Aug 13, 2012

Cardiovascular Disorders

Anatomy and Physiology - HEART

- Center of the thorax
- 300 g in weight; cone shaped and tilted forward and to the left
o Size and weight are influenced by
 Age
 Gender
 Body weight
 Physical condition
 Heart condition (disease)
- Pumps blood to the tissues and supplies them with oxygen and other nutrients
- Size of a fist
- Location: mediastinum
o In a rotated position
o Right ventricle > lies anteriorly, beneath the sternum
o Left ventricle > situated posteriorly
o Close proximity to chest wall > pulsation created by the normal ventricular contraction is easily
detected = Apical Pulse / Point of Maximum Impulse (PMI)
- Layers:
o Pericardium
 Thin, fibrous sac which encases the heart
 Layers:
 Visceral
o Adheres to the epicardium
 Parietal
o Envelops the visceral pericardium
o Tough fibrous tissue that attaches to the great vessels, diaphragm,
sternum and vertebral column
o Supports the heart in the mediastinum
 The space between visceral and parietal is called pericardial space
o Filled with about 20 ml of fluid
o Lubricates the surface of the heart
o Reduces friction during systole
 Pericardial space (between; consist the fluid)
o Epicardium
 Exterior layer
o Myocardium
 Heart muscle
 Responsible for the contractility (pumping action) and function of the heart
 Made up of muscle fibers
 Composed of specialized cells called Myocytes > which form an interconnected network
of muscle fibers
 Fibers encircle the heart in a figure-of-eaight pattern, forming a spiral from the
base (top_ of the heart to the apex (bottom)
 during contraction
 facilitates a twisting and compressive movement of the heart that begins in the
atria and moves to the ventricles
 Sequential and rhythmic pattern of contraction + muscle fibers relaxation =maximizes
the volume of blood ejected with each contraction.
 Controlled by the conduction system
o Endocardium
 Innermost layer
 Consist of endothelial tissue and lines the inside of the heart and valves
- Pumping action > accomplished by the rhythmic relaxation and contraction of the four chambers’
muscular walls
o Diastole
 Relaxation phase
 All four chambers relax simultaneously
 Allows the ventricles to fill in preparation for contraction.
 Period of Ventricular Filling
o Systole
 Refers to the events in the heart during contraction of the
 two top chambers (atria systole)
o Occurs first, just at the end of diastole
 Two bottom chambers (ventricular systole)
 o Follows the atria systole
o The process allows the ventricles to completely fill prior to ejection of blood from the chambers
- Heart Chambers
o Right Side
 Right Atrium and Right Ventricle
 Distributes venous blood (deoxygenated blood) to the lungs via the pulmonary artery
(pulmonary circulation) for oxygenation.
 Right Atrium
 Receives blood returning from the
o Inferior vena cava
o Superior vena cava
o Coronary sinus cardiac vein
 Right ventricle
o Contracts against a low pressure system within the pulmonary arteries
and capillaries
o Left Side
 Left atrium and left ventricle
 Distributes oxygenated blood to the remainder of the body via the aorta
 Left Atrium
 Receives oxygenated blood from the pulmonary circulation via four pulmonary
veins.
 Left ventricle
 2 ½ times more muscular than the right ventricle
 To overcome the high aortic and arterial pressure
o Valves
 Four valves
 Permit blood to flow in only one direction
 Composed of thin leaflets of fibrous tissue
 Open and close in response to the movement of blood and pressure changes within the
chambers
 Types:
 Atrioventricular Valves
o Separate the atria from the ventricles
o Tricuspid Valve
 Composed of 3 cusps or leaflets
 Separate the right atrium from the right ventricle
o Mitral / Bicuspid Valve
 Composed of 2 cusps
 Lies between the left atrium and the left ventricle
o During diastole
 Tricuspid + Mitral = open >allowing blood in the atria to flow
freely into the relaxed ventricles.
o Ventricular systole starts
 Ventricles contract
 Blood flows upward into the cusps or the tricuspid and mitral
valves > T + M = closes
 T and M pressure increase = the papillary muscles and the
chordae tendineae maintain valve closure.
 Papillary muscles
o located on the sides of the ventricular walls
o Connected to the valve leaflets buy thin
fibrous bands called Chordae Tendineae
 Contraction of papillary muscles
 Causes the chorea tendineae to become taut,
keeping the valve leaflets approximated and closed.
 Prevents backflow of blood into the artia
(regurgitation) as blood is ejected out into the
pulmonary artery and aorta

