Cardiovascular 41 to 50
Explain the electrophysiological changes that cause the ST segment elevation seen in a myocardial infarction?
Prompt: Time course? Cellular mechanism?
- Abnormally rapid repolarisation of the infarcted muscle (accelerated opening of K+ channels). Current flow out of infarct (normal region negative relative to infarct). Occurs within seconds of infarction and last a few minutes.
- Decreased resting membrane potential (due to loss of intracellular K+). Begins in first few minutes secondary to process above. Current flow into infarct during diastole (ECG configured to record as ST elevation).
- Slowed depolarisation of affected cells cf nomral cells. Occurs @ 30 minutes into infarct process. Current flow out of infarct.
- 2 of 3 to pass
Please draw the Frank Starling curve as it relates to human cardiac muscle
Prompt: What effect does EDV have on SV?
- To pass must be able to draw the FS curve including the hump and correctly label axes (SV or Pressure on y axis)
What factors influence the Frank-Starling curve?
- Circulating catecholamines
- Pharmacol depressants
- Loss of myocardium
- Intrinsic depressing
- Symp NS & PSym
- Fluid Status
- 4 Factors with correct influence
What are the ECG changes in Hyperkalaemia?
- Peaked T waves (repolarisation abnormality)
- P wave flattening
- Loss of P waves (progressive atrial paralysis)
- QRS widening/bizarre QRS (conduction abnormality)
- Sinusoidal ECG
- Ventricular arrhythmias
- 3/6 to pass
Describe the way the kidney handles the K+
Prompt: What happens to K+ in Proximal Tubule? What happens to K+ in Distal Tubule?
- K+ is filtered at the glomerulus
- Most filtered K+ is actively reabsorbed at the proximal tubules
- K+ is then secreted into the fluid by the distal tubules
- Rate of K+ secretion is proportionate to distal tubular fluid flow)
- At distal tubule: K+ secretion is passive and Na+ is reabsorbed
- In a healthy person
- the amount of K+ secreted = K+ intake and K balance is maintained
- Normally > 93% is reabsorbed by the kidneys
- K+ secretion & excretion alter depending on serum K+ and H+
- Bold to pass
What are baroreceptors?
- Stretch receptors in the adventitia layer of vessel
Where are they located?
- Aortic arch
- Carotid sinus
- Walls or right and left atria (SVC and IVC entrances)
- Pulmonary circulation
- Bold + 1 other
What is their mechanism of action in hypotension?
- In response to hypotension, the arterial baroreceptors are less stimulated because they are less stretched
- Reduced baroreceptor discharge travels via glossopharyngeal and vagus nerves to the medulla resulting in an overall increase in sympathetic discharge to increase heart rate and stimulate vasoconstriction and reduce vagal drive
- Bold to pass and understand inhibitory concept
What are the factors that determine cerebral blood flow?
- Intracranial pressure
- Mean arterial pressure
- Mean venous pressure at brain level
- Blood viscosity
- Local constriction/dilation of arterioles
- Bold + 1 other to pass
Describe the autoregulation of cerebral blood flow.
Prompt: What happens to cerebral blood flow when blood pressure changes?
- Maintains CBF at constant rate (~750 mL/min) across a range of perfusion pressures (MAP 65-140 mmHg)
- Bold to pass
A patient's bradycardia and hypertension are caused by a head injury. Describe the mechanism responsible.
- Cushing reflex
- Increased ICP compromises blood flow to medulla
- Sympathetic outflow from vasomotor centre
- Increases BP in attempt to restore medullary flow
- Stretch of baroreceptors
- Vagal stimulation
- Bold to pass
- Vagal stimulation OK instead of stretched baroreceptors
What is autoregulation of tissue blood flow?
Prompt: What are the main features if autoregulation?
Capacity of tissues to regulate their own blood flow, which remains relatively constant despite moderate changes in perfusion pressure. This is achieved by altering the vascular resistance.
- Bold concepts to pass
What are the proposed mechanisms involved in autoregulation?
- Myogenic: Intrinsic contractile response of smooth muscle to stretch. As pressure rises, vascular smooth muscles surrounding the vessels contract to maintain wall tension (La Place’s Law; T = P x R).
- Metabolic: Production of vasodilator metabolites by active tissues leads to vessel vasodilation and increased blood flow.
- Endothelial products:
- Vasoconstrictors (endothelin, thromboxane A2)
- Vasodilators (nitric oxide, prostacyclin)
- Circulating neurohumural substances:
- Vasoconstrictors (adrenaline, noradrenaline, vasopressin, angiotensin II)
- Vasodilators (kinins, VIP, ANP)
- Sympathetic (alpha-adrenergic receptors – vasoconstriction; beta-adrenergic receptors – vasodilation)
- Parasympathetic (muscarinic receptors – vasodilation).
- 3 Bold concepts to pass, with explanation.
What are some local factors that lead to vasodilation?
- Increased local temperature
- Increased lactate
- 4 to pass.
List some conditions that activate the renin-angiotensin system.
Activated in response to a deacrease in blood pressure/ECF volume or increased sympathetic activity. Examples:
- Cardiac failure
- Na+ depletion/diuretics
- Upright posture
- Pain, fear and arousal
- 4 conditions to pass.
What are some principal effects of angiotensin II?
Prompt: Where does angiotensin II act?
- Arterioles (AT1 receptor): Vasoconstriction leading to increased TPR
- Adrenal cortex (AT1 receptor): Increased aldosterone production leading to Na+/H20 retention
- Kidney: Direct effect to decrease GFR and increase Na+ reabsorption
- Brain: Decrease sensitivity of brain baroreceptor reflex leading to a potentiation of the pressor effect
- Pituitary gland: Increased ADH and ACTH secretion
- Bold to pass.
Describe the mechanism of venous return to the heart.
Prompt: In a healthy person.
- Thoracic pump:
- Inspiration fenerates negative intra-thoracic pressure and positive intra-abdominal pressure.
- Venous valves:
- One-way flow
- Heart beat:
- AV valves pulled downwards in systole increases the size of the atria and sucks blood into them.
- Muscle/arterial pump:
- Contraction of muscles and arteries adjacent to veins compresses them.
- Differential resistance:
- Less resistance in more proximal (larger) veins.
- Thoracic pump plus one other to pass.
What factors may affect CVP in a patient with septic shock?
- Decrease CVP
- Fluid loss (third spacing)
- Loss of arterial tone
- Loss of muscle pump
- Myocardial depression (from acidosis)
- Poor ventricular filling (due to tachycardia)
- Increase CVP
- Positive pressure ventilation (but will decrease venous return)
- Fluid replacement
- Vasopressor use
- 1 example from each bolded category.
What is the mean CVP in a healthy adult?
- 6-8 cm H2O or 4.6 – 5.8 mmHg
- Reasonable value.