Cardiovascular Unit

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Cardiovascular Unit

• By Pat Pence, RN, C, MSN

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Heart

• Located in mediastinum.
• Base (wider) is superior and under the 2nd rib.
• Apex (narrow) is inferior and slightly to the
  left between 5th and 6th ribs.

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Heart wall

• Composed of 3 layers.
• Pericardium transparent, thin layer, lines
  outside of heart, 2 layers that contain serous
  fluid to decrease friction.
• Myocardium middle, thickest and strongest,
  actual contracting muscle tissue.
• Endocardium innermost layer, thin layer of
  connective tissue.

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4 Heart chambers

• Right atrium receives deoxygenated blood from
  superior vena cava, inferior vena cava and
  coronary sinus.
• Right ventriclepumps blood to lungs via
  pulmonary artery.
• Left atrium receives O2 rich blood from lungs
  via pulmonary veins.
• Left ventricle PMI, thickest, most muscular,
  pumps blood to all parts of body via aorta.
• Separated by septum.

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4 Heart valves

• Heart functions as 2 separate pumps.
• Heart valves keep blood flowing forward and
  prevent backflow (regurgitation).
• Tricuspid valve and mitral valve (AV valves).
• Chordae tendineae and papillary muscles connect
  valves to walls of heart and promote a tight seal
  to prevent backflow.

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Semilunar valves

• Pulmonary semilunar valve between Rt ventricle
  and pulmonary artery.
• Aortic semilunar valve between left ventricle
  and aorta.

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Coronary blood supply

• Heart requires a constant supply of O2 rich blood
  and return of O2 poor blood from tissue to the
  lungs.
• Rt./Lt. Coronary arteries.
• Coronary vein and coronary sinus.
• Collateral circulation.

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Blood vessel pattern

• Artery largest, vessels that carry blood away
  from heart thicker, elastic and muscle tissue.
• Arteriole smooth muscle, deliver blood to
  tissues dilate or constrict in response to low
  O2/hi CO2, affect BP blood flow.
• Capillary endothelial cells, allow exchange of
  products no muscle or elastic tissue.

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• Venules small amounts of muscle and connective
  tissue.
• Veins larger veins have valves to prevent
  backflow of blood carry blood back to heart
  large diameter, thin walled.

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Pulmonary circulation

• Deoxygenated blood passes through pulmonary
  circulation to receive O2.
• Right ventricle, pulmonary semilunar valve,
  pulmonary artery, pulmonary capillaries,
  pulmonary veins, left atrium, bicuspid valve,
  left ventricle, aortic semilunar valve, and
  aorta.

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Systemic circulation

• Refers to blood pumped from lt ventricle to all
  parts of body and then to rt atrium.
• Aorta largest artery, main trunk of systemic
  arterial circulation.
• Vena cava returns deoxygenated blood to rt
  atrium.
• Superior vena cava from head, neck, chest, and
  upper extremities.
• Inferior vena cava from parts of body below
  diaphragm.

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Electrical conduction system

• Automaticity specialized ability to contract in
  rhythmic pattern.
• Irritability excitability or sensitivity.
• Hormones, ion concentration, changes in body
  temp. affect the conduction system.
• Depolarization contraction.
• Repolarization relaxation (resting state).

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Impulse pattern

• Initiated in SA node in Rt. Atrium. Pacemaker
  of heart. Internodal pathways to atria.
• AV node Rt atrium, slows impulses to allow
  atrium to contract and ventricles to fill.
• Bundle of His group of conduction fibers in base
  of rt atrium.
• Rt. and Lt. Bundle branches in septum.
• Perkinjes fibers surround ventricles.

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Cardiac cycle systole/diastole

• Refers complete heartbeat.
• Systole contraction, blood is pumped out of
  the ventricles. (depolarization).
• Atria relax to receive blood. (repolarization).
• AV valves close S1 first heart sound.
• Ventricles contract in response to electrical
  impulse having passed through.

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Diastole

• Diastole relaxation, blood enters the relaxed
  chambers.
• Ventricles fill.
• Semilunar valves close S2 2nd heart sound.
• Atria contract in response to electrical impulse.

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Stroke volume/cardiac output

• Stroke volume volume of blood ejected (pumped)
  during each ventricular contraction (heartbeat).
• Cardiac output amount of blood ejected (pumped)
  by each ventricle per minute.
• CO SV X HR.
• Numerous factors affect CO.

