THE CARDIOVASCULAR SYSTEM

The Cardiovascular System

y A closed system of the heart and blood vessels
y The heart pumps blood y Blood vessels allow blood to circulate to all parts of the body

y The function of the cardiovascular system is to deliver oxygen and nutrients and to remove carbon dioxide and other waste products
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The Heart

y Location
y Thorax between the lungs y Pointed apex directed toward left hip

y About the size of your fist

The Heart

Figure 11.1

Overview: Heart
Muscular pumping organ of the body Occupies most of the L mediastinum Weighs < 1 lb; approx. 300-400 g Resembles a closed fist Covered by serous membrane
Pericardium (parietal and visceral) - Serous fluid fills the space between the layers of pericardium Pericardial fluid = 10-20 cc; prevents friction rub

Overview: Heart
Layers Epicardium- outermost Myocardium- middle Endocardium- innermost

The Heart: Heart Wall

y Three layers
y Epicardium
y Outside layer y Connective tissue layer

y Myocardium
y Middle layer y Mostly cardiac muscle

y Endocardium
y Inner layer y Endothelium
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The Heart: Coverings

y Pericardium a double serous membrane
y Visceral pericardium y Next to heart y Parietal pericardium y Outside layer

External Heart Anatomy

Chambers 2 Atria- upper -receiving/collecting chambers 2 Ventricles- lower -pumping/contracting/ discharging chambers
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The Heart: Chambers

y Right and left side act as separate pumps y Four chambers
y Atria y Receiving chambers
y Right atrium y Left atrium

y Ventricles y Discharging chambers

y Right ventricle y Left ventricle
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Valves Prevent blood backflow Promote unidirectional flow

Overview: Heart

AV valves Tricuspid and Mitral Guards opening between atria and ventricles Closure p S1 sound Semilunar valves Pulmonic and Aortic Closure p S2 sound *Extra heart sounds: S3 (Ventricular gallop) p CHF S4 (Atrial gallop) p MI
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The Heart sounds 1. S1- due to closure of the AV valves 2. S2- due to the closure of the semilunar valves 3. S3- due to increased ventricular filling 4. S4- due to forceful atrial contraction

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The Heart: Valves

y Allow blood to flow in only one direction y Four valves
y Atrioventricular valves between atria and ventricles
y Bicuspid valve (left) y Tricuspid valve (right)

y Semilunar valves between ventricle and artery

y Pulmonary semilunar valve y Aortic semilunar valve
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The Heart: Valves

y Valves open as blood is pumped through y Held in place by chordae tendineae (heart strings) y Close to prevent backflow

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Operation of Heart Valves

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Blood Circulation

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Blood Circulation
Pulmonary circuit (from the heart to lungs then back to heart) RA Tricuspid Valve RV Pulmonic Valve PA Lungs PV LA Mitral Valve LV Aortic Valve Systemic Circuit circulation of blood to all body tissues via aorta parts of the body
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Coronary Circulation
y Blood in the heart chambers does not nourish the myocardium y The heart has its own nourishing circulatory system
y Coronary arteries y Cardiac veins y Blood empties into the right atrium via the coronary sinus
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Overview: Heart
Coronary Arteries Arises from base or aorta R and L main coronary arteries p supplies blood to myocardium (for nourishment)

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The Cardiovascular System

The Blood supply of the heart comes from the Coronary arteries 1. Right coronary artery 2. Left coronary artery

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Blood Vessels
1. Right coronary artery a. posterior interventricular b. marginal artery - supplies the RIGHT atrium, RIGHT ventricle, inferior portion of the LEFT ventricle, the POSTERIOR septal wall and AV (90%) and SA node (55%)
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2. Left coronary artery anterior interventricular a. circumflex arteries - left atrium and the posterior LEFT ventricle b. Left anterior descending artery anterior wall of the LEFT ventricle, the anterior septum and the Apex of the left ventricle
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The Coronary Arteries

Coronary Artery and its Branches Portion of Myocardium Supplied Portion of Conduction System Supplied

Right Posterior descending Right margin (AV nodal) Left Anterior descending (LAD) Circumflex (LCX)

Right atrium Inferior wall of right ventricle anterior surface of left ventricle Anterior surface of left ventricle Left atrium Lateral wall of left ventricle Part of right ventricle

AV node (90% of population) SA node ( > 55%) Bundle of His Posterior division of left bundle branch AV node (10%) SA node (45%) All bundle branches

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The Cardiovascular System

The venous drainage of the heart 1. Cardiac veins 2. Coronary sinus cardiac veins drain into the coronary sinus which in turn drain into right atrium
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The Heart: Conduction System

y Intrinsic conduction system (nodal system)

y Heart muscle cells contract, in a regular, continuous way

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Myocardial Cells
Myocardial Cell Types
Kinds of Cardiac Cells Myocardial cells Where Found Primary Function Primary Property Contractility

Contraction and Myocardium Relaxation Electrical conductio n system Generation and conduction of electrical impulses

Specialized cells of the electrical conduction system

Automaticity Conductivity

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The Heart: Conduction System

y Special tissue sets the pace y Sinoatrial node y Pacemaker y Atrioventricular node y Atrioventricular bundle y Bundle branches y Purkinje fibers
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Conduction System SA node Located at the junction of SVC and RA Primary pacemaker p 60-100 bpm AV node Located at interatrial septum There is a delay of electrical impulse of 0.08 millisec. To allow ventricular filling Bundle of His Located at interventricular septum Divides into R and L main bundle branches Purkinje fibers Located at the walls of ventricles p ventricular contraction

Overview: Heart

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Heart Contractions

y Contraction is initiated by the sinoatrial node y Sequential stimulation occurs at other auto rhythmic cells

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SA Node
natural pacemaker for the heart 60-100 impulses/min Junction of the right atrium and SVC sends the electrical impulse that triggers each heartbeat.

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AV Node
Located at the right atrial wall near tricuspid valve 40-60 impulses/min Receives impulse from the sinoatrial node atrioventricular node in turn sends an impulse through the nerve network to the ventricles.
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Purkinje system
Bundle of His Right and left bundle branch Purkinje fibers

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Physiology of conduction
Electrical activity due to movement of ions Resting state, inside cell membrane (-); outside cell membrane (+) Initiation of electrical impulse, Na moves inside, K goes outside to begin Depolarization (electrical activation of cell) Inside cell membrane, more (+) Stimulus incites neighboring cells to depolarize as well Contraction follows
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Repolarization (resting state) Refractory period phase where muscle cannot be restimulated to contract; protect heart from tetany 1. Absolute refractory period cannot be restimulated regardless of strength of stimuli 2. Relative refractory period stronger than normal stimulus can incite muscle to contract

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CARDIAC CYCLE
sequence of events that occur when the heart beats

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The Heart: Cardiac Cycle

y Atria contract simultaneously y Atria relax, then ventricles contract y Diastole = relaxation y Systole = contraction
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diastole
Ventricles are relaxed AV valves open Blood empties to atria then to ventricles End of diastole, atria contract d/t SA node Atrial pressure rises ejecting blood to ventricles

