hormones- ADH, aldosterone, epinephrine can increase BP; ANF can decrease BP

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Vascular System

Regulation of Stroke Volume (SV) 

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exercise - lowers resting heart rate (40-60) heat - increases heart rate significantly cold - decreases heart rate significantly tachycardia - HIGHER than nor mal resting heart rate (over 100); may lead to fibrillation bradycardia - LOWER than normal resting heart heart rate (below 60); parasympathetic drug side effects; physical conditioning; sign of pathology in non -healthy patient

Major function of the blood vessels isto supply the tissue with blood, remove wastes, & carry unoxygenated blood

End diastolic volume (EDV) - total blood collected in ventricle at end of diastole; determined by length of diastole and venous pressure (~ 120 ml) End systolic volume (ESV) - blood left over in ventricle at end of contraction (not pumped o ut); determined by force of ventricle contraction and arterial blood pressure (~50 ml)

back to the heart

Types of Blood Vessels

Arteries

SV (ml/beat) = EDV (ml/beat) - ESV (ml/beat) = 120 ml/beat - 50 ml/beat = 70 ml/beat Normal SV

Elastic-walled Elastic-walled vessels that can stretch during systole & recoil during diastole; they carry blood away from the heart & distribute oxygenated blood throughout the body

Frank-Starling Frank-Starling Law of the Heart - critical factor for stroke volume is "degree of stretch of cardiac muscle cells"; more stretch = more contraction force

Arterioles

Small arteries that distribute blood to the capillaries &

increased EDV = more contraction force slow heart rate = more time to fill exercise = more venous blood return

function in controlling systemic vascular resistance & therefore arterial pressure Capilliaries

The following exchanges occurs in the capilliaries

Regulation of Heart Rate (Autonomic, Chemical, Other)

O2 & CO2

1. Autonomic Regulation of Heart Rate (HR) 

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Solutes between the blood & tissue

Sympathetic - NOREPINEPHRINE (NE) increases heart rate (maintains stroke volume which leads to increased Cardiac Output)

Fluid volume transfer between the p lasma & interstitial space Venules

Parasympathetic - ACETYLCHOLINE (ACh) decreases heart rate

Small veins that receive blood from capillaries & function as collecting channels between the capillaries &

Vagal tone - parasympathetic inhibition of inherent rate of SA node, allowing normal HR

veins Veins

Baroreceptors, pressoreceptors - monitor changes in blood pressure and allow reflex reflex activity with with the autonomic nervous system

Low-pressure vessels with thin small & less muscles than arteries; most contains valves that prevent retrograde blood flow; they carry carry deoxygenated blood back to the

2. Hormonal and Chemical Regulation of Heart Rate (HR) 

heart. When the skeletal surrounding veins contract, the

epinephrine - hormone released by adrenal medulla during stress; increases heart rate

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thyroxine - hormone released by thyroid; increases heart rate in large qu antities; amplifies amplifies effect of epinephrine

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Ca++, K +, and Na+ levels very important; hyperkalemia - increased K + level; KCl used to stop heart on lethal injection hypokalemia - lower K + levels; leads to abnormal heart rate rhythms hypocalcemia - depresses heart function hypercalcemia - increases contraction phase


veins are compressed, promoting movement of blood back to the heart.

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Palpation:

Assessment of the Client with Cardiovascular Disorders

Nursing History Risk Factors A. Non – Non – Modifiable Modifiable Risk Factor  Age  Gender  Race  Heredity

Heart Sounds: Stethoscope Listening

B. Modifiable Risk Factor Stress  Diet  Exercise  Sedentary lifestyle  Cigarette smoking  Alcohol  Hypertension  Hyperlipidemia  DM   Obesity  Type A personality  Contraceptive Pills

Overview of Heart Heart Sounds (lub-du ; lub, dub )

Common Clinical Manifestations of Cardiovascular Cardiovascular Disorders

(pulmonic/aortic) valves S2 - due to the closure of the semi-lunar (pulmonic/aortic) - timing: diastole - loudest at the base

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d. e. f. g. h. i. j. k.

lub - closure of AV valves, onset of ventricular systole dub - closure of semilunar valves, onset of diastole    

Tricuspid valve (lub) - RT 5th intercostal, intercostal, medial Mitral valve (lub) - LT 5th intercostal, lateral Aortic semilunar valve (dub) - RT 2nd intercostal Pulmonary semilunar valve (dub) - LT 2nd intercostals

AV(mitral/tricuspid) valves S1 - due to closure of the AV(mitral/tricuspid) - timing: beginning of systole - loudest at the apex

Dyspnea - Exertional - Orthopnea - Paroxysmal Noctural Dyspnea - Cheyne-stokes Chest Pain Edema - Ascites - Hydrothorax - Anasarca Palpitation Hemoptysis Fatigue Syncope and Fainting Cyanosis Abdominal Pain Clubbing of fingers Jaundice

S3 – Ventricular Diastolic Gallop Mechanism: vibration resulting from resistance to rapid ventricular filling secondary to poor compliance Timing: early diastole Location: Apex (LV) or LLSB (RV) Pitch: faint and low pitched S4 - Atrial Diastolic Gallop Mechanism: vibration resulting from resistance to late ventricular filling during atrial systole Timing: late diastole ( before S1) Location: Apex ( LV) or LLSB (RV) Pitch: low ( use bell)

Physical Assessment Inspection: – Skin color – Neck vein distention distention

Heart Murmurs Murmur - sounds o ther than the typical "lub-dub"; typically caused by disruptions in flow

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Respirations Pulsations Clubbing Capillary refill

Incompetent valve - swishing sound just AFTER the normal "lub" or "dub"; valve does not completely close, some regurgitation of blood

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Stenotic valve - high pitched swishing sound when b lood should be flowing through valve; narrowing of outlet in the open state

Pericardial Pericardial Friction Rub   


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It is an extra heart sound o riginating from the pericardial sac Mechanism: Originates from the pericardial sac as it moves Timing: with each h eartbeat Abejo


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Location: over pericardium. Upright position, leaning forward Pitch: high pitched and scratchy. Sounds like sandpaper being rubbed together Significance: inflammation, infection, infiltration

2. Coagulation Screening Test

measures the ability to stop bleeding after a. Bleeding Time – measures small puncture wound used to identify b. Partial Thromboplastin Time (PTT) – used deficiencies of coagulation factors, prothrombin and fibrinogen; monitors heparin therapy.

Classification of Clients with Diseases of the Heart ( Functional Capacity )

determines activity and c. Prothrombin Time (Pro-time) – determines interaction of the Prothrombin group: factors V (preacclerin), VII (proconvertin), X (Stuart-Power factor), prothrombin and fibrinogen; used to determine dosages of oral anti-coagulant.

