|MEDICAL EDUCATION TEACHING NOTE
|Year : 2017 | Volume
| Issue : 1 | Page : 59-63
Common “transmission block” in understanding cardiovascular physiology
Hwee-Ming Cheng1, See-Ziau Hoe1, Amira Abd Jamil2
1 Department of Physiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia
2 Department of Pharmacy, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia
|Date of Submission||11-Apr-2017|
|Date of Acceptance||10-May-2017|
|Date of Web Publication||1-Jun-2017|
Department of Physiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur
Source of Support: None, Conflict of Interest: None
We obtained responses from 69 medical and 65 pharmacy students who had cardiovascular (CVS) physiology taught in the previous academic year. A real-time response exercise using an online game-based learning platform (Kahoot!) (https://getkahoot.com/) was conducted during a lecture class using true/false questions that cover certain core aspects of CVS physiology. Comments will be made on some of the common, incomplete understanding of CVS conceptual mechanisms. Some follow-up thoughts on our role as physiology educators in fine-tuning our teaching as we encounter persistent mistakes among our students' learning physiology.
Keywords: Cardiovascular physiology, educators, medical, pharmacy, students
|How to cite this article:|
Cheng HM, Hoe SZ, Jamil AA. Common “transmission block” in understanding cardiovascular physiology. BLDE Univ J Health Sci 2017;2:59-63
| Students' Responses to Cardiovascular (True/false) Statements|| |
Interestingly, for most of the test questions, the proportion of students that responded correctly is quite similar among the medical or pharmacy students [Table 1]. For the incorrect responses, this indicates that there are common misconceptions among students' learning cardiovascular (CVS) physiology.
The data in [Table 1] will be a useful resource for teachers to discuss the areas of lack in our students' understanding. The observations are useful information for us to think through how to improve our communication and transmission of CVS physiology to our students.
Here are some comments on the first eleven selected questions listed in [Table 1].
| Question 1: Electrocardiogram Wave Amplitude|| |
There were 42% of medical and only 22% of pharmacy students thought that cardiac sympathetic activity during physical activity increases the amplitude of the action potentials that depolarize the myocardium. As teachers we might presume that our students know well that action potentials are “all or nothing.” This principle of neurophysiology was covered in the first few weeks of their entry into university. Perhaps, our students do not go beyond their power points when we teach that action potentials in nerves and skeletal muscles have fixed amplitude in vivo since the transmembrane sodium gradient is maintained throughout the body. The myocardium, being an excitable muscle tissue, should also display this same action potential amplitude. This is a case perhaps of not thinking outside the PowerPoint boxes!
The increased strength of cardiac muscle contraction by sympathetic action during exercise is due to elevated intracellular calcium in the cardiomyocytes.
| Question 2: Calcium and Ventricular Function|| |
It is heartening to know that the majority of students (80% medical, 84% pharmacy) have knowledge of the role of calcium in the unique prolonged depolarization (or delayed repolarization) of cardiac ventricular muscle. The trigger extracellular calcium influx is needed for further release of sarcoplasmic reticular calcium. The combined rise in intracellular calcium then activates the actin-myosin sliding mechanism for cardiac muscle contraction.
| Questions 3 and 4: Heart Sounds and Cardiac Cycle|| |
Heart sounds are time points in the cardiac cycle, with the first sound being the beginning of systole and the second sound starting diastole. The cardiac cycle thus is either the duration between two first heart sounds or two second heart sounds. Temporal events are quite commonly unappreciated by students. This true/false statement that seemingly is not one of a high level of difficulty gave correct response in 66% of medical and 54% of pharmacy students.
This lack of focus with temporal matched physiologic events is also seen in the responses for the question on the PR interval. Both medical (66%) and pharmacy (73%) students with wrong answers appear to have forgotten that the PR duration includes the essential atrioventricular delay in cardiac impulse transmission.
