Vital Signs Flashcards
Blood pressure why is it important to use the right size cuff
- Use a blood pressure cuff that is of proper size to minimize errors in blood pressure determinations. The arm cuff should be at least 10cm wide; for the thigh, a width of 18cm is preferable. The length of the blood pressure cuff’s bladder (the inflatable part) should encircle at least 80% of the arm’s circumference.
Incomplete Occlusion: A small cuff may not fully occlude (block) the artery during measurement. This can result in some blood continuing to flow through the partially compressed artery, leading to a falsely high reading.
**If the clamp (cuff) is too small, you’d need to apply more pressure to stop the flow of water (blood). This excessive pressure can lead to inaccurately high readings because it compresses the artery too much.
If the clamp is just the right size, you’d apply the correct amount of pressure to stop the flow without squeezing the hose too tightly or leaving it too loose. This is analogous to using a properly sized cuff for blood pressure measurement, which gives accurate readings.
Conversely, if the clamp is too big, you wouldn’t need to apply much pressure because it naturally fits around the hose without squeezing it much. However, this can also lead to inaccurate readings because the cuff might not fully occlude the artery.
Blood pressure what to screen for before taking
Screen the patient to identify if patient has avoided caffeine and smoking 30 minutes prior to measurement. Also be aware that anxiety, “white coat syndrome”, rushing to make the appointment on time, bladder distension, chronic alcoholism, recent cigarette smoking and caffeine consumption can contribute to temporarily raised blood pressure in the absence of disease.
- The patient’s arm should be bare, free of clothing, and have no scarring, lymphedema, or arteriovenous (AV) fistulas. Keep the patients arm at the level of the heart.
Easy to remember if you understand to double for hypertension
Blood pressure what is normal, what are the different stages
Hypotension = low blood pressure (> 90/60 mm Hg)
Common Causes of hypo/hypertension
Clinical manifestations of low blood pressure can include fatigue, shortness of breath (SOB)/dyspnea on exertion (DOE), and light-headedness, especially on assuming an upright posture (orthostatic hypotension).
- The most common causes of low blood pressure are dehydration or decreased cardiac output.
- In patients with acute illness, hypotension with a systolic BP of <90 mm Hg can predict death in hospitalized patients in the intensive care unit (ICU) (LR+ 3.1) and in patients with bacteremia (LR+ 4.9) and pneumonia (LR+ 7.6); with a systolic BP of <80 mm Hg it can predict death in patients with myocardial infarction (LR+ 15.5). The APACHE (Acute Physiology and Chronic Health Evaluation) scoring system, which predicts the risk of hospital mortality among patients in the ICU, assigns more points (and thus a higher risk) to severe hypotension than to any other vital sign or laboratory variable.
- Hypotension also predicts other adverse outcomes. In patients with myocardial infarction, a systolic blood pressure less than 80 mm Hg predicts a much higher incidence of congestive heart failure (CHF), ventricular tachycardia and fibrillation, and complete heart block. In hospitalized patients, hypotension greatly increases the risk of serious adverse outcomes in the next 24 hours (≤90 mm Hg, LR+ 4.7; ≤85 mm Hg, LR+ 9; ≤80 mm Hg, LR+ 16.7)
HYPERTENSION = High Blood Pressure (>130 / 80)
- Blood pressures that are too high may cause end-organ damage with equally disastrous consequences. Heart attack, stroke, hypertensive renal failure, and retinopathy are all too familiar in the hypertensive population.
- Essential hypertension is defined as three or more blood pressure readings taken over three visits separated by weeks
- Blood pressure should be measured in every person, even when asymptomatic, because essential hypertension is common and treatable and because treatment reduces cardiovascular morbidity and overall mortality rates.
Orthostatic Hypotension what is it?
(aka. postural hypotension), is a drop in blood pressure upon standing.
**Positive findings: a decline of ≥ 20 mmHg in systolic or ≥ 10 mmHg in diastolic blood pressure within 3 minutes of standing.