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systole
Ventricular pressure rises AV valves close Blood ceases flowing from atria into ventricles and regurgitation into atria is prevented Rise in ventricular pressure opens semilunar valves Blood ejected into pulmonary artery and aorta End of systole, ventricular pressure decreases Pulmonary and aortic pressure decreases Closure of semilunar valves
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Filling of Heart Chambers the Cardiac Cycle

49

The Heart: Cardiac Cycle

y Cardiac cycle events of one complete heart beat
y Mid-to-late diastole blood flows into ventricles y Ventricular systole blood pressure builds before ventricle contracts, pushing out blood y Early diastole atria finish re-filling, ventricular pressure is low
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The Heart: Cardiac Output

y Cardiac output (CO)
y Amount of blood pumped by each side of the heart in one minute y CO = heart rate x stroke volume y CO = HR x SV

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Cardiac Output Regulation

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 Stroke volume
Volume of blood pumped by each ventricle in one contraction; amount of blood ejected per heartbeat Average resting stroke volume: 70 ml

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STROKE VOLUME
1. Preload degree of stretch at the end of diastole Inc volume inc stretch inc preload greater contraction and inc stroke volume Increased by inc blood volume and exercise, dec by diuretics 2. Afterload amount of resistance to ejection of blood from ventricle Also called systemic vascular resistance Inverse relationship with stroke volume

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3. Contractility force generated by contracting myocardium - Enhanced by SNS, digitalis, dopamine and dobutamine

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HEART RATE affected by ANS, baroreceptor activity, cathecolamines, thyroid hormone Tachycardia > 100 bpm Bradycardia < 60 bpm

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The Heart: Regulation of Heart Rate

y Increased heart rate
y Sympathetic nervous system y Crisis y Low blood pressure y Hormones y Epinephrine y Thyroxine y Exercise y Decreased blood volume
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The Heart: Regulation of Heart Rate

Decreased heart rate
Parasympathetic nervous system High blood pressure / blood volume Decreased venous return

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Blood Pressure
Cardiac output X peripheral resistance Control is neural (central and peripheral) and hormonal Hormones- ADH, aldosterone, epinephrine can increase BP; ANF/ ANP can decrease BP Baroreceptors in the carotid and aorta
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Baroreceptor reflexes - carotid sinus and aortic arch - causes vasoconstriction and increased blood pressure Dec arterial pressure SNS inc cardiac rate, contraction, contractility, circulating blood volume, constriction of renal arterioles and increased aldosterone
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- increased pressure on the arteries due to the contraction of the ventricles (heart pumping) - systolic pressure. - decreased pressure due to the relaxation of the ventricles (heart resting) - diastolic pressure. - Blood pressure is measured in mm mercury, with the systole in ratio to the diastole.

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 PERIPHERAL RESISTANCE - amount of friction encountered by blood as it flows through blood vessels -increased by constriction of blood vessels d/t SNS activity/ atherosclerosis, blood viscosity, blood volume; when increased along w/ cardiac output, inc BP

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Blood Pressure
y Measurements by health professionals are made on the pressure in large arteries
y Systolic pressure at the peak of ventricular contraction y Diastolic pressure when ventricles relax

y Pressure in blood vessels decreases as the distance away from the heart increases
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Blood Pressure: Effects of Factors

y Neural factors
y Autonomic nervous system adjustments (sympathetic division)

y Renal factors
y Regulation by altering blood volume y Renin hormonal control

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Blood Pressure: Effects of Factors

y Temperature
y Heat has a vasodilation effect y Cold has a vasoconstricting effect

y Chemicals
y Various substances can cause increases or decreases

y Diet
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Factors Determining Blood Pressure

Figure 11.19

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 ARTERIAL PULSE - alternating expansion and recoil of an artery w/ each beat of the left ventricle; creates a wave w/c travels through entire arterial system 60- 100 bpm influenced by activity, postural changes, and emotions temporal, facial, carotid, brachial, radial, femoral, popliteal, posterior tibial, dorsalis pedis a.
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Pulse
y Pulse pressure wave of blood y Monitored at pressure points where pulse is easily palpated
69 Slide 11.35

Vascular System

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COMPONENT PARTS
A. Blood vascular system Taking blood to the tissues and back y y y y y Arteries Arterioles Capillaries Venules Veins

B. Lymph vascular system lymphatic capillaries lymphatic vessels main lymphatic trunks: thoracic duct, right lymphatic duct lymphoid organs
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 arteries are vessels that carry blood away from the heart to the periphery The veins are the vessels that carry blood to the heart The capillaries are lined with squamous cells, they connect the veins and arteries lymphatic system collects extravasated fluid from the tissues and returns it to the blood
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MAJOR ARTERIES OF THE SYSTEMIC CIRCULATION

Aorta ascending, arch (left carotid, left subclavian and brachioephalic trunk gives rise to right common carotid and right subclavian; ), descending branch Subclavian artery axilary, brachial, radial, ulnar Common carotid artery - (internal. External, thoracic and abdominal aorta) Abdominal aorta branches into Common iliac internal and external iliac artery (femoral, popliteal, tibial, dorsalis pedis)
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Major Arteries of Systemic Circulation

Figure 11.11

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MAJOR VEINS OF THE SYSTEMIC CIRCULATION

1. Superior vena cava drains the head and upper extremities 2. Inferior vena cava drains the abdomen, pelvis & lower limbs 3. coronary sinus is large vein draining the heart muscle back into the heart Veins of the Head and Neck 1. External and Internal jugular veins drain the head and neck into the superior vena cava 2. Dural venous sinuses empty into internal jugular vein
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Major Veins of Systemic Circulation

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yBLOOD VESSEL: ANATOMY

yThree layers (tunics) yTunica intima ySingle layer of smooth endothelial cells yTunica media ySmooth muscle cells yControlled by sympathetic nervous system yAllows vessel to vasoconstrict and vasodilate yTunica adventitia/ externa yMostly fibrous connective tissue
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The Vascular System

Figure 11.8b

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Differences Between Blood Vessel Types

y Walls of arteries are the thickest y Lumens of veins are larger y Skeletal muscle milks blood in veins toward the heart y Walls of capillaries are only one cell layer thick to allow for exchanges between blood and tissue
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Movement of Blood Through Vessels

y Most arterial blood is pumped by the heart y Veins use the milking action of muscles to help move blood
(valves)
80 Slide 11.27

Capillary Beds
y Capillary beds consist of two types of vessels
y Vascular shunt directly connects an arteriole to a venule

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Capillary Bed
Diffusion at Capillary Beds
y True capillaries exchange vessels y Oxygen and nutrients cross to cells y Carbon dioxide and metabolic waste products cross into blood
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ASSESSMENT

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ASSESSMENT
Subjective Data Objective Data

