406 EXAM 2 STUDY GUIDE
Unit 2 Cardiovascular
History
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Use of:
o Tea and coffee
o Over-the-counter drug use: Ibuprofen, Acetaminophen, Benadryl
 OTC’s can cause blood pressure problems – like cold medicine – it’s okay just not long-term
o Smoking: Cigarettes, cigars, smokeless tobacco
o Exercise: What, and how often
o Sleep & dietary habits: Use of sleep aids
 Do they use a sleeping aid? CPAP or BIPAP?
o Use of illegal recreational drugs (e.g., cocaine)
o Use of alcohol (occasional/daily)
Lifestyle pattern and responsibilities: Working, relaxing, coping, cultural habits
Social support systems: Recent life changes within the past 12 months
Emotional state: is there any evidence of psychological stress, anger, anxiety, depression.
What is their perception of illness and its meaning for the future?
Risk factors:
o Gender/age/cultural identity
o Sedentary lifestyle
o Family history of premature CAD (age
o Obesity
under 65 years)
o Family History
o Smoking history
o CAD at age 65 years or younger
o Hypertension
o Myocardial infarction/early death of
o Hyperlipidemia
unknown etiology
o Cardiac Studies or Interventions Done in the Past:
 Cardiac catheterization
 Thrombolytic therapy
 Electrophysiology study
 PTCA
 Cardiac ultrasound
 Atherectomy
(echocardiogram)
 Stent placement
 12–Lead ECG
 Valvuloplasty
 Exercise electrocardiography
 Medical History
test (stress test)
 Childhood History:
 Murmurs, cyanosis, streptococcal infections, rheumatic fever
Surgical history
Allergies
o Especially to emergency medication (lidocaine, morphine), radiographic contrast agents, or iodine
(shellfish)
o Recent dental work or infection
Medications
o Have to have physician order to continue their home meds
 Hormone replacement therapy
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Oral contraceptives
Nonprescription medications/herbal remedies
Physical assessment
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Face: Tongue: Shows central cyanosis.
o Tongue is most important part of face – if tongue is blue-ish it often means they have central cyanosis
o Ask them to stick out tongue also shows neuro status
Thorax: Scars, bulges: Pacers/defib. Implants.
Abdomen: Distention/Ascites: Right -sided Heart Failure
Nail beds
o Clubbing: Sign of long standing central cyanotic heart disease or pulmonary disease with hypoxia.
Lower extremities
o Arterial Disease: Pale, shiny legs with spares hair growth. –Often ACUTE PAIN!
 No oxygen to tissues
o Venous Disease: Edematous limb. PAIN, but more CHRONIC!
 Feet swollen
 Red/brown discolorations
Posture/Mentation/JVD
o Posture: Notation of the effort to breathe.
 They need to sit up as straight as possible so we can assess their breathing
o Mentation: Signs of confusion/lethargy
 Could be a sign of hypotension, low cardiac output or hypoxemia.
o Jugular Veins: Distention is a sign of fluid overload and right ventricular dysfunction. (preload/CVP is
elevated)
 Measured as Central Venous Pressure or CVP. Normal is: 5-12.
 right side of heart (pulmonary side)
palpation of pulses
o PULSE PALPATION SCALE:
 0--Not palpable
 2+--Palpable (normal pulse)
 1+--Faintly palpable (weak and
 3+--Bounding (hyperdynamic
thready)
pulse)
o Which pulses does the nurse assess?
 Carotid, Apical, Radial and Pedal Pulses
 Can’t feel it? Get the Doppler.
Edema
Indentation Depth Scale
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Edema
0
1 Trace
2(Mild)
3 (Moderate)
4 (Severe)
Capillary refill
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Time to baseline
0
Rapid
10-15 sec
1-2 min
2-5 min
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o Evaluate arterial circulation to the extremity and overall perfusion.
o Normal is < 3 seconds.
Auscultation of heart sounds
o Normal: S1 and S2—heard at the apex
o S3 heard if ventricular way compliance is decreased—Abnormal:--CHF, Vavular Regurgitation. Could be
normal in adults < 30years
 Ask if they have ever been diagnosed with CHF
o S4—Heard with atrial systole—IF resistance to ventricular filling is present
 Abnormal—cardiac hypertrophy, disease, or ventricular wall injury
Cardiac Rubs
o Can occur 2-7 days after an MI.
o Due to inflammation on of the pericardial sac.
o Both systolic and diastolic you may hear it
o Often associated with chest pain.
o Ask them to lean forward and if chest pain goes away it is most likely pericarditis.
o Also can auscultate when leaning back for pericardial rub.
Electrolyte Imbalances with cardiac patients
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Restless: Hypomagnemsia
o Prolonged PR and QT interval. Presence of U waves, and T-Wave Flattening and Widened QRS
complex.
o Torsades de Points is a possible dysrhythmia.—Gold Standard Treatment for this is Magnesium
replacement!
o Check renal function!!!
o Need to get magnesium level and BUN/Creatinine
Irritability= Hypokalemia
o Commonly caused by GI losses, diuretic therapy with insufficient replacement, or chronic steroid
therapy.
o EKG changes: PVC’s that lead to V-Tach or V-Fib.
o Prolongs the ventricular repolarization this is noted
by a U wave—positive deflection following the T
wave on the EKG
o Replacing K
 High Alert Medication
 Must be diluted sufficiently
 If hypomagnesemia also exists—must correct
to have K+ corrected also
 K+ and Mag go hand in hand
 You can give at same time
 K+ you can give over an hour
 Mag over 2-4 hours
Hyperkalemia- Discontent
o Hyperkalemia: excess potassium administration, extensive skeletal muscle destruction
(rhabdomyolysis), tumor lysis syndrome, renal failure, and some drugs.
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Drugs: potassium-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitor drugs and
angiotensin receptor–blocker (ARB) drugs.
HR is slow (whiney)
Cannot contract effectively
Can cause V-fib and asystole if not treated
Effects:
 Hyperkalemia causes a prolonged PR interval, loss of P wave, widening of QRS
 If not corrected will lead to Ventricular Fibrillation and/or asystole.
Correction
 IV insulin/glucose infusion that pushes the K+ inside the cell and out of the serum---this is a
Temporary solution.
 Permanent removal of K+ is done through administration of Kayexalate. This is given PO or
through tube
Diagnostic Indicators of an AMI Cardiac Enzymes
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CPK-MB: Proteins that are released from damaged myocardial tissue.
o Elevate in 4-18 hours after injury
o Peak at 24 hours
o Return to baseline in 2-3 days after injury
o Serial samples Q 6 or 8 hours X3 to r/o DX. Of MI.
o Must be in conjunction with Troponin T and Troponin I
 Troponin is more specific to heart than any other enzyme
 Elevates 3-6 hours after injury.
 Remain elevated 5-14 days after injury
o Example
1450
2045
0320
0846
72
530
1103
1312
Trop. T 0.07
0.17
0.16
0.13
CPKMB 1.8
20.6
32.6
35.4
CK
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Blood cells
o Hbg and Hct- Important to keep them with in normal limits.
o INR—used with Warfarin/Coumadin.
o How long does it take for the INR to become therapeutic?
 3-5 days
o When should Warfarin be stopped prior to surgery?
 1 week, then do lab work to be sure
o What if?
 PT/INR rise above normal therapeutic levels?
 INR 3-5—reduce dosage
 INR 5-9?
 Temp Stop Warfarin and given oral Vit. K. (1-2.5mg)
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INR >9?
 9—oral Vit.K, (3-5mg)
 INR >20?
 20—Vit. K 10mg IV VERY SLOWLY (15 min IV push)! May give FFP’s and Prothrombin
Complex Concentrate
o has clotting factors in it
o aPTT—Related to Heparin infusion to assure therapeutic dosage. Normal 28-38 seconds.
o ACT (Activated Coagulation Time) is done at bedside. The normal is 120 sec or less. therapeutic: 150300 sec if on Heparin
o Lipids
 4 primary lipids to evaluate risk:
 Total cholesterol: <200mg/dl
 LDL: <130 mg/dl without CAD
o <100 mg/dl with CAD but not considered “high-risk”
o <70 mg/dl with CAD and considered “high risk” for future coronary events
 Triglycerides: <150 mg/dl
 HDL: >40 mg/dl (male)
o >50 mg/dl (female)
Diagnostic Exams
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Chest x-ray
o What the nurse should teach the patient:
 Take a deep breath when told to
 Remove tubing away from thorax of patient.
 Position patient sitting upright, if allowable
 Ensure patient is “straight” in bed.
o When should it be ordered?
