Week 3 Flashcards
1
Q
What is the typical diameter of capillaries?
A
5–10 µm
2
Q
What type of cells make up the wall of capillaries?
A
Single layer of thin, flattened endothelial cells
3
Q
What is the role of the basal lamina in capillaries?
A
Helps maintain the structural integrity of the capillary
4
Q
What are pericytes?
A
Contractile cells present along the outside of the basement membrane
5
Q
What is a key feature of capillary beds?
A
Form dense networks with a large total cross-sectional area
6
Q
Why is close proximity of capillaries to cells significant?
A
Facilitates efficient exchange
7
Q
What is the relationship between flow velocity and surface area in capillaries?
A
Low flow velocity, high surface area
8
Q
What characterizes continuous capillaries?
A
Endothelial cells joined by tight junctions
9
Q
What types of substances can pass through continuous capillaries?
A
Small water-soluble solutes, lipid-soluble substances, macromolecules via pinocytotic vesicles
10
Q
Where are continuous capillaries commonly found?
A
- Muscle tissue
- Central nervous system
- Lungs
- Skin
11
Q
What distinguishes fenestrated capillaries from continuous capillaries?
A
Numerous pores (fenestrations) in endothelial cells
12
Q
What is the permeability of fenestrated capillaries compared to continuous capillaries?
A
Greatly increased permeability to fluids and small solutes
13
Q
Where are fenestrated capillaries commonly located?
A
- Kidneys (glomeruli)
- Intestinal villi
- Endocrine glands
14
Q
What is the structure of sinusoidal (discontinuous) capillaries?
A
Large gaps between endothelial cells, discontinuous basement membrane
15
Q
What can pass through sinusoidal capillaries?
A
Large molecules and even cells
16
Q
Why is blood flow through sinusoids slower?
A
Allows time for exchange
17
Q
Where are sinusoidal capillaries typically found?
A
- Liver (hepatic sinusoids)
- Bone marrow
- Spleen
18
Q
What is the primary mechanism responsible for the movement of dissolved gases and small lipid-soluble substances across the endothelial cell membrane?
A
Diffusion
Diffusion is the primary process for gas exchange in capillaries.
19
Q
What does Fick’s Law of Diffusion state?
A
The rate of diffusion is proportional to the concentration gradient, membrane surface area, and permeability, and inversely proportional to membrane thickness.
This law helps predict how substances move across membranes.
20
Q
What is the difference between transcellular and paracellular pathways?
A
Transcellular: Lipid-soluble gases diffuse through endothelial cell membranes.
Paracellular: Small water-soluble substances diffuse through intercellular clefts.
These pathways describe how substances move across capillary walls.
21
Q
Define bulk flow in the context of capillary processes.
A
Movement of fluid (water + dissolved solutes) en masse from one compartment to another, driven by pressure differences.
Bulk flow is crucial for nutrient delivery and waste removal.
22
Q
Where does filtration predominantly occur in capillaries?
A
At the arteriolar end of capillaries, where capillary hydrostatic pressure is higher.
This is where fluid moves out into the interstitial space.
23
Q
What happens during the reabsorption process in capillaries?
A
Fluid moves back into capillaries from the interstitium, mainly at the venular end.
This occurs when blood colloid osmotic pressure predominates.
24
Q
What determines whether there is a net gain or loss of fluid from the capillary?
A
The balance between filtration and reabsorption.
Net filtration or reabsorption is critical for fluid homeostasis.
25
What is osmosis?
Movement of water across a semipermeable membrane from low solute concentration to high solute concentration.
## Footnote
Osmosis is essential for maintaining fluid balance in tissues.
26
What is the main osmotic force exerted in capillaries?
Plasma proteins, especially albumin, create an osmotic gradient (colloid osmotic pressure).
## Footnote
This gradient helps retain fluid within the vascular space.
27
What are the four Starling's forces that govern fluid exchange across the capillary?
* Capillary Hydrostatic Pressure (CHP)
* Interstitial Fluid Hydrostatic Pressure (IFHP)
* Blood Colloid Osmotic Pressure (BCOP)
* Interstitial Fluid Colloid Osmotic Pressure (IFCOP)
## Footnote
These forces are essential for understanding fluid dynamics in the circulatory system.