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Stroke volume factors

• Preload volume of blood within ventricles at end
  of diastole, comes from veins, before next
  contraction. Preload determines the amount of
  stretch placed on the myocardium.
• Afterload pressure that ventricles work against
  when they contract to eject blood from the heart.
  That pressure is located in arteries (peripheral
  resistance or arterial BP).

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• Normal heart overcomes afterload and maintains CO
  except when muscles have been damaged.
• Contractility increased by norepinephrine and
  epinephrine.
• Increased preload, afterload and contractility
  increase workload and O2 demand on heart.

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Inotropic state

• Inotropic state strength of myocardial
  contraction unrelated to blood volume.
• Affected by sympathetic stimulation, metabolic
  abnormality, hypoxemia, metabolic acidosis, drugs
  (epinephrine).

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Starlings law

• To a point the heart will pump out all blood it
  receives within certain limits.
• The more the fibers are stretched, the greater
  their force of contraction.
• If stretched beyond capacity- blood will
  accumulate in ventricles and back up into
  pulmonary system.

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Heart sounds

• Produced by closure of valves.
• Lubb (S1) long duration, low pitch, AV valves
  close.
• Dubb (S2) short duration, sharp sound, semilunar
  valves close.
• Murmur swishing sound, may be normal or abnormal.

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Cardiovascular assessment

• Subjective data past CV problems, health habits
  (smoking, diet, activity), current CV problems.
• History description of symptoms, when they
  occurred, course and duration, location,
  precipitating factors, relief measures.

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Pain

• Character, quality, radiation, associated
  symptoms.
• Rated on pain scale.
• Location chest, radiated to jaw, left shoulder.
• Description dull, sharp, pressure, squeezing,
  crushing, viselike, grinding, radiating.
• Precipitating onset.
• Pain in extremities or lack of sensation.

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Palpitations

• Characterized by rapid, irregular, or pounding
  heartbeat.
• Associated with dysrhythmias or ischemia.

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Dyspnea

• Exertional dyspnea is associated with decreased
  cardiac output.
• DOE, DAR, PND, orthopnea.

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Cough

• Dry, productive, irritating, spasmodic.
• May be associated with dyspnea.

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Fatigue

• Exhaustion/ activity intolerance.
• Associated with decreased cardiac output.
• Depression may associated with fatigue.

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Syncope

• Fainting brief lapse of consciousness.
• Caused by transient cerebral hypoxia.
• Sudden decrease in cardiac output to brain
  resulting from dysrhythmia or decreased pumping
  action of heart.
• Preceded by lightheadedness.

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Objective data

• Vital signs. LOC.
• Lung sounds. Bowel sounds. Sputum.
• Heart Apical pulse, heart sounds, carotid
  arteries, systemic with no bruit.
• Jugular veins not distended when sitting or
  standing.
• Extremities color, temp, moisture, edema, hair
  distribution, capillary refill, clubbing,
  peripheral pulses, Homans sign, turgor.

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Cyanosis

• Caused by excess of deoxygenated Hgb in blood.
• Results from decreased cardiac output and poor
  peripheral perfusion.

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Diaphoresis

• Profuse sweating associated with clamminess.
• Result of decreased cardiac output and poor
  peripheral perfusion.

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Edema

• Wt. Gain of more than 3lb. In 24 hours.
• Inability of heart to pump efficiently or accept
  venous return, causes backflow of blood and
  increased blood volume.
• Increased hydrostatic pressure results and an
  increase in fluid to interstitial spaces.

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Diagnostic Tests
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CBC

• Determination of RBCs, WBCs, platelets, Hgb, Hct.
• Low Hgb decreased O2 carrying capacity
• High WBC infection or inflammation.
• High RBC body compensating for chronic
  hypoxemia by stimulating RBC production in bone
  marrow, leading to secondary polycythemia.

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Cardiac enzymes

• Elevated amounts of enzymes (proteins, cardiac
  markers) are released into blood during cardiac
  muscle cell damage.
• These enzymes are helpful in determining the
  degree of myocardial damage and the timing of
  onset of damage.
• Some enzymes are more specific to cardiac muscle
  tissue.

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Creatine phosphokinase (CPK)

• Enzyme found in brain, skeletal muscle, and
  myocardium.
• Can be broken down into isoenzymes.
• CPK II (MB) is more specific to cardiac tissue.
  Levels gt 7.5 ng/ml associated c MI.
• Onset 3-6 hours peak 12-18 hours duration 3-4
  days.

