Ben's You Tubes Flashcards
(395 cards)
1
Q
What is a stroke?
A
An impairment of cerebral circulation causing damage to the brain.
2
Q
What’s the difference between a stroke and a TIA?
A
In a TIA, symptoms disappear within 2 hours with no permanent damage, while a stroke results in permanent brain damage.
3
Q
What are the two main types of stroke?
A
Ischemic stroke (obstruction of blood flow) and hemorrhagic stroke (rupture of a cerebral blood vessel).
4
Q
Which type of stroke is more common?
A
Ischemic stroke.
5
Q
Which type of stroke tends to be more fatal?
A
Hemorrhagic stroke.
6
Q
What are the two main types of ischemic stroke?
A
Thrombotic stroke and embolic stroke.
7
Q
What causes a thrombotic stroke?
A
A thrombus (blood clot) forming directly in a cerebral artery or intracranial vessel, blocking blood flow.
8
Q
What causes an embolic stroke?
A
A thrombus or fatty plaque that originates elsewhere in the body, travels through circulation, and lodges in a cerebral blood vessel.
9
Q
What is the most common form of embolic stroke?
A
Embolic stroke due to atrial fibrillation.
10
Q
Why does atrial fibrillation lead to stroke?
A
When the atrium doesn’t contract properly, blood becomes stagnant, forming clots that can travel to the brain.
11
Q
What are the two main types of hemorrhagic stroke?
A
Subarachnoid hemorrhage and intracerebral hemorrhage.
12
Q
What is a subarachnoid hemorrhage?
A
Bleeding into the subarachnoid space (below the arachnoid layer of the meninges).
13
Q
What is the typical symptom of subarachnoid hemorrhage?
A
“The worst headache of their life.”
14
Q
What is an intracerebral hemorrhage?
A
Bleeding directly into the brain tissue itself.
15
Q
If a clot forms in the right side of the heart, what condition might result?
A
Pulmonary embolism, not stroke.
16
Q
What is a TIA?
A
Temporary interruption of blood flow to the brain with symptoms that resolve within 2 hours without permanent damage.
17
Q
What is an ischemic stroke?
A
Stroke caused by obstruction of blood flow to the brain.
18
Q
What is a hemorrhagic stroke?
A
Stroke caused by rupture of a cerebral blood vessel.
19
Q
What is a thrombotic stroke?
A
Ischemic stroke caused by a blood clot forming directly in a cerebral artery.
20
Q
What is an embolic stroke?
A
Ischemic stroke caused by a clot or plaque from elsewhere in the body.
21
Q
What is a thrombus?
A
Blood clot that forms in a blood vessel.
22
Q
What is an embolus?
A
A particle (often a blood clot) that travels through the bloodstream and lodges in a blood vessel.
23
Q
What is atrial fibrillation?
A
Irregular heart rhythm where the atria don’t contract properly, increasing stroke risk.
24
Q
What is a subarachnoid hemorrhage?
A
Bleeding into the space between the arachnoid membrane and the brain.
25
What is an intracerebral hemorrhage?
Bleeding directly into the brain tissue.
26
What is infarction?
Death of tissue due to inadequate blood supply.
27
What is cerebral circulation?
Blood flow to and within the brain.
28
What are the meninges?
The three membranes (dura mater, arachnoid mater, and pia mater) that cover the brain and spinal cord.
29
What is the arachnoid layer?
The middle layer of the meninges.
30
What is the subarachnoid space?
The space between the arachnoid and pia mater layers filled with cerebrospinal fluid.
31
What is the circulation pathway?
Blood from lungs → left atrium → left ventricle → body (including brain).
32
What is the circulatory origin of strokes?
Left side of heart → Brain (can cause stroke); Right side of heart → Lungs (can cause pulmonary embolism, not stroke).
33
What is the severity relationship between stroke types?
Hemorrhagic strokes tend to be more fatal than ischemic strokes.
34
What is the time relationship for TIA and stroke?
TIA: Symptoms resolve within 2 hours; Stroke: Permanent damage.
35
What initiates the CNS ischemic response?
A cranial insult (blow to the head) leading to hemorrhage and vasogenic edema.
36
What happens to intracranial pressure following a cranial insult?
Intracranial pressure increases due to bleeding and swelling inside the skull.
37
How does increased ICP affect cerebral blood vessels?
It compresses cerebral arteries, reducing blood flow to the brain.
38
What happens to cerebral perfusion pressure when ICP increases?
Cerebral perfusion pressure decreases, as CPP = MAP - ICP.
39
According to the Monro-Kellie Hypothesis, what are the three components contained in the skull?
Brain tissue, blood, and cerebrospinal fluid (CSF).
40
What compensatory mechanism occurs according to the Monro-Kellie Hypothesis?
CSF shifts into the spinal cavity to create more space and relieve intracranial pressure.
41
What gas changes occur in the brain during cerebral ischemia?
Hypoxia (decreased oxygen) and hypercapnia (increased carbon dioxide).
42
How does the brain initially respond to hypoxia and hypercapnia?
With cerebral vasodilation to increase blood flow.
43
How does the sympathetic nervous system respond to decreased CPP?
It activates systemic vasoconstriction (everywhere except the brain).
44
How does systemic vasoconstriction affect blood pressure?
It increases total peripheral resistance (TPR), which increases blood pressure.
45
Why does the body increase blood pressure during cerebral ischemia?
To attempt to improve cerebral perfusion pressure (CPP) when ICP is elevated.
46
What seemingly contradictory cardiovascular signs occur in Cushing's Triad?
Increased systolic blood pressure with bradycardia (decreased heart rate).
47
Why does bradycardia occur despite sympathetic activation?
Baroreceptors in the aortic arch detect high blood pressure and trigger a parasympathetic response via the vagus nerve.
48
What type of breathing pattern is associated with brainstem compression?
Cheyne-Stokes respirations (irregular breathing patterns).
49
Why should respirations be counted for 30-60 seconds in patients with suspected increased ICP?
