Degree summary - Practical Only Flashcards
How is breathing controlled under normal circumstances?
Breathing is mediated by the medullary respiratory centre (MRC), which controls breathing depth and frequency according to inputs from chemoreceptors Central chemoreceptors in the medulla respond to changes in PH, whilst peripheral receptors in the carotid sinus and aorta are sensitive to changes in plasma that effect the partial pressure of oxygen (Pa02) and carbon dioxide (PaC02). PC02 provides the stimulus for breathing rather than pa02.
What type of drug is amiodarone?
Class III anti-arrhythmic and is a K+ channel blocker.
When is amiodarone indicated?
REFACTORY Ventricular Tachycardia or Ventricular Fibrillation in cardiac arrest (ie, if the patient remains in VT/VF post 3 cycles of CPR/shocks or if the patient has a tendency to revert to VT/VF on repeated conversions). In some cases it has also been used in tachyarrythmias such as AF and SVT.
What is the mechanism of action for amiodarone?
Amiodarone blocks some K+ channels resulting in slowed efflux of K+, thereby prolonging phase III of the cardiac action potential. This leads to slowed repolarisation, increased refractory period and increased QT interval, making it more likely that higher pacemaker cells (outside the ventricles) take over through the interruption of re-entrant tachycardia’s and suppressing ectopic activity.
It also has a minor action of blocking Na+ channels, Ca2+ channels and beta receptors, thus slowing HR and conduction through the AV node.
Does amiodarone improve survival?
Amiodarone has been shown to significantly improve the chances of survival to hospital. There is however, no benefit of amiodarone in survival to discharge or neurological outcomes. The ARREST and ALIVE (double blind randomised controlled trials) both concluded that amiodarone had higher rates of survival to hospital admission.
What are the 4 H’s?
- Hypoxia
- Hypovolemia
- Hypo/Hyper kalaemia and h+ hydrogen ions
- Hhypothermia
What are the four T’s?
- Toxins
- Tamponade
- Tension Pnemothorax
- Thrombosis.
What changes occur to metabolism during hypoxia?
Without oxygen, the body cannot facilitate aerobic metabolism (oxygen driven metabolism of fats, protein and carbohydrates). Anaerobic metabolism is VASTLY less efficient (way less ATP). It also has H+ ion byproducts predominatley due to lactic acid production associated with this process.
These H+ ions are converted to c02, and as pac02 increases, RR increases accordingly to expel it. Once biarbonate and respiration increases cannot compensate - metabolic acidosis occurs (later stage sign in MI for example).
What is the patho of an MI?
MI is commonly precipitated by a ruptured coronary atheroma, exposing a lipid core to platelets that aggregate and initiate a coagulation cascade (Brener 2006, p. 2). As a thrombus forms myocytes become ischemic and switch to anaerobic metabolic production, reducing availability of adenosine triphosphate (ATP) (Aymong, Ramanathan & Buller 2007, p. 705).
Contractile function is impaired and ionic dysregulation results in necrotic or oedematous myocytes (Aymong, Ramanathan & Buller 2007, p. 705). As cardiac output (HR x stroke volume - so only stroke volume is reduced) and mean arterial pressure (MAP) decline, heart rate, inotrope and systemic vascular resistance (SVR) increase, worsening ischemia and potentially expanding the infarct (Lilly 2012, p. 168).
Why is a BP potentially narrow in an MI?
Stroke volume and heart rate are the determinants of cardiac output. SV tends to decrease as ventricular contractile function is impaired, which occurs due to cellular deficits of ATP and the presence and propagation of necrotic tissue.
These processes cause a decrease in left ventricular ejection fraction and when paired with increases in systemic vascular resistance (SVR), they lead to a narrowed pulse pressure which may signal the onset of cardiogenic shock
What hormonal response occurs in MI, how does this effect the heart?
Increases in SVR occur in response to drops in MAP, which prompt sympathetic release of adrenaline and nor adrenaline causing systemic vasoconstriction, increased inotrope and increased chronotrope (Lilly 2012, p. 168). This response is maladaptive and increases afterload and the inotropic force necessary to eject blood from the left ventricle (Gowda, Fox & Khan 2008, p. 223).
Inotrope rises in accordance with this demand and widespread vasoconstriction enhances preload (Gowda, Fox & Khan 2008, p. 223). Subsequently there is a marked increase in ventricular wall tension and myocyte stretch in accordance with Starlings law, resulting in greater myocardial oxygen demand (MVO2) and exacerbation of ischemia (Gowda, Fox & Khan 2008, p. 223).
An increased HR also enhances MVO2, according to its inverse relationship with diastolic filling time (Gowda, Fox & Khan 2008, p. 223). As ischemia is worsened the function of myocytes tend to decline, promoting further maladaptive responses – which may lead to greater infarct size and cardiogenic shock (Gowda, Fox & Khan 2008, p. 224).
What are the three classifications of hypovolemia?
In a 70kg adult male:
Mild = 750ml or 15% of total blood volume
Moderate = 750-1500ml or
15-30%Severe = Above 2 litres of blood or >40%.
What are the three classifications of hypothermia?
mild = 35-32°C
Moderate 32°C- 28°C
Severe = <28°C
Hyperkalemia is a serum potassium level above?
it causes?
How is it detected in ECG?
- 5.5mmol.
Potassium plays a vital role in heart function, particularly in heart rhythm with its involvement in the SA node and influence on diastolic depolarization. In the AV node, the permeability of potassium determines the time required for depolarisation to reach the action potential voltage threshold, once reached the electrical conduction can be transmitted to the ventricles. During the recovery or repolorisation phase, hyperkalaemia can be detected on an ECG through its characteristic ‘peaked T-waves’, often an early sign.
Why does hypokalaemia matter? How is it detected on ECG?
hypokalaemia is a level <3.5mmol/L.
It is a less common cause of cardiac arrest; however, decreased extracellular potassium levels can lead to myocardial hyperexcitability potentially leading to the development of re-entrant arrhythmias. The presence of hypokalaemia is noted on an ECG through increased amplitude of the P wave, prolonged PR interval, T wave flattening/inversion and/or ST depression
DRSABCD is now wrong ONLY in traumatic arrest. Explain the new order
DRSCABDED -
D- Danger R - Response S - Send for help C- Circulation (only in traumatic cause - fluid bolus of 20 ml per kilo given because hypovolemia a likely cause) A - Airway B- Breathing D- Disability E - Environment
There are alpha cells and beta cells in the pancreas, what function does each one have? These cells are only found in the islets of langerhans and involve the ENDOCRINE function of the pancreas.
Alpha - Glucagon
Beta - Insulin.
What condition in in particular are type 2 diabetics prone to?
Hyperosmolar hyperglycemic state (HHS). The high levels of glucose in plasma increase the osmolarity of blood. Therefore, fluid is drawn from cells (cellular dehydration) increasing blood volume. As blood volume increases, more urine is produced (polu uria) and more drinking occurs for cell shrivelling due to dehydration (polydipsia). The brain gets dehydrated so they have MENTAL STATUS changes.
Why would someone with poorly controlled diabetes have weight loss
Glucose cant get into cells. So lipolysis occurs (fat burning for ATP) and protein breakdown (muscle tissue). This causes weight loss but paradoxically increased hunger.
