OXYGENATION UTILIZATION
that can cause mild to severe illness in people of
PROBLEMS - Supplemental
Resources
Pneumothorax -
The term spontaneous pneumothorax
refers to the presence of air in the pleural space
that is not caused by trauma or other obvious
precipitating factor (trauma or iatrogenic during
a procedure). While primary spontaneous
pneumothorax occurs without a clinically
apparent lung condition; secondary spontaneous
pneumothorax is a complication of preexisting
lung disease. To this date, there are only rare
mentions of pneumothorax as a complication of
COVID-19 viral pneumonia including few case
reports.
The proposed mechanism of
spontaneous pneumothorax in patients with
COVID-19 disease is thought to be related to the
structural changes that occur in the lung
parenchyma. These include cystic and fibrotic
changes leading to alveolar tears. In addition to
the increase in intrathoracic pressure resulting
from prolonged coughing and/or mechanical
ventilation. Herein we review the incidence and
outcomes of pneumothorax in over 3000 patients
admitted to our institution for suspected
COVID-19 pneumonia.
Pneumonia -
Pneumonia is an infection of the lungs
that can cause mild to severe illness in people of
all ages. Immunizations can prevent some types
of pneumonia. You can also help prevent
pneumonia and other respiratory infections by
following good hygiene practices.
Pneumonia is an infection of the lungs
all ages. However, some people are at increased
risk for getting pneumonia. Being a certain age,
having certain medical conditions, and smoking
can increase a person’s risk for pneumonia.
Causes of Pneumonia -
Viruses, bacteria, and fungi can all cause
pneumonia. In the United States, common
causes of viral pneumonia are:
● Influenza viruses
● Respiratory syncytial virus (RSV)
● SARS-CoV-2 (the virus that causes
COVID-19)
Common causes of bacterial pneumonia are
Streptococcus pneumoniae (pneumococcus) and,
especially in kids, Mycoplasma pneumoniae.
The bacteria and viruses that most commonly
cause pneumonia in the community are different
from those in healthcare settings. However,
clinicians are not always able to find out which
germ caused someone to get sick with
pneumonia.
Defining Types of Pneumonia
Community-acquired pneumonia is when
someone develops pneumonia in the community
(not in a hospital).
Healthcare-associated pneumonia is when
someone develops pneumonia during or
following a stay in a healthcare setting.
Healthcare settings include hospitals, long-term
care facilities,
and dialysis centers.
Ventilator-associated pneumonia is when
someone gets pneumonia after being on a
ventilator, a machine that supports breathing.
 Diagnosis and Treatment of Adults with
Community-acquired Pneumonia -
This document provides evidence-based
clinical practice guidelines on the management
of adult patients with community-acquired
pneumonia. Antibiotic recommendations for the
empiric treatment of CAP are based on selecting
agents effective against the major treatable
bacterial causes of CAP. Traditionally, these
bacterial pathogens include Streptococcus
pneumoniae, Haemophilus influenzae,
Mycoplasma pneumoniae, Staphylococcus
aureus, Legionella species, Chlamydia
pneumoniae, and Moraxella catarrhalis. The
microbial etiology of CAP is changing,
particularly with the widespread introduction of
the pneumococcal conjugate vaccine, and there
is increased recognition of the role of viral
pathogens.
COPD -
COPD is a chronic condition in the
lungs characterized by inflammation and severe
limitation of air flow in and out of the lungs.
Cigarette smoking is the leading cause of
COPD. Other factors can also contribute to
COPD such as long-term exposure to
second-hand smoke or irritants such as air
pollution, dust or workplace fumes.
Chronic Obstructive Lung Disease
(GOLD) has been producing reports that offer
recommendations on the management of chronic
obstructive pulmonary disease (COPD) since
2001. One of the key strengths of the GOLD
report is that, unlike the NICE guideline,1 it is
updated annually. Major revisions were
published in 2007, 2011, and 2017, and the 2021
report contains a new chapter on COPD and
COVID-19. GOLD published its 2022 report in
November 2021.
There have been no significant changes