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Class I . Patients with cardiac disease but without

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Class Class I I . Patients with cardiac disease resulting to slight

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Class Class I I I . Patients with cardiac disease resulting in

Normal Values

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marked limitation of physical activity. They are comfortable at rest. Class Class I V . Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort

Bleeding Time : 2.75-8 min Partial Thromboplastin Time (PTT ): 60 - 70 sec. Prothrombin Time (PT): 12-14 sec.

resulting limitations of ph ysical activity. limitation of physical activity

3. Erythrocyte Erythrocyte sedimentation sedimentation rate ( ESR) It is a measurement of the rate at which RBC’s settle out of anticoagulated blood in an hour It is elevated in infectious heart disorder or myocardial infarction

Diagnostic Assessment Purposes: 1. To assist in diagnosing MI 2. To identify abnormalities 3. To assess inflammation 4. To d etermine baseline value 5. To monitor serum level of medications 6. To assess the effects of medications

Normal Values 15-20 mm/hr Male: Female: 20-30 mm/hr

A. Blood Studies

4. CARDIAC Proteins and enzymes a.

CK- MB ( creatine kinase) kinase)  Most cardiac specific enzymes  Accurate indicator of myocardial dammage  Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 days  Normal value is 0-7 U/L or males 50-325 mu/ml Female 50-250 mu/ml

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Lactic Dehydrogenase (LDH) Most sensitive indicator of myocardial damage  Elevates in MI in 24 hours, peaks in 48-72 hours  Return to normal in 10-14 days  Normally LDH1 is greater than LDH2 Lactic Dehydrogenase (LDH)  MI- LDH2 greater than LDH1 (flipped LDH pattern)  (100 – 225 225 mu/ml)  Normal value is 70-200 IU/L (100 –

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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

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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! weeks!  Normal value for Troponin 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!

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SERUM LIPIDS Lipid profile measures the serum cholesterol,  triglycerides and lipoprotein levels levels Cholesterol= 200 mg/dL  Triglycerides- 40- 150 mg/dL  LDH- 130 mg/dL  HDL- 30-70- mg/dL   NPO post midnight (usually 12 hours)

1. Complete Blood Count a. RBC count- # of RBCs/ mm3 of blood, to diagnose anemia and ploycythemia b. Hemoglobin - # of grams of hgb/ 100ml of blood; to measure the oxygen-carrying capacity of the blood

expressed in %; measures the volume of RBCs in c. Hematocrit – expressed proportion to plasma; used used also to diagnose anemia anemia and polycythemia and abnormal abnormal hydration states d. RBC indices- measure RBC size and hemoglobin content a. MCV (mean corpuscular volume) b. MCH (mean corpuscular corpuscular hemoglobin) c. MCHC (mean corpuscular hemoglobin concentrarion) e. Platelet count - # of Platelet/ mm3; to diagnose thrombocytopenia and subsequent bleeding tendencies f. WBC count- of WBCs/ mm3 of b lood; to detect infection or inflammation g. WBC Differential count - determines proportion of each WBC in a sample of 100 WBCs; used to classify leukemias Normal Values

Women – 4.2-5.4 4.2-5.4 million/mm3 million/mm3 RBC: Women – Men – Men – 4.7-6.1 4.7-6.1 million/mm3 Women – 12-16 12-16 g/dl Hgb: Women – Men – Men – 13-18 13-18 g/dl Women – 36-42% 36-42% Hct : Women – Men – Men – 42-48% 42-48% WBC: 5000-10,000/mm3 Granulocytes Neutrophils: 55-70% Eosinophils: 1-4% Basophils: 0.5-1.0% Agranulocytes Lymphocytes: 20-40% Monocytes: 2-8% Platelets: 150,000-450,000/mm3


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B. Non-Invasive Procedure 1. Cardiac Monitoring / Electrocardiography Electrocardi ography (ECG) A non-invasive procedure that evaluates the electrical activity of the heart

a. Limb Leads

b. Precordial Leads

D eflecti flecti on Waves Waves of of E CG 1. P wave - in itial wave, demonstrates the depolarization from SA Node through both ATRIA; the ATRIA ATRIA contract about 0.1 s after after start of P Wave.

demonstrates the 2. QRS complex - next series of d eflections, demonstrates depolarization of AV node through both ventricles; the ventricles contract throughout the period of the QRS complex, with a short delay after the end of atrial contraction; repolarization of atria also obscured 3. T Wave - repolarization of the ventricles (0.16 s)

The precordial leads VI – VI – V6 V6 are part of the 12 lead EKG. They are not monitored with the standard limb leads

4. PR (PQ) Interval Interval - time period from beginning of atrial contraction to beginning of ventricular contraction (0.16 s)

c. 12 lead ECG

ventricular contraction contraction (about 0.36 s); 5. QT Interval - the time of ventricular from beginning of ventricular depolarization to end of repolarization.

2. Holter M onitoring onitoring A non-invasive test in which the client wears a Holter  monitor and an ECG tracing recorded continuously over a period of 24 hours Instruct the client to resume n ormal activities and  maintain a diary of activities and any symptoms symptoms that may develop

ECG Paper


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3. Stress Test     

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C. Invasive Procedure

A non-invasive test that studies the heart during activity and detects and evaluates CAD Exercise test, pharmacologic test and emotional test Treadmill testing is the most commonly used stress test Used to determine CAD, Chest pain causes, drug effects and dysrhythmias in exercise Pre-test: consent may be required, adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine During the test: secure electrodes to appropriate location on chest, obtain baseline BP and ECG tracing, instruct client to exercise as instructed and report any pain, weakness and SOB, monitor BP and ECG continuously, record at frequent interval Post-test: instruct client to notify the p hysician if any chest pain, dizziness or shortness of breath . Instruct client to avoid taking a hot shower for 10 -12 hours after the test

1. Cardiac Catheterization ( Coronary Angiography / Arteriography Arteriography ) Insertion of a catheter into the heart and surrounding  vessels Is an invasive procedure during which ph ysician  injects dye into coronary arteries and immediately immediately takes a series of x-ray films to assess the structures of the arteries Determines the structure and performance of the  heart valves and surrounding vessels Used to diagnose CAD, assess coronary atery  patency and determine determine extent of atherosclerosis atherosclerosis  Pretest: Ensure Consent, assess for allergy to seafood and iodine, NPO, document weight and height, baseline VS, blood tests and document the peripheral pulses  Pretest: Fasting for 8-12 hours, teachings, medications to allay anxiety  Intra-test: inform patient of a fluttery feeling as the catheter passes through the heart; inform the patient that a feeling of warmth and metallic taste may occur when dye is administered  Post-test: Monitor VS and cardiac rhythm  Monitor peripheral pulses, color and warmth and sensation of the extremity distal to insertion site  Maintain sandbag to the insertion site if required to maintain pressure  Monitor for bleeding and hematoma formation

4. Pharmacological stress test Use of dipyridamole  Maximally dilates coronary artery  Side-effect: flushing of face  Pre-test: 4 hours fasting, avoid alcohol, caffeine  Post test: report symptoms of chest pain 

5. ECHOCARDIOGRAM

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Non-invasive test that studies the structural and functional changes of the heart with the use of u ltrasound Client Preparation: instruct client to remain still during the test, secure electrodes for simultaneous ECG tracing, explain that there will be no pain or electrical shock, lubricant placed on the skin will be cool.

