OUR LADY OF GUADALUPE COLLEGES

COLLEGE OF NURSING
MS 5: Medical-Surgical Nursing
RESPIRATORY SYSTEM

RESPIRATION Parts of the Respiratory System

Oxygen – vital gas UPPER RESPIRATORY TRACT
Characteristics of O2 ● Entrance of O2
● Colorless NOSE
● Cilia – filters/purify air
● Odorless ● Frontal, Ethmoid, Sphenoid,
● Supports combustion SINUSES Maxillary (resonating chamber
● Dry gas — can lead to dryness of mucous and passageway of air)
membranes ● Deep Throat
PHARYNX ● Naso, Oro, Laryngopharnyx
(site of NGT)
NOTE!
Oxygen is prone to leakage ● Cover/lid of the trachea to
EPIGLOTTIS
prevent food going to the lungs
Nursing Interventions: OXYGEN THERAPY ● Windpipe
I. PROMOTE SAFETY ● Major airway
● “No smoking” sign ● Contains goblet cells –
● Open ventilation produces mucus to keep the
● Avoid static electricity TRACHEA humidity
● Avoid short circuits ● Contains cilia – remove
● Avoid flammable substances impurities
● Mucociliary Escalator –
II. MAINTAIN SKIN INTEGRITY cleansing mechanism
● Use of humidification (Distilled or Sterile LOWER RESPIRATORY TRACT
water) BRONCHUS ● Major airway
BRONCHIOLES ● Tiny twigs
● Terminal Airway
Complications of Prolonged O2 Use ● Made of Pneumoctyes
1. Retinopathy of Prematurity/ Retrolental Fibroplasia ○ Type I – Creates cell wall
➢ Retinal Detachment → Blindness (Alpha1 antritrypsin
ALVEOLI
○ Type II – Surfactant →
2. Respiratory Alkalosis Maintain stability of alveoli
➢ ↑ O2 Levels = Vasoconstriction → ↓Blood ○ Type III – Alveolar
flow → Headache/Lightheadedness, Macrophage
Tachycardia, Tachypnea LUNGS
PLEURA
RESPIRATORY SYSTEM
Function of the Respiratory System Protective Mechanism of the Lungs
● Supply O2 1. Goblet Cell
● Eliminate Co2 2. Cilia
● Maintain BP – Production of ACE → Partial 3. Mucocillary Escalator
Vasoconstriction 4. Surfactant
● Maintains Acid-Base Balance 5. Alpha 1 Antitrypsin
○ pH ↑ – Acidosis ← Hyperventilate 6. Alveolar Macrophage
○ pH ↓ – Alkalosis ← Hypoventiate 7. Cough

PULMONARY DIFFUSION

The alveoli are lined with a thin layer of epithelial

cells, and adjacent to them are capillaries with
endothelial cells. This thin membrane
(alveolar-capillary membrane aka blood gas barrier)
allows gases to diffuse (movement of particles
from high to low concentration) across it. Oxygen
moves from the alveoli into the capillaries, where it
binds to hemoglobin in red blood cells for transport
to tissues. Simultaneously, carbon dioxide moves
from the capillaries into the alveoli to be exhaled.
 4. MRI
ASSESSMENT OF THE RESPIRATORY SYSTEM ● More detailed than CT scan
INSPECTION 5. PET
● Symmetrical expansion ● Most detailed to outline lung problems
LUNG SYMMETRY ● No paradoxical breathing ● Can use to view metastasis of the lungs
● May affect the normal INVASIVE PROCEDURES
ABNORMAL
expansion of the lungs →
POSTURE 1. BRONCHOSCOPY
Decreased O2
● w/ anesthesia — informed consent
● Indicates ↓ O2 ● To determine presence or absence of disease
● 2 Types ● Instruct client to avoid driving and operating
○ Circumoral – cyanosis machinery
CYANOSIS
around the mouth
○ Peripheral – cyanosis on 2. LUNG BIOPSY
the extremities ● w/anesthesia — informed consent
PALPATION (Light and Deep) ● Before the operation the patient should be place
● Vibration on the non operative site – this reveals the
TACTILE
● (-) = Pleural Effusion or incision site.
FREMITUS
Pneumothorax ● Post-operative position should be on the
CREPITUS ● Grating sound operative site to prevent bleeding and entry of
● (+) = may indicate air.
MASS subcutaneous emphsyema ● Client should also not ambulate post-operatively
(air in the skin) to prevent bleeding
PERCUSSION (Direct and Indirect) ● WOF BLEEDING
DULL Liver, spleen
TYMPANIC Air-filled stomach
CLASSIFICATION OF LUNG DISEASES
Bone, muscle (+) Pleural
FLAT
effusion
OBSTRUCTIVE – problem is in the airway leading
RESONANCE Lungs (normal) to impaired gas exchange
Emphysematous Lungs or
HYPERESONANCE
Pneumothorax RESTRICTIVE – problem is in the restriction of the
AUSCULTATION (Direct and Indirect) structures external to the lungs affecting lung
COARSE Consolidation of fluids in the expansion leading to impaired gas exchange.
CRACKLES airway (pneumonia)
FINE Consolidation of fluids in the
CRACKLES lungs (pulmonary edema) EPIGLOTTITIS
Musical sound heard during ● Inflammation of the epiglottis
WHEEZING ● Emergency condition due to the obstruction of
expiration (asthma)
High-pitch sound due to the airway
STRIDOR ● Common in children
obstruction
Low-pitch sound due to ● Airway is obstructed
RHONCHI ● Cause: Haemophilus influenzae
obstruction
PLEURAL Grating of the pleura
FRICTION RUB Signs and Symptoms
● Drooling
● Dysphonia
DIAGNOSTIC TESTS
● Dysphagia
NON-INVASIVE PROCEDURES ● Tripod/Sniffing position (child sits upright, leaning
1. PULSE OXIMETRY forward with chin thrust out
● Infrared
● Most non-invasive
● Measures oxyhemoglobin

