PIDT Learning Review Flashcards
What are the phases of the pacemaker potential cells?
4 - There is a slow leak of Na+ into the cell. This creates an upwards slope. it reaches a point that triggers Ca+ voltage gates channels, but it is just beneath the pacemaker potential ‘all or nothing’ threshold.
0 - Voltage gated Ca+ voltage channels open! There is a an uptick of depolarization.
1 - Not present because the morphology of the cardiac action potential isnt there. So there is no ‘phase 1’ so to speak.
2- Not present because the morphology of the cardiac action potential isnt there. So there is no ‘phase 2’ so to speak.
3 - Peak voltage causes the same Ca+ channels to close! AND for the voltage gated K+ channels to open…Allowing for steep repolarisation (negative deflection in voltage). The cycle begins anew. The slope of phase 4 (the rate of sodium influx which can be modulated) determines the heart rate.
How does a pacemaker potential vary in comparison to a myocyte action potential?
- A myocyte action potential is sodium driven for depolarisation, where as pacemakers are driven by calcium.
- A mycocyte has automaticity and conductivity. But, it is a contractile cell. Pacemaker cells in the SA node and AV node have no contractility, and a faster automaticity than myocytes.
- Pacemaker potentials, arising from the SA node/AV node ect. never flatline, they just continuously go up and down…ca+ leak channels constantly allowing depolarisation at a steady rate until a voltage gate ca+ channel is triggered. MUST understand different wave-forms between the two. Action potential from cardiac myocyte is more like an ‘elephant under a blanket’.
Explain the phases of the myocyte action potential.
Phase 4 - Voltage gated K+ channels shut. True isolectric/flat line occurs as voltage maintained by the potassium / sodium leak channels and ATPase pump. The Na+/K+ pump uses ATP to push 3Na+ out and 2K+ in to maintain the resting membrane potential
Phase 0 - Influx of na+ triggers ‘all or nothing’ action potential response. Causing depolarisation -> positive voltage.
Phase 1 - Voltage gated potassium gates are triggered. Rapid Na+ gates are closed -> causes a slight dip in negative voltage as it starts to go down.
Phase 2 - The voltage flat lines up high, as potassium voltage channels are still remaining open which pushes the voltage down, whilst calcium voltage channels are opened in this phase. The calcium wants to make the potential more positive…the balance of potassium and calcium creates the ‘flat line’ of voltage just down from the peak in phase 0.
Phase 3 - Ca+ voltage channels close. Potassium gates K+ channels remain open…steep drop in voltage back down to isoelectric line.
What three areas have pacemaker cells?
- Bundle of His.
- Av node
- SA Node.
You are presented with a patient on his side, snoring, breathing and maintaining an airway. First step?
Place him supine and pop in an OPA.
ST elevation can occur outside of STEMI when?
It can occur in massive cerebral trauma such as in haemorrhagic stroke.
What is the difference pathologically between STEMI and N STEMI…how does it show on the ECG?
N STEMI - This is partial thickness injury, so necrosis has not dispersed throughout the entire myocardial wall. It is called a ‘sub-endocardial’ MI. Because there is still functional tissue, the delayed conduction that shows in ST elevation is not present. however the general ischemia is still present. So you WILL see potentially…T wave inversion, and ST depression.
STEMI - Transmural or full thickness. Goes through the entire wall and ST elevation evident. T wave inversion at times present as a leading indicator.
What are three big causes of MIs?
- Toxins - In particular smoking which over time is associated with significant vascular damage.
2) Fats/Cholesterol - Raised LDL in particular - Chronic disease - in particular hypertension and diabetes .
Explain the electrical conduction system of the heart?
SA Node -> internodal pathways -> AV Node -> bundle of HIS -> splits into left and right bundle branches -> perkinje fibres come off the bundle branches
Explain why pain may radiate to the jaw and within the chest cavity during an MI?
- Overall the pain mechanisms are not well understood
- Ischemic episodes excite chemo-sensitive and mechanoreceptive receptors in the heart.
- Stimulation of these receptors results in the release of adenosine, bradykinin, and other substances that excite the sensory ends of the sympathetic and vagal afferent fibers.
- Sympathetic Impulses are transmitted via the spinal cord to the thalamus and hence to the neocortex.
- Within the spinal cord, these afferent sympathetic nerve fibre may converge with other somatic thoracic structures. The convergence of these signals may be the basis for referred cardiac pain, for example, to retrosternally within the chest.
- In comparison, cardiac vagal afferent fibers synapse at the medulla, which can cause a descending impulse that excites the upper cervical spino-thalamic tract. This may contribute to the anginal pain experienced in the neck and jaw.
