CCRN REVIEW PART 1

Never let what you cannot do interfere with what you can do
- John Wooden -

Sherry L. Knowles, RN, CCRN, CRNI

CCRN REVIEW PART 1

TOPICS
Acute Coronary Syndromes Acute Myocardial Infarction Heart Blocks

ARDS Chronic Lung Disease Drowning

Heart Failure Cardiac Alterations Aortic Aneurysms Cardiomyopathy Shock States Peripheral Vascular Disease Hemodynamics

Pneumonia Pneumothorax Pulmonary Embolism Respiratory Failure Gastrointestinal Alterations GI Bleeding Pancreatitis

CCRN REVIEW PART 1

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

OBJECTIVES
Understand the different types of acute coronary syndromes. Identify basic coronary circulation and how it relates to different types of myocardial infarctions. Anticipate potential complications associated with an AMI. Identify the standard treatment of an AMI. Distinguish between various AV blocks. Recognize the signs & symptoms of heart failure. Identify the treatment of heart failure. Recognize the general definition and classifications of aortic aneurysms. Understand the different types of aortic dissections. Recognize the signs & symptoms of cardiomyopathy. Differentiate between the different types of cardiomyopathy. Identify the treatment for the different types of cardiomyopathy. Understand the different stages of shock. Differentiate between different types of shock.

CCRN REVIEW PART 1

15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26.

OBJECTIVES
Distinguish between arterial and venous peripheral vascular disease. Identify the various treatments for peripheral vascular disease. Define respiratory failure. Identify the various treatments for acute respiratory failure. Recognize the signs & symptoms and causes of various respiratory alterations. Identify the standard treatment for various respiratory alterations. Identify the components of cardiac output and stroke volume. Recognize the pulmonary artery catheter waveforms. Recognize the basic treatments used for commonly seen hemodynamic profiles. Explain the common causes of gastrointestinal bleeding. Describe the most commonly seen treatments for GI bleeding. Describe the signs & symptoms of acute pancreatitis and available treatments.

Cardiovascular Conditions

Acute Coronary Syndromes Acute MI Aortic Aneurysms Cardiac Alterations

Cardiomyopathy Heart Blocks Heart Failure

Shock States

Acute Coronary Syndrome

DEFINITIONS
Term used to cover a group of symptoms compatible with acute myocardial ischemia Acute myocardial ischemia is insufficient blood supply to the heart muscle usually resulting from coronary artery disease

Acute Myocardial Infarction

DEFINITION
Infarction occurs due to mechanical obstruction of a coronary artery (or branch) caused by a thrombus, plaque rupture, coronary spasm and/or dissection. STEMI vs. NSTEMI (non-STEMI)

Acute Myocardial Infarction

SIGNS & SYMPTOMS

Complains Vary

May include crushing chest pain (which may or may not radiate), back, neck, jaw, teeth and/or epigastric pain, SOB, nausea/vomiting and dizziness

ST elevations on ECG

Elevated cardiac enzymes

Acute Myocardial Infarction

SIGNS & SYMPTOMS

PAWP, CO, SVR, dysrhythmias, S4, cardiac failure, cardiogenic shock Diaphoresis, pallor, referred pains Diabetics and women often present abnormal symptoms

Coronary Circulation

12 Lead ECG
I II III II V AVR AVL AVF V1 V2 V3 V4 V5 V6

Acute Myocardial Infarction

ST ELEVATIONS
Anterior Wall MI

Leads V1-V4

Reciprocal changes in leads II, III, and aVF

Area supplied by the LAD

Inferior Wall MI

Leads II, III and aVF

Reciprocal changes in leads I, and aVL Area usually supplied by the RCA

Acute Myocardial Infarction

ST ELEVATIONS
Lateral Wall MI

I, aVL, V5 and V6

Area supplied by the Circumflex artery

Posterior Wall MI

Reflected on the opposite walls Opposite deflections

Coronary Arteries

Anterior Wall MI

Inferior Wall MI

Acute Myocardial Infarction

COMPLICATIONS
Dysrhythmias, heart failure, pericarditis,

ventricular aneurysms, ventricular thrombus,

VSD, mitral regurgitation, papillary muscle (or chordae tendineae) rupture, pericardial effusions, pericarditis

