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CRITICAL NURSING RESUME

PATHOPHYSIOLOGY, PHARMACOLOGY, AND DIET THERAPY IN CRITICAL

CASES WITH DISORDERS OF SHOCK, RESPIRATORY FAILURE

Supervisor : Ns. I Made Sukarja, S.Kep.,M.Kep

By :

Group 2 / 3B Str. Nursing

Members of the group :

1. Kadek Ayu Ananda Redita Darma (03/P07120221052)

2. Kadek Ayu Willie Mirah Maheswari (04/P07120221053)
3. Ni Ketut Dyah Okpiani (17/P07120221066)
4. Ni Komang Lisa Kastari (18/P07120221067)
5. Ni Nyoman Putri Redasponi (31/P07120221080)
6. Ni Nyoman Santi Pratiwi (32/P07120221081)
7. Ni Wayan Putriasih (44/P07120221093)
8. Rista Aprilia (51/P07120221100)

MINISTRY OF HEALTH REPUBLIC OF INDONESIA

DENPASAR HEALTH POLYTECHNIC
NURSING MAJOR
 ACADEMIC YEAR 2023
A. Pathophysiology in Critical Cases with Shock Disorders
1. Definition of Shock

Shock is a life-threatening condition with various underlying causes.

Pathophysiologically shock is a circulatory disorder which is defined as a condition of
inadequate oxygen transport to tissues or perfusion caused by hemodynamic
disturbances. These hemodynamic disturbances can be in the form of decreased
systemic vascular resistance, especially in the arteries, reduced blood return,
decreased ventricular filling and very small cardiac output.(Hardisman, 2013).

Shock is characterized by inadequate tissue perfusion and if not treated

immediately will result in cell death. During shock, the body struggles to survive,
activating all of its homeostatic mechanisms to restore blood flow and tissue
perfusion. In a state of shock, systemic blood flow is insufficient to provide oxygen
and nutrients to vital cells and organs. Adequate blood flow to tissues and cells
requires several components, namely: adequate heart pump, an effective circulatory or
vascular system, and sufficient blood volume. When one of the components is
disrupted, blood flow to tissues becomes limited and inadequate, resulting in poor
delivery of oxygen and nutrients to cells, cell death, organ dysfunction, then progress
to organ failure.

2. Hypovolemic Shock

Hypovolemic shock is shock that occurs due to reduced intravascular plasma

volume. This shock can occur due to heavy bleeding (hemorrhagic), trauma that
causes fluid shifts (extravasation) to non-functional body spaces, and severe
dehydration from various causes such as burns and severe diarrhea. The most
common cases of hypovolemic shock are caused by bleeding, so hypovolemic shock
is also known as hemorrhagic shock.(Hardisman, 2013).

The most common cause is bleeding due to external trauma or occult internal
bleeding following blunt or penetrating injuries. Bleeding can also occur due to
disseminated intravascular coagulation (DIC), aortic aneurysm, intra-operative
complications, placental abruption, placenta previa, postpartum uterine atony.
Hypovolemic shock can occur due to intravascular dehydration due to loss of fluid
 from blood vessels, such as polyuria, diarrhea, nonketotic hyperosmolar
hyperglycemic coma (HHNK), diabetes insipidus, Addison's crisis, removal of
accumulated fluids through paracentesis or thoracentesis. Hypovolemic shock can
also occur due to loss of fluid volume due to displacement of fluid from blood vessels
as in burns, ascites, and pleural effusion.

The most likely to be life-threatening in hypovolemic shock comes from

decreased intravascular blood volume, which causes decreased cardiac output and
inadequate tissue perfusion. Then the anoxia tissue encourages metabolic changes in
cells to change from aerobic to anaerobic. This causes accumulation of lactic acid
which causes metabolic acidosis. When these compensatory mechanisms fail,
hypovolemic shock occurs in the sequence listed below(Dewi & Rahayu, 2020):

a. Decreased intravascular fluid volume

b. Reduced venous return, which causes a decrease in preload and stroke volume
c. Decreased cardiac output
d. Decrease in Mean Arterial Pressure (MAP)
e. Impaired tissue perfusion
f. Decrease in oxygen and delivery of nutrients to cells
g. Multisystem organ failure

Clinical symptoms of bleeding may not be seen if the lack of blood is less than
10% of the total blood volume because at this time the body can still compensate by
increasing vascular resistance and the frequency and contractility of the heart muscle.
If the bleeding continues then the body is no longer able to compensate and cause
clinical symptoms. In general, hypovolemic shock causes symptoms of increased
heart rate and pulse (tachycardia), weak pulse filling, cold skin with poor turgor, cold
extremities and slow capillary refill.