Because irregular breathing patterns may be missed with shorter counting periods.
50
What is the final outcome of unresolved cerebral ischemia?
Excitotoxicity leading to neuronal death and eventually patient death.
51
What is a cranial insult?
A blow or injury to the head.
52
What is hemorrhage in the context of the cranial cavity?
Bleeding, in this context within the cranial cavity.
53
What is vasogenic edema?
Swelling caused by increased permeability of blood vessel walls, allowing fluid to leak into surrounding tissues.
54
What is intracranial pressure (ICP)?
The pressure inside the skull and thus in the brain tissue and cerebrospinal fluid.
55
What is cerebral perfusion pressure (CPP)?
The pressure gradient driving cerebral blood flow to the brain.
56
What is mean arterial pressure (MAP)?
The average pressure in arteries during one cardiac cycle.
57
What is the Monro-Kellie Hypothesis?
The principle that the skull contains a fixed volume, so an increase in one component must be offset by a decrease in another.
58
What is cerebrospinal fluid (CSF)?
Clear fluid that surrounds the brain and spinal cord, providing cushioning and nutrients.
59
What is hypoxia?
Reduced oxygen levels in tissues.
60
What is hypercapnia?
Elevated carbon dioxide levels in the blood.
61
What is cerebral vasodilation?
Widening of blood vessels in the brain.
62
What is the sympathetic nervous system?
Part of the autonomic nervous system that activates the 'fight or flight' response.
63
What is total peripheral resistance (TPR)?
The resistance to blood flow offered by all peripheral vasculature in the body.
64
What is cardiac output (CO)?
The amount of blood pumped by the heart per minute.
65
What is Cushing's Triad?
A clinical triad of increased systolic blood pressure, bradycardia, and irregular respirations, indicating increased ICP.
66
What are baroreceptors?
Sensory nerve endings that detect changes in blood pressure.
67
What is the vagus nerve?
The 10th cranial nerve, part of the parasympathetic nervous system.
68
What is bradycardia?
Abnormally slow heart rate (less than 60 beats per minute).
69
What are Cheyne-Stokes respirations?
An abnormal pattern of breathing characterized by alternating periods of deep and shallow breathing, sometimes with periods of apnea.
70
What is excitotoxicity?
Process by which nerve cells are damaged or killed by excessive stimulation by neurotransmitters.
71
What is the brainstem?
The part of the brain connecting the cerebrum with the spinal cord, controlling basic vital life functions.
72
What is systemic vasoconstriction?
Narrowing of blood vessels throughout the body (except in the brain during ischemia).
73
What is the parasympathetic nervous system?
Part of the autonomic nervous system responsible for 'rest and digest' functions.
74
Where are baroreceptors located?
Baroreceptors are located in the aortic arch (aortic sinus) and carotid sinuses.
75
How do baroreceptors detect hypotension?
Baroreceptors function as stretch receptors - they detect decreased stretch in the vessel walls during hypotension.
76
What are the two medullary centers involved in the sympathetic response to hypotension?
The cardioacceleratory center and the vasomotor center.
77
What catecholamines are released during the sympathetic response to hypotension?
Adrenaline (epinephrine) and noradrenaline (norepinephrine).
78
Where are these catecholamines released from?
From sympathetic nerve endings and the adrenal medulla.
79
What is the effect of sympathetic stimulation on blood vessels?
Sympathetic stimulation causes vasoconstriction of blood vessels via alpha-1 receptors, increasing total peripheral resistance.
80
What is a chronotropic effect?
A chronotropic effect changes the heart rate.
81
Which receptors mediate the cardiac effects of the sympathetic response?
Beta-1 (β1) receptors.
82
What is an inotropic effect?
An inotropic effect changes the contractility of cardiac muscle.
83
How does the sympathetic response affect stroke volume?
It increases stroke volume by increasing cardiac muscle contractility (positive inotropic effect).
84
What is a dromotropic effect?
A dromotropic effect changes the conduction velocity through cardiac tissue.
85
What is the formula for calculating cardiac output?
Cardiac Output = Heart Rate × Stroke Volume.
86
What is the formula for blood pressure?
Blood Pressure = Cardiac Output × Total Peripheral Resistance.
87
Where is the adrenal medulla located?
In the middle portion of the adrenal glands, which sit above the kidneys.
88
What does 'epi' in epinephrine refer to anatomically?
'Epi' means 'over/above,' referring to how the adrenal glands sit above the kidneys.
89
How does the sympathetic response to hypotension affect the SA and AV nodes?
It increases heart rate (chronotropic effect) and improves conduction velocity (dromotropic effect).
90
What is the overall goal of the sympathetic response to hypotension?
To restore normal blood pressure by increasing both cardiac output and total peripheral resistance.
91
Which division of the autonomic nervous system is activated in response to hypotension?
The sympathetic nervous system (fight-or-flight response).
92
How does alpha-1 receptor activation affect blood pressure?
Alpha-1 receptor activation causes vasoconstriction, which increases total peripheral resistance and therefore blood pressure.
93
How does beta-1 receptor activation affect cardiac output?
Beta-1 receptor activation increases both heart rate and stroke volume, which increases cardiac output.
94
What does RAAS stand for?
Renin-Angiotensin-Aldosterone System
95
What does ADH stand for?
Anti-Diuretic Hormone
96
What is the alternative name for ADH?
Vasopressin
97
What are the three triggers that activate RAAS?
(1) Decreased renal perfusion, (2) Sympathetic nervous system activation of juxtaglomerular cells, (3) Decreased solute concentration in distal convoluted tubule
98
Where is renin produced?
Juxtaglomerular cells of the kidney
99
What does renin convert and what is the product?
Renin converts angiotensinogen to angiotensin I
100
Where is angiotensinogen produced?
In the liver
101
What does ACE stand for?
Angiotensin Converting Enzyme
102
Where is ACE primarily produced?
Endothelial cells of the lungs
103
What does ACE convert and what is the product?
ACE converts angiotensin I to angiotensin II
104
What are the four major effects of angiotensin II?