Acute Myocardial Infarction

NURSING INTERVENTIONS
O2 Bedrest Serial ECGs Serial cardiac enzymes Keep pain free (NTG. MSO4) MONA (Morphine, O2, Nitroglycerin, Aspirin), Heparin, beta-blockers, and ace inhibitors. May also include thrombolytics or Gp2b3a inhibitors PCI, PTCA, IABP, CABG

Acute Myocardial Infarction

TREATMENT
Time Is Heart Muscle Prompt ECG Goals: Relieve pain, limit the size of the infarction and to prevent complications (primarily lethal dysrhythmias)

Acute Myocardial Infarction

TREATMENT
MONA (Morphine, O2, Nitroglycerin, Aspirin), Heparin, beta-blockers, and ace inhibitors. May also include thrombolytics or Gp2b3a inhibitors Cardiac Catheterization (with angioplasty, atherectomy and/or stent) IABP, CABG, Education

Balloon Angioplasty

Vascular Stent Deployment

Atherectomy

Acute Myocardial Infarction

SPECIFIC TREATMENTS
Inferior Wall (IWMI)

Fluids (with RV infarct) Inotropics Afterload reducing medications

Anterior Wall (AWMI)

Diuretics Inotropics Afterload reducing medications

Aortic Aneurysms

DEFINITION
A bulge or ballooning of the aorta

When the walls of the aneurysm include all three layers of the artery, they are called true aneurysms When the wall of the aneurysm include only the outer layer, it is called a pseudo-aneurysm

May be thoracic or abdominal

Aortic Aneurysms

CAUSES

Atherosclerosis Marfan syndrome Hypertension Crack cocaine usage

Smoking
Trauma

Aortic Aneurysms Rupture

An aortic aneurysm, depending on its size, may rupture, causing life-threatening internal bleeding The risk of an aneurysm rupturing increases as the aneurysm gets larger The risk of rupture also depends on the location of the aneurysm Each year, approximately 15,000 Americans die of a ruptured aortic aneurysm.

Aortic Aneurysms

CLASSIFICATIONS
Classified by shape, location along the aorta, and how they are formed May be symmetrical in shape (fusiform) or a localized weakness of the arterial wall (saccular)

Aortic Aneurysms

Aortic Aneurysms

SIGNS & SYMPTOMS

Often produces no symptoms If an aortic aneurysm suddenly ruptures it presents with extreme abdominal or back pain, a pulsating mass in the abdomen, and a drastic drop in blood pressure An increase in the size of an aneurysm means an increased in the risk of rupture

Aortic Aneurysms

THORACIC SIGNS & SYMPTOMS

Back, shoulder or neck pain Cough, due to pressure placed on the trachea

Hoarseness
Strider, dyspnea Difficulty swallowing

Swelling in the neck or arms

Aortic Dissections

DEFINITION
Tearing of the inner layer of the aortic wall, which allows blood to leak into the wall itself and causes the separation of the inner and outer layers Usually associated with severe chest pain radiating to the back

Aortic Dissections

A. Dissection beginning in the ascending aorta

B. Whenever the ascending aorta is not involved

Aortic Dissections

A. Dissection beginning in the ascending aorta

B. Whenever the ascending aorta is not involved

Aortic Dissections

Aortic Dissections

Aortic Aneurysms

COMPLICATIONS

Rupture

Peripheral embolization
Infection

Spontaneous occlusion of aorta

Aortic Aneurysms

TREATMENT

Medical management
Controlled BP (within specific range)

Surgical repair
> 4.5 cm in Marfan patients or > 5 cm in nonMarfan patients will require surgical correction or endovascular stent placement

Cardiomyopathy

DEFINITION
Diseases of the heart muscle that cause deterioration of the function of the myocardium

Cardiomyopathy

CLASSIFICATIONS
Primary / Idiopathic (intrinsic)

Heart disease of unknown cause, although viral infection and autoimmunity are suspected causes

Secondary (extrinsic)

Heart disease as a result of other systemic diseases, such as autoimmune diseases, CAD, valvular disease, severe hypertension, or alcohol abuse