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- If orthostatic hypotension is observed, an accompanying rise in heart rate of fewer than 15 beats per minute may indicate a neurogenic cause, and a rise in heart rate of more than 15 beats per minute may indicate a non-neurogenic cause.
- A pulse rate increase of ≥ 30 bpm may suggest hypovolemia, independent of whether the patient meets criteria for orthostatic hypotension.
- Pulse rate is not a specific indicator of the underlying cause and could be inaccurate (e.g. if the patient is on a beta-blocker).
Orthostatic hypotension etiology
Here’s how the baroreceptor reflex works:
Baroreceptor Activation: Baroreceptors are specialized sensors located in the walls of certain blood vessels, especially in the carotid sinus in the neck and the aortic arch in the chest. These receptors detect changes in blood pressure.
Signal to the Brain: When a person stands up, the decrease in blood pressure is sensed by the baroreceptors. They send signals to the brain, specifically to the cardiovascular control center in the medulla oblongata, which is part of the brainstem.
Autonomic Nervous System Response: The brain responds by activating the autonomic nervous system, which includes the sympathetic and parasympathetic branches. In the context of orthostatic hypotension:
Sympathetic Activation: The sympathetic nervous system is activated to increase heart rate and contractility (the strength of heart contractions). This helps maintain cardiac output despite the drop in blood pressure.
Parasympathetic Modulation: The parasympathetic nervous system may also be modulated to a lesser extent, reducing its inhibitory effect on heart rate and allowing the heart rate to increase further.
Now, regarding the rise in heart rate and its association with neurogenic versus non-neurogenic causes of orthostatic hypotension:
Neurogenic Causes: Neurogenic orthostatic hypotension is often related to dysfunction in the autonomic nervous system, particularly the sympathetic control of blood pressure and heart rate. In this case, the rise in heart rate of fewer than 15 beats per minute may indicate an inadequate sympathetic response, leading to a less pronounced compensatory increase in heart rate.
Non-Neurogenic Causes: Non-neurogenic orthostatic hypotension may be due to factors such as dehydration, medication side effects, blood volume deficits, or other systemic conditions. In these cases, the body’s compensatory mechanisms, including the baroreceptor reflex and sympathetic activation, may still function relatively normally. This can result in a more robust increase in heart rate (more than 15 beats per minute) to counteract the drop in blood pressure.
In summary, the rise in heart rate during orthostatic hypotension is a compensatory response mediated by the autonomic nervous system, particularly the sympathetic branch. The magnitude of the heart rate increase can provide insights into the underlying cause of the orthostatic hypotension, with a smaller increase potentially indicating a neurogenic cause and a larger increase indicating a non-neurogenic cause.
Orthostatic hypotension how to perform test
There are numerous ways but what is described below is the ‘classic’ orthostatic hypotension test
**Note: All measurements should be completed within 3 minutes of standing. Normally, the pulse change stabilizes after 45 to 60 seconds, and the blood pressure stabilizes after 1 to 2 minutes. Which is why we count the heart rate first (beginning at 1 minute), as it allows more time for the blood pressure to stabilize and improves accuracy of testing.
1. Clinician instructs patient to lie supine for 3-5 minutes. * Note: shorter periods of supine rest significantly reduce the sensitivity of postural vital signs in detecting blood loss. 2. Clinician measures the patient’s blood pressure and pulse rate in supine position. 3. Clinician assists patient to stand. Clinician asks patient about symptoms of dizziness, weakness, or visual changes associated with position change, as well as noting diaphoresis or pallor. 4. After 1 minute of standing, clinician takes patient’s pulse, followed by the patient’s blood pressure. * If patient is unable to stand, ask patient to sit upright with legs dangling over the edge of the treatment table. Note: sitting vital signs reduces ability to detect blood loss as cause of orthostatic hypotension. * If the patient experiences near syncope, the clinician should assist the patient back into the supine position. Clinician compares supine to standing vital signs.
What is the normal temperature of the human body? What is the life threatening temperature
Easy to remember clinical equivalents are: 35oC = 95oF, 37oC = 98.6oF, and 40oC = 104oF.
