The Client with Alterations in Cardiac Output

Lecture 9/26/05

Sherry Burrell, RN, MSNRutgers University

Nursing III

Assessment Parameters• Cardiac Output

• Measures the effectiveness of the heart’s pumping abilities.

• CO is defined as the amount of blood that leaves the heart in one minute.

CO = Stroke Volume (SV) X Heart Rate (HR)

• Normal CO: Approximately 4-8 liters/minute

• Cardiac Index: CO per square meter of BSA • CO ÷ body surface area = CI

C0= SV x HR• Stroke Volume (SV)

• The amount of blood that leaves the heart with each beat or ventricular contraction.• Not all blood ejected• Normal Adult 70 ml / beat

• Ejection Fraction (EF) • The percentage of end-diastole blood

actually ejected with each beat or ventricular contraction.

• Normal adult 55-70% (healthy heart)

Stroke Volume• Three factors regulate stroke volume:

• Preload• The degree of stretch of the ventricle at

the end of diastole.

• Contractility• Force of ventricular contraction (systole);

inotropy.

• Afterload• The amount of resistance the ventricular

wall must overcome to eject blood during systole.

Stroke Volume Cont.,• Preload

• The degree of ventricular stretch at end-diastole

• The Frank-Starling Law of the Heart Preload = Contractility (to a point)

• Factors Affecting Preload• Circulating volume • Body positioning • Atrial systole or “kick” • Medications

• Diuretics (i.e. Lasix)• ACE Inhibitors (i.e. Vasotec)• I.V. Fluids

Starling Curve

Stroke Volume Cont., • Contractility

• Positive inotropic agents Force of contraction

• Negative inotropic agents• Force of contraction

• Factors that affect contractility• Autonomic nervous system (ANS)• Medications:

• Digoxin (Lanoxin) • Beta-adrenergic blockers (i.e. metoprolol ) • Calcium channel blockers (i.e. verapamil )

Stroke Volume Cont., • Afterload

• Resistance to ventricular ejection during systole

• Factors that affect afterload• Outflow impedance

• Left side• High systemic blood pressures (SVR) • Aortic valve stenosis

• Right side• High pulmonary blood pressures (PVR) • Pulmonary valve stenosis

• Diameter of arterial vessels • Blood characteristics• Medications:

• ACE (angiotension converting enzyme) inhibitors

CO = SV x HR• Heart Rate: beats per minute (bpm)

HR = CO (to a point)• HR >160 bpm = CO

• Leads to inadequate diastolic filling time = time for coronary artery filling and an increase workload of the heart.

• Factors that affect heart rate • ANS• Medications

• Atropine sulfate • Digoxin (Lanoxin)• Beta-adrenergic blockers / calcium channel blockers

Assessment Considerations• General Cardiac Symptoms

• Fatigue• Chest pain or discomfort • Palpitations • Shortness of breath• Edema • Weight gain • Dizziness • Syncope, loss of consciousness

Assessment: Special Populations

• Gerontologic Considerations• Heart function is adequate at rest; limited ability to

respond to stress and takes longer to return to baseline.

• Decrease sensation of chest pain; tend to be under quantified or even absent.

• Gender Considerations • Women:

• Smaller hearts and coronary arteries• Tend to present with “atypical symptom” of CAD

• Other Considerations• Diabetes mellitus and cardiovascular disease

• Increased threat; decreased symptoms !!

Laboratory Analysis • Serum Enzymes • Blood Chemistry

• Lipid Studies• Electrolytes • Renal Function Studies

• Coagulation Studies • Hematologic Studies

Serum Enzymes: Cardiac • Creatine Phosphokinase (Total CK / CPK)

• Non-Specific: enzyme elevated with damage to heart or skeletal muscles and brain tissue.

• Elevates in 4 to 8 hours• Peaks in 15 to 24 hours • Returns to normal in 3 to 4 days

• Creatine Phosphokinase Isoenzyme (CPK-MB)• Specific: isoenzyme of CPK; elevated with

cardiac muscle damage. • Elevates in 4 to 8 hours • Peaks in 15 to 24 hours• Returns to normal in 3 to 4 days

Cardiac Enzymes • Myoglobin

• Non-specific: a heme protein found in muscle tissue; elevated with damage to skeletal or cardiac muscle.

• Elevates in 2 to 3 hours• Peaks 6-9 hours • Returns to normal 12 hours

• Lactic Acid Dehydrogenase (LDH)• Non-specific: enzyme elevated with damage to

many body tissues. (i.e. heart, liver, skeletal muscle, brain and RBC’s); Not frequently used today.