Cardiomyopathy

Hypertropic Cardiomyopathy Restrictive Cardiomyopathy Dilated Cardiomyopathy

Hypertropic Cardiomyopathy

Bizarre hypertrophy of the septum

Previously called IHSS

Idiopathic Hypertropic Subaortic Stenosis Hypertropic Obstructive Cardiomyopathy

Known as HOCM

Positive inotropic drugs Should Not Be Used

Contractility will outflow tract obstruction

Nitroglycerin Should Not Be Used

Dilation Will Worsen The Problem

Harley

Hypertropic Cardiomyopathy

TREATMENT
Relax the ventricles

Beta Blockers Calcium Channel Blockers

Slow the Heart Rate

Increase filling time

Use Negative Inotropes

Optimize diastolic filling

Dilation will worsen the problem

Do Not use NTG

Restrictive Cardiomyopathy

Rigid Ventricular Wall

Due to endomyocardial fibrosis

Obstructs ventricular filling

Least common form

Restrictive Cardiomyopathy

TREATMENT
Positive Inotropics Diuretics Low Sodium Diet

Dilated Cardiomyopathy

Grossly dilated ventricles without hypertrophy

Global left ventricular dysfunction Leads to pooling of blood and embolic episodes Leads to refractory heart failure Leads to papillary muscle dysfunction secondary to LV dilation

Dilated Cardiomyopathy

TREATMENT
Positive Inotropes Afterload Reducers Anticoagulants with Atrial Fib

Cardiomyopathies

Cardiomyopathy

GENERALIZED TREATMENT
Positive Inotropes

Except with Hypertropic Cardiomyopathy Except with Hypertropic Cardiomyopathy

Diuretics Beta Blockers Calcium Channel Blockers IABP Vasodilators (as indicated) Fluid Restriction

Vasodilators

Reduce Preload & Afterload

Daily weights, prn O2, planned activities, education, and emotional support
Consider Heart Transplant

CCRN REVIEW PART 1

BREAK!

Conduction Defects

STABLE VS UNSTABLE
Stable

Start with medications

Unstable

Shock (cardioversion or defibrillation)

Normal Sinus Rhythm

Heart Rate Rhythm P Wave PR Interval (in seconds) QRS (in seconds) 60 - 100 bpm Regular Before each QRS & identical 0.12 to 0.20 < 0.12

Atrial Fibrillation

AFib
Multifocal atrial impulses at rate 300-600/min Irregular conduction to ventricles

Atrial Flutter

AFL
Atrial impulses at rate of 250-350/min Regularly blocked impulses at the AV node Saw tooth flutter waves

Wandering Atrial Pacemaker

WAP
Multiple ectopic foci in the atria Three or more p wave morphologies Rate < 100

Supraventricular Tachycardia

SVT
Supraventricular rhythm at rate 150-250 P waves cannot be positively identified

Atrial Tach = supraventricular rhythm with p wave morphology that is noticeably different from the sinus p wave

Ventricular Tachycardia

VT
Ventricular rate of 100-250/min Wide QRS

Torsades de Pointes

Polymorphic VT
VT with alternating ventricular focus Often associated with prolonged QT Rate < 100

Heart Blocks (AV Blocks)

Sinus Rhythm with First Degree AV Block

Sinus Rhythm with Second Degree AV Block, Type 1

Sinus Rhythm with Second Degree AV Block, Type 2

Third Degree AV Block

Heart Failure

DEFINITION
A condition in which the heart cannot pump sufficient blood to meet the metabolic needs of the body Pulmonary (LVF) and/or systemic (RVF) congestion is present.

Heart Failure

DEFINITION
Pulmonary Edema

Fluid in the alveolus that impairs gas exchange by altering the diffusion between alveolus and capillary Acute left ventricular failure causes cardiogenic pulmonary edema Non-cardiogenic pulmonary edema is a synonym for Adult Respiratory Distress Syndrome (ARDS)

Heart Failure

COMPENSATORY MECHANISMS
Sympaththetic nervous system stimulation

Tachycardia Vasoconstriction and increased SVR

Renin-angiotensin-aldosterone system activation (RAAS)

Hypo perfusion to the kidneys (renin) Vasoconstriction (angiotensin) Sodium and water retention (kidneys) Ventricular dilation

Heart Failure

FUNCTIONAL CLASSIFICATIONS
Class I
(without noticeable limitations) (symptoms upon activity) (severe symptoms upon activity)

Class II
Class III

Class IV (symptoms at rest)

Heart Failure

COMPLICATIONS
Hypotension Dysrhythmias Respiratory Failure Progressive Deterioration

Acute Renal Failure

Fluid & Electrolyte Imbalances

Heart Failure

TREATMENT
Improve Oxygenation Decrease Myocardial Oxygen Demand Decrease Preload Decrease Afterload Increase Contractility Manage Dysrhythmias Educate!