(1) Vasoconstriction of arterioles, (2) Stimulation of thirst centre, (3) Aldosterone release, (4) Stimulation of ADH release
105
How does vasoconstriction affect blood pressure?
Vasoconstriction increases total peripheral resistance, which directly increases blood pressure
106
Where is aldosterone produced?
In the adrenal cortex
107
What is the effect of aldosterone on the kidney?
Aldosterone increases sodium reabsorption in the distal convoluted tubule
108
How does increased sodium reabsorption affect blood volume?
Water follows sodium (via osmosis), increasing blood volume and blood pressure
109
What are the two stimuli for ADH release?
(1) Angiotensin II stimulation, (2) Osmoreceptors in hypothalamus detecting increased blood osmolarity
110
Where is ADH produced and where is it released from?
ADH is produced in the hypothalamus and released from the posterior pituitary
111
What are the two primary effects of ADH?
(1) Vasoconstriction, (2) Increased water reabsorption from collecting ducts
112
How does alcohol affect ADH?
Alcohol inhibits ADH, resulting in increased urine production (diuresis)
113
What does 'juxtaglomerular' mean anatomically?
'Juxta' means 'sit beside' - juxtaglomerular cells sit beside the glomerulus in the kidney
114
Which part of the nephron is responsible for water reabsorption under ADH influence?
The collecting ducts
115
What happens to blood osmolarity when blood volume decreases?
Blood osmolarity increases (blood becomes more concentrated)
116
How does the blood pressure equation relate to vasoconstriction?
Vasoconstriction increases total peripheral resistance, and since BP = CO × TPR, blood pressure rises
117
What happens to urine concentration when ADH levels increase?
Urine becomes more concentrated as more water is reabsorbed
118
What happens in the distal convoluted tubule when aldosterone levels rise?
Increased sodium reabsorption, with water following sodium due to osmosis
119
What is hypotension?
Abnormally low blood pressure
120
What is the sympathetic nervous system responsible for?
Responsible for 'fight, flight, fright' responses
121
Where are alpha-1 (α1) receptors located?
In the smooth muscle of blood vessels around skin, abdominal organs, digestive tract, and kidneys
122
What is the effect of stimulating alpha-1 receptors during hypotension?
Vasoconstriction, which increases total peripheral resistance and raises blood pressure
123
Where are beta-1 (β1) receptors found?
In the heart and kidneys
124
What is the chronotropic effect?
An increase in heart rate that occurs when beta-1 receptors on the SA node are stimulated
125
What is a dromotropic effect?
An increase in electrical conduction speed through the AV node
126
What is the inotropic effect?
Change in contractility or force of heart muscle contraction
127
What is stroke volume?
Amount of blood pumped by the heart in a single contraction
128
What is total peripheral resistance (TPR)?
The resistance to blood flow offered by all blood vessels
129
What is vasoconstriction?
Narrowing of blood vessels that increases blood pressure
130
What are juxtaglomerular (JG) cells?
Specialised cells in the kidneys that release renin
131
What does RAAS stand for?
Renin-Angiotensin-Aldosterone System
132
What is angiotensinogen?
Protein produced by the liver that is converted to angiotensin I
133
What is angiotensin I?
Inactive precursor converted to angiotensin II by ACE
134
What is angiotensin II?
Active hormone that causes vasoconstriction and stimulates aldosterone release
135
What does ACE stand for?
Angiotensin Converting Enzyme
136
What is the role of aldosterone?
Hormone that increases sodium reabsorption in the kidneys
137
What is ADH?
Antidiuretic Hormone; increases water reabsorption
138
What do osmoreceptors detect?
Changes in osmotic pressure
139
What do baroreceptors detect?
Changes in blood pressure
140
What are aquaporin-2 channels?
Water channels in collecting ducts activated by ADH
141
What is the SA node?
Sinoatrial node; the heart's natural pacemaker
142
What is the AV node?
Atrioventricular node; delays electrical impulses in the heart
143
What are the two main types of receptors involved in the sympathetic response to hypotension?
Alpha-1 (α1) and Beta-1 (β1) receptors
144
What initiates the RAAS response to hypotension?
Baroreceptors detect reduced pressure, triggering juxtaglomerular cells to release renin
145
What does renin convert in the RAAS pathway?
Renin converts angiotensinogen to angiotensin I
146
What enzyme converts angiotensin I to angiotensin II?
Angiotensin Converting Enzyme (ACE)
147
List three effects of angiotensin II.
1) Vasoconstriction, 2) Stimulates thirst, 3) Prompts aldosterone secretion from adrenal cortex
148
How does aldosterone affect blood pressure?
It increases sodium reabsorption in distal tubules and collecting ducts, with water following passively due to osmotic pressure, thereby increasing blood volume
149
What stimulates ADH release during hypotension?
Osmoreceptors in the hypothalamus detect reduced blood pressure
150
Where is ADH produced and released?
Produced in hypothalamus, released from posterior pituitary
151
How does ADH increase water reabsorption?
By inserting aquaporin-2 channels in the collecting ducts, increasing water permeability
152
What additional effect does ADH have at higher concentrations?
Vasoconstriction, which increases peripheral resistance
153
How do RAAS and ADH complement each other to restore blood pressure?
Both systems increase blood volume through water retention, and both can increase peripheral resistance through vasoconstriction
154
Which system primarily affects sodium balance?
RAAS (via aldosterone)
155
Compare the primary actions of angiotensin II and ADH.
Angiotensin II primarily causes vasoconstriction and aldosterone release, while ADH primarily increases water reabsorption directly
156
What is the equation for blood pressure (BP)?
Blood Pressure (BP) = Cardiac Output (CO) × Total Peripheral Resistance (TPR)
157
What is the equation for cardiac output (CO)?
Cardiac Output (CO) = Heart Rate (HR) × Stroke Volume (SV)
158
What is the relationship between sympathetic stimulation and blood pressure?
