Shock Flashcards
1
Q
What is shock?
A
- CV system fails to adequately perfuse cells, tissues, and organs, resulting in widespread impairment of cellular metabolism and tissue function
- all types of shock are characterized by decreased oxygen delivery and/or increased tissue demand for oxygen
- cells become damaged and death my occur as a result of multiple organ failure
2
Q
What determines oxygen delivery?
A
- Blood Pressure: shock is not always associated with a decrease in BP but in order to perfuse tissues with blood a BP needs to be generated to keep blood moving around. BP = CO x SVR. SVR is needed to create a BP however too much will increase BP at the expense of tissue perfusion.
- Systemic Vascular Resistance: SVR= viscosity x length/radius^4. Radius contributes most to SVR- if radius of vessel is halved, resistance would increase by factor of 16.
- Cardiac Output: CO= SV x HR. HR largely regulated by autonomic input. SV regulated by preload, contractility, and afterload.
- Stroke Volume: affected by preload, contractility and afterload. Preload is related to amount of filling of ventricle during diastole. As it fills more it stretches which stimulates stronger contraction and increased SV. In hypovolemic shock, preload is less resulting in decline in SV and CO. Afterload is pressure ventricle must overcome. As afterload increases, SV decreases. More forceful contraction allows ventricle to generate more pressure which increases SV. Positive inotropes will increase contractility.
- Oxygen content: Partial pressure of oxygen and hemoglobin concentration contribute to oxygen content of the blood. Oxygen flows from high PP to low PP. 98.5% of oxygen in blood is bound to hemoglobin molecules in erythrocytes. Decrease in hemoglobin will cause a decrease in oxygen content. Respiratory disorders will affect the PPs or a decrease in blood flow to lungs will affect oxygen content.
3
Q
What increases oxygen demand from tissues?
A
BMR
- basal metabolic rate governs the rate at which tissues use oxygen
- largely regulated by thyroid hormone
- hyperthyroidism causes increased tissue demand for oxygen because BMR is elevated
- infection/fever is energy intensive so BMR increases
- signalling molecules released from immune cells signal to hypothalamus to change body temp and make immune cells more metabolically active
- increase in body temp also causes other body tissues to take in more oxygen at rest
- increased work of organs: kidneys and brain consume lots of energy at rest to generate ATP to keep ion pumps running, without these pumps we could not generate electrical impulses or rid body of waste
- heart and lungs account for 1/3 of energy expenditure at rest
- agitation or pain: increase in HR and respiratory rate, clench skeletal muscles, increases oxygen consumption at rest
4
Q
How is the heart affected by increased oxygen demand to the tissues?
A
- increased workload and thus increased oxygen demand at the heart
- increasing oxygen demand to a heart that is damaged by atherosclerosis or other things may damage the heart further
5
Q
How are cellular processes affected by shock?
A
- in the presence of oxygen cells break down glucose through aerobic respiration which yields 36 ATP per glucose molecule
- impaired delivery of oxygen to tissues causes a switch to anaerobic respiration which generates ATP from glucose without oxygen which yields 2 ATP per glucose and generates lactic acid
- leads to a deficit of ATP in the cell
6
Q
Describe the vicious circle in shock
A
- inadequate bloodflow to the organs leads to tissue hypoxia
- this leads to lactic acid accumulation and drop in pH
- metabolic acidosis ensues
- also occurs in the heart with low oxygen
- drop in pH is detrimental to heart contractility resulting in cardiac depression and reduced cardiac output
- this further impairs blood flow to organs causing further hypoxia
7
Q
What are the body’s responses to shock (ie. stages of shock)?
A
- initial stage: cellular alterations as a result of reduced oxygen delivery and utilization- no clinical symptoms except for elevated lactic acid
- compensatory stage: neural, hormonal, and chemical responses designed to improve tissue perfusion and oxygen delivery
- progressive: equivalent to multi organ failure (kidney, liver, GI tract are notable)
- refractory: permanent damage to myocardium and other tissue occurs, no longer able to maintain CO and death is inevitable
8
Q
What occurs during the compensatory stage of shock?
A
Neural
- neural responses activated immediately following a drop in BP originating from autonomic reflexes from baroreceptors
- baroreceptors detect drop in BP and send afferent impulses to CV system in brain, CV system will activate sympathetics which increase HR, contractility of myocardium, and vasoconstriction which causes an increase in peripheral vascular resistance, cardiac output, and BP
- reduced blood flow to kidneys, GI tract, and skin
Hormonal
- Adrenal Medulla: releases NE and EP to help increase peripheral vascular resistance, HR, myocardial contractility, CO, and BP
- Posterior Pituitary: releases ADH which increases renal water reabsorption, thereby increasing blood volume. ADH causes vasoconstriction increasing SVR. Both help to increase BP. ADH released when osmoreceptors detect drop in BP. Works over hours-days.
- RAA system: drop in blood volume/pressure reduces blood flow to kidneys. JG cells sense this reduction in BP and will start to release renin. Increased sympathetics or hyponatremia can also cause renin release. AII acts on vascular smooth muscle receptors to vasoconstrict which increases SVR. Stimulates release of aldosterone which promotes sodium and water retention.