Vascular Disease

Aorto/Iliac Disease: Pre & Post PTA/Stent

Peripheral Vascular Disease

SYMPTOMS PAIN PAIN RELIEF EDEMA
ARTERIAL Upon walking On resting, standing or dependent position of lower limbs None VENOUS While standing Elevation of extremities Present, edematous

PULSES
INTEGUMENT CHANGES

Decreased or absent
Hair loss Skin shiny Nail thickening Pallor when elevated Red when dependent

May be difficult to palpate

Brownish pigmentation May be cyanotic when extremities are dependent

ULCERS
SKIN TEMPERATURE SEXUAL ISSUES

Ulcers located on toes, lateral areas or site of trauma Gangrene possible

Cool Impotency Sexual dysfunction

Ulcers located on ankles, medial or pre-tibial areas

Normal or warm Not present

Peripheral Vascular Disease

TREATMENTS
Medical

Are they taking ASA, Coumadin, Ticlid, Plavix, Oral Contraceptives, Hormones?

Invasive

PTA, atherectomy, stents

Surgical

Grafts

Peripheral Vascular Disease

Bypass Grafts

Shock

DEFINITION
Inadequate perfusion to the body tissues

Low blood pressure with impaired perfusion to the end organs

May result in multiple organ dysfunction

Shock

TYPES OF SHOCK
Hypovolemic Shock
Cardiogenic Shock
Distributive Shock

Obstructive Shock

Shock

COMPENSATORY MECHANISMS
Tachycardia

Attempts to deliver more blood to the tissues Attempts to maintain adequate BP in order to adequately perfuse the body tissues

Vasoconstriction

Increased ADH Secretion

ADH makes the body hold onto water in an effort to maintain volume and thus enough blood pressure to perfuse the body tissues

Types of Shock

Hypovolemic Shock
Inadequate perfusion to the tissues due to insufficient intravascular volume

Cardiogenic Shock
Inadequate perfusion to the tissues due to heart failure

Distributive Shock
Inadequate perfusion to the tissues due to blood flow out of the intravascular space causing insufficient intravascular volume Anaphylactic, Septic, and Spinal Shock

Obstructive Shock
Inadequate perfusion to the tissues due to obstruction of blood flow

Hypovolemic Shock

SIGNS & SYMPTOMS

Low BP Orthostatic Hypotension Confusion Thirst Cool, Clammy Skin UOP PAWP SVR Tachycardia Restlessness Agitation (or listless) Pallor Resp. Rate CO CVP Lactate Levels

Hypovolemic Shock

TREATMENT
Volume (IVF, Blood)

Cardiogenic Shock

SIGNS & SYMPTOMS

Low BP Agitation (or listless) Tachycardia UOP PAWP (low with RVF) SVR JVD Ventricular Gallop (S3) Pulmonary Crackles Restlessness Confusion Pallor CO CVP Lactate Levels Peripheral Edema Dyspnea

Cardiogenic Shock

TREATMENT
Bedrest CO Preload & Afterload Vasodilators Myocardial Demand O2 Positive Inotropes Diuretics Positioning IABP

Anaphylactic Shock

SIGNS & SYMPTOMS

Low BP Restlessness Agitation (or listless) Pallor Pruritus Angioedema Wheezing Dyspnea UOP PAWP SVR Tachycardia Confusion Thirst Warm Feeling Hives Bronchoconstriction Laryngeal Edema Cool, Clammy Skin CO CVP Lactate Levels

Anaphylactic Shock

TREATMENT
Epinephrine IVF Vasoconstrictors Support/Maintain Airway

Obstructive Shock

SIGNS & SYMPTOMS

Low BP Restlessness Agitation (or listless) Cool, Clammy Skin Tachycardia Confusion Pallor CO , UOP

Symptoms related to cause

Obstructive Shock

CAUSES
Pulmonary Embolus Tension Pneumothorax Tamponade Aortic Aneurysm

TREATMENT
Treat the Cause

Shock Profiles
Parameter Hypovolemic Cardiogenic Neurogenic Anaphylactic Early Septic CVP/RAP PAWP CO BP SVR HR

Late Septic

or Norm Normal

Cardiogenic Shock is the only shock with PAWP Early (Hyperdynamic) Shock is the only shock with CO and SVR Neurogenic Shock is the only shock with Bradycardia Anaphylactic Shock has the definitive characteristic of wheezing due to bronchospasm

