Jack, an apartment superintendent, grabbed a quick cup of coffee ...

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Jack, an apartment superintendent, grabbed a quick cup of coffee and then put on his coat to shovel snow off the front sidewalk.
 
  He is 56 years old and has experienced two episodes of angina over the past 3 years. This time when he was shoveling the snow, he felt palpitations in his chest. It was as though his heart had stopped and then began to beat rapidly as if to catch up. Afraid of what he was feeling, he went inside and called for an ambulance. When the paramedics arrived, they took an ECG and told Jack he was going to be fine. He was taken to hospital to be seen by an emergency physician and was released later that afternoon.
 
  The ECG taken by the paramedics showed Jack was experiencing premature ventricular contractions. In general terms, how do PVCs appear on an ECG? What factors contributed to the onset of PVCs in Jack's situation?
 
  Describe the physiologic events in PVC. How is cardiac output disrupted with the presence of PVCs?
 
  Because of Jack's history, his PVCs leave him at risk for events such as ventricular tachycardia or ventricular fibrillation. Compare and contrast these two arrhythmias. Why are they particularly dangerous?

Question 2

Milo, a 19-year-old, lives in an inner-city apartment complex. One late night he was walking home after hanging out with his friends.
 
  Before he knew what was happening, someone jumped Milo from behind and tried to get his wallet. A fight broke out, and the thief stabbed Milo in the abdomen before taking off. When the paramedics arrived, Milo was pale, sweating, and rolling restlessly on the ground. His pulse was 94 beats/minute and his blood pressure 115/82 mm Hg. He was rushed to the hospital where his treatment began immediately.
 
  Why is Milo presenting with pallor, diaphoresis, and restlessness?
 
  In spite of his blood loss, Milo's blood pressure was only slightly affected when the paramedics first found him. Describe how cardiovascular compensatory mechanisms serve to maintain homeostasis as long as possible in the early stages of shock. How does ADH contribute to compensation?
 
  What are the disadvantages of prolonged vasoconstriction in hypovolemic shock?
 
  If Milo's respirations were to become progressively deeper and more rapid, what physiological changes in the body would that indicate?

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Answer to Question 1

Premature ventricular contractions present with normal beats interspersed by distorted QRS complexes. The PVCs in Jack's situation may have been triggered by the increased physical activity that generated an increased sympathetic response and heart rate. The coffee might have acted as an additional sympathetic stimulant. Finally, his history of previous cardiac events can be a predisposing factor to arrhythmia.

A premature ventricular contraction begins with an electrical event by a ventricular ectopic pacemaker. Because of the ectopic beat, the ventricles are unable to complete repolarization before the next SA impulse. The result is a delay, or compensatory pause, in ventricular systole. PVCs cause a decrease in diastolic filling and therefore a reduction in cardiac output.

Ventricular tachycardia originates within the conduction system and/or the muscles of the ventricular wall. It involves abnormal QRS complexes on the electrocardiograph and a heart rate falling within 70 to 250 beats/minute. It may be sustained or may spontaneously rectify itself. Ventricular fibrillation creates a series of sine-wave patterns on the electrocardiograph and involves a quivering of the ventricular walls instead of contraction.
Ventricular tachycardia is clinically significant because it inhibits the proper function of the atrial pacemaker and decreases the diastolic filling time. With ventricular fibrillation, cardiac output and pulses are nonexistent.

Answer to Question 2

Hypovolemia creates a sympathetic response in the body in an attempt to maintain homeostasis in the presence of fluid loss. Increased sympathetic activity stimulates sweat gland activity and generates restlessness. The sympathetic response also causes vasoconstriction of the dermal vasculature. In concert with a decline in red blood cells, the skin and mucous membranes appear pale as a result.

The heart, under sympathetic influence, beats faster and with greater contractility as a means to maintain homeostasis in the presence of fluid loss. Arteriolar constriction occurs to ensure systemic resistance, while venous constriction ensures venous return to the heart. An added benefit of venous constriction is the movement of blood that has been stored in the capacitance portion of the circulation. Fluid loss also stimulates the release of ADH from the posterior pituitary. ADH stimulates thirst centers in the hypothalamus and assists in the generation of peripheral vasoconstriction. It also has a strong effect on the kidneys and stimulates water resorption by renal tubules.

As fluid loss continues, vasoconstriction intensifies as a means to maintain vascular resistance and perfusion to the major organs. Prolonged vasoconstriction, however, limits tissue perfusion and oxygenation. Tissue cells revert to anaerobic metabolism, which over time leads to lactic acid production and cellular damage.

Increased rate and depth of respirations indicate the presence of metabolic acidosis, a result of the shift from aerobic to anaerobic cellular respiration. A decrease in the oxygen-carrying capacity of the blood (due to volume loss) is an additional factor for the alteration in ventilation.