• Elevates in 1 to 3 days • Peaks in 2 to 5 days • Returns to normal 10 to 14 days

Cardiac Enzymes Cont.,• Troponin I / T

• Specific: a contractile protein released with cardiac muscle damage; not normally present in serum.

• Elevates in 4 to 6 hours• Peaks in 10 to 24 hours• Returns to normal in 10 to 15 days

• Sensitivity superior to CK-MB within the first 6 hours of event.

• Has replaced LDH for client’s who delay seeking treatment.

Other Serum Enzymes • C-Reactive Protein

• Protein marker of acute inflammatory reactions• Increased serum levels associated with increased risk of

acute cardiovascular events.

• Homocysteine• Amino acid; presence in serum suggests

increased risk of cardio-vascular events. • Natriuretic Peptides

• Hormone-like substances released into bloodstream with cardiac chamber distention.

• Atrial Natriuretic Peptide (ANP)• Brain or B-type Natriuretic Peptide (BNP)

Blood Chemistry Analysis • Lipoprotein (Lipid) Profile

• Total Cholesterol• Normal < 200mg/dl

• Triglyceride• Normal < 150 mg/dl

• Low Density Lipoproteins (LDL)• Normal <130 mg/dl / “Optimal”

<100mg/dl• High Density Lipoproteins (HDL)

• Normal: > 40 mg/dl > 60 mg/dl cardio-protective

Blood Chemistry Analysis Cont.,

• Serum Electrolytes• i.e. Na, K, Ca and Mg• Glucose / Hemoglobin A1C

• Coagulation Studies• PTT / aPTT• PT / INR

• Hematologic Studies • CBC

• Renal Function Studies • BUN• Creatinine

Diagnostic Testing • Electrocardiography *

• 12-Lead EKG• Continuous bedside monitoring • Ambulatory monitoring

• Stress Tests• Thallium Scans

• Echocardiograms• Cardiac Catheterizations

* Previously Discussed

Cardiac Stress Tests • Stressing the heart to monitor performance• Assists in Determining

• Coronary artery disease• Cause of chest pain• Functional capacity of heart• Identify dysrhythmias • Effectiveness of medications• Establish goals for a physical fitness routine

Cardiac Stress Tests Cont., • Types of Stress Tests

• Exercise• Treadmill (most common)• Bike• Arm crank

• Pharmacological• Vasodilating agents to mimic the effects of

exercise • Persantin• Adenosine

• Mental / Emotional (new; under investigation) • Simulated public speaking • Mental arithmetic test

Cardiac Stress Tests Cont.,• Thallium Scan

• Often combined with stress tests • Radiological exam to assess how well

the coronary arteries perfuse the myocardium.

• Images are taken 1 to 2 minutes prior to end of stress test and again 3 hours later.

• Nursing Considerations • NPO• IV Access

Cardiac Stress Tests Cont.,• Nursing Considerations

• Explain procedure to client• Maintain NPO status 4 hour before test• Instruct client to avoid stimulants (i.e.

chocolate, caffeine and cigarettes) • Hold certain medications before testing

• Exercise: i.e. beta-adrenergic blockers • Pharmacologic: i.e. Theophylline (24-48 hours

prior)

• I.V. access must be obtained

Echocardiogram • Ultrasound procedure of the heart

combined with an electrocardiogram (EKG).• Assesses

• Cardiac geometry (size & shape)• Motion of structures (chamber walls / valves)

• Simultaneous EKG assists in interpretation• Can be done in conjunction with stress

testing• Referred to as a stress echocardiography or

exercise echocardiography

Echocardiogram Cont., • Types of Echocardiograms

• Transcutanoeous• Non-invasive / painless

• Transesphogeal (TEE)• Invasive / Clearer images • Nursing Considerations:

• Explain procedure• NPO 6 hours prior procedure• I.V. access• NPO 4 hours post-procedure• Monitor for complications

Cardiac Catheterization • “Gold Standard” of cardiac diagnostics• Invasive procedure to assess

• Cardiac chamber pressures & oxygen saturations• Detect congenital or acquired structural defects• Ejection fraction

• Often Includes: • Coronary arteriography: to assess coronary

artery patency

• Using X-ray technique called fluoroscopy • Requiring the use of I.V. contrast / dye

Cardiac Catheterization Cont.,

• Nursing Care• Prior to procedure

• Explain procedure • NPO prior to procedure (8 to 12 hours) • Check allergies (I.V. dye / shellfish / iodine)• Laboratory tests

• During procedure• I.V. access• Hemodynamic monitoring • Arterial and venous access via catheters

(sheaths) • Femoral (most common) or brachial

Cardiac Catheterization Cont.,• Post-Procedure Nursing Care

• Maintain Client Bedrest for 6 to 8 hours• Extremity straight & HOB up < 30 degrees

• Maintain Adequate Hydration• IV Fluids (if ordered)• Encourage Fluids

• Frequent Monitoring For Complications • Vital signs• Puncture site• Distal pulses• Laboratory results

The Client with Alterations in Cardiac Output

Lecture II9/30/05

Sherry Burrell, RN, MSNRutgers University

Nursing III

Coronary Artery Disease (CAD)

• An insidious, progressive disease resulting in coronary artery narrowing or total occlusion.• Atherosclerosis

• Most common cause of CAD• The abnormal accumulation of plaques on

the vessel wall; involves inflammatory process.

