Chapter 35
This presentation is the property of its rightful owner.
Sponsored Links
1 / 107

Chapter 35 PowerPoint PPT Presentation


  • 110 Views
  • Uploaded on
  • Presentation posted in: General

Chapter 35 . Cardiac Disorders. Learning Objectives. Label the major parts of the heart. Describe the flow of blood through the heart and coronary vessels. Name the elements of the heart’s conduction system. State the order in which normal impulses are conducted through the heart.

Download Presentation

Chapter 35

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -

Presentation Transcript


Chapter 35

Chapter 35

Cardiac Disorders


Learning objectives

Learning Objectives

  • Label the major parts of the heart.

  • Describe the flow of blood through the heart and coronary vessels.

  • Name the elements of the heart’s conduction system.

  • State the order in which normal impulses are conducted through the heart.

  • Explain the nursing considerations for patients having

    procedures to detect or evaluate cardiac disorders.


Learning objectives1

Learning Objectives

  • Identify nursing implications for common therapeutic

    measures, including drug, diet, or oxygen therapy; pacemakers

    and cardioverters; cardiac surgery; and cardiopulmonary

    resuscitation.

  • Explain the pathophysiology, risk factors, signs and symptoms,

    complications, and treatment for selected cardiac

    disorders.

  • List the data to be obtained in assessing the patient with

    a cardiac disorder.

  • Assist in developing nursing care plans for patients with

    cardiac disorders.


Anatomy and physiology of the heart

Anatomy and Physiology of the Heart


Anatomy

Anatomy

Chambers

Two upper atria (right and left)

Two lower ventricles (right and left)

Muscle layers

Endocardium, myocardium, and epicardium

Valves

Atrioventricular valves

Mitral and tricuspid

Semilunar valves

Aortic and pulmonic


Heart sounds

Heart Sounds

The first heart sound (S1), referred to as lub, occurs when the ventricles contract during systole and when the mitral and tricuspid valves close

The second heart sound (S2), called dub, occurs during ventricular relaxation or diastole and is caused by the closing of the aortic and pulmonic valves


Chapter 35

Figure 35-1


Coronary blood flow

Coronary Blood Flow

Left coronary artery and the right coronary artery

Left coronary artery branches into the left anterior descending and circumflex arteries

Right coronary artery branches to supply the sinoatrial (SA) and the atrioventricular (AV) nodes, the RA and RV, and the inferior part of the LV


Coronary blood flow1

Coronary Blood Flow

Venous system parallels the arterial system: the great cardiac vein follows the left anterior descending artery and the small cardiac vein follows right coronary artery

Veins meet to form the coronary sinus (largest coronary vein), which returns deoxygenated blood from the myocardium to the right atrium


Chapter 35

Figure 35-2


Chapter 35

Figure 35-3


Conduction

Conduction

SA node, called the pacemaker, initiates the impulse

The impulse is carried throughout the atria to the AV node, located on the floor of the RA

Impulse is delayed in the AV node, then transmitted to the ventricles through the bundle of His

The bundle is made up of Purkinje cells and is located where the atrial and ventricular septa meet

Bundle of His divides into left and right bundle branches

Left branch divides into anterior and posterior branches: fascicles

Terminal ends of right and left branches: the Purkinje fibers

When impulse reaches Purkinje fibers, ventricles contract


Chapter 35

Figure 35-4


Conduction1

Conduction

Cardiac innervation

Heart innervated by sympathetic and parasympathetic fibers of the autonomic nervous system

Sympathetic fibers distributed throughout the heart

Sympathetic stimulation results in increased heart rate, increased speed of conduction through the AV node, and more forceful contractions

Parasympathetic fibers (part of the vagus nerve) found primarily in the SA and AV nodes and the atrial tissue

Parasympathetic stimulation results in slowing of heart rate, slowing of conduction through the AV node, and decreased strength of contraction


Cardiac function

Cardiac Function

Cardiac cycle

Contraction and relaxation of the heart make up one heartbeat

Cardiac output

Amount of blood (in liters) ejected per minute

Factors that affect stroke volume: preload, contractility, and afterload

Myocardial oxygen consumption

Myocardial tissue routinely needs 70% to 75% of the oxygen delivered to it by the coronary arteries