2. CHEST X-RAY
● Outline the lungs — to see impurities in the lung
● No jewelries
● No metal
● No to pregnant women

3. CHEST CT SCAN
● Determine lung symmetry
● Plain or w/contrast
● Ask allergies to iodine and shellfish
Diagnostic Test
● Lateral Neck X-Ray
Management Pathophysiology: ASTHMA
● Hospitalization STAT — Emergency
● Prepare tracheostomy set at bedside Asthma Triggers (Allergens)
● IVF for hydration – No oral fluids because the ↓
patient is at risk for aspiration Stimulates the release of chemical mediators
● Antibiotic (Cephalosporins) for 7-10 days (Bradykinin, Cytokine, Histamine, Leukotrine,
● Corticosteroids PRN – Reduces the Prostaglandin)
inflammation of the epiglottis ↓
● Prevention: Immunization with Haemophilus Triggers inflammation and mucus production
influenzae type b (Hib) vaccine ↓
Mucus fills and blocks airways
↓
DO NOT PUT ANYTHING IN THE MOUTH Air trapping
The epiglottis is the covering of the trachea that Signs and Symptoms
closes upon swallowing to prevent anything from ● Absent or diminished breath sounds
entering the airway. It opens when we breathe, then ● Respiratory Acidosis (initially Respiratory
closes when we swallow. Therefore a person Alkalosis)
cannot breathe and swallow at the same time, ● Oxygen Desaturation
preventing the occurrence of choking. ● Tachycardia, Tachypnea
● Hypoxemia
In patients with epiglottitis, the airway is obstructed. ● Hyperrosonance
For the patient to continue breathing, they use their ● Restlessness
mouth which is why putting anything in the mouth ● Wheezing and Crackles
can put the patient at risk for choking.

Suctioning of secretions is also contraindicated as PATIENTS WITH ASTHMA ARE INITIALLY

this can aggravate the inflammation. To facilitate ALKALOTIC
drainage of secretions, repositioning the client is
more appropriate. Insertion of ET tube is also Hypoxemia
contraindicated ↓
Activation of the Sympathetic Nervous System
(SNS)
↓
A PATIENT TAKING CORTICOSTEROIDS
Bronchodilation
↓
Do not give anything fresh (e.g., flowers, fresh
Increase RR
vegatables) to the client because of the presence of
↓
microorganisms
Increased O2 Saturation
↓
A patient taking corticosteroids has a low immune
Alkalosis
system and is prone to infection. Corticosteroids
can cause agranulocytosis.
But since clients with asthma has mucus
production, the lung will compensate by increasing
Avoid crowded places – Reverse Isolation
the respiration rate. But since there is mucus in the
airway, it traps the air leading to decreased entry of
ASTHMA oxygen in the body (Acidosis)
● Chronic inflammatory disorder causing airway
obstruction Buffer Systems: Buffer System, Lungs, Kidneys
(maintains acid-based balance)
Risk Factors: ASTHMA
● Animal dander and allergens (dust/fumes) Acidosis → Increase RR (Hyperventilate) →
● Smoking and Stress Expulsion of carbonic acid → Decreased levels of
● Temperature changes of weather CO2
● Hormonal changes (pregnancy)
● Molds Alkalotic → Decrease RR (Hypoventilate) →
● Acetylsalicylic Acid (Aspirin) Retain carbonic acid → Increase level of CO2