 Semilunar Valves
o Composed of three leaflets which are shaped like half-moons.
o Pulmonic Valve
 Valve between right ventricle and pulmonary artery
o Aortic Valve
 Valve between the left ventricle and aorta
o Closed during diastole
 Pressure in the pulmonary artery and orta decreases
  Causing blood to flow back toward the semilunar
valves
o Fills the cusps with blood and closes the
valves
o Forced open during ventricular systole as blood is ejected from the R
and L ventricles into the pulmonary artery and aorta.
o Coronary Arteries
 L and R arteries and the branches > supply arterial blood to the heart
 Arteries > originate from the aorta just above he aortic valve leaflets
 Heart > high metabolic requirements, extracting approximately 70% to 80% of the
Oxygen delivered
 Are perfused during diastole
 Heart rate increases = diastole time is shortened > may not allow adequate time for
myocardial perfusion.
 Result > patient at risk for myocardial ischemia (HR>100), esp. patient with CAD
 L Coronary Artery
 Has three branches
o Left main coronary artery
 Artery from the point of origin to the first major branch
 Two branches arises
 Left anterior descending artery
o Courses down the anterior wall of the heart
 Circumflex artery
o Circles around to the lateral left wall of the
heart
Three Vessels involved in ASHD CAD 3:
1. R Coronary Artery
2. Left Anterior Descending Artery
3. Left Circumflex

 Right Coronary Artery

 Leads to the inferior wall of the heart
 Posterior wall > receives blood supply by an additional branch from the R
coronary artery call posterior descending artery
 Coronary Veins
 Superficial to the coronary arteries
 Venous blood returns to the heart primarily through the coronary sinus
(located posteriorly in R atrium)

Coronary Circulation
- Needs a constant supply of O2 and nutrients to contract efficiently and conduct impulses
- Major blood vessels
- Blood flow through myocardium is greatest during relaxation (diastole) and reduced during contraction
(systole)
- Rapid/prolonged contractions interfere with blood supply to the heart
- Anastomoses (connections) – btw RCA and LCA
- Potential to open up and provide collateral circulation
- Collateral circulation – alternative source of blood
- When obstruction develops gradually, other capillaries tend to enlarge to meet metabolic needs
- RCA – supplies R side of heart and inferior part of LV – SV node, AV node
- anterior descending – anterior wall of ventricles, anterior septum, bundle branches
- L Circumflex – L atrium, lateral and posterior walls of LV
- Implications
o RCA blockage -> conduction disturbances of AV node (arrhythmias)
o LCA - > Impair pumping ability of LV (CHF )

Cardiac Cycle
- Refers to the alternating sequence of diastole (relaxation) and systole (contraction) coordinated by the
conduction system
- Cycle
o 2 atria relaxed and filing with blood
o AV valves open because of pressure and ventricles are relaxed
o Blood flows into ventricles almost emptying atria
o Conductions system stimulates atrial muscle to contract forcing any blood into the ventricles
o Atria relax
o 2 ventricles contract and pressure increases in V
o AV valves closed
o (Brief moment) – all valves closed, ventricular myocardium continues to contract building up
pressure (isovulmetric phase)
o Increasing pressure opens up the semilunar valves(blood forced into pulmonary and aorta)
 o Contraction needs to be strong to overcome opposing pressure in the artery
o Atria fills again, ventricles relax
o Start the cycle again

Pulse
- The pulse indicated the heart rate
- During ventricular systole, it expands the arteries
- Weakness or irregularity is in a peripheral pulse (radial) indicates a problem
- Apical pulse – rate measures at the heart itself
- Pulse deficit – difference between apical and radial
- Common causes: coartation of aorta / stenosis

Cardiac Output
- Blood ejected from L ventricle / minutes
- Ave: 5.6 L / min
- CO = stroke vol x HR
o Stroke volume: blood ejected / heartbeat
o Increased amt of blood returns to the heart (SNS stimulation), heart stretched more and force of
contraction increases proportionately
o Preload: venous return
o Afterload: resistance to L Ventricular ejections (peripheral resistance)

Vascular System
- Arteries
- Arterioles (smallest)
- Capillaries (site of diffusion, O/CO2 exchange, supply of nutrients)
- Venules
- Veins
- Valves
- Lymphatics – drains the lymph fluids