↑ Sympathetic Stimulation → ↑ Heart Rate + ↑ Contractility → ↑ Cardiac Output → ↑ Blood Pressure
159
What is the relationship between alpha-1 receptor activation and blood pressure?
↑ α1 Receptor Activation → ↑ Vasoconstriction → ↑ Total Peripheral Resistance → ↑ Blood Pressure
160
What is the relationship between beta-1 receptor activation in the heart and blood pressure?
↑ β1 Receptor Activation (Heart) → ↑ Heart Rate + ↑ Stroke Volume → ↑ Cardiac Output → ↑ Blood Pressure
161
What is the relationship between beta-1 receptor activation in the kidney and blood pressure?
↑ β1 Receptor Activation (Kidney) → ↑ Renin → ↑ Angiotensin II → ↑ Aldosterone → ↑ Na+ Reabsorption → ↑ Water Retention → ↑ Blood Volume → ↑ Blood Pressure
162
What is the relationship between blood pressure and ADH release?
↓ Blood Pressure → ↑ ADH Release → ↑ Aquaporin-2 Channels → ↑ Water Reabsorption → ↑ Blood Volume → ↑ Blood Pressure
163
What is the definition of shock?
A life-threatening condition characterised by inadequate oxygen delivery and consumption at a cellular level.
164
What are the four main types of shock?
Hypovolaemic, Obstructive, Cardiogenic, and Distributive shock.
165
What causes hypovolaemic shock?
Decreased blood volume due to plasma loss, whole blood loss, or extracellular fluid loss.
166
Name three examples of causes of hypovolaemic shock.
Burns (plasma loss), trauma with external bleeding, GI bleeding, vomiting, diarrhoea, dehydration.
167
What is obstructive shock?
Shock caused by a mechanical obstruction to blood flow.
168
Name three causes of obstructive shock.
Pulmonary embolism, cardiac tamponade, and tension pneumothorax.
169
What is cardiac tamponade?
A condition where fluid accumulates between the pericardial layers, compressing the heart and preventing proper filling.
170
What is a tension pneumothorax?
A condition where air gets trapped in the pleural space through a 'trap door' mechanism, creating pressure on the heart and major vessels.
171
What is cardiogenic shock?
Decreased cardiac output despite adequate blood volume due to problems with the heart itself.
172
What are the three main causes of cardiogenic shock?
Myocardial infarction, valve problems (stenosis or regurgitation), and arrhythmias.
173
How does valve stenosis contribute to cardiogenic shock?
The valves don't open enough ('creaky doors'), decreasing cardiac output.
174
How does valve regurgitation contribute to cardiogenic shock?
The valves allow blood to flow backwards, decreasing cardiac output.
175
What is distributive shock?
Shock caused by enlarged vascular compartment or displacement of vascular volume away from central circulation due to massive vasodilation.
176
What are the three subtypes of distributive shock?
Septic shock, anaphylactic shock, and neurogenic shock.
177
What causes septic shock?
A dysregulated host response to infection causing systemic inflammation and widespread vasodilation.
178
What is anaphylactic shock?
A type 1 hypersensitivity reaction mediated by IgE antibodies (like peanut or bee sting allergies) resulting in massive vasodilation.
179
What is neurogenic shock?
Shock caused by decreased sympathetic tone and increased parasympathetic tone, resulting in vasodilation.
180
What causes neurogenic shock?
High spinal cord injury, CNS depressant drugs, hypoxia of CNS, general anaesthesia, or severe hypoglycaemia.
181
Why does a high spinal cord injury cause neurogenic shock?
It disrupts sympathetic outflow (from thoracic region) while leaving parasympathetic tone (via vagus nerve) intact, resulting in vasodilation.
182
What is 'cool shock' and which types of shock fall into this category?
Shock states where the body compensates with peripheral vasoconstriction; includes hypovolaemic, obstructive, and cardiogenic shock.
183
What is 'warm shock' and which type of shock falls into this category?
Shock characterized by vasodilation with blood rushing to the periphery; distributive shock.
184
How does the body compensate in 'cool shock' states?
By increasing sympathetic response, increasing heart rate, and peripheral vasoconstriction to redirect blood to vital organs.
185
How would you clinically differentiate between 'cool shock' and 'warm shock'?
'Cool shock' presents with increased capillary refill time and cool extremities, while 'warm shock' presents with rapid capillary refill time and warm extremities initially.
186
What is the underlying pathophysiology of all shock types?
Inadequate oxygen delivery and consumption at a cellular level.
187
Using the petrol station analogy, how would you explain hypovolaemic shock?
Running out of fuel.
188
Using the petrol station analogy, how would you explain obstructive shock?
Blockage in the pipes.
189
Using the petrol station analogy, how would you explain cardiogenic shock?
Problem with the pump.
190
What is sepsis?
A life-threatening condition characterised by a dysregulated host response to infection, leading to widespread systemic inflammation that can cause organ dysfunction and potentially death.
191
What receptors on white blood cells initially detect pathogens?
Toll-like receptors (TLRs)
192
Name three plasma-derived inflammatory mediators.
Complement system, coagulation factors, and kinin system.
193
Name four cell-derived inflammatory mediators.
Histamine, pro-inflammatory cytokines, tumour necrosis factor, interleukin-1, leukotrienes, prostaglandins, platelet activating factor, nitric oxide. (Any four correct answers)
194
What are the five processes involved in a local inflammatory response?
Vasodilation, increased capillary permeability, chemotaxis, increased clotting factors, and increased temperature.
195
What is vasodilation and what is its purpose in local inflammation?
Vasodilation is the enlargement of blood vessels to increase blood flow to the affected area, allowing more immune cells to reach the infection site.
196
What is the purpose of increased capillary permeability in inflammation?
To allow white blood cells to exit blood vessels and reach the pathogen in the tissues.
197
What is chemotaxis?
The process by which inflammatory mediators attract more white blood cells to the area of infection.
198
Why does local inflammation cause increased clotting?
To form localised clots that contain the pathogen and prevent its spread.
199
What are the four clinical signs of local inflammation?