Sepsis Syndrome

SIRS Infection

Sepsis

Severe Sepsis

Septic Shock

MODS

Death

Sepsis Syndrome

Sepsis
SIRS response with presumed/confirmed infection

Severe Sepsis
Sepsis associated with organ dysfunction, hypoperfusion (lactic acidosis, oliguria, altered mental status etc.), or hypotension (SBP < 90 mmHg or SBP > 40 mmHg)

Septic Shock
Sepsis with perfusion abnormalities and hypotension despite adequate fluid resuscitation

Septic Shock

EARLY STAGE (Hyperdynamic)

Normal BP Confusion Respiratory Rate Normal Color Normal PAWP Tachycardia Agitation (or listless) Temperature Normal or UOP CO SVR Tachycardia Restlessness Agitation (or listless) Pallor UOP PAWP SVR

LATE STAGE (Hypodynamic)

Low BP Orthostatic Hypotension Confusion Thirst Cool, Clammy Skin CO CVP Lactate Levels

Homeostasis Gets Lost

Treatment for Sepsis

1. Stabilize The Patient
Fluids (lots of fluids) 150ml/hr or more Vasoconstrictors

2.

Treat The Cause

Pan culture, antibiotics Seek primary site of infection Direct therapy to primary cause Prevent organ dysfunction Treat temp as needed

3.

Improve Perfusion

HEMODYNAMICS

Invasive PA Catheter

CONTRAINDICATIONS

Mechanical Tricuspid or Pulmonary Valve Right Heart Mass (thrombus and/or tumor) Tricuspid or Pulmonary Valve Endocarditis

Basic Concepts

CO = HR X SV
BP = CO x SVR

CO and SVR are inversely related

CO and SVR will change before BP changes

Stroke Volume

Components Stroke Volume

Preload: the volume of blood in the ventricles
at end diastole and the stretch placed on the muscle fibers

Afterload: the resistance the ventricles must

overcome to eject its volume of blood

Contractility: the force with which the heart

muscle contracts (myocardial compliance)

PAC Insertion Sequence

Phlebostatic Axis

4th ICS Mid-chest, regardless of head elevation

Normal Hemodynamic Values

RAP (CVP) RVP PAP PAWP SVR

0-8 mmHg 15-30/0-8 mmHg 15-30/6-12 mmHg 8 - 12 mmHg 700-1500 dynes/sec/cm2

Normal Hemodynamic Values

Values normalized for body size (BSA)

CI:

2.5 4.5 L/min/m2

SVRI:

1970 2390 dynes/sec/cm-5/m2

35 60 mL/beat/m2

SVI or SI:

EDVI:

60 100 mL/m2

Mixed Venous Oxygen Saturation SvO2

End result of O2 delivery and consumption

Measured in the pulmonary artery

An average estimate of venous saturation for the whole body. Does not reflect separate tissue perfusion or oxygenation

Stroke Volume Variation (SVV)

Minimally Invasive Flo Trac

Measured through Arterial Line

Measures preload responsiveness

SVV > 10-15 % = preload responsive (responsive to fluids)

SVV > 10-15% = pulsus paradoxus

SVV < 1015% = not preload responsive

Measuring PA Pressures

Measure All Hemodynamic Values at End-Expiration

Patient Peak
Vent Valley

Spontaneous Respirations

Measuring PA Pressures

Measure all pressures at end-expiration

At top curve with Spontaneous Respiration

patient-peak

Intrathoracic pressure decreases during spontaneous inspiration

Negative deflection on waveforms

Intrathoracic pressure increases during spontaneous expiration

Positive deflection on waveforms

Measuring PA Pressures

Measure all pressures at end-expiration At bottom curve with mechanical ventilator

Vent-Valley

Intrathoracic pressure increases during positive pressure ventilations (inspiration)

Positive deflection on waveforms

Intrathoracic pressure decreases during positive pressure expiration

Negative deflection on waveforms

PAWP Waveform

a-wave
Atrial contraction Correct location for measurement of PAWP Average the peak & trough of the a-wave Begins near the end of QRS or at the QT segment Delayed ECG correlation from CVP since PA catheter is further away from left atrium

PAWP Waveform

c-wave
Rarely present Represents mitral valve closure

v-wave
Represents left atrial filling Begins at about the end of the T wave

PAWP Waveform

CCRN REVIEW PART 1

BREAK!