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The Cardiovascular System

Cardiac History Interview Focused assessment

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CARDIAC ASSESSMENT
Health History Obtain description of present illness and the chief complaint Chest pain or discomfort Shortness of breath/ dyspnea Edema and weight gain Palpitations Fatigue Dizziness and syncope or LOC Assess risk factors
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Cardiovascular Assessment
Cardiac signs and symptoms
Chest Pain Most common Due to Ischemia or MI, angina, valvular disease Angina, Precipitated by stress or can be relieved by Nitroglycerin (NTG) In MI, it is more intense, unrelated to activities and cant be relieved by NTG If it occurs during breathing, suspect respiratory problems
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Cardiac & Non Cardiac Causes of CHEST PAIN

ANGINA PECTORIS Substernal/ retrosternal spreasing across the chest; may radiate to inside of arm, neck, or jaw 5-15 min Usually related to exertion, emotion, eating, cold Relieved with rest, nitroglycerine, oxygen MYOCARDIAL INFARCTION Substernal pain or pain over the precordium; may spread widely throughout the chest; may have pain in shoulders and hands >15 min Occurs spontaneously or sequela to unstable angina Relieved by Morphine SO4, successful reperfusion of blocked coronary artery

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CHEST PAIN
PERICARDITIS Sharp, severe, substernal, to the left of the sternum; may be felt in the epigastrium; may be referred to neck, arms and back Intermittent Sudden; increases with inspiration, swallowing, coughing, rotation of the trunk Relieved by analgesia, sitting upright, antiinflammatory medications PLEURITIC PAIN Pain arises from inferior portion of pleura; may be referred to costal margins or upper abdomen; patient may be able to localize pain 30+ min Occurs spontaneously; increases with inspiration Relieved with rest, time, treatment of underlying cause, bronchodilators

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CHEST PAIN
ANXIETY Pain over chest, may be variable; does not radiate; patient may complain of numbness, tingling of the hands and mouth 2-3 min Stress, emotion Relieved with removal of the stimulus, relaxation ESOPHAGEAL PAIN (Reflux esophagitis or spasm, hiatal hernia) Substernal pain; may be projected around chest to shoulders 5-60 min Precipitated by recumbency, cold, liquids, exercise; may occur spontaneously Relieved with food/ antacid; NTG relieves spasm

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Dyspnea Difficulty of breathing subjective feeling (inability to get enough air) May be due to MI, HF Dyspnea on exertion is due to increased O2 myocardial demand. Orthopnea (DOB while lying down) is related to blood pooling in the pulmonary bed; suspect Pulmonary Edema. Any sudden or acute dyspnea may be a sign of Pulmonary Embolism Paroxysmal nocturnal dyspnea (PND): person suddenly awakens, is sweating and is having DOB.

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Cyanosis Bluish discoloration of the skin and mucous membrane Sat O2 is below 94% Fatigue May be due to Anemia or related to decreased Cardiac Output, severe cardiovascular disorder
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Palpitations Awareness of rapid or irregular heart beat Autonomic Nervous System and Adrenal Glands response (stress) Syncope Transient loss of consciousness Due to decreased cerebral tissue perfusion
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Edema May be due to HF Due to: Increased Hydrostatic Pressure (HP) Decreased Colloidal Oncotic Pressure (COP) Obstructed Lymphatic or Vascular System Related to Inflammatory reaction
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 Bilateral edema = CHF or Renal Failure Unilateral edema = Vascular or Lymphatic obstruction Non-pitting edema = Inflammatory Pitting edema = HP and COP derangement
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History
Health perception and management - how patient perceives his current health status; risk factors Nutrition and metabolism height, weight, eating habits; BP, lab results; fod preferences - impt: dietary modification, exercise, weight loss (HPN, hyperlipidimia, hyperglycemia) Elimination nocturia (awakening at night to urinate- HF) -straining/ Valsalva maneuver dec HR Activity and exercise changes in pattern of activity in the last 6 -12 months; exercise/ cardiac rehab program

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History
Sleep and rest PND (awakening short of breath at night), nocturnal angina (awakening with angina) - HF Cognition and perception- read/ comprehend (determine the patients mental capacity to manage safe and effective selfcare) Self perception & self concept Type A behavior Roles and relationships support systems Sexuality and reproduction- changes in sexual activity: fear of another attack/ sudden death, untoward symptoms, impotence, depression; advised against pregnancy Coping and stress tolerance- stressors and coping ability Prevention strategies- identify patients modifiable risk factors and measures taken by the patient to prevent disease

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RISK FACTORS FOR HEART DISEASE

NONMODIFIABLE RISK FACTORS (+) Family History for premature coronary artery disease Gender ( men and postmenopausal women) Race (> incidence in African Americans than in Caucasians)
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RISK FACTORS FOR HEART DISEASE

MODIFIABLE RISK FACTORS Hyperlipidemia Hypertension Cigarette smoking Elevated blood glucose level (ie, DM) Obesity Physical inactivity Type A personality characteristics, particularly hostility Use of oral contraceptives
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CARDIAC ASSESSMENT
Physical Examination - Performed to confirm the data obtained in the health history - Should include the evaluation of the following: a. Effectiveness of the heart as a pump (dec if reduced pulse pressure, cardiac enlargement, murmurs and gallop)

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CARDIAC ASSESSMENT
b. Filling volumes and pressures - Estimated by the degree of jugular vein distention and the presence or absence of congestion in the lungs, peripheral edema and postural changes in BP that occur when the individual sits up or stands

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CARDIAC ASSESSMENT
c. Cardiac output - Reflected by cognition, heart rate, pulse, pressure, color and texture of the skin and urine output d. Compensatory mechanisms e.g., to help maintain cardiac outputincreased filling volume and elevated heart rate 103

CARDIAC ASSESSMENT
Findings on PE -correlated with data obtained from diagnostic procedures, such as hemodynamic monitoring (use of monitoring devices to measure cardiovascular function; e.g., CVP)

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CARDIAC ASSESSMENT
Physical examination covers:
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. General appearance Cognition Skin Blood pressure Arterial pulses Jugular venous pulsation and pressures Heart Extremities Lungs abdomen
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General Appearance and Cognition

Indication of hearts ability to propel oxygen to the brain (cerebral perfusion) Patients level of distress Level of consciousness Thought processes Put the anxious patient at ease. (Emotional effects on CV status)
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Inspection of the skin

Pallor- lack of oxyhemoglobin; result of anemia or decreased arterial perfusion Peripheral cyanosis- decreased flow rate of blood to a particular area; bluish tinge of the nails, skin of the nose, lips, extremities and earlobes; in HF; anxiety; may be normal in peripheral vasoconstriction associated with a cold environment Central cyanosis- bluish tinge in the tongue and buccal mucosa; venous blood passes through the pulmonary circulation without being oxygenated; serious cardiac disorder, eg, pulmonary edema, CHD
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Inspection of the skin

Xanthelasma- yellowish, slightly raised plaques in the skin; along the nasal portion of 1 or both eyelids and may indicate elevated cholesterol levels (hypercholesterolemia) Reduced skin turgor- dehydration and aging Temperature and moistness- normal: skin is warm and dry; under stress: cool and moist; cardiogenic shock: cold and clammy; MI: diaphoresis
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Inspection of the skin