3. Septic Shock

Septic shock is shock due to severe infection in which large amounts of toxins
enter the bloodstream. Escherichia coli is a germ that often causes this shock. In
general, septic shock is invasion of the bloodstream by any organism that has the
potential to cause a general host reaction to toxins. The result is a state of inadequate
 tissue perfusion that is life threatening. Septic shock often occurs in newborns, over
50 years of age, and in people with compromised immune systems. Risk factors for
septic shock include chronic diseases (such as diabetes, blood cancer, urinary-genital
tract, liver, bile, intestine, and infections), long-term use of antibiotics, and medical or
surgical procedures (Rahmi, Upik., 2022).

The pathophysiology of septic shock is when the immune response evokes the
activation of various chemical mediators that have several effects that lead to leakage
of fluid from the capillaries. In addition, what leads to septic shock is when increased
capillary permeability leads to seepage of fluid from the capillaries as well as
vasodilation. Prior to the occurrence of septic shock, usually, it is preceded by a septic
infection. Sepsis infection can be caused by gram-positive and gram-negative
bacteria. In gram-negative bacteria, lipopolysaccharide (LPS) plays a role. On the
other hand, in gram-positive bacteria, components of the bacterial cell wall in the
form of lipoteichoic acid (LTA) and peptidoglycan (PG) are cytokine inducers.

Sepsis is a complex process of infection and inflammation initiated by endo or

exotoxin stimulation of the immune system. Furthermore, there is activation of
macrophages, secretion of various cytokines and mediators, as well as activation of
complement and neutrophils resulting in endothelial dysfunction and damage. Then,
activation of the coagulation system and platelets leads to impaired perfusion to
various tissues and multiorgan dysfunction or failure. The spread of severe gram-
negative bacterial infection has the potential to give a clinical syndrome called septic
shock. The cause of septic shock occurs due to toxins produced by certain bacteria
and due to cytokinesis (substances made by the immune system to fight an infection).
The toxins released by the bacteria can cause tissue damage and circulatory disorders.

4. Cardiogenic Shock

Cardiogenic shock is a disorder caused by a decrease in systemic cardiac

output in the presence of sufficient intravascular volume, and can result in tissue
hypoxia. Cardiogenic shock occurs when the heart fails to pump an adequate volume
of blood, and develops when the heart loses its pumping power. The main signs and
symptoms of cardiogenic shock are decreased urine output, impaired mental function,
cold extremities, increased JVP, hypotension with evidence of pulmonary and
systemic (venous) congestive (Sutjahjo, Ari., 2015).
 Mechanical complications due to acute myocardial infarction can lead to
shock. Among these complications are ventricular septal rupture, papillary muscle
rupture or dysfunction, and myocardial rupture, all of which can result in cardiogenic
shock. Meanwhile, right ventricular infarction without infarction or left ventricular
dysfunction can cause shock. Another common cause of cardiogenic shock is
recurrent tachyarrhythmias or bradyarrhythmias, which are usually the result of left
ventricular dysfunction, and can coexist with supraventricular or ventricular
arrhythmias. Cardiogenic shock may also occur as a late-stage manifestation of
progressive myocardial dysfunction, including as a result of ischemic heart disease.
and hypertrophic and restrictive cardiomyopathy.

B. Pathophysiology in Critical Cases with Respiratory Failure

Respiratory failure is a condition in which insufficient oxygen enters the blood

from the lungs. Organs, such as the heart and brain, need oxygen-rich blood to work
properly. Respiratory failure can also occur if the lungs are unable to remove carbon
dioxide from the blood. Too much carbon dioxide in the blood can harm the organs. In
respiratory failure there is an increase in arterial partial pressure of carbon dioxide
(PaCO2) greater than 50 mmHg and arterial partial pressure of oxygen (PaO2) less than
60 mmHg.