2. Nuclear Cardiology  Are safe methods of evaluating left ventricular muscle function and coronary artery blood distribution.  Client Preparation: obtain written consent, explain procedure, instruct client client that fasting fasting may be required for a short period before the exam, assess for iod ine allergy.  Post Procedure: encourage client to drink fluids to facilitate the excretion of contrast material, assess venipuncture site for bleeding or hematoma.  Types of N uclear Cardiology Multigated acquisition (MUGA) or cardiac o blood pool scan  Provides information on wall motion during systole and diastole, cardiac valves, and EF. Single-photon emission computed o tomography tomography (SPECT) Used to evaluate the myocardium at  risk of infarction and to determine infarction size. Positron emission tomography (PET) o scanning  Uses two isotopes to distinguish viable and nonviable myocardial tissue.

6. Phonocardiography  Is a graphic recording of heart sound with simultaneous ECG.


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Perfusion imaging with exercise testing  Determines whether the coronary blood flow changes with with increased activity. Used to diagnose CAD, determine  the prognosis in already diagnosed CAD, assess the physiologic significance of a known coronary lesion, and assess the effectiveness of various therapeutic modalities such as coronary artery bypass surgery, percutaneous coronary intervention, intervention, or thrombolytic therapy.

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CARDIAC DI S ORDE R CORONARY ARTERIAL DISEASE ISCHEMIC HEART DISEASE

D. Hemodynamics Monitoring 1. CVP ( Central Venous Pressure ) Reflects the pressure of the blood in the right atrium.   Engorgement is estimated by the venous column that can be observed as it rises from an imagined angle at th point of manubrium ( angle of Louis).  With normal physiologic condition, the jugular venous column rises no higher than 2-3 cm above the clavicle with the client in a sitting position at 45 degree angle.

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Client Preparation: obtain consent, insertion is under strict sterile technique, usually at the bedside, explain to client the sterile drapes may cover the face, assists to position client flat or slight T-postion as tolerated and instruct to remain still during the procedure Nursing Care During Insertion: Monitor and document HR,BP and ECG during the procedure

Results from the focal narrowing of the large and medium-sized coronary arteries due to deposition of atheromatous plaque in the vessel vessel wall

Stages of Development of Coronary Artery Disease 1. 2. 3.

CVP is a measurement of: - cardiac efficiency - blood volume - peripheral resistance Right ventricular pressure – a catheter is passed from a cutdown in the antecubital, subclavian jugular or basilica vein to the right atrium and attached to a prescribed manometer or tranducer. NORMAL CVP is 2 -8 cm h20 or 2-6 mm Hg Decrease indicates dec. circulating volume, increase indicates inc. blood volume or right heart beat failure. To Measure: patient should be flat with zero point of manometer at the same level of the RA which corresponds to the mid-axillary line of the patient or approx. 5 cm below the sternum. Fluctuations follow patients respiratory function and will fall on inspiration and rise on expiration due to changes in intrapulmonary pressure. Reading should be obtained at the highest point of fluctuation.

Myocardial Injury: Atherosclerosis Myocardial Ischemia: Angina Pectoris Myocardial Necrosis: Myocardial Infarction

I. ATHEROSCLEROSIS ATHEROSCLEROSIS

ARTERIOSCLEROSIS

Narrowing of artery Lipid or fat deposits Tunica intima

Hardening of artery Calcium and protein deposits Tunica media

A. PRESDISPOSING FACTORS 1. Sex: male 2. Race: black 3. Smoking 4. Obesity 5. Hyperlipidemia 6. Sedentary lifestyle 7. Diabetes Mellitus 8. Hypothyroidism 9. Diet: increased saturated fats 10. Type A personality

2. Pulmonary Artery Pressure ( PAP) Monitoring  Appropriate for critically ill clients requiring more accurate assessments of the left heart p ressure  Swan-Ganz Catheter / Pulmonary Artery Catheter is use

B. SIGNS AND SYMPTOMS 1. Chest pain 2. Dyspnea 3. Tachycardia 4. Palpitations 5. Diaphoresis C. TREATMENT Percutaneous Percutaneous Transluminal Transluminal Coronary Angioplasty and Intravascular Intravascular Stenting  Mechanical dilation of the coronary vessel wall by compresing the atheromatous plaque.  It is recommended for clients with single-vessel coronary artery disease.


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Prosthetic intravascular cylindric stent maintain good luminal geometry after ballon deflation and withdrawal. Intravascular stenting is done to prevent restenosis after PTCA

Nursing Management: 

Nitroglycerine is the the drug of choice for relief relief of pain from acute ischemic attacks Instruct to avoid over fatigue  Plan regular activity program  For Saphenous Vein Site:  Wear support stocking 4-6 week postop  Apply pressure dressing or sand bag on the site  Keep leg elevated when sitting 3 Complications of CABG 1. Pneumonia: encourage to perform deep breathing, coughing exercise and use of incentive spirometer 2. Shock 3. Thrombophlebitis

II. ANGINA PECTORIS Transient paroxysmal chest pain produced b y insufficient blood flow to the myocardium myocardium resulting to myocardial myocardial ischemia Clinical syndrome characterized by paroxysmal chest pain that is usually usually relieved by rest or nitroglycerine due to temporary myocardial ischemia Types of Angina Pectoris  

Coronary Arterial Bypass Graft Surgery 



Stable Angina: pain less than 15 minutes, recurrence is less frequent. mins.,but not less Unstable Angina : pain is more than 15 mins.,but than 30 minutes, recurrence is more frequent and the intensity of pain increases. Variant Angina ( Prinzmetal’s Angina ): Chest pain is on longer duration and may occur at rest. Result from coronary vasospasm. that occur when Angina Decubitus: paroxysmal chest pain that the client sits or stand. A.

PRESDISPOSING FACTORS 1. Sex: male 2. Race: black 3. Smoking 4. Obesity 5. Hyperlipidemia 6. Sedentary lifestyle 7. Diabetes Mellitus 8. Hypertension 9. CAD: Atherosclerosis 10. Thromboangiitis Obliterans 11. Severe Anemia 12. Aortic Insufficiency: heart valve that fails to open & close efficiently 13. Hypothyroidism 14. Diet: increased saturated fats 15. Type A personality

B.

