ILA Mr Johnson Flashcards
Cardiovascular System
What is blood pressure?
The force exerted by blood on the walls of vasculature.
What is the normal range of BP in a healthy person? and does this vary for age and why?
General healthy BP: 120/80 mmHg
Systolic healthy range: 90-140 mmHg
Diastolic healthy range: 60-90 mmHg
For individuals over 65+, healthy BP is less than 130 mmHg systolic & 80 mmHg diastolic.
As you age, it is common for HR and BP to rise due to a drop in vessel elasticity and heart weakness.
Other factors affecting BP include medications.
How is BP measured? What factors may affect the measurements taken?
sphygmomanometer to track systolic and diastolic pressure in mmHg.
The BP cuff compresses the branchial artery within the arm. During maximum compression of the ventricles and the branchial artery, systolic BP is measured. After the release of the compression, diastolic BP is measured.
If you use the wrong-sized cuff, you can get incorrect readings. For people without arms, you can use thigh cuffs - also come in different sizes.
What structures are involved in maintaining BP in a healthy individual? How does each of them work in maintaining BP in a healthy individual?
- Baroreceptors (in the carotid sinus and aortic arch) detect changes in blood pressure and send signals to the cardiovascular control center to adjust heart rate and vessel dilation.
The Cardiovascular Control Center in the brain coordinates responses by modulating sympathetic or parasympathetic activity, releasing hormones like adrenaline and noradrenaline to adjust heart rate and vessel tone. - Blood Vessels (mainly arterioles) regulate resistance through vasoconstriction (increasing BP) or vasodilation (decreasing BP), influenced by intrinsic factors (e.g., temperature, histamine) and extrinsic factors (e.g., hormones).
- The Heart adjusts blood pressure by varying its strength, rate, and output.
- Blood viscosity, affected by its composition (RBCs, lipids), directly influences resistance and blood pressure.
- The Kidneys regulate BP through fluid and sodium balance, with mechanisms like the renin-angiotensin-aldosterone system (RAAS) adjusting blood volume in response to changes in salt levels or pressure.
- Endocrine system - Adrenal medulla and the chromaffin cells play a role in the release of Ad and NAd. Other hormones involved include aldosterone, vasopressin (a potent vasoconstrictor), and angiotensin I and II.
What processes (short term and long term control processes; hormones) involved in maintaining pressure in a healthy individual?
Short term:
1. Baroreceptor reflex
Senses acute changes in blood pressure.
Involves the carotid sinus and aortic arch baroreceptors.
Baroreceptors send signals to the cardiovascular control center in the medulla, which adjusts the ratio between sympathetic and parasympathetic activity.
Effects:
Elevated BP: Increases parasympathetic and decreases sympathetic activity.
Low BP: Increases sympathetic and decreases parasympathetic activity.
- SNS and ParaNS
Parasympathetic Stimulation:
Decreases heart rate, reducing cardiac output (CO) and lowering BP.
Sympathetic Stimulation:
Increases heart rate and contractility to raise CO.
Causes vasoconstriction in arterioles and veins, increasing total peripheral resistance (TPR) and venous return, thus increasing BP.
Long term:
1. Renin-Angiotensin-Aldosterone System (RAAS):
Triggered by low blood pressure, detected via low sodium/chloride in the kidneys.
Renin is released by the kidneys, converting angiotensinogen into Angiotensin I.
Angiotensin I is converted to Angiotensin II (AngII) by ACE.
AngII actions include:
Aldosterone release: Increases sodium and water reabsorption, raising blood volume and BP.
Stimulates ADH release: Enhances water reabsorption in the kidneys, increasing blood flow and BP.
- Antidiuretic Hormone (ADH):
Released from the posterior pituitary in response to AngII.
Promotes water reabsorption in the kidneys, increasing blood volume. - Adrenaline & Noradrenaline:
Released from the adrenal gland.
Adrenaline: Causes vasoconstriction, increasing BP.
What changes occur to BP and HR when there is a change in posture from lying down to standing up? and why do these changes occur?