Respiratory failure can be caused by intrapulmonary and extrapulmonary

disorders. Intrapulmonary disorders include disorders of the lower airways, pulmonary
circulation, interstitial tissue, and alveolar capillaries. Extrapulmonary disorders are
abnormalities in the respiratory center, neuromuscular, pleural and upper respiratory tract.
Respiratory failure is generally caused by ventilation failure which is characterized by
CO2 retention, accompanied by an abnormal decrease in pH and decrease in PaO2.
Ventilation failure can be caused by hypoventilation due to extrapulmonary disorders and
severe ventilation-perfusion imbalance in intrapulmonary disorders.

Respiratory failure is preceded by a compensatory stage. In this condition, there is

an increase in work of breathing which is characterized by respiratory distress (use of
additional respiratory muscles, retraction, tachypnea and tachycardia). An increase in
respiratory effort occurs in an effort to maintain airflow even though lung compliance
decreases. Conversely, the decompensated stage appears later, characterized by decreased
respiratory effort.
 Pathophysiology of respiratory failure can be differentiated based on the type of
respiratory failure, namely hypoxemia and hypercapnia. Respiratory failure
typeHypercapnia occurs in extrapulmonary disorders. In this type of hypercapnic
respiratory failure, there is a decrease in airflow between the atmosphere and the lungs
without abnormalities in gas exchange in the lung parenchyma. Thus an increase in
PaCO2 will be obtained. Ventilation failure in patients with pulmonary disease occurs as
follows: some alveoli experience a decrease in ventilation relative to perfusion, while
some have an increase in ventilation relative to perfusion. Initially, areas with low
ventilation can be compensated with areas with high ventilation so that there is no
increase in PaCO2. But if the ventilation imbalance is getting worse, the compensatory
mechanism fails resulting in ventilation failure which is characterized by an increase in
PaCO2. Meanwhile, hypoxemic-type respiratory failure occurs in intrapulmonary
disorders and is not caused by extrapulmonary causes. The mechanism of hypoxemia is
caused by ventilation-perfusion imbalance, whereas diffusion disorders may be a co-
factor, not the dominant factor.

C. Pharmacology in Critical Cases With Shock Disorders

1. Pharmacology in critical cases with hypovolemic shock disorder
In cases of hypovolemic shock (shock due to decreased blood or fluid volume), drugs
are not used to correct hypotension. Administration of fluids or blood products or both
is the only acceptable way to treat hypovolemic shock.
2. Pharmacology in critical cases with septic shock disorder
If resuscitation fails to restore blood pressure to normal, pharmacologic measures to
increase blood pressure are needed. The target mean arterial pressure is between 60
and 65 mmHg. Blood pressure measurement is important to evaluate overall perfusion
based on SpO2, urine output, and resolution of increased arterial lactate. Because
adrenergic receptor function is decreased in sepsis, the required pressor dose is higher
than the others.
a. Dopamine and norepinephrine are the most commonly used pressors for the
treatment of septic shock. Dopamine is the direct precursor of endogenous
norepinephrine. At lower doses (2-5µg/kg per minute), dopamine increases
cardiac contractility and cardiac output without increasing heart rate, blood
pressure, or systemic vascular resistance. Renal blood flow and urine output
increase at doses of 0.5–2 µg/kg per minute as a result of selective stimulation of
 dopaminergic receptors. When the dose reaches 10µg/kg per minute, dopamine
has a chronotropic effect and an inotropic effect. Metabolic effects of dopamine
administration include decreased aldosterone secretion, inhibition of thyroid
stimulation, release of hormone and prolactin, and inhibition of insulin secretion.
Because it increases cardiac output, Dopamine can increase pulmonary shunting
by increasing flow to poorly ventilated areas of the lung. After ensuring adequate
fluid resuscitation, dopamine infusions are usually started at 5 µg/kg per minute
and continued until blood pressure improves. Epinephrine is used, in low doses,
to support blood pressure by its vasoconstrictive effect.
b. Dobutamine has a predominant β-adrenergic inotropic effect, with a relatively
small chronotropic effect resulting in a smaller increase in heart rate and
peripheral vascular resistance. Dobutamine tends to lose its hemodynamic effects
after prolonged administration, possibly due to receptor downregulation.
However dobutamine is a better choice for long term infusion.
c. Alpha-adrenergic agents, phenylephrine and norepinephrine are needed if, after
resuscitation and increased cardiac output, blood pressure remains depressed.
both agents increase systemic vascular resistance. In low doses, epirephrine has a
main β-adrenergic effect, which increases cardiac contractility, conduction
velocity, and heart rate. At higher doses, both α- and β-adrenergic effects occur,
which include peripheral vasoconstriction, increased cardiac contractility,
cardiac work, and stroke volume. Norepinephrine causes splanchnic
vasoconstriction which can lead to organ ischemia.
d. The antidiuretic hormone vasopressin, normally released by the hypothalamus,
produces vasoconstriction of vascular smooth muscle. At low concentrations it
causes vasodilation of coronary, cerebral and pulmonary vessels. Vasopressin
levels rise early and then fall as sepsis worsens. When administered in doses of
0.01–0.04 units/min, vasopressin infusion increases serum vapressin levels and
reduces the need for other vasopressors. At these doses, urine output may
increase, and pulmonary vascular resistance decreases. Doses higher than 0.04
units/min can cause unwanted vasoconstrictive effects.
3. Pharmacology in critical cases with cardiogenic shock disorders

