Type of shock Flashcards
Question 1: What is the definition of shock?
Answer: Shock is any situation in which there is inadequate tissue perfusion, resulting in decreased oxygen delivery to the tissues, leading to ischemia and, over a long period of time, necrosis.
Question 2: How does shock progress?
Answer: Shock is a progressive process.
- It starts with a compensatory stage where blood pressure decreases.
- If not reversed, it progresses to a refractory stage where blood pressure cannot be restored despite exhaustive efforts, which can be deadly.
Question 3: What causes hypovolemic shock?
Answer:
Hypovolemic shock is caused by a decrease in blood volume.
- The causes include blood loss (such as from gastrointestinal bleeding, ruptured abdominal aortic aneurysm, trauma, postpartum hemorrhage, ectopic pregnancy),
- non-blood fluid loss (such as severe burns, excessive vomiting or diarrhea, bowel obstruction, acute pancreatitis, diabetic ketoacidosis).
Question 4: How can blood loss lead to hypovolemic shock?
Answer: Blood loss can lead to hypovolemic shock as it reduces the overall blood volume in the body, resulting in decreased cardiac output (CO) due to a decrease in stroke volume (SV) or heart rate (HR), or increased systemic vascular resistance (SVR) or total peripheral resistance (TPR).
Question 5: Provide examples of non-blood fluid loss causing hypovolemic shock.
Answer:
severe third-degree burns,
excessive vomiting or diarrhea,
bowel obstruction,
acute pancreatitis, and
diabetic ketoacidosis. (DIK)
Question 6: What is the pathophysiology of compensation in hypovolemic shock?
Answer:
- vasoconstriction,
- increased heart rate,
- increased contractility of the heart,
- and activation of the renin-angiotensin-aldosterone system.
These compensatory responses aim to maintain perfusion to vital organs and restore blood volume.
Question 1: How does the body compensate for decreased blood volume in hypovolemic shock?
Answer:
activation of baroreceptors in the aortic and carotid sinus, which stimulate the medullary center. The medulla then sends out action potentials that lead to various responses:
- Vasomotor center:
- It stimulates smooth muscle in the tunica media of blood vessels, resulting in vasoconstriction.
- This is achieved through the release of epinephrine, leading to an increase in systemic vascular resistance (SVR) and subsequently increasing blood pressure (BP).
- Heart:
- The medulla also sends signals to the heart, increasing heart rate (HR).
- However, even with increased contractility, the decreased end-diastolic volume (EDV) due to reduced blood volume results in a decreased stroke volume (SV) and, therefore, a decreased cardiac output (CO).
- Kidneys:
- The medulla stimulates the kidneys to increase blood volume.
- This is achieved through the release of renin, which converts angiotensinogen into angiotensin I and then angiotensin II.
- Angiotensin II causes vasoconstriction in renal vessels (increasing SVR), stimulates the adrenal cortex to produce aldosterone (increasing sodium and water reabsorption), triggers the release of antidiuretic hormone (ADH) to increase water reabsorption, and activates the thirst center.
Question 2: What are the manifestations of hypovolemic shock on complete blood count (CBC)?
Answer:
- Increased hematocrit (HCT):
- This is not due to an increase in red blood cell (RBC) count but rather a result of plasma loss, leading to hemoconcentration.
- The composition of the blood becomes more concentrated with a higher proportion of RBCs to plasma.
- Decreased hematocrit (HCT):
- Blood loss can cause a decrease in hematocrit levels.
- This decrease in blood volume can lead to cyanosis, which is characterized by a bluish cast on the fingertips, toes, lips, tongue, and mucous membranes.
- It occurs due to decreased tissue perfusion resulting from reduced blood volume.
Question 3: What are the treatments for hypovolemic shock?
Answer:
- Resuscitate blood volume: This can be achieved through intravenous (IV) administration of fluids.
Central line IV or large-bore IVs with bigger gauge needles may be used to infuse fluids faster.
The choice of fluids includes crystalloids like normal saline or lactated Ringer’s solution, as well as plasma volume expanders such as albumin or hetastarch.
- Prevent hypothermia: Hypovolemic shock can lead to a decrease in internal body temperature regulation. Preventing hypothermia is important to maintain optimal physiological function.
