1. Fill in the chart below. Use “+” if the patient’s vital sign is higher than normal, “−” if the sign is lower than normal, or “x” if the sign is normal. If you need to, use your text or another resource to determine normal values.
Vital Sign Increase/Decrease/Normal
Respiration Rate +
Heart Rate +
Blood Pressure –
2. If you were the doctors on the scene, what diagnosis would you give this patient? (You may use the internet to help diagnose the patient.)
I would question as to whether he has any allergies. The heart rate and respiration elevation, and low blood pressure can be present in allergic reactions.
3. Jot down some notes about your diagnosis, and bring these to class with you for discussion.
Does the patient have allergies? Is he taking any medication (obviously the anesthesia).
Assignment 2
3. In the above article, what is the “veritable metabolic storm” that the author refers to? What molecular changes are reported in pig muscles during a MH state?
The “veritable metabolic storm” refers to rapid heart rates and breathing,
abnormal muscle stiffening, blotchy blueness of the skin, and a rapid rise in temperature. The pig muscles lose adenosine triphosphate and release a tremendous amount of acid and potassium, which helps to stop their hearts.
The Essay on Rate Of Contractions Heart Angina Blood
What is Angina what is the cure RESPONSE: Angina refers to the pain arising from lack of adequate blood supply to theheart muscle. Typically, it is a crushing pain behind the breastbone in the center of the chest, brought on by exertion and relieved by rest. It may at times radiate to or arise in the left arm, neck, jaw, left chest, or back. It is frequently accompanied by sweating, palpitations ...
4) Arrange muscle contraction cards:
1. Neuron action potential arrives at end of motor neuron
2. ACH is released
3. ACh binds to receptors on motor end plate
4. Permeability of sarcolemma changes (Na rushes in)(an action potential is produced) 5. Muscle action potential sweeps into the T tubules triggering 6. release of Ca from the cisternae of the sarcoplasmic reticulum 7. CA binds to troponin
8. Troponin changes shape and shifts tropomyosin to expose binding sites of actin 9. myosin binds to actin (cross bridge is formend)(ADP released from myosin) 10. Myosin head pivots (pulling actin)
11. Myosin releases from actin (cross bridge is broken)(another ATP binds to myosin) 12. Myosin re-extends into “ready” position (ATP->ADP+Pi)(ADP is bound to myosin) 5) Steps that require ATP:
– ATP binding – myosin releases from actin.
– ATP hydrolysis – myosin head swings and binds to a new actin – Release of Pi initiates the power stroke
Steps that require Ca24:
release of Ca from the cisternae of the sarcoplasmic reticulum Ca binds to troponin
Assignment 3
1. Predict if healthy muscle or muscle with MH will contract with the most force.
The MH muscles generates excessive contraction.
3. Even though screening tests exist, most people aren’t checked for the disease. Why not? What types of people (or what populations) would be most
likely to be screened before they had their first surgery?
The testing takes time, and often people need to be admitted for surgeries quickly. Cost may also be a prohibitive factor for the poor or elderly. Assignment 4
2) Answers to Emily’s questions:
1) How do muscles contract?
-Action potential arrives at axon terminal of motor neuron;
-Acetylcholine (ACh) is released and binds to receptors on sarcolemma; -The sarcolemma’s Ion permeability changes;
The Term Paper on Skeletal Muscle Myosin Actin Calcium
... of the inhibitory action of troponin I. Troponin I blocks the affinity of actin to interact with myosin. When calcium binds to troponin C ... it causes fusion of acetylcholine-containing vesicles with neurolemma and release of Ach. Into the cleft space (about 300 vesicles / ... is- slow or fast. All muscles are mixed; there are no pure "fast" muscles or "slow" muscles. All muscles are slow and fast mixed ...
-depolarization occurs locally in the sarcolemma;
-This local change in membrane voltage ignites Action Potential in sarcolemma; -Action Potential travels across the entire sarcolemma and along the T tubules; -Sarcoplasmic Reticulum (SR) then releases Calcium which binds to troponin in the thin filament, exposing myosin-binding sites; -Myosin heads bind to actin causing contracytion to begin.
2) What is MH?
Malignant Hyperthermia is a hereditary condition in which a person, upon receiving certain types of anesthesia, has their muscles contract vigorously causing a rapid increase in body temperature. 3) How is MH triggered?
MH is triggered by certain anesthetics often used during surgery, once administered to a person with this condition. 4) What is the metabolic storm?
Metabolic Storm refers to the symptoms that occur in MH: patient’s muscles become rigid, respirations become very rapid, heart begins to beat fast and irregularly, skin becomes mottled, body temperature increases extremely, and blood pressure lowers to dangerous levels quickly. 5) How does malignant hyperthermia disrupt muscle physiology? In MH, the SR in the skeletal muscle cell is affected, causing Calcium to be released into the cell, resulting in a drastic increase in intracellular Calcium levels and muscle contraction. This causes a cycle where muscle maintains contraction.
6) Why does body temperature rise during malignant hyperthermia? During MH,
body temperature rises because of the heat that is produced by the severe muscle contractions that are occurring in the person’s body.
7) Why does body temperature rise during malignant hyperthermia? The standard test for MH is through a muscle biopsy (CHCT).
In CHCT, they remove a large portion of the muscle from the patient in surgery and immediately take it to the lab for testing. There is genetic testing for this condition available, but it only detects about 30%. People usually find out they have this condition when they receive the anesthetic for the first time during an invasive procedure requiring anesthesia. 8) What drug is used to treat MH?
The drug used to treat MH is Dantrolene, a skeletal muscle relaxant. It acts on the muscle by interfering with the release of Calcium from the SR, therefore stopping the excitation-coupling process which leads to muscle contraction. 9) Why doesn’t the antidote to malignant hyperthermia impact smooth or cardiac muscle? The drug only affects skeletal muscles.
The Essay on Malignant Hyperthermia
Clinical signs are; Increased end tidal CO2 production which is an early sign, tachycardia, tachypnea, trunk or total body rigidity, masseter (jaw) muscle rigidity after succinylcholine which occurs commonly in children, marked temperature elevation (maybe a late sign), respiratory and metabolic acidosis, myoglobinuria(MHAUS, 2011). If left untreated the patient will experience cardiac arrest, ...