28
Define Capillary Hydrostatic Pressure (CHP)
The fluid (blood) pressure within the capillary lumen
## Footnote
CHP tends to push fluid out of the capillary, favoring filtration.
29
What is the typical value of Capillary Hydrostatic Pressure (CHP) at the arteriolar end?
~35 mmHg
## Footnote
This value can vary by tissue and physiological state.
30
What is the typical value of Capillary Hydrostatic Pressure (CHP) at the venular end?
~15 mmHg
## Footnote
This value can vary by tissue and physiological state.
31
Define Interstitial Fluid Hydrostatic Pressure (IFHP)
The hydrostatic pressure of the fluid within the interstitial (tissue) space
## Footnote
IFHP tends to push fluid into the capillary if positive, or favors outward movement if negative.
32
What is the typical value of Interstitial Fluid Hydrostatic Pressure (IFHP) under normal conditions?
Around 0 mmHg or slightly negative
## Footnote
This value can influence fluid movement into or out of the capillaries.
33
Define Blood Colloid Osmotic Pressure (BCOP)
Also called 'plasma oncotic pressure,' primarily generated by plasma proteins, especially albumin
## Footnote
BCOP draws water into the capillary, favoring reabsorption.
34
What is the typical value of Blood Colloid Osmotic Pressure (BCOP) under normal physiological conditions?
~25 mmHg
## Footnote
This pressure is crucial for maintaining fluid balance in the capillaries.
35
Define Interstitial Fluid Colloid Osmotic Pressure (IFCOP)
Oncotic pressure due to proteins present in the interstitial space
## Footnote
IFCOP draws water out of the capillary, favoring filtration.
36
What is the typical value of Interstitial Fluid Colloid Osmotic Pressure (IFCOP)?
Usually low (~1–5 mmHg)
## Footnote
This value can rise significantly if vascular permeability is increased.
37
Write the equation for Net Filtration Pressure (NFP).
NFP = (CHP - IFHP) - (BCOP - IFCOP)
## Footnote
NFP determines whether net filtration or net reabsorption occurs.
38
What occurs when Net Filtration Pressure (NFP) is positive?
Net filtration occurs
## Footnote
This means fluid is moving out of the capillaries into the interstitial space.
39
What occurs when Net Filtration Pressure (NFP) is negative?
Net reabsorption occurs
## Footnote
This indicates fluid is moving from the interstitial space back into the capillaries.
40
What is the average amount of fluid filtered from capillaries that is not reabsorbed?
~2–3 L/day
41
What role does the lymphatic system play in relation to excess fluid?
Collects excess fluid and returns it to the venous circulation via the thoracic duct or right lymphatic duct
42
What are lymph nodes responsible for?
Filtering pathogens, debris, and foreign antigens
43
Which immune cells are involved in immune responses within lymph nodes?
Lymphocytes and macrophages
44
How does the lymphatic system regulate interstitial protein oncotic balance?
Helps clear proteins from interstitial fluid to prevent excess accumulation
45
What can excessive accumulation of proteins in tissue space lead to?
Increased interstitial fluid colloid osmotic pressure (IFCOP) and fluid retention
46
What is lymphedema?
Accumulation of excess fluid in the interstitium due to inadequate lymphatic drainage
47
What are some causes of lymphatic blockage?
Filariasis, tumor invasion
48
Fill in the blank: The lymphatic system returns excess fluid to the venous circulation via the _______.
[thoracic duct or right lymphatic duct]
49
True or False: The lymphatic system has no role in immune functions.
False
50
Define Oedema
Oedema refers to the excess accumulation of fluid in the interstitial spaces or within cells, leading to tissue swelling.
## Footnote
Clinically recognized by palpable or visible increase in tissue fluid volume.
51
What physiological factors regulate fluid exchange between capillaries and interstitial compartments?
Starling’s forces, which include:
* Capillary hydrostatic pressure
* Capillary oncotic pressure
* Interstitial fluid hydrostatic pressure
* Interstitial fluid oncotic pressure
## Footnote
Also influenced by lymphatic drainage.
52
What is localized oedema?
