Critical Care Nursing Assignment

The provided assignment is a detailed document that covers various aspects of critical care nursing. It includes references to medical texts, journals, and online resources, providing in-depth information on topics such as septic shock treatment, pathophysiology of fluid imbalance, and the ABCDE primary assessment. The document also discusses the importance of early goal-directed therapy in treating severe sepsis and septic shock. The assignment is likely intended for students pursuing a degree in nursing or a related field, providing them with a valuable resource for understanding critical care concepts and practices.

RUNNING HEAD: SEPTIC SHOCK 1
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Students name
Institutional affiliation

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A case study of a seventy-seven-year-old patient admitted to the ward through the
emergency department for lower lobe pneumonia at night. She had a past history of
hypertension, hypercholesterolemia and ischemic heart disease. She was on Ramipril 10mg,
aspirin 100mcg, spironolactone 50mg and atorvastatin 80mg nocte.
On arrival to the emergency department, she presented with shortness of breath. She was
put on oxygen and given ceftriaxone (antibiotics) which relieved this symptom. The patient had a
calm night. In the morning the patient had shortness of breath and used accessory muscle to aid
her in breathing. Her breathing rate was 36 breaths per minute. She was confused. Her blood
pressure was 90/65 mmHg and heart rate of 120 bpm. She had a low-grade fever. Her oxygen
saturation was at 91%. She complained of pain in the left lower chest on deep inspiration. The
indwelling catheter that was inserted on admission has drained 30mls of urine.
The above presentations were alarming so the medical emergency team was called to
intervene. The team inserted a central catheter in her subclavian vein which was secured so as to
prevent her from removing it. She was started on two liters of 0.9% normal saline. She was
started on azithromycin 500mg and the oxygen therapy was increased from two liters per minute
to five liters.
The present paper will give, one, a detailed and structured primary assessment of
Catherine. The ABCDE assessment, that is airway, breathing, cardiovascular, disability, and
exposure assessment. Each assessment will be having a scientific rationale. The second part will
focus on the finding obtained from the primary assessment. With this finding, a focused
assessment will be done. Scientific rationale will explain the importance of each step done when
assessing patient Catherine. Three, identify the type of shock that Catherine is experiencing. The

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pathophysiology of this shock and the clinical manifestation presented by Catherine that supports
that she is experiencing the type of shock identified above. Four, explain the nursing
interventions to be carried out. Prioritize the interventions giving a scientific rationale. Five,
summarize the work above.
Primary assessment
According to Olgers, Dijkstra, Drost-de Klerck, & Maaten, (2017), the ABCDE approach
is the primary assessment performed on the critically ill or injured patient. This approach helps in
early detection of life-threatening illnesses hence timely treatment/resuscitation. It provides life-
saving modalities, breaks down the complex clinical circumstances into manageable situations. It
gives a treatment guide/resuscitation guide.
A- involves the airway assessment on Catherine. This is done so as to assess the airway
patency. It should be the first one because if it gets obstructed it causes severe hypoxia which
leads to cardiac arrest. The ques used when assessing the airway are as follows; the patient's
voice, ability to communicate verbally, the breathing sounds, skin color, inspect the mouth for
obstruction and assessment of the cervical spine injury. When there is airway obstruction there is
a change in voice, the patient uses accessory muscle for breathing and they produce noisy sounds
when breathing. All the above is as a result of narrowing of the airway making it had for the air
to rush in or out (Thim, Krarup, Grove, & Lofgren, 2012). Catherine’s primary assessment
should include, inspection of the mouth, assess the breathing sounds, inspection of the skin color,
voice and communication abilities. The only significant findings on primary assessment on
airway done on Catherine is that she talks in short sentences. This indicates some aspects of
airway obstruction. To treat this, the patient’s oxygen therapy is increased.

