Academic Week 7 Flashcards
What is cardiogenic shock?
Cardiogenic shock is inability of the heart to circulate blood which causes tissue hypoxia. This is defined as a systolic BP under 90 with urine output lower than 20ml/hr and normal or elevated LV filling pressure. The pathophysiology is caused by reduced stroke volume.
Cardiogenic shock can be non-obstructive or obstructive. Non obstructive causes are MI, arrhythmia, acute valvular failure, acute VSD and drug overdose. Obstructive causes are tension pneumothorax, cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, and PE.
What is hypovolaemic shock?
Hypovolaemic shock is loss of over 20% of intravascular fluid volume which is classified as haemorrhagic or non-haemorrhagic. Haemorrhagic causes include trauma, GI bleed, aortic dissection and PPH whereas non-haemorrhagic causes include GI loss, burns, acute pancreatitis, and renal fluid loss such as adrenal insufficiency, salt wasting nephropathies and drug induced diuresis.
What is distributive shock?
Distributive shock is where there is capillary leakage and vasodilation causes. This is seen in sepsis, neurogenic shock, and anaphylactic shock. Sepsis is life-threatening organ dysfunction due to a dysregulated response to infection, septic shock is sepsis and low BP despite adequate fluid replacement.
What is neurogenic shock?
Neurogenic shock is autonomic failure (usually because of a brain injury) as the loss of sympathetic vascular tone causes peripheral dilation and hence distributive shock. The causes include traumatic brain injury, spinal cord injury, cerebral haemorrhage, poisoning and spinal anaesthesia. This is a rare cause of shock.
What is anaphylactic shock?
Anaphylactic shock is a type 1 hypersensitivity reaction characterised by systemic vasodilation and increased capillary leakage. Common causes are drug reactions, bee stings, food allergies and contrast medium.
How should cardiogenic shock be treated?
- MI = PPCI, ACS treatment and diuretics
- Arrythmias = cardioversion
- Valvular failure = repair
- Drug OD = Dependent on the drug
- Tension pneumothorax = decompression
- Tamponade = pericardiocentesis
- PE = Anticoagulation and thrombolysis (altepase)
How is hypovolaemic shock treated?
- Initial resuscitation
- Blood
- Haemostasis
- Aggressive fluid for burns and pancreatitis
How is distributive shock treated?
- Sepsis: Sepsis 6
- Neurogenic: Atropine and vasopressors
- Anaphylaxis: adrenaline IM, steroids and nebs
Define opiate and opioid
An opiate is a substance which produces morphine like effects (analgesia and euphoria) and can be blocked by antagonists such as naloxone. An opioid is used to describe synthetic morphine-like drugs with non-peptide structures. All opioids are considered opiates but not all opiates are opioids.
How do opioids work?
The mechanism of action is through inhibition of excitatory neurones which reduces pain. They also stimulate the descending inhibitory pathways which prevent pain transmission.
Opioids excite neurones in the periaqueductal grey matter (PAG) and the nucleus reticularis paragigantocellularis (NRPG). These actions lead to inhibitory effects on transmission from the dorsal horn. Opioids also have a direct inhibitory effect on the dorsal horn and peripheral terminals of nociceptive afferent neurones.
There are three receptors which mediate the main pharmacological effects of opiates:
- U-receptors (Mu) are responsible for most of the analgesic effects and the main unwanted side effects
- Ō receptors (delta) may contribute to the analgesic effects but more important in the periphery
- K-receptors (kappa) contribute to analgesic effects at spinal level. Activity of these receptors produces few side effects and does not contribute to development of tolerance.
These are all g-protein coupled receptors. They inhibit adenylyl cyclase expression which reduces cAMP formation which in turn affects cell function. They also promote opening of potassium channels and inhibit opening of voltage gated calcium channels which reduces neuronal excitability and transmitter release. The overall effect is inhibition at a cellular level.
What is the antagonist to opioids?
Naloxone
What type of pain should opioids be used for?
Opioids are effective in both acute and chronic pain but are less useful in neuropathic pain. The main adverse effect is respiratory depression which is mediated by the action of u-receptors. Respiratory depression is associated with decrease in the sensitivity of the respiratory centre to CO2. One of the most troublesome side-effects of opioids and can occur at therapeutic doses.
What are the additonal side effects and therapeutic effects of opioids?
Pupil constriction is an adverse effect mediated by u and k receptor stimulation of the oculomotor muscles. Pinpoint pupils are an important diagnostic feature of opioid toxicity.
Reduced GI motility is an adverse effect because opioids increase tone and reduce motility in much of the GI tract leading to constipation. All three receptors are involved in reduced GI motility as the local effect of opioids on neurones in the myenteric plexus is inhibitory.
