Detailed Analysis of Heart Failure, Asthma, Shock, and Sepsis

This assignment comprehensively covers the pathophysiology, clinical features, and management of several critical medical conditions, including heart failure, asthma, various types of shock (hypovolemic, cardiogenic, neurogenic, and septic), sepsis, and multi-organ dysfunction syndrome (MODS). It delves into the mechanisms of heart failure, exploring concepts like preload, afterload, cardiac output, and the Frank-Starling law, as well as the renin-angiotensin-aldosterone system (RAAS). The asthma section discusses airway resistance, ventilation, and the role of inflammatory mediators, alongside management strategies including beta-2 agonists and corticosteroids. The shock section details the stages of shock and its management. The sepsis section defines sepsis, septic shock, and MODS, examining the roles of inflammatory mediators and organ dysfunction. The assignment also includes diagnostic tools, pharmacological interventions (e.g., diuretics, ACE inhibitors, antibiotics), and clinical manifestations. It emphasizes the importance of early recognition, fluid resuscitation, and supportive care in managing these complex and life-threatening conditions.

1. Heart failure pathophysiology
Congestive Cardiac Failure - “Heart failure is a complex
clinical syndrome that is frequently, but not exclusively,
characterised by an underlying structural abnormality or
cardiac dysfunction that impairs the ability of the left ventricle
(LV) to fill with or eject blood, particularly during physical
activity. Symptoms of CHF can occur at rest or during physical
activity.
CCF is the inability of the heart to maintain an output, at rest or
during stress, necessary for the metabolic needs of the body.
End Diastolic Volume (EDV) - The amount of blood returning
to the heart and filling the ventricle
End Systolic Volume (ESV) - The volume of blood that
remains in the ventricle at the end of systole
Stroke Volume (SV) - Volume of blood pumped out of the
heart by the left ventricle with each beat (measured in mL), Not
all the blood that is in the ventricle is ejected, usually just over
half or 1mL/kg.
SV= EDV-ESV
=120mL/beat- 50 mL/beat
=70 mL/beat
Preload - The amount of blood at the end of diastole prior to
contraction AND A measure of the degree of the ventricular
stretch at the end of diastole prior to contraction (is influenced
by the factors just prior to ventricular contraction and is
determined by the end-diastolic volume (and the associated
end-diastolic pressure).

Contractility - Ability of the myocardial fibres to shorten or
contract when loaded. Determines the force of contraction
Afterload - The force which the ventricle must overcome to eject blood.
The resistance to the ejection of blood from the left ventricle. E.g.
Systemic Vascular Resistance (SVR)
Cardiac Output (CO) - The amount of blood pumped around the body in one
minute.
CO = SV x Heart Rate (HR)
E.g for a healthy person weighing 70kg SV 70mL x HR 70bpm = CO 4.9L/minute
Frank-Starling law of the heart - ↑ stretch= ↑cardiac output, more
volume (blood) in the left ventricle increases the stretch of the cardiac
myocytes, which will increase the force of contraction
Ejection Fraction (EF) - Percentage of blood the left ventricle pumps
out with each contraction OR blood ejected during systole.
E.g. In a healthy person weighing 70kg, Normal End Diastolic Volume
(EDV) is about 120mls and SV 70mls the EF is 58%
Normal EF is 55-70%
Causes of HR: disorders that increase the workload of the heart and
disorders that interfere with the pumping ability of the heart.
When RASS is activated, the JUXTA GLOMERULAR cells in the
kidneys produce RENIN which converts to
ANGIOTENSINOGEN in the liver to ANGIOTENSIN 1.
ANGIOTENSIN 1 is then converted to ANGIOTENSIN 2 using the
enzymes called Angiotensin-converting enzyme (ACE).

Angiotensin 2 now stimulates the adrenal cortex to produce
ALDOSTERONE. It also stimulates the PITUITARY GLAND to
produce anti-diuretic hormone (ADH). Both of these INCREASE
the reabsorption of sodium water. This increases the
reabsorption of the BLOOD VOLUME and the cardiac output.
Renin Angiotensin Aldosterone (RAAS) is one of the
compensatory mechanisms in early stages of heart failure.
RAAS causes - increased reabsorption of sodium and water.
Stroke volume can be calculated using: End-diastolic volume
and end-systolic volume.
Increased venous return is caused by stimulation of: Alpha
receptors
* Read Module 2 download Part 2
2. Heart failure clinical features and management
Decreased contractility causes left heart myocardial damage
releasing B-NATRIUERETIC PEPTIDE from the atria. This
reduces the EJECTION FRACTION of the left ventricle. Blood
backs up into the pulmonary circulation using an increase in
PULMONARY VENOUS PRESSURE. This causes an increase
in the HYDROSTATIC PRESSURE which causes the fluid to
move into the interstitial space. This results in PULMONARY
EDEMA. This DECREASES the gas exchange. Hypoxia is
sensed by CHEMORECEPTORS sending signals to the
respiratory centre in the medulla oblongata which in turn
INCREASES the respiratory rate.