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Lactic dehydrogenase (LDH)

• Found in many body tissues (cardiac, kidneys,
  RBCs, brain, stomach, skeletal muscle). Normal lt
  100 U/L.
• Late indicator of damage.
• Rises in 24-72 hours peaks in 3-4 days returns
  to normal levels in about 14 days.
• Not as specific as other enzymes.

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Myoglobin

• Small O2 binding protein found in cardiac and
  skeletal muscle.
• Because it is smaller when compared to larger
  enzymes, it is detected earlier.
• 1-4 hours after onset. Peak 6-9 hrs.
• Must be done within 1st 18 hrs after onset.
• Normal lt 92 men lt 76ng/ml women.

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Troponin

• Protein located on cardiac and skeletal muscle
  tissue.
• 3 forms. Troponin I is more specific found
  exclusively in cardiac tissue.
• Onset 3-6 hours peaks 14-20 hours returns to
  normal in 5-7 days.
• Elevated levels of Troponin I is diagnostic of
  MI. Range 0 - 0.4ng/mL.

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Serum Lipids

• Cholesterol fatty substance coated with 2 types
  of proteins. LDL or HDL.
• Total cholesterol level is sum of all
  cholesterols. Level should be lt 200mg/dl.
  (nonfasting test).
• Associated with diet high in saturated fat,
  cholesterol and calories.

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• Hyperlipidemia elevated levels of any or all of
  lipids in plasma.
• Triglycerides Mixture of fatty acids.
• Normal 40-190 ng/dl.

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HDL/LDL

• HDL and LDL need to fast 12 hrs.
• High-density lipoprotein good cholesterol.
  More protein than fat.
• Removes cholesterol from vessels and transports
  to liver for removal.
• Higher the level less risk of CAD.
• Desirable level 35 or gt.

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LDL

• Low-density lipoprotein bad cholesterol.
  Promotes CAD.
• Equal amount of fat and protein.
• Transports cholesterol from the liver to body
  tissues, accumulating in vessel walls.
• Level lt 160mg/dl (c no risk factors). Higher the
  level greater risk of CAD. Desired level for
  LDL depends on the risk factor profile of pt.
  More risks a goal for a lower LDL level. (ex.
  100mg/dl)

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EKG

• A graphic representation of the hearts
  electrical activity reflected by changes in the
  electrical potential at the skin surface.
• Recorded as a tracing on a strip of paper.
• Resting EKG over lt one minute.
• Telemetry continuous visualization on a screen
  (monitor).

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Purposes

• Identify rhythm disturbances.
• Provides information about the position of the
  heart in the chest and the size of the chambers.
• Detects electrolyte imbalances.
• Monitors the effectiveness of pacemakers and
  cardiotonic meds.

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Holter monitor

• Ambulatory EKG a type of portable EKG which
  records 12- 48 hours of usual pt.s activities
  with normal stress.
• Pt keeps a diary of activities and symptoms.
• Purposes determines exercise tolerance post-MI.
  Provides more diagnostic information.

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• Inpatient or outpatient basis.
• Detects intermittent arrythmias c ADLs c
  associated manifestations of dizziness,
  palpitations, chest pain.
• Guages antiarrythmic meds.
• Instruct pt to update diary regularly and note
  any symptoms not to get monitor wet.

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EKG waveforms

• P wave depolarization or contraction of the
  atria. SA node fires impulse, delay by AV node
  seen as space after P wave.
• QRS complex ventricles depolarize or contract,
  atria repolarize (relax), strong signal because
  of greater mass of ventricles.
• T wave ventricles repolarize or relax.

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• Intervals are the length of time it takes the
  impulse to travel from one area of heart to
  another.
• Cardiac dysrhythmias result of abnormal pacemaker
  function.

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Cardiac dysrhythmias (arrhythmia)

• Any cardiac rhythm that deviates from normal
  sinus rhythm.
• The result of alteration in the formation of
  impulses through the sinoatrial node.
• Results from irritability of myocardial cells
  that generate impulses.
• SS and treatment vary depending on type and
  severity.

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• Classified according to origin (atrial or
  ventricular),
• Mechanism bradycardia, tachycardia, or both.

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Normal sinus rhythm

• Originates in SA node.
• Characterized by
• Rate 60-100 beats/min.
• P waves precede each QRS complex. (atrial
  depolarization)
• P-R interval interval between atrial and
  ventricular repolarization.