Chemical Response
- hypoxemia and acidosis will stimulate an increase in respiratory depth and rate in an effort to improve blood oxygenation and to blow off CO2 to correct for the acidosis
- chemoreceptors in aortic arch and carotid bodies send afferent signals to respiratory centres of brainstem
- proton and bicarbonate are converted to carbonic acid which dissociates into water and CO2
- as you breathe out more CO2, buffer system will create more CO2 which will reduce amount of H+
9
Q
Describe the compensatory mechanisms for hypovolemic shock (flow chart)
A
10
Q
What is cardiogenic shock?
A
- cardiogenic: comes about due to failure of the pump including MI, cardiac conduction problems (arrhythmias), or disease of the heart muscles (cardiomyopathy), severe valve problems–> inability of heart to contract or contract in a coordinated manner
- reduced SV (or HR)
11
Q
What is obstructive shock?
A
- obstructive: obstruction to blood flow which either impedes filling or emptying of the heart.
- Common causes are pulmonary embolism (impedes blood flow through pulmonary circuit), pericardial effusion ie. cardiac tamponade which impedes proper filling of the heart, or tension pneumothorax (collapsed lung) which obstructs filling of heart by causing collapse of vena cava and right atrium
- impaired blood flow
12
Q
What is hypovolemic shock?
A
- reduction in total blood volume
- can be related to bleeding (trauma or ulcer) or excessive loss of body fluids (dehydration- heat shock, diuretics, diarrhea, emesis)
- reduced preload
13
Q
What is distributive shock?
A
- profound vasodilation that increases capacity of vascular system such that one’s normal blood volume may not be sufficient to fill the space and maintain a BP
- vasodilation is often accompanied by increase in capillary permeability so fluid starts to leak from BVs into the tissues
- common causes are sepsis, anaphylaxis, acute spinal cord injury (loss of symp to BVs), venoms, overactive thyroid
- low SVR
14
Q
What types of shock present with cyanosis?
A
- cardiogenic, hypovolemic, obstructive
- reduction in blood flow to skin and hypoxemia (due to poor/absent blood flow to lungs) so appear cyanotic
- in cardiogenic, lack of pumping of heart and intense peripheral vasoconstriction means there is little/no blood flow to skin, sweating from increased symp output; cool and clammy skin
- in obstructive, interruption of blood flow means it does not pass to lungs to get oxygenated, present profoundly blue
- in hypovolemic, compensatory mechanisms shunt blood from skin to make it available for heart and brain, peripheral pulse not palpable
- distributive shock there is an increased perfusion of blood to the skin from widespread vasodilation which results in flushed skin, heart pumps against little SVR so patients can’t maintain good diastolic BP resulting in bounding peripheral pulses, CO may be greater but lack of vascular tone makes it so that there is insufficient flow to tissues
15
Q
A 65 year old man with a history of hypertension was admitted with severe, sudden-onset chest pain. His physical examination showed sinus tachycardia, low systolic pressure, cool extremities, low urine output, and altered mental status. Blood test for cardiac enzymes and ECG findings were suggestive of an MI.
A
- cardiogenic shock
- inability of heart to pump adequate blood to tissues and organs
- CO decreases which causes RAA activation, neurohormonal stimulation, and SNS activation
- emergency requiring immediate resuscitative therapy to prevent irreversible tissue/organ damage
- key to good outcome is rapid diagnosis and prompt initiation of pharmacologic therapy to maintain BP and CO
- PCI to reestablish blood flow to myocardium
16
Q
29 year old pregnant lady was admitted to LAD following rupture of her membranes. Despite progress in labour, the patient underwent a C-section as baby was breech. There was an unusual amount of blood loss during surgery. About 30 mins after the end of the operation, patient’s BP fell and she entered cardio-pulmonary arrest. CPR was performed and heart was restarted but patient was unstable. Despite several blood transfusions, the patient died the following day.
A
- hypovolemic shock
- loss of blood volume either whole blood, plasma (burns), or interstitial fluid (diaphoresis, diabetes, emesis, dehydration)
- develops when intravascular volume has decreased by 15%
- catecholamine release to increase HR and SVR, RAA activation to improve blood volume and BP
- emergency and treatment should be started immediately
- oxygen delivery and controlling bleeding and volume support/replacement are gold standard
17
Q
A 46 year old man with a history of tuberculosis. RR=40, BP=75/40, pitting edema in lower limbs. Chest auscultation revealed crackles at both bases. The heart sounds were muffled and jugular venous distention was visible. Evidence of excessive pericardial fluids on CXR. Pericardial fluid was positive for TB.
A
- obstructive shock (cardiac tamponade)
- cardiac tamponade occurs from buildup of fluid in pericardial space
- fibrous pericardium largely resists stretching
- results in increased pressure that compresses the heart and prevents it from properly expanding during filling phase
- when pericardial fluid accumulates slowly as with TB, pericardial sac will expand over time before cardiac tamponade ensues
- can get venous overload in systemic and pulmonary circuits
18
Q
While eating an ice cream Jason receives a bee sting. The site becomes red and inflamed and Jason begins to feel lightheaded and short of breath. He suddenly falls to the ground. His pulse is rapid and weak.
A
- distributive shock
- overall decrease in SVR
- often accompanied by increase in CO
- sepsis and anaphylaxis are the 2 most common etiologies of distributive shock