Ecchymosis- bruise, purplish-blue color fading to green, yellow or brown over time -blood outside the vessels; caused by trauma; unexplained ecchymosis in patients with anticoagulant therapy (prolonged clotting time- PT & PTT) Wounds, scars and tissue surrounding implanted devices- adequate healing; thinning (erosion)

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BP
Affected by cardiac output, distention of arteries, volume, velocity and viscosity of the blood Normal adult values: (?) 100/60 to 140/90 mmHg Hypertension hypotension
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Pulse pressure
Difference b/w systolic and diastolic pressures Normal: 30 40 mmHg How well the patient maintains cardiac output Increased in - conditions that elevate the SV (anxiety, exercise, bradycardia); reduce systemic vascular resistance (fever); reduce distensibility of the arteries (atherosclerosis, aging, HPN) Decreased in -abnormal condition reflecting reduced SV, ejection velocity (shock, HF, hypovolemia, mitral regurgitation) or obstruction to the blood flow during systole (mitral/ aortic stenosis)
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Postural Blood Pressure Changes

Postural orthostatic hypotension BP drops significantly after the patient assumes an upright position accompanied by dizziness, lightheadedness, or syncope Normal: HR inc of 5- 20 bpm above resting rate unchanged systolic pressure or slight decrease of up to 10 mmHg slight increase of 5 mmHg in diastolic pressure
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Postural Blood Pressure Changes

Suspect decrease in the amount of blood or fluid increased HR and either a decrease in systolic pressure by 15 mmHg or a drop in diastolic pressure by 10 mmHg

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Arterial Pulses
Pulse rate Pulse rhythm pulse deficit: radial vs apical (atrial fibrillation, atrial flutter, PVC, heart block) Pulse Quality: 0 - +4 (absent to strong/ bounding Pulse configuration
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Jugular Venous pulsations

Internal jugular vein Not apparent 30 degrees (+) obvious distention with the patients head at 45 90 degrees: abnormal increase in volume of the venous system Right sided HF (less common: obstruction of BF to SVC; acute massive pulmonary embolism)
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Heart Inspection & Palpation

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Surface Anatomy

Auscultation

Tricuspid Valve

lies behind right half of the right half of the lower end sternum; opposite the 4th of the body of the ICS sternum lies behind the left half of apex beat (5th LICS MCL) the sternum; opposite the 4th costal cartilage Lies behind the medial end Medial end of the 2nd left of the 3rd left costal cartilage ICS & the adjoining part of the sternum Behind left half of sternum; Medial end of the 2nd right opposite 3rd ICS ICS
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Mitral Valve

Pulmonary Valve

Aortic Valve

Cardiac IPPA
Inspection and Palpation PMI (left 5th ICS MCL) Bruits and Thrills murmurlike; vascular in origin palpate a thrill, auscultate a bruit Percussion displaced apical pulse
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Heart Sounds
S1 - closure of AV valves (lub); apex of heart S2 - closure of SL valves (dub); base of the heart S3 rapid diastolic filling; heard after S2; normal in children and young adults; may be heard when ventricles fail to eject all of their blood on systole S4 is heard prior to S1; atrial contraction; associated w/ CAD, HPN, aortic stenosis
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Heart Sounds
Murmurs - turbulence of blood flow; if positive watch out for FVE and regurgitation; normal until 1 year old Pericardial Friction Rub -grating sound; suspect pericardial effusion if this is heard Muffled Heart Sound - if positive rule out Cardiac Tamponade and other similar problems like Effusion

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Extremities
Extremities capillary refill, edema, loss of pulse, vascular changes (numbness, decrease in temperature, pain, pallor) Clubbing CHD

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OTHER SYSTEMS: Abdomen hepatomegaly d/t RVF - liver engorgement - decreased urine output Lungs: tachypnea (HF/ pain) hemoptysis (acute pulmonary edema) Cheynes Stokes respiration LVF dry hacking cough HF pulmonary congestion Crackles- HF Wheezing- pulmonary edema
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CARDIAC ASSESSMENT
3. Laboratory and diagnostic studies CBC Cardiac catheterization Lipid profile Arteriography Cardiac enzymes and proteins CXR CVP ECG Holter monitoring Exercise ECG

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The Cardiovascular System Laboratory Test Rationale 1. To assist in diagnosing MI 2. To identify abnormalities 3. To assess inflammation

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The Cardiovascular System Laboratory Test Rationale 4. To determine baseline value 5. To monitor serum level of medications 6. To assess the effects of medications
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LABORATORY PROCEDURES
CARDIAC Proteins and enzymes

CK- MB ( creatine kinase) Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 days
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LABORATORY PROCEDURES
CARDIAC Proteins and enzymes

CK- MB ( creatine kinase) Normal value is 0-7 U/L

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LABORATORY PROCEDURES
CARDIAC Proteins and enzymes

Lactic Dehydrogenase (LDH) Elevates in MI in 24 hours, peaks in 48-72 hours Normally LDH2 is greater than LDH1
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LABORATORY PROCEDURES
CARDIAC Proteins and enzymes

Lactic Dehydrogenase (LDH) MI- LDH1 greater than LDH2 (flipped LDH pattern) Normal value is 70-200 IU/L

138

LABORATORY PROCEDURES
CARDIAC Proteins and enzymes

Myoglobin Rises within 1-3 hours Peaks in 4-12 hours Returns to normal in a day
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LABORATORY PROCEDURES
CARDIAC Proteins and enzymes

Myoglobin Not used alone Muscular and RENAL disease can have elevated myoglobin

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LABORATORY PROCEDURES Troponin I and T Troponin I is usually utilized for MI Elevates within 3-4 hours, peaks in 4-24 hours and persists for 7 days to 3 weeks! Normal value for Troponin I is less than 0.6 ng/mL
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LABORATORY PROCEDURES
Troponin I and T REMEMBER to AVOID IM injections before obtaining blood sample! Early and late diagnosis can be made!
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LABORATORY PROCEDURES SERUM LIPIDS Lipid profile measures the serum cholesterol, triglycerides and lipoprotein levels Cholesterol= 200 mg/dL Triglycerides- 40- 150 mg/dL

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LABORATORY PROCEDURES

SERUM LIPIDS LDL- 130 mg/dL HDL- 30-70- mg/dL NPO post midnight (usually 12 hours)
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LABORATORY PROCEDURES ELECTROCARDIOGRAM (ECG) A non-invasive procedure that evaluates the electrical activity of the heart Electrodes and wires are attached to the patient
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LABORATORY PROCEDURES

ELECTROCARDIOGRAM (ECG) Tell the patient that there is no risk of electrocution Avoid muscular contraction/movement
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LABORATORY PROCEDURES Holter Monitoring A non-invasive test in which the client wears a Holter monitor and an ECG tracing recorded continuously over a period of 24 hours
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The Cardiovascular System LABORATORY PROCEDURES Holter Monitoring Instruct the client to resume normal activities and maintain a diary of activities and any symptoms that may develop