- Control hemorrhage: Addressing the source of bleeding and performing transfusions, if necessary, can help control ongoing blood loss.
Question 1: What are the causes of cardiogenic shock?
Answer:
- Myocarditis: Inflammation of the myocardium, often caused by the Coxsackie B virus.
Massive/multiple/severe myocardial infarction: Extensive damage to the heart muscle due to a lack of blood supply. - Aortic valve stenosis and mitral valve stenosis: Narrowing of the aortic or mitral valves, which increases the workload on the heart and weakens its pumping ability.
- Arrhythmias: Abnormal heart rhythms, including tachyarrhythmias (increased heart rate without enough time for proper filling and ejection) and bradyarrhythmias (decreased cardiac output).
Question 2: What is the pathophysiology of cardiogenic shock?
Answer:
In cardiogenic shock, the problem arises from the heart’s inability to generate sufficient power to pump an adequate volume of blood into the circulation.
The pathophysiology involves the following events and responses:
- Pump (ventricular) failure: Decreased contraction of the heart leads to a reduced ability to propel blood into the systemic, peripheral, and pulmonary circulation.
-
Decreased volume of circulating blood: This results in systemic hypotension (low blood pressure) and decreased cardiac output (CO), as blood becomes congested within the heart.
Decreased oxygen delivery to tissues: Insufficient blood flow leads to reduced oxygen delivery to tissues, resulting in decreased ATP production, increased lactic acid production, and metabolic acidosis. - Compensatory responses: The body compensates by increasing heart rate (tachycardia) and activating the renin-angiotensin-aldosterone system (RAAS) and antidiuretic hormone (ADH) system to increase systemic vascular resistance (SVR). However, these compensatory mechanisms are insufficient to overcome the underlying problem.
Question 3: What are the treatment options for cardiogenic shock?
Answer: The treatment of cardiogenic shock involves various approaches:
- Treating the underlying disease: For example, in the case of myocardial infarction, interventions such as angioplasty or thrombolytics may be used to restore blood flow to the affected coronary vessels.
- Administering oxygen: Providing supplemental oxygen is a crucial aspect of managing cardiogenic shock.
- Small amount of isotonic fluids: Intravenous administration of isotonic fluids may be used to support blood circulation.
- Vasopressors: Medications like epinephrine, dobutamine, and amrinone may be used to improve heart contractility and increase systemic vascular resistance.
- Atropine: Atropine, a medication that reduces the effects of the parasympathetic nervous system, may be administered to increase heart rate.
- Intra-aortic balloon pump: This device, placed in the abdominal aorta, assists with cardiac function by inflating during diastole and deflating during systole, improving coronary blood flow and reducing myocardial damage.
Question 1: What are the causes of obstructive shock?
Answer:
Obstructive shock occurs when there is an internal or external obstruction that affects the heart, its chambers, or the blood flow going into or out of the heart’s great vessels.
Some causes of obstructive shock include:
- Tension pneumothorax: This occurs when there is damage to the parietal pleura, leading to air accumulation in the pleural cavity. The increased pressure in the pleural cavity compresses the heart and blood vessels, impeding blood flow.
- Pericardial tamponade: In this condition, fluid accumulates in the pericardial cavity, between the visceral and parietal layers of the pericardium. The increased fluid restricts the filling of the heart chambers, leading to decreased blood volume and impaired cardiac function.
Question 2: What are the clinical manifestations of tension pneumothorax?
Answer: Tension pneumothorax can present with the following clinical manifestations:
- Tympanitic tap: Upon percussion, a loud, low-pitched, hyperresonant sound is heard, indicating the presence of gas or air in the pleural cavity.
* Decreased breath sounds on the affected side: The collapsed lung due to increased pressure prevents adequate air movement and decreases breath sounds.
- Increased jugular venous pressure (JVP) or distended neck veins: Compression of the superior vena cava (SVC) by the increased intrapleural pressure leads to decreased blood flow into the heart, causing venous congestion.
- Tracheal deviation: The trachea may be shifted contralaterally due to the pressure exerted by the accumulated air in the pleural cavity.