Asthma attack often occurs at night or early in

the morning or exercise-induced
Management Pathophysiology
● Low-flow O2 Support Risk factors
● Identify risk factors ↓
● High-fowler’s position Airflow limitation is progressive, associated with
● Mast cell stabilizer (Cromolyn Sodium) abnormal inflammatory response to noxious particles
● Bronchodilator (Theophylline, Aminophylline, or gases
Epinephrine) – Common side effect is ↓
tachycardia Chronic inflammation damages tissue
↓
Stepwise Approach for Managing Asthma Scar tissue in airways results in narrowing
Quick-relief medications Scar tissue in the parenchyma decreases elastic recoil
● Short-acting beta2-adrenergic agonists (SABA) (compliance)
● Anticholinergics Scar tissue in pulmonary vasculature causes thickened
vessel lining and hypertrophy of smooth muscle
Long-acting medications (pulmonary hypertension)
● Corticosteroids (Inhaled Budesonide)
● Mast cell stabilizer (Cromolyn sodium) – prevents Risk Factors
the subsequent release of inflammatory mediators ● Cigarette Smoking – MAJOR RISK FACTOR
● Long-acting beta2-adrenergic agonists (LABA) ● Allergens – Severe allergic reaction can lead to
● Leukotriene modifiers COPD
● Immunomodulators ● Long-term pulmonary infection – eg., Pulmonary
Tuberculosis
● Age – older adults
AN ASTHMA PATIENT WITH O2 SUPPORT ● Genetic Makeup – Alpha1 Antitrypsin Deficiency
In administering O2 support to a patient with CHRONIC BRONCHITIS (BLUE BLOATERS)
asthma, a low-flow (2-3 lpm) system is only allowed. ● Ciliary function is reduced, bronchial walls thicken,
High-flow oxygen can further reduce respiratory bronchial airways narrow, and MUCOUS MAY
drive and increase the risk of retaining carbon PLUG AIRWAYS – leads to airway obstruction
dioxide due to the suppression of hypoxic ○ Cough and sputum production for at least 3
respiratory drive. months in each of 2 consecutive years
● Alveoli become damaged, fibrosed, and alveolar
macrophage function diminishes
BRONCHODILATORS ● The patient is more susceptible to respiratory
infections (pneumonia)
Administer bronchodilators first, followed by ● Primary Affected Structure: MAJOR BRONCHI
corticosteroids (inhalers) then proceed to provide
O2 support. This makes the airway to be dilated, Major Characteristics of Chronic Bronchitis
facilitating more effective delivery of medication and 1. Inflammation
oxygen. 2. Excess Mucus Production
3. Bronchospasm

Complication
● Status Asthmaticus – a type of asthma that DISTINGUISHING CHARACTERISTICS: CB
does not respond to conventional treatment.
○ Management: Intubation, Sputum production and productive cough that lasts
Epinephrine (intratracheal) for more than 3 months

COPD/ CHRONIC AIRFLOW LIMITATION (CAL)

● Slowly and Progressive respiratory disease of BLUE BLOATER: Why? Due to cyanosis and
airflow obstruction edema
● COPD is not infectious but inflammatory
● Umbrella term for long-term pulmonary disorders Chronic smoking
characterized by increased airway resistance ↓
● Preventable and treatable but not fully reversible Inflammation of the bronchus
● The goal of management is to prevent the ↓
progression of the condition Decreased O2 Supply → Hypoxemia → Hypoxia →
● Primary structures affected: AIRWAYS, Cyanosis
PULMONARY PARYENCHYMA, or both ↓
● 2 Types: Chronic Bronchitis (Blue Bloaters) and Heart pumps more forcefully
Emphysema (Pink Puffers) ↓
Pulmonary Hypertension
↓
 Right Ventricular Hypertrophy of the Heart Rupture of Bullae can lead to Closed
↓ Pneumothorax. This rupture is caused by various
Cor Pulmonale events such as extrinsic trauma, coughing, and
↓ CPT. This is why not all patients with secretions can
Right-Sided Heart Failure be CPTd.
↓
Edema
Signs and Symptoms
Cor Pulmonale – condition characterized by the ● DYSPNEA – primary manifestation
enlargement and failure of the right ventricle of the ○ progressive, persistent, worse with exercise)
heart due to increased pressure in the pulmonary ● Increased size of accessory muscles
arteries (pulmonary hypertension) ● BARREL CHEST – characteristic of emphysema
○ The AP is equal (1:1) to the transverse
diameter – to accommodate the
Signs and Symptoms accumulation of air
● Cyanosis w/ edema ● Hyperresonance upon percussion
● Inflammation of the bronchi ● Hypercarbia → Acidosis
● Increased mucus production ● Cardiac Dysrhythmias
● Airway obstruction ● Hypoxemia
● Productive cough ● Orthopnea
● Crackles ● Prolonged expiration
● Increased airway resistance → Impaired gas ● Pulmonary HPN
exchange ● Decreased vital capacity and pulmonary function
● Dirty lung appearance in X-ray test
● Complication: Cor Pulmonale ● Weight loss – use of accessory muscles can
lead to fatigue
EMPHYSEMA (PINK PUFFERS) ● Use of accessory muscles leading to hypertrophy
● Acyanotic w/ compensatory pursed lip breathing – There are overdeveloped accessory muscles
● Break down of lung elasticity
● No Alpha1 Antitrypsin (prevents enzymatic Management
reactions) – Caused by chronic smoking ● Smoking cessation – Most important
● Decrease lung recoil ● Chest physiotherapy – Only if advised by the
● Lung overdistension → AIR TRAPPING → Barrel PHCP
chest ● Reduce risk factors
● Impaired gas exchange ● Corticosteroids – relieves inflammation
● DEAD SPACE – refers to the alveoli that is no ● Bronchodilators – dilates bronchus
longer functioning and ineffective for gas exchange ● Cough suppressant – To prevent the rupture of
● Primary Affected Structure: TERMINAL bullae. Secretions can be eliminated through
BRONCHIOLES and ALVEOLI suctioning
● Low flow O2 support (2-3 lpm)
● Increase OFI unless contraindicated – To loosen
PINK PUFFERS: Why? Pink = No Cyanosis; Puffers: secretions
pursed lip breathing like a puffer fish ● Pneumococcal vaccine – to prevent pneumonia
Destruction of alveolar cell wall (blood gas barrier)
(given every 5 years)
↓ ● Influenza vaccine – administered annually
Formation of bullae ● Pursed lip breathing
↓ ● Postural drainage
Impairment of gas exchange due to the destruction of the ● Diet (high calorie, high protein, low carbs)
blood gas barrier ● Bed rest
↓
Oxygen is trapped (air trapping)
↓
Barrel chest
↓
Increased pressure in the lungs
↓
Pursed lip breathing as a compensatory mechanism