 Post insertion of:
 ET tube or Chest Tube
 CVP/CVC Catheter (any kind of central line)
 Pulmonary Artery Catheter
 Peripheral Intravenous Continuous Catheter (PICC)
 Feeding tube
o Feeding tube has an internal weight inside tube to help it go down past pyloric
sphincter
o NG tube does not – that’s the difference
 Intra-Aortic Balloon Pump (IABP)
 Pacemaker or Defibrillator
Cardiac catheterization
o Pre-op nursing considerations
 Pre-op check list completed and consent forms signed
 Patient educated
 Pre-op meds are given
 Benadryl
 Zantac
 Valium
 Lab work done
 BUN/Creatinine to determine kidney function because of dye
 Bleeding times
 NPO
 Baseline pulses
 Hold Metformin (Glucophage)
 can cause BUN/Creatinine to skyrocket with the dye
 can cause acute renal failure
 Shave (clip)/wash/clean groin area
o Peri-op nursing considerations
 Observation and assisting physician
 Specialized nurse
o Post-op nursing considerations
 Either will have sheath pulled or it will stay in if stent has been placed
 Sheath is a large plastic catheter in artery and it’s connected to tubing and transducer
and a pressure bag
 Patient:
 Do not lift head (no
 Keep leg still
greater than 30˚)
 Lay flat
 Nurse:
 We can put soft restraints on ankle if needed – need order
 Vital signs Q 15 minutes for 1 hour, then 30 mins for one hour, then hourly until sheath
comes out
 Lift dressing and make sure there is no bleeding or hematomas
 Palpate pulses distal to femoral – mostly pedal pulse
o Observe color of foot and temperature
 Log roll onto bedpan if bathroom is needed
 When sheath is coming out:
o Bleeding time needs to be okay
o BP needs to be < 140
o They need to be relaxed
o Two people need to be there
o Need suture removal kit
 Snip sutures and tweeze them out
o Need elastoplast tape (2-3 pieces)
o 4x4’s
o Need atropine at bedside just in case HR drops from vagal nerve stimulation
o Apply pressure two fingerbreadths above site so you can observe site and not
dislodge clot – possible test question
o Second nurse is checking pedal pulses to make sure not too much pressure is
being applied
o Hold pressure for thirty minutes
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o Apply pressure dressing
 Lay flat for six hours
 Observe vital signs same as above (q 15 min x 1 hr, q 30 min x 1 hr, hourly x 6 hrs)
o Radial Cardiac Catheterization
 Less recovery time – hardly any mobility issues
 This is not for interventional (angioplasty, stent)
 For a “clean” patient
Other diagnostic exams
o TTE: Transthroacic Echocardiography
 Transducer is placed in the third or fourth intercostal space to the left of the sternum
 Nursing care:
 Monitoring patient during procedure
 Reassure this is completely noninvasive
 Explain purpose of test
 Can take about 30-60 minutes
o TEE Transesophageal Echocardiography
 Transducer is mounted onto flexible shaft similar to endoscope and is advanced into esophagus
 Cardiac structures can be clearly visualized – high quality images
 Patient needs to be NPO for six hours prior to TEE to prevent n/v
 Medications can be given to inhibit salivary secretions, reduce fear/anxiety, to provide
retrograde amnesia
 Need to have emergency resuscitation equipment at bedside just in case vagal nerve
stimulation and also suction in case of aspiration
Heart Diseases
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Manifestations of Coronary Artery Disease
o Sudden cardiac death
o The development of heart failure
o Angina pectoris
o Chronic arrhythmias
o Myocardial infarction
o Conduction disturbances
Angina Pectoris
o Symptoms: Mainly Secondary to a blockage or a spasm of the coronary artery.
 Hypotension or other factors that cause ischemia to the muscle:
 Aortic stenosis (narrowing of aorta) or insufficiency
 Anemia
 Polycythemia - too many blood cells so it is sluggish
o Characteristics of pain:
 Pain is usually relieved by rest and nitroglycerin
 Anaerobic metabolism creates a buildup of lactic acid - creates pain
o Types of Angina
 Unstable
 Defined as a change in the previously established stable pattern of angina or new onset
severe angina.
 Pain relief usually requires more than nitrates.
 This type of angina requires medical attention.
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Variant or Prizmetal’s Angina
 Caused by a coronary artery spasm with or without the presence of arteriosclerotic
lesions.
 May be precipitated by smoking tobacco and ingesting alcohol and cocaine.
 Usually associated with ST segment elevation.
 Treatment includes vasodilators such as nitrates and calcium channel blockers
o Can give Calcium channel blockers UNLESS they have had an MI!! It increases
mortality rate.
 “broken-heart syndrome” - caused by great emotional stress (death of a loved one)
 Clear arteries, but it spasms/collapses
 Can be caused by vasoconstricting drugs
 Treat with vasodilators
 Silent
 Defined as: ECG changes of myocardial ischemia without the patient experiences
symptoms (chest pain).
 What comorbid condition is often accompanied with this?
o Diabetes due to nerve damage
o Treatment
 Increase coronary artery perfusion
 Oxygen
 Vasodilators
 Nitrates (nitroglycerin)
 thrombolytic
 Decrease myocardial workload
 bed rest
 calcium channel blockers
 beta blockers
 morphine
 ACE inhibitors
 Prevent myocardial infarction
 All above interventions
 reduce CAD risk factors
Women and heart disease
o Women often complain of chest pressure or pain that can extend to left arm, jaw, and/or back. SOB,
Nausea, Sudden sweating, Jaw pain, Light-headedness and weakness
o Warning signs for Women: In addition to the others) Significant fatigue, disproportionate to the
activity level engaged in. Obvious decrease in functional capacity.
o When do women start to have serious signs of heart disease?
 10-15 years after men
 Due to protective hormones (estrogen and progesterone)
o Post-menopausal women are at higher risk of CAD and MI.
o HRT (Hormone Replacement Therapy):
 Old science>5 years ago—not recommended for HRT.
 New science < 5 years---HRT with progesterone and estrogen combined.
 Decreases menopausal symptoms and decreases the risk for CAD and MI in women
 Weigh pros and cons with HRT
o Homocysteine : elevated levels increase risk of CAD, CVA, and PAD in women
 high inflammatory system (response)
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inflammation of blood vessels caused by:
 Increased blood sugar.
 Elevated blood lipids.
 Nicotine.
 Hypertension
o All arteries are affected
o Coronary arteries are so much smaller than others – they will be affected first
STEMI
o Defined as irreversible myocardial necrosis resulting from an abrupt decrease or cessation of coronary
blood flow to an area of the heart
o ST elevation is present on 12 lead EKG
o Treatments
Medications/Treatments for STEMI
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Oxygen
o Increases supply of oxygen to ischemic tissue
o New requirements state to keep O2 saturation >94% when AMI is suspected
o Start with nasal cannula at 2 L/min
o Remember one word: oxygen-IV-monitor
o Watch Out!
 Rarely COPD patients with hypoxic
ventilatory drive will hypoventilate
Nitrates (nitroglycerin)
o Decreases pain of ischemia
o Decreases preload and cardiac
o Increases venous dilation
oxygen consumption
o Decreases venous blood return to heart
o Dilates coronary arteries
o Increases cardiac collateral flow
 Collateral flow – if my main artery closes off, if I have enough circulation around that artery it
may help sustain enough oxygen to the tissue
o Indications
 First 24 to 48 hours in patients with ST-segment elevation or depression including:
 LV failure (acute pulmonary edema or CHF)
 Elevated BP (especially with signs of LV failure)
 Large anterior infarction
 Persistent ischemia
 Suspected ischemic chest pain
 Unstable angina (change in angina pattern)
 Acute pulmonary edema (if BP >90 mm Hg systolic)
o Dosing
 Max dose is 50 mcg
 Sublingual: 0.4 mg; repeat every 5 minutes
 Spray inhaler: 2 metered doses at 5-minute intervals
 IV infusion: 5 to 10 mcg/min infusion, titrated
o Precautions
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Use extreme caution if systolic BP <90 mm Hg
Use extreme caution in RV infarction
 Give NS at 100 ml/hr with low dose of Nitro with RV infarction
 Suspect RV infarction with inferior ST changes
 Right ventricle is all by gravity – low pressure
Watch for headache, drop in BP, syncope, tachycardia
Tell patient to sit or lie down during administration
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beta blockers
o Mechanism of action
 Blocks catecholamines from binding to
ß-adrenergic receptors
 Reduces HR, BP, myocardial contractility
 Decreases AV nodal conduction
 Decreases incidence of primary VF
 Caused by ischemia
o Absolute contraindications
 Severe CHF/PE
 Acute asthma (bronchospasm)
 SBP <100 mm Hg
 2nd- or 3rd-degree AV block
o cautions
 Mild/moderate CHF
 IDDM
 HR <60 bpm
 Severe peripheral vascular
 History of asthma
disease
ACE inhibitors
o Mechanism of action
 Reduces BP by inhibiting angiotensin-converting enzyme (ACE)
 Alters post-AMI LV remodeling by inhibiting
tissue ACE
 Lowers peripheral vascular resistance
by vasodilatation
 Reduces mortality and CHF from AMI
morphine
o Why? (Actions)
 To reduce pain of ischemia—by dilating smooth muscle.