in the chapter on diagnosis and initial
assessment. A diagnosis of COPD is based on
the presence of symptoms and airflow
obstruction, which is demonstrated by a
postbronchodilator forced expiratory volume in
1 second (FEV1) to forced vital capacity (FVC)
ratio of less than 0.7 on spirometry.2 The goals
of assessment are to determine the level of
airflow limitation, the impact of the disease on
the patient’s health, and the risk of future events,
such as exacerbations, hospital admissions, or
death. To achieve these goals, the GOLD report
recommends that assessment of people with
suspected COPD must consider:2
● the presence and severity of the
spirometric abnormality
● the current nature and magnitude of the
patient’s symptoms
● history of moderate and severe
exacerbations, and future risk
● the presence of comorbidities.
Cystic Fibrosis -
Cystic fibrosis is a monogenic disease
considered to affect at least 100 000 people
worldwide. Mutations in CFTR, the gene
encoding the epithelial ion channel that normally
transports chloride and bicarbonate, lead to
impaired mucus hydration and clearance.
Classical cystic fibrosis is thus characterised by
chronic pulmonary infection and inflammation,
pancreatic exocrine insufficiency, male
infertility, and might include several
comorbidities such as cystic fibrosis-related
diabetes or cystic fibrosis liver disease.
Cystic fibrosis is a monogenic disease
considered to affect at least 100 000 people
worldwide. Mutations in CFTR, the gene
encoding the epithelial ion channel that normally
transports chloride and bicarbonate, lead to
impaired mucus hydration and clearance.
Classical cystic fibrosis is thus characterised by
chronic pulmonary infection and inflammation,
pancreatic exocrine insufficiency, male
infertility, and might include several
comorbidities such as cystic fibrosis-related
diabetes or cystic fibrosis liver disease.
Oxygenation Cardio Tests & Assessment -
A thorough assessment of the heart
provides valuable information about the function
of a patient’s cardiovascular system.
Understanding how to properly assess the
cardiovascular system and identifying both
normal and abnormal assessment findings will
allow the nurse to provide quality, safe care to
the patient.
Before assessing a patient’s
cardiovascular system, it is important to
understand the various functions of the
cardiovascular system. In addition to the
information provided in the “Review of Cardiac
Basics” section, the following images provide an
overview of the cardiovascular system.
Figure 1. Structure of the Heart
Figure 2. Blood Flow Through the Heart
Assessing the cardiovascular system
includes performing several subjective and
objective assessments. At times, assessment
findings are modified according to life span
considerations.
Subjective Assessment
The subjective assessment of the
cardiovascular and peripheral vascular system is
vital for uncovering signs of potential
dysfunction. To complete the subjective
cardiovascular assessment, the nurse begins with
a focused interview. The focused interview
explores past medical and family history,
medications, cardiac risk factors, and reported
symptoms.
Symptoms related to the cardiovascular
system include chest pain, peripheral edema,
unexplained sudden weight gain, shortness of
breath (dyspnea), irregular pulse rate or rhythm,
dizziness, or poor peripheral circulation. Any
new or worsening symptoms should be
documented and reported to the health care
provider.
Oxygenation Cardiac Disorder -
Supplemental oxygen has been a
cornerstone of supportive care in cardiovascular
medicine for decades. In the scenario of acute
myocardial infarction (MI), the mnemonic
MONA has been taught to medical students and
professionals for generations, helping them to
remember the initial treatment morphine,
oxygen, nitroglycerin, and aspirin. Specifically,
the utility of supplemental oxygen has been
challenged lately, questioning the need for this
ubiquitous therapy based on limited scientific
evidence.
 The rationale behind supplemental
oxygen in the acute setting has been to increase
oxygen delivery to the ischemic heart, brain, or
other organs. In the hypoxemic patient
(hypoxemia defined as oxygen saturation
<90%), this approach seems reasonable.

