Week 2

Reflection

Using the Gibb’s Reflective Model I will reflect on the second lab session we had for this semester. It took place on the 9^th of September.

Description: This week I was given a scenario about a 19 year old male with right sided chest pain. I assessed the patient and obtained his history, however, I didn’t know what his diagnosis was. I thought it was a muscle strain or a rib fracture. In the end, I was told that the patient had tension pneumothorax. That’s when I realized I had missed auscultating the pt.’s chest. In tension pneumothorax, breath sounds will not be equal in both lungs with decreased breath sounds on the side of the pneumothorax. In this case, the right side. Furthermore, we discussed the case and learned about the three definitive signs of tension pneumothorax, called the Virchow’s triad. This includes: Difficulty breathing, chest pain and hypoxia. In the second hour of the lesson, we discussed the different drug groups and were required, as a homework, to find two examples of each group.

Feelings: At first, I was confused but later on, when my teacher explained the signs and symptoms of tension pneumothorax, I understood the case. I felt very interested in the new facts I learned, and more aware  of the importance of conducting a thorough vital signs assessment. Moreover, it was intriguing to learn about the different drug groups.

Evaluation: It was a very good experience to be thrown into an unknown scenario and feel the confusion and then have everything explained. It showed me how much I still needed to learn and made the learning process exciting and interesting. It was very bad of me to miss auscultating the patient’s chest. That is because it would have given me a major hint to what the patient’s diagnosis was. Furthermore, it was really good to learn about the different drug groups and expand our knowledge about them.

Analysis: A good patient assessment equals the best patient outcome. Not auscultating lead me to miss the tension pneumothorax which caused me to misdiagnose the patient. This could have caused the patient to die.

Conclusion: In conclusion, I should have done a full patient assessment, including auscultating the pt.’s chest.

Action Plan: For next time, I will have the Virchow’s triad memorized and will conduct a complete and thorough patient assessment from the start. This will help me avoid missing any facts and will allow me to have a more accurate diagnosis and, as a result, provide the right treatment. Moreover, I plan to have more knowledge about the different drug groups.

Picture 1: Drug groups and two examples of each

Domain Knowledge: This week's lecture covered blood pressure, perfusion, factors affecting them both, preload, afterload, different types of hypertension, HT management, and the percentage of blood in different vessels. The following are my notes for this lecture:

First off, there are some definitions i learned this week and they include:

Pressure: Force per unit area exerted on vessel walls by the contained blood (mmHg).

Blood flow: Amount of fluid moved per unit time (L/min).

Resistance: Opposition of force. This is accomplished by change in the radius, length, and diameter of the vessel and the viscosity of blood. Length, diameter and viscosity have an inverse relation with blood flow. However, the radius is directly related to blood flow where Flow∝r⁴  

^{Velocity: Distance traveled by blood in unit of time. (increase area causes decrease in velocity in capillaries).}

^{Laminar flow: Smooth flow in layers (normal)}

^{Turbulent flow: whorls and eddy currents (abnormal)}

^{Compliance: increased volume causes vessel increases in size. (veins can store more volume, veins more compliant).}

^{Perfusion: Passage of blood through the vessels of organs reliant on blood flow and BP.}

^{Also, there are different types of pressures:}

Hydrostatic pressure: Mechanical force of H₂O pushing against cell membranes.

Oncotic pressure: Due to proteins (albumin), pulls water into circulatory system.

Passive transport: Such as osmosis (osmotic pressure)

Moreover, tonicity plays an important role in pressure control. There are three types of tonicity: Isotonic, hypertonic and hypotonic. These affect the direction of flow of fluid which causes changes in pressure.

Some formulas covered were:

CO= HRxSV

BP=COxR

Pulse Pressure= SBP-DBP

MAP= 1/3(2xDBP+SBP)

Picture 2: PSA and factors affecting it

Starling's law: increased venous return -> increased EDV -> increased preload -> increase in myocardial contraction force -> increase in SV, CO and BP

BP is regulated by: 1- Neural control (cardiac center, baroreceptors, chemoreceptors)

                                2- Hormonal (Adrenal medulla, RAAS, ADH)

                                3- Renal mechanisms

Picture 3: RAAS action flowchart

Blood flow is controlled by precapillary sphincters which contract and relax.