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B-breathing is assessed through oxygen saturation, auscultation of the lungs, assessment
of the respiratory rate, inspection of use of axillary muscles for breathing and the chest symmetry
when breathing. This is done so as to detect inadequate breathing early and intervene before any
complication arises. Inadequate breathing causes inadequate tissue perfusion which can translate
to cardiac arrest. Patient Catherine presents with difficulties in breathing. She uses the accessory
muscle for breathing. She is hyperventilating, her respiration rate is 36 breaths per minute. Her
oxygen saturation is 91%. She feels pain on deep inspiration on the right lower part of the chest.
This clearly shows that she has difficulty in breathing. This means that tissue perfusion is being
compromised. The immediate intervention is oxygen therapy and treating the cause. The
breathing difficulty is as a result of sepsis. She has been started on broad-spectrum antibiotics to
treat it. The oxygen volume she is receiving has been increased (Fein, 2014).
C-circulation is assessed through capillary refill time, systolic and diastolic blood
pressure, the pulse rate, mucosal membrane and the temperature feel of the extremities. This
assessment is important as it focusses on circulation. It allows early detection of circulation
issues so as to remedy early. Patient’s Catherine blood pressure is 90/65mmHg with a heart rate
of 120beats per minutes. This pulse is weak and thready. Her skin is flushed and sweaty. Her
capillary refill is three seconds. All this indicates that there is inadequate tissue perfusion. This is
life-threatening as can cause cell death and organ dysfunction. To avoid this the patient is to be
infused with blood expanders, 0.9% normal saline. The patient is on broad-spectrum antibiotics
to treat the sepsis which is causing hypotension. The patient also needs to lie in the supine
position with her legs propped to ease venous return (Kumar et al., 2013).
D-disability is assessed through the level of consciousness. This is achieved through
AVPU method, Glasgow Coma Score, the limb movement, the pupil reflexes to light and the

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blood glucose level. This assessment is important as the unconsciousness has effects on
breathing and airway patency. Patient Catherine has a GCS of 14/15 and she is confused. Her
pupils react on light and dilate at 3mm. This indicates that the patients’ needs close monitoring
of the airway and breathing can be compromised (Barrett, Barman, & Boitano, 2017).
E-exposure is assessed through body temperature and then a head to toe physical
assessment examining signs of skin reactions, trauma, and deep venous thrombosis. This is
important as it allows early detection of hypothermia, hyperthermia, trauma, or/and allergic
reaction. Patient Catherine has a low-grade fever; exposure will help in reversing. While
exposing the patient, her dignity should be observed (Hinkle & Cheever, 2013).
Focused assessment
This is the nursing assessment of specific body systems as pertaining to the presenting
complaints. Since it is a case of circulatory shock, it is the cardivascular system that will be
thoroughly assessed. The presenting complaints in the cardiovascular system include
palpitations, difficulty breathing, chest pain, dysponea and syncope (Glynn & Drake, 2014).
On inspection, the overall appearance of the patient is noted. The patient could be
confused, sick looking or in obvious pain. Look at the chest to assess symmetry and movement
with respiration. Palor and obvious cyanosis are observed as in septic shock hypoperfuion and
hypoxia could lead to this. The hands are inspected for stigmata of cardiovascular disease such as
finger clubbing, splinter hemorrhages, nicotine stains, cyanosis, anemia, coldness or hotness of
the skin and oedema. The pulses are then measured as in septic shock the circulating volume is
relatively reduced due to vasodilation. It is measured in relation to rate, rhythm, volume, and