• Causes narrowing then eventually blockages in the coronary arteries that reduces myocardial blood flow = CAD

• Asymptomatic until 75% occlusion of coronary artery lumen.

Coronary Artery Disease Cont.,

• Basis of CAD Management • Framingham Study (1948- cont. today)

• Identified specific risk factors and life-style habits that increase one’s risk for developing atherosclerotic heart disease.

CAD: Risk Factors • Modifiable

• Cigarette smoking• Hypertension

(HTN)• Hyperlipidema• Physical inactivity• Diabetes Mellitus• Obesity• Stress / Anxiety• Diet

• Non-Modifiable• Increasing Age

• Males >45 years old • Females >55 years old

• Gender• Affects both men and

women; #1 killer is U.S.

• Genetics• Strong genetic

component

• Ethnicity• Non-whites increased

incidences versus whites

CAD: Interventions • Smoking Cessation• Diet• Exercise• Weight Management• Cholesterol

Management • Lipid Profile

• Normal: every five years

• Medications:• i.e Zocor, Crestor &

Niaspan

• HTN Management• BP Screenings • Medications:

• i.e. antihypertensives & diuretics.

• Diabetes Management • Blood glucose testing • Medications:

• i.e. oral hypoglycemics & insulin

Angina Pectoris • As CAD progresses the atherosclerotic

plagues become significant, reducing blood flow to portions of the myocardium = Ischemia.• Myocardial ischemia clinically manifests

most often as angina or chest pain.• Angina pectoris is defined as myocardial

ischemia without cellular death.• Imbalance between myocardial oxygen

supply and demand

O2

Myocardial Oxygen Supply and Demand Balance

Demand

Supply

O2

ArterialOxygenContent

Preload Afterload CoronaryArtery

Blood flowContractilityHeart Rate

Precipitating Factors: Angina

• Any situation where oxygen demands are increased:• Physical exertion• Tachycardia• Dysrhythmias • Cold weather• Eating a heavy meal • Stress or emotional states

Angina Pectoris • Signs and Symptoms

• Chest Discomfort or Pain• Can occur anywhere in chest; most commonly

behind sternum; poor localization • Pain may radiate to the back, arms (left most

common), shoulder, neck or jaw.• Described as pressure, tightness or burning

sensation • Often precipitated by physical exertion or stress • Maybe associated with a few of the following

symptoms: • SOB, weakness, anxiety, diaphoresis, N/V,

dizziness or numbness in upper extremities

Types of Angina• Stable Angina

• Predictable, consistent pain with physical exertion & relieved with rest; “my usual chest pain”• Rest & NTG; can be managed medically for years

• Unstable Angina • Last longer than stable angina, new onset

or increased frequency / intensity of symptoms; pain at rest• Preinfarction or Crescendo Angina

• Lasting longer than 15 minutes /unrelieved by NTG x3 is a medical emergency!

• Call 911 / hospitalization for management

Types of Angina Cont.,• Variant / Prinzmetal Angina

• Pain at rest; maybe cyclic, + ST segment elevation (reversible); usual cause is coronary artery vasospasm with or without atherosclerotic plaques• Nitrates & calcium channel blockers

• Silent Angina• No signs or symptoms; + ST segment

elevation • Nitrates, beta blockers, calcium channel

blockers & lifestyle changes

Management: Unstable Angina

• Goals of Medical Management• Increase O2 supply & decrease O2 demand to the

myocardium. • Prevent MI and death• To actively intervene !!