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• QRS ventricular depolarization.
• T wave ventricular repolarization.
• Rhythm regular.

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Sinus Tachycardia

• A rapid regular rhythm.
• Originates in SA node.
• Rate 100 or gt.
• SS occasional palpitations, hypotension,
  angina.
• Most are asymptomatic.

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Sinus Bradycardia

• A slow rhythm.
• Originates in SA node.
• Rate lt60.
• SS fatigue, lightheadedness, syncope.
• Some are asymptomatic.

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Atrial fibrillation

• A very rapid production of atrial impulses.
• Atria beat chaotically resulting in improper
  contraction.
• Rate 350-600.
• SS pulse deficit, palpitations, dyspnea,
  angina, lightheadedness, pulmonary edema,
  decreased cardiac output.
• May cause emboli or CHF.

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Premature Ventricular Contractions

• PVCs early ventricular beats that occur in
  conjunction with regular rhythm.
• Originates in more than one location in
  ventricles.
• SS depend on frequency of PVCs and their effect
  on ability of heart to pump effectively.

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• Some are asymptomatic.
• Palpitations, weakness, lightheadedness,
  decreased cardiac output.
• PVCs that last long enough to cause ventricular
  tachycardia may lead to death.

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Ventricular Tachycardia

• A regular or slightly irregular rhythm in which 3
  or more successive premature ventricular
  contractions occur.
• Rate 140-240.
• Life threatening.
• May lead to ventricular fibrillation and death.

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Ventricular fibrillation

• Ventricular muscles are quivering.
• Characterized by rapid and disorganized
  ventricular pulsation.
• Medical emergency.
• SS are a result of no cardiac output.
• Loss of consciousness, lack of pulse, loss of BP
  and respirations, possible seizures, and sudden
  death if untreated within 3 min.

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Cardiac arrest

• A sudden cessation of cardiac output and
  effective circulation.
• Usually precipitated by ventricular fibrillation
  or ventricular asystole.
• Asystole a life threatening cardiac conduction
  characterized by absence of electrical and
  mechanical activity in heart. SS lack of pulse
  and breathing.

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• Atrial arrhythmias prevent proper filling of
  ventricles and decrease CO.
• Ventricular arrhythmias prevent proper filling of
  ventricles, decrease or absent CO.
  Life-threatening.
• V Tach is likely to result in V Fib and death.

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Arteriogram

• Series of radiographs taken after an injection of
  radiopaque dye into a coronary artery.
• Diagnose vessel occlusion, pooling in chambers of
  heart, and congenital anomalies.

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Stress Test

• Exercise EKG.
• Types Treadmill walking, then increase speed
  and incline until pt reaches a target HR, has
  chest pain, fatigue, extreme dyspnea, vertigo, or
  claudication (calf pain c walking, relieved c
  rest).
• Stationary bicycle.

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• MUGA (multigated acquistion scan) use of
  computers with EKG during scanning.
• Persantine pharmacological stress test.
  Vasodilator. No caffeine 12 hrs. prior.
• Thallium nuclear agent used during scan.
• Purpose To evaluate CV fitness prior to an
  exercise program,
• To diagnose exercise induced symptoms and
  arrythmias,
• To evaluate the effectiveness of meds.

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• Nursing care No eating, drinking, or smoking 2
  hours prior.
• Wear comfortable clothes.
• Continue all meds.
• Vitals, monitor.
• The earlier manifestations developed more
  serious the heart disease is.

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Cardiac catheterization

• Invasive procedure used to visualize heart
  chambers, valves, great vessels, and coronary
  arteries in order to determine the degree of
  blockage.
• Catheter is inserted through a peripheral vessel
  and advanced to heart chambers.
• Dye injected to assist in examining structure and
  motion of the heart.

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• Measure pressure within heart.
• Measure blood-volume relationship to cardiac
  competence.
• Determine valvular defects, arterial occlusion,
  or congenital anomalies.
• Blood samples obtained.

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Nursing care

• Check for allergy to iodine (used as contrast
  medium).
• Consent. NPO. Give sedative as ordered.
• Instruct will feel warmth/fluttering sensation as
  catheter is passed.
• Post-procedure Pressure dressing and 5-10lb.
  sandbag used to provide pressure over site to
  prevent hemorrhage.

