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Which individual is likely experiencing the manifestation of acute coronary syndrome (ACS)? A client whose most recent ECG indicates that silent myocardial ischemia has occurred A client who occasionally experiences persistent and severe chest pain when at rest A client who sometimes experiences chest pain when climbing stairs A client who has recently been diagnosed with variant (vasospastic) angina
A client who occasionally experiences persistent and severe chest pain when at rest The onset of ST-elevation myocardial infarction (STEMI) involves abrupt and significant chest pain. The pain typically is severe, often described as being constricting, suffocating, and crushing. Substernal pain that radiates to the left arm, neck, or jaw is common, although it may be experienced in other areas of the chest and back. Unlike that of angina, the pain associated with myocardial infarction (MI) is more prolonged and not relieved by rest or nitroglycerin. Any angina that occurs at rest, is of new onset, or is increasing in intensity or duration denotes an increased risk of MI and should be evaluated immediately. Silent MI, stable angina, and variant, or vasospastic, angina are subtypes of chronic ischemic coronary artery disease.
Two months following a myocardial infarction (MI), a client visits the health care provider with reports of severe fatigue, shortness of breath, and frequent episodes of palpitations. A 12-lead ECG reveals the client has atrial fibrillation with a heart rate of 120. Which medications should the health care provider consider prescribing for this client? Select all that apply. Thrombolytics Anticoagulants Analgesics Antiarrhythmics Inhalers
Anticoagulants Antiarrhythmics Atrial fibrillation (AF) is a rhythm that involves quivering of the atrium rather than contracting rhythmically, causing pooling of blood in the atrium that can lead to the development of thrombi along with a decrease in cardiac output. Anticoagulants are used to decrease the ability of the blood pooling in the atrium to develop clots that could break off and become emboli that lodge in blood vessels elsewhere in the body; these emboli could cause ischemia, often to the brain, causing strokes. Antiarrhythmics are used with atrial fibrillation to either convert the rhythm to normal sinus or to control the rate, which gives the ventricles more time to fill.
Although pressure pulses usually are not transmitted to the capillaries, there are situations in which this does occur. Under what conditions do cardiac pulsations occur? Select all that apply. Aortic regurgitation Cerebrovascular accidents Myocardial infarction Patent ductus arteriosus
Aortic regurgitation Patent ductus arteriosus Capillary pulsations occur in conditions that cause exaggeration of aortic pressure pulses, such as aortic regurgitation or patent ductus arteriosus.
Which conditions reflect failure of the circulatory system? Select all that apply. Orthostasis Circulatory shock Renal dysfunction Suppression of the renin-angiotensin-aldosterone system (RAAS) Heart failure
Circulatory shock Heart failure Heart failure and circulatory shock are both failures of the circulatory system to provide an adequate supply of oxygen and nutrients to all body tissues. Orthostasis is a temporary decrease of blood flow to the central nervous system, causing dizziness. Renal dysfunction can be a result of impaired blood flow to the kidneys. Suppression of RAAS can cause vasodilation and decreased blood volume but usually does not completely disrupt systemic circulation.
What are the physiologic clinical manifestations of cardiogenic shock? Select all that apply. Decrease in mean arterial blood pressures Increased urine output related to increased renal perfusion Rise in central venous pressure (CVP) Hypercapnic lips and nail beds Increased extraction of O2 from hemoglobin
Decrease in mean arterial blood pressures Rise in central venous pressure (CVP) Hypercapnic lips and nail beds Increased extraction of O2 from hemoglobin Signs and symptoms of cardiogenic shock include indications of hypoperfusion with hypotension, although a preshock state of hypoperfusion may occur with a normal blood pressure. The lips, nail beds, and skin may become cyanotic because of stagnation of blood flow and increased extraction of oxygen from the hemoglobin as it passes through the capillary bed. Mean arterial and systolic blood pressures decrease due to poor stroke volume, and there is a narrow pulse pressure and near-normal diastolic blood pressure due to arterial vasoconstriction. Urine output decreases due to lower renal perfusion pressures and the increased release of aldosterone. Elevation of preload is reflected in a rise in CVP and pulmonary capillary wedge pressure. Neurologic changes, such as alterations in cognition or consciousness, may occur due to low cardiac output and poor cerebral perfusion. The other physiologic occurrences are not signs or symptoms of shock.