Localized oedema may reflect local injury or inflammation, such as in an inflamed joint or around a site of infection.
53
What is generalized oedema?
Generalized oedema, such as anasarca, often points to systemic disorders like heart failure, liver disease, or nephrotic syndrome.
54
What is the core mechanism behind increased capillary hydrostatic pressure?
Excessive fluid filtration into tissues due to elevated blood pressure in capillaries.
55
What are common causes of increased capillary hydrostatic pressure?
* Elevated venous pressures (e.g., heart failure)
* Venous obstruction (e.g., deep vein thrombosis)
* Excess fluid retention (e.g., renal failure)
## Footnote
Particularly seen in right-sided heart failure.
56
What does decreased plasma oncotic pressure cause?
Diminished inward pulling force that normally retains fluid in the vascular space.
57
List common causes of decreased plasma oncotic pressure.
* Hypoalbuminemia
* Liver disease (decreased albumin synthesis)
* Nephrotic syndrome (loss of protein through urine)
* Malnutrition (inadequate albumin production)
## Footnote
Leads to fluid shifting into the interstitial compartment.
58
What is the core mechanism of increased capillary permeability?
Damage or disruption of the endothelial barrier allows proteins and fluid to move freely into the interstitial space.
59
What are common causes of increased capillary permeability?
* Inflammation/Infection
* Allergic reactions (e.g., anaphylaxis)
* Burns or trauma
## Footnote
Results in higher interstitial fluid colloid osmotic pressure, drawing fluid into tissues.
60
What is the core mechanism behind lymphatic obstruction?
Blockage of lymphatic vessels prevents the return of excess interstitial fluid and proteins to the venous circulation.
61
List common causes of lymphatic obstruction.
* Malignancy (tumor growth)
* Infections (e.g., filariasis)
* Surgical disruption (e.g., lymph node removal)
## Footnote
Leads to accumulation in the tissue, often presenting as non-pitting oedema.
62
What are common causes of elevated venous pressures?
* Congestive heart failure
* Deep venous thrombosis
* Hepatic cirrhosis with portal hypertension
## Footnote
Characterized by pitting peripheral oedema and jugular venous distension.
63
What is a characteristic clinical manifestation of peripheral oedema?
Often noticed in the ankles and feet due to gravity-dependent fluid accumulation.
64
What is pitting oedema?
When pressed, a temporary indentation persists.
65
What are clinical correlations of pulmonary oedema?
* Dyspnea (especially orthopnea)
* Paroxysmal nocturnal dyspnea
* Crackles (rales) on lung auscultation
## Footnote
Often a hallmark of left-sided heart failure.
66
What is ascites?
Fluid accumulation in the peritoneal cavity.
67
List clinical presentations of ascites.
* Abdominal distension
* Fullness
* Discomfort
* Shifting dullness on percussion
* Fluid wave sign
## Footnote
Commonly associated with portal hypertension or hypoalbuminemia.
68
What is hepatomegaly?
Enlargement of the liver, which may be tender or non-tender on palpation.
69
What is raised JVP (Jugular Venous Pressure)?
Visually assessed by looking at the neck veins in a semi-recumbent position.
70
What does an elevated JVP indicate?
Increased central venous pressure.
71
True or False: Increased capillary permeability can be caused by trauma.
True
72
Define Heart Failure
Heart Failure is a clinical syndrome in which the heart fails to pump sufficient blood to meet the body’s metabolic demands or can only do so at the cost of elevated filling pressures.
## Footnote
Common manifestations include fluid retention and inadequate organ perfusion.
73
What are common manifestations of Heart Failure?
* Fluid retention (leading to oedema and/or pulmonary congestion)
* Inadequate organ perfusion (leading to fatigue, reduced exercise tolerance, and end-organ dysfunction)
74
What physiological changes occur in Heart Failure?
Compensatory mechanisms such as sympathetic activation, RAAS stimulation, and ventricular remodeling eventually become maladaptive, exacerbating the syndrome.
75
What is Systolic Heart Failure (HFrEF)?
Heart Failure with reduced Ejection Fraction (EF typically <40%), primarily due to impaired myocardial contractility.
76
What is Diastolic Heart Failure (HFpEF)?