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LABORATORY PROCEDURES
ECHOCARDIOGRAM Non-invasive test that studies the structural and functional changes of the heart with the use of ultrasound No special preparation is needed

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LABORATORY PROCEDURES Stress Test A non-invasive test that studies the heart during activity and detects and evaluates CAD Exercise test, pharmacologic test and emotional test
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The Cardiovascular System LABORATORY PROCEDURES Stress Test Treadmill testing is the most commonly used stress test Used to determine CAD, Chest pain causes, drug effects and dysrhythmias in exercise
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The Cardiovascular System LABORATORY PROCEDURES Stress Test Pre-test: consent may be required, adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine

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The Cardiovascular System LABORATORY PROCEDURES 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

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The Cardiovascular System LABORATORY PROCEDURES Pharmacological stress test Use of dipyridamole Maximally dilates coronary artery Side-effect: flushing of face

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LABORATORY PROCEDURES Pharmacological stress test Pre-test: 4 hours fasting, avoid alcohol, caffeine Post test: report symptoms of chest pain

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LABORATORY PROCEDURES CARDIAC catheterization Insertion of a catheter into the heart and surrounding vessels Determines the structure and performance of the heart valves and surrounding vessels

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LABORATORY PROCEDURES CARDIAC catheterization Used to diagnose CAD, assess coronary artery patency and determine extent of atherosclerosis

161

LABORATORY PROCEDURES Pretest: Ensure Consent, assess for allergy to seafood and iodine, NPO, document weight and height, baseline VS, blood tests and document the peripheral pulses

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LABORATORY PROCEDURES

Pretest: Fast for 8-12 hours, teachings, medications to allay anxiety

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LABORATORY PROCEDURES 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

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LABORATORY PROCEDURES 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

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LABORATORY PROCEDURES Maintain strict bed rest for 6-12 hours Client may turn from side to side but bed should not be elevated more than 30 degrees and legs always straight Encourage fluid intake to flush out the dye Immobilize the arm if the antecubital vein is used Monitor for dye allergy

166

LABORATORY PROCEDURES CVP The CVP is the pressure within the SVC Reflects the pressure under which blood is returned to the SVC and right atrium

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LABORATORY PROCEDURES CVP Normal CVP is 0 to 8 mmHg or 4-10 cm H2O

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LABORATORY PROCEDURES CVP Elevated CVP indicates increase in blood volume, excessive IVF or heart/renal failure

169

LABORATORY PROCEDURES CVP Low CVP may indicate hypovolemia, hemorrhage and severe vasodilatation

170

LABORATORY PROCEDURES Measuring CVP 1. Position the client supine with bed elevated at 45 degrees (CBQ) 2. Position the zero point of the CVP line at the level of the right atrium. Usually this is at the MAL, 4th ICS 3. Instruct the client to be relaxed and avoid coughing and straining.

171

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CARDIAC IMPLEMENTATION 1. Assess the cardio-pulmonary status VS, BP, Cardiac assessment 2. Enhance cardiac output Establish IV line to administer fluids

173

CARDIAC IMPLEMENTATION 3. Promote gas exchange Administer O2 Position client in SEMI-Fowlers Encourage coughing and deep breathing exercises

174

CARDIAC IMPLEMENTATION 4. Increase client activity tolerance Balance rest and activity periods Assist in daily activities Provide strict bed rest if indicated Soft foods Assistance in self-care

175

CARDIAC IMPLEMENTATION

5. Promote client comfort Assess the clients description of pain and chest discomfort Administer medication as prescribed Morphine for MI Nitroglycerine for Angina Diuretics to relieve congestion (CHF)

176

CARDIAC IMPLEMENTATION 6. Promote adequate sleep 7. Prevent infection Monitor skin integrity of lower extremities Assess skin site for edema, redness and warmth Monitor for fever Change position frequently

177

CARDIAC IMPLEMENTATION

8. Minimize patient anxiety Encourage verbalization of feelings, fears and concerns Answer client questions. Provide information about procedures and medications

178

Activity Intolerance

Monitor TPR and BP Space activities in the day Permit rest periods before activity Limit activity 1 hour before meals Teach energy conservation measures like bed rest Instruct patient to avoid constricting garments Instruct to elevate edematous areas Instruct patient to avoid dependent positions Teach patient to prepare low sodium meals Apply anti-embolic stockings Instruct patient to stop activity when pain occurs Administer nitroglycerine for angina Pace activities within patients limits Instruct patient to avoid cold temperatures and smoking Instruct to report unrelieved pain immediately
179

Edema

Pain

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Cardiac Disorders
CAD Angina MI Cardiac Dysrythmias CHF Cardiogenic shock Cardiac Tamponade
181

Hyperlipidemia
group of metabolic disorders that lead to: elevated serum total cholesterol (hypercholesterolemia) elevated low density lipoprotein elevated triglycerides (hypertriglyceridemia)

182

1. Primary: Genetic 2. Secondary: DM Hypothyroidism Nephrotic Syndrome Liver Disease Obesity Dietary Intake Pregnancy Use of Beta Blockers and Diuretics

183

Coronary Artery Disease (CAD)

Accumulation of fatty deposits in the inner layer of coronary arteries. due to hypercholesterolemia Incomplete occlusion of the coronary arteries lead to Angina (ischemia) Complete occlusion of the coronary arteries lead to Myocardial Infarction Manifestations depend on the severity of coronary arterial occlusion
184

Risk Factors
Age above 45/55 Sex- Males and post-menopausal females
Race Family History Hypertension Cigarette Smoking Diabetes Mellitus Obesity Sedentary Lifestyle Stress Atherosclerosis
185

Pathophysiology
Fatty streak formation in the vascular intima T-cells and monocytes ingest lipids in the area of deposition atheroma narrowing of the arterial lumen reduced coronary blood flow myocardial ischemia

186

Angina
Chest pain resulting from coronary atherosclerosis or myocardial ischemia Types:

Stable exertional; relieved by rest, drugs; severity does not change Unstable Occurs unpredictably during exertion and emotion; severity increases with time and pain may not be relieved by rest and drug Prinzmetal (variant) pain at rest with vasospasm
187

Manifestations
Characteristic of chest pain - Substernal or retrosternal pain that radiates to arms, neck and jaws - Squeezing, heavy, burning, tight chest - Precipitated by cold, eating, emotions, exertion - Lasts a few minutes and then subsides

188

Diaphoresis Nausea and vomiting Cold clammy skin Sense of apprehension and doom Dizziness and syncope

189

Diagnostic Tests
NTG test (relief from pain) ECG (ST depression and T wave elevation) Cardiac catheter atherosclerotic lesions Thallium 201 Imaging Technetium Imaging

190

Nursing Diagnosis
Pain related to imbalance in myocardial oxygen demand Decreased cardiac output related to reduced preload and afterload Anxiety related to pain, uncertain prognosis and threatening environment

191

Management
Relieve pain Place in comfortable position Administer O2 Decrease Anxiety PTCA - percutaneous transluminal coronary angioplasty
To compress the plaque against the vessel wall, increasing the arterial lumen