Age related changes

Age-Related Changes

Heart

Increased density of connective tissue and decreased elasticity

Number of pacemaker cells in the SA node decreases, as does the number of nerve fibers in the ventricles

Blood vessels

The number of pacemaker cells in the SA node decreases, as does the number of nerve fibers in the ventricles


Nursing assessment of cardiac function

Nursing Assessment of Cardiac Function


Chief complaint and history of present illness

Chief Complaint and History of Present Illness

Symptoms related to cardiac disorders include fatigue, edema, palpitations, dyspnea, and pain

Note when symptoms occur, what aggravates them, and what relieves them


Medical history

Medical History

Hypertension, kidney disease, pulmonary disease, stroke, rheumatic fever, streptococcal sore throat, and scarlet fever

Document previous cardiac disorders and hospitalizations. List recent and current medications and note allergies in appropriate records


Family history

Family History

Assess whether immediate relatives have had hypertension, coronary artery disease (CAD), other cardiac disorders, or diabetes mellitus


Review of systems

Review of Systems

Systematically assess whether the patient has experienced the following: weight gain, fatigue, dyspnea (shortness of breath), cough, orthopnea (difficulty breathing in a supine position), paroxysmal nocturnal dyspnea (sudden dyspnea during sleep), palpitations, chest pain, syncope (fainting), concentrated urine, or leg edema


Functional assessment

Functional Assessment

Determine how this illness has affected the patient’s ability to carry out usual activities

Activity and rest patterns and usual diet

Ask about sources of stress and coping strategies


Physical examination

Physical Examination

Vital signs

Blood pressure, pulses, and respirations

Skin

Heart sounds

Heart murmurs

Extremities


Chapter 35

Figure 35-5


Diagnostic tests and procedures

Diagnostic Tests and Procedures

Electrocardiogram (ECG)

Ambulatory ECG (Holter monitor)

Implantable loop monitor/recorder (ILR)

Echocardiogram (heart sonogram)

Transesophageal echocardiogram (TEE)

Magnetic resonance imaging (MRI)

Multiple-gated acquisition scan


Diagnostic tests and procedures1

Diagnostic Tests and Procedures

Stress test (exercise tolerance test)

Perfusion imaging

Thallium imaging

Ultrafast computed tomography

Cardiac catheterization

Electrophysiology study (EPS)


Chapter 35

Figure 35-6


Laboratory tests

Laboratory Tests

Arterial blood gases

Pulse oximetry

Cardiac enzymes

Creatine phosphokinase

Cardiac protein markers

Complete blood count

Lipid profile

B-type natriuretic peptide (BNP)

C-reactive protein (CRP)


Chapter 35

Figure 35-7


Drug therapy

Drug Therapy

Cardiac glycosides

Antianginals

Antidysrhythmics

Angiotensin-converting enzyme (ACE) inhibitors (ACEIs)

Diuretics

Anticoagulants


Drug therapy1

Drug Therapy

Heparin

Low-molecular-weight heparin (LMWH)

Warfarin

Antiplatelet agents

Fibrinolytic agents (also called thrombolytics)

Lipid-lowering agents

Analgesics


Diet therapy

Diet Therapy

Low-fat, high-fiber diet

Well-balanced diet

Emphasis on fruits, vegetables, grains, and proteins low in fat (fish, legumes, poultry, lean meats)

Cholesterol intake should be limited to

200 mg/day; foods with trans fatty acids, limited to 8

Exercise program may help achieve optimal weight


Diet therapy1

Diet Therapy

Sodium

A diet containing sodium 2 g/day most often prescribed

Potassium

Patients taking potassium-wasting diuretics need adequate potassium in the diet


Other therapeutic measures

Other Therapeutic Measures

Oxygen therapy

Pacemakers

Temporary

Permanent

Cardioversion


Cardiac surgery

Cardiac Surgery

Common surgical procedures

Pacemaker insertion

Repair or replace valves or septa or remove tumors

Coronary artery bypass surgery


Cardiac surgery1

Cardiac Surgery

Preoperative nursing care

Interventions

Fear and Anxiety


Cardiac surgery2

Cardiac Surgery

Postoperative nursing care

Interventions

Ineffective Breathing Pattern

Pain

Ineffective Thermoregulation

Decreased Cardiac Output

Risk for Infection

Anxiety


Cardiac disorders

Cardiac Disorders


Coronary artery disease cad

Coronary Artery Disease (CAD)