Patients with underlying lung disease or

pulmonary congestion leading to an excessive
risk of hypoxemia may potentially benefit from
prophylactic oxygen supplementation, whereas
patients with chronic obstructive pulmonary
disease might be at risk to develop hypercarbia
from respiratory suppression.

Types of CAD -
Nursing Management - MI

● Relieving fluid overload symptoms. ● substernal radiating to left arm, neck or

● Relieving symptoms of anxiety and jaw
fatigue. ● severe crushing, constricting, “someone
● Promoting physical activity. sitting on my chest”
● Increasing medication compliance. ● prolonged (>35mins) & not relieved by
● Decreasing adverse effects of treatment. rest
● Teaching patients about dietary ● Shortness of breath, profuse perspiration
restrictions. ● Feeling of impending doom
● Teaching patient about self-monitoring
of symptoms. Management
• Initial: O.M.E.N.
Myocardial Infarction - • Thrombolytic Therapy
• Anti-arrhythmic
ST-Segment Elevation MI (Heart Attack) • Anticoagulants
❖ Causes: atherosclerotic plaque disruption or • Stool softeners
significant CHD, cocaine use (risk factor) ❖ • Surgery
Defining guidelines: (3 presentations)
1. Symptoms at rest (usually prolonged, i.e.. OTHER THERAPEUTIC
>20mins) MANAGEMENT:
2. New onset exertional angina (increased in
severity of at least 1 class – to at least class III) 1. Emergent Percutaneous Coronary
in <2months Intervention (PCI)
3. Recent acceleration of angina to at least class 2. Cardiac Rehabilitation
III in <2months • Improve cardiac function and
❖ Dx: based on pain severity & presenting return to normal life as possible.
symptoms, ECG findings & serum cardiac
markers PHASES OF CARDIAC REHAB:
❖ Unremitting chest pain for >20mins,
STSegment Elevation MI is usually considered ● PHASE 1: Admission and diagnosis
FOCUS: Self-Care; Low-level activities;
Angina HT: Signs and Symptoms
● precipitated by increased work demands ● PHASE 2: Discharged FOCUS:
of the heart Outpatient program 4-6 weeks HT:
● precordial or substernal chest area < Lifestyle modification.
15mins constricting, squeezing, or ● PHASE 3: Maintaining cardiovascular
suffocating sensation stability: long term conditioning
● Usually steady, increasing in intensity at
the onset & end of attack Congestive Heart Failure
● May radiate to left shoulder, arm, jaw, or
other chest areas Left-sided
● Relieved by rest or by NTG
● Coughing
 ● Hemoptysis
● Orthopnea
● Pulmonary
● congestions

Right Sided

● Hepatomegaly
● Edema
● Ascites
● Distended neck
● Vein

Pharmacologic
Management

• ACE inhibitors
• Nitrates – Hydralazine (Apresoline) +
Isosorbide
dinitrate (Isordil)
• ACE inhibitors + Beta blockers –
recommended
w/ACE Inhibitors (titrated dose every 2wks)
• Diuretics
• Digitalis
• Calcium channel blockers
Fluids & Electrolytes: Hypertonic

Renal Regulation- ● solute concentration higher than the

solute concentration of the serum
● Kidneys are the most important ● infusion causes an increase in the solute
regulators of volume and composition of concentration of the serum, pulling fluid
body fluids from the interstitial space to the vascular
● Hormonal Control space through osmosis
● ADH
● Renin – angiotensin - aldosterone
system (RAAS) Electrolyte Imbalance
● Natriuretic factors
● Signs and symptoms
Fluid Balance - ● Depend largely on the physiological role
of the electrolyte affected
● Solutions (liquid solvents) containing
dissolved substances (solutes) are Electrolytes
classified according to their
concentration (or tonicity) ● Major intracellular electrolytes
● Hypertonic ● Potassium (cation)
● Isotonic ● Phosphorus (anion)
● Hypotonic
Major extracellular electrolytes
Intravenous Fluids
● Sodium (cation)
● Crystalloids ● Chloride (anion)
● Hypertonic ● Sodium is the determinant of (tonicity)
● Isotonic since it is the major ECF cation
● Hypotonic Sodium

Colloids ● Controls water flow across cell

membrane
● Albumin ● Conduction of neuromuscular impulses
● Hetastarch ● Helps regulate acid-base balance
● Dextrans