Once volume status is optimized, drugs to increase myocardial performance are

required.
a. Dobutaine is the inotropic drug of choice for the management of congestive
heart failure and cardiac arrest. At moderate doses (5-10 µg/kg per minute)
dopamine improves cardiac function and increases blood pressure without
increasing myocardial oxygen consumption. At higher doses (>10 µg/kg per
minute) dopamine increases systemic vascular resistance by stimulating α-
adrenergic receptors and increases heart rate by stimulating β-adrenergics. An
average dose of 17 µg/kg per minute is required to optimize coronary perfusion
pressure in patients with cardiogenic shock after myocardial infarction.
Dopamine at these doses increases myocardial oxygen demand resulting in
tachycardia, and can limit renal perfusion.
b. Digoxin has an inotropic effect, given only when atrial fibrillation occurs with
a rapid ventricular response. Intravenous digoxin in small doses can increase
diastolic filling time and increase cardiac output.
c. Norepinephrine at low doses causes beta stimulation of the heart and increases
blood pressure and cardiac output. At higher doses, it affects alpha adrenergic
receptors and increases blood pressure by increasing systemic vascular
resistance. At higher doses it also tends to produce tachycardia, arrhythmias,
and peripheral visceral ischemia.
d. Glucagon increases cardiac contractility and decreases peripheral vascular
resistance. A test dose of 4-6 mg should be given intravenously to determine if
an effect is produced. If successful, continue with constant infusion of 4-12
mg/hour. Glucagon is useful in the treatment of cardiogenic shock and left
ventricular failure. But it has a side effect of hyperglycemia.
e. Vasolidator drugs, used to reduce left ventricular afterload, which reduces
myocardial oxygen consumption. Its use is limited because of its hypotensive
effect, which can compound the difficulties associated with peripheral oxygen
delivery. Nitroprusside is started at 5-10 µg/min and increased in increments of
2.5-5 µg/min every 10 minutes until heart rate increases and the dose should be
reduced if systolic blood pressure falls below 90 mm Hg. Doses above 3
µg/min can cause toxicity especially if the drug is used for more than 3 days
which causes anaerobic metabolism and increased lactate.
f. The nitrate derivative nitroglycerin reduces preload, which reflexively reduces
left ventricular filling. Besides that, it has the effect of dilating coronary blood
vessels and is the drug of choice when cardiogenic shock is caused by
 ischemia. Can cause hypovolemia, because it increases venous capacity,
decreases venous return and further decreases cardiac output. The normal
starting dose is 10 µg/min, which may be increased by 10 µg/min every 5-10
minutes up to a total dose of 50-100 µg/min.
D. Pharmacology in Critical Cases with Respiratory Disorders

According to(Volta, Hanafi, & et al, 2022)Pharmacological therapy for clients with
respiratory failure can be given by administering drugs in the following ways:

1. Bronchodilators
Bronchodilators are inhaled drugs that are often used to help widen the airways by
causing bronchial smooth muscle relaxation in bronchospasm patients. According
to(Rasmawati & Hartawan, 2017)Bronchodilators can be further divided into
sympathomimetic drugs (β-adrenergic agonist drugs) and parasympatholytic drugs
(anticholinergic drugs).
a. Adrenergic agonist
The adrenergic agonists used to treat bronchospasm, wheezing, and airflow
obstruction are β-adrenergic agonists. Clinical uses of β-adrenergic agonists are
usually administered via inhalers or nebulizers, are β2 selective and are divided
into short-acting and long-acting therapies. Short acting β2 agonist therapies
called SABAs (short acting beta-2 agonists) are effective for relieving wheezing,
airflow obstruction and they are prescribed for bronchospasm caused by COPD,
bronchial asthma, or emphysema. Long acting β2 agonists or what are called
LABA (long acting beta-2 agonists) are used for maintenance therapy to improve
lung function and reduce symptoms and the risk of an attack.
Short-acting β2 agonists such as albuterol, levalbuterol, metaproterenol, and
pirbuterol have an onset of action within minutes and a duration of action of 4-6
hours, so they are intended as a relief or savior therapy for the symptoms of
bronchospasm and other airway obstructions, which can threaten the patient's
life.
Long acting β2 agonists have the same mechanism, but have a longer duration
of action. This is related to drug binding with receptors that can last longer and is
indicated as a maintenance treatment of bronchoconstriction in patients with
COPD, chronic bronchitis, and emphysema. Long acting β2 agonists include
salmeterol, formoterol, and arformoterol.
 b. Inhaled Choligergic Antagonists

Anticholinergics are commonly used for maintenance therapy or control

therapy and acute attack therapy in obstructive airways diseases. The
parasympathetic system plays a major role in regulating bronchomotor tone and
inhaled anticholinergics act on muscarinic receptors in the airways to reduce
muscle tone. The use of inhaled anticholinergics in COPD cases as maintenance
and treatment of acute attacks has been considered as standard therapy. In the
case of anticholinergic asthma, it is recommended to treat acute attacks only.

There are two inhaled anticholinergics specifically approved for the

treatment of obstructive airways disease, namely:

 Ipratropium
Ipratropium is classified as a short-acting anticholinergic which is usually
used to treat COPD (acute attack and maintenance) and asthma (acute
attack). Patients treated with ipratropium experienced increased exercise
tolerance, decreased shortness of breath, and improved ventilation.
 Tiotropium
Tiotropium is classified as a long-acting anticholinergic that can be given
as maintenance therapy in COPD. The use of tiotropium can reduce the
occurrence of attacks/acute exacerbations of COPD, respiratory failure,
and other causes of mortality.
2. Corticosteroids

Corticosteroids are anti-inflammatory glucocorticoids that are used primarily

for asthma patients, but may also be used in COPD (especially for patients with
severe COPD and frequent exacerbations). Corticosteroids inhibit many cells involved
in the inflammatory response (such as eosinophils, T lymphocytes, mast cells, and
dendritic cells and help increase the diameter of the airways by reducing swelling. By
inhaling these drugs, patients minimize their many systemic side effects, which can
include hypothalamic, pituitary, and adrenal gland suppression; osteoporosis; mood
swings; fluid retention; hypertension; increased white blood cell count and normal
differential shift, cushingoid appearance, and growth restriction.
Nonetheless, some side effects are associated with inhaled steroids. These
include oral candidiasis, hoarseness and voice changes, and coughing. This problem
 can be minimized through the use of a spacer with a metered-dose inhaler (MDI),
along with brushing and rinsing to help reduce drug residue in the oropharynx after
using inhaled medications. Recently developed inhaled steroids provide long-term
drug protection that do not require the patient to take multiple puffs of the inhaler,
helping to improve adherence. Fluticasone, budesonide, and most recently
mometasone have become popular as effective steroids that reduce the number of
puffs needed; mometasone, for example, can be effective for some patients using just
one puff of 220 µg at night.
3. diuretic

According to drugs - diuretic drugs can be given if there is left or right heart
failure. The dosage and method of administration depend on the clinical condition of
each client. Generally given 20 mg Furosemide intravenously and can be repeated
every 30 minutes until the diuretic is reached or stopped as needed or when side
effects occur.