Arteriosclerosis

Abnormal thickening, hardening, loss of elasticity of arterial walls

Atherosclerosis

Form of arteriosclerosis; inflammatory disease that begins with endothelial injury and progresses to the complicated lesion seen in advanced stages of the disease process

Progression of lesions

Fatty streak

Fibrous plaque

Complicated lesions

Collateral circulation

Branches grow from existing arteries; provide increased blood flow


Coronary artery disease cad1

Coronary Artery Disease (CAD)

Risk factors

Nonmodifiable

Age, gender, heredity, and race

Modifiable

Increased serum lipids, high blood pressure, cigarette smoking (nicotine), diabetes mellitus with elevated blood glucose, obesity, sedentary lifestyle

Other factors

Stress, sex hormones, birth control pills, excessive alcohol intake, high homocysteine levels


Angina pectoris

Angina Pectoris

The most common symptom of CAD

Demand for oxygen by myocardial cells exceeds supply

Stable angina

Occurs with exercise or activity and usually subsides with rest

Unstable angina

Pain more severe, occurs at rest or with minimal exertion, is often not relieved by NTG or requires more frequent NTG administration, and is not predictable

Variant angina

Caused by coronary artery spasm; may not be associated with CAD

Unpredictable and often occurs at rest


Angina pectoris1

Angina Pectoris

Medical treatment

Initial therapy for patients with angina

A Aspirin and antianginal therapy

B Beta-blocker and blood pressure

C Cigarette smoking and cholesterol

D Diet and diabetes

E Education and exercise


Acute myocardial infarction

Acute Myocardial Infarction

Risk factors for AMI

Obesity, smoking, a high-fat diet, hypertension, family history, male gender, diabetes mellitus, sedentary lifestyle, and excessive stress


Acute myocardial infarction1

Acute Myocardial Infarction

Pathophysiology

Begins with occlusion of a coronary artery

Over 4-6 hours, ischemia, injury, infarction develop

Ischemia results from a lack of blood and oxygen to a portion of the heart muscle

If ischemia is not reversed, injury occurs

Deprived of blood and oxygen, the affected tissue becomes soft and loses its normal color

Continued ischemia: infarction of myocardial tissue

Ischemia lasting 20 minutes or more is sufficient to produce irreversible tissue damage


Acute myocardial infarction2

Acute Myocardial Infarction

Complications

Heart failure, cardiogenic shock, thromboembolism, and ventricular aneurysm/rupture

Signs and symptoms

Pain

Heavy or constrictive pain located below or behind sternum

May radiate to the arms, back, neck, or jaw

Patient becomes diaphoretic and lightheaded and may experience nausea, vomiting, and dyspnea

The skin is frequently cold and clammy

Patient experiences great anxiety; feeling of impending doom


Acute myocardial infarction3

Acute Myocardial Infarction

Medical diagnosis

History and the physical signs and symptoms

Laboratory evidence and ECG changes

Cardiac markers

Troponin, myoglobin, and cardiac enzymes

Electrocardiogram

Ischemia: ST segment depressed; T wave is inverted

If there has been total occlusion of a coronary artery, the ECG will show ST elevation (STEMI)

Following infarction, another change often seen on the ECG waveforms is a significant Q wave


Chapter 35

Figure 35-8


Acute myocardial infarction4

Acute Myocardial Infarction

Medical treatment

Drug therapy

Sublingual or intravenous nitroglycerin

Morphine or Demerol

Oxygen

Fibrinolytic therapy

Aspirin and beta-adrenergic blockers

Percutaneous coronary intervention (PCI)

Intracoronary stents

Coronary atherectomy

Laser angioplasty

Radiation therapy

Coronary artery bypass graft surgery


Chapter 35

Figure 35-9


Chapter 35

Figure 35-10


Chapter 35

Figure 35-11


Acute myocardial infarction5

Acute Myocardial Infarction

Assessment

Ask patient to describe the pain, including type, location, duration, and severity

Interventions

Pain

Decreased cardiac output

Anxiety

Cardiac rehabilitation


Heart failure

Heart Failure

Etiology and risk factors

Two types

Disorders that increase the workload of the heart

Disorders that interfere with heart’s pumping ability

Patients at risk for HF: those with CAD, AMI, cardiomyopathy, hypertension, COPD, pulmonary hypertension, anemia, disease of the heart valves, and fluid volume overload