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character. Thee jugular venous pressure is also measured to have an indication of cardiac
function and any volume or pressure defects.The blood pressure is also measured as hypotension
is a hallmark of septic shock and also the patient was a known hypertensive.
Palpation involves location and decription of the apex beat of the heart. It is described as
displaced or not displaced from its normal position in an adult at fifth intercoastal space, mid-
clavicular line. The patient is palpated to also note any masses and skin. The apex is displaced in
heart enlargement. Also heaves and taps can be felt by the palm in heart enlargement. Catherine
might have an enlarged heart due to hypertension.
Auscultation is the final step in the examination whereby a stethoscope is used to listen to
heart sounds and over the aorta. Since the patient has suspected myocardial depression as
expected in septic shock, the quality of the heart sounds should be noted and the heart rate
charted Any added heart sounds and murmers can be described as thay point to a specific cardiac
pathology (Colledge, Walker & Ralston, 2013). One should also listen for friction rubs as this is
a common phenomena in pericarditis.
Septic shock
In order to develop septic shock, one has to develop sepsis. Sepsis is multisystem organ
dysfunction due to a response to infection in the host. it is in itself life-threatening. Septic shock
occurs in a division of those with sepsis as the infection causes circulatory insufficiency with
underlying metabolic and cellular derangements. The risk of sepsis and therefore septic is
increases in pneumonia and bacteremia but can occur following most infections including
intraabdominal infections, infections involving indwelling catheters, skin, and wound infections.

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Pathophysiology of septic shock
The pathophysiology of septic shock is a complex interplay of immune responsiveness,
inflammation, and end-organ involvement. The hallmarks of septic shock include hypotension,
vasodilation and increased endothelial permeability on a background of severe inflammation.
There is also an activation of the coagulation cascades (McConnell & Coopersmith, 2016).
Powerful initiators of this inflammatory response include lipopolysaccharide (LPS) and
endotoxins of gram-negative bacteria including E. coli, shigella etc. Another initiator is
exotoxins and superantigens released by gram-positive bacteria including S. aureus, S.
pneumonia, and H. influenza. The patient has lobar pneumonia which is commonly caused by
gram-positive bacteria hence septic shock is feasible. Lipopolysaccharide of gram-negative
bacteria binds to a binding site on macrophages as the initial stage of the inflammatory response.
The binding initiates a signal pathway that activates a proinflammatory state with the release of
powerful inflammatory mediators. Cytokines releases include interleukins-1, interleukin-2,
interleukin-6, interleukin-8, interleukin-12, tumor necrosis factor and platelet activating factor.
The interplay of this cytokines with the vessel walls and endothelium at a massive multiorgan
level causes the dramatic manifestations of sepsis. The cytokines interact with the hypothalamus
resetting the body’s thermoregulatory setting giving the patient fever. This is an important
clinical presentation as it helps differentiate septic shock from other forms of shock like
hypovolemic shock where the skin is cold and clammy unlike the hot skin of a septic shock
patient. On the endothelium, the cytokines induce nitric oxide synthesis through endothelial
damage. Nitric oxide is a powerful vasodilator hence it leads to profound vasodilation. The
endothelial regulatory mechanisms are also dysfunction so, despite high levels of circulating
catecholamines to try and offset the vasodilation, it persists hence the reduced peripheral

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resistance. Vasodilation has an important role in the pathogenesis of shock. Due to vasodilation,
the intravascular space is increased leading to a relative hypovolemia. Endothelial damage also
causes increased capillary permeability and further extravasation of fluid from the intravascular
space (Kalil, 2018).
Damage to the endothelial cell causes activation of the coagulation cascade. Damaged
endothelial cells cause neutrophil margination and platelet aggregation and by releasing tissue
factor (TF) also activate the complement pathway. Endothelial cells also express immune
receptors explaining their role in activation of coagulation. There is defective fibrinolysis
coupled with inflammation and pro coagulation leads to hemostatic derangements including clot
and end-organ damage due to ischemia. The procoagulant state leads to disseminated
intravascular coagulation (DIC) (Kalil, 2018).
Clinical manifestations
The clinical manifestations can be largely divided into three sections: signs and
symptoms of sepsis, signs, and symptoms of the specific infection and signs of specific end-
organ dysfunction.
1. Signs and symptoms of sepsis
Signs of sepsis are usually nonspecific. They include fever, fatigue, anxiety, confusion, nausea,
and vomiting. Fever is due to cytokines produced by macrophages in response to the infection
resetting the thermoregulatory control of the hypothalamus. Catherine had a fever of 38.90 C.
mental status is usually altered with anxiety, confusion, and agitation. Catherine was confused
and removed her IV line necessitating the team to suture the central line in place.
2. Signs and symptoms of the specific infection.