A more challenging and engaging question to pose for our students along this temporal line is to ask them to match the ventricular action potential on the same time scale as the electrocardiogram. Then, we can help them to see that the ST segment coincides with the unique prolonged action potential that stretches from the associated QRS depolarization complex to the T repolarization wave.
| Question 5: Myocardial Hypoxia and Coronary Perfusion|| |
Only around 50% of both medical and pharmacy students agreed with the statement of myocardial hypoxia being a major contributor to increased coronary blood flow. The role of vasodilator autonomic nerves is not established in cardiac muscles, unlike in skeletal muscles. The coronary vessels through innervated by sympathetic fibers do not vasodilate in response to neural stimulation. The action of sympathetic action increases cardiac metabolism as the heart rate and stroke volume are higher. Metabolite vasodilators, for example, adenosine and the local tissue hypoxia then decrease the coronary vascular resistance to match the blood perfusion with the greater metabolic demands.
| Question 6: Right and Left Ventricular Outputs|| |
This question highlights the essential view of the CVS as a closed, fixed volume space. Seventy-one percent of medical students thought wrongly that the less muscular right ventricular cardiac ejects less cardiac output (CO) compared with the left ventricle that pumps into the systemic circulation. The integrated cardiorespiratory physiology is important here. Physiologically, both ventricular outputs must be equalized to prevent vascular congestion. If the right CO is less than that from the left ventricle, this is akin to a right ventricular failure. Peripheral congestion and edema will consequently develop.
Students need to recall that the pulmonary circulation has a low pressure with a matched low-resistance hemodynamics. Thus, the pulmonary blood flow from the “weaker” right cardiac pump is equal to the left ventricular CO.
| Question 7: Stroke Volume in Denervated Heart|| |
The denervated, donor heart still responds inotropically to circulating adrenaline that binds to the same beta-adrenergic receptors in the myocardium that are activated by the sympathetic neurotransmitter noradrenaline. The adrenal medulla secretes the catecholamines on sympathetic nerve stimulation. A quarter of medical students (25%) and a third of pharmacy students (33%) still fail to see the alternative hormonal stimulus that is available in vivo in the absence of the cardiac sympathetic nerve.
In addition, the stroke volume can also be heightened by an increased in ventricular filling, independent of neural or hormonal excitement (Starling's phenomenon).
| Question 8: Mean Aortic/arterial Blood Pressure|| |
If the student just takes the equation (blood pressure = CO í total peripheral resistance) at face value, the arterial pressure will indeed be the driving pressure for CO. The essential missing fact likely missed in 12% of medical students is that the heart is not a constant pressure pump. The rhythmic cardiac pump has a ≈0 mmHg intraventricular pressure during diastolic relaxation. In the subsequent systolic contraction, the aortic pressure presents an “afterload” against which the cardiac work is expended to sustain peripheral blood flow. As such, with increasing arterial pressure, the counterforce of the afterload on cardiac ejection is exerted. The CO, therefore, does not increase proportionately with the mean arterial pressure for a rhythmic heart pump. It is interesting that for the pharmacy students who likely have less exposure to clinical cases in hospitals, the percentage of wrong responses (90%) was surprisingly high.
| Question 9: Blood Flow Is Volume Per Minute|| |
Physiology is a dynamic science. In both blood and fluid flow, quantitative aspects are perhaps sometimes lacking in our teaching, reflected by the high rate of incorrect responses (78% in medical, 71% in pharmacy). Units in physiology should be highlighted for our students' learning. This question also reminds students of the closed circulatory loop, with the systemic and pulmonary vasculature in series. Blood flow is like traffic flow, and we do use vascular and traffic congestion with the same scenario in mind. In a closed circulatory loop, the right and left cardiac ventricular pumps are in series. Since the venous return and the CO for both ventricles must be equalized over time, the blood flow (volume/min) ought to be the same throughout every segment of the complete vascular circuit.