CABG - coronary artery bypass graft

To improve the blood flow to the myocardial tissue

Explain the reasons for hospitalization, diagnostic tests and therapies

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Give antianginal drugs

Aspirin- prevent thrombus formation Beta-blockers- reduce BP and HR Calcium-channel blockers- dilate coronary artery and reduce vasospasm Nitrates- to dilate the coronary arteries
194

 Put one nitroglycerin tablet under the tongue Wait for 5 minutes If not relieved, take another tablet and wait for 5 minutes Another tablet can be taken (third tablet) If unrelieved after THREE tablets seek medical attention
195

Myocardial Infarction
Absence of O2 supply to the myocardium Necrosis or death to the myocardial tissue Attack may be sudden or gradual

196

Etiology
1. CAD 2. Coronary vasospasm 3. Coronary artery occlusion by embolus and thrombus 4. Conditions that decrease perfusion- hemorrhage, shock
197

Risk factors
1. Hypercholesterolemia 2. Smoking 3. Hypertension 4. Obesity 5. Stress 6. Sedentary lifestyle
198

Pathophysiology
Interrupted coronary blood flow myocardial ischemia anaerobic myocardial metabolism for several hours myocardial death depressed cardiac function triggers autonomic nervous system response further imbalance of myocardial O2 demand and supply

199

Chest pain: Severe, steady crushing and squeezing substernal pain Radiates to the neck, arm, jaw and back Not relieved by rest or NTG May continue for 15-30 minutes May produce anxiety and fear resulting to increased HR, BP and RR
200

dyspnea Diaphoresis cold clammy skin N/V restlessness, sense of doom tachycardia or bradycardia hypotension dysrhythmias
201

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Diagnostic Evaluation
Chest pain cannot be relieved by NTG ST segment depression and T wave inversion, Q wave

Cardiac enzymes: increased Troponin, CK MB, LDH CBC- may show elevated WBC count
203

Nursing Diagnosis
Pain related to an imbalance in oxygen supply and demand Anxiety related to chest pain, fear of death and threatening environment Decreased cardiac output related to impaired contraction of the heart

204

 Altered tissue perfusion (myocardial) related to coronary stenosis Activity intolerance related to insufficient oxygenation Risk for injury (bleeding) related to dissolution of clots Ineffective individual coping related to threats to self esteem
205

Management
Oxygen therapy Provide adequate rest periods Minimize metabolic demands Provide soft diet Provide a low-sodium, low cholesterol and low fat diet Passive ROM Minimize anxiety Reassure client and provide information as needed
206

Pharmacologic Therapy
Thrombolytic agents - Dissolve clots in the coronary artery allowing blood to flow ie TPA tissue plasminogen activator (Alteplase), Streptokinase (streptase), Urokinase Anticoagulant prevents formation of new blood clots ie Heparin, Warfarin
207

 Antiplatelet hypersensitivity to aspirin ie Ticlopidine, Clopidogrel Beta adrenergic blocking agents reduce myocardial O2 demand by blocking sympathetic stimulation; dec HR, contractility, BP ie Propranolol Calcium channel blockers dec contraction, HR; relax blood vessels ie Diltiazem
208

 Morphine - reduces pain and anxiety - Relaxes bronchioles to enhance oxygenation ACE Inhibitors - Prevents formation of angiotensin II which causes vasoconstriction; dec O2 demand Limits the area of infarction

209

Surgical revascularization: Percutaneous Transluminal Coronary Angioplasty (PTCA); coronary artery bypass graft (CABG ) After the condition had been stabilized: - CBR without BP (complete bedrest without bathroom privilege) - Gradual resumption of ADL to full recovery

210

Congestive Heart Failure CHF

A syndrome of congestion of both pulmonary and systemic circulation caused by inadequate cardiac function and inadequate cardiac output to meet the metabolic demands of tissues
211

Predisposing Factors
Myocardial Infarction Arrhythmias Pregnancy Pulmonary Embolism Anemia Renal Failure CAD Valvular heart diseases Hypertension Cardiomyopathy Pericarditis and cardiac tamponade

212

New York Heart Association

Class 1 Ordinary physical activity does NOT cause chest pain and fatigue No pulmonary congestion Asymptomatic NO limitation of ADLs Class 2 SLIGHT limitation of ADLs NO symptom at rest Symptom with INCREASED activity Basilar crackles and S3

213

Class 3 Markedly limitation on ADLs Comfortable at rest BUT symptoms present in LESS than ordinary activity Class 4 SYMPTOMS are present at rest

214

PATHOPHYSIOLOGY

LEFT Ventricular pump failure back up of blood into the pulmonary veins increased pulmonary capillary pressure pulmonary congestion

215

LEFT ventricular failure decreased cardiac output decreased perfusion to the brain, kidney and other tissues oliguria, dizziness

216

PATHOPHYSIOLOGY RIGHT ventricular failure blood pooling in the venous circulation increased hydrostatic pressure peripheral edema

217

RIGHT ventricular failure blood pooling venous congestion in the kidney, liver and GIT

218

LEFT SIDED CHF ASSESSMENT FINDINGS

1. Dyspnea on exertion 2. PND 3. Orthopnea 4. Pulmonary crackles/rales 5. cough with Pinkish, frothy sputum 6. Tachycardia

219

7. Cool extremities 8. Cyanosis 9. decreased peripheral pulses 10. Fatigue 11. Oliguria 12. signs of cerebral anoxia

220

RIGHT SIDED CHF ASSESSMENT FINDINGS

1. Peripheral dependent, pitting edema 2. Weight gain 3. Distended neck vein 4. hepatomegaly 5. Ascites 6. Body weakness 7. Anorexia, nausea 8. Pulsus alternans
221

Diagnostics
EKG - heart strain Chest X-ray - cardiomegaly and pleural effusion CVC Central Venous Catheter and SwanGanz Catheter are able to record high pressure in the chambers and pulmonary capillaries. Echocardiogram may show hypokinetic heart ABG and Pulse oximetry may show decreased O2 saturation

222

Nursing Considerations
goal of treatment - improve pump function and reverse the compensatory mechanism of the heart. complete bed rest and reduce myocardial oxygen demand. FVE management and prevent complications Diuretics and Digoxin, vasodilators and hypolipidemics LOW sodium diet Limit fluid intake Monitor daily weight and report signs of fluid retention

223

Complications: Acute Pulmonary Edema Treatment: Bed rest and maintain high fowlers position O2 therapy Morphine administration to dilate blood vessels Dopamine to increase myocardial contractility and CO Diuretics to reduce blood volume Steroids to reduce inflammation

224

Cardiac Arrhythmias
Disturbances in regular rate and rhythm due to changes in electrical automaticity or conduction Irregular HR, rhythm and regularity

225

 Premature atrial contraction (PAC) more than 100 bpm Atrial flutter 250-300 bpm Atrial fibrillation higher than 500 bpm Premature ventricular contraction (PVC) most common; due to dec. K, dec. Calcium and MI Ventricular tachycardia (vtach) 3 or more PVCs Ventricular fibrillation (vfib) extremely rapid and erratic impulse formation
226