Arteries and Veins

- 3 Layers
o Tunica Intima
 Endothelial cells – secretes substances that can adjust the dilatation and constriction of
blood vessels
o Tunica Media
 Smooth muscle that controls the diameter and lumen size of the blood vessels
o Tunica Adventitia
 Outermost

Autoregulation
- Localized vasodilation and vasoconstriction regulated by reflex and adjustment
- Decrease in pH and O and increased CO2 and release of chemical mediators > vasodilation
- Norepinephrine / Epinephrine, angiotensin > systemic vasoconstriction (Alpha 1 receptions)

Blood Pressure
- Pressure of blood against systemic arterial walls
- Systolic pressure – pressure exerted by the blood when ejected by the LV
- Diastolic pressure – pressure that occurs when the ventricles are relaxed
- BP = CO x PR
- Peripheral resistance:
o Decrease lumen
o Vasoconstriction
o Obstruction of blood vessels
- Blood Pressure Controls
o Baroreceptors (Pressoreceptors) – aortic arch and carotid sinus
o Stretch Receptors – vena cava and right atrium
o Anti-diuretic hormone
o Aldosterone: primary fx: Na Reabsorption with Water
o Renin-Angiotensin System

Properties of Cardiac Muscle

- Automaticity
- Excitability
- Conductivity
- Contractility

Cardiac Conduction System

Conduction system
 - Atrial contraction – depolarization in the P wave
- Ventricular contraction – depolarization in the ventricles (QRS)
- T-Wave – ventricular repolarization

ECG
Control of Heart
- Heart rate and force of contraction controlled cardiac control center (medulla)
- Baroreceptor (aorta and carotid) – changes in BP > cardiac center > SNS/PNS
- SNS – increase heart rate and contractility and vasoconstrictions
- PNS – vagus nerve stimulation – slows heart rate
- Beta – receptors in the heart

Nursing History
- Non modifiable
o Age
o Gender
o Race
o Heredity
- Modifiable
o Stress
o Diet
o Exercise
o Cigarette
o Alcohol
o HPN
o Hyperlipidaemia
o DM
o Obesity
o Contraceptive pill
o Personality type

Physical Examination
- Inspection
o Skin color
o JV distention
o Respiration
o PMI
o Edema
- Palpate
o Peripheral pulses
o Apical pulse
- Auscultate
o Heart sounds (s1-apex, AV closure, s2-base, semilunar valve closure, s3, s4)
o Murmurs
o Pericardial friction rub
- Percussion
o Note: dullness (heart is a solid organ)
- Common clinical manifestation
o Dyspnea
 Dyspnea on exertion
 Orthopnea
 Paroxysmal dyspnea
o Chest pain
o Edema
o Syncope – caused by narrowing of blood vessels; common carotids supply the brain (anterior
part of the brain)
o Palpitation – because of the abnormality of the conduction and contractility of the heart
o Fatigue - related to Oxygen – hypoxemia

Diagnostic Tests
- Cardiac Enzymes
Enzyme Onset Peek Normal Values
CPK – MB 4-5 hours 18-24 hours 0 – 4.7 ng/ml
LDH Within 24 hours 48-72 hours 70-200 IU / L
Troponin Within 3 hours Up to 7 days Less than 0.6 ng/ml
Myoglobin 1 hour 4-6 hours 0-85 g / ml

- Complete Blood Count

- Serum Lipids
 o Cholesterol
o Triglycerides
o HDL/LDL
- Electrolytes
o Any imbalance can result to arrhythmias and dysrhythmias
Increase Decrease
Potassium Vent dysrhythmia Vent dysrhythmia assystole