Typical posture of a patient with emphysema

Pharmacological Management ● Open Pneumothorax – occurs when there is a
1. BRONCHODILATORS through MDIS large chest wall wound allowing air to pass freely
● Beta-adrenergic agonists: Mimics the in and out of the thoracic cavity. This passing air
sympathetic response (bronchodilation) produces a sucking sound which is referred to as
○ Salbutamol, Albuterol Terbutaline, sucking chest wound
Salmeterol ○ Can lead to Mediastinal Shift on the
● Muscarinic antagonists unaffected side
(anticholinergics):Prevents parasympathetic
response (bronchial constriction)
○ Ipratropium bromide Tension Pneumothorax – air is drawn into the
pleural space from a lacerated lung or through a
2. INHALED CORTICOSTEROIDS small opening. In contrast with open
● Budesonide, fluticasone proprionate pneumothorax, here, the air inspired is trapped and
cannot be expelled due to a small opening. This
3. COMBINATION SABA AND ANTICHOLINERGIC increases the positive pressure in the affected
AGENTS pleural space which can lead to lung collapse and
● Salbutamol/ipratropium (Combivent) mediastinal shift.
● Short-acting – effects 30minutes-1hr but shorter
duration
Signs and Symptoms
● Dyspnea
4. COMBINATION INHALED CORTICOSTEROIDS
● Tachycardia
AND LABA
● Sudden pleuritic pain
● Budesonide/formoterol (Symbicort)
● Diminished breath sound
● Long-acting – effects hours but longer duration
● Asymmetric lung expansion
● Desaturation
Other Medications:
● Shallow rapid respiration → Increased ITP
● Alpha1-antitrypsin augmentation therapy,
● Decreased cardiac output → Obstructive shock
antibiotic agents, mucolytics, antitussives,
vasodilators and narcotics
Complications
● Tracheal deviation
Patient Education on MDI usage
● Atelectasis
1. If without spacer, the mouthpiece should be
● Obstructive shock
1inch away from the mouth
● Recurrent effusion
a. Instruct the patient to open their mouth
wide
Management
b. Press the tube and then inhale deeply and
● Chest tube drainage if the fluid if >1 liter
hold the breath for 10 seconds – to allow
○ Insertion of the tube is between the 3rd and
the powder to enter the terminal
4th ICS
bronchioles not in the mouth.
● Thoracentesis if <1 liter
c. After usage, instruct the patient to perform
● High flow O2 support
oral care to prevent fungal/yeast infection
● Fowlers position
● Apply dressing for open chest wound
PNEUMOTHORAX ● PLEURODESIS – pleural binding of the parietal
● The pleural space normally has a negative or and visceral pleura
subatmospheric pressure (lower than atmospheric
pressure) – This difference in pressure allows air to FLAIL CHEST
flow into the lungs during inhalation.
● A complication of blunt trauma (injury caused by a
● Pneumothorax occurs when the parietal or visceral
forceful impact or collision WITHOUT PENTRATION
pleura is breached and the pleural space is
OF THE SKIN)
exposed to positive atmospheric pressure
● Crushing chest injury of three or more adjacent ribs
resulting in free-floating rib segments
SIMPLE/SPONTANEOUS/CLOSED PNEUMOTHORAX
● Ruptured bleb or bullae Signs and Symptoms
● It may also be associated with diffuse interstitial lung ● Paradoxical Breathing – results in increased
disease and severe emphysema deadspace, reduction in alveolar ventilation,
decreased lung compliance
OPEN/TRAUMATIC/TENSION PNEUMOTHORAX ● Retained airway secretions
● Laceration of the lung causes air to escape and ● Hypoxemia – due to the impairment of gas
enters the pleural space exchange, tissues are inadequately perfused with
● Trauma, surgery (biopsy) → positive pressure oxygen
enters ● Respiratory Acidosis – due to the impairment of
● A traumatic pneumothorax that is caused by a major gas exchange, CO2 is retained
injury can also be accompanied by Hemothorax or ● Decreased cardiac output – due to impaired gas
Hemopneumothorax exchange
● Respiratory Distress
 Prevention
● Frequent turning
● Early mobilization
● Strategies to expand the lungs
● Secretion management techniques