PRESIPITATING FACTORS 4 E’s of Angina Pectoris 1. Excessive physical exertion: heavy exercises, sexual activity 2. Exposure to cold environment: vasoconstriction 3. Extreme emotional response: fear, anxiety, excitement, strong emotions 4. Excessive intake of foods or heavy meal

C.

SIGNS AND SYMPTOMS 1. Levine’s Sign: Sign: initial sign that shows the hand clutching the chest 2. Chest pain: characterized by sharp stabbing p ain located at sub sterna usually radiates from neck, back, arms, shoulder and and jaw muscles usually usually relieved by rest or taking nitroglycerine(NTG) 3. Dyspnea 4. Tachycardia 5. Palpitations 6. Diaphoresis

Greater and lesser saphenous veins are commonly used for bypass graft procedures

Objectives of CABG 1. Revascularize myocardium 2. To prevent angina 3. Increase survival rate 4. Done to single occluded vessels 5. If there is 2 or more occluded blood vessels CABG is done Medical and Surgical Nursing

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

D.

E.

F.

DIAGNOSTIC PROCEDURE 1. History taking and physical exam 2. ECG: may reveals ST segment depression & T wave inversion during chest pain 3. Stress test / treadmill test: reveal abnormal ECG during exercise 4. Increase serum lipid levels 5. Serum cholesterol & uric acid is increased



C.

MEDICAL MANAGEMENT 1. Drug Therapy: if cholesterol is elevated Nitrates: Nitroglycerine Nitroglycerine (NTG) Beta-adrenergic blocking agent: Propanolol Calcium-blocking agent: nefedipine Ace Inhibitor: Enapril 2. Modification of diet & other risk factors 3. Surgery: Coronary artery bypass surgery 4. Percutaneuos Transluminal Coronary Angioplasty (PTCA)

 

4. 5. 6. 7. 8.

NURSING INTERVENTIONS 1. Enforce complete bed rest 2. Give prompt pain relievers with nitrates or narcotic analgesic as ordered 3. Administer medications as ordered: A.

Nitroglycerine(NTG): when given in small doses will act as venodilator, but in large doses will act as vasodilator  Give 1st dose of NTG: sublingual 3-5 minutes  Give 2nd dose of NTG: if pain persist after giving 1st dose with interval of 3-5 minutes  Give 3rd& last dose of NTG: if pain still persist at 3-5 minutes interval

9.

NT G Table Tablets ts(sublingual) (sublingual) 

 

 

 

Keep the drug in a d ry place, avoid moisture and exposure to sunlight as it may inactivate the drug Change stock every 6 months Offer sips of water before giving sublingual nitrates, dryness of mouth may inhibit drug absoprtion Relax for 15 minutes after taking a tablet: to prevent dizziness Monitor side effects: orthostatic hypotension, flushed face. Transient headache & dizziness: frequent side effect Instruct the client to rise slowly from sitting position Assist or supervise in ambulation

  

B.

 

Administer oxygen inhalation Place client on semi-to high fowlers position Monitor strictly V/S, I&O, status of cardiopulmonary fuction & ECG tracing Provide decrease saturated fats sodium and caffeine Provide client health teachings and d ischarge planning  Avoidance of 4 E’s  Prevent complication (myocardial infarction)  Instruct client to take medication before indulging into physical exertion to achieve the maximum therapeutic effect of drug  Reduce stress & anxiety: relaxation techniques & guided imagery  Avoid overexertion & smoking Avoid extremes of temperature  Dress warmly in cold weather  Participate in regular exercise program  Space exercise periods & allow for rest periods  The importance of follow up care  Instruct the client to notify the physician immediately if pain occurs & p ersists despite rest & medication administration

Death of myocardial cells from inadequate oxygenation, often caused by sudden complete blockage of a coronary artery Characterized Characterized by localized formation of necrosis (tissue destruction) with subsequent healing by scar formation & fibrosis Heart attack Terminal stage of coronary artery disease characterized characterized by malocclusion, necrosis & scarring. Types of M.I  Transmural Myocardial Infarction: most dangerous type characterized characterized by occlusion of both right and left coronary artery  Subendocardial Myocardial Infarction: characterized by occlusion of either right or left coronary artery

Nitropatch is applied applied once a day, usually in the morning. Avoid placing near hairy areas as it may decrease drug absorption Avoid rotating transdermal patches as it may decrease drug absorption Avoid placing near microwave ovens or during defibrillation as it may lead to burns (most important thing to remember)

The Most Critical Period Following Diagnosis of Myocardial Myocardial Infarction 6-8 hours because majority of death occurs due to arrhythmia leading to premature ventricular contractions (PVC)

Beta-blockers: decreases myocardial oxygen demand by decreasing heart rate, cardiac ou tput and BP Propanolol Metropolol Pindolol Atenolol Assess PR, withhold if dec.PR Administer with food ( prevent GI up set )


Calcium – Calcium – Channel Channel Blockers: relaxes smooth cardiac muscle, reduces coronary vasospasm Amlodipine ( norvasc ) Nifedipine ( calcibloc calcibloc ) Diltiazem ( cardizem ) Assess HR and BP Adminester 1 hour before meal and 2 hours after meal ( foods delay absorption )

III. MYOCARDIAL INFARCTION

N TG Ni trol or or T r ansde ansdermal pat patch ch 

Propanolol: not given to COPD cases: it causes bronchospasm and DM cases: cases: it cause hypoglycemia Side Effects: Nausea and vomiting, mental depression and fatigue

A.

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PREDISPOSING FACTORS 1. Sex: male 2. Race: black 3. Smoking 4. Obesity 5. CAD: Atherosclerotic 6. Thrombus Formation 7. Genetic Predisposition 8. Hyperlipidemia Abejo


9. 10. 11. 12. 13. B.

C.

2. 3.

4. 5. 6.

SIGNS AND SYMPTOMS 1. Chest pain Excruciating visceral, viselike pain with sudden onset located at substernal& rarely in precordial Usually radiates from neck, back, shoulder, arms, jaw & abdominal muscles (abdominal ischemia): severe crushing Not usually relieved relieved by rest or by nitroglycerine 2. N/V 3. Dyspnea 4. Increase in blood pressure & pulse, with gradual drop in blood pressure (initial sign) 5. Hyperthermia: elevated temp 6. Skin: cool, clammy, ashen 7. Mild restlessness & apprehension 8. Occasional findings: Pericardial friction rub Split S1& S2 Rales or Crackles upon auscultation S4 or atrial gallop

7. 8. 9. 10. 11. 12. 13.

DIAGNOSTIC PROCEDURED 1. Cardiac Enzymes CPK-MB: elevated Creatinine phosphokinase(CPK):elevat phosphokinase(CPK):elevated ed Heart only, 12 – 12 – 24 24 hours Lactic acid dehydrogenase(LDH): is increased Serum glutamic pyruvate transaminase(SGPT): is increased Serum glutamic oxal-acetic transaminase(SGOT): transaminase(SGOT): is increased 2. Troponin Test: is increased 3. ECG tracing reveals ST segment elevation T wave inversion Widening of QRS complexes: indicates that there is arrhythmia in MI

4. 5. D.