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• Supine position 4- 8hrs. Then elevate HOB 30
  degrees.
• Inspect site for bleeding and swelling.
• Monitor vital signs, heart and lung sounds,
  peripheral pulses, color and sensation.
• Encourage fluids to eliminate dye.
• Monitor IO, labs.
• Advise pt. to report chest pain.

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Percutaneous transluminal coronary angioplasty
(PTCA)

• Invasive surgical procedure performed in cardiac
  cath lab.
• Consent required.
• Balloon tipped catheter is guided by fluoroscopy
  from the femoral or brachial artery to the
  coronary arteries.
• Balloon is inflated intermittently and opens
  narrowed vessel to improve blood flow.

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• 1-2 hour procedure.
• Mild sedative is given.
• Post procedure monitor catheter insertion site
  for hemorrhage.
• Risk for complications.

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Stent Placement

• Used to treat abrupt or threatened vessel
  occlusion following PTCA.
• Expandable, meshlike structures compress against
  vessel wall.
• Potential for thrombus formation must be on
  anticoagulants for 3 months.
• Complications hemorrhage, injury, dysrhythmias.

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Risk factors for CV disease

• Nonmodifiable family history,
• Age gt with elderly.
• Sex men gt risk, but incidence increasing in
  women.
• Race African-American males (high BP, CVA),
  Hispanics with diabetes, Caucasians have highest
  rate of CV disease, higher total cholesterol
  levels.

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Modifiable factors

• Smoking 2-3 X gt risk than nonsmokers. More
  Caucasian women smoke than other women.
• Hyperlipidemia diet, exercise, meds.
• Hypertension BP gt 140/90 mm Hg.
• Diabetes mellitus related to elevated BS levels,
  altered lipid metabolism c elevated cholesterol
  and triglycerides.

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• Obesity increases workload. Increased obesity
  among Americans.
• Sedentary lifestyle exercise lowers BS levels,
  improves ratio of HDL to LDL, reduces Wt., BP,
  stress, and improves well-being.
• Stress releases catecholamines, results in
  vasoconstriction.

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• Oral contraceptives
• Psychosocial factors Type A personality.
• Asthma more prone to heart disease meds side
  effects or chronic lung inflammation damages
  arteries.
• Homocysteine elevated levels triple your risk
  amino acid associate with folate deficiency.

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Dietary Modifications

• Total fat intake lt 30 of total calories.
• Saturated fats lt 10 of total calories.
• Sodium under 1g of sodium for every 1,000
  calories consumed.
• Cholesterol lt 300mg. (eggs, meat, butter, whole
  milk)
• Alcohol moderation.

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• Polyunsaturated fats lower both LDL and HDL (corn
  oil).
• Monounsaturated fats lower only LDL. (olive oil,
  canola oil).
• Dietary supplements Vitamin E, antioxidant.

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Common cardiac drugs

• Adrenergics
• Adrenergic blockers.
• Diuretics.
• Beta-blockers.
• Calcium channel blockers.
• ACE inhibitors.
• Vasodilators.

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Adrenergics

• Stimulate the sympathetic nervous system.
• Act on one or more of adrenergic receptor sites.
• Alpha 1-receptor increases force of contraction
  of heart vasoconstriction, increases BP.
• Alpha 2-receptor inhibits release of
  norepinephrine, vasodilator, decreases BP.

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• Beta1- receptor increases HR/force of
  contraction, renin secretion and BP.
• Beta 2- receptor bronchodilation.
• Many of adrenergic drugs stimulate more than one
  receptor site.
• Epinephrine sc or IV, inhalation, topically. Not
  po. Used in shock, cardiac arrest.

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• Dopamine to correct hypotension.
• Ephedrine HCL hypotension. (OTC meds).
• Norepinephrine bitartrate shock, potent
  vasoconstrictor.
• Side effects hypertension, tachycardia,
  palpitations, dysrhythmias, tremors, dizziness,
  difficulty urinating, nausea, vomiting.

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Nursing implications

• Monitor vitals and for side effects.
• Monitor urinary output for retention.
• Check IV site for tissue necrosis.
• Offer food to avoid N/V.
• Instruct pt. to read med labels.

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Adrenergic Blockers

• Stimulate alpha2 receptors , decrease sympathetic
  response, decrease epinephrine, norepinephrine
  and renin release, resulting in decreased
  peripheral vascular resistance.
• (promote vasodilation to decrease BP)
• Minimal effect on CO and renal blood flow.
• Can cause Na/H2O retention. Given c diuretic.