• 12-Lead Electrocardiogram (EKG)• Significant CP without EKG changes; + changes

treated as an MI.• Laboratory Tests

• Electrolytes• Cardiac Enzyme Panel

• Rule-out MI: every 8 hours x 3 / 6 hours x4

Management: Unstable Angina• Relief of Chest Pain: “MONA”

• Morphine (drug of choice)• Oxygen• Nitroglycerine

• Increase Coronary Artery Blood Flow • Antiplatelet medications

• ASA• Glycoprotein (GP) IIb/IIIa Inhibitors• Heparin

• Percutaneous Coronary Intervention (PCI)

Management of Unstable AnginaDemand

O2

Beta Blockers

Ca ChannelBlockers

ACE I

Preload

NTGACE I

Morphine

Supply

Blood FlowNTG

Ca Channel Blockers

ASAAnticoagulants

Morphine

Open OccludedArteries

O2

PCI

Contractility

HR

Afterload

Nursing Interventions: Unstable Angina

• Early Identification of Chest Pain• Assessment of Chest Pain

• Chest Pain: Intensity- Scales (0-10) & Characteristics- “OLD

CART”

• Mentation, overall tissue perfusion

• Vital signs, heart rhythm, pulse oximetery

• Diagnostics: 12- lead EKG and Laboratory tests

• Management of Chest Pain =“MONA”

Nursing Interventions: Unstable Angina

• Calm Environment• Anxiety and fear of impending doom (death)

• Activity Restrictions • Avoid the valsalva maneuver

• Patient Education• Risk factors for CAD • Signs and symptoms of angina • Medications• When to call the doctor• Stress management techniques

See pp.403 box 16-8 Thalen

Acute Coronary Syndromes (ACS)

• Umbrella term to describe a wide range of clinical presentations of CAD from unstable angina to acute myocardial infarction (MI). • Continuum, Not separate disorders!

UnstableAngina

AcuteMyocardial Infarction

Myocardial Infarction (MI)• An MI is defined as irreversible necrosis

(death) of myocardial tissue, resulting from an abrupt decrease or total lack of coronary blood supply.• An abrupt and severe disruption of O2

supply and demand to the myocardium.• Causes:

• Coronary artery thrombosis (most common)• Coronary artery vasospasm• Cocaine• Trauma• Severe and abrupt hypotension

Myocardial Infarction (MI) Cont.,

• Signs and Symptoms: • Chest Pain

• Severe and unrelenting substernal chest pain; often radiating to the back, left arm or jaw.

• Lasting for 30 minutes or more• Only relieved by opioids • Occurs without a know precipitating event;

usually occurring in the morning• Associated Symptoms

• SOB, weakness, anxiety, diaphoresis, N/V, dizziness or numbness in upper extremities.

Myocardial Infarction Cont.,

• Pathophysiology • Irreversible cell death within 20-40

minutes of cessation of blood flow.• Wavefront of cellular death proceeds from

endocardium to epicardium.• EKG changes associated with an MI:

• Ischemia: T wave inversion• Injury: ST segment elevation• Infarction: Pathological Q waves

Types of Myocardial Infarctions

• Classified according to muscle layer affected:• Q wave MI

• Transmural: full thickness muscle wall necrosis• Often associated with a more prolonged MI

• Non-Q wave MI• Partial-thickness muscle wall necrosis• Often associated with smaller, less complete

occlusions. • i.e. Subendocardial- necrosis of the inner 1/3 to

1/2 of the muscle wall.

Types of Myocardial Infarctions • According to anatomical location

• Left Ventricle • Anterior Wall

• Left Anterior Descending (LAD)• Associated with left ventricular failure,

pulmonary edema & cardiogenic shock• Inferior Wall

• Right Coronary Artery (RCA)• Associated with dysrhythmias & conduction

disturbances • Posterior Wall

• RCA or Circumflex Artery

• Right Ventricle• Portion of the RCA; Rare

Complications: Post-Acute MI• Dysrhythmias (Most Common)

• Sinus Bradycardia• Occurs in about 40% of clients after an

acute MI• Sinus Tachycardia

• Must be corrected !!• Atrial

• PAC’s or Atrial fibrillation common• Ventricular

• PVC’s and ventricular tachycardia (VT) • AV Heart Blocks

• Most common with inferior wall MI

Complications: Post-Acute MI • Ventricular Aneurysm

• Non-contractile, thin ventricular wall = SV• Leads to acute heart failure, emboli and VT

• Ventricular Septal Defect• Rupture of septum; shunting of blood

• S/Sx: Severe CP, syncope, BP & holosystolic murmur

• Medical emergency; high mortality; surgery to correct

• Pericarditis• An inflammation of the pericardial sac

• S/Sx: Pain, friction rub (left sternal border)• Treatment: NSAIDS and ASA

CAD / Angina / MI: Nursing Diagnoses

• Acute pain related to an imbalance between myocardial oxygen supply and demand.

• Anxiety related to fear of unknown or death.

• Ineffectual coping related to effects of acute illness and major lifestyle changes.

• Activity intolerance related to fatigue (secondary to an imbalance between oxygen supply and demand).

• Knowledge deficit related to CAD /angina / MI and its treatments.