Sedentary lifestyle Diabetes Mellitus Hypothyroidism Diet: increased saturated fats Type A personality

14. Provide client health teaching & discharge planning concerning: a. Effects of MI healing p rocess & treatment regimen b. Medication regimen including time name purpose, schedule, dosage, side effects c. Dietary restrictions: low Na, low cholesterol, avoidance of caffeine d. Encourage client to take 20 – 20 – 30 30 cc/week of wine, whisky and brandy:to induce vasodilation e. Avoidance of modifiable risk factors f. Prevent Complication Arrhythmia: caused by premature ventricular contraction Cardiogenic shock: late sign is oliguria Left Congestive Heart Failure Thrombophlebitis: homan’s sign Stroke / CVA Dressler’s Syndrome(Post Syndrome(Post MI Synd rome):client is resistant to pharmacological agents: administer 150,000-450,000 units of streptokinase as ordered g. Importance of participation in a pro gressive activity program h. Resumption of ADL particularly sexual intercourse: is 4-6 weeks post cardiac rehab, post CABG & instruct to:

Serum Cholesterol & uric acid: are both increased CBC: increased WBC

NURSING INTERVENTIONS

Goal: Decrease myocardial myocardial oxygen demand 1.

Decrease myocardial workload (rest heart) Establish a patent IV line Administer narcotic analgesic as ordered: Morphine Sulfate IV: provide pain relief(given IV because after an infarction there is poor peripheral perfusion & because serum enzyme would be affected by IM injection as ordered) Side Effects: Respiratory Depression Antidote: Naloxone (Narcan) Side Effects of Naloxone Toxicity: is tremors


Administer oxygen low flow 2-3 L / min: to prevent respiratory arrest or dyspnea & prevent arrhythmias Enforce CBR in semi-fowlers position without bathroom privileges(use bedside commode): commode): to decrease decrease cardiac workload Instruct client to avoid forms of valsalva maneuver Place client on semi fowlers po sition Monitor strictly V/S, I&O, ECG tracing & hemodynamic procedures Perform complete lung / cardiovascular assessment Monitor urinary output & report output of less than 30 ml / hr: indicates decrease cardiac output Provide a full liquid d iet with gradual increase to soft diet: low in saturated fats, Na & caffeine Maintain quiet environment Administer stool softeners as ordered:to facilitate facilitate bowel evacuation & prevent straining Relieve anxiety associated with coronary care unit(CCU)environment Administer medication as ordered: a. Vasodilators:Nitroglycirine Vasodilators:Nitroglycirine (NTG), Isosorbide Dinitrate, Isodil (ISD): sublingual b. Anti Arrythmic Agents: Lidocaine (Xylocane), Brithylium Side Effects: confusion and dizziness c. Beta-blockers: Propanolol (Inderal) d. ACE Inhibitors: Captopril (Enalapril) e. Calcium Antagonist: Nefedipine f. Thrombolytics / Fibrinolytic Agents: Streptokinase, Urokinase, Tissue Plasminogen Activating Factor (TIPAF) Side Effects:allergic reaction, urticaria, pruritus Nursing Intervention: Monitor Monitor for bleeding time g. Anti Coagulant Heparin Antidote: Protamine Sulfate Nursing Intervention: Check Check for Partial Thrombin Time (PTT) Caumadin(Warfarin) Antidote:Vitamin Antidote:Vitamin K Nursing Intervention: Check Check for Prothrombin Time (PT) h. Anti Platelet: PASA (Aspirin): Anti thrombotic effect Side Effects:Tinnitus, Heartburn, Indigestion / Dyspepsia Contraindication:Dengue, Peptic Ulcer Disease, Unknown cause of headache

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j. k.

Make sex as an appetizer rather than dessert Instruct client to assume a non weight bearing position Client can resume sexual intercourse: if can climb or use the staircase Need to report the ff s/sx: Increased persistent chest pain Dyspnea Weakness Fatigue Persistent palpitation Light headedness Enrollment of client in a cardiac rehabilitation rehabilitation program Strict compliance to mediation & importance of follow up care

Aminophylline to reduce bronchospasm caused by severe congestion. Vasodilators to reduce venous return Diuretics to decrease circulating volume V. PERICARDITIS / DRESSLER’S SYNDROME

Is the inflammation of the pericardium which occurs approximately 1 – 1 – 6 6 weeks after AMI. Results as an antigen – antigen – antibody antibody response. The necrotic tissues play the role of an antigen, which trigger antibody formation. Inflammatory process follows. Constrictive Pericarditis is a condition in which a chronic inflammatory thickening of the pericardium compresses the heart so that it is unable to fill normally during diastole.

IV. CARDIOGENIC SHOCK ( POWER/PUMP FAILURE ) A.

SIGNS AND SYMPTOMS 1. Pain in the anterior chest, aggravated by coughing, yawning, swallowing, twisting and turning the torso, relieved by upright, leaning forward position. 2. Pericardial friction rub rub – – scratchy, scratchy, grating or cracking sound 3. Dyspnea 4. Fever, sweating, chills 5. Joints pains 6. Arrhythmias

B.


Is a shock state which result from pro found left ventricular failure usually from massive MI. It result to low cardiac output, thereby systemic hypoperfusion. A.

B.

C.

SIGNS AND SYMPTOMS 1. Decrease systolic BP 2. Oliguria 3. Cold, clammy skin 4. Weak pulse 5. Cyanosis 6. Mental lethargy 7. Confusion

1. 2. 3.

MEDICAL MANAGEMENT 1. Counterpulsation ( mechanical cardiac assistance / diastolic augmentation ) Involves introduction of the intra – intra – aortic aortic balloon catheter via the femoral artery artery Intra Aortic Balloon Pump augments diastole, resulting in increased perfusion of the coronary arteries and the myocardium and a decrease in left ventricular workload. The balloon is inflated during diastole, it is deflated during sytole. Indications: Cardiogenic shock  AMI  Unstable Angina  Open heart surgery 

4. 5.

VI. CARDIAC TAMPONADE

Also known as pericardial tamponade, is an emergency condition in which fluid accumulates in the pericardium (the sac in which the heart is enclosed). If the fluid significantly elevates the pressure on the heart it will prevent the heart's ventricles from filling properly. This in turn leads to a low stroke volume. The end result is ineffective pumping of blood, shock, and often death.


1. 2. 3. 4.

5. 6. 7.