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• Side effects orthostatic hypotension,
  tachycardia, bradycardia, dry mouth, drowsiness
  and dizziness.
• Not used as frequently.
• Methyldopa (Aldomet) one of 1st drugs widely used
  in controlling hypertension.
• Clonidine 7 day transdermal patch.

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Alpha adrenergic blockers

• Block alpha adrenergic receptors to promote
  vasodilation and decrease BP.
• Benefits do not affect BS, lipids, or
  respiratory function.
• Prazosin HCL (Minipress) selective
• Diuretic added to reduce edema.
• Side effects hypotension, tachycardia, wt. Gain,
  nausea, drowsiness, nasal congestion.

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• If taken with NTG can cause syncope.
• If taken with other hypertensive drugs or alcohol
  can cause hypotension.
• Monitor for fluid retention.
• Encourage pt to decrease salt intake.
• Therapeutic effect takes 4 weeks.

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• Beta-adrenergic blockers decrease HR, BP, CO,
  and force of contractions.
• Inderal nonselective (beta1 and 2) many side
  effects- bronchoconstriction.
• Metaprolol (Lopressor) cardioselective.
• Uses cardiac dysrhythmias, hypertension,
  tachycardia, and angina.

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Side effects

• Beta-adrenergic blockers bradycardia, dizziness,
  hypotension, HA, mood changes.
• Nursing Monitor vital signs, assess lung sounds,
  instruct to avoid stopping med and to avoid
  orthostatic hypotension.

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Alpha/beta blockers

• Causes vasodilation, decreased HR and
  contractility of heart.
• Large doses increase airway resistance- decreased
  dosage necessary in asthma pts.
• Labetalol HCL (Trandate, Normadyne).
• May cause orthostatic hypotension, palpitation
  and syncope.

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Diuretics

• Thiazides
• Loop diuretics
• Osmotic diuretics
• Carbonic anhydrase inhibitors
• Potassium-sparing diuretics

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Diuretics

• Purpose to decrease BP and edema.
• Single or combination therapy.
• Produce diuresis by inhibiting Na and H2O
  reabsorption in one or more segments of the renal
  tubules.
• Diuretics that act closest to the glomeruli have
  the greatest effect on Na loss.
• Potassium-wasting or sparing.

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• Combination diuretics may promote both K wasting
  and sparing.
• 5 categories thiazide/thiazide-like
• loop
• osmotic
• carbonic anhydrase inhibitor
• potassium-sparing

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Thiazides

• Act on the distal convoluted tubule to promote Na
  and H2O excretion and cause vasodilation to
  decrease BP.
• Used in pts. c normal renal function.
• Not for immediate treatment.
• Increases BS. Monitor BS.

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• Should be taken in am (long half-life) to avoid
  nocturia.
• Can elevate lipids and uric acid.
• Can cause hypokalemia and hypocalcemia (potential
  for digitalis toxicity).
• HCTZ is usually 1st one in this group ordered.
  Inexpensive/ well tolerated.

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Nursing implications

• Assess vital signs, wt., urine output, labs, BS,
  edema.
• Advise to take in am and c food.
• Instruct to include foods rich in K or may need
  K supplement.
• Instruct pt. regarding potential for postural
  hypotension.

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Loop diuretics

• Potent drugs that act on ascending loop of Henle
  by inhibiting Cl transport of Na into
  circulation.
• No effect on BS.
• Edecrin is most potent and rarely used.
• Bumex is more potent than Lasix.
• Can be used in pts.c renal disease.

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• Main side effects fluid and electrolyte
  imbalances, high uric acid, elevated lipids.
• Digitalis toxicity can result due to loss of K.
• Lasix PO onset of action 30-60 IV- 5.

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Osmotic diuretics

• Act by increasing concentration of plasma and
  fluid in renal tubules, Na, Cl, K, and H2O loss.
• Used to prevent kidney failure, decrease ICP and
  IOP.
• Mannitol IV potent K wasting diuretic used in
  emergency.

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• Uses to prevent acute renal failure
• decrease cerebral edema
• reduce IOP in narrow-angle glaucoma
• promoted diuresis in chemotherapy pts.

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Carbonic anhydrase inhibitors

• Act by blocking the action of enzyme carbonic
  anhydrase which causes increased Na, K, and
  bicarbonate excretion.
• Potential for metabolic acidosis high BS, uric
  acid, and Ca levels.
• Uses decrease IOP, for edema, seizures.
• Diamox PO or IV.