Redness, heat, swelling, and pain.
200
Name three reasons why a local infection might progress to systemic sepsis.
High pathogen load, high virulence of pathogen, or pathogen spreads throughout bloodstream.
201
What host factors can increase the risk of developing sepsis?
Advanced age, very young age, immunosuppression, or multiple comorbidities.
202
What is a 'cytokine storm'?
An excessive release of inflammatory cytokines leading to a dysregulated inflammatory response that occurs throughout the body.
203
How does the body initially compensate for widespread vasodilation in sepsis?
With a compensatory increase in heart rate to maintain blood pressure.
204
What happens to the white blood cell count initially in sepsis?
It increases as white blood cells are released to fight the infection.
205
What happens to the white blood cell count as sepsis progresses to septic shock?
It decreases (leucopenia) due to exhaustion of white blood cell production.
206
What is septic shock?
A condition where the circulatory system fails to maintain adequate blood pressure and organ perfusion despite fluid resuscitation, due to severe vasodilation and capillary leakage.
207
Why does body temperature eventually drop in late septic shock after the initial fever?
Because the body shifts from aerobic to anaerobic metabolism, which generates less heat.
208
What metabolic process dominates in septic shock due to inadequate oxygen delivery?
Anaerobic metabolism.
209
What is a major metabolic by-product of anaerobic metabolism in septic shock?
Lactic acid, leading to metabolic acidosis.
210
What is MODS?
Multiple Organ Dysfunction Syndrome - the progressive failure of two or more organ systems due to septic shock.
211
Name three causes of organ failure in MODS.
Microthrombi blocking blood flow to organs, decreased oxygen transport due to shock, inflammatory damage to tissues, and metabolic acidosis impairing cellular function.
212
What is ARDS?
Acute Respiratory Distress Syndrome - a condition characterised by alveolar and capillary damage in the lungs, leading to pulmonary oedema and hypoxia.
213
What is DIC?
Disseminated Intravascular Coagulation - a condition in which widespread clot formation throughout the body consumes clotting factors, leading to simultaneous clotting and bleeding.
214
What are the four key principles of managing sepsis?
Early recognition, aggressive fluid resuscitation, appropriate antimicrobial therapy, and vasopressors when indicated.
215
What is the correct sequence of the sepsis continuum?
Local Infection → Sepsis → Severe Sepsis → Septic Shock → MODS/ARDS/DIC → Death
216
How does sepsis affect the coagulation system initially?
Initially causes hypercoagulability with formation of microthrombi throughout the body.
217
How does sepsis affect the coagulation system in later stages?
Leads to thrombocytopenia and DIC due to consumption of clotting factors.
218
Name two compensatory mechanisms the body uses to maintain blood pressure in early sepsis.
Increased heart rate and activation of the renin-angiotensin-aldosterone system (RAAS).
219
What causes the shift from aerobic to anaerobic metabolism in septic shock?
Inadequate oxygen delivery to tissues due to poor perfusion.
220
What is sepsis?
A dysregulated host response to infection leading to life-threatening organ dysfunction.
221
What are Toll-like receptors (TLRs)?
Receptors on white blood cells that detect pathogens.
222
What are inflammatory mediators?
Chemical substances that initiate and regulate inflammatory responses.
223
What is vasodilation?
Widening of blood vessels resulting in increased blood flow.
224
What is capillary permeability?
The ability of substances to pass through capillary walls.
225
What is chemotaxis?
The movement of cells directed by chemicals in their environment.
226
What is a cytokine storm?
Excessive release of cytokines causing widespread inflammation.
227
What is septic shock?
Life-threatening condition with severe hypotension despite fluid resuscitation.
228
What is leucopenia?
Abnormally low white blood cell count.
229
What is thrombocytopenia?
Abnormally low platelet count.
230
What is Disseminated Intravascular Coagulation (DIC)?
Condition with simultaneous clotting and bleeding.
231
What is Multiple Organ Dysfunction Syndrome (MODS)?
Progressive failure of two or more organ systems.
232
What is Acute Respiratory Distress Syndrome (ARDS)?
Severe respiratory condition with fluid in alveoli.
233
What is anaerobic metabolism?
Energy production without oxygen.
234
What is lactic acidosis?
Buildup of lactic acid in the bloodstream.
235
What are microthrombi?
Tiny blood clots in small blood vessels.
236
What is total peripheral resistance?
The resistance to blood flow offered by all peripheral vasculature.
237
What is the renin-angiotensin-aldosterone system (RAAS)?
Hormonal system that regulates blood pressure and fluid balance.
238
What is pulmonary oedema?
Fluid accumulation in the air spaces of the lungs.
239
What is hypoxia?
Inadequate oxygen supply to tissues and cells.
240
What is the formula for Cardiac Output?
Cardiac Output = Heart Rate × Stroke Volume
241
What is the formula for Blood Pressure?
Blood Pressure = Cardiac Output × Total Peripheral Resistance
242
What is the Fick Principle?
VO₂ = CO × (CaO₂ - CvO₂)
243
What is the formula for Oxygen Delivery?
Oxygen Delivery = Cardiac Output × Arterial Oxygen Content × 10
244
What is the Lactate Production in Anaerobic Metabolism?
Glucose + 2 ADP + 2 Pi → 2 Lactate + 2 ATP + 2 H₂O + 2 H⁺
245
What is the Simplified Sepsis Risk Equation?
Sepsis Risk ∝ (Pathogen Load × Pathogen Virulence) ÷ Host Immune Competence
246
What is anaphylaxis?
A life-threatening allergic reaction affecting two or more body systems, involving the release of inflammatory mediators from mast cells and basophils.
247
What are the two main pathophysiological effects of anaphylaxis?
Massive vasodilation leading to blood pressure drop, and bronchoconstriction causing difficulty breathing.
248
What is another name for adrenaline?
Epinephrine.
249
What does 'epi' in EpiPen stand for?
Epinephrine.
250
What are the three main types of adrenergic receptors involved in anaphylaxis treatment?