Perform hemodynamic monitoring Administer oxygen therapy Correct hypovolemia. Administer IV fluids as ordered Pharmacology: a. Vasodilators: Nitroglycerine b. Inotropic agents:Digitalis, Dopamine c. Diuretics : Furosemide d. Sodium Bicarbonate, Relieve lactic acidosis Monitor hourly urine output, LOC and arrhythmias Provide psychosocial support Decrease pulmonary edema a. Auscultate lung fields for crackles and wheezes b. Note for dyspnea, cough , hemoptysis hemoptysis and orthopnea c. Monitor ABG for hypoxia and metabolic acidosis d. Place in fowler’s position to reduce venous return e. Administer during therapy as ordered: Morphine sulfate to reduce venous return.


Elevate head of bed, place pillow on the overbed table so that the patient can lean on it. Bed rest Administer prescribed pharmacotherapy. a. ASA to suppress inflammatory process b. Corticosteriods for more severe symptoms Assist in pericardiocentesis if cardiac tamponade is present. Pericardiocentesis Pericardiocentesis is aspiration of blood or fluid from pericardial sac.

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A.

PREDISPOSING FACTORS 1. Chest trauma ( blunt or penetrating ) 2. Myocardial ruptured 3. Cancer 4. Pericarditis 5. Cardiac surgery ( first 24 – 24 – 48 48 hours ) 6. Thrombolytic therapy

B.

SIGNS AND SYMPTOMS 1. Beck’s Triad  Hypotension  Jugular venous distension  Muffled heart sound 2. Pulsus paradoxus ( drop of at least 10 mmHg in arterial BP on inspiration ) 3. Tachycardia 4. Breathlessness 5. Decrease in LOC

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3.

1. 2.

4. 5.

3. 4.

5. 6.

Administer oxygen Elevate head of bed, place pillow on the overbed table so that the patient can lean on it. Bed rest Administer prescribed pharmacotherapy. c. ASA to suppress inflammatory process d. Corticosteriods for more severe symptoms Assist in pericardiocentesis and thoracotomy Pericardiocentesis is aspiration aspiration of blood o r fluid from pericardial sac.

B.

SIGNS AND SYMPTOMS (Venous congestion) 1. Jugular vein distention 2. Pitting edema 3. Ascites 4. Weight gain 5. Hepatosplenomegaly 6. Jaundice 7. Pruritus/ urticaria 8. Esophageal varices 9. Anorexia 10. Generalized body malaise

C.

DIAGNOSTICS 1. CXR – CXR – cardiomegaly cardiomegaly 2. CVP – measures pressure in right atrium; N = 410cc H2O  During CVP: trendelenburg  to prevent pulmo embolism and to promote ventricular filling  Flat on bed post CVP, check CVP readings  fluid challenge Hypovolemia – fluid  diuretics (loop) Hypervolemia – diuretics 3. Echocardiography – Echocardiography – reveals reveals enlarged heart chamber  Muffled heart sounds  cardiomyopathy  Cyanotic heart diseases TOF  “tet” spells  cyanosis with hypoxemia Tricuspid valve stenosis Transposition of aorta Acyanotic  PDA – PDA – machine-like machine-like murmur  DOC: indomethacin  SE: corneal cloudiness 4. Liver enzymes  SGPT up  SGOT up

D.

NURSING MANAGEMENT

CONGESTIVE HEART FAILURE

Inability of the heart to pump blood towards systemic circulation I.

LEFT-SIDED HEART FAILURE A.

PREDISPOSING FACTORS 1. 90% - Mitral valve stenosis  RHD Inflammation of mitral valve Anti-streptolysin O titer (ASO) – (ASO) – 300 300 todd units Penicillin, PASA, steroids  Aging 2. MI 3. IHD 4. HPN 5. Aortic valve stenosis

B.

SIGNS AND SYMPTOMS 1. Pulmonary edema/congestion Dyspnea, PND (awakening at night d/t  difficulty in breathing), 2-3 pillow orthopnea Productive cough (blood tinged)  Rales/crackles  Bronchial wheezing   Frothy salivation 2. Pulsus alternans (A unique pattern during which the amplitude of the pulse changes or alternates in size with a stable heart rhythm.)This is common in severe left ventricular dysfunction.) dysfunction.) 3. Anorexia and general body malaise 4. PMI displaced laterally, cardiomegaly 5. S3 (ventricular gallop)

C.

Goal: increase myocardial contraction  increase CO; Normal CO is 3-6L/min; 3-6L/min; N stroke volume is 60-70ml/h2o

1.

DIAGNOSTICS 1. CXR – – cardiomegaly cardiomegaly 2. PAP – pulmonary pulmonary arterial pressure  Measures pressure in right ventricle  Reveals cardiac status 3. PCWP – pulmonary pulmonary capillary wedge pressure  Measures end-systolic and end-diastolic pressure (elevated) (elevated)  Done through cardiac catheterization (SwanGanz) 4. Echocardiograph – reveals reveals enlarged heart chamber 5. ABG analysis reveals elevated PCO2 and decreased PO2 (respiratory acidosis)  hypoxemia and cyanosis

CVP  reveals fluid status; Normal = 4-10cm H2o; right atrium PAP – PAP – cardiac cardiac status; left atrium ALLEN’S test – collateral collateral circulation Cardiac Tamponade: pulsus paradoxus, muffled heart sounds, HPN

2. 3. 4. 5. 6. 7. 8.

RIGHT SIDED HEART FAILURE A.

PREDISPOSING FACTORS 1. Tricuspid valve stenosis 2. COPD


Administer medications as ordered Cardiac glycosides Digoxin (N=.5-1.5, tox=2)  Tox: Anorexia, N&V; A: Digibind Digitoxin – Digitoxin – given given if (+) ARF; metabolized in liver and not in kidneys Loop diuretics  Lasix – Lasix – IV IV push, mornings Bronchodilators  Aminophylline (theophylline) Tachycardia, palpitations   CNS hyperactivity, agitation  Narcotic analgesics analgesics Morphine sulfate – sulfate – induces induces vasodilation  Vasodilators NTG and ISDN Anti-arrhythmic agents  Lidocaine (SE: dizziness and confusion) Bretyllium   YOU DON’T GIVE BETA-BLOCKERS TO THESE PATIENTS Administer O2 inhalation at 3-4 L/minute via NC as ordered  high flow High fowler’s, fowler’s, 2-3 Pillows Restrict Na and fluids Monitor strictly VS and IO and Breath Sounds Weigh pt daily and assess for pitting edema abdominal girth daily and notify MD provide meticulous skin care care 

Tracheostomy  for severe respiratory distress and laryngospasm  performed at bedside within 10-15 10-15 minutes

II.

Pulmonary embolism (char by chest pain and dyspnea) Pulmonic stenosis Left sided heart failure

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9.

provide a dietary intake which is low in saturated fats and caffeine 10. Institute bloodless phlebotomy  ROTATING TOURNIQUET Rotated clockwise every 15 minutes to promote a decrease in venous return 11. Health teaching and discharge planning Prevent complications : Arrhythmia, Shock,  Thrombophlebitis, MI, Cor pulmonale – RV hypertrophy Regular adherence to medications  Diet modifications  Importance of ffup care 

B.