Explain why you might experience nausea in an MI?
- Ischemic episodes excite chemo-sensitive and mechanoreceptive receptors in the heart.
- Stimulation of these receptors results in the release of adenosine, bradykinin, and other substances that excite the sensory ends of the sympathetic and vagal afferent fibers.
- Vagal stimulation results in nausea
Explain how vomiting works in the body, and how anti-emetics exert their effect?
- The vomiting centre is located in the central medulla and this co-ordinates the complex events behind vomiting.
- It projects to the vagus nerve and spinal motor neurons, which innervate the abdominal muscles.
- The chemoreceptor trigger zone (CTZ) is ALSO located within the medulla oblongata in a different location….BUT…primarily recieves inputs from blood-borne drugs or hormones, and communicates with the vomiting center to initiate vomiting.
Mainly triggered by
- Drugs
- Toxins
- Chemicals
- The vomiting centre contains muscarinic (acH) and histamine receptors. Comparatively, the CTZ is rich in dopamine (D2) and 5-HT3 b (seratonin) receptors. Hence antiemetic drugs such as ondansatron only effect the CTZ, because they are 5-ht-3 receptor antagonists.
The vomiting centre can recieve inputs for vomiting from the limbic system and other areas within the cortex. It also links with the vestibular system (the inner ear responsible for balance/vertigo).
***The limbic system is the part of the brain involved in our behavioural and emotional responses, especially when it comes to behaviours we need for survival: feeding, reproduction and caring for our young, and fight or flight responses.
The vomiting centre is triggered by
- Pain
- Fear
- Olfactory
Which leads correspond with which vessels within the heart?
II, III and AvF = RCA (Right coronary artery)
V1, V2, V3, V4 = LAD (Left anterior descending)
V5, V6, 1, AvL = LcX (left circumflex) or obtuse marginal.
Why might a patient with a heart attack breath quicker?
- Not enough oxygen is delivered to tissue -> Change to anaerobic respiration. Increased lactic acid production
- This is buffered in blood, converted to carbonic acid, and then c02 to be blown off at the lungs.
- This increase in pac02 is picked up by the aortic arch receptors and the carotid sinus receptors
- They feed into the MRC - The muddulary respiratory centre to increase breathing and remove the c02.
Explain which leads correspond on the ECG, with which areas of the heart?
II, III, AvF = Inferior
V1, V2 = Septal
V3, V4 = Anterior
1, AvL, V5, V6 = Lateral
Explain the maladaptive haemodynamic responses to MI, and what hormones drive this?
The hormones are all the adrenergic hormones, all of them. So Alpha 1, Beta 1, Beta 2 and Alpha 2.
The maladaptive response:
- MAP and CO goes down
- Hormones released. Inotrope increased. Chronotrope increased. SVR increased.
- Afterload increases. Mv02 demand increases.
- More ischemia, less CO. Cycle begins anew.
Within the cell, what is the primary regulator of vascular tone…how does it exert its effect?
- GTN interacts with other nitrate groups within the body, ultimately forming nitric oxide.
- nitric oxide is a potent activator of cyclic guanosine mono phosphate (cGMP). cGMP is formed via gaunosine triphosphate.
- cGMP is a secondary messenger. It is the primary regulator of vascular tone. Noitric oxide increases the intracellular concentration of cGMP. This cGMP uses kinase dependent processes, to cause de-phosphoralisation of myosin CHAINS. This causes efflux of calcium, thereby decreasing troponin binding with ca+ and therefore muscle relaxation occurs.
- Link this with myosin/actin actions. Lack of calcium means that the tropamyosin cannot be moved out of the way, and muscle contraction cannot occur.
How do myosin heads act?
- ATP binds to myosin heads (little golf club like proteins) and this ‘releases’ the myosin head from the actin filament.
- ATP is broken down, into ADP and one phosphate group. This ‘cocks the spring’ of the myosin head. Puts it into high energy state.
- Phosphate is released from the myosin head. This chemical energy is converted into physical action as the myosin head crawls along the actin filament.
- ADP is released and the cycle begins anew.
Explain actin, myosin, tropamyosin, and tropanin. How does calcium play a role?
- Actin is the filament that myosin heads crawl along.
- Myosin are the heads that move along the actin filament. In order to perform their action there needs to be an ‘open’ actin filament.
- At rest the tropamyosin blocks the binding site for myosin heads. It moves out of the way when the toponin ‘bolts’ are activated with calcium.
- Troponin is activated when calcium binds to the troponin. This releases the tropomyosin rope, allowing myosin to engage with the actin filament using ATP to crawl along it.