 To reduce anxiety
 To reduce extension of ischemia by reducing oxygen demands
o When? (Indications)
 Continuing pain
 Systolic blood pressure >90 mm
 Evidence of vascular congestion
Hg
(acute pulmonary edema)
 No hypovolemia
o How? (Dose)
 2 to 4 mg titrated to effect
 Goal: Eliminate pain
o Watch out for (Precautions)
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Drop in blood pressure,
 Depression of ventilation
especially in patients with
 Nausea and vomiting (common)
 Volume depletion
 Bradycardia
 Increased systemic resistance
 Itching and bronchospasm
 RV infarction
(uncommon)
o Prevent myocardial infarction
 All above interventions
 reduce CAD risk factors
aspirin
o Why?
 To decrease platelet aggregation
o When? (Indications) As soon as possible!
 Standard therapy for all patients with new pain suggestive
of AMI
 Give within minutes of arrival
o How? (Dose)
 160- to 325-mg tablet taken as soon as possible
o Watch Out! (Precautions)
 Relatively contraindicated in patients with active peptic ulcer
disease or asthma
 Contraindicated in patients with known aspirin hypersensitivity
 Bleeding disorders
 Severe hepatic disease
Heparin
o Mechanism of action
 Indirect thrombin inhibitor (with AT III)
o Indications
 PTCA or CABG
 With fibrin-specific-lytics
 High risk for systemic emboli
 Conditions with high risk for systemic emboli, such as large anterior MI, atrial fibrillation, or LV
thrombus
Antiplatelet agents
o How do they work?
 Not the same as aspirin
 Blocked receptors cannot attach to fibrinogen
 Fibrinogen cannot aggregate platelets to platelets
o Indications: ACS with NSTEMI: NO ST-segment elevation:
 Non–Q-wave MI
 Unstable angina managed medically
o Examples: abciximab (ReoPro), eptifibitide (Integrilin), tirofiban (Aggrastat)
o Thienopyridines: class of drugs that prevent platelet aggregation.
o Clopidigrel—first generation—prior to intervention needs 6 hours to convert to active drug.
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o Prasugrel- clinical trials show marked improvement in reducing clinical events but increased bleeding.
(not used in pt’s with active bleeding,>70 years old, hx. Of CVA, wt. <60Kg)
o Have to be discontinued 7 days prior to surgery
Fibrinolytic therapy
o Treatment for STEMI
o Breaks up the fibrin network that binds clots together
o Indications: ST elevation >1 mm in 2 or more contiguous leads or new LBBB or new BBB that obscures
ST
 Time of symptom onset must be <12 hours
 Caution: fibrinolytics can cause death from brain hemorrhage
 Do not give to someone who is at risk for brain hemorrhage (someone who had a stroke
in last 30 days)
o 5 agents currently available: alteplase (tPA, Activase).
o Meds
 Fibrinolytic drugs are administered to STEMI patients with ST-segment elevation, and onset of
symptoms less than 12 hours earlier.
 Before administration of fibrinolytic therapy, rule out neurologic contraindications
 Rule out facial trauma, uncontrolled hypertension, or ischemic stroke within the last 3 months.
 If contraindications to fibrinolysis are present, PCI is the preferred method of reperfusion.
 Via stent instead of fibrolyntic therapy
 What is active bleeding? - do not give if active bleeding
 GI bleeds, trauma and bleeding behind eye, lacerations
 What is not active bleeding?
 Menstruation
 Reperfusion PVCs
 This will happen after this treatment
 May become irritable due to sudden O2
 This is a positive sign
Reperfusion of STEMI
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o Serum CK-MB Levels rise dramatically initially!!
o Reperfusion dysrhythmias also occur…often PVC’s—3-5 at times. Must WATCH to make sure not
Vtach!
o Warn patient they may have pain, and they need to tell you when they do
Percutaneous Transluminal Coronary Angioplasty
o Direct treatment
o Mechanical reperfusion of infarct-related coronary artery
o Best outcome achieved for patients with AMI plus cardiogenic shock
o Will have chest pain when balloon is inserted, so can give nitroglycerin
Post-op care
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Monitor Heart rate: Epicardial pacing Wires are in place post-surgery if needed.
o They stop heart during surgery with cardioplegic solution
 It is cold potassium solution
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 Allows surgeon to operate on the heart
o Epicardial wires are for when heart does not start up correctly
 Right underneath sternum and is connected to a pacemaker (outside the body) – it is off – only
turn on if needed
 Epicardial wires are d/c’d when patient is awake, oriented, alert, doing well, etc.
Monitoring chest tube patency and output: No stripping …only milking
o Chest tubes lie in pleural space with fluid
 Pulling out any possible air in the pleural space
o Mediastinal chest tubes are right under sternum
 These go in pericardial sac
 Keeps cardiac Tamponade from happening by draining any kind of bleeding going on in there
 Maintain patency – there will be clots
Monitor for Cardiac Tamponade: Monitoring Hemodynamic pressures.
Monitoring pulmonary status- all patients are ventilated
Monitor Neuro status—Post-cardiotomy delirium
Possible CVA
Bleeding
Infection
Kidney Function—Maintain normal
o If they are ischemic in surgery, they can have renal ischemia
Dysthymias- high risk for Atrial Fibrillation in post CABG pt.
If low preload in the Postoperative cardiac pt: Low Cardiac Output—Treated with Blood Transfusion, or a
crystalloid/colloid fluid.
o Due to 3rd spacing – not in vascular space, in interstitial space
o May need fluid and diuretics to push into vascular system and equalize fluid status
If preload is too elevated: Cardiac Output will be low
o needs to be treated with just diuretics (Lasix).
Complications of CABG
o HEART RATE:
 Can be regulated with medications and pacing (Epicardial Pacer wires)
 Can be too high or too low
o Cardiac Tamponade and Effusion
 When the pericardium fills with blood and causes the heart muscle to be unable to stretch or
beat well. Compression of heart by fluid in pericardial sac.
 All pressures will be high and CO will be low due to heart not having any room to beat
 CO - ↑Preload - ↑Afterload
 Symptoms:
 Dyspnea
 Chest Pain
 Fatigue
 Syncope
 Orthopnea
 Signs
 Distended neck veins (JVD)
 Hyperdynamic JVP
 Pulsus Paradoxus
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Faint heart sounds
Chest tubes dumping large amounts of blood then sudden cessation of drainage.
o Most physicians want you to monitor every 15 minutes for first hour, then every
30 minutes for second hour, then hourly for 12-24 hours
 Tachycardia – compensatory mechanism
 Falling arterial pressure – due to decreased perfusion – staying in pericardial sac and not
going to systemic
 Narrow Pulse Pressure
 Hypotension
 Cyanosis – late sign
 Treatment
 Needle aspiration immediately if hemodynamically unstable!
 Sterntomy in the ICU
o Open up sternum
o Always try aspiration first
 Surgery to evacuate the clot
o There will be a clot eventually due to blood just sitting there
 Treat the underlying cause:
o Bleeding – re-suture in OR
o Trauma – 3rd spacing in pericardial sac
o Valve problem
 Preferred tests
 ECHO
 CXR- Shows a cardiac shadow
o Bleeding
 Most commonly with IMA (Internal Mammary Artery) grafts
 Due to extensive chest dissection.
 If Chest Tubes dump >150mL/hr: intervention is needed.
 CVP: low
 HR: elevated
 SVR :low
 BP: low
 Bleeding of 500mL in one hour or 300mL in 2 consecutive hours despite normal bleeding times,
indicates need for surgical investigation.
 What to do?