RISK FACTORS 1. Family history 2. Age 3. High salt intake 4. Low potassium intake 5. Obesity 6. Excess alcohol consumption 7. Smoking 8. Stress

C.

SIGNS AND SYMPTOMS 1. Headache 2. Epistaxis 3. Dizziness 4. Tinnitus 5. Unsteadiness 6. Blurred vision 7. Depression 8. Nocturia 9. Retinopathy

D.

TREATMENT STRATEGIES

HYPERTENSION

Is an abnormal elevation of Bp, systolic pressure above 140 mmHg and or diastolic pressure above 90mmHg at least two readings WHO: BP >160/95 mmHg AHA: BP >140/90 mmHg In hypertension, vasoconstriction – vasospasm – increases PVR – PVR – decrease decrease blood flow to the organ. Target Organs:  Heart : MI, CHF, Dysrhythmias  Eyes: blurred / impaired vision, retinopathy, cataract.  Brain: CVA, encephalopathy  Kidneys : renal insufficiency, RF Peripheral Bloods Vessels – aneurysm,  gangrene

N on-phar on-phar macolo macologi gi c therapy 1. 2. 3. 4. 5. 6. 7.

Stepped Care Progressive addition of drugs to a regimen, o starting with one, usually a diuretic, and adding, in a stepwise fashion, a sympatholytic, vasodilator, and sometimes an ACE inhibitor. Monotherapy Advantageous because of its simplicity, better o patient compliance, compliance, and relatively relatively low incidence of toxicity.

Optimal <120 mmHg / <80 mmHg Recheck in 2 years.

Normal 120-129 mmHg / 80-84 mmHg Recheck in 2 years. High normal 130-139 mmHg / 85-89 mmHg o Recheck in 1 year. Stage 1 (mild) HPN 140-159 mmHg / 90-99 mmHg o Confirm in 2 months. Stage 2 (moderate) HPN 160-179 mmHg / 100-109 mmHg o Evaluate within a month. Stage 3 (severe) HPN 180-209 mmHg / 110-119mmHg o Evaluate within a week. Stage 4 (very severe) HPN 210 mmHg / >/=120 mmHg Evaluate Evaluate o o

A.

CATEGORIES OF ANTI-HYPERTENSIVE ANTI-HYPERTENSIVE DRUGS

Drugs that alter sodium and water balance  Diuretics. Loop diuretics Thiazides Spironolactone and Triamterene

Drugs that alter sympathetic nervous system function  Sympatholytic Sympatholytic drugs. Centrally-acting Centrally-acting sympatholytics  Clonidine  Guanabenz  Guanfacine  Methyldopa Peripherally-acting Peripherally-acting sympatholytics  Guanadrel  Guanethidine  Reserpine a-blockers  Doxazosin  Prazosin b-blockers  Acebutolol - Labetalol Atenolol - Metoprolol   Betaxolol - Nadolol Bisoprolol - Penbutolol  Carteolol - Pindolol  Carvedilol - Propranolol  Esmolol - Timolol 

CLASSIFICATION  Essential / Idiophatic / Primary HPN, accounts for 90 – 95% of all cases of HPN, cause is unknown  Secondary HPN, due to known causes ( Renal failure, Hypertension )  Malignant Hypertension, is severe, rapidly progressive elevation in BP that causes rapid onset of end organ complication  Labile HPN, intermittently elevated BP Resistant HPN, does not respond to usual  treatment White Coat HPN, elevation of B only during  clinic or hospital visits


Low salt diet. Weight reduction. Exercise. Cessation of smoking. Decreased alcohol consumption. Psychological methods: Relaxation / meditation. Dietary decrease in saturated fat.

D r ug therapy therapy

CLASSIFICATION OF BP FOR ADULTS 18 YRS AND OLDER (PHIL. SOCIETY OF HPN)

o

Hypertensive Crisis, situation that requires immediate blood pressure lowering 240mmHg / 120 mmHg

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Vasodilators Direct vasodilators  Diazoxide  Minoxidil  Fenoldopam Calcium channel blockers  Amlodipine  Diltiazem  Felodipine  Isradipine  Manidipine  Lacidipine Lercanidipine 

- Hydralazine - Nitroprusside

- Nifedipine - Nimodipine - Nisoldipine - Nitrendipine - Nicardipine - Verapamil - Gallopamil

AGENTS THAT BLOCK THE PRODUCTION OR ACTION OF ANGIOTENSIN ACE inhibitors   Benazepril - Moexipril  Captopril - Quinapril  Enalapril - Perindopril  Fosinopril - Ramipril  Lisinopril - Trandolapril AT1-receptor blockers  Irbesartan - Losartan  Telmisartan - Valsartan  Candesartan - Eprosartan  Olmesartan DRUGS FOR HYPERTENSIVE EMERGENCIES OR CRISES Trimethaphan 1 mg/ml mg/ml IV infusion; titrate; o instantaneous onset Sodium nitroprusside 5-10 mg/L IV infusion; titrate; o instantaneous onset Diazoxide 300-600 mg Rapid IV push; o instantaneous onset Nifedipine 10-20 mg Sublingual or chewed; o onset within 5-30 min. Labetalol 20-80 mg IV at 10-minute intervals (max.dose: o 300mg); immediate onset MECHANISMS OF DRUG ACTION

PRINCIPLES OF DRUG THERAPY

Monotherapy is generally reserved for mild to moderate HPN; it has gained popularity because of its simplicity, fewer side effects, and improved patient compliance. More severe HPN may require treatment with several drugs that are selected to minimize adverse effects of combined regimen. Treatment is initiated with any of 4 drugs depending on individual patient: Diuretic, b-blocker, b-blocker, ACEI, and a Cachannel blocker; if BP is inadequately controlled, a 2nddrug is then added. HPN may co-exist with other disease that may be aggravated by some of the anti-HPN agents. Lack of patient compliance is the most common reason for failure of anti-HPN therapy; it is important to enhance compliance by carefully selecting a drug regimen that minimizes adverse effects. Therapy is directed at preventing disease that may occur in the future, rather than in relieving present discomfort of the patient.