Deviation of temperature by more than 4oC above or below normal can produce life-threatening cellular dysfunction.
104°F (40°C) or above can lead to heat-related illnesses such as heat exhaustion and heatstroke.
Temperatures above 106°F (41.1°C) can result in severe heatstroke, causing life-threatening cellular damage, organ failure, and central nervous system dysfunction.
33°C or 91.4°F and lower can lead to severe hypothermia, which can result in cardiac arrhythmias, respiratory failure, and metabolic derangements. Severe hypothermia can also cause life-threatening cellular dysfunction and complications.
What is the range of normal respiration rates?
12-20 Respirations
>20 Tachypnea
- occurs with exertion, fear, cardiac insufficiency, pain, pulmonary embolism, acute respiratory distress from infections, pleurisy anemia and hyperthyroidism
< 12 Bradypnea
- - Occurs with hypothyroidism, respiratory failure, medication and drug use (i.e. opiods), or brain injuries
In the Heart what can the different heart sounds suggest
S1: AV valves closing, marking the start of ventricular contraction.
S2: Semilunar valves closing, marking the end of ventricular contraction.
S3: Rapid ventricular filling in early diastole, can indicate increased blood volume or decreased ventricular compliance.
S4: Atrial contraction in late diastole, often associated with ventricular hypertrophy or stiffness.
Why S3 sounds are sometimes considered normal and in what populations?
S3 can be a normal finding in certain circumstances, such as in young children, adolescents, and well-conditioned athletes. Here are some reasons why S3 may be considered normal in these populations:
Rapid Ventricular Filling: In young individuals with healthy hearts, especially children and adolescents, the ventricles can fill rapidly during diastole due to their efficient and well-functioning cardiovascular systems. The rapid filling of blood into the ventricles during early diastole can contribute to the creation of an audible S3 sound.
Increased Cardiac Output: Athletes and individuals who engage in regular physical exercise often have well-conditioned hearts with increased cardiac output. The increased blood volume and cardiac output can lead to a more forceful filling of the ventricles during diastole, potentially resulting in the detection of an S3 sound.
**Normal Ventricular Compliance: **Young individuals and athletes typically have hearts with good ventricular compliance, meaning that the ventricular walls are flexible and can expand easily to accommodate blood volume. This normal ventricular compliance allows for efficient and rapid ventricular filling, which may contribute to the presence of S3 without indicating underlying heart pathology.
Absence of Pathological Signs: In these populations, the presence of an S3 sound is often accompanied by other signs of normal cardiac function, such as absence of symptoms, normal heart rates, and absence of other abnormal heart sounds or murmurs.
It’s important to note that while S3 may be considered normal in certain circumstances, its presence alone does not necessarily indicate pathology. Clinical assessment, including a thorough history, physical examination, and additional diagnostic tests if needed, is crucial to differentiate between normal and abnormal findings and to assess overall cardiac health.
When does S4 occur and what could be the cause
S4 and Ventricular Filling Patterns: The S4 heart sound occurs during late diastole, just before the atria contract. It is caused by the rapid and forceful filling of blood into a ventricle that is stiff or less compliant than normal.
Let’s clarify the role of the atria in the S4 heart sound. While the atria do play a part in generating the S4 sound, the primary cause of S4 is related to the properties of the ventricles rather than the atria.
Here’s a breakdown of how S4 is generated:
Atrial Contraction (Atrial Systole): During the cardiac cycle, atrial contraction (atrial systole) occurs just before ventricular contraction (ventricular systole). This atrial contraction is responsible for pushing the remaining blood into the ventricles before they contract and pump blood out of the heart.
Primary Cause in Ventricles: The main factor contributing to S4 is the properties of the ventricles themselves. Conditions that lead to ventricular hypertrophy (thickening of ventricular walls) or decreased ventricular compliance (stiffness) can result in abnormal ventricular filling patterns.
Atrial Contribution: While the atria contract and push blood into the ventricles during atrial systole, it is the characteristics of the ventricles (such as stiffness or hypertrophy) that lead to the creation of the S4 sound.