Alpha-1 receptors, Beta-1 receptors, and Beta-2 receptors.
251
Where are alpha-1 receptors located and what is their action when stimulated by adrenaline?
Located on smooth muscle of blood vessels; they cause vasoconstriction.
252
How does alpha-1 receptor stimulation help during anaphylaxis?
It increases total peripheral resistance, which helps maintain blood pressure (counteracting vasodilation).
253
Where are beta-1 receptors located?
In the SA node and myocardium of the heart.
254
What are the three effects of beta-1 receptor stimulation?
Increased heart rate (chronotropic), increased electrical conduction speed (dromotropic), and increased contractility/stroke volume (inotropic).
255
How do beta-1 effects help in anaphylaxis?
They increase cardiac output, which helps increase blood pressure.
256
What are the two main actions of beta-2 receptor stimulation?
Stabilising mast cells and causing bronchodilation of bronchial smooth muscle.
257
How does mast cell stabilisation help in anaphylaxis?
It prevents further degranulation and release of inflammatory mediators like histamine.
258
How does beta-2 mediated bronchodilation help in anaphylaxis?
It opens airways, making breathing easier.
259
What does 'chronotropic effect' refer to?
Effect on heart rate.
260
What does 'dromotropic effect' refer to?
Effect on electrical conduction speed in the heart.
261
What does 'inotropic effect' refer to?
Effect on myocardial contractility.
262
What is the '3C' memory device for adrenaline's action in anaphylaxis?
1) Constricts vessels (α1), 2) Cardiac stimulation (β1), 3) Clear airways + Calm mast cells (β2).
263
Why is adrenaline considered the first-line treatment for anaphylaxis?
Because it rapidly addresses all major pathophysiological changes: it reverses hypotension (via α1 and β1) and improves breathing (via β2) while limiting the allergic response (via β2).
264
What is a pulmonary embolism?
A substance traveling through the bloodstream that lodges in the pulmonary circulation, blocking blood supply to a portion of the lungs.
265
What is the difference between a pulmonary embolism and airway obstruction?
A pulmonary embolism blocks blood vessels in the lungs, not airways.
266
What are the five possible compositions of emboli?
Blood clot (thrombus), fat, air, tumour, and amniotic fluid.
267
What path does blood follow through the heart to the lungs?
Superior/inferior vena cava → right atrium → right ventricle → pulmonary arteries → lungs.
268
What is DVT and how does it relate to pulmonary embolism?
DVT (Deep Vein Thrombosis) is a blood clot in a deep vein, typically in the leg. It can dislodge and travel to the lungs, causing a pulmonary embolism.
269
How does atrial fibrillation contribute to pulmonary embolism?
In atrial fibrillation, the atrium doesn't contract properly, causing blood to stagnate and form clots that can travel to the lungs.
270
How can bone fractures lead to pulmonary embolism?
Fat from bone marrow can be released into the bloodstream after a fracture, travel to the lungs, and cause a fat embolism.
271
What are the five main clinical presentations of pulmonary embolism?
Hypoxia, dyspnoea (shortness of breath), unilateral chest pain, tachycardia, and hypotension.
272
Why does pulmonary embolism cause tachycardia?
The heart increases its rate to compensate for reduced oxygen delivery and decreased cardiac output.
273
Why does pulmonary embolism cause hypotension?
Less blood returns to the left side of the heart due to blocked pulmonary circulation, reducing cardiac output.
274
Why is pulmonary embolism considered a medical emergency?
It can lead to right heart failure, severe hypoxia, and has high mortality if untreated.
275
What is the relationship between immobility and PE risk?
Prolonged immobility (like during long flights) can cause blood to stagnate in the legs, increasing the risk of DVT formation, which can lead to PE.
276
What does 'pulmonary' refer to?
Relating to the lungs.
277
What is an embolism?
A substance traveling through the bloodstream that lodges and causes obstruction.
278
What is a thrombus?
A blood clot formed in a blood vessel.
279
What is hypoxia?
Decreased oxygen level in the blood.
280
What is dyspnoea?
Shortness of breath or difficulty breathing.
281
What is tachycardia?
Abnormally rapid heart rate.
282
What is hypotension?
Abnormally low blood pressure.
283
What is DVT (Deep Vein Thrombosis)?
Blood clot formed in a deep vein.
284
What is AF (Atrial Fibrillation)?
Irregular heart rhythm where the atria don't contract properly.
285
What is the superior vena cava?
Large vein carrying blood from upper body to the heart.
286
What is the inferior vena cava?
Large vein carrying blood from lower body to the heart.
287
What are pulmonary arteries?
Blood vessels carrying deoxygenated blood from heart to lungs.
288
What does unilateral mean?
Affecting only one side.
289
What is cardiac output?
The volume of blood pumped by the heart per minute.
290
What is the relationship between PE risk factors?
Immobility + Hypercoagulability + Venous Stasis = Increased PE Risk.
291
What is the compensatory mechanism in pulmonary embolism?
↓ Oxygenation → ↑ Heart Rate (tachycardia).
292
What is the hemodynamic effect of pulmonary vessel obstruction?
Pulmonary vessel obstruction → ↓ Blood return to left heart → ↓ Cardiac output → Hypotension.
293
What is the progression of DVT to PE?
DVT → Dislodgement → Embolus → Right heart → Pulmonary artery → PE.
294
What is the clinical severity correlation in pulmonary embolism?
Size of embolus + Extent of circulation blocked = Severity of symptoms.
295
What are the two layers of pleura surrounding the lungs?
Parietal pleura (outer layer) and visceral pleura (inner layer)
296
What does 'parietal' refer to in relation to pleura?
It means 'wall' - this pleura is on the outside, closer to the chest wall
297
What does 'visceral' mean in relation to pleura?
It means 'organ' - this pleura is wrapped around the organ (lung)
298
What is a haemothorax?
Blood in the pleural cavity
299
What is a pneumothorax?
Air or gas in the pleural cavity
300
What causes a tension pneumothorax?
