question: Why does your heart drop when terrified or jump scared?
comment: That dropping sensation isn't really your heart. When you are scared,your body is alert. In a second, it puts itself into overdrive to "survive". This means stopping blood flow to your stomach (since you don't want to lose valuable resources digesting your food when you can run away or fight). That is why you get that funny feeling.
passages: Some of the hormones involved during the state of fight-or-flight include epinephrine, which regulates heart rate and metabolism as well as dilating blood vessels and air passages, norepinephrine increasing heart rate, blood flow to skeletal muscles and the release of glucose from energy stores, and cortisol which increases blood sugar, increases circulating neutrophilic leukocytes, calcium amongst other things.
   BULLET::::1. On one end of the spectrum is the cardioinhibitory response, characterized by a drop in heart rate (negative chronotropic effect) and in contractility (negative inotropic effect) leading to a decrease in cardiac output that is significant enough to result in a loss of consciousness. It is thought that this response results primarily from enhancement in parasympathetic tone.
   The cranium dysfunction mechanical changes in the gut can compress the vagus nerve at any number of locations along the vagus, slowing the heart. As the heart slows, autonomic reflexes are triggered to increase blood pressure and heart rate.
   A subject's blood volume pulse (BVP) can be measured by a process called photoplethysmography, which produces a graph indicating blood flow through the extremities. The peaks of the waves indicate a cardiac cycle where the heart has pumped blood to the extremities. If the subject experiences fear or is startled, their heart usually 'jumps' and beats quickly for some time, causing the amplitude of the cardiac cycle to increase. This can clearly be seen on a photoplethysmograph when the distance between the trough and the peak of the wave has decreased. As the subject calms down, and as the body's inner core expands, allowing more blood to flow back to the extremities, the cycle will return to normal.
   BULLET::::2. On the other end of the spectrum is the vasodepressor response, caused by a drop in blood pressure (to as low as 80/20) without much change in heart rate. This phenomenon occurs due to dilation of the blood vessels, probably as a result of withdrawal of sympathetic nervous system tone.
  
  BULLET::::3. The majority of people with vasovagal syncope have a mixed response somewhere between these two ends of the spectrum.
  
  One account for these physiological responses is the Bezold-Jarisch reflex.
  
  Vasovagal syncope may be an evolution response, specifically the fight-or-flight response.
  
  Section::::Diagnosis.
   Section::::Reactions.:Startle and orienting response.
  
  Startle response interrupts and disengages the organism from ongoing activity, directs attention to stimuli, and protects the organism from potential harmful stimuli. Orienting response is an organism’s innate reaction to a novel stimulus, and it is a defensive response. Heart rate increases after the onset of startle stimuli. The heart rate decreases during the orienting response.
  
  Section::::Measurement techniques for body reactivity.
  
  Section::::Measurement techniques for body reactivity.:Electroencephalography.
   Some patients describe this experience as a 'flip' or a 'jolt' in the chest, or a 'heart hiccups', while others report dropped or missed beats. Ectopic beats are more common during periods of stress, exercise or debility; they may also be triggered by consumption of some food like alcohol, strong cheese, or chocolate.
  
  It is a form of cardiac arrhythmia in which ectopic foci within either ventricular or atrial myocardium, or from finer branches of the electric transduction system, cause additional beats of the heart. Some medications may worsen the phenomenon.
   In regard to the characters present onstage, a reduced startle response has been associated with a passive defense, and the diminished initial heart rate response has been predicted to have a greater tendency to dissociation. 
  
  Further, note that heart rate is an accurate measure of stress and the startle response which can be easily observed to determine the effects of certain stressors.
  
  Section::::Physiology.:Factors influencing heart rate.:Factors decreasing heart rate.
   According to the SMH, two distinct pathways reactivate somatic marker responses. In the first pathway, emotion can be evoked by the changes in the body that are projected to the brain—called the "body loop". For instance, encountering a feared object like a snake may initiate the fight-or-flight response and cause fear. In the second pathway, cognitive representations of the emotions can be activated in the brain without being directly elicited by a physiological response—called the "as-if body loop". For instance, imagining an encounter with a snake would initiate a similar flight-or-fight response "as-if" you were in that particular situation (albeit perhaps a much weaker one). In other words, the brain can anticipate expected bodily changes, which allows the individual to respond faster to external stimuli without waiting for an event to actually occur.
   Section::::In humans.:Goose bumps.
  