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With a diagnosis of lobar pneumonia on treatment, Catherine still has signs and symptoms of
pneumonia. She has a fever, difficulty in breathing as shown by the use of accessory muscles and
the high respiratory rate and chest pain which is worse on breathing meaning it is most likely a
pleuritic chest pain due to the setting of pleuritis. These symptoms can be explained by the
disease process in pneumonia that causes lung consolidation and impaired respiratory function
(Colledge, Walker & Ralston, 2013)
3. Signs and symptoms of end-organ dysfunction
Septic shock will affect virtually all organ systems as hypoperfusion is global. In the
cardiovascular system, the main sign is hypotension (Russell, Rush, & Boyd, 2018). This is due
to the massive vasodilation that increases the intravascular compartment leading to a relative
hypovolemia. The capillary endothelium is damaged losing some local regulation of peripheral
resistance, one of the determinants of blood pressure together with cardiac output. Myocardial
depression also contributes to hypotension (Bridges & Dukes 2015). It is postulated that several
factors cause myocardial depression in septic shock including ischemia due to hypoperfusion,
inflammatory cytokines, and coronary vessel dysfunction e.g. due to clots from a procoagulant
state and any underlying heart disease. Catherine developed hypotension as on presentation her
blood pressure was 140/90 mmHg but at review 6 hours later was at 90/55 mmHg. She has a
history of ischemic heart disease and is hypertensive. These are risk factors for her as she can
easily develop heart failure, myocardial infarction, and hypertension can mask the hypotensive
state of shock hence giving a false impression of severity. She also has a tachycardia of 120bpm
due to compensation as the heart tries to maintain perfusion in the setting of low intravascular
volume. Catecholamines are responsible for this reflex.

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In the respiratory system, tachypnea and hyperventilation arise. These set in as the alveoli
become hypoperfused and reduce the production of surfactant which is important in keeping
them open leading to a fall in oxygen saturation. Pulmonary capillaries leak due to direct injury
to the capillary endothelium leading to pulmonary edema and alveoli collapse (Russell, Rush, &
Boyd, 2018). This is denoted as acute lung injury or acute respiratory distress syndrome.
Breathing difficulty becomes a concern as the patient becomes unable to maintain oxygen
saturation. Catherine had a respiratory rate of 26 at presentation and 36 6 hours later both
showing higher than normal rates. She was also using accessory muscles and was short of breath.
The metabolic manifestations of hyperventilation and confusion are due to metabolic
acidosis. Due to hypoperfusion and hypoxia, tissues revert to anaerobic respiration producing
lactic acid that accumulates due to impaired renal function causing lactic acidosis. The body tries
to compensate by more excretion of carbon dioxide through hyperventilation. However,
hyperventilation can lead to overcompensation with the development of respiratory alkalosis that
gives the patient confusion (Vincent & Ferreira, 2016).
Central nervous system manifestations include altered mental status as shown by
agitation, confusion, and anxiety and ischemic events e.g. stroke. This is due to brain
hypoperfusion and hypoxia in the setting of relative low intravascular volume. Catherine was
confused and agitated, removing her IV line. Her GCS score deteriorated from 15/15 at 0130 to
14/15 six hours later.
Renal system manifestations include a low urine output. This is due to hypoperfusion and
hypotension. An acute renal failure may ensue due to severe hypoxia leading to renal ischemia.
Other mechanisms include activation of neutrophils and cytokines that have an effect on tubular

