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