 The use of PEEP with ventilation will increase intrathoracic pressure enough to affect
Tamponade of oozing mediastinal vessels.
o This may decrease ability to bleed and then they clot (in a good way) - Internal
scabbing
 Rewarming the patient reverses the depressed manufacture and release of clotting
factors that occurs with cooling the patient.
o When patient is really cold, clotting factors go into hibernation, so when we
warm them up then they are released and more likely to clot
 Infuse clotting factors: FFP, Fibrinogen and Platelets.
 Infusing of PRBC
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Amicar: 5 gm over 1 hour followed by continuous infusion of 1 gm/hr for 8 hours or until
bleeding is controlled.
 Desmopressin acetate (DDAVP): 0.3mg/kg IV over 20-30 min.
 Protamine Sulfate: 25-50mgIV slowly over 10 min
o Reverses heparin
 Auto-Transfusion: of blood
o A device that collects and re-infuses shed mediastinal blood. Pumps it back
through intravenously.
o No longer a routine intervention because it may further exacerbate bleeding
 More heparin, another filter, blood that comes back is not very good
blood – doesn’t coagulate very well
 Also increased risk of infection
Pulmonary Care- Post CABG
 Extubation within 24 hours post-surgery. (people without lung problems)
 Early Extubation 4-8 hours- multidisciplinary approach – nurse, surgeon, pulmonologist,
respiratory therapist, etc. all need to be on board.
 Small amounts of opioids for pain and anxiety can be used.
 History of pulmonary disease or problems will prolong Extubation.
 Post Extubation: supplemental oxygen, pain meds for incisional pain and splinting with
cough and deep breathing.
 Incentive spirometry is effective also, but needs to be motivated to perform.
Neurological complications
 Transient neurologic dysfunction related to decreased cerebral profusion, cerebral
micro emboli, and systemic inflammatory response.
 Co-morbid conditions of CVA, diabetes, and cognitive impairment.
 Environmental factors of sensory deprivation and overload are also contributing factors
Kidney issues
 Development of Acute Renal Failure is often due to ischemia intra-operatively.
 Postoperative fluid retention requires frequent diuresis
 Frequently monitoring of Urine output, BUN/CR, and K+
Treatment for cognitive impairment
 Use of Benzodiazepines or Haldol.
 Modifications to noise control.
 Restoring day/night lighting patterns.
 Placing familiar objects at the bedside.
 Open visiting hours to allow family at bedside.
 Organizing nursing care to optimize sleep and wake cycles.
Infection
 Post op fever is common due to temperature rebound and inflammatory process
o However persistent temperature elevation grater that 101 degrees must be
investigated.
o Get specimens
 Sternal wound infections and infective endocarditis are the most devastating
complication.
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Leg wound infections, pneumonia, and urinary tract infections can also occur.
Patients with diabetes are at greater risk of infections.
Prevention:
o Maintaining a blood glucose concentration between 80-110 in the postoperative
period by means of continuous insulin drip – check BS every hour
o Washing hands is extremely important.
o Patient assignment considerations need to addressed.
 Should not be taking care of post-op bypass patient and also an MRSA
patient at the same time (common sense)
o Cleansing wounds with ordered wound care products.
o Vitamin C 500mg BID is helpful in wound healing
 Thermoregulation
 Hypothermia can depress myocardial contractility.
 Use of warming blankets, water blankets, or warm air blankets (bear hugger)
 Massive vasodilation will occur with rewarming.
o BP may drop and increased bleeding may occur
 Remove blankets when temp reaches 98.6 or greater degrees
o Patient education
 Valve Surgery antibiotic prophylaxis before invasive procedures (for the rest of their life) and
specific instructions pertaining to their anticoagulation regimen
 Not to lift anything greater than 10 lbs post-surgery for 4-6 weeks. At least until their initial
post hospital visit.
 Take their medications as ordered.
 Weigh themselves every day
 Call nurse if gains >2 lbs a week.
Complications of AMI

Heart failure
o CHF: 20-30% mortality rate of all hospitalized AMI patients.
o Left ventricular failure
 Paroxysmal nocturnal dyspnea
 Pulmonary capillary wedge
pressure will be elevated
 Crackles/wheezing
 SOB
 Fatigue
 Cough with blood tinged sputum
o Right ventricular failure
 Fatigue
 Increased peripheral venous
pressure
 Ascites
 Enlarged liver and spleen
o BNP- Test for Heart Failure
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Restless
Confusion
Orthopnea
Tachycardia
Exertional dyspnea
cyanosis
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JVD
Anorexia and GI distress
Swelling in hands and fingers
Dependent edema – feet down =
swelling
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o Treatment
 Positive inotropic medication (Dobutamine)
 Diuretic
 Oxygen
 NO USE OF A BETA BLOCKER – they decrease contractility
Papillary muscle rupture
o They’ve had such a massive heart attack that the papillary muscles become like tiny strings and they
rupture and contractility is affected.
o Need positive inotropes to increase contractility
Ventricular septal defect
o When patient has an MI in the septal area
o Septal area is thinned out so much from ischemia that a hole is created
o Mixture of oxygenated and deoxygenated blood
o Can be repaired if the hole is not too big
Dysrhythmias
o 95% of all AMI patients will experience dysrhythmias.
o Site of the infarction will determine type of dysrhythmias:
 right coronary artery- bradycardia, heart blocks, PVCs
 left anterior descending- PVCs, BBB, 2nd degree blocks
 circumflex- PVCs
Ventricular Free Wall Rupture
o 3-4% of all AMI deaths result from Ventricular free wall rupture.
o Usually left ventricle
o Wall thins out so much that it tears
o Usually occurs around the 5th post-MI day when leukocyte scavenger cells are removing necrotic trash.
This thins the ventricular wall resulting in rupture.
o Cardiac Tamponade, cardiogenic shock, and death are eminent.
Pericarditis
o Inflammation of the pericardial sac secondary to irritation
o Signs and Symptoms:
 pain (usually greater with deep inspiration)
 when they lean forward it goes away
 pericardial friction rub at the sternal boarder
o Treatment:
 aspirin or other NSAID’s
Hemodynamic Lines

arterial blood pressure
o Direct measure of the blood pressure.
o Often in the radial or femoral arteries.
o When assisting with physician, must maintain sterility.
o Creates a wave form:
 Systolic - peak
 Dyastolic - Dicrotic notch (closure of the aortic valve)
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o Complications of Direct BP Monitoring
 Exsanguination – excessive
 Loss of limb.
bleeding (bleeding out)
 Loss of feeling/function of limb,
 Hematoma Development
distal to catheter site. (check cap
 Bleeding around site. (bruising)
refill)
 Nerve compression.
 Thrombus/embolus.
Perfusion pressure (mean arterial pressure)
o Normal is 70-100
o Must be >60 to perfuse coronary artereies!!
o Must be 90-100 mmHg if pt has had neurovascular surgery to keep Cerebral Profusion Pressure
adequate!
Cardiac output
o Cardiac output = heart rate X stroke volume
o Normal cardiac output ranges from 4-6 liters per minute.
o Variances in CO are caused by either changes in HR or SV
Stroke volume control
o Stroke volume is the volume of blood ejected from the ventricle with each beat and is influenced by
three factors.
 Preload---also called filling pressure, CVP, and right ventricular diastolic pressure!
 Volume of blood in the right ventricle at end diastole. (when the ventricle fills – right
before it is ejected)
 Amount of myocardial stretch placed on the ventricle as a result.
 Preload is measured clinically by observing the central venous pressure (right ventricular
preload). With a pulmonary artery catheter in place.
 Preload=Measured in R Atrium=CVP (central venous pressure)
o Elevated preload could indicate cardiac failure or hypervolemia.
o Reduced preload could indicate hypovolemia.
o Normal CVP is 5-12
 Alterations in Central Venous Pressure.
o Increased blood
o Cardiac
volume
tamponade
o CHF
o Positive pressure
o Right ventricular
ventilation
failure
o Vasoactive drugs
o Tricuspid valve
that cause
disease
constriction
o Pulmonary HTN
 Potential problems with CVP monitoring
o Pneumothorax
o Fluid volume
o Phlebitis
overload
o Air embolus
o Arrhythmias
o Pulmonary
o Sepsis
embolus
o Micro electric
shock
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Afterload—Also Called SVR or Systemic Vascular Resistance
 Defined as: the pressure the ventricle generates to overcome the resistance to eject
blood. The resistance is from the arteries and arterioles.
 If the arteries are contracted and the ventricle is attempting to eject blood – the SVR will
be high
 If the arteries are dilated/wide open, and the ventricle is attempting to eject blood – the
SVR will be low
 Normal SVR is 600-1200
MAP - CVP
X 80 = SVR
CO
 In general the lower the SVR the higher the CO!