How do PDE-5 inhibitors interact with GTN in a negative way?
- Phosphodiesterase-5 is an enzyme that regulates cGMP within the cell.
- It is an enzyme that causes hydrolysis of cGMP. The downsteam effect of cGMP, is to use kinase dependent processes, to dephosphoralise myosin chains, hence increasing ca+ efflux and causing smooth muslce RELAXATION.
- Therefore PDE-5 inhibitors such as viagra, REDUCE the availability of PDE-5 - > increasing cAMP and allowing for vasodilation and therefore erections.
- If you give GTN, this drug INCREASES cGMP via nitric oxide. Therefore the two together can cause a pathological increase in cGMP, massive vasodilation and a code brown.
What are some of the signs and symptoms in terms of ECG for pericardial effusion?
- Sinus tachycardia
- Low QRS voltages
- Electrical alternans (beat to beat variation in QRS height). This happens because the heart swings side to side within the pericardial cavity.
What would you expect on an ECG if the patient was hyperkalaemic?
- Bradycardia
- Flattening/loss of P waves ( https://lifeinthefastlane.com/wp-content/uploads/2010/01/ECG_Hyperkaemia_L.jpg )
- Peaked T waves (this is the main symptom).
What is the acronym that is useful for AMA’s (Against medical advice)?
VIRCA
V - Voluntary - Free decision, no coercion or undue influence
I - Informed - The person is informed of the possible risks or consequences of refusal.
R - Relevant - The refusal must be relevant, in that it relates to the treatment that has been recommended.
C - Capacity - The person has capacity, and understands the nature and consequence of the decision to refuse
Advice - The patient has been provided with advice for safety, comfort and follow up given the refusal of service.
In what type of MI might you see bradycardia?
It can be a sign of inferior infarcts, because they involve the RCA (right coronary artery) which feeds the right ventricle, and right atrium.
Ischemia within the R) atrium can lead to poor electrical conduction and hence effects the SA node. Slower rate—-> Bradycardia is the result.
When describing any kind of ‘rate related’ or ‘preload dependent’ rhythm in a VIVA, how do you describe and think about the potential consequences?
Always relate it back to cardiac output. CO = HR x SV
What are the two primary features of PE pathology, and how does this effect your thoughts on GTN?
The two primary effects:
- Hypoxaemia due to a significant V/Q mismatch (good ventilation and poor perfusion).
- Hypotension - Massive reduction in preload to the left ventricle, due to the ‘backed up’ blood flow from the RV that is potentially not getting through efficiently.
Therefore PE is a PRELOAD dependent rhythm! You want to be sure someone is not having a PE and poor perfusion before giving GTN!!
Explain the oxygen/hameglobin dissassociation curve?
https://www.medicalexamprep.co.uk/understanding-oxygen-dissociation-curve/
The curve has on the y axis, sp02. Or the amount of haemoglobin that is bound to oxygen -> forming oxyhaemoglobin. The X axis, has the pa02. Or the amount of free oxygen floating around.
The lower the p02, the less oxygen floating around, there is a propensity for oxy-haemoglobin to form haemoglobin and release the 02 molecule.
The reason there is a signmoid shape on the graph, is the concept of co-operative binding. Co-operative binding means that haemoglobin has a greater ability to bind oxygen after a subunit has already bound oxygen. Haemoglobin is, therefore, most attracted to oxygen when 3 of the 4 polypeptide chains are bound to oxygen.
If you took the thigh for example -> this area is low in pa02 and so you would expect the sp02 to be lower in this area, as oxyhaemoglobin releases oxygen molecules to form haemoglobin.
- So low pa02 (the o2 dissassociation curve) is one reason for 02 delivery.
- Another reason is the bohr effect -> The Bohr Effect refers to the observation that increases in the carbon dioxide partial pressure of blood or decreases in blood pH result in a lower affinity of hemoglobin for oxygen.
This bohr effect shifts the curve to the RIGHT. High temps and acidity shifts to the right.
A rightwards shift assists in the natural inclination of 02 to bind less aggressively at lower pa02 levels.
A leftward shift would be alkalinity and colder temperatures. This would increase the binding affinity and compromise oxygen delivery.
What is the haldane effect
In the presence of oxygen, there is a decrease in the affinity of hameoglobin for c02. And hence, more c02 is released (for example at the lungs -> high 02 environment) and delivered to tissue for expulsion.
How heme binding sites are there for oxygen molecules?
4
What is KVO rate?
30 ml per hour
Or
10 drops per minute
Why do we get free radicals or reactive oxygen species?