A client with a history of Wolff-Parkinson-White (WPW) syndrome is admitted for symptomatic tachyarrhythmias resistant to medications. Which cause can result in the development of reentry circuits abnormalities? Select all that apply. Hyperkalemia Myocardial ischemia Hyperglycemia Myocardial infarction Hypothyroidism
Hyperkalemia Myocardial ischemia Myocardial infarction Many tachyarrhythmias are caused by reentry rhythms which interrupt the normal organized, sequential electrical impulse conduction through the myocardium. These reentry circuits occur in the presence of slow conduction, which enables previously depolarized cells to repolarize to the point where they can respond to stimuli, and unidirectional blocks, which block the normal impulse from extinguishing the reentry circuit. Hyperkalemia, along with myocardial ischemia and infarction, can contribute to the development of reentry circuits.
Which factor is the primary factor of local control of blood flow? Action potential Nutritional needs of the tissue involved Cardiac contractility and preload Feedback from arterial baroreceptors and chemoreceptors
Nutritional needs of the tissue involved The major factor that governs local control of blood flow is the nutritional needs of the tissue in question. Action potentials, cardiac contractility, and preload are all aspects of overall circulation, but these heart-related factors do not govern local control. Similarly, feedback from arterial baroreceptors and chemoreceptors inform the neural control of systemic blood pressure but not local control of blood flow.
Malignant hypertension causes injuries to the walls of the arterioles. Because hypertension is a chronic disease and is associated with autoregulatory changes in the blood flow to major organs, what would be the initial treatment goal for malignant hypertension? Partial reduction in blood pressure to less critical values Reduction to normotensive levels of blood pressure Rapid decrease in blood pressure to less critical levels Slow, gradual decrease in blood pressure to normotensive blood pressures
Partial reduction in blood pressure to less critical values Because chronic hypertension is associated with autoregulatory changes in coronary artery, cerebral artery, and kidney blood flow, care should be taken to avoid excessively rapid decreases in blood pressure, which can lead to hypoperfusion and ischemic injury. Therefore, the goal of initial treatment measures should be to obtain a partial reduction in blood pressure to a safer, less critical level, rather than to normotensive levels.
Persons with hypertension secondary to hyperaldosteronism may be treated with which medication? Beta adrenergic blockers Alpha adrenergic antagonists Potassium-sparing diuretics Angiotensin-converting enzyme (ACE) inhibitors
Potassium-sparing diuretics Persons with hyperaldosteronism will exhibit hypokalemia as aldosterone stimulates renal sodium for potassium exchange. Potassium sparing diuretics such as spironolactone will inhibit this action of aldosterone and will increase sodium excretion and mitigate the loss of potassium. ACE inhibitors will not alter the excessive level of aldosterone, which emanates directly from an overactive adrenal gland or an adenoma. Alpha or beta antagonists will not affect the excessive sodium and water retention induced by aldosterone.
The circulatory system is divided into two parts. What does the pulmonary circulation include? Select all that apply. Right heart Pulmonary artery Pulmonary veins Aorta Vena cava
Right heart Pulmonary artery Pulmonary veins The pulmonary circulation consists of the right heart, the pulmonary artery and the pulmonary veins. The systemic circulation includes the aorta, left side of heart, and vena cava.
An important factor in the mortality of severe shock is acute renal failure. What impacts the extent of renal damage in shock? Loss of perfusion and duration of shock Loss of perfusion and degree of immune-mediated response Severity and duration of shock Severity of shock and degree of immune-mediated response
Severity and duration of shock The degree of renal damage in shock is related to the severity and duration of shock. None of the other answers relate to the damage to the renal system in shock.
A group of vascular disorders called vasculitides cause inflammatory injury and necrosis of the blood vessel wall (vasculitis). Which condition is the most common of the vasculitides? Polyarteritis nodosa Raynaud disease Temporal arteritis Varicose veins
Temporal arteritis Temporal arteritis (i.e., giant cell arteritis), the most common of the vasculitides, is a focal inflammatory condition of medium-sized and large arteries. It predominantly affects branches of arteries originating from the aortic arch, including the superficial temporal, vertebral, ophthalmic, and posterior ciliary arteries. Neither polyarteritis nodosa nor Raynaud disease are the most common of the vasculitides. Varicose veins are not vasculitides.