 Postoperative hypertension is transient and most like is due to:
o hypothermia
 Warm them slowly
 SVR and BP will drop
o vasoconstriction
 This can cause the workload on the LV to be high!
 Treat with NTG or Nipride to vasodilate
 this will decrease the SVR/Afterload.
 Postoperative hypotension—peripheral vasodilatation and low SVR.
o Often due to systemic inflammatory response (SIRS) to the surgery.
o Treat with fluids, vasopressors, such as vasopressin or dopamine
 What meds decrease afterload?
o Nipride
o IV Hydralazine –
o High doses of NTG
short acting
(nitroglycerin)
o PO ACE inhibitors
>30mcg
 Meds increase afterload?
o Norepinephrine
o Levophed
o Dopamine (at the correct dose)
 These meds are vasoconstricting. These cause peripheral as well as
systemic constriction and cause the mean arterial pressure to increase
therefore affecting the SVR.
 What does the nurse assess frequently when adjusting these medications
 Cap refill
 Necrosis
 HR
Degree of contractility
 Enhances by Positive inotropic support
 Intraaortic Balloon Pump (IABP) to help circulation.
 Warming the pt will also help. This is does with a warm air blanket (bear hugger)
 Optimizing contractility=optimizing CO
o Positive inotropic medications such as Dobutamine, Primocor, and Inocor
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o Negative inotropic meds – Inderal and Cardizem
Preload or CVP is affected by: Constriction or Dilation!
o Constriction- CVP will be High.
o Dilation-- CVP will be Low.
Afterload or SVR is affected by: Constriction or Dilation!
o Constriction- Hypertension PAWP will be high.
o Dilation– Fluid deficit or Shock- PAWP will be low
Pulmonary artery pressure monitoring
o Indications
 When specific hemodynamic and intracardiac information is required
 Diagnosis and evaluation of heart disease, shock states, and medical conditions that
compromise cardiac output or fluid volume
 Used to evaluate patient response to treatment
 Post-surgery/procedure
 Drug titration
o PAP measurement
 Systolic – normal is 20-30
 Diastolic – normal is 5-20
 Look up in hemodynamic monitoring book (page 73 or 74?)
o Catheter info
 The traditional PA catheter was invented by Doctors Swan and Ganz
 has 4 lumens
o RAP or CVP
 Proximal lumen
 situated in RA
 Uses:
 IV fluids
 CVP measurement
 withdrawal of venous blood samples
 injection of fluid of CO determinants
o PA pressures
 Pulmonary artery lumen – distal lumen
 located at the tip of the catheter
 situated in pulmonary artery
 it is used to record PA pressures
 can be used for withdrawal of blood samples to measure SVO2
o PAWP – pulmonary wedge pressure
 Balloon lumen
 opens into a latex balloon
 balloon inflates with 0.8 - 1.5 ml of air
 inflates during insertion through RA and RV and for PAWP readings
 When open reads the PAOP or PAWP or “Wedge pressure”
 Normal wedge pressure is 5-12mmHg--just like the CVP!
o CO - Thermistor lumen
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used to measure the blood temperature and measures CO
located 4cm from the tip of the catheter
used to measure thermo-dilution CO
the connector end of this lumen is attached directly to the CO
computer/transducer cable
 Multi-function catheters may have additional lumens
 for IV infusions
 to measure mixed venous oxygen saturation (SVO2)
o If continuous Svo2 is measured, the catheter has an additional fiberoptic lumen
that exits at the tip of the catheter
 RV volumes
 Continuous CO measurement
 transvenous pacing
Pulmonary artery wedge
o During insertion, the physician will ask that the balloon be inflated and deflated as he floats the
catheter into the pulmonary artery
 this helps him “position” the catheter/balloon in the proper zone of the pulmonary vasculature
o The balloon will occlude a pulmonary vessel so that the PA catheter lumen is exposed only to the left
atrial pressure and is protected from the pulsatile influence of the PA.
 This decides how well the left ventricle is doing
o When the balloon is deflated, the catheter should spontaneously float back into the PA.
o When the balloon is re-inflated, the wedge tracing should be visible.
o The normal PAWP ranges from 5 - 12 mmHg
Post PAP catheter insertion care
o The physician will suture the catheter in place.
 Dress and secure appropriately.
o A portable chest x-ray is taken to confirm positioning.
 If the catheter is too far advanced the patient is at risk for pulmonary infarction.
o If the catheter is not sufficiently advanced into the PA, it will not be useful for PAWP readings.
 In many critical care units, if the patient’s PAD and PAWP values are “close” (within 0-3 mmHg),
the PAD is reliably used to follow to trend the LV filling pressures.
o Care must be taken to prevent accidently balloon inflation - turn slide valve off or closed, leave syringe
attached
o NEVER LEAVE BALLOON INFLATED! ONLY INFLATE TO GET READING THEN DEFLATE. MUST BE LESS
THAT 5 SECONDS!!
o Be aware of the factors that can adversely affect the PA measurement reliability:
 Positioning of patient: supine with head of bed elevated at 0-60 degrees.
 a stabilization of 5 minutes is required before taking pressure readings after a patient
changes positions.
 Respiratory variation - (PAD and PAWP)
 always read measurements at the end of expiration
 PEEP: Can create an artificially high Wedge pressure reading.
Removal of the catheter
o Avoiding complications (rare):
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
 Ventricular dysrhythmias – most common out of these
 Endocarditis
 Valvular damage
 Cardiac rupture
 Cardiac Tamponade
o Avoiding pulmonary complications
 Rupture of a pulmonary artery
 Pulmonary artery thrombosis
 Embolism
 Hemorrhage
o Infarction of a segment of the lung---Spontaneous wedge --pull back carefully (without the balloon
inflated) if hospital policy allows.
Continuous SVO2
o Can be measured at the tip of the CVC or the tip of the Pulmonary Artery Catheter:
 The SVO2 is measurement of venous oxygen saturation. So it shows the nurse the balance of
oxygen supply and demand for the individual patient.
o Procedure: Blood is drawn from these catheters and sent to the lab for analysis.
o Normal values: 75% (with a range of 60% -80%)
o So…the more the pt is under stress--with fever, shivering, serve infection, labored breathing,
suctioning…etc--the supply of oxygen will be decreased and consumption will be high. – SVO2 will be
low.
IABP (Intra-Aortic Balloon Pump)
o Temporary mechanical circulatory assist device for supporting failing circulation
o Usually inserted in femoral artery
o Have to lay flat
o Indications
 Left ventricular failure after cardiac surgery
 Unstable angina refractory to medications
 Recurrent angina after acute myocardial infarction
 Complications of acute myocardial infarction
 Cardiogenic shock – most common reason
 Papillary muscle dysfunction or rupture with mitral regurgitation
 Ventricular septal rupture
 Refractory ventricular dysrhythmias
o Assessment
 Monitor for dysthymias
 Peripheral ischemia
 Urine Output at least Q hour– due to possible occlusion of renal artery
 Pulses at least Q hour: Pedal and radial pulses
 Bleeding
 Hematoma
 Neurovascular Assessment
 Anxiety
o Weaning
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Weaning is done with in one - four days post insertion intervention.
During diastole the balloon inflates and during systole it deflates
Starts out at a 1:1 ratio with each heartbeat
Decrease in triggering from 1:1-1:2, then 1:3- 1:4 and so on then
Once IABP is on 1:4—it must be removed with in 30minutes.
 Currently Physicians are only allowed to remove these. Due to the extreme possible
complications!
o Complications
 Peripheral Ischemia: Pedal, Left radial, femoral
 The balloon may have slipped past the renal arteries and is blocking blood flow to the kidney
 Acute aortic dissection and the development of pseudoaneurysms at the catheter insertion site.
 Whole artery balloons out
 Need surgery
 Emergency: Balloon Perforation due to calcified plaque on the aorta (as the balloon inflates and
deflates and is in contact with the plaque)
Pacemakers
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Simple electrical circuit consisting of a pulse generator and a pacing lead - with one, two, or three electrodes.
Pulse generator is designed to generate an electrical current that travels through the pacing lead and exits
through an electrode that is in direct contact with the heart.
Leads
o Bipolar---two electrodes + and – in direct contact with myocardium.
o Unipolar—one electrode – in direct contact with heart muscle.
Permanent pacemakers
o Purpose: to simulate, as much as possible, normal physiologic cardiac depolarization and conduction.
o Types: Rate-responsive pacing---response to sensed atrial activity or in response to a variety of
physiologic sensors (body motion, QT interval, and minute ventilation).
o Insertion is done in the Cath. Lab.