Sodium H20 Toxicity Diuretics use / HF

Calcium AV block/Tachycardia Prolonged of interval vent

Shortened at interval tachycardia
Muscle weakness

MG Hypotension Fibrillation
Prolonged PR interval
Wide QRS complex

- BUN
o Renal fx
 Creatinine
- Chest X-Ray
o Silhouette of the heart
o Left ventricular hypertrophy image – retrosternal fullness
o Right ventricular hypertrophy image – retrocardia fullness
- ECG
o 0.04 sec and 0.1 millivolt – 1 box
o 6 chest leads
 V1-V6
 V1-V3 – Septal defect – Septal Wall (Atrium or Ventricular = multiple vessels)
 V1-v4 – Anterior Defects
 V5-V6 – Lateral Wall Defects
 2-3 ABF – Inferior wall ischemia/infarction – Right coronary Artery
 1 ABL – High lateral wall infarction – Left Coronary Artery
o Initial dx and monitoring of arrhythmias
o Non invasive
o Holter-monitor – worn to record ECG changes while pursuing daily activities; what activities of
the px can induce arrhythmia
o Echocardiagraphy – reflected sound waves records the image of the heart and valve movements;
Heart structure and valve movement
- Invasive Hemodynamic Monitoring
o Central Venous Pressure
 Monitors right side of the heart
 The tip of the catheter is inside the Right atrium
 Common with px with hypervolemia
 Nursing responsibility
 Consent
 Explain the procedure
 Patient must be relaxed
o The reading will be altered if patient is tachypnic or brachydic
 0 point of manometer at level of R atrium
 Record initial reading must be done in the same position
 Concurrent reading must be done in the same position
 Change dressing, IV fluid bag, manometer and tubing every 24 hours
 Hold breath when cath is changed
 Check daily for infection
o Pulmonary Artery Pressure (PAP) / Pulmonary Capillary Wedge Pressure (PCWP)
 For patients with Cor Pulmonale
 Nursing responsibility
 Consent
 Explain procedure
 Check baseline VS or attach to ECG monitor
 Position: Supine
 Adjust transducer at phlebostatic axis or sternal notch
 Observe insertion site for information, swelling and bleeding
 Deflate balloon after reading
o If a balloon is left inflated, no blood will enter from the R ventricle to
enter the pulmonary circulation
o Cardiac Catheterization
 Passing a catherter to the blood vessel to:
  Visualize the inside of the heart
 Measure pressures
 Asses valve and heart function
 Right Sided Catheterization
 Antecubital or femoral vein
 Measures R atria and ventricle pressure
 Left Sided Catheterization
 Retrograde catheterization
 Transseptal Catheterization
 Nursing Responsibilities
 Pre procedure:
o Consent
o Explain procedure
o Asses allergies to seafoods and iodine
o Document wt and ht
o Baseline VS
o Inform of fluttery feeling / warm, flushed feeling and desire to cough
 Post procedure
o VS q 30 mins for 2 hours
o Asses for chest pain or dysrhythmias
o Monitor for bleeding and hematoma
o Keep extremely extended for 4-6 hours
o CBR for 6-12 hours
o Increase fluid intake
o Cardiac angiography
 Contrast dye injection to visualize blood flow and any obstructions
o Blood flow in peripheral vessels can be assessed with Doppler studies (microphone that records
the sound of blood flow)