Heart Failure with preserved Ejection Fraction (EF >50%), often due to decreased ventricular compliance and relaxation abnormalities.
77
What is Borderline Heart Failure (HFmEF)?
A 'mid-range' EF category (41–49%) recognized in some guidelines.
78
List major risk factors for Heart Failure.
* Hypertension
* Coronary Artery Disease
* Diabetes Mellitus
* Obesity
* Valvular Heart Disease
* Advanced Age
79
What are the primary etiologies of Heart Failure?
* Ischemic Heart Disease
* Hypertension
* Valvular Disorders
* Cardiomyopathies
* Arrhythmias
* Other Causes
80
What is the pathophysiology of Forward Failure in Left Heart Failure?
The left ventricle fails to effectively pump blood into the systemic circulation, reducing cardiac output and tissue perfusion.
81
What is Backward Failure in Left Heart Failure?
Elevated left ventricular end-diastolic pressure transmits back into the left atrium and pulmonary veins, causing pulmonary congestion.
82
What are common clinical features of Left Heart Failure?
* Dyspnea on exertion and orthopnea
* Paroxysmal nocturnal dyspnea
* Bibasilar Crackles (Rales)
* Fatigue and Reduced Exercise Tolerance
* S3 Heart Sound
83
What is the pathophysiology of Right Heart Failure?
Secondary to Left-Sided Failure or isolated right-sided failure from primary pulmonary disease.
84
List clinical features of Right Heart Failure.
* Peripheral Edema
* Jugular Venous Distension (JVD)
* Hepatomegaly
* Ascites
* Congestion of Visceral Organs
85
What are the ACC/AHA stages of Heart Failure?
* Stage A: High risk for developing HF but no structural heart disease
* Stage B: Structural heart disease present but no symptoms
* Stage C: Structural heart disease with prior or current symptoms
* Stage D: Refractory HF requiring specialized interventions
86
What is the NYHA Functional Classification of Heart Failure?
* Class I: No limitation of physical activity
* Class II: Slight limitation of physical activity
* Class III: Marked limitation of physical activity
* Class IV: Symptoms at rest
87
True or False: The ACC/AHA stages focus on functional limitations.
False
88
What are key takeaways regarding Heart Failure?
* Heart Failure is a complex syndrome
* Stages track the evolution of disease
* Left HF manifests with pulmonary symptoms
* Right HF features systemic venous congestion
89
What is Cardiac Remodeling?
A spectrum of molecular, cellular, and structural adaptations in the heart in response to chronic injury or hemodynamic stress.
## Footnote
Includes changes in size, shape, and function of the myocardium affecting myocytes and the extracellular matrix.
90
What is the difference between Physiological and Pathological Remodeling?
Physiological remodeling occurs with regular exercise or pregnancy, while pathological remodeling is triggered by sustained pressure or volume overload, ischemia, or toxic insults.
## Footnote
Physiological remodeling typically preserves or improves cardiac function, whereas pathological remodeling impairs it.
91
What are some underlying molecular/chemical mediators of Cardiac Remodeling?
* Neurohormonal Activation
* Growth Factors and Cytokines
* Genetic Reprogramming of Myocytes
## Footnote
Examples include TGF-β and Endothelin-1 influencing gene expression.
92
What are the causes of Cardiac Remodeling?
* Pressure Overload
* Volume Overload
* Myocardial Infarction (MI)
* Neurohormonal Factors
## Footnote
Each cause leads to specific structural and functional alterations in the heart.
93
What is Pressure Overload in the context of Cardiac Remodeling?
Long-standing hypertension or aortic stenosis requiring the ventricle to generate higher pressures.
## Footnote
This prompts changes in cardiomyocyte architecture, such as adding sarcomeres in parallel.
94
What is Volume Overload in the context of Cardiac Remodeling?
Chronic valvular regurgitation or chronic anemia leading to chamber dilation.
## Footnote
The ventricle accommodates greater blood volume, adding sarcomeres in series.
95
What is Concentric Remodeling?
A pattern where ventricular wall thickness increases, often resulting in reduced chamber diameter or volume due to pressure overload.