Heart failure1

Heart Failure

Pathophysiology

The LV, RV, or both fail as pumps

Usually left side of heart fails first; right side fails as a result of the left-sided failure

Compensation

Sympathetic compensation

Renal compensation

Natriuretic peptides

Ventricular hypertrophy


Heart failure signs and symptoms

Heart Failure: Signs and Symptoms

Left-sided heart failure

Anxious, pale, and tachycardic

Consecutive blood pressure readings may show a downward trend

Auscultation of the lung fields reveals crackles, wheezes, dyspnea, and cough

S3 and S4 heart sounds heard


Heart failure signs and symptoms1

Heart Failure: Signs and Symptoms

Right-sided heart failure

Increased central venous pressure, jugular venous distention, abdominal engorgement, and dependent edema

Anorexia, nausea, and vomiting from the abdominal engorgement

Fatigue, weight gain, decreased urinary output


Heart failure2

Heart Failure

Medical diagnosis

History, physical examination, radiographs, and laboratory test results


Heart failure3

Heart Failure

Medical treatment

Drug therapy

ACE inhibitors, diuretics, beta-adrenergic blockers, inotropic agents, cardiac glycosides, and nitrates. In addition, certain patients will benefit from B-type natriuretic peptide

Intra-aortic balloon pump (IABP)

Ventricular assist devices (VADs)

Biventricular pacing

Surgery

Coronary artery bypass grafting, valve repair or replacement, partial left ventriculectomy, and cardiac transplantation


Heart failure4

Heart Failure

Assessment

Heart sounds, rate, and rhythm

Jugular vein distention

Baseline respiratory assessment of rate, rhythm, and breath sounds is vital

Measure weight and blood pressure accurately

Inspect skin and palpate for turgor and edema

Intake and output records and daily weights


Heart failure5

Heart Failure

Interventions

Decreased Cardiac Output

Impaired Gas Exchange

Fluid Volume Excess

Activity Intolerance

Anxiety


Infective endocarditis

Infective Endocarditis

Etiology and risk factors

Primarily affect the valves

Incidence has decreased with the use of antibiotics, but there has been a resurgence of the problem in intravenous drug abusers

Patients with valvular disease also at risk


Infective endocarditis1

Infective Endocarditis

Pathophysiology

Pathogens, usually bacteria, enter the bloodstream by any of the previously mentioned means

The pathogen accumulates on the heart valves and/or the endocardium and forms vegetations


Infective endocarditis2

Infective Endocarditis

Complications

Heart failure and embolization

Signs and symptoms

Fever, chills, malaise, fatigue, and weight loss

Chest or abdominal pain; may indicate embolization

Petechiae inside the mouth and on the ankles, feet, and antecubital areas

Osler’s nodes on the patient’s fingertips or toes


Infective endocarditis3

Infective Endocarditis

Medical diagnosis

History, physical examination, results of lab studies

Echocardiography

Serial blood cultures; elevated WBC

Medical treatment

Antimicrobials, rest, limitation of activities

Prophylactic anticoagulants

Surgery to replace an infected prosthetic valve


Infective endocarditis4

Infective Endocarditis

Assessment

Review patient’s history for risk factors, recent invasive procedures, pathologic cardiac conditions, and onset of symptoms

Assess for temperature elevation, heart murmur, evidence of HF (cough, peripheral edema), and embolization


Infective endocarditis5

Infective Endocarditis

Interventions

Administer prescribed antibiotics

Assess cardiac output and monitor for complications

Teach patient about the medications prescribed and any restrictions imposed

Encourage adequate rest


Pericarditis

Pericarditis

Etiology and risk factors

Inflammation of the pericardium

May be primary disease or associated with another inflammatory process

The disease may be acute or chronic

Acute pericarditis caused by viruses, bacteria, fungi, chemotherapy, or AMI (Dressler’s syndrome)

Chronic pericarditis caused by tuberculosis, radiation, or metastases


Pericarditis1

Pericarditis

Pathophysiology

In acute pericarditis, inflammatory process increases amount of pericardial fluid and inflammation of the pericardial membranes