CNS Neuron – neurons in the brain and spinal cord

PNS Neuron – neurons in the muscle
Dendrites – going to the brain
Axon Terminal – away from the brain
Complications
● Atelectasis GUILLAINE-BARRE SYNDROME – ascending
paralysis (destruction of the myelin sheet) –
Management electrical impulse can’t go to the brain causing the
● Promote O2 support non-release of ACTH (no ACTH no contraction)
● PRIORITY: Maintain a patent airway – ● Caused by infection
intubation ● Viral Mimicry – the virus mimics the
● Controlling pain neuron, therefore the immune system
● Clearing secretions also attacks the true neurons
● Surgery
MYASTHENIA GRAVIS – descending paralysis
CARBON MONOXIDE POISONING (destruction of the ACTH receptors and
● CO2 takes up the space of O2 in the RBC → neuromuscular junction)
Hypoxia
● Exposure to inadequately vented combustion device Normal Flow of Electrical Impulse
Electrical Impulse
Signs and Symptoms ↓
● SORD CNS Neurons (Dendrites)
● Headache ↓
● Vertigo Alpha and Delta and C Fiber
● Paralysis ↓
Spinal Cord
Management ↓
● Hyperbaric pressure Spinothalamic Tract
● Remove patient immediately from the area of ↓
poisoning Brain
● Initiate CPR immediately ↓
● Administer O2 support Electrical Response
● Monitor VS ↓
● Intubation Corticospinal Tract
● Mechanical Ventilation ↓
Nerves
↓
ATELECTASIS
PNS Neurons
● Collapse of the alveoli ↓
● Complications of lung problems Muscle
↓
Causes Response
● Altered breathing patterns (GBS, MG)
● Retained secretions
● Prolonged supine positioning Management
● Reduced lung volume ● Endotracheal intubation
● Surgical procedure ● Mechanical ventilation
● Presence of fluid in the pleural space ● Treat underlying causes

Signs and Symptoms

● Progressive dyspnea
● Flat during percussion
● Absent or diminished breath sounds
 ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) Cause
● A form of pulmonary edema that can lead to acute ● Ventilatory failure
respiratory failure ○ Impairment of CNS – head trauma, CVA,
infection
Risk Factors ○ Neuromuscular Dysfunction – Amyotropic
● Anaphylaxis lateral sclerosis (ALS), Guillan-Barre
● Aspiration Syndrome (GBS), Myasthenia Gravis (MG)
● Respiratory trauma (fat embolism, lung contusion, ○ Muscular Dysfunction – chest trauma,
radiation) malnutrition, kyphosis
● Disseminated vascular coagulation ● Oxygen failure
● Drug overdose/ ○ Constrictive lung diseases, pneumothorax,
● Drowning pleural effusion
● Diffused pneumonia
● Sepsis Signs and Symptoms
● Shock ● Tachycardia
● Smoking ● Tachypnea
● Air Hunger
● Cyanosis
Pathophysiology ● Diaphoresis
● Alterations of LOC
Assault in the Respiratory System
↓ Complication
Damaged pulmonary blood vessels ● Respiratory arrest
↓
Destroyed type 2 cells of the lungs Management
↓ ● Aim the cause, treat the cause
Alveolar collapsed ● O2 support
↓ ● ET intubation
Platelet aggregation ● Mechanical ventilation
↓ ● Monitor respiratory status
Inflammatory response → Release of chemical
mediators CYSTIC FIBROSIS (MUCUVISIDOSIS)
↓ ● Chronic disorder resulting to hyperactivity of the
Increased capillary permeability exocrine gland
↓ ● Most common life-shortening inherited disease
Pulmonary edema ● Can lead to: chronic airway obstruction, Infection,
↓ Malabsorption
Respiratory distress (tachypnea, dyspnea,
hypoxemia, decreased oxygen saturation and Signs and Symptoms
carbon dioxide) ● Failure to pass meconium (meconium ileus)
↓ ● Signs of respiratory distress
Decreased lung compliance ● Thick mucus production
↓ ● Cyanosis
Severe respiratory failure ● Clubbing
● Recurrent plug infection → Steatorrhea
Management ● Recurrent long infection
● Aim the cause, treat the cause ● Frosting of the skin or salty taste sweat
● Antibiotic therapy
● Anticoagulant Diagnostic Test
● Respiratory Support ● Iontophoresis or Pilocarpine Test (sweat chloride
● Restrict fluids test) – <60 meq/L
● Diuretics
● Dopamine Management
● Corticosteroids ● Promote effective airway
● CPT
ACUTE RESPIRATORY FAILURE ● Reduce risk factors for respiratory infection
● Lifestyle modification
● Deterioration of the gas exchange function of the
● Supplemental oxygen
lungs → failure in ventilation/oxygenation
mechanism
Pharmacotherapy
● Antibiotic
● Anti-inflammatory
● Leukotriene (mast cell inhibitor)
 CHEST TUBE DRAINAGE SYSTEM Types
● If air or fluid is >1L ● Hemothorax (blood) ← trauma, metastasis
● 1st Bottle – DRAINAGE BOTTLE ● Pyothorax (pus) ← long term pulmonary infection
○ NI: Monitor for the color, amount, and (PTB)
consistency of drainage – record ● Hydrothorax (serous fluid) ← unknown cause but
can occur due to cellular aberations (Malignant
● 2nd Bottle – WATER SEAL BOTTLE Hydrothorax)
○ NI: Prevent positive pressure
○ CONTINUOUS BUBBLING – it indicates air Signs and Symptoms
leak; check high suction ● Sudden sharp pain upon inhalation
○ INTERMITTENT BUBBLING – Normal; there is ● Tachycardia
tidaling and fluctuating when the patient inhales ● Tachypnea
○ NO BUBBLING – indicates obstruction, the ● Dyspnea
tube is kinked – milk the tube towards the bottle ● Absent or diminished breath sounds
and reposition the pt ● Asymmetric lung expansion — paradoxical chest
movement
● 3rd Bottle – SUCTION BOTTLE ● Flat sound upon percussion
○ If no continuous bubbling, check suction,
dressing may be dry, or mass (crepitus) – Complications
indicates subcutaneous emphysema – mark the ● Atelectasis
site and refer ● Hypovolemic Shock
○ CONTINUOUS BUBBLING – if the suction
machine is open Management
○ NO CONTINUOUS BUBBLING – check the ● Chest Tube Drainage (5th-6th ICS/ 8th and 9th
suction if it is plugged. ICS)
○ CONTINUOUS then Suddenly gone – check ● Thoracentesis
the pressure of the suction machine, obstruction, ● High fowlers
kinking of the tube. ● Oxygen
● Pain Management