Blood back up in the inferior vena cava can result in:
Hepatomegaly
Crackles in the lungs are typically due to fluid in this space:
Interstitial
Inability to breathe in supine position is called: Orthopnoea
Congestion in the superior vena cava can result in distension of
this vein: Jugular
ECHOCARDIOGRAM is the most useful investigation to
determine heart failure.
FRUSEMIDE is a common loop diuretic used in patients with
heart failure.
CAPTOPRIL is an example of an ACE inhibitor used for heart
failure.
DIGOXIN is a cardiac glycoside used in heart failure.
Daily weighs are used to adjust the dosage of
FRUSEMIDE/DIURETIC medication administered in heart
failure.
Side effects of DIGOXIN toxicity is: DYSRYTHMIAS.
HYPERKALEMIA is a side-effect of ACE inhibitor group of
medications.

* Read Module 2 download Part 3
Read Module 2 download Part 4
3. Asthma pathophysiology
Elastic recoil is the tendency of the lungs to return to the
resting state after inspiration, in a similar way that an elastic
band springs back into place after being stretched.
Compliance is the measure of lung and chest wall distensibility
(stretchiness) and is defined as volume change per unit of
pressure change.
Airway resistance is determined by the length, radius and
cross-sectional area of the airways and density, viscosity and
velocity of the gas (Poiseuille's law).
Ventilation is the mechanical movement of gas or air into and
out of the lungs.
Tidal volume: The amount of gas inspired or exhaled each
breath
Partial pressure: is directly proportional to the percentage of
that gas in the mixture of gases
The partial pressure of arterial oxygen is less than the partial
pressure of arterial carbon-dioxide in deoxygenated blood
entering the lungs for gas exchange. True

Decreased level of oxygen at the tissue level is called
hypoxemia. False
In a normal lung the ventilation perfusion ratio will be 4:5. True
Mast cells _____ to release histamines, leukotrienes, and
prostaglandins. Degranulate
These predominantly release cytokines and leukotrienes in
asthma. Eosinophils
Cell-mediated immune response is also called Type 1 _____.
Hypersensitivity
The effect of inflammatory mediators on the bronchus causes
_____. Bronchoconstriction
The functional unit of lungs: Alveoli
The oxygen haemoglobin dissociation curve shifts in asthma
towards the: right.
The cause of mucosal oedema can be attributed to which of the
following factors: leukotrienes, histamines, prostaglandins
Wheezing occurs due to: Inability of air to move in and out
through obstructed passage.

4 Asthma management and acute respiratory
failure
Beta 2 agonists ACTIVATES Beta 2 adrenergic receptors. They
couple with G protein and adenylyl cyclase and increase the
levels of intracellular CYCLIC ADENOSINE MONOPHOSPHATE
which RELAXES the smooth muscles. This will result in
bronchodilation. The most common side effects are: TREMORS
and PALPITATION.
TYPE 2 – HYPERCAPNIA is found in respiratory failure.
As a result of bronchial inflammation, airflow resistance
INCREASES.
As a result of lung injury, surfactant production DECREASES.
TYPE 1 – High concentration of oxygen should be administered
in TYPE 1 respiratory failure.
Which of the following reduces inflammation of the airways?
HYDROCORTISONE
Endothelial damage in lung injury can result in: PULMONARY
OEDEMA
Silent chest occurs in: acute life-threatening asthma
5. SHOCK
Shock is the clinical condition of organ dysfunction resulting
from an