External trauma creating a one-way 'flap' where air enters but cannot escape the pleural space
301
What is mediastinal shift?
The pushing of mediastinal structures toward the opposite side of the chest due to pressure from a tension pneumothorax
302
What structures are contained in the mediastinum?
The heart and great vessels (superior/inferior vena cava, aorta, pulmonary arteries)
303
What type of shock can result from a significant haemothorax?
Hypovolaemic shock
304
What type of shock can result from a tension pneumothorax?
Obstructive shock
305
Why does a tension pneumothorax cause obstructive shock?
Pressure obstructs the filling of the heart and blood flow through the great vessels
306
How does a tension pneumothorax mechanism work?
Air enters the pleural space through a 'trap door' but cannot escape, causing increasing pressure with each breath
307
What are the two main life-threatening consequences of a haemothorax?
Hypovolaemic shock and impaired oxygenation from lung collapse
308
What happens to the affected lung in a pneumothorax?
It collapses due to the increased pressure in the pleural space
309
What is pleura?
The membrane surrounding the lungs
310
What is parietal pleura?
The outer layer of pleura near the chest wall
311
What is visceral pleura?
The inner layer of pleura wrapped around the lung
312
What is tension pneumothorax?
A severe form of pneumothorax where air cannot escape
313
What is mediastinum?
The middle compartment of the chest containing the heart and great vessels
314
What is mediastinal shift?
Displacement of mediastinal structures due to pressure
315
What are the great vessels?
Major blood vessels including superior/inferior vena cava, aorta, and pulmonary arteries
316
What is hypovolaemic shock?
Shock resulting from significant blood loss
317
What is obstructive shock?
Shock resulting from obstruction of blood flow to or from the heart
318
What is a trap door/flap?
One-way valve mechanism that allows air to enter but not escape
319
What is pleural cavity/space?
The potential space between the parietal and visceral pleura
320
What is the relationship between haemothorax and hypovolaemic shock?
Haemothorax → Blood in pleural space → Lung collapse → Hypovolaemic shock + Impaired oxygenation
321
What is the relationship between pneumothorax and impaired oxygenation?
Pneumothorax → Air in pleural space → Lung collapse → Impaired oxygenation
322
What is the relationship between tension pneumothorax and obstructive shock?
Tension pneumothorax → One-way valve → Increasing pressure → Lung collapse + Mediastinal shift → Obstructive shock + Severe impaired oxygenation
323
What is the relationship between mediastinal shift and obstructive shock?
Mediastinal shift → Compression of heart and great vessels → Obstructed blood flow → Obstructive shock
324
What is the primary driver of breathing in healthy individuals?
Central chemoreceptors responding to CO₂ levels and pH changes (hypercapnic drive)
325
Where are central chemoreceptors located?
In the brainstem (medulla oblongata)
326
Where are peripheral chemoreceptors located?
In the carotid bodies and aortic arch
327
What do peripheral chemoreceptors primarily detect?
Low oxygen levels (hypoxia)
328
What is the 'hypoxic drive theory' and is it accurate?
The theory suggests COPD patients breathe primarily due to low O₂ levels. It's largely a myth; even in COPD, the hypercapnic drive remains the main breathing stimulus.
329
What is pulmonary vasoconstriction in COPD?
A protective mechanism where blood vessels constrict in poorly ventilated areas, redirecting blood to healthier lung regions with better gas exchange.
330
What are the two main mechanisms that cause CO₂ buildup when COPD patients receive excessive oxygen?
Ventilation/perfusion (V/Q) mismatch and the Haldane effect.
331
How does high-flow oxygen affect the V/Q mismatch in COPD?
It reverses protective pulmonary vasoconstriction, causing blood vessels in poorly ventilated areas to dilate, redirecting blood to damaged lung tissue with poor gas exchange.
332
What is the Haldane effect?
When oxygen binds to haemoglobin, it reduces haemoglobin's ability to carry CO₂, causing more CO₂ to be released into the bloodstream.
333
How does CO₂ buildup lead to respiratory acidosis?
CO₂ reacts with water to form carbonic acid (H₂CO₃), lowering blood pH and making it more acidic.
334
What are symptoms of CO₂ narcosis?
Confusion, drowsiness, slurred speech, decreased level of consciousness, and in severe cases, respiratory depression and coma.
335
What is the recommended SpO₂ range for oxygen therapy in COPD patients?
88-92%
336
Why is the SpO₂ target range lower for COPD patients compared to healthy individuals?
To prevent excessive oxygen leading to CO₂ retention while still preventing dangerous hypoxia.
337
What happens if a COPD patient's blood vessels in damaged lung areas vasodilate?
Blood is redirected away from healthy tissue to poorly ventilated areas, worsening gas exchange and causing CO₂ buildup.
338
Should oxygen be withheld from hypoxic COPD patients?
No, oxygen should still be given but carefully titrated to maintain SpO₂ of 88-92%.
339
What are central chemoreceptors?
Sensors in the brainstem that detect CO₂ levels and pH changes.
340
What are peripheral chemoreceptors?
Sensors in the carotid bodies and aortic arch that detect oxygen levels.
341
What is hypercapnic drive?
The primary breathing stimulus triggered by elevated CO₂ levels.
342
What is hypoxic drive?
A secondary breathing stimulus triggered by low oxygen levels.
343
What is ventilation/perfusion (V/Q) mismatch?
Imbalance between airflow and blood flow in the lungs.
344
What is pulmonary vasoconstriction?
Narrowing of blood vessels in poorly ventilated areas of the lungs.
345
What is the Haldane effect?
Phenomenon where increased oxygen binding to haemoglobin reduces its ability to carry CO₂.
346
What is respiratory acidosis?
A condition where increased CO₂ in the blood leads to increased acidity (lower pH).
347
What is CO₂ narcosis?
A state of decreased consciousness caused by elevated CO₂ levels affecting brain function.
348
What is desensitisation?
When receptors become less responsive to a stimulus due to chronic exposure.
349
What is SpO₂?
Oxygen saturation as measured by pulse oximetry.