  The pilomotor reflex, more commonly known as goose bumps, was originally a reflex that assured the raising of fur for additional insulation against cold. When scared, this response also made the frightened animal seem bigger and a more formidable enemy.
  
  Section::::In humans.:Hypnic jerk.
  
  The sudden startled arm-jerking response sometimes experienced when on the verge of sleeping is known as the hypnic jerk.
   The central brain structure through which fear-associated responses are mediated has been determined to be the amygdala, which is located in the brain's temporal lobe. When the central nucleus of the amygdala is stimulated - what is popularly referred to as the "fight-or-flight" response is activated - the organism in question reacts passively (is rendered frozen in its tracks, becomes hyper-vigilantly attentive, etc.), or displays a physiological reaction geared toward facilitating an aggressive reaction (e.g., increased heart-rate/pulse, rapid breathing). These fear-induced reactions result from communication between the amygdala and a variety of other brain regions (such as the brain stem and hypothalamus), resulting in a variety of physiological responses in the organism. For instance, communication between an activated amygdala and the lateral hypothalamus results in increased blood pressure and dilation of the pupils; the initiation of the central grey via communication from the amygdala results in the organism's becoming frozen in its tracks; communication between the activated amygdala and the paraventricular nucleus of the hypothalamus releases hormones associated with stress.
   Medullary ischemic reflex
  
  The medullary ischemic reflex is a big response to a drop in blood pressure in the brain particularly in the medulla, where the lack of oxygen due to decreased perfusion triggers an autonomic response from the cardiac and vasomotor centers. The cardiac and vasomotor centers respond to the decrease in blood pressure with sympathetic outflow to the heart and blood vessels. This outflow causes increased heart rate and force of contraction, as well as bodywide vasoconstriction. Together these responses increase blood pressure and perfusion rate to the brain, ending the feedback loop.
   There have been a number of other studies supporting Tinbergen's short neck hypothesis with some as recent as the 1980s such as Helmut C. Mueller and Patricia G. Parker, in 1980, demonstrated that naive mallard ducklings shows a greater variance in heart rate to the hawk models over the goose models. They concluded that cardiac response is an excellent measurement of fear and controlled for learned behavior by maintaining the ducklings in a brooder until they were transported to their laboratory in opaque containers and in 1982, Elizabeth L. Moore and Helmut C. Mueller found that a chick’s heart rate was of greater variance in response to the hawk model without prior, pertinent experience, suggesting a greater innate fear response to the hawk over the goose. Obvious behavioral responses to fear were not identified.
   Bowditch effect
  
  The Bowditch effect is an autoregulation method by which myocardial tension increases with an increase in heart rate. Also known as the Treppe phenomenon, Treppe effect or staircase effect. It was first observed by Henry Pickering Bowditch in 1871.
   The small window of vulnerability explains why it is a rare event. Considering that the total cardiac cycle has a duration of 1 second (for a base cardiac frequency of 60 beats per minute), the probability of a mechanical trauma within the window of vulnerability is 1 to 3% only. That also explains why the heart becomes more vulnerable when it is physically strained by sports activities:
  
  BULLET::::1. The increase in heart rate (exercise tachycardia) may double the probability above (e.g., with 120 beats per minute the cardiac cycle shortens to 500 milliseconds without fundamentally altering the window-of-vulnerability's size)
   BULLET::::- Atropine — The process of intubation can cause massive stimulation to vagus nerve, causing bradycardia (low heart rate). The people who are at increased risk of bradycardia are neonates and children. This does not happen in adults because sympathetic stimulation overpowers the vagal response. However, for those adults who have received drugs such as beta blocker, calcium channel blocker, and digoxin has an increased risk of developing bradycardia. Atropine is a muscarinic receptor antagonist, thus blocking the vagal response. The dose is 0.01 mg/kg. It has quick onset of action, and common side effects are: increased heart rate, dry mouth, flushing, and urinary retention.
   An example of premature ventricular contraction, is the classic athletic heart syndrome. Sustained training of athletes causes a cardiac adaptation where the resting SAN rate is lower (sometimes around 40 beats per minute). This can lead to atrioventricular block, where the signal from the SAN is impaired in its path to the ventricles. This leads to uncoordinated contractions between the atria and ventricles, without the correct delay in between and in severe cases can result in sudden death.
  