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NURSING INTERVNTIONS Teaching and Counselli Counselling ng 1. Patient Teaching  Teaching about HPN and its risk factors Stress therapy  Low NA and low saturated fat  Avoid stimulants ( caffeine, alcohol, smoking )  Regular pattern of exercise  Weight reduction if obese  2. Teaching about medication The most common side effects of diuretics are  potassium depletion and and orthostatic hypotension. The most common side effect of the different  antihypertensive drugs is orthostatic hypotension. Take anti – anti – hypertensive hypertensive medications at regular  basis  Assume sitting or lying position for few minutes  Avoid very warm bath  Avoid prolonged sitting and standing  Avoid alcoholic beverages  Avoid tyramine – tyramine – rich rich foods ( proteins ) as follows: ( this may cause hypertensive crisis ) Aged cheese Liver Beer Wine Chocolate Pickles Sausages Soy sauce eventing N on-com on-compliance 3. Pr eve  Inform the client that absence o f symptoms does not indicate control of BP Advise the client against abrupt withdrawal of  medication, rebound hypertension may occur. Device ways to facilitate remembering of  taking medications

D.

MEDICAL / SURGICAL MANAGEMENT 1. Hypertensive Medication 2. Surgery if aneurysm is greater than 4 cm  Teflon graft  Dacron graft  Gortex graft

E.

NURSING INTERVENTIONS 1. Monitor the following  VS  Hemodynamic measurements  Urine output  BUN and creatinine  Bowel sounds  Passage of flatus  Peripheral pulses 2. Promoting Fluid Volume  Check dressing for excessive drainage  Assess for abdominal pain or backpain  Assess Hgb and Hct values

PERIPHERAL VASCULAR DISORDERS

ANEURYSM ARTERIAL ULCERS

It is the localized, irreversible dilatation of an artery secondary to an alteration in the integrity of its wall. Most common type is AAA ( abdominal aortic aneurysm ) The most common cause is hypertension A.

I.

CLASSIFICATIONS Fusiform Aneurysm , involves outpouching of the both side of the artery Saccular Aneurysm , outpouching of only one side  of the artery.  Dissecting Aneurysm, involves separation or tear in the tunica intima and tunica media 

B.

RISK FACTOR 1. Age 2. Tobacco use 3. HPN 4. Atherosclerosis 5. Race 6. Gender 7. Family history

C.

SIGNS AND SYMPTOMS

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

A.

B.

C.

Pulsating mass over abdomen (AAA) Presence of the bruit sound Low back pain Lower abdominal pain Flank pain Shock


THROMBOANGITIS OBLITERANS ( Buerger’s Dse. ) – acute inflammatory condition affecting the smaller and medium sized arteries and veins of the lower extremities. IDIOPATHIC

17

PREDISPOSING FACTORS 1. High risk group  men 30 years old above 2. Chronic smoking SIGNS AND SYMPTOMS  Consistent to all arterial diseases 1. Intermittent claudication – leg pain upon strenuous walking r/t temporary ischemia 2. Cold sensitivity and skin color changes White/pallor  bluish/cyanosis  red/rubor  (+) especially post smoking  3. Decreased peripheral peripheral pulses’ volume particularly in dorsalis pedis and posterior tibial 4. Trophic changes 5. Ulceration 6. Gangrene formation DIAGNOSTICS 1. Oscillometry – reveals a decrease in peripheral pulse volume 2. Doppler UTZ – decrease decrease in blood flow to affected extremity 3. Angiography – site site and extent of malocclusion

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D.

II.

NURSING MANAGEMENT 1. Encourage slow progressive physical activity  Walking 3-4x/day Out of bed 3-4x/day  2. Medications as ordered Analgesics  Vasodilators  Anticoagulants  3. Instruct patient to avoid smoking and exposure to cold environment 4. Institute foot care management Avoid barefoot walking  Straight nails   Lanolin cream for feet (-) constricting clothes  5. Assist in surgery: BKA

PREDISPOSING FACTORS 1. Hereditary 2. Congenital weakness of veins 3. Thrombophlebitis 4. Cardiac diseases 5. Pregnancy 6. Obesity 7. Prolonged immobility  prolonged standing and sitting

B.

SIGNS AND SYMPTOMS 1. Pain after prolonged standing 2. Dilated tortuous skin veins which are warm to touch 3. Heaviness in the legs

C.

DIAGNOSTICS 1. Venography 2. Trendelenburg’s Trendelenburg’s test – reveals that veins distend quickly < 35 seconds  incompetent valves

D.

NURSING MANAGEMENT (consistent to all venous ulcers) 1. Elevate legs above heart level  increased venous return (2-3 pillow elevation) 2. Measure circumference of leg to determine swelling 3. Anti-embolic stocking, full support panty hose 4. Medications as ordered  analgesics 5. Assist in surgery  Vein stripping and ligation (more effective, no recurrence)  Sclerotherapy For spider-web varicosities Cold solution injection  SE: thrombosis

characterized by acute episodes REYNAULD’S DISEASE – characterized of arterial spasms involving the digits of hands and fingers

II. A.

B.

C.

D.

PREDISPOSING FACTORS 1. High risk group  women 40 years old up 2. Smoking 3. Collagen diseases SLE  RA  4. Direct hand trauma Piano playing  Excessive typing (tsk tsk! Lagot!)  Carpal tunnel syndrome  Operating chainsaw (nyek!)  Writing (tsk tsk, kaya dapat may module eh!  Grr!) SIGNS AND SYMPTOMS 1. Intermittent claudication 2. Cold sensitivity and skin color changes  White/pallor  bluish/cyanosis  red/rubor  (+) especially post smoking 3. Trophic changes 4. Ulceration 5. Gangrene formation DIAGNOSTICS 1. Oscillometry – reveals a decrease in peripheral pulse volume 2. Angiography – site site and extent of malocclusion NURSING MANAGEMENT 1. Administer medications as ordered  Analgesics  Vasodilators 2. Encourage pt to wear gloves 3. Instruct: avoid smoking and exposure to cold environment

VENOUS ULCERS

I.

A.

THROMBOPHLEBITIS / DEEP VEIN THROMBOSIS (DVT) A.

PREDISPOSING FACTORS 1. Smoking 2. Obesity 3. Prolonged use of OCPs 4. Chronic anemia 5. Diet high in saturated fats 6. DM 7. CHF 8. MI 9. Post-cannulation (insertion of various catheters) 10. Post-surgical operation 11. Sedentary lifestyle

B.

SIGNS AND SYMPTOMS 1. Pain at the affected extremity 2. Presence of cyanosis 3. Dilated tortuous veins 4. (+) HOMAN’ HOMAN’S S  pain on calf on do rsiflexion

C.

DIAGNOSTICS 1. Venography 2. Doppler UTZ 3. Angiography

D.

NURSING MANAGEMENT 1. Elevate the legs above heart level 2. Apply warm moist pack to relieve lymphatic congestion 3. Measure circumference of leg muscles to determine if it is swollen 4. Anti-embolic stockings 5. Administer medications as ordered  Analgesics Anticoagulants – Anticoagulants – heparin heparin  6. Prevent complications Pulmonary embolism 

abnormal dilation of the veins of the VARICOSE VEINS – abnormal lower extremities d/t incompetent valves leading to increased venous pooling and venostasis  decreased venous return


18

Abejo

Cardio Nursing.pdf

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