## Footnote
This is characterized by wall thickening and increased wall-to-cavity ratio.
96
What are the complications of Concentric Remodeling?
* Diastolic Dysfunction
* Progression to Systolic Dysfunction
* Increased Myocardial Oxygen Demand
## Footnote
These complications can lead to heart failure with preserved ejection fraction (HFpEF).
97
What is Eccentric Remodeling?
A pattern where the ventricular chamber dilates, often with relative wall thinning or normal wall thickness due to volume overload.
## Footnote
It is characterized by increased internal diameter of the ventricle.
98
What are the complications of Eccentric Remodeling?
* Systolic Dysfunction
* Increased Wall Stress and Valvular Compromise
* Arrhythmias
## Footnote
These complications can lead to reduced ejection fraction (HFrEF) and disrupt normal electrical conduction.
99
How does Concentric Remodeling differ from Eccentric Remodeling?
Concentric remodeling is associated with pressure overload and diastolic dysfunction, while eccentric remodeling is linked to volume overload and systolic dysfunction.
## Footnote
The progression of heart failure symptoms can occur in both types of remodeling.
100
What role does neurohormonal blockade play in cardiac remodeling?
Therapies like ACE inhibitors, beta-blockers, and ARNI can slow or partially reverse remodeling by reducing chronic RAAS and sympathetic stimulation effects.
## Footnote
Understanding these therapies is critical for managing heart failure progression.
101
What is the hallmark symptom of heart failure?
Dyspnea (shortness of breath) on exertion
## Footnote
Dyspnea is a key indicator of heart failure severity.
102
What does orthopnea refer to in heart failure patients?
Dyspnea when lying flat, often measured by the number of pillows needed to sleep comfortably
## Footnote
This symptom indicates worsening heart failure.
103
What is Paroxysmal Nocturnal Dyspnea (PND)?
Sudden nighttime episodes of severe shortness of breath
## Footnote
PND often occurs during sleep due to fluid redistribution.
104
What are common signs of fluid retention in heart failure?
Edema or weight gain, especially swelling in ankles, legs, or abdomen
## Footnote
Fluid retention is a direct consequence of heart failure.
105
What does Jugular Venous Distension (JVD) indicate?
Elevated right-sided filling pressures
## Footnote
JVD is assessed during physical examination for heart failure.
106
What do pulmonary crackles (rales) signify in heart failure?
Fluid in the alveolar spaces from pulmonary venous congestion
## Footnote
Crackles are indicative of heart failure-related pulmonary issues.
107
What does an S3 Gallop indicate?
Volume overload and reduced left ventricular function
## Footnote
The S3 sound is often found in patients with heart failure.
108
What is the gold standard diagnostic test for heart failure?
Echocardiogram
## Footnote
It evaluates ejection fraction, chamber sizes, and valvular function.
109
What does an elevated BNP or NT-proBNP level indicate?
Presence of heart failure; levels correlate with disease severity
## Footnote
These biomarkers help differentiate cardiac from non-cardiac causes of dyspnea.
110
What is the significance of a Chest X-Ray in diagnosing heart failure?
Assesses cardiac silhouette for cardiomegaly and signs of pulmonary congestion
## Footnote
CXR is a quick, non-invasive method to evaluate fluid overload.
111
What does the presence of Kerley B lines on CXR indicate?
Interstitial edema in the interlobular septa
## Footnote
These lines are characteristic of heart failure.
112
What is the relationship between heart failure and renal impairment?
Hypoperfusion leads to reduced glomerular filtration rate (GFR) and fluid retention
## Footnote
This condition is known as cardiorenal syndrome.
113
What is congestive hepatopathy?
Hepatic congestion due to elevated central venous pressure from right-sided heart failure
## Footnote
It can lead to liver dysfunction and coagulopathy.
114
What arrhythmia is commonly associated with advanced heart failure?
Atrial fibrillation
## Footnote
It exacerbates heart failure symptoms and can lead to rapid ventricular rates.
115
What complication can arise from chronic pulmonary congestion in heart failure?
Increased risk of infections or impaired gas exchange
## Footnote
Chronic congestion can lead to significant pulmonary complications.
116
What does a reduced cardiac output in severe heart failure lead to?