PLEURAL EFFUSION
● Excessive accumulation of fluids in the pleural space

THORACENTESIS

Due to the gravity, fluid usually accumaltes in the

lower segment of the lungs. Therefore, the puncture
will be on the lower segment also. In contrast, in
pneumothorax, it will be on the upper side because
air is lighweight it tends to accumulate in the upper
segment.

During CTT, the client will have to undergo chest

x-ray before and after insertion of the tube. The
initial x-ray is used to identify where the fluids are
accumulating. The second x-ray will be done after
insertion to check if the tubing is patent or if air has
entered the tube.
 CARDIOVASCULAR SYSTEM
● Delivers oxygen CARDIAC TAMPONADE
● Eliminate waste products
● Helps in metabolism A medical emergency that takes place when
● Parts: Heart, Blood Vessels, Blood abnormal amounts of fluid accumulate in the
pericardial sac compressing the heart and leading
to a decrease in cardiac output and shock.
HEART
● Pumping station of the body
● Size of a fist
● Location: 2nd rib, 5th ICS, Midclavicular Line,
Inferior Mediastinum
● Layers: Epicardium, Myocardium, Endocardium
● Covering: Pericardium

Layers of the Heart

Epicardium
● Outermost layer
● Epicarditis

Myocardium Signs and Symptoms (BECK’S TRIAD)

● Middle layer ● Narrowed pulse pressure (hypotension)
● Contracting part ○ Pulsus Paradoxus – decrease of >10
● Myocarditis – most dangerous, because this mm Hg systolic blood pressure during
layer is responsible for contraction. inspiration.
!EMERGENCY ● Distended jugular vein
○ S/sx: Fatigue ● Muffled heart sound
Endocardium Cause
● Inner most part ● Trauma
● Endocarditis
Management
PANCARDITIS ● Pericardiocentesis – puncture of the
Inflammation of all layers of the heart pericardial sac to aspirate pericardial fluid

Pericardium VALVES OF THE HEART

● Covering of the heart ● Promotes unilateral flow and prevent backflow of
● Contains pericardial fluid (5-20mL) – to decrease blood.
friction for the beating heart and to prevent friction ● Atrioventricular Valve – Tricuspid (right) and Mitral
rub (left) valve
● Semilunar Valve – Pulmonary and Aortic valve
PERICARDITIS
● Inflammation of the pericardium CHAMBERS OF THE HEART
● 4 Chambers
Causes: ● RA, RV, LA, LV
● Viral/Bacterial Infecion
● Surgery (e.g., coronary artery bypass graft
(CABG), percutaneous transluminal coronary Cardiac Output – amount of blood pumped by the
angioplasty (PTCA) heart in one full minute
● Lung Metastasis HR x SV = CO