Indications
o Brady arrhythmia
o Sick Sinus Syndrome
o Drug toxicity
o Arial Fibrillation with RVR
o Electrolyte imbalances
o Heart Blocks
Routes
o Transcutaneous
o Transvenous
o Epicardial
o Permanent
Modes
o Synchronous: (Demand Pacing)-Delivers a stimulus when the heart's intrinsic pacemaker fails to
function
o Asynchronous: (Fixed Rate)-Delivers a pacing stimulus at a set or fixed rate regardless of the heart rate
Settings
o Rate: number of impulses sent to the heart per minute: 60-80/min.
o Output control: amount of electrical current (MA) delivered to the heart.
o Sensitivity control: The ability of the pacer to detect the heart’s intrinsic electrical ability
Where is it?
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o Atria
 Pacemaker hits before p-wave
o Ventricle
 Pacemaker hits right on QRS
o Both
 Pacemaker hits both areas
Problems
o Failure to capture
 Failure to spike or they’re not regular spikes (where they need to be)
 Rationale and nursing interventions
 Reasons: Failure of the pulse generator or its battery
o A loose connection
o Broken lead wires
o Stimulus inhibition as a result of EMI (extra electrical medical interference)
 What to do?
o Tightening connections, replacing the batteries or the pulse generator itself, or
removing the source of EMI may restore pacemaker function. Position pt on the
left side!
o Over-sensing: Extra pacer spikes
 Presence of Tall Peaked T waves, EMI in the critical care environment.
 What to do? Decrease Gain on EKG, lower the sensing (if temporary pacemaker)
o Pacer is inhibited to initiate spike causing abnormal pauses.
 Source: Sensitivity is too low so it is not picking up intrinsic rate
 What to do? Moving the sensitivity control toward 20 mV stops the pauses.
o Under-sensing:
 Why? Inadequate wave amplitude, inappropriate mode selection, lead displacement, loose
cable connections, and pulse generator failure.
 What to do? Increasing the sensitivity
Cardiac Resynchronization therapy
o CRT: atrial pacing, (biventricular pacing), to optimize atrial and ventricular mechanical activity.
o Severe Heart Failure patient’s: ventricular delays - Prolonged QRS duration or BBB.
ICD: Internal Cardioverter Defibrillators
o Who? Those who are at risk for SCD (Sudden Cardiac Death). Primary prevention of SCD in patients
with coronary artery disease (CAD), previous myocardial infarction, or left ventricular dysfunction
when VT or VF was inducible during an electrophysiology study (EPS).
o Sensing electrodes to see dysrhythmia and defibrillation electrodes—deliver shocks.
o Nursing management
 Monitoring for ICD-associated complications
 Monitor for infection, possible broken leads, and the system may sense SVT resulting in
unneeded shocks
 Be prepared to check a shockable rhythm in the event the ICD malfunctions
 Do not place pads or paddles over generator if having to shock pt.
 Providing patient education: If the shocks are associated with SOB or other symptoms of heart
failure= trip to the emergency department for monitoring.
Cardiac Infective Disorders

Infective endocarditis (IE): bacterial or fungal organism in the bloodstream that successfully colonizes the
cardiac endothelium.
o FATAL –if not treated.
o Most common organism: Staphylococcus aureus.
o Treatment is long and intensive.—usually 6 weeks.
 Due to way bacteria colonizes around the valves – can encapsulate
o Clinical manifestations
 Fever, Splenomegaly, Hematuria, Petechiae
 Cardiac murmurs
 Easy fatigability
 Osler nodes (small, raised, tender areas most commonly found in pads of fingers and toes)
 Splinter hemorrhages in nail beds
 Roth spots (round or oval spots consisting of coagulated fibrin; seen in the retina and lead to
hemorrhage)
o What does the nurse do?
 Orders for Blood Cultures, CBC, CXR.
 Prepare client for possible TTE.
 Get antibiotics or antifungal started STAT!!
 Control fever and pain.
 Teach infection control
 In many cases antibiotic therapy is not enough to cure IE. Clients must have Cardiac surgery to
excise the damaged native or prosthetic valve.
 Many pt’s sent home before surgery to continue medications through PICC Lines until
stable to go to surgery.
o Assessment
 Nursing assessment includes : signs of worsening infection= persistent temperature elevation
 malaise
 weakness
 easy fatigability
 night sweats
 new emboli (roth spots) on hands or feet
o Early detection of changes you need to know!
 Level of consciousness
 Visual changes
 Complaints of headache
o Patient education
 Activity tolerance: increase activity as tolerated; rest periods as needed
 Heart failure: if symptoms of heart failure are present, education is given on fluid and sodium
restriction, fluid balance, diuretic management, daily weight, and controlling breathlessness
 Follow-up care after discharge
 Symptoms to report to a health care professional
 Temperature elevation
Cardiac Effusions/Tamponade
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Cardiac Tamponade is a complication of a procedure or surgery.
When the pericardium fills with blood and causes the heart muscle to be unable to stretch or beat well.
Compression of heart by fluid in pericardial sac .
Symptoms
o Dyspnea
o Chest Pain
o Fatigue
o Syncope
o Orthopnea
Preferred tests
o Echo
o Chest x-ray – shows a cardiac shadow
Signs
o Distended neck veins (JVD)
o Tachycardia
o Hyper dynamic JVD
 Falling arterial pressure
o Pulsus Paradoxus
 Narrow Pulse Pressure
o Faint heart sounds
o Hypotension
o
o Cyanosis
Treatment
o Needle aspiration immediately if hemodynamically unstable!
o Treat the underlying cause:
 Bleeding
 Trauma
 Valve problem
Valvular Heart Disease
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Mitral Valve
o Stenosis: narrowing of the mitral valve orifice.
 Left ventricle does not fill very well
 Causes: aging Valvular tissue and acute rheumatic fever.
o Regurgitation
 Causes retrograde flow of blood into the left atrium with each ventricular contraction.
 Chronic: the left atrium will have dilated or accommodate the additional regurgitate volume
and the left ventricle is dilated or hypertrophied to maintain an adequate stroke volume and
cardiac output.
 Acute MR (acute mitral valve regurgitation)
 Acute: is precipitated by papillary muscle rupture secondary to an acute MI or trauma.
 This is a MEDICAL EMERGENCY!!
 The left ventricle cannot handle the increase in volume and pressure.
 IABP and inotropic drug to stabilize then surgical repair or replacement.
Aortic valve
o Stenosis
 Caused by: aging rheumatic valvulitis or deterioration of a congenital bicuspid valve.
 Less perfusion to peripheral circulation


What happens?
 The impedance of LV ejection into the aorta results in increased left ventricular systolic
pressure, left ventricular hypertrophy and eventually left ventricular dilation.
 Symptoms of angina, dyspnea, syncope and the other symptoms of heart failure occur
 critical intervention is needed to decrease the damage to the left ventricle. An aortic
calve replacement is needed.
o Regurgitation
 What happens?
 Reflux of blood back into the left ventricular during ventricular diastole. To
accommodate this extra volume, the left ventricle initially dilates and then
hypertrophies in an attempt to empty more completely and to meet the meds of the
peripheral circulation. Pt will have hypertension!
 Causes:
 Rheumatic fever, systemic hypertension, marfan syndrome, syphilis, rheumatoid
arthritis, aging valve tissue or discrete sub aortic stenosis.
 Aortic valve replacement is the treatment of choice
Patient education and nursing management of valve disorders
o Must report this to all providers due to infection control
o Infection control: prophylactic antibiotics related to dental work or other invasive procedures
o Heart failure: if symptoms of heart failure are present, education is provided on fluid and sodium
restriction, fluid balance, diuretic management, daily weight, and controlling breathlessness
o Surgery: if open heart surgery was performed, information about postsurgical recovery is provided
o Medications: medications may be complex, and information must be in writing, as well as oral
Cardiomyopathy

Hypertrophic
o Genetic—affects the myocardial sarcomere.
o Progressively causes the LV to stiffen, become noncompliant, and hypertrophied, sometimes in an
asymmetrical way.
o Develops 2 ways:
 Manifestation of a stiff, noncompliant myocardial muscle with LV hypertrophy and bizarre
cellular forms.
 Generalized LV hypertrophy, but the septum is not more enlarged than the rest of the
myocardium.
o Symptoms
 Fatigue
 s/s of heart failure or mild myocardial ischemia
 SVT
 Chest pain and other symptoms are more severe with exercise
o Management
 Beta-Blockers in small doses to decrease afterload.