Respiratory Alterations

ARDS Drowning

Chronic Lung Disease Pneumonia Pulmonary Embolism

Pneumothorax
Respiratory Failure

ARDS

DEFINITIONS
Severe respiratory failure associated with pulmonary infiltrates (similar to infant hyaline membrane disease)

Pulmonary edema in the absence of fluid overload or depressed LV function (Non-cardiogenic pulmonary edema)
Originates from a number of insults involving damage to the alveolar-capillary membrane

Acute Respiratory Distress Syndrome

ARDS

PATHOPHYSIOLOGY
Inflammatory mediators are released causing extensive structural damage

Increased permeability of pulmonary microvasculature causes leakage of proteinaceous fluid across the alveolar capillary membrane Also causes damage to the surfactant-producing type II cells

ARDS

CXR CHARACTERISTICS
Normal size heart No pleural effusion

Ground Glass appearance

Often normal early in the disease but may rapidly progress to complete whiteout

ARDS

ARDS

SIGNS & SYMPTOMS

Symptoms develop 24 to 48 hours of injury

Sudden progressive disorder Pulmonary edema Severe dyspnea Hypoxemia REFRACTORY to O2 Decreased lung compliance Diffuse pulmonary infiltrates

Symptoms may be minimal compared to CXR Rales may be heard

ARDS

RISK FACTORS
Common Risk Factors Sepsis Massive Trauma Shock Multiple Transfusions Pneumonia Aspiration Infection Other Risk Factors Smoke inhalation Inhaled toxins Burns Near Drowning DKA Pregnancy Eclampsia
Amniotic Fluid Embolus

Drugs

Acute Pancreatitis DIC Head Injury ICP Fat Emboli Blood Products Heart/Lung Bypass Tumor Lysis Pulmonary Contusion Narcotics

ARDS

TREATMENT
Respiratory Support

PEEP, CPAP

Chronic Lung Disease

COPD
Presents with hyper-inflated lung fields

Due to chronic air trapping

May be barrel chested

May lead to cor pulmonale (right-sided heart failure)

Due to chronic high pulmonary pressures

Often hypercarbic (high pCO2)

Often dependent upon hypoxic drive

Chronic Lung Disease

COPD TREATMENT
Avoid overuse of oxygen (except in emergencies) Bronchodilators

Steroids
Hydration Education

Pursed Lip Breathing

Leaning Upright

Near Drowning

Salt Water
Causes body fluids to shift into lungs

Osmosis: From low to high concentration Results in hemoconcentration & hypovolemia

Results in acute pulmonary edema

Fresh Water
Fluids shift into body tissues

Results in hemodilution & hypervolemia Can result in gross edema May lead to pulmonary edema

Damaged alveoli fill with proteinaceous fluid

Pneumonia

Lung infection (bacterial, viral, or fungal)

Most commonly caused by Streptococcus pneumoniae

Symptoms include fever, pleuretic chest pain, productive cough, and tachypnea
Often presents bronchial breath sounds over the lung area

Treatment involves giving the right antibiotic

Pneumothorax

DEFINITIONS
Simple pneumothorax

Results from buildup of air or pressure in the pleural space

Spontaneous pneumothorax

May be due to blebs that rupture The 2 key risk factors are increased chest length and cigarette smoking

Tension pneumothorax

Involves a buildup of air in the pleural space due to one-way movement of air
Progressively worsens Requires immediate intervention

Pneumothorax

Tension Pneumothorax

Pneumothorax

CAUSES
Barotrauma

Injury
Blebs

Pneumothorax

SIGNS & SYMPTOMS

Standard Pneumothorax

Sharp "pleuritic" chest pain, worse on breathing Sudden shortness of breath Dry, hacking cough (may occur due to irritation of the diaphragm) May cause mediastinal shift

Tension pneumothorax

Signs of standard pneumothorax with signs of cardiovascular collapse Immediately life threatening May cause mediastinal shift

Pneumothorax

TREATMENT
Spontaneous pneumothorax
Depends on symptoms & size of pneumothorax Provide respiratory support May need chest tube or needle decompression

Some resolve without intervention

Tension pneumothorax
Requires immediate intervention
May cause cardiovascular collapse May need chest tube or needle decompression

2nd intercostal space

Pneumothorax

TREATMENT Pleurodesis

Chemical or surgical adhesion of the lung to the chest wall

Used for multiple collapsed lungs or persistent collapse

Flail Chest

Pulmonary Embolism

Definition
Arterial embolus that obstructs blood flow to the lung

Signs & Symptoms

Symptoms include sudden dyspnea, cough, chest pain, hemoptysis and sinus tachycardia Blood gas shows low pO2 & low pCO2