In chronic pericarditis, scarring of the pericardium fuses the visceral and parietal pericardia together

Loss of elasticity results from the scarring

Constrictive process prevents adequate ventricular filling


Pericarditis2

Pericarditis

Complications

Pericardial effusion or accumulation of fluid in the pericardial space

May lead to cardiac tamponade

Signs and symptoms

Chest pain

Most severe on inspiration

Sharp and stabbing but may be described as dull or burning

Relieved by sitting up and leaning forward

Dyspnea, chills, and fever


Pericarditis3

Pericarditis

Medical diagnosis

Serial ECGs

Echocardiogram

CPK-MB

Blood cultures

Medical treatment

Analgesics, antipyretics, anti-inflammatory agents, and antibiotics

Surgical creation of a pericardial window for chronic pericarditis with effusion


Pericarditis4

Pericarditis

Assessment

Assessment of heart sounds especially important

Interventions

Rest and reduction of activity

Administer and teach patient about medications

Emotional support

Vital signs; auscultate for pericardial friction rub

Note pain characteristics and response to analgesics and anti-inflammatory agents

Monitor the ECG for dysrhythmias


Cardiomyopathy

Cardiomyopathy

Disease of the heart muscle

Cause often unknown; may be secondary to another disease process

Usually leads to heart failure

Three types: dilated, hypertrophic, and restrictive

Risk factors with dilated CMP are excessive use of alcohol, pregnancy, and infections

Hypertrophic CMP: common in younger individuals

Amyloidosis, sarcoidosis, and other immunosuppressive disorders may predispose individuals to restrictive cardiomyopathy


Chapter 35

Figure 35-12


Cardiomyopathy1

Cardiomyopathy

Pathophysiology

Dilated cardiomyopathy: dilation of the ventricle and severely impaired systolic function

Hypertrophic cardiomyopathy: LV hypertrophies and there is thickening of the ventricular septum

Restrictive cardiomyopathy: the myocardium becomes rigid and noncompliant


Cardiomyopathy2

Cardiomyopathy

Signs and symptoms

Dilated cardiomyopathy: dyspnea, fatigue, left-sided heart failure, and moderate-to-severe cardiomegaly

Hypertrophic cardiomyopathy: dyspnea, orthopnea, angina, fatigue, syncope, palpitations, ankle edema, and S4 sounds

Restrictive cardiomyopathy: dyspnea, fatigue, right-sided HF, S3 and S4 sounds, and mitral valve regurgitation


Cardiomyopathy3

Cardiomyopathy

Medical diagnosis

Echocardiography

Chest radiography


Cardiomyopathy4

Cardiomyopathy

Medical treatment

Dilated cardiomyopathy: positive inotropic drugs, diuretics, ACE inhibitors and vasodilators; heart transplant

Hypertrophic cardiomyopathy: antidysrhythmics, antibiotics, anticoagulants, calcium channel blockers, beta-blockers; surgical interventions; implantable cardioverter-defibrillator

Restrictive cardiomyopathy: similar to that of HF therapy. Heart transplantation may be considered


Cardiomyopathy5

Cardiomyopathy

Assessment

Primarily for heart failure

Be alert for dyspnea, cough, edema, dysrhythmias, and decreased cardiac output

Interventions

Similar to that of patients with HF

A hopeful atmosphere and careful explanation of care requirements

Encourage the family to support the patient

Guide the patient to make lifestyle changes

Encourage patient to make decisions and choices


Chapter 35

Figure 35-13


Sudden cardiac death

Sudden Cardiac Death

When heart activity and respirations cease abruptly

Most common reason is coronary heart disease

Often preceded by ventricular tachycardia or ventricular fibrillation and occasionally by severe bradydysrhythmias

Sudden cardiac death may be the first indication of CAD

Other causes: left ventricular dysfunction, cardiomyopathy, hypokalemia, antidysrhythmics, liquid protein diets, and high alcohol consumption

Those who survive sudden cardiac death need extensive testing to determine its nature and cause


Sudden cardiac death1

Sudden Cardiac Death

Implantable cardioverter/defibrillator

For patients with life-threatening recurrent ventricular fibrillation who are unresponsive to medications or pacemakers

The device senses heart rate, diagnoses rhythm changes, and treats ventricular dysrhythmias