  Section::::Autorhythmicity.:Regulation by the autonomic nervous system.
   In a majority of specific phobias, affected individuals experience heightened anxiety when exposed to a phobic trigger. While BII-phobics experience a similar reaction initially upon exposure, most ultimately respond to a trigger with a biphasic, or two-phase, fainting response. In the first phase, phobics often experience an anxiety reaction characterized by elevated heart rate and heightened blood pressure, as occurs in most other phobias. This is the result of increased activation of the sympathetic nervous system. However, with BII phobia, a second phase usually follows closely, in which the phobic individual experiences a massive dip in heart rate and blood pressure known as vasovagal response. Stimulation of the vagus nerve, a part of the parasympathetic nervous system, is responsible for promoting the lowered heart rate and decreased blood pressure. These physiological changes limit blood flow to the brain and can promote pre-syncope (lightheadedness, feelings of faintness) and syncope (fainting): categorized in this instance as vasovagal fainting. This second, fainting phase is not common to other phobias. 
   The perception of a "threat" may also trigger an associated ‘feeling of distress’.
  
  Physiological reactions triggered by mind cannot differentiate both the physical or mental threat separately, Hence the "fight-or-flight" response of mind for the both reactions will be same.
  
  Section::::Duration of threat and its different physiological effects on the nervous system..
   First-degree heart block does not require any particular investigations except for electrolyte and drug screens, especially if an overdose is suspected.
  
  Section::::Treatment.
   During systole, the ventricles contract, pumping blood through the body. During diastole, the ventricles relax and fill with blood again.
   The first cell to produce the action potential in the SA node isn’t always the same, this is known as pacemaker shift. In certain species of animals, for example, in dogs, a superior shift (i.e. the cell that produces the fastest action potential in the SA node is higher than previously) usually produced an increased heart rate whereas an inferior shift (i.e. the cell producing the fastest action potential within the SA node is further down than previously) produced a decreased heart rate.
  
  Section::::Clinical significance.
   BULLET::::- Second-degree atrioventricular block - The heart’s electrical signals between the upper and lower signals of the heart are slowed by a much greater rate than in first-degree atrioventricular block. Type 1 (a.k.a. Mobitz 1, Wenckebach): Progressive prolongation of PR interval with dropped beats (the PR interval gets longer and longer; finally one beat drops) . Type 2 (a.k.a. Mobitz 2, Hay): PR interval remains unchanged prior to the P wave which suddenly fails to conduct to the ventricles.
   Both surprise and stress induce physiological response: elevate heart rate substantially. In a study conducted on 8 female and male student actors ages 18 to 25, their reaction to an unforeseen occurrence (the cause of stress) during a performance was observed in terms of heart rate. In the data collected, there was a noticeable trend between the location of actors (onstage and offstage) and their elevation in heart rate in response to stress; the actors present offstage reacted to the stressor immediately, demonstrated by their immediate elevation in heart the minute the unexpected event occurred, but the actors present onstage at the time of the stressor reacted in the following 5 minute period (demonstrated by their increasingly elevated heart rate). This trend regarding stress and heart rate is supported by previous studies; negative emotion/stimulus has a prolonged effect on heart rate in individuals who are directly impacted. 
   During stage 4 of an action potential, the inside of a cardiac muscle cell rests at −90 mV. As the inner muscle cell potential rises towards −60 mV, electrochemical changes begin to take place in the voltage-gated rapid sodium channels, which permit the rapid influx of sodium ions. When enough sodium channels are opened, so that the rapid influx of sodium ions is greater than the tonic efflux of potassium ions, then the resting potential becomes progressively less negative, more and more sodium channels are opened, and an action potential is generated. The electrical potential at which this occurs is called the threshold potential.
  
presuppositions: Heart drops when you are scared. The heart drops when someone is terrified.
corrections: That is just a feeling, your heart doesn't actually move. The heart doesn't drop when someone is terrified, but blood flow to the stomach stops.
raw_presuppositions: Heart drops when you are scared. The heart drops when someone is terrified.
raw_corrections: That is just a feeling, your heart doesn't actually move. The heart doesn't drop when someone is terrified, but blood flow to the stomach stops.