HEART DISEASES
- Coronary Artery Disease (CAD)
o Narrowing or obstruction of one or more coronary arteries as result of
 Atherosclerosis – Dyslepedemia
 Arteriorsclerosis – immune defects
o Common with narrowing of arteriosclerosis
 Signs and symptoms
 Chest pain
 Palpitation
 Difficulty in breathing / dyspnea
 Syncope / loss of consciousness
 Cough or hemoptysis
 Excessive fatigue
o Management
 Nitrates
 Antiplatelets
 Antilipemics
 Beta adrenergic blockers
 Calcium Channel Blockers
 Surgery
 PTCA
 Atherectomy
 CABG
o Nursing Management
 Encourage to reduce the risk by modifying lisfestyle
 Admin prescribed meds
 Diet: low fat, low cholesterol, low Na
- Angina Pectoris
o Types:
 Stable
 Unstable
 Prinzmetal – exposure to cold weather
 Intractable – unrelieved by any type of meds; very suggestive of MI
o Causes:
 Exertion
 Emotion
 Exposure to cold
 Excessive smoking
 Excessive eating
o Assessment:
 Pain patterns
  Mild to moderate
 Retrosternal – choking, heartburn, pressing, bursing squeezing
 Radiating to neck, jaw, shoulder, arms L
 3-5 minutes
 Relieved by rest and nitroglyceride
 Pallor, diaphoresis, dizziness, palpitation
 ECG change – ST depression, T wave inversion
o Medications
 Vasodilators
 Nitroglycerine, amyl nitrate, isosorbide
 B-Adrenergic
 Propranolol, metoprolol
 Ca channel blocker
 Verapamil, nifedipine, diltiazem
 Pit – aggregating inhibitors
 ASA, dypiridamole, ticlopidine
 Anticoagulants
 Heparin Na, Warfarin NA (Coumadin), dicumarol
 Thrombus – thrombolytics
o Nursing Responsibilities
 Anticipate postural hypotension
 Take max of 3 doses at 5 min interval
 SL prep has nursing or stinging sensation
 Avoid OH - tachycardia
 Advise client to carry 3 tabs in his pocket; store nitroglycerine in a cool, dry, dark placel
replace stock every 3-6 months
 Nitropatch applied OD in AM, rotating sites
 Do not give NTG if px took Viagra or any drug for erectile dysfunction
 Evaluate effectiveness (if not MI)
o Interventions
 Beta blockers, calcium channel blockers
- Myocardial Infarction
o Sudden dec of oxygenation due to absence of coronary blood flow that results to destruction of
myocardial tissue in regions of the heart
o Right coronary -> arrhythmia
o Left Coronary -> DEAD; comprises the cardiac output immediately
o Causes:
 Thrombus
 Emboli
 Atherosclerosis
o Location
 L anterior descending artery – anterior or septal wall MI or both
 Circumflex artery - posterior wall MI or lateral wall MI
 Right coronary artery – inferior wall MI
o Diagnostic Studies
 Total CK levels
 Cardiac enzymes
 AST
 ECG
 T wave inversion – zone of hypoxia
 ST elevation – zone of injury
 Pathologic Q wave – zone of infarction
o Assessment
 Pain pattern: sever crushing substernal pain; knife like, viselike
 May radiate to jaw, back and left arm
 Fever
 N/V
 Anxiety
 Crushing chest pain
 Dyspnea
 Pallor
o Nursing responsibilities
 Admin prescribed meds
 Morphine, Nitrogen, Oxygen, Aspirates
 Lidocaine – Xylocaine
 Beta blockers – propranolol, timolol
 Thrombolytics – risk for bleeding; streptokinase and uroinase
 Anticoagulants – heparin, warfarin/Coumadin
 Oxygen at 2-4 L/min
 Stool softeners and soft diet – to avoid valsalva
  Diet: liquid / small frequent meals; low fat, cholesterol and Na
 Pos: semi fowlers to promote lung expansion
 Emotional rxns: anxiety, denial, depression
 Monitor thrombolytic therapy
 Check for signs of bleeding
 Used within 3-4 hours after onset of Sxs
 6 hours – golden period
 Following acute episode:
 Maintain CPR
 Provide ROM
o Progressive Cardiac rehab
 Progress to ambulation
 Rehabilitation:
 Early activity
o 1-2 metabolic act on tas (MET)
o Hospitals discharge: 14th day
o ADL’s: 6 weeks after
o Sex: 4-8 weeks after
 Guidelines
 Resume if bale to climb 2 flights of stairs
 Before: rest is impt / avoid large meals/ wear loose fitting clothes/ nitro before
sex / usual envi / sex at rm temp/ foreplay
 During: comfortable position
 Female position: side lying
 Male position: sitting position
o Usual complications
 Cardiogenic shock – pumping ability of the LV severely impaired
 Cardiac Arrhythmias – lack of O causes conduction problems
 CHF
- Cardiac Dysrhythmias
o Abnormal cardiac rhythms that can be due to abnormal automaticity of conduction or both
o Most common complications and major cause of MI
o Most common dysrhythmia in MI is PVC’s