 Anti-dysrthymics
 Anticoagulation with Atrial Fib - inhibits clot formation.
 Diuretics- decrease preload.
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Inotropic meds- increase contractility.
Interventional Procedure: Internal Cardiac Defibulator (ICD)—Decreases risk of Sudden Cardiac
Death (SCD).
Percutaneous Alcohol Ablation of the intraventricular septum—To decrease the size of septal
wall. Temporary solution.
Ultimate cure is a transplant
Restrictive
o Causes: Idiopathic and occurs secondary to known causes.
o What happens?
 Ventricular wall rigidity from myocardial fibrosis
 This causes diastolic inhibition of ventricular filling
o S/S = diastolic heart failure: Low cardiac output, dyspnea, orthopnea, and liver engorgement.
o Management
 Beta blockers- decrease afterload
 Diuretics- manage preload
 Low Na+ diet
 Most common nursing diagnosis for this Cardiomyopathy is Impaired Gas Exchange
 This is due to the ventilation/perfusion mismatching that occurs. (intrapulmonary
shunting)
o Patient education
 Fluid balance: low-salt to reduce fluid retention; intake and output measurement; signs of fluid
overload, such as peripheral edema
 Daily weight: increase or loss of 1 to 2 pounds in a few days is a sign of fluid gain or loss, not
true weight gain or loss
 Breathlessness: increasing shortness of breath, wheezing, and sleeping upright on pillows are
symptoms that must be monitored and reported to a health care professional.
 Activity: activity conservation with rest periods as heart failure progresses
Dilated
o Gross dilation of BOTH ventricles with our muscle hypertrophy.
o Septum becomes very thin
o TYPES:
 1. Ischemic Dilated Cardiomyopathy: repeated myocardial injury or infarction from CAD, s/s of
systolic heart failure and low EF
 2. Familial Dialed Cardiomyopathy: Idiopathic, some are r/t genetic causes.
o Other causes:
 valvular disease/dysfunction
 infections= myocarditis
Nursing management of cardiomyopathy
o Achievement of stable fluid balance.
o Monitoring the effects of medications.
o Safety increasing mobility.
o Providing patient and family education.
Pulmonary Hypertension
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Types
o Idiopathic: Unknown cause.
o Familial: Associated with other diseases.
o Pulmonary Hypertension Associated with Left Heart Disease: Atrial or ventricular disease, Valvular
disease (e.g., mitral stenosis)
o Pulmonary Hypertension Associated with Lung Diseases and/or Hypoxemia : (COPD), interstitial lung
disease (ILD)
Causes
o Sleep-disordered breathing, alveolar hypoventilation
o Chronic exposure to high altitude
o Developmental lung abnormalities
o Chronic Thrombotic and/or Embolic Disease
o Pulmonary embolism in the proximal or distal pulmonary arteries
o Embolization of other matter, such as tumor cells or parasites
Symptoms
o Physical examination clues that reveal right ventricular failure
o Pt c/o SOB and fatigue: Hypoxia and decreased CO.
o Later: Syncope, angina, intestinal edema=constipation, abdominal pain, malabsorption and anorexia.
Diagnostic exams
o 12 lead ECG
o Echo
o Right sided heart Cath.
o PAH, the mean PAP must be greater than 25 mm Hg at rest and above 30 mm Hg with exercise.
Treatment
o Anticoagulation meds
o Oxygen
o Diuretics
o Endothelia-receptor antagonists
 Bosentan (oral)
 Sitaxsentan (oral)
 Ambrisentan (oral)
Other Medications
o Phosphodiesterase inhibitors:
 Sildenafil
 ProstanoidsEpoprostenol (IV)
 Treprostinil (SC)
 Iloprost (inhaled)
Aortic Aneurisms and Dissection
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Result from progressive artherosclerotic disease and systemic arterial hypertension, blunt trauma, Marfan
syndrome (genetic), pregnancy
Aortic Aneurysm: localized dilation of the arterial wall that results in a change in vessel shape and blood flow.
Most often in older adults, abdominal aortic aneurysm is four times more common than thoracic aneurysms.
Dissections
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o Classified according to location of tear. (arch, thoracic, abdominal)
o Classic clinical manifestation is a sudden onset of intense severe tearing pain, which may be localized
initially in the chest, abdomen, or back. As the tear extends the pain radiated to the back or distally
toward the lower extremities.
o Pt may present with hypertension and the goal is control the pressure.
 The more HTN the more they tear
o Pt presents with hypotension, poor organ perfusion, and shock - need immediate care to stabilize and
treat the problems.
Assessment and diagnosis
o Aortic Aneurysm is detected during routine abdominal examination as a palpable, pulsatile mass
located in the umbilical region of the abdomen to the left of the midline.
o A thoracic aneurysm may be identified on a routine chest x–ray film.
o An aortic dissection is usually identified emergently by the onset of acute pain.
o TTE (transthorasic echo)
o CT chest or abdomen.
Symptoms
o Most pts with AAA are asymptomatic.
o Most are managed until become larger than 5.5 cm. Then surgical intervention must be done.
Ascending vs. descending
o Ascending aortic dissection produces pain in the central chest or mid-scapular region of the back.
o A descending aortic dissection usually manifest by pain that radiates down the back, abdomen or legs.
Treatment
o Traditional Open abdominal aortic aneurysm repair.(AAA)
o Newer minimally invasive alternative: endovascular aneurysm repair (EVAR)
 Must meet certain criteria
 Contraindications for EVAR:
 Poor aortic neck (above the aneurysm)
 Poor circulation to the mesenteric artery
 Significant iliac occlusive disease and tortuous iliac vessels.
Post-op care
o Monitor femoral artery sites for bleeding, expanding hematoma, and lower extremities for alterations
in neurovascular status.
o Monitor pedal pulses
o Pt. education at discharge (24-48 hours): s/s of infection at femoral sites.
o Teach them s/s of neurovascular problems.
o Full activity can be tolerated after discharge within 2-3 days.
o Follow up CT scans at 3,6,12 months, then yearly.
Peripheral Arterial Disease (PAD)
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Thrombotic occlusion
Post-operative Bypass
Both require critical care admission
Caused by:
o Arthrosclerosis
o Diabetes
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Risks:
o Smoking,
o Hyperlipidemia
o Hypertension,
o Male gender
Assessment/diagnostics
o Ankle Brachial Index: noninvasive test used to estimate the severity of arterial disease in the leg by
comparing it to the measured on the arm.
o Intermittent Claudication: Arterial occlusion obstructs blood flow to the distal extremity.
o Pain at rest occurs as the disease progresses.
o Pain threatens the viability of the limb and requires immediate catheter or surgical intervention.
S/s
o Acute occlusion: sudden onset of acute pain, loss of pulses, collapse of superficial veins, coldness,
pallor, and impaired motor and sensory function.
o Chronic: Changes in skin; thickening, of nails and drying of skin. Hair loss is common on the lower leg,
feet, and toes. Skin ulcerations and gangrene can occur.
Nursing management
o Assessment of peripheral pulses, limb color, and temperature.
o Should keep legs in a dependent position.-to maximize blood flow to the limbs.
o Skin integrity: healing is impaired. Use of cotton or lamb’s wool placed between the toes can protect
skin.
o Pain control: removal of thrombus is the only solution for pain relief. Morphine is used for pain also.
Medical interventions
o Percutaneous Trans-luminal Angioplasty
o Surgical Bypass
o Stent Grafts
o Amputation
Hypertensive Emergencies
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Acute BP elevation > 180/120 (sustained) complicated by impending or progressive target organ dysfunction.
Etiology:
o Acute Renal Failure
o Pregnancy Induced HTN
o Acute central nervous system events:
o Phenochromocytoma
Subarachnoid
o Drug Induced HTN
o Hemorrhage or a stroke.
o Food and Drug Interactions
o Acute Aortic Dissection
S/S
o CNS compromise: H/A, Blurred vision, Change in LOC, or coma
o CV: chest pain, AMI, Aortic dissection
o Acute Kidney Failure: sudden absence of urine output.
o Catecholamine excess
Diagnostics
o Blood pressure measurement in both arms and/or Arterial line placement.
o 12-lead ECG
o Lab work to show catecholamine levels
Medical management
o Drug therapy should be to target the specific condition
 Nipride is the Drug of Choice due to its short half-life.
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Procardia/labetalol combination less likely to cause cerebral compromise
 Aortic dissection: Short acting Beta Blockers
 Heart Failure: ACE inhibitors drugs are best.
 Chest Pain: NTG drip.