Nursing care

Nursing Care

Promote psychosocial adaptation

Body image change and a fear of shocks

Patients and families need teaching and support

Family instructed in CPR

ID bracelet and a card with instructions about the ICD setting carried at all times

Advise to avoid strong magnetic fields


Valvular disease

Valvular Disease

Mitral stenosis: narrowing of the opening in the mitral valve that impedes blood flow from the LA into the LV

Mitral regurgitation: allows blood to flow back into the LA during diastole

Mitral valve prolapse: one or both leaflets enlarges and protrudes into the LA during systole

Aortic stenosis: valve cusps become fibrotic and calcify

Aortic regurgitation: fibrosis and thickening of the aortic cusps progress until the valve no longer maintains unidirectional blood flow


Cardiac transplantation

Cardiac Transplantation

The first heart transplantation was performed in 1967 in South Africa by Dr. Christiaan Barnard

Today in the United States, approximately 2500 are done annually for end-stage heart disease

Donor must meet the criteria for brain death, have no malignancies outside the central nervous system, be free of infection, and not have experienced severe chest trauma


Cardiac transplantation1

Cardiac Transplantation

Donor and recipient organs carefully matched

Recipient must be free of infection at the time of transplantation

Patient prepped as any open-heart procedure

Cardiopulmonary bypass initiated; recipient’s heart is removed except for the posterior portions of the atria

Donor heart trimmed and anastomosed to the remaining native heart

Patient removed from bypass, heart restarted, and chest is closed


Cardiac transplantation2

Cardiac Transplantation

Aftercare similar to that of coronary artery bypass surgery

Hemodynamic monitoring, ventilation, cardiac assessment, care of chest tubes, and accurate intake and output measurements are vital

Modified protective isolation used

Patients and families taught sign/symptoms of infection, to avoid crowds and others with infections

Lifelong immunosuppression

Rejection monitored by endomyocardial biopsies


Electrocardiogram monitoring

Electrocardiogram Monitoring

12-lead electrocardiogram

Looks at heart from 12 directions or perspectives

Permits more precise evaluation of the heart’s electrical activity

Continuous ECG monitoring

Most units that perform continuous monitoring use the five-lead system with four limb electrodes and a chest electrode


Chapter 35

Figure 35-15


Electrocardiogram monitoring1

Electrocardiogram Monitoring

Interpretation of electrocardiograms

Heart’s electrical activity represented by deflections, positive and negative, from the baseline

P wave, QRS complex, and T wave

Criteria for interpreting electrocardiograms

Rate calculation

Rhythm

P waves

PR interval

QRS complex

T waves

QT interval


Electrocardiogram monitoring2

Electrocardiogram Monitoring

Interpretation of electrocardiograms

Normal sinus rhythm

The most common cardiac rhythm is sinus in origin because the impulse originates in the SA node; is conducted normally

Common dysrhythmias (rhythm disturbance from problem in the conduction system)

Atrial dysrhythmias

Junctional or escape rhythms

Ventricular dysrhythmias


Chapter 35

Figure 35-17


Chapter 35

Figure 35-18


Chapter 35

Figure 35-19


Chapter 35

Figure 35-20


Chapter 35

Figure 35-21


Chapter 35

Figure 35-22


Chapter 35

Figure 35-23


Chapter 35

Figure 35-24


Chapter 35

Figure 35-25


Chapter 35

Figure 35-26


Chapter 35

Figure 35-27


Chapter 35

Figure 35-28


Chapter 35

Figure 35-29


Chapter 35

Figure 35-30


Hemodynamic monitoring

Hemodynamic Monitoring

Central venous catheter

Placed through the skin, into a venous access (brachial, femoral, subclavian, or jugular sites), and threaded into the RA

Catheter may have 1 to 3 lumens

Mixed venous oxygen saturation


Hemodynamic monitoring1

Hemodynamic Monitoring

Pulmonary artery catheter

Swan-Ganz catheter

Longer than the central venous catheter

Inserted like the central venous catheter and is threaded through the RA, tricuspid valve, RV, pulmonic valve, and into pulmonary artery

Cardiac output

Measured continuously or by thermodilution


Hemodynamic monitoring2

Hemodynamic Monitoring

Arterial line

Provides a direct measurement of systolic and diastolic blood pressures


  • Login