o PVC of >6/min is life threatening
o Predisposing factors are
 Tissue ischemia
 Hypoxemia
 CNS and PNS influences
 Lactic acidosis
 Hemodynamic abnormalities
 Drug toxicities
 Electrolyte imbalance
o Types
 Sinus
 Atrial
 Ventricular
 Conduction
o Bradycardia – regular, slower rate <60
o Tachycardia – regular, faster rate >100
o Atrial flutter – 160-350 / min, less filling time
o Atrial fibrillation – rate >300, uncoordinated, muscle contractions, no output – carding standstill,
no filling
o PVC’s – may induce fibrillation
o Bundle branch block – delayed conduction to BB
o 1st degree Heart Block – delayed conduction AC node
o 2nd degree HB – some beats go to AV, some don’t
o 3rd degree HB – no conduction to AV node, ventricles slowly contract, some independent atrial
contractions
- Sinus Dysrhythmias
o Types
 Sinus Tachycardia
 Digitalis
 Sinus Bradycardia
 Atropine
- Atrial Dysrhythmias
o Premature Atrial Contaction (PAC)
o Paroxysmal Atrial Tachycardia
o Atrial Flutter
o Atrial Fibrilation
o Meds
  Quinidine
 Ca Channel Blockers
 Cardioversion
 The electrical impulse waits for the R wave at the peak of the QRS complex
 Pacemaker
 Long term management
- Ventricular Dysrhythmia
o Premature Ventricular Contraction
o Vantricular Tachycardia
 Widen QRS
 Rapid firing
o Ventricular Fibrillation
 Chaotic discharge rate >300
 May result to clinical death
 Tx: immediate defibrillation then CPR
 Epinephrine
o Pacemakers
 Electronic device that causes cellular depolarization and cardiac contraction
 It initiates and maintains HR
 Pacing modes
 Demand
 Fixed Rate
 Precautions
 DO NOT MRI
 Nursing interventions
 Monitor ECG ff implantation, include VS
 Make sure all the equipment in the clients unit is grounded
 Observe for signs of pacemaker failure
o Cardioversion / Defibrillation
 Cardioversion
 Synchronous application of shock during R wave
 Defib
 Asynchronized electric shock to terminate VF or V tachycardia without pulse
 Nursing intervention
 Client in firm, flat surface
 Apply interface materials to the paddle
 Grasp paddle only by insulated handles
 Give command to STAND clear
 Apply one of the paddles at precordium, other R parasternal area 3 rd ICS
 For defibrillation, release 200-360 joule; for cardioversion, lower energy is
required
 Defibrillation is done prior to CPR
 Diazepam – sedative
 CPR
 Indications
o CP Arrest / clinical death (breathlessness / pulselessness)
o CPR should be started < 5 mins after arrest
 Types
o Basic Life Support – use of mouth, hands
o Advance Cardiac Support – BLS and equipment
 When to stop?
o When the client is revived
o When EMS has been activated
o When the rescuer is exhausted
o When client is dead
- CHF
o Causes
 Hypervolemia
 Arteriosclerosis
 MI
 Valvular problems
o Types
 Right sided CHF (Systemic Sx)
 Fatigue
o Distended jugular veins
 Ascites
 Left side heart failure (Pulmonary Sx)
 Cardiomegaly
o Blood tinged sputum
 Chronic cough
 o Acute pulmo edema
 Exertional dyspnea
o Cyanosis
 Orthopnea
o Weight loss
o Managements
 Rest – minimize O2 consumption
 High fowler’s or sitting
 Decrease fluids and Na
 Medications
 Cardiac glycosides – (+) inotropy / (-) chronotropy
 Digitalis / digozin (Lanoxin) / digitoxin (Crystodigin)/ Lanatoside
o Guidelines
 Check HR
 ^ K intake
 Normal level: 0.5-2 ng/ml
 Toxicity
o Antidote
 Digoxin Immune Fab (Digibind) = Antibodies that bind to digoxin
 Diuretics = H2O and Na + excretion
 Loop Diuretics – Furosemide (Lasix)
 Potassium sparing – spironolactone (Aldactone)
 Guidelines:
 Give in the AM
 Monitor IO
 S/E: Hypoalemia / hyponatremia/ dehydration/hypotension
o Rotating Tourniquet
 Principles:
 Apply 3 tourniquet
 Inflate cuff 10 mm above diastolic pressure
 Rotate q 15
 Check distal pulses
 Remove 1 at a time q 15 mins interval
- Inflammatory Disease of the Heart
o Pericarditis
 Acute or chronic inflammation of the pericardium
 Assessments
 Precordial pain
 Pain (inspiration, coughing, and swallowing)
 Pain worse when supine
 Pericardial friction rub
 Fever and chills
 Management
 Pos: side liying, high fowlers, upright or leaning forward
 Admin: analgesic, corticosteroids, NSAID’s
 Avoid aspirin and anticoagulants
 Antibiotics
 Diuretics and digoxin
 Monitor for complications: cardiac tamponade
o Over accumulation of pericardial fluid
o Pericardial effusion occurs when the space bet. The parietal and