 Renal Failure: Dopamine receptor antagonist (DA1) fenoldpam
 Eclampsia: Hydralazine/Labetalol - IV Drug of choice because it does not pass over the
placenta and labetalol.
 Phenochromocytoma crisis : Alpha blocker - Phentolamine.
 Fluid overload: Lasix
Nursing management
o Monitoring Patient to observe closely for clinical manifestation in other organ systems.
o Change in LOC, myocardial ischemia, dysrhythmias, Urine Output, BUN, Creatinine
o Monitor medications.
o Assessment of Arterial line
Blocked carotid arteries
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Diagnostic tests
o Ultra sound Doppler
o CT Angiography Magnetic Resonance Imaging
Carotid Endarterectomy
o Surgical removal of fatty deposits in the carotid arteries and Carotid Stenting: Similar to Coronary
Stenting.
o Done if there is a 50% blockage or if they’re having severe s/s
o Nursing Care Post Operatively:
 Neuro. checks q 15 x4, q30 x2 then q 1 hour up to the second day post operatively or as
ordered.
 Monitoring of V/S especially Blood pressure.
 Avoid hypertension which often leads to stress on the suture line and may lead to bleeding.
 Monitor for hypotension: which may often lead to inadequate cerebral perfusion and potential
neuro. Deficits
 Monitor for bleeding.
 Monitor for compromised airway--monitor for tracheal deviation and stridor, or wheezing.
 Bradycardia is common as a result of baroreceptor stimulation
Left Ventricular Assist Device (LVAD)
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Bridge to Recovery: Persistent cardiac failure, but have potential for regaining normal heart function if heart
has time to rest.
Bridge to Transplantation: Those patients with decompensated chronic heart failure who need circulatory
support until transplantation.
Destination Therapy: Severe Heart Failure who are not candidates for heart transplantation and the LVAD may
provide survival and quality of life.
Heart transplant
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Indications
o The most common conditions necessitating heart transplantation are cardiomyopathies of various
origins (idiopathic, viral, Valvular) and coronary artery disease.
o patients generally are evaluated for the presence of familial or social support, absence of chemical
dependence (illicit drugs), and commitment to adhering to a strict, lifelong medical regimen and
follow-up
contraindications
o Advanced age
o Recent pulmonary infarction
o Significant systemic or multisystem
o Cachexia or obesity
disease
o Psychiatric illness
o Fixed severe pulmonary hypertension
o Drug or alcohol abuse
o Active infection
Techniques
o Biatrial Technique
o Bicaval Technique
Post-op infection
o Development of fever is aggressively investigated, with systematic blood, wound, and respiratory tract
cultures, chest radiographs, and observation.
o Because steroids are known to suppress the body's inflammatory reaction, an elevated temperature
generally is considered significant when it reaches 38° C (100.4° F).
o Nurses must be suspicious of any new productive cough, dry cough, change in type of secretions, or
change in chest roentgenogram findings
o CMV
 CMV is a particular threat to transplant recipients.
 CMV is a herpes virus that can produce latent infection that persists throughout life.
 An antiviral agent, ganciclovir, can inhibit viral replication and ameliorate symptoms and is used
in the prophylaxis and treatment of CMV infections.
 CMV immune globulin is being used increasingly for the prevention of primary CMV disease and
for treatment of CMV disease.
Post-op teaching – test questions!
o Postoperative care includes educating the patient regarding compliance and record keeping.
o Education is provided on the immunosuppressive medication regimen, risks and signs and symptoms of
infection, myocardial biopsy, and symptoms of heart failure.
o Patients may be required to check their blood glucose, blood pressure, temperature, and daily weight
at home.
o At first, frequent clinic visits are needed to monitor progress and adjust medications.
o As the patient progresses, a schedule is established for routine laboratory tests and clinic visits to
ensure long-term success of the transplant
Long-term immunosuppression
o Poor outcomes
o Often transplanted hearts develop CAD which is often diffuse and rapidly progressive. Not able to do
an angioplasty or stent the arteries. Must be transplanted.
o Many patient have denervated hearts and cannot feel angina. More often, their symptoms are graft
ischemia, heart failure or sudden death.
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o Proliferation signal inhibitors such as sirolimus and everolimus are sometimes used as prophylaxis
against graft vasculopathy
Post-transplant
o 95% report no activity limitations at 5 years after transplantation.
o Less than 35% return to work.
o Many who do are unable to find suitable employment due to employer concerns of liability, lack of
health insurance, and the need to qualify for medical disability.
o Leading causes of mortality 3-5 years post transplantation: malignancy, graft vasculopathy, graft
failure.
Unit 3 Shock
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Cardiovascular stability is maintained by the interaction of three elements:
o The heart (cardiovascular shock)
o Blood vessels (distributive shock)
o Fluid and blood volume (hypovolemic shock)
Shock syndrome: Complex cycle of compensatory responses resulting in inadequate tissue perfusion, cellular
dysfunction, and end organ failure
Stages of shock
o Compensatory Stage
 Neurohormonal responses to maintain cardiac output.
 Increased heart rate and contractility
 Arterial and venous vasoconstriction
 Decreased urine output
o Progressive Stage
 The compensatory mechanisms begin to fail and tissue perfusion is compromised.
 Tissues switch from aerobic to anaerobic metabolism.
 Anaerobic metabolism produces lactic acid and we have decreased bicarb levels
because the bicarb binds with lactic acid to get rid of it
 Tissue hypoxia also causes increased capillary permeability resulting in increased hypovolemia.
(systemic inflammatory response).
o Refractory Stage
 Shock is now unresponsive to therapy and is considered irreversible.
 Individual organ systems fail due to hypoxia.
Early s/s of shock
o Decreased pulse pressure
o Respiratory alkalosis due to ↑RR
o Deceased urine output
o Restlessness, anxiety
Late s/s of shock
o Decreased systolic BP
o Cold clammy skin due to
o Metabolic acidosis due to using up all
vasoconstriction
our Bicarb stores
o Oliguria to anuria
o Decreased level of consciousness
o Decreased cardiac output
Types of shock
o Hypovolemic – no fluid
 The most commonly occurring shock.
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Results from loss of circulating fluid volume in the intravascular space.
Etiology: Bleeding, dehydration, burns, etc
 Dehydration from:
o massive diruesis
o vomiting
o diarrhea
 hemodynamics:
 low CO, CI, PAP, CVP, PAWP
 elevated SVR due to vasoconstriction (compensatory mechanism)
 interventions
 Lower extremity elevation – increases preload
 Fluid and Red blood cell replacement
 Colloid replacement
 Crystalloid replacement
 Vasopressors used after fluid volume replacement to increase preload
o Cardiogenic – pump is destroyed
 Results from the hearts inability to pump blood forward.
 Etiology: ventricular ischemia, structural problems, dysrhythmias.
 The most common cause is AMI resulting in the loss of > 40% of the functional myocardium
 Hemodynamics
 low CO, CI (cardiac index)
 elevated SVR, PAP, CVP, PAWP
 interventions
 Optimize hemodynamics
o Positive inotropes
o Vasodilators to decrease SVR
 Control rhythm disturbances
 Assist with pericardiocentesis (if pericarditis)
o Distributive – have fluid but it’s not getting to the right place
 Septic
 A complex response that is initiated by the invasion of a microorganism and stimulates
the inflammatory/immune responses
 Hemodynamics:
o low CO, CI, PAP, CVP, PAWP, SVR
 interventions:
o Treat infective process
o Treat Hypovolemia due to vasodilation
o Inotropic support
o Temperature control
 Anaphylactic
 A severe systemic reaction to an antigen that leads to decreased tissue perfusion and
initiation of the general shock response.
 Difference with this distributive shock is that it causes smooth muscle constriction!!
 Hemodynamics:
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o low CO, CI, PAP, CVP, PAWP, SVR
 interventions
o Epinephrine
o Diphenhydramine (Benadryl)
o Corticosteroids
o Fluid Therapy
o Alpha-adrenergic support
 Vasopressors
 Bronchodilators
Neurogenic
 Results from a loss of sympathetic tone (fight or flight).
 Etiology: spinal cord injury, spinal anesthesia, drugs, emotional stress, pain, CNS
dysfunction
 Hemodynamics
o low CO, CI, PAP, CVP, PAWP, SVR
 interventions
o Positioning with cervical spine precautions
o Fluid therapy to maintain systolic BP
o Maintain body temperature
o Vasopressor support
o Atropine for persistent bradycardia
o Corticosteroids – decreases inflammatory process (new research has shown this
isn’t the best standard of care anymore)