CAD / Angina / MI: Nursing Diagnoses

• Powerlessness related to the lack of control over current situation or disease progression.

• Ineffective (cardiopulmonary) tissue perfusion related to impaired arterial blood flow.

• Decreased cardiac output related to altered… • Preload• Afterload• Contractility• Heart rate / rhythm

Acute MI: Management• Goals of Medical Management

• Chest pain control• To preserve the myocardium• Prevention or management of complications• Pharmacological / intervention-based therapies

• EKG• Positive changes and/or severe CP despite

medical therapies• Laboratory Tests

• Electrolytes• Cardiac Enzyme Panel

• Rule-in MI and then to monitor response to treatments

Thrombolytic Therapy• Preserves the ischemic myocardium; limits

the size of infarction by restoring blood flow quickly; can be done in emergency room.• Thrombolytic Agents

• Work by causing lysis of clots; “clot busters”• i.e. Alteplase (t-PA) or Reteplase (r-PA)

• Eligibility Criteria• CP >30 minutes• < 12 hours from onset (many institutions < 6

hours) • Positive EKG changes• CP unrelieved with medical therapies (i.e. NTG)

Thrombolytic Therapy Cont.,• Exclusion Criteria

• History of CVA or any bleeding disorder• Active internal bleeding or recent surgery

• Complications• Bleeding and reperfusion dysrhythmias

• Nursing Role• I.V. Access• Baseline labs• Monitoring

• Subsequent labs, vital signs & for complications• Bleeding Precautions

Percutaneous Coronary Intervention

• Umbrella term for all various of interventional cardiac catheterization procedures. • Indications

• Angina refractory to medical therapies• Proximal coronary artery stenosis; single or

double vessels disease• Procedure & Nursing Care

• Much the same as cardiac catheterizations • Except: venous & arterial catheters; larger

lumen with interventional catheterizations (i.e. stents)

Percutaneous Coronary Intervention• Procedural Variations

• Angioplasty• Percutaneous Transluminal Coronary Angioplasty

(PTCA)• Balloon tipped-catheter; expanded to dilate vessel• Laser- UV pulse laser to “vaporize” lesion

• Atherectomy• Removal of plaque from vessel

• Coronary Artery Stenting• Tiny metal mesh tubes

• Drug-eluting Stents: Coated with Rapamune• Brachytherapy

• For in-stent re-stenosis; gamma radiation therapy

PCI Cont., • Nursing Care

• Prior to procedure• Explain procedure • NPO prior to procedure ( 8 to 12 hours) • Check allergies (I.V. dye / shellfish / iodine)• Laboratory tests

• During procedure• I.V. access• Hemodynamic monitoring • Arterial and venous access via catheters

(sheaths) • Femoral (most common) or brachial

PCI Cont.,• Post-Procedure Nursing Care

• Maintain Client Bedrest for 6 to 8 hours• Extremity straight & HOB up < 30 degrees

• Maintain Adequate Hydration• IV Fluids (if ordered)• Encourage Fluids

• Frequent Monitoring For Complications • Vital signs• Puncture site• Distal pulses• Laboratory results

PCI: Complications• Acute Coronary Artery Occlusion

• Thrombosis /emboli or persistent vasospasm• Impaired circulation to distal extremity

• Distal arterial emboli • “Blue toe syndrome”

• Disrupted plaques occludes small vessels; pulses and circulation checks are good but, severe pain.

• Hemorrhagic Event • i.e. Arterial tear: retroperitoneal bleeding

• Puncture Site Complications• i.e. Bleeding or hematoma formation

• Reperfusion DysrhythmiasSee pp. 735 table 28-7; Smeltzer & Bare

Cardiac Surgery• Coronary Artery Bypass Graft (CABG)

• A surgical revascularization procedure; blockages are bypassed using internal mammary artery or great saphenous vein.

• Indications• Angina unrelieved by medical therapies• Left main disease• Triple vessel disease• Single or double vessel disease not

amendable to PCI or failed PCI

Cardiac Surgery: CABG• Different Surgical Approaches

• On-Pump (Traditional CABG)• Cardiopulmonary bypass machine (extracorporeal

circulation); heart stopped during procedure

• Off-Pump• “Beating heart” procedure; uses “octopus device”

to stabilize the myocardium during procedure

• Minimally Invasive Direct CABG (MIDCABG)• Single vessel disease not amendable by PCI

procedures• Small thoracotomy incision; off-pump approach

Cardiac Surgery: CABG• Complications

• Stroke (2% post-bypass reperfusion)• Hypertension• Hypotension• Bleeding• Dysrhythmias• Cardiac Tamponade