Hypotension and end-organ hypoperfusion
## Footnote
This condition may result in cardiogenic shock.
117
What is a key diagnostic feature of heart failure on an echocardiogram?
Measurement of ejection fraction (EF)
## Footnote
EF is crucial for classifying heart failure into HFrEF and HFpEF.
118
True or False: An ECG is definitive for diagnosing heart failure.
False
## Footnote
While helpful, ECG is not definitive but guides further evaluation.
119
Fill in the blank: Elevated BNP levels can differentiate cardiac causes of dyspnea from _______.
[non-cardiac causes]
## Footnote
BNP aids in distinguishing between cardiac and non-cardiac dyspnea.
120
What findings on a chest radiograph may indicate elevated pulmonary venous pressures?
Alveolar edema, upper lobe diversion, cardiomegaly, pleural effusions
## Footnote
These findings are characteristic of heart failure.
121
What is acute decompensated heart failure (ADHF)?
ADHF typically manifests with worsening congestion, hypoperfusion, or both.
122
What are the principal goals in the acute management of ADHF?
Stabilize the patient, relieve symptoms, restore adequate tissue perfusion.
123
What does the acronym ABCs stand for in acute management?
Airway, Breathing, Circulation.
124
When should non-invasive positive pressure ventilation be considered?
If the patient is significantly hypoxic or in severe respiratory distress.
125
What positioning is recommended to reduce pulmonary congestion?
Upright positioning.
126
What are loop diuretics used for in ADHF?
Provide rapid volume reduction by promoting diuresis.
127
Name three examples of loop diuretics.
* Intravenous furosemide
* Bumetanide
* Torsemide
128
What is the mechanism of action of vasodilators in ADHF?
Reduce preload and afterload, improving cardiac output.
129
What are two examples of vasodilators used in ADHF?
* Nitroglycerin
* Sodium nitroprusside
130
What is the indication for oxygen and non-invasive ventilation in ADHF?
If the patient is hypoxic (O₂ saturation <90–92%).
131
When are intravenous inotropes used in ADHF?
In patients with low output and poor end-organ perfusion.
132
What should be monitored during diuretic therapy?
* Renal function
* Electrolytes
* Blood pressure and hemodynamics
133
True or False: Intravenous morphine is commonly used in ADHF management.
False
134
What is the primary goal of chronic heart failure management?
Slow disease progression, reduce morbidity and mortality, improve quality of life.
135
What are two lifestyle modifications recommended for chronic heart failure?
* Sodium restriction
* Regular moderate exercise
136
Name two classes of pharmacological agents used in chronic heart failure.
* ACE Inhibitors (or ARBs)
* Beta-Blockers
137
What is the mechanism of action of ACE inhibitors?
Reduce afterload and ventricular remodeling by inhibiting angiotensin II.
138
What is an example of an Angiotensin Receptor-Neprilysin Inhibitor?
Sacubitril/valsartan (Entresto).
139
What is the clinical benefit of beta-blockers in chronic heart failure?
Improved survival, especially in systolic heart failure.
140
Fill in the blank: Mineralocorticoid Receptor Antagonists (MRA) block _______’s effects.
aldosterone
141
What is the indication for hydralazine and isosorbide dinitrate?
Beneficial in African American patients with HFrEF.
142
What is the rationale for Cardiac Resynchronization Therapy (CRT)?
Improves synchrony of contraction and cardiac function in patients with conduction delays.
143
What is the indication for an Implantable Cardioverter-Defibrillator (ICD)?
Patients with significantly reduced ejection fraction (<35%) at high risk for life-threatening arrhythmias.
144
What is essential for titration and monitoring of ACE inhibitors and ARBs?
Monitor renal function and potassium.
145
What is the focus of management in acute decompensated heart failure?
Stabilization, rapid relief of congestion, inotropic support if perfusion is low.
146
What are the long-term therapies emphasized in chronic heart failure management?
* Neurohormonal blockade
* Diuretic use
* SGLT2 inhibitors
* Lifestyle modifications
* Device therapy
147
What should be tailored to patient comorbidities in heart failure management?
Therapies should be individualized.
148
What is the definition of shock?