Crystalloids Hyponatremia

● Isotonic ● CAUSES
● osmolarity equals serum ● Decreased intake and adrenal
● stays in the intravascular space thus insufficiency
expanding the volume ● Inappropriate ADH
● good choice for hydration ● Diaphoresis with water replacement
● Diuretic therapy

MANIFESTATIONS
● Cellular swelling with cerebral edema
leading to headache, stupor and coma;
muscle weakness; decreased thirst;
edema if secondary to hypervolemia
Sodium
● Decreased intake, adrenal cortex
hyperfunction and diuretic therapy
● Alkalosis
● Vomiting/gastric suction
MANIFESTATIONS
● Cardiac arhythmia (lower T and
appearance of U wave due to slow
repolarization) and muscle weakness

● Principle active solute in the Potassium

extravascular space
● Determines the volume of both the
intravascular and interstitial spaces
Hypernatremia
● Must be ingested daily
● It is not stored
● Kidneys can excrete excess K+
● Can’t selectively retain K+

CAUSES Hyperkalemia
● Increased intake or renal failure
● Water deprivation CAUSES
● Decreased ADH secretion ● Increased intake or renal failure and
● Increased aldosterone hypoaldosteronis
● Liver failure ● Acidosis
● Hypothalamic lesion ● RBC hemolysis

MANIFESTATIONS
● Cellular shrinking with increased CNS MANIFESTATIONS
irritability; increased thirst; hypotension ● Cardiac depression (shallow, wide QRS
with oliguria if secondary to with elevated T due to exaggerated
hypovolemia repolarization)
● Paresthesia and/or paralysis
Potassium

● Maintenance of cellular osmotic Hypocalcemia

pressure
● Facilitation of neuromuscular activity CAUSES
● Glucose uptake ● Decreased intake (10), vit. D deficiency,
● Regulation of acid-base balance hypoparathyroid
● Hypoalbuminemia
Hypokalemia ● Alcohol abuse or liver failure

CAUSES MANIFESTATIONS
 ● Increased neuromuscular activity
(possible convulsions); skeletal muscle
tetany
CAUSES
Hypercalcemia ● renal insufficency, or PO4 release from
cell due to widespread cell necrosis
CAUSES ● Hypocalcemia
● Increased intake ● increase intake of alkali (baking soda)
● Immobility ● Addison’s disease
● Hyperparathyroidism ● Vitamin D excess
● Bone malignancies
● Renal failure Magnesium

● Second most abundant intracellular

MANIFESTATIONS cation
● Decreased neuromuscular activity ● Cofactor for enzyme reactions involving
(stupor to coma); renal calculi; increased ATP
fracture risk ● Membrane pump for electrical gradient
Hypophosphatemia across cell membranes
● Activity of electrically excitable tissues
CAUSES ● Regulates calcium flux in smooth
● resp.alkalosis muscle cells
● beta agonist bronchodilators ● Plasma levels poorly reflect body stores
● Sepsis
● phosphorus binding agents Hypomagnesemia
(carafate/amphogel)
● diabetic ketoacidosis CAUSES
● malabsorption ● excessive diuretics, starvation,
alcoholism, antibiotics, drugs,
MANIFESTATIONS malabsorption, GI losses, diabetes, acute
● often clinically silent-impaired MI, cisplatin Rx, acute/chronic
myocardial contractility and decreased pancreatitis, hypokalemia hypocalcemia
CO, hemolytic anemia, shift in the
oxyhemoglobin dissociation curve to the MANIFESTATIONS
left, muscle weakness ● confusion, seizures, coma,
arrhyhmias(PVC, Vfib, torsadesde
Hyperphosphatemia pointes), hyperreflexia

MANIFESTATIONS
● not well documented except for
formation of insoluble
calcium-phosphate complexes that are
deposited in soft tissues and promote
tissue damage
Hypermagnesemia
CAUSES
● CRF, inc.intake (laxatives/antacids),
Addison’s disease, aspiration on salt
 water, hyperparathyroidism,
hypothyroidism, dehydration

MANIFESTATIONS
● confusion, feeling of warmth/sweat
followed by severe depression,
hypotension, SB, heart block, muscle
weakness, flaccid paralysis, respiratory
muscle paralysis, hypoactive DTR