May present positive Homans Sign

May present loud S2

Pulmonary Embolism

Diagnostic Tests
CXR VQ Scan

Spiral CT
Pulmonary arteriogram/angiogram Venous ultrasound of the lower extremities

ABG with low pO2 & low pCO2

D-Dimer

Pulmonary Embolism

Treatment
Requires immediate intervention Provide respiratory support Treat pain & comfort

Usually includes intravenous heparin

Heparin reduces risk of secondary thrombus formation while clot is reabsorbed

May require embolectomy

May require thrombolysis

May need umbrella filter May need long term anticoagulants

Respiratory Failure

DEFINITIONS
Failure to maintain adequate gas exchange

Inadequate blood oxygenation or CO2 removal

PaO2 < 50 mmHg and/or PaCO2 > 50 mmHg and/or pH < 7.35 on Room Air

Respiratory Failure
TYPE I Hypoxemia without hypercapnia

TYPE II Hypoxemia with hypercapnia

Respiratory Failure

CAUSES
V/Q Mismatching

Intrapulmonary Shunting
Alveolar Hypoventilation

Respiratory Failure

V/Q MISMATCHING
COPD

Interstitial Lung Disease

Pulmonary Embolism

Respiratory Failure

PULMONARY SHUNTING
AV fistulas/malformations

Alveolar collapse (atelectasis)

Alveolar consolidation (pneumonia)

Excessive mucus accumulation

Respiratory Failure

SIGNS & SYMPTOMS

Restlessness / Agitation Confusion / LOC Tachycardia / Dysrhythmias Tachypnea / Dyspnea Cool, clammy, pale skin

Respiratory Failure

ARTERIAL BLOOD GASES

pH 7.30 / pO2 45 / pCO2 80

pH 7.30 / pO2 55 / pCO2 65

pH 7.32 / pO2 50 / pCO2 50 pH 7.55 / pO2 65 / pCO2 22

Respiratory Failure

TREATMENT
Ensure Adequate Ventilation FiO2

Ineffective with shunting Prolonged O2 > 40% causes O2 toxicity Must use caution with CO2 retainers
Chronic hypercapnia causes CO2 retainers to use hypoxic drive Too much O2 can depress respirations

CCRN REVIEW PART 1

BREAK!

Gastrointestinal Alterations

GI Bleed

Pancreatitis

Gastrointestinal Bleeding

CAUSES
UGI Bleeding

Includes the esophagus, stomach, duodenum

Peptic Ulcer Disease (PUD), or Esophageal Varices
ASA, NSAIDs, Anticoagulants, Alcohol H. Pylori

LGI Bleeding

Includes the jejunum, ileum, colon, rectum

Colorectal cancer, Polyps, Hemorrhoids, IBD

Gastrointestinal Bleeding

Gastrointestinal Bleeding

Hematemesis vomiting of blood (or coffee ground

material) (indicates bleeding above the duodenum )

Melena passage of black tarry stools > 50ml (indicates

degradation of blood in the bowel)

Hematochezia passage of red blood (rectal bleeding)

Occult Bleeding bleeding that is not apparent to the
patient and results from small amounts of blood

Obscure Bleeding occult or obvious but source not

identified

Gastrointestinal Bleeding

Hematemesis always UGI source

Melana indicates blood has been in GI tract
for extended periods
Mostly UGI Small bowel Rt colon (if bleeding relatively slow)

Hematochezia
Mostly colon Massive UGI bleeding (not enough time for degradation)

Gastrointestinal Bleeding

TREATMENT
Find the underlying cause Fluid volume replacement Endoscopy or colonoscopy Medical and /or surgical therapy

Somatostatin IV or intra-arterial vasopressin Sclerotherpay Angiography with embolization Electrocoagulation Band ligation Balloon tamponade (Sengstaken-Blackmore tube)

The Pancreas

The Pancreas secretes digestive enzymes, bicarbonate, water, and some electrolytes into the duodenum via the pancreatic duct
Lipase, Amylase, Trypsin

The Pancreas also produces and secretes insulin

Pancreatitis

DEFINITION
An autodigestive process resulting from premature activation of pancreatic enzymes

Pancreatitis

PATHOSHYSIOLOGY
Inactive pancreatic enzymes are activated outside of the duodenum