 AV Block - Impulse is delayed from SA node to AV node 1st degree atrial impulses conducted slower than normal 2nd degree some atrial impulses conducted into ventricles Mobitz type I asymptomatic (ventricular contraction is adequate) Mobitz type II critical (atrial contraction is not synchronized with the ventricle) 3rd degree no atrial impulse conducted to Av node
227

Treatment
Increase CO Cardiovascular drugs and mechanical equipment Cardiovascular Drugs: IV Dopamine (vasopressor) IV Dobutamine (diuretic effects) IV Epinephrine (vasoconstrictor) IV Nitroprusside (vasodilator)
228

 Mechanical: IABP intra aortic balloon pump (improves coronary perfusion) Defibrilator (arrhythmias can be stopped) Cardiac monitor (to detect arrhythmias)

229

CARDIOGENIC SHOCK
Heart fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion ETIOLOGY Massive MI Severe CHF Cardiomyopathy Cardiac trauma Cardiac tamponade

230

HYPOTENSION oliguria (less than 30 ml/hour) tachycardia narrow pulse pressure weak peripheral pulses cold clammy skin changes in sensorium/LOC pulmonary congestion

231

LABORATORY FINDINGS
Increased CVP
Normal is 4-10 cmH2O

232

Management
modified Trendelenburg (shock ) position IVF, vasopressors and inotropics such as DOPAMINE and DOBUTAMINE, diuretics, nitrates Administer O2 Morphine is administered to decrease pulmonary congestion and to relieve pain Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganz cath and IABP Monitor urinary output, BP and pulses
233

CARDIAC TAMPONADE
heart is unable to pump blood due to accumulation of fluid in the pericardial sac (pericardial effusion) restricts ventricular filling resulting to decreased cardiac output Acute tamponade - sudden accumulation of more than 50 ml fluid in the pericardial sac

234

Risk Factors
Cardiac trauma Complication of Myocardial infarction Pericarditis Cancer metastasis

235

Manifestations
BECKs Triad- Jugular vein distention, hypotension and distant/muffled heart sound Pulsus paradoxus Increased CVP decreased cardiac output Syncope anxiety dyspnea Percussion- Flatness across the anterior chest
236

Diagnostics
Echocardiogram CXR

237

Management
Assist in PERICARDIOCENTESIS Administer IVF Monitor ECG, urine output and BP Monitor for recurrence of tamponade
238

CARDIOMYOPATHIES

Heart muscle disease associated with cardiac dysfunction

239

CARDIOMYOPATHIES

1. Dilated Cardiomyopathy 2. Hypertrophic Cardiomyopathy 3. Restrictive cardiomyopathy

240

DILATED CARDIOMYOPATHY ASSOCIATED FACTORS 1. Heavy alcohol intake 2. Pregnancy 3. Viral infection 4. Idiopathic
241

DILATED CARDIOMYOPATHY
PATHOPHYSIOLOGY Diminished contractile proteins poor contraction decreased blood ejection increased blood remaining in the ventricle ventricular stretching and dilatation. SYSTOLIC DYSFUNCTION
242

HYPERTROPHIC CARDIOMYOPATHY

Associated factors: 1. Genetic 2. Idiopathic

243

HYPERTROPHIC CARDIOMYOPATHY Pathophysiology Increased size of myocardium reduced ventricular volume increased resistance to ventricular filling diastolic dysfunction
244

RESTRICTIVE CARDIOMYOPATHY

Associated factors 1. Infiltrative diseases like AMYLOIDOSIS 2. Idiopathic

245

RESTRICTIVE CARDIOMYOPATHY

Pathophysiology Rigid ventricular wall impaired stretch and diastolic filling decreased output Diastolic dysfunction
246

CARDIOMYOPATHIES
Assessment findings 1. PND 2. Orthopnea 3. Edema 4. Chest pain 5. Palpitations 6. dizziness 7. Syncope with exertion

247

CARDIOMYOPATHIES
Laboratory Findings 1. CXR- may reveal cardiomegaly 2. ECHOCARDIOGRAM 3. ECG 4. Myocardial Biopsy

248

CARDIOMYOPATHIES
Medical Management 1. Surgery= heart transplant 2. pacemaker insertion 3. Pharmacological drugs for symptom relief
249

CARDIOMYOPATHIES
Nursing Management 1. Improve cardiac output Adequate rest Oxygen therapy Low sodium diet
250

CARDIOMYOPATHIES
Nursing Management 2. Increase patient tolerance Schedule activities with rest periods in between

251

CARDIOMYOPATHIES
Nursing Management 3. Reduce patient anxiety Support patient Offer information about transplantations Support family in anticipatory grieving
252

Infective endocarditis

Infection of the heart valves and the endothelial surface of the heart
253

Infective endocarditis

Can be acute, sub-acute or chronic

254

Infective endocarditis

Etiologic factors 1. Bacteria- Organism depends on several factors 2. Fungi

255

Infective endocarditis
Risk factors 1. Prosthetic valves 2. Congenital malformation 3. Cardiomyopathy 4. IV drug users 5. Valvular dysfunctions
256

Infective endocarditis
Pathophysiology Direct invasion of microbes microbes adhere to damaged valve surface and proliferate damage attracts platelets causing clot formation erosion of valvular leaflets and the clot and vegetation can embolize

257

Infective endocarditis
Assessment findings 1. Intermittent high grade fever 2. anorexia, weight loss 3. cough, back pain and joint pain 4. splinter hemorrhages under nails

258

Infective endocarditis

Assessment findings 5. Oslers nodes- painful nodules on fingerpads 6. Roths spots- pale hemorrhages in the retina
259

Infective endocarditis

Assessment findings 7. Heart murmurs 8. Heart failure= usually acute heart failure

260

Infective endocarditis

Prevention Antibiotic prophylaxis if patient is undergoing procedures like dental extractions, bronchoscopy, surgery, etc.
261

Infective endocarditis

Prevention Any invasive procedure that is associated with transient bacteremia may cause the microrganism to lodge in the damaged, irregular valves
262

Infective endocarditis
LABORATORY EXAM Blood Cultures to determine the exact organism Usually, 3 culture specimens are obtained and antibiotic sensitivity done

263

Infective endocarditis
Nursing management 1. Regular monitoring of temperature, heart sounds 2. Manage infection 3. Long-term antibiotic therapy is given to ensure eradication of bacteria
264

Infective endocarditis

Medical management 1. Pharmacotherapy IV antibiotic for 2-6 weeks Antifungal agents are given amphotericin B
265

Infective endocarditis

Medical management 2. Surgery Valvular replacement

266

Vascular Disorders
Venous Thrombosis CVI Arterosclerosis Raynauds Phenomenon Aneurysm Hypertension

267

Venous Thrombosis
Due to: Stasis of blood Injury to the vessel wall Altered blood coagulation