CABG: Post-Operative Nursing Care

• Maintain airway patency • Continuous bedside monitoring• Mediastinal chest tube management

• Monitor drainage & avoid kinks in tubing • Assess pain levels frequently and provide relief

• Provide relief from anxiety and fear

• Assess the surgical incisions for s/sx of infection

• Assess the extremity from which vessel harvested • Look for signs impaired circulation & edema

• Monitor for complications

Management of an Acute MI Demand

O2

Beta Blockers

Ca ChannelBlockers

ACE I

Preload

NTGACE I

Morphine

Supply

Blood FlowNTG

Ca Channel Blockers

ASAAnticoagulants

Morphine

Open OccludedArteries

O2

PCIThrombolytics

CABG

Contractility

HR

Afterload

Cardiac Rehabilitation• Education and support for client and

family• Initiated once client is free of symptoms• Focuses:

• Education• Psychological Support• Physical Conditioning

• Goals: • Maximize QOL• Limit progression of CAD• Prevent further cardiac events

Cardiac Rehabilitation • Phases of Cardiac Rehabilitation

• Phase I: Inpatient (post-event)• Education on medications, rest-activity balance,

follow-up appointments & when to call doctor or “911”.

• Low-level physical conditioning i.e. self-care & mobilization.

• Phase II: Outpatient Supervised• Physical conditioning & education on risk factor

modification

• Phase III: Outpatient Self-Directed• Maintain cardiovascular stability & long-term

physical conditioning

The Client with Alterations in Cardiac Output

Lecture III10/10/05

Sherry Burrell, RN, MSNRutgers University

Nursing III

Hemodynamics • Describe the intravascular pressures and the

flow occurring when the myocardium contracts and blood is pumped via the vascular system through-out the body.

• Basic Principles • Blood flow throughout the cardiovascular

system from area of higher pressures to areas of lower pressures.• Pressures created by cardiac cycle: systole &

diastole • Pressures: Cardiac chambers and vessels

Hemodynamic Monitoring

• Two Major Categories • Non-Invasive

• i.e. Taking a blood pressure or a pulse

• Invasive• Intra-arterial blood pressure monitoring (A-lines)• Central venous pressures (CVP) catheters • Pulmonary artery (PA) catheters (Swan-Ganz)

Invasive Hemodynamic Monitoring

• Three Components: • Transducer: Converts fluid waves into electrical

signals • Amplifier: Increases the size of the electrical signal • Monitor / Recorder: Displays the signal and saves

data

• Specialized Equipment: • Catheter access to client • Semi-rigid (high pressure) tubing

• Three-way stop cock • Intraflow or In-line flow device

• Inflatable pressurized sleeve / bag • I.V. Solution: 0.9 % NSS with heparin added

Invasive Hemodynamic Monitoring Cont.,

• Calibration of Equipment • Leveling:

• Transducer at the level of right atrium

• Zeroing: • Atmospheric pressure

Let’s see how it’s done…

http://www.eonreality.com/demos/e-learning/ccn/unit3_4demo/e2_electdemo.html

Intra-arterial BP Monitoring

• Indicated for direct, continuous blood pressure monitoring in the critically ill client. • Measures systolic, diastolic & mean arterial

pressures (MAP)• Allows for serial samplings of ABG’s• Considered “low-risk”• More accurate than cuff pressures in low CO

and shock (not affected by vasoconstriction) • NEVER USED TO GIVE MEDICATIONS !!

Intra-arterial BP Monitoring Cont.,

• Insertion Sites:• Radial (most common)• Brachial • Femoral

• Insertion Techniques:• Percutaneous • Cut-down (if necessary)

• Insertion Assessment:• Distal Blood Flow

• Doppler Ultrasound• Allen’s Test

Intra-arterial BP Monitoring Cont., • Nursing Considerations

• Monitor for complications• Compromised blood flow to distal extremity

• i.e. thrombosis or arterial spasm

• Insertion Site• i.e. Infection, bleeding, hematoma or skin

breakdown

• Maintenance of System• Sterile dressing changes• Tubing, caps and flush bag changes

Central Venous Pressure (CVP) Catheters

• Measures the pressures in the right atrium.• Used to assess right ventricular function

and venous blood return to heart.

• CVP / Right Atrial Pressures: Reflection of right ventricular filling pressures (preload).

• Normal Limit: 2- 6 mm Hg• Increased CVP = Fluid Overload• Decreased CVP = Hypovolemia

CVP Catheters Cont., • Insertion Sites

• Internal Jugular• Subclavian Vein

Tip advanced to the Superior Vena Cava

• Prior to Use:• Chest X-Ray

• Confirm placement• Rule-out pneumo- or hemo- thorax

CVP Catheters Cont., • Complications

• Dislodgement • Infection• Air Embolism• Cardiac dysrhythmias

• Nursing Care• Sterile dressing changes• Tubing, caps and fluid bag changes • Flushing of lumens; never tie off !!