350
What is titration?
The process of adjusting oxygen therapy to maintain target SpO₂ levels.
351
What is the medulla oblongata?
Part of the brainstem containing central chemoreceptors.
352
What is vasodilation?
Widening of blood vessels.
353
What is COPD?
Chronic Obstructive Pulmonary Disease, a progressive lung disease that includes emphysema and chronic bronchitis.
354
What is the equation for CO₂ and its relationship to acidosis?
CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻
## Footnote
This equation shows how CO₂ leads to acidosis.
355
What is the normal SpO₂ for healthy individuals?
> 92% for healthy individuals.
356
What is the target SpO₂ for COPD patients?
88-92%.
357
What is the primary respiratory drive relationship?
Primary driver = Hypercapnic drive (CO₂/pH)
Secondary driver = Hypoxic drive (O₂)
358
What is the gas exchange efficiency relationship?
Optimal gas exchange requires matching ventilation (V) with perfusion (Q). V/Q mismatch leads to impaired gas exchange and CO₂ retention.
359
What is the Haldane effect relationship?
↑ O₂ binding to haemoglobin → ↓ CO₂ carrying capacity → ↑ free CO₂ in blood.
360
What is cor pulmonale?
Right-sided heart failure due to pulmonary hypertension that originates from a respiratory/lung disorder.
361
What does the term 'cor' refer to in cor pulmonale?
'Cor' refers to cardiac or heart.
362
What does 'pulmonale' refer to in cor pulmonale?
'Pulmonale' refers to the lungs or pulmonary system.
363
Name three common causes of cor pulmonale.
COPD, asthma, emphysema, chronic pulmonary emboli, cystic fibrosis (any three).
364
What type of heart failure is cor pulmonale primarily classified as?
Diastolic heart failure (problem with relaxing and filling).
365
What is the primary circulatory problem that leads to cor pulmonale?
Pulmonary hypertension (increased pressure in the pulmonary circulation).
366
Why does the body cause vasoconstriction around poorly ventilated alveoli?
To avoid a ventilation/perfusion (V/Q) mismatch by diverting blood away from poorly ventilated areas.
367
What happens to the right ventricle in response to increased pulmonary resistance?
It undergoes hypertrophy (muscle thickening) to overcome the increased resistance.
368
How does right ventricular hypertrophy contribute to heart failure?
The thickened walls reduce chamber size, decreasing preload and limiting the ability of the heart to fill with blood properly.
369
What are three clinical signs that might be observed in a patient with cor pulmonale?
Jugular venous distension, ascites (abdominal oedema), peripheral oedema.
370
What is the sequence of blood flow through the normal heart and lungs?
Right atrium → right ventricle → pulmonary arteries → lungs → pulmonary veins → left atrium → left ventricle → aorta → body.
371
What causes hypoxia in the initial stages of conditions leading to cor pulmonale?
Decreased ventilation around alveoli (air sacs in the lungs).
372
When vasoconstriction is widespread throughout the lungs, what circulatory effect does this have?
Increased resistance to blood flow, leading to pulmonary hypertension.
373
Where does blood 'back up' when right-sided heart failure occurs?
Into the right atrium, vena cava, and systemic circulation.
374
How does decreased preload affect cardiac output in cor pulmonale?
Less preload means less blood to eject from the heart, resulting in decreased cardiac output.
375
What is cor pulmonale?
Right-sided heart failure resulting from pulmonary hypertension due to respiratory disorders.
376
What is pulmonary hypertension?
Abnormally high blood pressure in the arteries of the lungs.
377
What is vasoconstriction?
Narrowing of blood vessels resulting from contraction of the muscular wall of the vessels.
378
What is hypoxia?
A condition in which tissues are deprived of adequate oxygen supply.
379
What is V/Q mismatch?
Ventilation-perfusion mismatch; occurs when areas of the lung are ventilated but not perfused with blood, or perfused but not ventilated.
380
What is diastolic heart failure?
Heart failure caused by impaired relaxation and filling of the ventricles, rather than impaired contraction.
381
What is right ventricular hypertrophy?
Enlargement/thickening of the right ventricular muscle in response to increased workload.
382
What is preload?
The volume of blood in the ventricle at the end of diastole, just before contraction begins.
383
What is afterload?
The pressure against which the heart must pump to eject blood.
384
What is jugular venous distension?
Abnormal bulging of the jugular vein in the neck, indicating increased central venous pressure.
385
What is ascites?
Abnormal accumulation of fluid in the peritoneal cavity, causing abdominal swelling.
386
What is peripheral oedema?
Swelling in the limbs, especially the lower legs and ankles, due to fluid accumulation.
387
What is COPD?
Chronic Obstructive Pulmonary Disease; a progressive lung disease that causes obstructed airflow from the lungs.
388
What is the relationship between hypoxia and vasoconstriction?
In poorly ventilated areas of the lung, hypoxia triggers vasoconstriction to redirect blood to better-ventilated areas.
389
What is the relationship between widespread vasoconstriction and pulmonary hypertension?
When vasoconstriction affects large areas of the lungs, the resistance to blood flow increases, causing pulmonary hypertension.
390
What is the relationship between pulmonary hypertension and right ventricular afterload?
Increased pressure in the pulmonary circulation creates higher afterload for the right ventricle.
391
What is the relationship between increased afterload and right ventricular hypertrophy?
The right ventricle responds to increased afterload by developing muscle hypertrophy to generate more force.
392
What is the relationship between right ventricular hypertrophy and decreased chamber size?
As the ventricular wall thickens, the internal chamber volume decreases.
393
What is the relationship between decreased chamber size and reduced preload?
A smaller ventricular chamber can accommodate less blood during filling, reducing preload.
394
What is the relationship between reduced preload and decreased cardiac output?
Less blood filling the ventricle (preload) results in less blood ejected during contraction.
395
What is the relationship between right-sided heart failure and systemic congestion?
Failure of the right ventricle leads to blood backing up into the venous system, causing systemic congestion (oedema).