268

High Risk: Fractures, cast and joint replacement Obesity and smoking Immobilized patient Heart problems

269

May progress to: Phlebitis-inflammation of the vessel wall Superficial thrombophlebitis - greater and lesser saphenous veins affected. Deep vein thrombosis - deep veins affected; pulmonary embolism is a complication

270

Manifestations
(+) Homans sign fever and chills swelling and cyanosis of the affected leg or arm Diagnostics: Venous duplex ultrasound Impedance plethysmography RF testing (radioactive fibrinogen) fibrinogen I 125 Venography Coagulation Profiles: APTT PT/INR
271

Management
Prevent complications Bed rest for 5 days Prevent muscle contraction if possible to prevent dislodging the clot Elevation of affected part 10-20 degree above the heart Anti-embolic stockings Anticoagulant Thrombolytic Green-field filter (IVC) Thrombectomy

272

Chronic Venous Insufficiency

Destruction of the valves because of chronic blood pooling or trauma. Venous return is decreased chronic venous stasis edema formation veins becomes distorted or tortuous (varicosities) stasis ulcer, cellulites and recurrent thrombosis manifest later
273

Manifestations
Edema Altered pigmentation Pain Stasis dermatitis Dilated superficial veins Stasis ulcers

274

Management
Elevate legs Elastic compression stockings Skin should be kept clean and dry

275

Raynauds Phenomenon
Arteriolar vasospastic disease with unusual sensitivity to cold or emotional stress. cause is unknown but may be secondary to Autoimmune Diseases

276

ASSESSMENT
Pallor then cyanosis Hyperemia when blood returns to digits after vasospasm Numbness, tingling and burning pain

277

Management
Avoid primary stimuli (cold, tobacco) Ca channel blocker Nifedipine for vasospasm Safety measures

278

Arteriosclerosis
hardening of the arterial blood vessel walls related to aging. Atherosclerosis-common type of arteriosclerosis due to atheromas.

279

Aging and atheromas impeding the lumen of the arterial walls (incomplete or incomplete occlusions ) systemic effects depending on the blood vessel affected

280

asymptomatic or may manifest if damaged is obvious systemic effects PVR to heart strain to hypertension weakening the muscles of the wall that leads to aneurysm
281

TIA to CVA Angina to MI ATN to Renal Failure Retinopathy to Blindness Peripheral Occlusive Disease (TAO) to Gangrene Formation Hepatic Infarction Pulmonary Infarction
282

Diagnostic Evaluation:
Arteriography CT Scan MRI Duplex UTZ EKG

283

Management:
Modification of risk factors (CAD and hyperlipidemia) Anticoagulants Antiplatelets Lipid Lowering Agent Antihypertensive Vascular Rehabilitation/Exercise
284

Surgical Intervention:
PTA-Percutaneous Transluminal Angioplasty Laser Angioplasty Embolectomy-removal of clot from the artery Thrombectomy-removal of thrombus from the artery Endarterectomy-removal of plaque from the artery Bypass Graft
285

Aneurysm
Dilation involving an artery formed at a weak point in the vessel wall Saccular= when one side of the vessel is affected Fusiform= when the entire segment becomes dilated
286

RISK FACTORS
1.Atherosclerosis 2.Infection= syphilis 3.Connective tissue disorder 4.Genetic disorder= Marfans Syndrome

287

PATHOPHYSIOLOGY
Damage to the intima and media weakness outpouching Dissecting aneurysm tear in the intima and media with dissection of blood through the layers

288

Manifestations:
1. Asymptomatic 2. Pulsatile sensation on the abdomen 3. bruit Diagnostics CT scan Ultrasound X-ray Aortography
289

Management
Anti-hypertensives Synthetic graft Nsg: Administer medications Emphasize the need to avoid increased abdominal pressure No deep abdominal palpation Remind patient the need for serial ultrasound to detect diameter changes
290

Hypertension
Silent killer disease of vascular regulation that leads to high blood pressure due to alteration of Central Nervous System, Renin-Angiotensin-Aldosterone System, Extracellular Fluid Volume

291

Primary or Essential Hypertension

Other causes are absent Average BP exceeds the upper limits (taken at rest 3x with several days interval) Diastolic is 90 mm Hg or higher Represents 95% of patients with hypertension

292

Secondary Hypertension
Due to: Renal Pathology Coarctation of the Aorta Endocrine Disturbance Drugs (estrogens, sympathomimetics, NSAIDs, steroids) Malignant Hypertension - It is a combination of both where in BP is uncontrolled.

293

Risk Factors
Old age male Race Overweight Family History Smoking Sedentary Lifestyle Diabetes Mellitus
294

Manifestations
1. Headache 2. Visual changes 3. chest pain 4. dizziness 5. N/V
295

Diagnostic Evaluation
Monitor BP EKG, Blood Sugar, Blood Chem etc. Management: Control of all risk factors:.
Lose weight, limit alcohol, cut sodium to 2.4 g/day, stop smoking, reduce dietary saturated fat and cholesterol, reduce coffee intake.

296

Despite lifestyle changes and BP remains high drug therapy should be started:

Diuretics Beta blockers Calcium channel blockers ACE inhibitors A2 Receptor blockers Vasodilators
297

Nursing Management
Health teaching on:
Lifestyle changes ie activities, nutrition, weight, diet (low fat, low Na), cessation of smoking treatment regimen ie drugs BP monitoring Follow up

298

Cardiovascular Drugs:
Anti Anginal
Opiate Analgesic Morphine Sulfate cardiac workload and BP, improve LOC and sedative effect

Vasodilators
Nitroglycerin NTG Relax smooth muscle, dec. BP and alleviate headache Increase blood vessel diameter and improves blood flow

S.E. dizziness and flushing Can be given SL or IV (Isordil) and topical (Nitrobid)

299

 Calcium Channel Blockers

Nifidepine (Procardia) Diazepam (Cardizem) Decrease muscle tone, interferes contraction, decrease BP S.E. bradycardia, diarrhea and rashes

Beta Blocking Agent

Propranolol Decrease workload Blocks beta receptors and capable of decreasing HR

S.E. vomiting, nausea and depression

300

 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) S.E. GIT disturbance, CNS depression and flashes of light Dopamine diuresis effect - Increase Na excretion (kidney) Dobutamine - Increase CO - More potent on contraction
301

 Diuretics - Spironolactone (Aldactone) K sparer - Furosemide (Lasix) K waster

ACE inhibitors Captopril (Capoten)

302

 Anti dysrhythmic drug

Lidocaine (Xylocaine) for PVC Atropine for Mobitz type I Isoproterenol (Isuprel) for sinus bradycardia Norepinephrine (Levophed) powerful vasoconstrictor Epinephrine increase conduction, contractility and automaticity Quinidine for atrial fib

303

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

304

 Blood thinner
Heparin prevent formation of new clot (4-8T IU/30 min)

Antidote Protamine Sulfate Warfarin (Coumadine) decrease viscosity of blood (PO) home meds Dont give to pregnant women Antidote Vitamin K

305

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308

Salamat po.

309