The swelling pancreas causes fluids to shift into the retro peritoneum and bowel
Fluid shifts can cause severe hypovolemia and hypotension Inflammation cause commotion around pancreas

Pancreatitis

MANY CAUSES
Alcoholism Biliary Disease Hypercalcemia Peptic Ulcer Disease

Gallstones
Infections Hyperparathyroidism

Cystic Fibrosis
Vascular Disease Multiple Drugs Much Much More

Hypertriglyceridemia

Pancreatitis

SIGNS & SYMPTOMS

Abdominal Pain Nausea & Vomiting Hematemesis Grey Turners Sign

Abdominal Distention
Jaundice Malnutrition

Cullens Sign
Elevated Amylase, Lipase, LDH, AST, WBCs

BUN, and Glucose

Pancreatitis

COMPLICATIONS
Hypocalcemia Hypotension Acute Tubular Necrosis DIC Obstructive Jaundice Erosive Gastritis Paralytic Ileus Pseudocyst or Abscess Bowel Infarction Internal Bleeding Fat Necrosis Pleural Effusion (left) Pulmonary Infiltrates Hypoxemia Atelectasis ARDS Pericardial Effusion Mediastinal Abscess Hyperglycemia Hypertriglyceridemia Encephalopathy

Pancreatitis

TREATMENT
Stabilization

Monitor For Complications Monitor Blood Sugar Drug Therapies

Correct Fluid And Electrolyte Status

Respiratory Support Control Pain

Demerol

Somatostatin, Anticholinergics

NG Tube

NPO
Restricted Diet

Watch For Signs Of Infection Pray

TPN

Pancreatitis

FULMINATING PANCREATITIS
Overwhelming form Necrotizing form Extreme symptoms Seen with ESRF patients May lead to ARDS & DIC

Pancreatitis

FULMINATING PANCREATITIS
Signs & Symptoms

Tachycardia & low BP (may be the only sign) Pulmonary & cerebral insufficiency Acute diabetic ketosis or oliguria Hemorrhagic pancreatitis may appear

CCRN REVIEW

THE END
PART 1

CCRN REVIEW PART 1

THANK YOU

References

American Heart Association. (2005). Guidelines 2005 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Available at: www.americanheart.org.
Bridges EJ.(2006) Pulmonary artery pressure monitoring: when, how, and what else to use. AACN Adv Crit Care. 2006;17(3):286303. Chulay, M., Burns S. M. (2006). AACN Essentials of Critical Care Nursing. McGraw-Hill Companies, Inc., Chapter 23. Finkelmeier, B., Marolda, D. (2004) Aortic Dissection, Journal of Cardiovascular Nursing: 15(4):1524. Hughes E. (2004). Understanding the care of patients with acute pancreatitis. Nurs Standard: (18) pgs 45-54.

Sole, M. L., Klein, D. G. & Moseley, M. (2008). Introduction to Critical Care Nursing. 5th ed. Philadelphia, Pa: Saunders.
Thelan, L. A., Urden, L. D., Lough, M. E. (2006). Critical care: Diagnosis and Treatment for repair of abdominal aortic aneurysm. St. Louis, Mo.: Mosby/Elsevier. pg 145-188.

References Continued

Urden, L., Lough, M. E. & Stacy, K. L. (2009). Thelan's Critical Care Nursing: Diagnosis and Management (6th ed). St. Louis, Mo.: Mosby/Elsevier.
Woods, S., Sivarajan Froelicher, E. S., & Motzer, S. U. (2004). Cardiac Nursing. 5th ed. Philadelphia, Pa: Lippincott Williams & Wilkins. Wynne J, Braunwald E. (2004). The Cardiomyopathies in Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine (7th Edition). Philadelphia: W.B. Saunders, vol. 2, pps. 16591696, 17511803. Zimmerman & Sole. (2001). Critical Care Nursing (3rd Edition). WB Saunders., pgs. 41-80, 176-180, 242-266. Anderson, L. (July 2001). Abdominal Aortic Aneurysm, Journal of Cardiovascular Nursing:15(4):114, July 2001. Irwin, R. S.; Rippe, J. M. (January 2003). Intensive Care Medicine. Lippincott Williams & Wilkins, Philadelphia: pgs. 35-548. Wung, S., Aouizerat, B. E. (Nov/Dec 2004). Aortic Aneurysms. Journal of Cardiovascular Nursing. Lippincott Williams & Wilkins, Inc.:19(6):409-416, 34(2).