BMS 360 Lecture Notes - Cardiac Output, Afterload, Heart

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lemondog142

22 May 2014

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Understand how pressure-volume loops are generated, how they describe cardiac function, and why this is important. Coordinated activity of the chambers and valves of the heart. Atrial systole isovolumetric contraction ventricular systole ventricular diastole. Stroke volume = end-diastolic volume end-systolic volume. Same things happen on left and right side of heart, but right side is lower pressure. The end-systolic pressure-volume relationship (espvr) is used most frequently to describe cardiac contractility. Afterload pressure against which heart has to pump (aorta) Lv volume (ml) vs lvp (mmhg) on graph. Makes a loop left side isovolumteric relaxation, bottom ventricular filling, right side isovolumetric contraction, top ejection: p and v at the end of ventricular filling. As the ventricle begins to contract but before the aortic valve opens, lvp increases by lv volume remains the same. Isovolumetric contraction: when lvp exceeds aortic diastolic pressure, the aortic valve opens and ejection of blood occurs, the aortic valve closes, ejection ceases.

Related Questions

Effects of electrical stimulation of ventricle at various time points during a Frog cardiac cycle:

1. at which time points of the cardiac cycle can an electrical stimulation induce extra systole?

2. explain how the extra systole can appear during this manipulation in terms of the refractory period of the ventricular action potential.

3. Stannius ligature experiment: what will happen to the beating rate of the two atria (right and left) versus the ventricle during the ligature?)

4. explain how these changes occur in the beating rate during the stannius ligature.

5. now the heart is completely devoid of neural or hormonal input. What will happen to the beating rate of all three chambers? What about the chamberâs beating rate when they are surgically separated? explain possible mechanisms for the changes in the beating rate for each chamber.)

6. describe the effects of the following drugs on the heart rate and the force of ventricular contraction:
acetylcholine(1%), atropine (0.5%), Pilocarpine (2.5%), nicotine (0.2%), Epinephrine (0.1%), Isoproterenol (0.1%)

also, explain how each of the 6 chemicals above either mimic or inhibit the cardiac function

Need 150 word response to the below discussion post

The heart is the most important muscle in your body. The heart is just like a pump that moves the blood throughout the body. This action is what keeps us alive. We are typically taught about the danger of a heart attack, and what we must change in our lives to prevent it; but just like many people, I am at a high risk for heart disease because of family history as well as because of my firefighter career, as heart disease is the number one killer of firefighters (Fire Engineering, 2012). According to the American Heart Association, âboth the risk of heart disease and risk factors for heart disease are strongly linked to family historyâ (American Heart Association, 2016). However, even though your family history provided a picture or marker for possible issues, it is up to us to lower the risk by making changes in our lifestyles.

Heart attacks are caused by blockage that stops blood flow to the heart. A heart attack is when there is damage or death to the heart muscle tissue due to loss of blood supply and this does not necessarily result in an individual's death. A heart attack can show symptoms, such as radiating chest pain or discomfort, dizziness or nausea, sweating, anxiety, stomach pain and shortness of breath. Women have the same symptoms, but they do show some difference in that they describe the pain in their stomach and shoulder blades. In the field we treat heart attack by treating the symptoms; we use IV fluids, baby aspirin, as well as nitroglycerin.

There is another silent killer that most people do not hear much about or they think it is the same thing as a heart attack. As a medic, I deal with this life and death situation all the time, and it interesting to see how many people are not aware of the difference of a heart attack and a sudden cardiac arrest. Sudden cardiac arrest is the abrupt loss of heart function in a person who may or may not have diagnosed heart disease. This can happen at any time, its unexpected and occurs instantly, or seconds after symptoms occur. Cardiac arrest is caused when the heartâs electrical system malfunctions. This causes the heart to go into and irregular heart rhythm (ventricular fibrillation). When this happens, the hearts lower chambers suddenly start quivering and this stops the pump of blood in the heart. The only thing that can reverse cardiac arrest is early defibrillation and CPR. Most people think that a defibrillator can be used on heart attack patients, but this is not the case. The defibrillator is used to shock the heart and restore the normal heart rhythm, if the heart stops, then CPR has to be performed.

Unlike a heart attack, sudden cardiac arrest can happen to anyone, no matter how health or fit they are. According to the American Heart Association âcardiac arrest is a leading cause of death, nearly 360,000 out-of-hospital cardiac arrest occur annually in the United Statesâ (American Heart Association, 2016).

blackbeetle526

Question 1. Increased peripheral edema could be caused by:

a. blocked lymph vessels

b. decreased capillary blood pressure

c. increased concentration of albumin in the blood

d. slowed heart rate

Question 2. The pulse pressure of a healthy student is most likely to be:

a. 5 mm Hg

b. 30 mm Hg

c. 95 mm Hg

d. 120 mm Hg

Question 3. beta-blockers inhibit the activity of beta-adrenergic receptors and change the function of the heart by:

a. increasing heart rate and increasing contractility

b. increasing heart rate and decreasing contractility

c. decreasing heart rate and increasing contractility

d. decreasing heart rate and decreasing contractility

Question 4. In cardiac pacemaker cells, the L-type calcium channels:

a. open during diastole

b. close when the membrane potential rises above threshold

c. are located in the cell membrane

d. pump Ca2+ ions into the sarcoplasmic reticulum

Question 5. Dr. Campbell used an elliptical trainer for 40 minutes at the gym. Although the workload remained constant, Dr. Campbellâs heart-rate rose to 150 beats per minute during the first 5 minutes, stayed at that level for the next 25 minutes and then started to rise. It was 180 beats per minute at the end of the exercise period.

What was the time interval between QRS complexes when Dr. Campbellâs heart rate was 180 beats per minute?

a. 3.3 ms

b. 33 ms

c. 333 ms

d. 3333 ms

Question 6. In the question 5 above, Dr. Campbellâs heart rate is most likely to have risen during the last 10 minutes of exercise because his:

a. lungs were becoming congested

b. atrial cells were fatigued

c. extracellular Ca2+ concentration had increased

d. hematocrit increased due to sweating

Question 7. A Physiology student is sitting still in a cold igloo. After 30 minutes, she stands up, walks slowly around the igloo, and suddenly starts to shiver.

The student preserved their core temperature while they were sitting by:

a. depressing their Frank-Starling mechanism

b. decreasing the extracellular Ca2+ concentration

c. relaxing smooth muscles in their peripheral circulation

d. increasing the resistance of arterioles in their arms and legs

Question 8. In the question 7 above, the student started to shiver soon after walking because:

a. their atria started to fibrillate

b. their ventricles started to fibrillate

c. blood moved to the periphery, became cold, and chilled the core when it returned to the chest

d. the ATP concentration in their skeletal muscles had dropped to zero

Please use the following scenario for answering the questions 9 and 10.

A newly discovered drug binds to myosin molecules in cardiac muscle (and nowhere else) and increases the probability that myosin molecules in ventricular cells will bind to actin filaments when the intracellular Ca2+ concentration rises. The drug is being tested as a potential therapy for patients with heart failure.

Question 9. This drug might help people who have low cardiac output by:

a. increasing peripheral resistance

b. increasing the force developed by ventricular cells

c. increasing the isovolumic contraction time

d. increasing heart rate

Question 10. The increased binding of cardiac myosin molecules to actin might prevent the drug from being a useful treatment by:

a. slowing ventricular relaxation

b. decreasing the duration of systole

c. decreasing resistance of capillaries

d. slowing heart rate

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BMS 360 Lecture Notes - Cardiac Output, Afterload, Heart

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