When a person stands up from a lying position, gravity causes blood to pool in the lower body, reducing venous return and leading to a drop in BP. Baroreceptors quickly detect this change and initiate compensatory mechanisms like increased HR, vasoconstriction, and the activation of skeletal and respiratory pumps to restore BP to normal levels. The overall goal is to maintain adequate cerebral blood flow and prevent symptoms like dizziness or fainting.
- Veins can stretch to accommodate increased blood volume in the legs
- Skeletal muscle pump – pumps blood back to heart against gravity to ensure venous return to the heart,
- Respiratory pump: diaphragm moves down during inhalation, reducing pressure in thoracic cavity, increase pressure in abdominal cavity. Then abdominal veins compress, forcing blood against gravity and toward the heart. During exhalation, the one way venous valves stop backflow
- Cardiac suction – heart moves up during contraction and moves down during diastole which generates suction that increases venous return
- One way venous valves – ensures there is no backflow of blood when skeletal muscle pumps relax
- Veins are a low pressure system, veno constriction ANS
Metabolic activity – lowered when lying down.
How does being dehydrated/hydration levels affect maintenance of BP?
Dehydration is defined as a decrease in total body water, which can result from insufficient water intake or excessive loss through sweating, vomiting, or diarrhea. These conditions cause a loss of both sodium and water because sodium acts to retain water in the body. When sodium and water are depleted, blood volume decreases, leading to a reduction in venous return and lower cardiac output, ultimately causing a drop in blood pressure. In response, the Renin-Angiotensin-Aldosterone System (RAAS) is activated: renin is released by the kidneys, converting angiotensinogen into angiotensin I, which is further converted into angiotensin II. Angiotensin II constricts blood vessels and stimulates aldosterone release from the adrenal glands. Aldosterone promotes sodium and water reabsorption by the kidneys, thereby increasing blood volume and pressure back to normal levels. Concurrently, the Anti-Diuretic Hormone (ADH) is released by the pituitary gland, enhancing water reabsorption and decreasing urine output to maintain blood volume. Blood is composed of ~60% plasma (which is ~90% water), meaning that changes in water levels directly impact blood volume. Increased blood volume exerts more pressure on vessel walls, raising venous return and cardiac output, thereby elevating blood pressure, while decreased blood volume leads to lower venous return, reduced cardiac output, and decreased blood pressure. This relationship explains why dehydration results in low blood volume, reduced venous return, and low BP, triggering compensatory mechanisms like RAAS and ADH to restore homeostasis.
What changes to the structures and processes that maintain BP occur as we age?
As individuals age, arteries become stiffer and less elastic, increasing systolic BP and pulse pressure while diastolic BP decreases due to reduced recoil and vascular calcification. Baroreceptor sensitivity declines, impairing the ability to regulate BP and increasing the risk of orthostatic hypotension and unstable BP. Cardiac muscles weaken, leading to reduced contractility, lower stroke volume (SV), and cardiac output (CO), which may require increased heart rate to compensate. In patients like Mr. Johnson, these changes lead to a higher risk of syncope and BP instability, especially with positional changes.
How does prolonged bed rest affect homeostatic mechanisms for maintaining BP?
& give some examples related to a patient like Mr Johnson.
Prolonged bed rest affects BP regulation by causing decreased baroreceptor sensitivity due to lack of positional changes, impairing BP detection and response. Muscle atrophy reduces skeletal muscle pump function, decreasing venous return and stroke volume (SV). Heart Rate Variability (HRV) decreases due to autonomic imbalance, lowering cardiovascular adaptability. Renal function declines, reducing RAAS activity, which decreases blood volume and BP. For Mr. Johnson, these changes result in weaker muscles, lower venous return, reduced SV, and unstable BP, increasing the risk of orthostatic hypotension.
How does temperature/climate affect homeostatic mechanisms for maintaining BP?
