WEEK 3: Shock Flashcards
What is a shock?
Inadequate tissue/organ perfusion to meet metabolic demands.
A1: Shock is a condition in which inadequate tissue perfusion results in insufficient delivery of oxygen to meet the body’s metabolic needs
What is the relationship between shock and hypotension?
A2: Inadequate perfusion in shock is often associated with hypotension or relative hypotension
Q3: What happens at the tissue level in shock?
A3: In shock, there is inadequate oxygen delivery at the tissue level, leading to cellular and tissue hypoxia
State the determinants of blood pressure.
Factors
*Circulating blood volume
*Cardiac output (pump function)
*Capacity/state of the blood vessels
BP = CO x SVR
CO: cardiac output
SVR: systemic vascular resistance
State the determinants of cardiac output.
The determinants of cardiac output include:
Heart Rate (HR): A higher heart rate increases cardiac output by multiplying with stroke volume.
Stroke Volume (SV): Determined by three factors:
*Preload:
Increased preload leads to an increase in stroke volume. Preload depends on factors like intrathoracic pressure, atrial contribution, central venous pressure, mean systemic filling pressure, ventricular compliance, and duration of ventricular diastole.
*Afterload:
Factors affecting afterload include ventricular radius, ventricular wall thickness, transmural pressure, intrathoracic pressure, ventricular cavity pressure, outflow impedance, aortic input impedance, arterial resistance, vessel radius, blood viscosity, length of the arterial tree, and influence of reflected pressure waves.
*Contractility:
Increased contractility improves stroke volume at any given preload or afterload value. It’s affected by heart rate, afterload, preload, cellular and extracellular calcium concentrations, and temperature
NOTE:
Preload: Refers to the amount of blood already in the ventricles before pumping. DEPENDS ON BLOOD VOLUME.
Afterload: Refers to the resistance the heart faces when pushing blood into the systemic circulation.
Discuss Pathophysiology of Shock.
1. At cellular level
2. At tissue level
- At the cellular level, shock results when oxygen delivery is insufficient to meet oxygen demand for aerobic metabolism
- In this delivery-dependent state, cells transition to anaerobic metabolism.
Lactic acid, inorganic phosphates, and oxygen radicals start to accumulate as a result of the mounting oxygen debt - Release of damage-associated molecular patterns (known as DAMPs or alarmins), including mitochondrial DNA and formyl peptides, incites a systemic inflammatory response.
- ATP supplies dwindle, cellular homeostasis ultimately fails, and cell death ensues through necrosis from membrane rupture, apoptosis, or necroptosis.
- At the tissue level, hypovolemia and vasoconstriction cause hypoperfusion and end-organ damage in the kidneys, liver, intestine, and skeletal muscle, which can lead to multiorgan failure in survivors.
- In extreme hemorrhage with exsanguination, pulselessness results in hypoperfusion of the brain and myocardium, leading to cerebral anoxia and fatal arrhythmias within minutes.
- Shock ultimately also causes endothelial dysfunction throughout the body
NOTE: Exsanguination is a term used to describe death caused by the loss of blood.
Depending on an individual’s health, people usually die from losing half to two-thirds of their blood; a loss of roughly one-third of the blood volume is considered very serious
70 yo female brought by her family. She was confused when they went to call on her this morning in the village.
VS: BP 80/60, HR 160, temp 36.8
General: pale, ill appearing, eyes closed
Oral: Dry Mucous Membranes: (DEHYDRATION)
Neck: supple
Abdo: soft, non-tender, bowel sounds decreased
Lungs: crackles at bases (SHOWS FLUID)
Neuro: Opens eyes to voice and pain, then mumbles incoherently. Moves all extremities
Skin: no rashes. (RULES OUT SEPTIC SHOCK)
Cool hands and feet. Body is warm. (CENTRALISATION OF BLOOD FLOW: blood to more important from less important organs)
Does the patient have hypotension?
Does the patient have shock?
Why might the patient be in shock?
What tissue/organ is not getting enough blood?
Why is her heart rate fast?
Why are her hands and feet cold? (it is summer)
- Yes
- Yes
Remember: BP = SVR x CO (= stroke volume x HR)
Something in the above equation is not working
Remember the main determinants of BP & perfusion:
*Blood volume (impact on stroke volume and CO)
*Heart contractility (impact on stroke volume and CO)
*Vascular tone: Impact on SVR
What could be affecting the above?
- Brain, liver, kidney, spleen, lungs, heart
- To compensate for hypotension by increasing cardiac output
- Centralization of blood to the more important organs
State the types and causes of shock.
Blood Volume: Hypovolemic shock
Heart Contractility: Cardiogenic shock
Vascular Tone: Distributive shock
*“warm” shock with warm extremities
Discuss the causes of hypovolemic shock.
Blood Volume Problem
1. Blood loss: hemorrhagic shock
2. Diarrhea/vomiting/poor fluid intake: hypovolemic shock
3. Preload obstruction: obstructive shock
Can result in Pulmonary embolism or tension pneumothorax
What is Hemorrhagic shock?
Hemorrhagic shock is a form of hypovolemic shock in which severe blood loss leads to inadequate oxygen delivery at the cellular level.
If hemorrhage continues unchecked, death quickly follows.
Discuss causes of cardiogenic shock.
Critical decrease of cardiac output,
Due to decrease of contractility of heart as a whole
(i.e. failure of cardiac pump)
Mechanisms:
1. Necrosis / large part of heart muscle is lost (most frequently extensive anterior MI), supposed loss of >40% myocardium or less in already altered myocardium (repeated MI, chronic heart failure, cardiotoxic substances / medicaments, metabolic factors)
- Malignant tachy / brady-arrhythmia (ventricular fibrillation x extreme bradycardia),
- Wall, papillary muscle or chordae tendineae rupture
Heart Contractility Problem
*Myocardial infarction
*Dysrhythmia (rhythm that is too fast or too slow)
*Toxins or toxic metabolites
*Drugs (e.g., beta blockers)
Discuss the causes of Obstruction (Obstructive shock).
Obstruction (Obstructive shock): preload problem
Pump is not filled, stroke volume decreases
Examples: Pulmonary embolism, tension pneumothorax, Cardiac tamponade.
NOTE:
*Pulmonary embolism: This occurs when a blood clot (usually from the legs) travels to the pulmonary arteries, blocking blood flow from the right-sided heart chambers to the left-sided heart chambers. The result is decreased cardiac output.
*Tension pneumothorax: In this condition, air accumulates in the pleural space, causing pressure to rise within the chest. This pressure reduces blood returning to the heart, leading to shock.
*Cardiac tamponade, also known as pericardial tamponade, is an emergency condition in which fluid accumulates in the pericardium (the sac in which the heart is enclosed).
Discuss the causes of a Distributive Shock.
Vascular Tone Problem
- Anaphylactic shock: allergic reactions
Release of histamine and other vasodilators - Neurogenic shock: spinal injuries
Loss of CNS stimulus to vasculature - Sepsis: overwhelming infection
Bacterial endotoxins & inflammatory response cytokines - Other: cortisol deficiency, toxins
State the Most common cause of distributive shock.
Sepsis or septic shock
Most common cause of distributive shock
Documented infection + SIRS with organ failure = Septic shock
Diagnosis of SIRS (Systemic inflammatory response syndrome)
Fever: > 38
Tachycardia: > 90 beats/min
Tachypnea: > 20breaths/min
PaCo2: <32mmHg
Elevated white blood count: 12000/mm3 or <4000mm3
I/T ratio: >10%
SIRS diagnosis
Presence of SIRS indicated by presence of minimum 2 of described signs. (Bone et al., 1992).