A 54-year-old man with a long-standing diagnosis of essential hypertension is meeting with his physician. The client's physician would anticipate that which phenomenon is most likely occurring? The client's juxtaglomerular cells are releasing aldosterone as a result of sympathetic stimulation. Epinephrine from his adrenal gland is initiating the renin-angiotensin-aldosterone system. Vasopressin is exerting an effect on his chemoreceptors and baroreceptors, resulting in vasoconstriction. The conversion of angiotensin I to angiotensin II in his lungs causes increases in blood pressure and sodium reabsorption.
The conversion of angiotensin I to angiotensin II in his lungs causes increases in blood pressure and sodium reabsorption. Angiotensin conversion in the lungs is a component of the renin-angiotensin-aldosterone system that ultimately increases blood pressure and sodium reabsorption. Juxtaglomerular cells release renin, and epinephrine (vasopressin) is responsible for neither initiating the renin-angiotensin-aldosterone system nor directly influencing chemoreceptors and baroreceptors.
Which inotropic drugs increase cardiac contractility by increasing the influx of free extracellular calcium ions in the vicinity of the actin and myosin filaments? Cardiac glycosides Beta blockers ACE inhibitors Calcium channel blockers
Cardiac glycosides The ions directly involved in the cardiac action potential are sodium, calcium, and potassium. Although cardiac muscle cells require calcium for contraction, they have a less well-defined sarcoplasmic reticulum for storing calcium than do skeletal muscle cells. Thus, cardiac muscle relies more heavily than skeletal muscle on an influx of extracellular calcium ions for contraction. Cardiac glycosides (e.g., digoxin) are inotropic drugs that increase cardiac contractility by increasing the free calcium concentration in the vicinity of the actin and myosin filaments.
During ventricular systole, closure of the atrioventricular (AV) valves coincides with which physiologic event? Atrial chamber filling Aortic valve opening Isovolumetric contraction Semilunar valves opening
Isovolumetric contraction Ventricular systole is divided into two parts: isovolumetric contraction when the AV valves close and ventricles fill; and the ejection period, when the semilunar valves open and blood is ejected through the aortic valve into circulation. Immediately after closure of the AV valves, there is a 0.02- to 0.03-second period during which the pulmonic and aortic valves remain closed. During this period, the ventricular volume remains the same while the ventricles contract, producing an abrupt increase in pressure. At the end of systole, the ventricles relax, causing a precipitous fall in intraventricular pressures. As this occurs, blood from the large arteries flows back toward the ventricles, causing the aortic and pulmonic valves to snap shut—an event marked by the second heart sound.
What does it mean when a client is in second-degree atrioventricular block and there is a relationship between the P waves and the QRS complex resulting in recurring PR intervals? The association of P waves and QRS complexes is not random. The relationship between the P waves and the QRS complexes is a widening PR interval. The association of P waves and QRS complexes is random. The relationship between the P waves and the QRS complexes is a narrowing PR interval.
The association of P waves and QRS complexes is not random. A distinguishing feature of second-degree atrioventricular block is that conducted P waves relate to QRS complexes with recurring PR intervals; that is, the association of P waves with QRS complexes is not random.
A 23-year-old college basketball player is brought to the emergency room following a syncopal episode The paramedic giving report reveals the initial rhythm demonstrated a heart rate of 250 (via AED) with differently shaped QRS complexes that rotated "around a point" and spontaneously converted to normal sinus rhythm. What does the nurse identify as a likely initial rhythm? Paroxysmal atrial fibrillation Torsades de pointes Recurrent atrial flutter Acquired torsades de pointes
Torsades de pointes This client most likely has inherited torsades de points, which is a ventricular dysrhythmia that is often caused by a prolonged QT interval. The hallmark of this rhythm is wide QRS complexes that appear to be twisting around a point as it changes negativity. There are two forms; in the genetic form persons with the acquired form involves defects in either the potassium or sodium ion channel defects. The acquired form has a variety of causes, such as electrolyte imbalance, subarachnoid hemorrhage, cocaine use, and many antiarrhythmic medications. There is no information in the question to suggest an acquired form.