imbalance between cellular oxygen supply and demand. It can
be defined
as a level of oxygen delivery that fails to meet the metabolic
requirements
of the tissues.
Impaired oxygen delivery to the tissues results in ANEROBIC
metabolism.
In a state of shock, the cellular metabolism only produces TWO
ATP from one molecule of glucose compared to the normal 38
ATP molecules.
Shock is a state of organ dysfunction resulting from supply and
demand issue of OXYGEN.
Vasodilation occurs in Obstructive type of shock. False
HYPOVOLEMIC shock results in “third spacing”. True
PULMONARY EMBOLISM is an example of Cardiogenic shock.
False
Stages of Shock
Initial - anaerobic metabolism and lactic acidosis are evident
due to
decreased oxygen delivery and increased carbon dioxide
retention.
Compensatory (reversible) - the neurochemical responses are
triggered, clinical signs and symptoms of shock are present.
Progressive - stage occurs when the body’s attempt to return to

homeostasis fails
Refractory - is the final stage of shock and is irreversible. At this
point, cellular damage leads to necrosis.
Management priorities of shock includes: recognize the shock
early, restore oxygen and identify the type of shock.
HYPOVOLEMIC SHOCK can result to: burns, trauma, and
gastrointestinal bleeding.
A common medication used in the management of anaphylactic
shock is: ADRENALINE
The modified TRENDLENBERG position is used in the
management of: NEUROGENIC SHOCK
The organ dysfunction in earlier stages of shock is reversible by
using: SUPPLEMENTAL OXYGEN
6. SEPSIS
Systemic Inflammatory Response Syndrome
(SIRS) is a systemic inflammatory response to a variety of
insults
• infection
• ischemia
• Infarction
• injury
Generalised inflammation in organs remote from the initial
insult

characterises SIRS
* Read Module 6 Sepsis Part 1 download
SEPSIS is defined as dysregulated host immune response to
infection.
When SEPSIS progresses, it can lead to SEPTIC SHOCK.
Sepsis is suspected when the bacteria is SOFA SCORE greater
than two.
SEPSIS is due to FUNGAL infections are common in
immunocompromised patients.
Common group of bacteria leading to sepsis from intravascular
catheters is: STAPHYLOCCUS AUREUS
Septic shock is suspected if serum lactate level is over 2
mmol/L despite fluid resuscitation.
Tissue plasminogen activator is blocked due to damage of the:
ENDOTHELIUM
Inflammatory mediators in sepsis cause: VASODILATION
Organ failure in sepsis is because of: HYPOPERFUSION
Disseminated intravascular coagulopathy is due to alteration in
the pathway of: COAGULATION

Sepsis is a type of distributive shock. TRUE
Stimulation of MAST CELLS release all: histamines, leukotrienes
and cytokines.
Except PLASMIN.
ENDOTOXIN is a toxic substance released by: GRAM NEGATIVE
BACTERIA
Decreased tissue factor activates the coagulation pathway in
Sepsis: FALSE
APOPTOSIS can occur in sepsis. TRUE
SEPSIS - is a life-threatening organ dysfunction caused by a
dysregulated host response to infection.
SEPTIC SHOCK – a subset of sepsis in which underlying
circulatory and cellular/metabolic abnormalities lead to
substantially increased mortality risk.
* Read Module 6 Sepsis Part 3 download
Sepsis diagnosis and clinical features.
VASODILATION results in profound hypotension in sepsis.
NON-CARDIOGENIC PULMONARY EDEMA results from interstitial
fluid extravasation

ENDOTHELIAL DAMAGE results in acute kidney injury in sepsis.
HEPATIC ENCEPHALOPATHY occurs due to SEPSIS induced liver
failure.
Inflammation, shortened red blood cells survival, and
haemolysis or destruction of blood cells in the setting of DIC in
severe sepsis contributes to ANEMIA in patients.
Cytokine mediated lung injury results in ACUTE RESPIRATORY
DISTRESS SYNDROME.
* Module 6 Sepsis Part 4 download
Haematological manifestations in sepsis results in all except:
POLYCYTHEMIA
The manifestations are: thrombocytopenia, anaemia and
disseminated intravascular coagulopathy
Patients with sepsis induced hepatic dysfunction can present
with: CONFUSION
SEPSIS is an example of hypovolemic shock: FALSE
SEPTIC shock is reversible: FALSE