Most likely, students mixed up or interchange blood velocity (distance/min) with blood flow rate (volume/min). A faster or slower flow rate is subtlely not the same as a higher or lower flow rate.
| Question 10: Downstream/upstream Vascular Resistance Effects|| |
Only 31% of medical students answered correctly this question on the effect of arteriolar constriction on capillary hydrostatic pressure. The effect of arteriolar vasoconstriction increases the total peripheral resistance. The resultant gain in arterial blood pressure is an “upstream effect.” The capillary pressure will experience a resultant decreased “downstream” hydrostatic pressure.
This reduced intracapillary pressure, however, contributes to the compensatory “transcapillary fluid shift” during hypovolemia when the baroreflex-activated sympathetic vasoconstriction takes place.
| Question 11: Hypovolemia, Renal Sympathetic Nerve, and Renin|| |
Only about 40% of medical students agreed with this pathway of renin secretion. The other two inputs to renin secretion from the juxtaglomerular (JG) cells are the macula densa signal and the direct sensing of renal perfusion pressure by the intrarenal baroreceptors located at the preglomerular afferent arteriole.
The CVS and renal physiology are taught in different modules. For any cardiorenal mechanisms relating to blood volume/pressure regulation, we should prime and emphasize to our students to think renal even as the cardio reflexes are trigged. The volume/baroreceptor reflexes are categorized as rapid control and the renal compensation mechanisms are described as long-term measures. However, any volume/pressure activation of the increased general discharge of sympathetic activity will already target the kidneys. The JG cells that secrete renin are stimulated by the renal sympathetic fibers.
| Some Summary Thoughts for Teachers|| |
When we observe common misperceptions in physiology among our students, it should make us, as teachers, think. We should go beyond just brushing aside these common occurring errors by concluding that these are more difficult areas for students to grasp. Perhaps, the focus ought to be redirected at our teaching approach, and our PowerPoint contents could be better when we take to heart these students' responses. The author coined the phrase “homeostatic teaching” in a recent presentation during the South Asian Association of Physiology conference in Dhaka, Bangladesh. Our students are our best teachers. Their common struggle with certain mechanisms ought to spur us to innovate our teaching to address and help them understand and make physiologic sense of these specific difficulties.
CVS mechanisms are diverse, and dynamic and integrative teaching can help our students to appreciate the bigger homeostatic picture. For example, the rapid volume receptor/baroreceptor reflexes and “intermediate” capillary dynamic compensations are not completely sequential but overlap. The increased, effector sympathetic activity triggered by hypovolemia indirectly reduces the capillary hydrostatic pressure due to arteriolar vasoconstriction. The new balance of capillary Starling's forces leads to a beneficial “autotransfusion” of interstitial fluid or what is called “transcapillary fluid shift.”
A second example of integrative teaching is the intrinsic Starling's mechanism of the heart. The textbook usually shows graphically the mechanism of a single ventricle, with stroke volume along the y-axis and end-diastolic volume along the x-axis. Both the right and the left ventricles obviously demonstrate this cardiac myocardial inherent property. The whole body's importance of Starling's law of the heart relates to the equalization of the left and right COs in a closed systemic/pulmonary circuit. This is indeed the Starling bird's eye view of an essential aspect of CVS physiology.
[Table 2] is a selected list of ten major CVS concepts that are needful for the students to build their physiologic foundations.
The authors welcome feedback to this article and look forward to hearing from teaching colleagues on their own learning journeys with their students.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Cheng HM. Thinking Through Physiology. Kuala Lumpur: Pearson Malaysia; 2012.
Cheng HM. Physiology Question-Based Learning: Cardio, Respiratory and Renal Systems. London: Springer International Publishing Switzerland; 2015.
Cheng HM, Hoe SZ. Students' convoluted trouble with renal autoregulation: A teaching note for students and physiology educators. BLDE Univ J Health Sci 2016;1:25-7. [Full text]
Cheng HM, Hoe SZ. The 14th
Inter-medical School Physiology Quiz: Observations of ommon errors in the written test among students of 81 medical schools from 24 countries. BLDE Univ J Health Sci 2016;1:139-42. [Full text]
[Table 1], [Table 2]