CCRN Review Part 1 (of 2)

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  ARDS
 Acute Myocardial Infarction  Chronic Lung Disease
 Heart Blocks  Drowning
 Heart Failure  Pneumonia
 Cardiac Alterations  Pneumothorax
 Aortic Aneurysms  Pulmonary Embolism
 Cardiomyopathy  Respiratory Failure
 Shock States  Gastrointestinal Alterations
 Peripheral Vascular Disease  GI Bleeding
 Hemodynamics  Pancreatitis

CCRN REVIEW PART 1
 OBJECTIVES
1. Understand the different types of acute coronary syndromes.
2. Identify basic coronary circulation and how it relates to different types
of myocardial infarctions.
3. Anticipate potential complications associated with an AMI.
4. Identify the standard treatment of an AMI.
5. Distinguish between various AV blocks.
6. Recognize the signs & symptoms of heart failure.
7. Identify the treatment of heart failure.
8. Recognize the general definition and classifications of aortic
aneurysms.
9. Understand the different types of aortic dissections.
10. Recognize the signs & symptoms of cardiomyopathy.
11. Differentiate between the different types of cardiomyopathy.
12. Identify the treatment for the different types of cardiomyopathy.

CCRN REVIEW PART 1
 OBJECTIVES
13. Understand the different stages of shock.
14. Differentiate between different types of shock.
15. Distinguish between arterial and venous peripheral vascular disease.
16. Identify the various treatments for peripheral vascular disease.
17. Define respiratory failure.
18. Identify the various treatments for acute respiratory failure.
19. Recognize the signs & symptoms and causes of various respiratory
alterations.
20. Identify the standard treatment for various respiratory alterations.
21. Explain the common causes of gastrointestinal bleeding.
22. Describe the most commonly seen treatments for GI bleeding.
23. Describe the signs & symptoms of acute pancreatitis and available
treatments.

Cardiovascular Conditions
 Acute Coronary  Cardiomyopathy
Syndromes
 Acute MI  Heart Blocks

 Aortic Aneurysms  Heart Failure

 Cardiac Alterations  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)

 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

↑ PAWP, ↓ CO, ↑ SVR, dysrhythmias, S4,
cardiac failure, cardiogenic shock

– Diaphoresis, pallor, referred pains

– Diabetics and women often present abnormal
symptoms

12 Lead ECG

I AVR V1
V4

II AVL V2 V5

III AVF V3 V6

II

V

 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

 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

 COMPLICATIONS
– Dysrhythmias, heart failure, pericarditis,
ventricular aneurysms, ventricular thrombus,
VSD, mitral regurgitation, papillary muscle (or
chordae tendineae) rupture, pericardial
effusions, pericarditis

 NURSING INTERVENTIONS
– O2
– Bedrest
– Serial ECG’s
– 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

 TREATMENT
– Time Is Heart Muscle

– Prompt ECG

– Goals: Relieve pain, limit the size of the
infarction and to prevent complications
(primarily lethal dysrhythmias)

 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

 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
– 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 B. Whenever the
beginning in the ascending aorta
ascending aorta is not involved

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 non-
Marfan 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
– Known as HOCM
 Hypertropic Obstructive Cardiomyopathy

 Positive inotropic drugs Should Not Be Used
↑ Contractility will ↑ outflow tract obstruction
 Nitroglycerin Should Not Be Used
– Dilation Will Worsen The Problem

Hypertropic Cardiomyopathy
 TREATMENT
– Relax the ventricles
 Beta Blockers
 Calcium Channel Blockers

– Slow the Heart Rate
 Increase filling time
– Use Negative Inotropes
 Optimize diastolic filling
– Do Not use NTG
 Dilation will worsen the problem

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

Cardiomyopathy
 GENERALIZED TREATMENT
– Positive Inotropes
 Except with Hypertropic Cardiomyopathy
– Vasodilators
 Except with Hypertropic Cardiomyopathy
– Reduce Preload & Afterload
– Diuretics
– Beta Blockers
– Calcium Channel Blockers
– IABP
– Vasodilators (as indicated)
– Fluid Restriction
– 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 60 - 100 bpm
Rhythm Regular
P Wave Before each QRS & identical
PR Interval (in seconds) 0.12 to 0.20
QRS (in seconds) < 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
 Hypo perfusion to the kidneys (renin)
 Vasoconstriction (angiotension)
 Sodium and water retention (kidneys)
 Ventricular dilation

Heart Failure
 FUNCTIONAL CLASSIFICATIONS
– Class I (without noticeable limitations)

– Class II (symptoms upon activity)

– Class III (severe symptoms upon activity)

– 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 ARTERIAL VENOUS

PAIN Upon walking While standing

PAIN RELIEF On resting, standing or Elevation of extremities
dependent position of lower limbs
EDEMA None Present, edematous
PULSES Decreased or absent May be difficult to palpate

INTEGUMENT Hair loss Brownish pigmentation
Skin shiny May be cyanotic when
CHANGES Nail thickening extremities are dependent
Pallor when elevated
Red when dependent
Ulcers located on toes, lateral Ulcers located on ankles,
ULCERS areas or site of trauma medial or pre-tibial areas
Gangrene possible

SKIN TEMPERATURE Cool Normal or warm

SEXUAL ISSUES Impotency Not present
Sexual dysfunction

 TREATMENTS
– Medical
 Are they taking ASA, Coumadin, Ticlid, Plavix,
Oral Contraceptives, Hormones?