Pulmonary Artery (PA) Catheters

• Used to assess left ventricular function.• “Multi-Tasking” Catheters

• Right Atrial Pressures (same as CVP)• Pulmonary Artery:

• Pulmonary artery systolic pressures (PAS)• Pulmonary artery diastole pressures (PAD)• Pulmonary artery mean pressure (MAP)

• Left Atrial Pressures: • Pulmonary artery occluded pressures

(PAOP)• Normal limit = 5-13 mmHg• Reflection of left ventricular filling pressures

(preload)

PA Catheters Cont., • “Multi-Tasking” Catheters Cont.,

• Intermittent Cardiac Output

• Specialized PA Catheters• Additional Features

• Continuous I.V. infusions • Continuous CO monitoring • Continuous venous mixed oxygen saturation

monitoring• Represents venous blood saturations from many body

tissues• Monitors balance between O2 supply and demand

• Temporary transvenous pacing wires

PA Catheters Cont., • Insertion Sites:

• Internal Jugular• Subclavian Vein

Threaded into the right atrium, to right ventricle finally resting in the pulmonary artery.

• Prior To Use:• Chest x-ray

• Ensure proper placement• R/O pneumo- or hemo- thorax

PA Catheters Cont., • Complications

• Dislodgement • Infection• Air embolism• Cardiac Dysrhythmias • Thromboembolism• Pulmonary Artery rupture

• Nursing Care• Sterile dressing changes• Tubing, caps and fluid bag changes • Flushing of lumens; Never tie off !!

Heart Failure • The inability of the heart to pump

adequate amounts of blood to meet body’s needs for oxygen & nutrients.• Common causes:

• CAD• HTN• Cardiac Infections • Cardiomyopathy• Valvular Disorders• Myocardial Infarction• Dysrhythmias

Classification of Heart Failure

• Onset:• Acute heart failure • Chronic heart failure

• Affected portion of the cardiac cycle:• Diastolic heart failure• Systolic heart failure

• Affected side of the heart: • Left heart failure • Right heart failure

• Stages of heart failure severity:• New York Heart Association • American Heart Association/American College of

Cardiology

Acute or Chronic Heart Failure• Describes the speed of onset of heart

failure• Acute Heart Failure

• Sudden onset• No compensatory mechanisms• May experience acute pulmonary

edema,CO or cardiogenic shock

• Chronic Heart Failure• Gradual (insidious) Onset • Presence of compensatory mechanisms

• Structural heart chamber changes (dilation or hypertrophy)

• Fluid overload & sodium and water retention• Ongoing process; may deteriorate into acute HF

• i.e. Onset of dysrhythmias or cessation of medications

Heat Failure: Compensatory Mechanisms

• Sympathetic Nervous System:• Decreased tissue perfusion results in activation of the

sympathetic nervous system, resulting in: • ↑ Heart rate• ↑ Contractility• Vasoconstriction of arteries, arterioles & veins

(↑afterload & ↑preload) • RAAS: Renin-Angiotension-Aldosterone

System• Decreased renal perfusion stimulates the increased

release of renin→ angiotensin II production, resulting in:• Vasoconstriction (↑ afterload)• Release of aldosterone: Na+ & water retention

(↑preload)

Heat Failure: Compensatory Mechanisms

• Ventricular Remodeling:• Final compensatory mechanism • The ventricles change in size & shape in order

to overcome the ↑ resistance (afterload) of heart failure. • Hypertrophy

• The ventricles thicken and become stiff resulting in impairing filling during diastole.

• Dilation• The heart muscle becomes over-stretched resulting

in a decreased force of contraction during systole.

• Overtime these mechanisms may actually worsen heart failure !!

Myocardial Disease / InjuryImpaired Ventricular Performance

Cardiac Output

↑ SNS↑ HR

↑ Contractility Vasoconstrictio

n

↑ RAASVasoconstriction

Na/H2O Retention

CardiacWorkload

Ventricular

RemoldingDilation &

Hypertrophy

Vicious Cycleof

Heart Failure

Systolic or Diastolic Heart Failure

• Described HF based on cardiac cycle• Diastolic Heart Failure

• Disorder of ventricular filling• Structural changes: usually ventricular

hypertrophy• Normal Ejection Fraction

• Systolic Heart Failure (more common)• Disorder of ventricular contraction• Structural changes: usually ventricular dilation Ejection Fraction (< 40%)

• Combined diastolic & systolic impairments are common.