EMPIRICAL BROAD-SPECTRUM ANTIBIOTICS are administered in
suspected SEPSIS: TRUE
30ml/kg IV fluids should be administered immediately to
patient’s on recognising sepsis. TRUE
Antibiotics needs to be administered after blood cultures have
been obtained for septic screening. False
Sepsis can lead to altered MENTAL STATUS. True
7. MULTI-ORGAN DYSFUNCTION
MODS is the failure of two or more organ systems, unable to
maintain homeostasis without intervention.
* Watch SHOCK AND SEPSIS, MEdCram video.
Acute lung injury in MODS results from: HYPOXEMIA
Massive systematic vasodilation causes increase in: HEART
RATE
This contributes significantly to inability to clot in later stages of
MODS: THROMBOCYTOPENIA
One of the complications that occurs due to altered blood flow
in MODS: CLOTTING

The initial clinical sign of renal insult is: OLIGURIA
The THREE MAIN TYPES of SHOCK are: SEPTIC, CARDIOGENIC
AND HYPOVOLEMIC
Vital organs are: heart, brain and lungs
HYPOXEMIA refers to low level of OXYGEN in your blood. This
results in HEMOGLOBIN circulating with no oxygen attached to
it. This is evident when the SpO2 is undertaken as part of a
patient’s observations. Remember a low haemoglobin means
there isn’t enough for oxygen to attach to, but the SpO2 will
still show the normal value. In this situation, the SpO2 will still
appear normal because the monitor MEASURES the number of
O2 attached to the available haemoglobin.
HYPOXIA is a measurement of oxygenation at TISSUE LEVEL.
The way we measure this in clinical setting is via ABG.
Shock occurs when the VITAL ORGANS do not get enough
OXYGEN. Oxygen is important for the activation of ATP. ATP is
the energy source for all cells and without the supply of oxygen
ATP does not occur and cell death arises.
Uncorrected HYPOVOLEMIA will result in a lack of oxygen
supply to organs and shock. TRUE
SEPTIC SHOCK is also known as DISTRIBUTIVE SHOCK. When
this occurs, dysregulated blood flow resulting in a low OXYGEN
level at the tissue level.

In terms of hypovolemia (low intravascular volume), the
observations you take on your patient would show, tachycardia,
low BP, lower end of normal temperature. TRUE
In cardiogenic shock, the initial observations you would see in
your patient are temperature low end of normal, tachycardia,
hypotension. TRUE
When the body is overwhelmed by bacterial or viral infection
sepsis occurs. Part of the sepsis response is the release of
cytokines. Cytokines are released and the immune system is
activated, in sepsis this system continues uncontrolled, and
dysregulation occurs causing a decrease in SVR, increased HR,
hypotension. TRUE
8. Neurology
Brain structures
• Cerebrum – occupies most of the cranium, two hemisheres,
copus callosum and four lobes of the brain.
• Diencephalon - Thalamus, pituitary gland and hypothalamus.
• Cerebellum
• Brain stem – mid brain, pons, medulla oblongata and spinal
cord
Vascular System – circle of Willis, blood brain barrier and
meninges.

FRONTAL LOBE – this lobe sits directly behind the forehead; it is
the largest lobe. The most common site of injury for traumatic
brain injury and responsible for thoughts, personality,
emotions, behaviour and speech.
OCCIPITAL LOBE - the primary area of visual reception, it allows
visual interpretation such as colour, motion, and the formation
of objects.
TEMPORAL LOBE – this lobe is responsible for the for auditory
reception, receptive speech (language) and information
retrieval (memory). It is the organiser of sensory input.
PARIETAL LOBE – this lobe is responsible for processing,
sensory output, sensory discrimination and motor orientation of
self. IT process touch, taste, and temperature.
Nervous system
• Cranial nerves
• Spinal cord
• Dermatomes
Ventricular system
• CSF
• Reticular activating system
• Munroe Kellie Doctrine – brain tissue, cerebral blood and
cerebrospinal fluid
Reticular Activating System (RAS)

•Arousal
•Cortex
•Awareness
* Watch video about MENINGITIS by Osmosis
The cerebrum occupies the majority of the cranium. It is
divided into the right and left hemispheres. The corpus and
callosum connects the right and left hemispheres allowing
for communication between the 2 hemispheres.
8.5
Neurology
The cerebrum occupies the majority of the cranium. It is divided into the right and left
hemisphere. The callosum and corpus connects the right and left hemispheres allowing
for communication
between the 2 hemispheres.
Motor impulses from the CEREBRAL CORTEX to PONS and
SENSORY IMPULSES from the SPINAL CORD to the THALAMUS
via: MIDBRAIN
The regulation of blood flood within the CEREBRUM is
maintained by the: CIRCLE OF WILLIS
Increased CO2 in brain causes: VASODILATION
The DURAMATER is the outer layer of the MENINGES.
GLUCOSE is the only source of energy used by the BRAIN.