– Invasive
 PTA, atherectomy, stents

– Surgical
 Grafts


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
–Vasoconstriction
 Attempts to maintain adequate BP in order to
adequately perfuse the body tissues
–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
Low BP Tachycardia
Orthostatic Hypotension Restlessness
Confusion Agitation (or listless)
Thirst Pallor
Cool, Clammy Skin ↑ Resp. Rate
↓ UOP ↓ CO
↓ PAWP ↓ CVP
↑ SVR ↑ Lactate Levels

Hypovolemic Shock

 TREATMENT

–Volume (IVF, Blood)

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

Cardiogenic Shock

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

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

Anaphylactic Shock

 TREATMENT
– Epinephrine
– IVF
– Vasoconstrictors
– Support/Maintain Airway

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

Symptoms related to cause

Obstructive Shock
 CAUSES
Pulmonary Embolus Tamponade
Tension Pneumothorax Aortic Aneurysm

 TREATMENT
Treat the Cause

Sepsis Syndrome

SIRS Sepsis Severe Septic MODS Death
Infection Sepsis Shock

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 Tachycardia
↑ Respiratory Rate Temperature
Normal Color Normal or ↑ UOP
Normal PAWP ↑ CO ↓ SVR
 LATE STAGE (Hypodynamic)
Low BP Tachycardia
Orthostatic Hypotension Restlessness
Thirst Pallor
Cool, Clammy Skin ↓ UOP
↓ CO ↓ PAWP
↓ CVP ↑ SVR
↑ Lactate Levels

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
3. Improve Perfusion
– Prevent organ dysfunction
– Treat temp as needed

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 it’s volume of blood
– Contractility: the force with which the heart
muscle contracts (myocardial compliance)

Phlebostatic Axis

4th ICS Mid-chest, regardless of head elevation

Normal Hemodynamic Values

 RAP (CVP) 0-8 mmHg
 RVP 15-30/0-8 mmHg
 PAP 15-30/6-12 mmHg
 PAOP
8 - 12 mmHg

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
 SVI or SI: 35 – 60 mL/beat/m2
 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

Measuring PA Pressures

 Measure All Hemodynamic Values
at End-Expiration

– “ Patient Peak”

– “ Vent Valley”

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

PAOP Waveform
 a-wave
– Atrial contraction
– Correct location for measurement of PAOP
 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

PAOP Waveform
 c-wave
– Rarely present
– Represents mitral valve closure
 v-wave
– Represents left atrial filling
– Begins at about the end of the T wave

Shock Profiles
Parameter Hypovolemic Cardiogenic Neurogenic Anaphylactic Early Septic Late Septic

CVP/RAP      
PAWP      or Norm 
CO      
BP      
SVR      
HR     Norm al 
 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

Respiratory Alterations
 ARDS  Chronic Lung
Disease
 Drowning
 Pneumonia
 Pneumothorax

 Pulmonary
 Respiratory
Embolism
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
– 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
Other Risk Factors
Factors
Sepsis Smoke inhalation Acute Pancreatitis
Massive Inhaled toxins DIC
Trauma Burns Head Injury
Shock Near Drowning ↑ ICP
Multiple DKA Fat Emboli
Transfusions Pregnancy Blood Products
Pneumonia Eclampsia Heart/Lung Bypass
Aspiration Amniotic Fluid Embolus Tumor Lysis
Infection Drugs 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
– Damaged alveoli fill with proteinaceous fluid
 May lead to pulmonary edema

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
 CAUSES
– Barotrauma

– Injury

– Blebs

Pneumothorax
– 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

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 Homan’s Sign
– May present loud S2

Pulmonary Embolism
 Diagnostic Tests
– CXR
– VQ Scan
– Spiral CT
– Pulmonary arteriogram
– 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
– 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

Gastrointestinal Alterations

 GI Bleed

 Pancreatitis

Gastrointestinal Bleeding
 CAUSES
– UGI Bleeding
 Includes the esophagus, stomach, duodenum
– Peptic Ulcer Disease (PUD), or Esophageal Varices
– ASA, NSAID’s, Anticoagulants, Alcohol
– H. Pylori

– LGI Bleeding
 Includes the jejunum, ileum, colon, rectum
– Colorectal cancer, Polyps, Hemorrhoids, IBD

 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


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)

 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 – Hypercalcemia
– Biliary Disease – Peptic Ulcer Disease
– Gallstones – Cystic Fibrosis
– Infections – Vascular Disease
– Hyperparathyroidism – Multiple Drugs
– Hypertriglyceridemia – Much Much More

Pancreatitis
– Abdominal Pain – Hematemesis
– Nausea & Vomiting – Grey Turner’s Sign
– Abdominal Distention – Cullen’s Sign

– Jaundice – Elevated Amylase,

– Malnutrition Lipase, LDH, AST, WBC’s
BUN, and Glucose

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

Pancreatitis
 TREATMENT
– Stabilization – Monitor For Complications
 Correct Fluid And – Monitor Blood Sugar
Electrolyte Status
– Respiratory Support – Drug Therapies
– Control Pain  Somatostatin,
 Demerol Anticholinergics
– NG Tube – Watch For Signs Of
 NPO Infection
– TPN – Pray
 Restricted Diet

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):286–303.
 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):15–24.
 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. 1659–1696, 1751–1803.
 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):1–14, 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).

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