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Potassium-sparing diuretics

• Mild diuretic that is weaker than thiazides and
  loop diuretics.
• K supplements should NOT be used.
• Act in collecting tubules and interfere c NaK
  pump controlled by aldosterone.
• More effective if used c K wasting diuretic
  (Aldactone and HCTZ).

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Nursing implications

• Side effects hyperkalemia.
• Should not be taken c ACE inhibitor because both
  spare K.
• Instruct pt. to avoid foods rich in K.
• Monitor for hyperkalemia labs, EKG, vital signs,
  nausea, diarrhea, ABD cramps.

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Vasodilators

• Potent antihypertensive drugs that cause
  vasodilation.
• Peripheral edema results due to Na/H2O retention
  given c diuretic.
• Reflex tachycardia results due to vasodilation
  given c beta blocker.

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• Diazoxide (Hyperstat) and Sodium nitroprusside
  (Nipride, Nitropress) used in hypertensive
  emergency.
• Hydralazine HCL (Apresoline) used for
  hypertension.

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ACE Inhibitors

• Act by inhibiting angiotensin-converting enzyme,
• Inhibits formation of angiotensin II (prevents
  vasoconstriction)
• Blocks release of aldosterone (Na retaining
  hormone) resulting in Na and H2O excretion.
• Used to treat hypertension or CHF.

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• African-Americans and elderly need a diuretic
  added to achieve therapeutic response.
• 10 different drugs in this category.
• 1st drug Captopril (Capoten).
• Most drugs end in pril.

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• Side effects hypotension and hyperkalemia.
• Nursing implications Should not be given c
  Potassium-sparing diuretics or salt substitutes
  containing potassium.
• Captopril is given 20 to 1 hr ac.

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Angiotensin II blockers

• New drugs similar to ACE inhibitors.
• Block angiotensin II from receptors.
• Cause vasodilation and decreased peripheral
  resistance.
• Losartan (Cozaar).
• Can cause angioedema.
• Not as effective c African-Americans.

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Calcium channel blockers

• Decrease calcium levels and promote vasodilation
  decreased BP.
• Better BP response in African-Americans.
• Verapamil (Calan), Diltiazem (Cardizem),
  Nifedipine (Procardia).
• Side effects dizziness, bradycardia,
  hypotension, HA.

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Cardiac glycosides

• 3 effect on heart
• 1. Positive inotropic action (increases
  myocardial contraction, CO).
• 2. Negative chronotropic action (decreases HR).
• 3. Negative dromotropic action (decreases
  conduction of heart cells).

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• Used to treat CHF, atrial flutter or atrial
  fibrillation.
• Nursing Check apical pulse for 1. HOLD if lt60.
• Potassium-wasting diuretics and cortisone c
  digoxin can result in hypokalemia and digoxin
  toxicity.

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• Digitoxin (potent cardiac glycoside c long
  half-life) vs Digoxin.
• Ensure that correct drug is given.
• Check serum digoxin levels.
• Normal level 0.5- 2.0 ng/mL.
• Check serum K levels.

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• Instruct pt. to eat foods rich in K.
• Monitor for signs of digoxin toxicity anorexia,
  nausea, vomiting, bradycardia, cardiac
  dysrhythmias, visual disturbances.
• Monitor response to med decreased HR, decreased
  rales.
• Teach pt to take pulse and when to call MD.

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Antianginal drugs

• Nitrates
• Beta blockers
• Calcium channel blockers

124

• Increase blood flow by increasing O2 flow or
  decreasing O2 demand.
• Nitrates relax coronary arteries and dilates
  veins.
• Beta blockers decreases HR/contractility to
  decrease O2 demand.
• Calcium channel blockers relax coronary
  arteries, dilates arterioles, decrease
  HR/contractility.

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Nitrates

• Nitroglycerin (NTG) 1st drug to treat angina.
• Must be given SL, ointment, patch, IV.
• Give NTG 1 tab (0.4mg or gr1/150) SL q 5 up to 3
  doses until chest pain relieved. Call MD if pain
  not relieved by the 3rd dose.
• Monitor BP and pulse.
• May have stinging/biting sensation.

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• Side effects HA (most common), dizziness or
  faintness.
• Nitrobid ointment not used as much due to effect
  lasts only 6-8hrs.
• Transderm Nitro patch applied daily. Rotate
  sites.
• Tylenol can be given for HA.
• Taper dose of ointment and patch.