Cold temperatures cause vasoconstriction, increasing vascular resistance and BP, while hot temperatures lead to vasodilation, reducing BP. Each 1°C change in temperature can alter systolic BP by 0.31 mmHg indoors. Maintaining an office temperature of at least 18°C is recommended to prevent BP instability and fainting risk.
Should office temperature be controlled?
an indoor temperature setting of at least 18ºC is recommended by Public Health England and WHO (Umishio et al. 2019). if temperature in office is too high (e.g. ac broken) à patients bp lower, risk of fainting
What are the First Aid procedures in Australia for managing a patient who has collapsed?
- Indicate the procedures for patient who remains Conscious
1. Stop all dental treatment
2. If the patient is in the dental chair, tilt the chair back to a horizontal position to lie the patient down (supine). If the patient is not in the dental chair, ask them to lie down. (a seated position is not enough)
3. Ensure the patient’s legs are positioned above their heart only slightly above head because if the legs are too high it triggers an autonomic response = increasing in HR.
4. Measure the patient’s heart rate
5. Talk to the patient to assess their consciousness (Therapeutic Guidelines 2019).
6. Look for signs of ANS: sweating, pupils dilated. If their HR is high, you won’t be surprised because of the ANS.
7. Explain to pt what has happened and get them to stay down e.g. “Mr Johnson you are in the clinic, you have just fainted, please lay down we don’t want you hurting yourself again”
8. Before getting pt to sit up, get them to take a few deep breaths and wriggle their toes. Can give pt a sip of water – not too much bc they will aspirate if their ANS drive is high.
9. Have someone on both sides when standing them up
10. Can look at nails for peripheral vasoconstriction (blue)
11. Ask how they are feeling before dismissing pt. Check if they have fainted before, what triggered it last time. How they will be getting home. Ask DA to talk to pt.
12. Debrief with pt’s emergency contact or whoever is there to pick them up.
13. SLS report. - Indicate the procedures for patient who becomes Unconscious
Stop all dental treatment and lie the patient back so that their legs are elevated, and their head is below their heart. Measure their blood pressure and heart rate.
What are the responsibilities of dentists and the dental team in managing a medical emergency in the dental clinic?
- immediate response to emergency situations
- Adequate documentation of the incident.
- Post emergency follow up
If a patient collapses (but remains conscious) whilst they are in the dental chair during treatment – what are all the sequence of steps that need to be taken immediately and afterwards?
In emergencies, practitioners should quickly assess the situation, prevent further harm (analgesics, CPR, emergency services), check response to stimuli, ensure proper airway and breathing, and control bleeding if present. After initial care, follow up with medical practitioners, contact the patient post-incident, review and reflect on management, consider additional training for staff, complete an SLS report, and update the patient record with adjustments for future treatments. Immediate care focuses on emergency response, while subsequent care ensures patient recovery and practice improvement.
Explain what happened physiologically during Mr Johnson’s dental appointment specifically regarding his collapse and the recovery?
Orthostatic hypertension is a condition characterized by an inadequate response to gravity-induced blood shifts when moving from a horizontal to vertical position, defined by a drop of ≥20 mmHg systolic or ≥10 mmHg diastolic BP within three minutes of standing. Mr. Johnson, who was supine for an extended period, experienced blood pooling in his legs upon standing, leading to decreased venous return, stroke volume, and blood pressure, ultimately resulting in insufficient cerebral perfusion and collapse. Recovery involves baroreceptor activation, increased sympathetic drive, elevated heart rate, cardiac output, and total peripheral resistance, restoring BP to normal levels.
What steps can you take to prevent this from occurring for your patients.
To prevent syncope in patients, practitioners should raise the chair slowly, allow the patient to lie down, and then assess if they feel stable before standing. If needed, assist the patient by allowing them to use the armrest. Encourage them to drink water and sit at the chair’s edge for a minute before standing. Conduct a thorough medical history to identify risk factors like self-medication or past syncope episodes. Monitor for presyncope symptoms (e.g., sweating or dizziness) and recommend physical counterpressure techniques (e.g., arm tension, leg crossing). Reduce stress through rapport building and positive distraction techniques during procedures.