Signs and Symptoms 4-6L of blood is pumped per minute

● Chest pain that radiates at the back – the reason SV — amount of blood pumped per beat (average
why it radiates at the back is because the resting SV=60-130mL)
pericardium covers the heart from front to back
● Friction Rub – grating or scratching in the left
sternal border
● ↑Pericardial fluids → Pericardial effusion – a fluid
>20mL → Can lead to cardiac tamponade
 BLOOD SUPPLY OF THE HEART
BLOOD FLOW IN THE HEART Aorta
Deoxygenated blood from the upper part of the ↓
body enters the SVC and then to the right atrium; Coronary Artery (Left and Right)
Deoxygenated blood from the lower part of the body ↓
enters the IVC and then to the right atrium Right Coronary Artery → Right side and Inferior part of
↓ the heart
Tricuspid Valve ↓
↓ Left Coronary Artery → Left Anterior Descending
Right Ventricle Artery and Circumflex Artery
↓
Pulmonary Valve
↓ LEFT ANTERIOR DESCENDING ARTERY
Pulmonary Artery Common site of Coronary Artery Disease (CAD)
↓
Lungs (Gas Exchange)
↓ CORONARY ARTERY DISEASE
Pulmonary Vein (now oxygenated) ● Build up of plaque (atheroma/fat deposit) in the
↓ arteries that supplies blood to the heart (coronary
Left Atrium artery)
↓ ● Atherosclerosis – build up of plaque in the artery –
Mitral Valve this fat can be diluted through exercise
↓
Left Ventricle
↓
Aortic Valve
↓
Aorta
↓
Oxygenated blood will be delivers all over the body
Complications
Ventricular Filling – filling of blood in the ventricles 1. Angina Pectoris
(occurs during diastole) 2. Myocardial Infarction

Risk Factors
HEART SOUNDS ● Familial History (Genetics)
● Closure of the AV Valves ● Alcohol
S1 “Lub” ● Ventricular SYSTOLE ● Cigarette Smoking – cigarettes contrains nicotine
(contract) that has a vasopressin effect (narrowing of blood
● Closure of the SL Valves vessels)
S2 “Dub” ● Ventricular DIASTOLE ● Type B Personality – Hyperactive people, people
(relax) that easily gets panic
● VENTRICULAR GALLOP ● Obesity
S3 “Lub Dub DEE” ● Race – common in african americans
● Indicator of CHF
● ATRIAL GALLOP ● Sedentary Lifestyle – can lead to hyperlipidemia
S4 “DEE Lub Dub”
● Indicator of Hypertension
TYPE B PERSONALITY
PROPERTIES OF THE HEART
● Ability to maintain rhythm These are people that are hyperactive. When a
person is hyperactive, their adrenal medulla
releases catecholamines (epinephrine and
norepinephrine) – these emergency hormones has
RHYTHMICITY a vasocontriction effect.

HYPERLIPIDEMIA

Normal LDL = <130 mg/dl

Normal HDL
EXCITABILITY ● Ability to respond to impulse ● Male = 35-65 mg/dl
● Ability to transmit electrical ● Female 35-85 mg/dl
CONDUCTABILITY
impulses
CONTRACTABILITY ● Ability to contract Female, naturally, has higher levels of fats
● Ability to initiate/generate
AUTOMATICITY
impulse
 Total Cholesterol should be <200 mg/dl, if it is Nursing Intervention
higher than 200, a client is at high risk of CAD ● Administer the drug at 5 minutes interval for 3
doses
● If the pain is not relieved after the 3rd dose, do
ANGINA PECTORIS not give another dose – the patient already
● Chest pain that is brought about by myocardial has met the maximum effect
ischemia ● Administer the drug in reclining or sitting
● When oxygen supply is insufficient, cells switch to position to ensure safety – the patient is at risk
anaerobic metabolism, resulting in the production of for fall (headache and hypotension)
lactic acid as a byproduct. This buildup of lactic ● Avoid alcohol while taking this drug
acid contributes to the discomfort and pain ● If given topically (NTG patch), the nurse
characteristic of angina episodes. should wear gloves

STABLE ANGINA (PREDICTABLE OR EXERTION ANGINA) UNSTABLE ANGINA

● Predictable and consistent pain that occurs on (PREINFARCTION OR CRESCENDO ANGINA)
exertion and is relieved by rest and/or ● Chest pain more than 15 minutes
nitroglycerin ● Not relieved by RON (Rest, Oxygen, Nitroglycerin)
● DOC: Morphine Sulfate
Risk Factors ● Risk for: Acute Coronary Syndrome (95% occlusion
1. Exercise (Sex) of the artery that can lead to MI)
2. Eating Heavy Meal
3. Extreme Emotion PATTERN
CAD
Signs and Symptoms ↓
● Chest pain that stay for 5-10 minutes Ischemia (Angina Pectoris)
↓
Management ACS
● Rest ↓
● Oxygen (1-2 lpm) MI
● Nitroglycerine – a potent vasodilator (in a large
dose it can dilate artery) SILENT ANGINA (PRINZMETAL ANGINA)
● (-) Chest pain
SEXUAL ACTIVITY
Management
A patient asked, “I have a heart disease, can I still
● 24-hour Holter Monitoring (24-hour Ambulatory
have sex with my wife?”
ECG)
○ NI: Take a bath before application of the
Answer:
machine.
For a patient who have recently sufferd from MI,
they should wait at least 6-8 weeks. Sexual activity
Other Management for Angina Pectoris
is best in the morning because the BP is low (came
1. Beta Blockers - ↓ Heart rate → ↓ Cardiac
from sleep). A client also should not have sex after
Workload → ↓ O2 Demand
a heavy meal because the stomach is distended –
this will lead to the heart pumping more forcefully
2. Calcium-Channel Blockers
● Nicardipine, Amplodipine, Nifedipine,
Felodipine
NITROGLYCERINE ADMINISTRATION ● Dilates blood vessels → ↓heart rate → ↓
● Given sublingual – there is increased absorption Cardiac demand
because there is presence of blood vessels in the
soft the frenulum MYOCARDIAL INFARCTION
● (+) Irreversible necrosis in the heart
Effectiveness
● If pain is relieved or decreased pain Signs and Symptoms
● Chest pain (squeezing, crushing)
Freshness Indicator ● Feeling of impending doom
● There is burning sensation under the tongue ● Pain radiating in the left arm, neck, and jaw