- During cellular respiration, normal oxygen molecules lose an electron, making them hyper reactive. The process in which ATP is produced, called oxidative phosphorylation, involves the transport of protons (hydrogen ions) across the inner mitochondrial membrane by means of the electron transport chain. In the electron transport chain, electrons are passed through a series of proteins via oxidation-reduction reactions, with each acceptor protein along the chain having a greater reduction potential than the previous.
The last destination for an electron along this chain is an oxygen molecule. In normal conditions, the oxygen is reduced to produce water; however, in about 0.1–2% of electrons passing through the chain oxygen is instead prematurely and incompletely reduced to give the superoxide radical. In aerobic organisms the energy needed to fuel biological functions is produced in the mitochondria via the electron transport chain.
In addition to energy, reactive oxygen species (ROS) with the potential to cause cellular damage are produced. ROS can damage lipid, DNA, RNA, and proteins, which, in theory, contributes to the physiology of aging.ROS are produced as a normal product of cellular metabolism. In particular, one major contributor to oxidative damage is hydrogen peroxide (H2O2), which is converted from superoxide that leaks from the mitochondria.
How is C02 transported in the body?
I thought it relevant to explain the manner in which c02 is predominately transported as bicarbonate ions within plasma. C02 is carried in three ways within the body:
- It dissolves directly into blood (5-7%)
- It binds directly to haemoglobin without disassociation into bicarbonate (10%)
- It dissociates into bicarbonate and a hydrogen ion. It is broken up essentially into two molecules which can combine to recreate c02. This is responsible for transporting 82% of c02). I will deal with the third mechanism:Diffusion is the driving force for c02, which moves from plasma into red blood cells (rbc’s), and as this occurs it comes into contact with a water molecule.
This sets off a reaction identical to that of the bicarbonate buffer system, however carbonic anhydrase (which sits inside the red blood cell) essentially speeds up the reaction. As C02 combines with water carbonic acid (H2c03) is formed momentarily, in order to produce both Hc03- (bicarbonate) and H+. In order to maintain electrical neutrality within the cell, the bicarbonate is exchanged for Cl- in a mechanism termed the chloride shift, and cl- enters the RBC in this process, whilst the bicarbonate diffuses out of the RBC into plasma. This bicarbonate by-product plays a crucial role in maintaining the high ratio of bicarbonate in blood that serves as our buffer system against acids.
The ratio of bicarbonate to carbonic acid in plasma is approximately 20:1 according to the vast majority of processes within the body that generate acid by-products. The left over H+ ion binds to the haemoglobin for transport to the lungs where the reaction is reversed, bicarbonate is exchanged for chloride and both water and C02 diffuses across the RBC membrane.
This allows for expulsion of c02 and this important mechanism is also central to the maintenance of PH within blood. For example, if enough acid were added to soak up half of the available bicarbonate our PH would drop from 7.4 to 6.0 within plasma. But the ability to convert excess carbonic acid (h2c03) into c02, as well as enhancing respiration rate allows PH to only drop from 7.4 to 7.2.
What role does the kidney play in maintaining blood PH?
It reclaims bicarbonate. 80-90% of bicarbonate is filtered through the glomerulus and reabsorbed within the proximal tubule. H+ Secretion and Bicarbonate Generation.
Importantly, excretion of hydrogen ions by the kidneys is molecularly coupled to novel generation of bicarbonate which is subsequently added to the extracellular fluid, thus replenising the ECF bicarbonate buffer. The specific molecular mechanisms and regulation of these processes are covered in Renal Acid Excretion.
Bicarbonate Excretion: The bicarbonate buffer is the principal physiological buffer of the extracellular fluid. As discussed in bicarbonate buffer, the extracellular pH is largely determined by the ratio of the Weak Acid (CO2) to Weak Base (HCO3-) form of this buffer. The kidneys can influence the extracellular pH by regulating urinary excretion of bicarbonate HCO3- as discussed in renal bicarbonate excretion. It should also be pointed out that as mentioned above, the kidneys can also synthesize and add novel bicarbonate to the ECF as part of renal acid excretion.
Fixed Acid Elimination: As discussed in physiological acid production, normal and pathological metabolic processes can generate a number of strong acids which are added to the extracellular fluid. Although these acids immediately release a free hydrogen ion which can be eliminated by other processes, the remaining molecule must also be eliminated to prevent its gradual build up in the extracellular fluid. The only organ which can ultimately eliminate these fixed acids is the kidney which does so through their urinary excretion.
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 are the 4 H’s?
- Hypoxia
- Hypovolemia
- Hypo/Hyper kalaemia and h+ hydrogen ions
- Hhypothermia