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injury. Catherine has renal injury as shown by low urine output of the only 30ml in the last six
hours.
Hematologic manifestations include bleeding tendencies and thrombosis. The
procoagulant state in sepsis leads to disseminated intravascular coagulation a complication of the
deranged coagulation system. Impaired fibrinolysis predisposes the patient to thrombus
formation leading to end organ damage including pulmonary emboli, myocardial infarction, gut
ischemia, deep venous thrombosis, and stroke.
Nursing intervention
A patient in shock regardless the specific type, the major nursing diagnosis include one,
the risk for metabolic acidosis as a result of inadequate perfusion which makes the cells to
respire anaerobically. Two, fluid volume deficit. Three, tissue perfusion inadequacy. Four, self-
care inadequacy and anxiety (Hinkle & Cheever, 2013).
The nursing care interventions aim at restoring effective tissue perfusion, maintaining the
fluid volume within the normal range, stabilizing the patient’s vitals, and keeping the patient
conscious and alert. This is achieved through, one, ensuring safe infusion of the intravenous
fluids. Two, proper drug administration. Three, increasing the oxygen volume received by the
patient per minute. Four, close monitoring of the patient’s vitals. Five, the nurse should monitor
the patient’s weight and intake and output regularly.
The nurse should ensure that patient’s safety is observed during intravenous infusion. The
medical team ordered the patient to be infused 2 liters of 0.9% normal saline. This is a volume
expander as it increases the osmotic pressure in the intravascular drawing water from the

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extracellular compartment. This helps in tissue perfusion by increasing blood volume which
increases blood pressure (Choi, Yip, Quinonez, & Cook, 2014). While infusing patient
Catherine, the signs and symptoms of cardiovascular overload should be monitored regularly.
These signs and symptoms include coughing, shortness of breath, generalized body swelling and
rapid weight gain. Early detection gives room for resuscitations (Kreimeirer, 2016).
Proper drug administration. Patient Catherine has been prescribed azithromycin 500mg.
The nurse should ensure that the ten rights of medication administration are followed. The right
medication, right dosage, right time, right route, and the right patient should be observed. When
this is observed, the drug efficiency is increased. The patient is having septic shock.
Azithromycin will help in treating the sepsis which will, in turn, reverse shock. It is therefore
important for the nurse to observe the medication rights (Rauen & Munro, 2015).
Increase oxygen therapy dosage. Initially, Catherine was receiving 2 liters of oxygen per
minute. The medical ordered the oxygen level to be increased. The aim of the nursing
interventions as mentioned earlier is to restore adequate tissue perfusion. The nurse should
increase oxygen volume being received by the patient to about 5litres per minute. This will
increase tissue perfusion as more oxygen will reach the cells (Gotts & Matthay, 2015).
The nurse should monitor the patient’s vitals regularly. This is so as to detect when the
patient condition is deteriorating. Patient Catherine is critically ill; her vitals should be monitored
every fifteen minutes. This will help in detecting changes in her condition which will allow
timely intervention. The vitals include the respiration rate, blood pressure, pulse rate,
temperature, and pain.

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The nurse should monitor Catherine’s input and output closely. The patient has shock,
which interferes with tissue perfusion to the kidneys. This causes renal insufficiency hence fluid
and wastes retention. So as to detect when renal failure sets in the nurse should monitor the
input/output of the patient. The nurse should weigh the patient regularly so as to detect fluid
retention. When renal failure is detected early, hemodialysis and reduction or halt fluid intake
can reverse this condition (Hinkle & Cheever, 2013).
Conclusion
The paper focusses on patient Catherine who has septic shock. Primary assessment and
focused assessment was done on the patient. The ABCDE approach which assesses the patient
condition in a glimpse allowing timely detection and management was done. The focused
assessment of the respiratory system was done. Details and rationales on how and why the
assessment was done have been explained above. The pathophysiology of shock and to be
specific septic shock has been explained. The manifestation of shock has been explained and
lastly, the nursing interventions have been discussed.

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