Picture 4: Notes talking about preload and factors affecting it.

Picture 5: Notes discussing afterload and its relation with aortic pressure.

SVR is PVR and the resistance in the pulmonary circuit.

Hypertension:

Picture 6: Table showing the normal values of BP for different age groups. Adopted from (Patel & Curtis, 2011).

 Hypertension:

Picture 7: Table showing factors affecting BP. Adopted from (Patel & Curtis, 2011).

HT can cause stroke, CHF, renal failure, AMI, and CVD doubles for every increase of 20/10 in BP above 115/75.

HT Management:

Picture 8: Different drugs used in the management of HT

Picture 9: Percentage of blood in vessels.

Reference

Patel, L., & Curtis, K. (2011). Patient assessment and essentials of care. In K. Curtis & C. Ramsden (Eds.), Emergency and trauma care for nurses and paramedics (pp.233-265). Chatswood, NSW: Elsevier.

Enquiry and Research:

Picture 10: Definition of HT and its different types. Information retrieved from (Brashers, 2012).

Through reading, i found out the following information:

• Blood flow through individual body organs may vary widely in accordance with their immediate needs.  
• BP is the systemic arterial BP in the largest arteries near the heart. 
• Pressure gradient is what drives the blood to keep moving from an area of higher pressure to an area of lower pressure, through the body.
• Turbulent flow occurs when there is an abrupt change in the vessel's diameter, such as in atherosclerosis. This increases the resistance dramatically.
• F=P2-P1/R. ( Flow is directly proportional to difference in pressures of two points in a vessel. Flow is inversely proportional to resistance.)
• Pumping action of heart causes blood flow. Pressure is the result of resistance opposing that flow.
• Systolic pressure due to lt. ventricle contracting. It is the peak aortic pressure. During diastole, walls of aorta recoil, maintaining sufficient pressure to keep the blood moving forward towards the smaller vessels.
• P2-P1= COx R. BP varies directly with CO and R. Changes in one variable that threatens the BP homeostasis is quickly compensated by changes in the other variables.
• Vasomotor center transmits impulses along vasomotor fibers. These fibers innervate the smooth muscle of blood vessels. They are behind the vasomotor tone of blood vessels. Decreased impulses from the vasomotor center causes vasodilation, decreased PVR and MAP.
• Hypotension is BP below 90/60 mmHg. Only a concern if it causes inadequate blood flow to tissues. Hypothyrodism can cause chronic hypotension.
• Blood flow can be autoregulated by the automatic adjustment of the flow to meet the tissue's requirement. This is accomplished independent of nerves and hormones.
• When blood flow is too low to meet tissue's metabolic demands, oxygen level declines and metabolic products accumulate. This serves as the autoregulation stimuli to increase blood flow to the tissues. This stimulus causes the release of nitric oxide by the vascular endothelial cells. Nitric oxide is a powerful vasodilator, which dilates the precapillary sphincters, increasing blood flow to the area.
• Hypovolemic shock: Circulatory shock due to large-scale blood/fluid loss.BP normal at first but eventually drops if blood loss continues.
• Vascular shock: Blood volume is normal but circulation is poor because of extreme vasodilation.
• Cardiogenic shock: Heart is inefficient and cannot sustain adequate circulation (Marieb &Hoehn, 2014).

References

Brashers, V.L. (2012). Alterations of cardiovascular function. In S.E. Huether & K.L. McCance (Eds.), Understanding pathophysiology (pp. 585-642). St. Louis, MO: Elsevier.

Marieb, E.N., & Hoehn, K.N. (2014). The cardiovascular system: Blood vessels. In E.N. Marieb & K.N. Hoehn (Eds.), Human anatomy and physiology (pp. 759-778). Essex, England: Pearson Education