4. Sedation and analgesia

Sedation is necessary in many patients to help maintain adequate ventilation.
And can be used to calm the patient and reduce the work of breathing. Analgesia
should be administered to control pain and anxiety in the patient.
5. Neuromuscular blocking agent
Neuromuscular blocking agentIt is frequently used in anesthesia to facilitate
endotracheal intubation, optimize surgical conditions, and assist mechanical
ventilation in patients with reduced pulmonary compliance. Neuromuscular blocking
agents (NMBAs) come in two forms: depolarizing neuromuscular blocking agents
(eg, succinylcholine) and nondepolarizing neuromuscular blocking agents (eg,
rocuronium, vecuronium, atracurium, cisatracurium, mivacurium). The class of
NMBA used to achieve neuromuscular blockade must be chosen carefully based on
patient factors, type of procedure performed, and clinical indications.
E. Diet Therapy In Critical Cases With Shock Disorders

1. Fluid Therapy
The most common initial treatment for critical cases with shock disorders is fluid
therapy. Fluid therapy is a therapeutic option that can be used for the successful
management of critical patients with shock disorders. Fluid therapy aims to maintain
circulation or control adequate fluid and electrolyte balance in patients who are unable
to control fluid balance in their bodies, so as to create beneficial outcomes for the
patient's condition. In implementing advanced life support, an important step that can
be carried out simultaneously with other initial steps is drug and fluid treatment. In
patients who experience significant fluid loss such as shock, these initial steps can
save the patient.
a. Fluid Therapy in Patients With Hypovolemic Shock
In hypovolemic shock, administration of fluids aims to expand
intravascular volume and restore venous return. The initial fluids that can be
given are isotonic fluids (normal saline and Ringer's lactate) which are
warmed by 1-2 L for adults and 20 ml/kg for pediatric patients. This type of
fluid provides transient vascular expansion and further stabilizes vascular
volume by replenishing fluid losses in the interstitial and intracellular spaces.
Rapid fluid resuscitation is the mainstay of therapy in hypovolemic
shock. Fluids are administered at a rate sufficient to rapidly correct the deficit.
In younger patients, maximum infusion can usually be given. But in patients
who are older or who have a history of heart disease, the infusion should be
slowed after the expected response to prevent complications of hypervolemia.
Two or more catheters are required for rapid fluid replacement and restoration
of hemodynamic instability. Intravenous fluids are infused at high rates until
the systolic blood pressure or CVP rises to optimal levels or until there is
improvement in the patient's clinical condition. Infusion of lactated Ringer's
solution is useful initially because it approximates plasma electrolyte
composition and osmolality.
The goal of resuscitation in a patient with hypovolemic shock is to
restore perfusion to the target organs. This is achieved by using resuscitation
fluids and blood products to replace lost intravascular volume. However, keep
in mind that if the blood pressure rises too quickly before the bleeding can be
controlled, more severe bleeding can result. Target MAP below 60-75 mm Hg
is still acceptable in patients with acute bleeding without overt neurological
disorders with the aim of reducing blood loss and coagulopathy until bleeding
can be controlled.
Blood transfusion may be considered in patients with ongoing bleeding
and a hemoglobin level <10 mg/dl. Resuscitated patients generally develop
 coagulopathy due to the absence of clotting factors in the crystalloid solution
and PRC administered during resuscitation.
b. Fluid Therapy in Patients with Septic Shock
Severe septic and septic shock are disorders that are often faced by
clinicians in the ICU. Patients with severe sepsis and septic shock generally
experience a decrease in the effectiveness of the arterial circulation due to
vasodilation along with impaired cardiac output. The management of septic
shock uses comprehensive management to improve outcomes, namely the
EGDT (Early Goals Directed Therapy) protocol. The EGDT protocol starts