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Other nitrates

• Isosorbide dinitrate (Isordil) PO, SL, chewable,
  SR forms. Flushing may occur.
• Isosorbide mononitrate (Imdur) PO, SR.
• Tolerance to nitrates may develop. SR Imdur form
  provides continued delivery and decreases
  tolerance.

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Nursing implications.

• Have pt sit or lie down when giving initial dose
  and when giving NTG.
• Monitor vital signs.
• Give sip of water prior to NTG to enhance
  absorption.
• Instruct pt when to call MD.

129
Drugs for Circulatory disorders

• Anticoagulants/antiplatelets
• Thrombolytics
• Antilipemics
• Peripheral vasodilators

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Anticoagulants

• Used to inhibit new clot formation in veins.
• Do NOT dissolve clots already formed.
• Heparin binds c antithrombin III, inactivates
  thrombin, inhibits conversion of fibrinogen to
  fibrin.
• Must be given subcut for prophylaxis, IV to treat
  acute thrombosis.

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• Monitor PTT.
• Monitor for bleeding.
• Protamine sulfate IV is antidote.
• Side effects itching and burning.

132
Low molecular weight heparins

• Lower risk of bleeding. Protamine sulfate is
  antidote.
• More stable response. Can be started inpt. and
  taught to give injections at home.
• PTT not needed.
• Binds to antithrombin III.
• Enoxaparin (Lovenox), dalteparin (Fragmin).

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• Given subcut BID in ABD.
• Prefilled syringes.
• Instruct pt not to take other antiplatelet drugs
  (ASA).

134
Coumadin

• Long term oral anticoagulant.
• Inhibit hepatic synthesis of Vit K and affecting
  clotting factors.
• Warfarin (Coumadin) most commonly used form.
• Monitor PT/INR. (INR 2-3)
• Monitor for bleeding. (Vit K/blood or platelets
  are given as antidote).

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Antiplatelets

• Prevents thrombosis in arteries by suppressing
  platelet aggregation.
• Used to prevent MI or CVA.
• ASA, dipyridamole (Persantine), ticlopidine
  (Ticlid).
• DC ASA one week prior to any surgery.

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Thrombolytics

• Used to dissolve clots by converting plasminogen
  to plasma.
• Reduces tissue necrosis caused by blocked
  artery.
• Used to treat coronary artery thrombi, DVT,
  pulmonary embolism.
• 5 drugs ex. Streptokinase.

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• Must by given IV and within 4-6 hrs.
• Side effects hemorrhage, allergic reaction.
• Contraindications recent bleeding (CVA, trauma,
  taking anticoagulants or ASA) and severe
  hypertension.
• Antidote aminocaproic acid (Amicar).
• Labs CBC, PT, EKG. Monitor vitals and for signs
  of bleeding.

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Antilipemics

• Lower abnormal lipid blood levels when diet,
  exercise and smoking cessation are ineffective.
• Resins bind c bile acids in intestine.
  Cholestyramine (Questran) Colestipol (Colestid).
  Powder mixed c water or juice. Side effects
  constipation, peptic ulcer.
• Fibric acid derivatives gemfibrozil (Lopid).

139

• Nicotinic acid (Niacin, Vit B2) very effective
  but has many side effects (flushing, GI).
  Requires large doses. Careful monitoring.
• Statins inhibit enzyme HMG CoA reductase in
  cholesterol synthesis in liver.
• Reduces cholesterol within 2 weeks.
• Names end in statin.

140

• Ex Lovastatin (Mevacor), atorvastatin (Lipitor),
  simvastatin (Zocor), pravastatin (Pravachol).
• Statins are contraindicated in liver disease.
• Nursing implications for all antilipemics
• Give c water/meals. Monitor liver enzymes, lipid
  levels, vital signs. Instruct pt. drug therapy is
  lifetime commitment. Not a replacement for
  diet/exercise.

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Peripheral vasodilators

• Increase blood flow to extremities and promote
  vasodilation.
• Used in peripheral vascular disease.
• Ex. Vasodilan.
• Side effects tachycardia, hypotension, flushing,
  HA dizziness, GI.

142
Nursing implications

• Assess vital signs and circulation to
  extremities.
• Instruct pt. not to smoke, drink alcohol, or use
  ASA like drugs without MD approval.
• Take med with meals.