Shock is a pathophysiological state of inadequate tissue perfusion leading to cellular hypoxia and organ dysfunction.
149
What is the primary issue shared by all forms of shock?
Impaired oxygen delivery to tissues.
150
What are the major types of shock?
* Hypovolemic Shock
* Cardiogenic Shock
* Distributive Shock
* Obstructive Shock
151
What causes hypovolemic shock?
Insufficient intravascular volume due to hemorrhage, severe dehydration, or third-spacing of fluids.
152
What is the pathophysiology of hypovolemic shock?
Reduced preload → decreased stroke volume and cardiac output → hypotension and poor tissue perfusion.
153
What compensatory mechanisms are activated in hypovolemic shock?
* Tachycardia
* Intense peripheral vasoconstriction
* RAAS activation to retain sodium and water
154
What causes cardiogenic shock?
Cardiac pump failure due to conditions like myocardial infarction or severe arrhythmias.
155
What is a key feature of cardiogenic shock?
Pulmonary edema, elevated jugular venous pressure, and hypotension.
156
What is the pathophysiology of distributive shock?
Marked vasodilation and inappropriate blood distribution cause a relative hypovolemia.
157
What are the subtypes of distributive shock?
* Septic Shock
* Anaphylactic Shock
* Neurogenic Shock
158
What triggers septic shock?
Systemic infection and inflammatory response.
159
What is the cause of obstructive shock?
A mechanical obstruction to cardiac filling or ejection.
160
What are examples of conditions that cause obstructive shock?
* Pulmonary embolism
* Tension pneumothorax
* Cardiac tamponade
161
What are the three stages of shock?
* Initial (Compensated) Stage
* Progressive (Decompensated) Stage
* Irreversible (Refractory) Stage
162
What physiological changes occur in the initial stage of shock?
* Sympathetic activation
* RAAS stimulation
* Sodium and water retention
163
What clinical presentations are seen in the initial stage of shock?
Blood pressure may be normal or slightly reduced; cold, clammy extremities; mild tachypnea.
164
What occurs during the progressive stage of shock?
Worsening hypoperfusion leads to tissue hypoxia and organ dysfunction.
165
What are the clinical features of the progressive stage of shock?
* Marked tachycardia
* Hypotension
* Confusion or lethargy
* Cool/clammy skin
166
What characterizes the irreversible stage of shock?
Severe cellular and tissue damage; multiple organ dysfunction syndrome (MODS).
167
What are the clinical presentations in the refractory stage of shock?
* Profound hypotension
* Rapid deterioration in mental status
* Multi-organ failure
168
What is the primary mechanism of cardiogenic shock?
Primary cardiac dysfunction leading to low cardiac output and poor end-organ perfusion.
169
What are the clinical hallmarks of cardiogenic shock?
* Pulmonary edema
* Elevated jugular venous pressure
* Marked hypotension
170
What are key clinical features of the compensatory stage of cardiogenic shock?
* Tachycardia
* Cool/clammy skin
* Mild hypotension
171
What occurs during the progressive stage of cardiogenic shock?
Marked hypotension and confusion; signs of metabolic acidosis.
172
What are the clinical features of the refractory stage of cardiogenic shock?
* Profound hypotension
* Severe organ failures
* Risk of arrhythmias or cardiac arrest
173
What is an important aspect of managing cardiogenic shock?
Improving cardiac output and restoring coronary perfusion.
174
What types of fluids are used cautiously in the management of cardiogenic shock?
IV Fluids.
175
What are examples of inotropes used in cardiogenic shock management?
* Dobutamine
* Milrinone
176
What is the role of vasopressors in cardiogenic shock?
Used if hypotension is profound and not responsive to inotropes.
177
What is necessary for monitoring patients in cardiogenic shock?
Continuous monitoring of ECG, invasive blood pressure, and urine output.
178
What is the purpose of mechanical circulatory support in cardiogenic shock?
To provide support to the failing ventricle or to improve coronary perfusion.
179
What does shock represent in clinical terms?
A life-threatening condition where tissue perfusion is inadequate to sustain normal cellular metabolism.
180
What are critical aspects of managing shock?
Timely intervention and definitive treatment of the underlying cause.