with initial fluid resuscitation in patients with septic shock using Crystalloid,
the patient is given a 500-1000 mL fluid bolus. Because of the extent of
massive peripheral vasodilatation, the patient requires large amounts of fluids.
A central venous pressure catheter is performed to guide therapy.
Volume bolus administration should be titrated to maintain central venous
pressure between 8 and 12 mm Hg. If a pulmonary artery flotation catheter is
used, it is necessary to increase the PCWP to a higher-than-normal level
before adequate cardiac output and blood pressure are achieved. Ongoing
capillary leak requires aggressive fluid replacement. The infusion should be
monitored for signs of pulmonary edema and congestive heart failure.
The choice of resuscitation fluid in septic shock is still a controversial
topic. Crystalloids tend to be less expensive, rapidly fill the intravascular and
extravascular compartments, increase target organ perfusion, and have a
minimal risk of anaphylactoid reactions. While colloids rapidly increase
intravascular volume and oncotic pressure, resuscitation can thus require less
time and fluid volume. Resuscitation with colloids can increase oxygen
transport, myocardial contractility, and cardiac output. However, several
studies have shown that HES, which is a type of colloid, increases the risk of
death and the need for renal replacement therapy compared to the use of
crystalloids.
c. Fluid Therapy in Patients With Cardiogenic Shock
When cardiogenic shock results from acute myocardial infarction,
initial efforts should be directed at controlling the extent of infarction. Fluid
therapy remains the way to go, although cardiogenic shock can occur in
patients who are fluid overloaded, and may also be hypovolemic. If the PCWP
 is less than 10-12 mm Hg, balanced saline should be administered in an
attempt to increase the filling pressure. Cardiac output should be measured
after every 2-3 mm Hg change in PCWP. Filling pressures approaching 20 mm
Hg may be required before cardiac output increases. If laboratory tests show
that the patient is hypoxemic, supplemental oxygen should be administered.
Intubation with PEEP may be necessary, if pulmonary edema is present, but
should be considered, as it adversely affects preload and cardiac output.
2. Low Salt Diet
This diet can be used as a form of prevention of cardiogenic shock. The following
modifications are made to the normal diet:
a. Salt is used in minimal amounts (no more than ½ teaspoon or 2grams a day) in
cooking time
b. Consumption of cow's milk should be limited and no more than 500 ml per
day. If possible, replace cow's milk with vegetable milk, such as soy milk,
which contains very little sodium
c. The following foods should also be avoided: salty foods, pickled vegetables
and fruits, various flavoring additives (salt, cooking spices, baking soda, soy
sauce, ketchup etc.),
d. To overcome the bland taste on a low salt diet, it is recommended to use spices
that do not contain sodium such as sugar, vinegar, shallots, garlic, ginger,
turmeric and salam.
3. Restricted Low Fat Diet
A number of studies comparing populations in various parts of the world have shown
that high blood cholesterol levels are one of a number of factors associated with an
increased incidence of coronary heart disease that can lead to cardiogenic shock.
Reducing blood cholesterol levels is possible by reducing the consumption of animal
fats. Consumption of cholesterol every day can be controlled by:
a. Limiting eating egg yolks, especially domestic chicken eggs (broiler) have a
high fat cholesterol content. It is better to choose free-range chicken eggs and
the amount of red eggs eaten does not exceed two eggs per week. Egg whites
are eaten freely
b. Replace the habit of full cream milk with skim milk or soy milk
c. Food should be boiled or sautéed in a little oil. The use of thick coconut milk
should also be avoided (warm, curry, curry)
 d. Fish can be eaten as a substitute for meat if you like it. White-fleshed fish have
a low fat content.
e. Avoid foods that are rich in cholesterol (brain and internal organs such as liver,
kidney, intestine and tripe, Lapis legit, tarcis, pastries, fried foods)