visceral layers of the pericardium fill with fluid
o Etiology
 Stab wound
 Effusion
 Heart surgery
o Assessment
 Beck’s triad:
 Distended neck veins
o Compressed heart due to the cardiac
tamponade, no space to accommodate the
blood coming from the venous system,
cannot enter the R atrium
 Muffled heart sounds
o Interface of the fluid – not good conductor
of sound
 Hypotension
o Inability of the heart to contract
 Paradoxical Pulse
 More than 10 mm
  Chest pain
 Cardiogenic shock
 Increased CVP
 Management
 CC for hemodynamic monitoring
 PERICARDIOCENTESIS
o Spinal needle will enter the medistianum and aspirate the pericardial
fluid
 Admin IV fluid as prescribed
o Myocarditis
 Acute/chronic inflammation of the myocardium
 Etiology:
 Bacterial
o Staphylococcus /pneumococcal
 Viral
o Mumps / influenza
 Parasitic:
o Toxoplasmosis
 Radiation / Lead exposure
 Assessment
 Fever
 Pericardial friction rub
 Gallop rhythm
 Murmur
o Infective endocarditis
 S/S of HF
 Chest pain
 Management
 Pos: bed rest/ sitting up or leaning forward
 Monitor the pulse rate and rhythm
o Can result to arrhythmia
 Admin of NSAID / analgesics / salicylates for fever and pain
 Limit activities
o Prevent fatigue
 Admin digoxin / antidysrhythmic / antibiotics as prescribed
o Endocarditis
 Inflammation of the inner lining of the heart
 Expect valvular problem
 Assessment
 Fever
 Anorexia
 Wt loss
 Fatigue
 Cardiac murmur
 Janeway’s lesions
 Ossler’s Nodes
 Petechiae
 Splinter haemorrhages in nail beds
 Splenomegaly
 Rheumatic heart fever (valve)
 Management
 Balance activity with intermitted rest
 Antiembolic stockings
 Monitor emboli
o Splenic – sudden abd pain radiating to L shoulder / rebound
tenderness on palpitation
o Renal – flank pain radiating to the groin, hematuria and pyuria
o Cardiomyopathy
 Myocardium around left ventricle becomes flabby, altering cardiac function > decreased
CO2
 Inc HR and inc muscle mass compensate in early but later stage > HF
 Types
 Dilated (congestive)
o Dilated chambers contract poorly causing blood to pool and reducing
CO
 Hypertrophic (Obstructive)
o Hypertrophied LV cant relax and fill properly
 Assessment
 Chest pain
 Dyspnea
  Enlarged heart
 Crackles
 Dependent putting edema
 Enlarge liver
 Jugular vein distension
 Murmur
 Gallops
 Syncope
 Management
 Low Na diet
 Dual chamber pacing
 Surgery
 Heart transplant
 Cardiomyoplasty
o Valvular Heart disease
 3 types of mechanical disruption from VHD
 Stenosis or narrowing
o Doesn’t open the valve
 Insufficiency
o Incomplete
 Mitral insufficiency
o Same + peripheral edema
 Tricuspid insufficiency
o R sided HF
 Treatment
 Na restrictions
 Open heart surgery using CP bypass for valve replacement
 Medications
 Anticoagulants
 Nursing management
 Monitor for sign of HF or pulmo edema and monitor for adverse rxns from drug
therapy
 Place in upright position to relieve dyspnea
 Maintain bed rest
 If patient undergoes surgery, watch for hypotension
- Peripheral Arterial and Venous Disease
o Arterial Disease
 Buerger’s Disease
o Occlusive disease of the median and small arteries and veins
accompanied by clot formation
 Etiology
 Unknown
 Smoking
 Males
 Assessment
 Intermittent claudication
 Ischemic pain occurring in the digits while at rest
 Cool number tingling sensation
 Diminished pulse at distal extremitiy
 Ulceration
o Lower extremity
 Management
 Amputation
 Removal of the thrombus / clot supplying the area
 Instruct to stop smoking
 Monitor pulses
 Avoid injury to extremities
 Admin vasodilators ad prescribed
o Reynaud’s Disease
 Vasospasm of the arterioles and arteries of extremities
 Etiology:
 Cold
 Stress
 Smoking
 Management
 Stop smoking
 Vasodilators
 Avoid precipitating factors
 Warm clothing
 Avoid injuries to hands and fingers
 o Venous Diseases
 Thrombophlebitis
 Clots lead to vein inflammation
 Phlebothrombus
 A thrombus w/o inflammation
 Common in the antecubital area
 Phlebitis
 Vein inflammation usually assoc. with invasive procedures
 Deep Vein Thrombosis
 Pain (calf or groin tenderness)
 Positive Homan’s sign
 Warm skin and tender to touch
 Varicose Veins
 Distended protruding veins that appear darkened and tortuous; vein wall
weaken and dilate, the valves become incompetent
 Etiology
o Prolonged standing
o Pregnancy
o Obesity
o Congenital
 Incidence
o female
o 35-40 y/o