Systolic & Diastolic Heart Failure: Remodeling

(Jessup & Brozena, 2003)

Left & Right Sided Heart Failure

• Describes Heart failure based on the side of the heart that is affected.• Left-Sided Failure

• Left ventricular failure• Pulmonary congestion

• Sign/Symptoms: i.e. fatigue, SOB, dyspnea, PND, orthopena, crackles, dry cough, & tachycardia

• Right-Sided Failure• Right ventricular failure• Systemic congestion

• Signs/Symptoms: i.e. weakness, peripheral edema, weight gain, JVD, hepatomegaly, anorexia & N/V.

NYHA: Functional Classification of HF

I No symptoms and no limitation in ordinary physical activity.

II Mild symptoms and slight limitation during ordinary activity. Comfortable

at rest.IIIMarked limitation in activity due to

symptoms, even during less-than-ordinary activity. Comfortable only at rest.

IV Severe limitations. Experiences symptoms even while at rest.

AHA/ACC: Classification System of HF

(Jessup & Brozena, 2003)

Heart Failure: Nursing Diagnoses

• Impaired gas exchange related to ventilation perfusion imbalance.

• Decreased cardiac output related to altered… • Preload• Contractility• Afterload• Heart rate /rhythm

• Activity intolerance related to fatigue (secondary to by an imbalance between oxygen supply and demand).

• Ineffective (cardiopulmonary) tissue perfusion related to impaired arterial blood flow.

Heart Failure: Nursing Diagnoses

• Excess fluid volume related to excess fluid or sodium intake and retention of fluid secondary to heart failure and its treatments.

• Anxiety related to breathlessness and / or restlessness secondary to inadequate oxygenation.

• Powerlessness related to inability to perform usual role responsibilities.

• Knowledge deficit related to heart failure and its treatments.

Nursing Management: Heat Failure

• Nursing Considerations • Respiratory

• Supplemental oxygen • Good lung assessment

• Monitoring • Hemodynamic Monitoring • Daily Weights• I & O’s • Laboratory Results

• i.e. electrolytes, BNP & digoxin levels

• Maintain • Small frequent meals; low in salt • Skin integrity

Nursing Management: Heat Failure

• Nursing considerations Cont.,• Promote rest and avoid fatigue • Assess for peripheral edema

• Client Education• Medications • Lifestyle changes

• i.e. low-sodium diet & activity-rest balance • Daily weights • S/Sx of worsening heart failure to report • Importance of follow-up care

Heart Failure Management• Goals of management

• Relief of health failure symptoms• Enhance cardiac performance

• Pharmacologic Management • Reduce Cardiac Workload

• Diuretics: Preload; watch for hypokalemia• Nitrates: Preload • ACE I / ARB’s: Preload & Afterload• Beta blockers / ACE I: Enhance reverse

remolding

• Increase Positive Inotropic Effects• i.e. Digoxin (Lanoxin)

Heart Failure Management • Mechanical Assist Devices

• Intra Aortic Balloon Pump (IABP)• Most widely used temporary assist

device• Augments diastolic coronary

artery blood flow, enhances renal perfusion & reduces afterload

• Used to reduce cardiac workload when medical therapies are refractory

• i.e. Acute MI, after cardiac surgery or heart Failure

Heart Failure Management• Ventricular Assist Devices

• Provide flow assistance to the failing ventricle• Three types available

• Left ventricular assist devices (LVAD); Most Common

• Bilateral ventricular assist devices (BiVAD)• Right ventricular assist devices (RVAD)

• Categories of use• Support to pending recovery• Bridge to transplantation• Destination therapy

Heart Failure Management• Surgical Interventions

• Correct Underlying Problem• Revascularization; CABG• Valvular repair or replacement

• Artificial, human or animal valves• Cardiac support devices

• ACORN CorCap

• Heart transplantation• UNOS Stats (2003 U.S.)

• 3,519 wait listed• 2,055 transplanted Not enough to go around !!

Complications of Heart Failure

• Electrolyte Imbalances• i.e. Hypokalemia

• Medication Toxicity • i.e. Digoxin

• Dysrhythmias • Cardiac Tamponade • Cardiogenic Shock • Pulmonary Edema

Pediatric Considerations• Most causes of heart failure are

congenital heart defects.• Three categories of signs & symptoms

• Impaired Myocardial Function• Tachycardia, gallop rhythm (S3 & S4) &

diaphoresis

• Pulmonary Congestion• Tachypnea*, dyspnea, costal retractions &

developmental delays

• Systemic Congestion• Hepatomegaly*, JVD, weight gain & peripheral

edema * See Box 34-1, pp. 1478 Wong