F. Diet Therapy in Critical Cases with Respiratory Failure

1. Oxygen Therapy
Oxygen therapy which can be defined as treatment that provides you with extra
oxygen for your body to work properly will be given in the face of respiratory failure.
Since respiratory failure is divided into two types, so the oxygen given to each of
them is different accordingly. Oxygen therapy is given through mechanical
ventilation which can be further divided into two, invasive ventilation and non-
invasive ventilation.
a. Invasive Ventilation
Mechanical ventilation requires an interface between the patient and the
ventilator. In the past, this always occurred via an endotracheal tube or
tracheostomy, but there is a growing trend towards noninvasive ventilation,
which can be achieved using either a full face mask (which covers the nose and
mouth) or a nasal mask. Endotracheal tube care includes correct tube placement,
maintenance of proper cuff pressure, and suctioning to maintain a patent airway.
After intubation, tube position in the airway (not the esophagus) should
be confirmed by auscultation of the chest and, ideally, by a carbon dioxide
detector. As a general rule, the endotracheal tube should be inserted to an
average depth of 23 cm in males and 21 cm in females (measured at the incisor
tooth). Confirming proper placement of the endotracheal tube with a chest
radiograph is recommended. The tube must be secured to prevent accidental
extubation or migration into the mainstem bronchus, and the endotracheal tube
balloon pressure must be monitored periodically. The pressure in the cuff should
generally not exceed 25 mm Hg. Endotracheal suctioning can be achieved
through either open circuit or closed circuit suction catheters. Routine suctioning
is not recommended, as suctioning may be associated with a variety of
complications, including desaturation, arrhythmias,
b. Non Invasive Ventilation
 Supportive ventilation via a nasal or full face mask rather than via an
endotracheal tube (see image below) is increasingly being used for patients
with acute or chronic respiratory failure. Noninvasive ventilation should be
considered in patients with mild to moderate acute respiratory failure. The
patient must have an intact airway, airway-protective reflexes, and be alert
enough to follow commands.
In a large randomized trial comparing NPPV with a standard ICU
approach, use of NPPV was shown to reduce complications, duration of ICU
stay, and death. In patients whose NPPV failed, mortality was similar to that of
the intubated group (25% vs 30%). In acute hypoxemic respiratory failure,
NPPV also helps maintain an adequate PaO2 until the patient improves.
Cardiogenic pulmonary edema, NPPV increases oxygenation, reduces the work
of breathing, and can increase cardiac output.
When applied continuously to patients with chronic ventilation failure,
NPPV provides sufficient oxygenation or elimination of carbon dioxide to
sustain life by reversing or preventing atelectasis or resting the respiratory
muscles.
2. Diet Therapy
The diet in patients with respiratory failure is as follows:
A high-calorie, high-protein diet is a diet that contains energy and protein above
normal requirements. The diet is given in the form of liquid food plus high protein
source foods such as milk, eggs and meat.
a. Dieting goals:
The goals of a high-calorie, high-protein diet are:
1) Meet the increased energy and protein needs to prevent and reduce damage to
body tissues
2) Add BB to reach normal BB
3) Giving excessive energy to patients with respiratory disease can increase the
metabolic rate so that the pattern of consumption of oxygen and carbon
dioxide,
b. Dietary Requirements:
The requirements for a high-calorie and high-protein diet are:
1) High in calories, namely 40-45 kcal / kg BW
2) High in protein, namely 2–2.5 grams/kg BW
 3) Adequate fat, namely 10-25% of keb. Total energy
4) Adequate carbohydrates, namely the rest of keb. Total energy
5) Vitamins and minerals are sufficient according to keb. Normal
6) Food is given in easily digestible form
c.According to the situation, the patient can be given one of two types of high-
calorie, high-protein diets as follows:
1) High protein high calorie diet I: 2600 kcal energy/calories, 100 g protein
(2g/kg BW)
2) High protein high calorie diet II: 3000kcal energy, 125 g protein (2.5g/kg
BW)
d. Recommended and not recommended ingredients:
1) Sources of carbohydrates:-Rice, bread, noodles, macaroni and processed
flour Sources of protein: Beef, chicken, fish, eggs, milk, cheese and yogurt
It is not recommended to cook with oil/condensed coconut milk
2) Vegetable protein sources are all legumes such as tempeh, tofuIt is not
recommended to cook with oil / thick coconut milk
3) Vegetables: All types of vegetables, especially spinach, beans, cassava
leaves, long beans, chayote, carrots, boiled/steamed.
It is not recommended to cook with oil / thick coconut milk.

e. When dealing with patients with respiratory problems, it is better to give them
a liquid diet. The type of food given depends on the patient.Liquid food is
given to patients who have problems chewing, swallowing, or digesting solid
food, for example mouth or throat surgery or decreased consciousness. This
food can be given orally or NGT.
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