Assessment (in comparison with arterial diseases)

Arterial Venous
Intermittent claudication Heaviness and leg cramps
Cyanosis Redness
Coldness Warmth
Absent pulse Unpalpable pulse due to edema
Loss of sensation No loss of sensation
Gangrene ulcers Venous stasis ulcers
Decreased capillary refill (+) Trendelenburg test

 Intervention (Peripheral)
o Lower down legs
o Wear warm socks
o Beurger – Allens Exercise
o Avoid tight clothing
o Avoid obesity
o Avoid crossing legs
o Avoid smoking and cold weather
o Femoral artery bypass
o Angioplasty
o Amputation
 Intervention (Venous)
o Elevate legs
o Wear elastic stockings
o Ankle push up
o Avoid obesity
o Avoid crossing legs
o Avoid tight clothing
o Avoid smoking and prolong standing
o Vein striping and ligation
o Post op care
 Elevate legs
 CBR for 24 hrs
 Elastic compression
 Check for haemorrhage
 Prevent thrombophlebitis
o Aortic Aneurism
 Abnormal dilation of the arterial wall caused by localized weakness and stretching in the
medial layer or wall of the artery
 Types
 According to morphology or form
o Fusiform
o Saccular
o Dissecting
o False (Pseudoanuerysm)
 According to location
 o Thoracic aortic aneurysm
 S/s
 Pain
 Syncope
 Dyspnea
 Inc pulse
o Abdominal aortic aneurysm
 S/s
 Pulsating mass in the abd
 Systolic bruit over the aorta
 Tenderness on deep palpation
 Abdominal or lower back pain
o Cerebral aneurysm
 s/s
 headache
 vomiting
 ^ICP
 Intervention
o Prevent rupture
 Antihypertensive medications
 Modify risk factors
o Surgery
 Resection of aneurysm with Teflon/Dacron Graft
o Post Op
 Monitor for haemorrhage
 Flat pos / avoid SF pos
 O2 as ordered
 Coughing / breathing exercise
 Check distal pulses
 Avoid hip-knee flexion
 HYPERTENSION
 Abnormal elevation of BP above 140/90 mmHg based on at least 2 readings on
same condition
 Brain
o Cerebrovascular accidents
 Eyes
o Hypertensive retinopathy
 Heart
o L ventricular Hypertrophy resulting to HF or Cardiomyopathy
(Hypertophic)
 Kidneys
o Hypertensive Nephrosclerosis
 Types
 Primary / Essential / Idiopathic
o Most common
o 90-95 percent of cases
o Unknown cause
 Secondary
o With known cause
o Endocrine
 Neochromocytoma
 Hyperthyroidism
o Cardiovascular
 Artherosclerosis
o Renal
 Secondary to activation of renin angiotensin system
 Renal artery stenosis
o Pregnancy
 Increase in blood volume
 Vasospasm
 Preeclampsia
 Labile
o Intermittenly elevated BO
 Malignant
o Sever, rapidly progressing and sustained > leads to rapid end organ
complication
 White coat
o Elevation of BP only during clinical visits
 Assessments
 Signs and symptoms
 o Headach
o Depression
o Dizziness
o Nocturia
o Unsteadiness
o Tinnitus
o Blurred vision
o Memory loss
 Asymptomatic, L ventricular hypertrophy, cerebral ischemia, renal failure, visual
disturbances including blindness, epistaxis
 Management
 Step care approach
o Joint Committee on Detection, Evaluation and Treatment of High
blood Pressure pp 898
 Lifestyle modification
 Single Drug Therapy
 Mild hypertension – diuretics (thiazide) beta blockers
 Multi Drug Therapy
 Add: ACE Inhibitors
 Inc Dosage of Beta Blockers
 Add beta blocker to diuretics (Thiazides)
 Substitute vasodilators
 All receptor blockers (sartans)
 Anti-lipemics (statins)
 Add: vasodilator or slow calcium channel blocker to current regimen
 Add: sympatholytic / Antiadrenergics – central acting
 Major side effects
 Orthostatic hypertension
 Dizziness
 Cardiac rate alteration
 Sexual disturbance
 Drowsiness
 Health teachings
 Emphasize compliance
 Therapy is usually for life
 Monitor BP
 Do not increase of decrease dose without doctor’s order
 Do not abruptly discontinue meds