Side Effects Diagnostic Tests

● Cephalgia (Headache) ● ECG
● Hypotension ○ Zone of Ischemia – Inverted T Wave
○ Zone of Injury – ST Segment Elevation
○ Zone of Necrosis – Pathologic Q Wave
● LDH (Lipid) – <130 mg/dL
 ● TROP I — ↑ within 3hrs and persists up to 7-10
days (Normal: <0.1-0.5 ng/mL) malformation of the baby
● TROP T — ↑ 3-4hrs and remains elevated for for
10-14 days (Normal: <0.2 ng/mL) Nursing Interventions
● MYOGLOBIN – ↑ 2-4hrs after cell death with a ● Monitor PT (Normal Prothrombin Time: 11-12
rapid decline after 7hrs seconds)
○ Normal Male: 20-90 ng/mL
○ Normal Female: 12-75 ng/mL Antidote – Vitamin K
● BRAIN NATRIURETIC PEPTIDE (BNP) — >100
ng/L
● Thrombolytic – dissolves clot (clot buster)
● CBC – ↑WBC, ↑CK-MB (6hrs from the onset of
○ Streptokinase, Eurokinase, Tissue
pain - 2 days)
Plasminogen Activator (TPA)
○ Male CK-MB: 2-6 ng/mL
○ Female CK-MB: 2-5 ng/mL
Other Management for Myocardial Infarction
● Beta-blockers
● Calcium-channel blockers

CONGESTIVE HEART FAILURE

● Decreased pumping ability of the heart

TYPES OF CHF
Signs and Symptoms (Systemic)
● Bipedal Edema
RIGHT-SIDED
● Weight Gain
HF
● Jugular Vein Distention (JVD)
● Ascites
● First to be impaired
● Most common

Signs and Symptoms (Pulmonary)

● Non-productive cough
● Pink frothy sputum – there
presence of fluids in the alveoli,
Management when the client cough, there
● Morphine Sulfate (Narcotic Analgesic LEFT-SIDED may be small amount of blood
○ Given to promotes peripheral vasodilation to HF ● Pulmonary edema
decrease the workload of the heart – BEST ● Orthopnea
○ Relieve of Pain ● Bilateral lung fine crackles
○ Relieve Anxiety ● Cyanosis (late sign- –
● Antidote: Naloxone (Narcan) respiratory distress
● NI: Check RR before administration (if less than
12, hold the medication, assess the pt, and report Management
to the physician) ● Intubation (ET)
● Oxygen Therapy ● Ready suction
● Antiplatelet – to prevent platelet aggregation to
prevent further thrombus formation Management for CHF
○ Aspirin, Clopidogrel, Ticlopidine ● Diet – LSLF
● Anticoagulant – to prevent coagulation process ● Limit OFI – 1L a day (divided into 200mL)
○ Heparin, Warfarin ● Digoxin (Lanoxin)
● Diuretics – Furosemide (Lasix)
HEPARIN
● Given subcutaneously
● Yes to pregnant women

Nursing Interventions
● Monitor PTT (Normal Partial Thromboplastin
Time: 22-35 seconds)

Antidote – Protamine Sulfate

WARFARIN
● Given per orem
● No to pregnant women – can lead to craniofacial
 DIGOXIN (LANOXIN)

Positive Inotropic – ↑ force of contraction

Negative Chronotropic – ↓HR

Nursing Intervention
● Check HR before administration

Digitalis Toxicity
● Normal Serum Value: 0.5-2 nanogram/dL
○ Digoxin has a narrow therapeutic index

Signs and Symptoms (Digitalis Toxicity)

● Visual Disturbances (xanthopsia)
● GI Distrubances (constipation)
● Hypokalemia

Antidote – Digitalis Immune Fab (Digibind)

FUROSEMIDE (LASIX)
● Given per orem

Signs of Toxicity
● Ototoxicity (Tinnitus)
○ Rationale: The ear has fluids in the
endolymph and perilypmh. Administration
of furosemide can reduce this and can
lead to dryness.
● Potassium-Wasting – Hypokalemia

NOTE!
Digoxin and Furosemide can be given
simultaneously. Both drugs can cause hypokalemia
but this decrease in serum potassium is associated
with Digitalis Toxicity. Administer DG bind