Euphoria is a therapeutic effect although it may factor in development of dependence. Opioids produce a strong feeling of contentment which helps to reduce anxiety and agitation associated with pain. This is mediated by u-receptors and balanced by the dysphoric effects of the k-receptor. This means the level of euphoria differs depending on the opioid.
Nausea and vomiting are related to chemical stimulation of the chemoreceptor trigger zone. It usually occurs are initiation or dose change.
Inhibition of the cough reflexes is a possible benefit and is especially seen in codeine, the mechanism of action for this is unclear. Itching is an adverse effect caused by histamine release from mast cells unrelated to action of the opioid receptors. Hypotension is another adverse effect which is thought to occur with large doses due to the action on the medulla.
How does tolerance develop to opioids?
- Opioids inhibit adenyl cyclase expression
- Leading to reduced cAMP formation
- A secondary rise in adenyl cyclase then occurs
- cAMP formation recovers in the presence of morphine
- Tolerance occurs
- Increased doses of opioid are required to achieve the same effect
How does naloxone work?
Naloxone is a short acting pure opioid antagonist with affinity for all 3 opioid receptors. It produces a rapid reversal of the effects of both endogenous and synthetic opioids. Clinical use is to treat respiratory depression resulting from opioid toxicity. Care should be taken as it can precipitate withdrawal symptoms in opioid addicts and chronic users. Naltrexone is a long-acting opioid antagonist which is used for previous opioid addicts who have been detoxified.
Define syncope
Syncope is defined as the sudden transient loss of consciousness and postural tone with spontaneous recovery. The loss of consciousness occurs within 10 seconds of hypoperfusion of the reticular activating system in the mid brain.
What is a syncopal prodrome?
Syncopal prodrome is common although loss of consciousness may occur without any warning symptoms. Typical presyncope symptoms include dizziness, light-headedness, faintness, weakness, fatigue, and visual/auditory disturbances.
What are the causes of syncope?
Syncope can be neurally mediated, orthostatic, cardiac arrhythmia, structural cardio-pulmonary or non-cardio-vascular.
Neural: Vasovagal, carotid sinus, situation such as cough or micturition
Orthostatic: Drug induced or autonomic nervous system failure
Cardiac arrhythmia: Brady (sick sinus and AV block) or Tachy (VT or SVT) or long QT syndrome.
Structural Cardio-pulmonary: Aortic stenosis, HOCM, pulmonary hypertension
Non-cardio-vascular: Psychological, hyperventilation or neurological
What are the causes of cardiac syncope?
Cardiac syncope is caused by severe obstruction to cardiac output or rhythm disturbance. Exertional syncope is a common manifestation of all types of heart disease in which output is fixed. Aortic stenosis is a fixed cardiac output cause of syncope. HOCM may present with VT. VT is the most common cause of cardiac syncope and generally occurs in known organic heart disease or long QT. It is unlikely for coronary artery disease to present with syncope.
Complete heart block can cause syncope and this is known as Stokes-Adam syndrome.
A trifascicular block is a combination of right bundle branch block, left anterior or posterior fascicular block and first AV block (prolonged PR interval). This is a precursor to complete heart block which can cause syncope.
In vasovagal syncope the normal sympathetic tone is inhibited which causes hypotension and bradycardia causing the syncope.
What is micturition syncope?
Micturition syncope is often seen in younger men after rising from the bed early in the morning and men who with sudden LOC during or immediately following voiding. The mechanism is similar to the vasovagal response caused by mechanoreceptors in the bladder. Risk factors include fatigue, alcohol, recent UTI or bladder pathology.
What is defaecation syncope?
Defaecation syncope usually occurs in older people and is caused by mechanoreceptors in the gut wall and risk factors include alcohol, fatigue, decreased food intake and GI pathology.
What is cough syncope?
Cough syncope usually follows a severe bout of coughing. The mechanism of syncope is through the pulmonary mechanoreceptors. The severe coughing increases intrathoracic pressure which decreases the venous return and thus cardiac output. Cough syncope may be related with Mobitz II and obstructive cardiomyopathy.
Describe carotid sinus hypersensitivity
Carotid sinus hypersensitivity presents with profound bradycardia and hypotension with compression of the carotid sinus in susceptible individuals. This causes spontaneous fainting in, usually, older men. The mechanism is through the carotid sinus and activating the parasympathetic and inhibiting the sympathetic tone through the vagal and sympathetic efferent fibres. There are three types including the cardioinhibitory type, vasodepressor type and mixed type.
What is orthostatic syncope?
Orthostatic syncope is a decline of systolic (>20) and diastolic (10) upon assuming an upright posture. This hypotension leads to light-headedness, blurring of vision, and weakness. These symptoms are usually worst in the morning, after meals or exercise.