Question 3: What is Beck’s triad, and how does it relate to pericardial tamponade?
Answer: Beck’s triad is a set of clinical signs associated with pericardial tamponade. It includes the following:
- Jugular vein distention or increased jugular venous pressure (JVP): The compression of the superior vena cava (SVC) by the accumulated fluid in the pericardial cavity leads to elevated JVP and jugular vein distention.
- Hypotension or decreased blood pressure: The restricted filling of the heart chambers due to the increased pericardial fluid leads to decreased cardiac output and hypotension.
- Distant heart sounds: The accumulation of fluid in the pericardial cavity causes the heart sounds to be muffled and distant.
Question 1: What is a massive pulmonary embolism (PE), and how does it contribute to obstructive shock?
Answer:
refers to the presence of a large clot, often known as a saddle embolism, that obstructs the pulmonary trunk, blocking blood flow through the pulmonary artery.
- This obstruction leads to decreased fluid going into both the right and left ventricles,
- resulting in decreased end-diastolic volume (EDV), stroke volume (SV), cardiac output (CO),
- and blood pressure (BP).
- The pressure accumulates beyond the embolus, leading to an increase in pulmonary capillary wedge pressure (PCWP).
- In severe cases, this can cause rupture of capillaries, resulting in hemoptysis (coughing up blood).
While massive pulmonary embolism is more commonly associated with obstructive shock, it can also contribute to cardiogenic shock.
Question 2: How does a massive pulmonary embolism affect the V/Q ratio and oxygenation?
Answer:
A massive pulmonary embolism affects the ventilation-perfusion (V/Q) ratio in the lungs.
- The V/Q ratio represents the ratio of alveolar ventilation (V) to pulmonary blood flow (Q).
- With a massive pulmonary embolism, blood flow is significantly impaired in the affected area, resulting in a decrease in the Q component of the V/Q ratio.
- This leads to a V/Q mismatch, where ventilation exceeds perfusion.
- The overall V/Q ratio becomes greater than the normal value of 0.8.
- The decreased blood flow and impaired gas exchange result in respiratory distress, decreased oxygenation (hypoxemic hypoxia), and decreased delivery of oxygen to tissues,
- which can lead to ischemia, organ failure, and increased lactic acid production.
Question 3: How is a massive pulmonary embolism treated?
Answer: The treatment of a massive pulmonary embolism involves managing the underlying condition and addressing the obstruction. Some treatment approaches include:
- Thrombolytics: Medications such as heparin can be administered to dissolve the clot and restore blood flow.
- Embolectomy: In severe cases, surgical intervention may be required to remove the embolism.
- Oxygen administration: Supplemental oxygen is given to improve oxygenation and tissue perfusion.
- Isotonic fluids: Intravenous fluids may be administered to maintain fluid balance and support blood pressure.
- Vasopressors: These medications can increase the contractility of the heart and constrict blood vessels, which helps to improve cardiac output and blood pressure.
a. Aortic dissection
b. Massive pulmonary embolism
c. Pericardial tamponade
d. Dilated cardiomyopathy
Question 2: Which of the following defines Cardiogenic Shock?
a. Elevated Filling pressure or PCWP
b. Atrial failure
c. Systolic dysfunction
d. None of the above
Question 3: What is the mechanism behind multi-organ hypoxia in patients who go into shock?
a. Increased O2 utilization
b. Low cardiac output
c. Reduced O2 consumption
d. Severe peripheral vasodilation
Question 4: In the previous question, what treatment should you administer?
a. Epinephrine
b. Increased IV fluids to compensate for the low cardiac output
c. Treat the underlying disease and administer oxygen
d. A & C
e. All of the above
Answer: The most probable cause of her shock is c. Pericardial tamponade.
Answer: The correct answer is a. Elevated Filling pressure or PCWP.
Answer: The mechanism behind multi-organ hypoxia in patients who go into shock is b. Low cardiac output.
Answer: The treatment that should be administered in the previous question is d. A & C - Treat the underlying disease and administer oxygen.
What are the two possible causes of decreased blood pressure in shock?
Decreased cardiac output (CO)
Decreased systemic vascular resistance (SVR)