The BLOOD BRAIN barrier stops pathogens entering the brain
tissue.
CEREBRO-SPINAL FLUID acts as a “cushion” for the CORTEX,
providing a basic mechanical and immunological protection to
the brain inside the skull.
Intra cranial pressure is PRESSURE exerted within the skull by
the brain tissue, CSF, and blood.
When doing a GCS, central stimuli is assessed by?
Supra-orbital pressure, trapezius pinch, sternal rub
GCS assesses:
pupillary function, cerebral function, limb strength
An increase in ICP causes an alteration of blood flow to the
brain: TRUE
Antibiotic stewardship promotes the optimal use of
antimicrobials to maximise treatment efficacy in individuals,
while minimising the impact of antimicrobial resistance on
communities. TRUE
Headache in patients with meningitis is caused by: containing
air, increased ICP, inflammation of the meninges.
The most severe form of meningitis is: BACTERIAL

Meningitis alters intracranial physiology causing: cerebral
oedema, increased permeability of the blood brain barrier,
raised ICP.
Which of the below is not indicative of meningitis? NEGATIVE
KERNIG’s SIG
Indicative Meningitis: Positive Kernig’s sig, Photophobia,
Positive Brudzinski’s sign
1. Meningitis
Inflammation of the meninges. The meninges consist of three layers: dura
mater, pia mater, arachnoid mater.
2. CSF
Cerebrospinal Fluid. This is fluid surrounding the brain and going into the
spinal cord that provides cushioning. CSF specifically looks at neutrophils,
lymphocytes, proteins, glucose. When these are all outside the normal
levels, it indicates (but does not diagnose) inflammation from a variety of
causes. This, together with the patient's history and clinical assessment,
are what leads us to a diagnosis.
3. ICP
Intracranial pressure. This is the pressure within the brain. The normal
range is 0–15mmHg.
4. Nuchal stiffness
The neck is generally a mobile area. The meninges cover the brain and
run through the neck and torso area. As the layers of the meninges
become inflamed within the relatively small space, this impacts on nerves,
causing pain and rigidity.
5. Photophobia
The mechanism of photophobia is not understood.
6. Vomiting
The mechanism of vomiting is also not understood. In Traumatic Brain
Injury (TBI) there is a definite relationship between skull fracture and
vomiting, but the mechanism is still unknown.
7. Headache

(Increased ICP) Inflammation of the meninges within the cranium causes
pain just as inflammation elsewhere in the body does, by impacting on
nerve fibers. The added problem here is there is limited space for
continued inflammation and the AIR continues.
8. Glucose
Glucose cannot be stored in the brain, which requires a constant supply
via blood flow.
9. petechial rash
This is caused by bleeding usually on the of end capillaries. Its
distinguishing feature is that when you press on them, they do not
disappear and then reappear (there is no blanching).
10. Kernig's sign
Lie the patient flat and have them bend one knee to a ninety-degree
angle. When the patient is asked to then straighten leg, they cannot do so
as they feel tight.
11. Brudzinski sign
Lying the patient flat and having them flex their head forward causes their
knees to flex.
12. lumbar puncture
The purpose of a lumbar puncture (LP) is to get a CSF sample to rule in or
rule out conditions.
LPs are performed in suspected meningitis or encephalitis. LPs are risky
and not diagnostic. There is a risk of infection and adverse outcomes such
as:
 failure to obtain a specimen
 post-dural puncture headache (fairly common) - up to 5-15%
 transient/persistent paraesthesia/numbness (very uncommon)
 respiratory arrest from positioning (rare)
 spinal haematoma or abscess (very rare)
LPs are rarely performed. If the patient is going to receive antibiotics
regardless of the result of the LP, then the LP won’t be done because it
will not change treatment.
*Read the DOWNLOAD about Burns.
Loss of fluids from burnt skin results in: HYPOVOLEMIA

Common formula used for fluid replacement in burns is:
PARKLAND
The TOTAL BODY SURFACE AREA affected by burns is assessed
using the: RULE OF NINES
Type of burn injury that takes place due to exposure of the skin
to excessive heat: THERMAL
The central zone of burns injury with the greatest damage is
the zone of: COAGULATION