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Andy Rodriguez
Impulse is generated somewhere near the AV node. Impulses can travel up or down causing absent or inverted P wave – sometimes after the QRS. QRS is normal and tight.
Premature Junctional Contraction (PJC)
Junctional Escape Rhythm
Accelerated Junctional Rhythm
Junctional Tachycardia
Supraventricular Tachycardia (SVT)
Paroxysmal Supraventricular Tachycardia (PSVT)
Some exam review for Respiratory emergencies:
1. A person who experiences sharp chest pain followed by increasing dyspnea after he or she coughs MOST likely has:
Choose one answer.
A. pleurisy.
B. acute pneumonia.
C. a pleural effusion.
D. a pneumothorax.
2. An otherwise healthy adult whose normal hemoglobin level is 12 to 14 g/dL typically will begin to exhibit cyanosis when: Choose one answer. A. hemoglobin levels fall below 12 g/dL. B. about 5 g/dL of hemoglobin is desaturated. C. his or her oxygen saturation falls below 50%. D. 10% of his or her hemoglobin is desaturated.
2. An otherwise healthy adult whose normal hemoglobin level is 12 to 14 g/dL typically will begin to exhibit cyanosis when:
A. hemoglobin levels fall below 12 g/dL.
B. about 5 g/dL of hemoglobin is desaturated.
C. his or her oxygen saturation falls below 50%.
D. 10% of his or her hemoglobin is desaturated.
3. Intrapulmonary shunting occurs when:
A. hyperinflated alveoli retain high levels of carbon dioxide.
B. resistance to airflow increases due to bronchoconstriction.
C. nonfunctional alveoli inhibit pulmonary gas exchange.
D. the volume of anatomic dead space suddenly increases.
4. A patient with status asthmaticus commonly presents with: Choose one answer. A. compensatory respiratory alkalosis and stridor. B. physical exhaustion and inaudible breath sounds. C. audible expiratory wheezing and severe cyanosis. D. accessory muscle use and inspiratory wheezing.
4. A patient with status asthmaticus commonly presents with:
A. compensatory respiratory alkalosis and stridor.
B. physical exhaustion and inaudible breath sounds.
C. audible expiratory wheezing and severe cyanosis.
D. accessory muscle use and inspiratory wheezing.
5. __________ breath sounds are the MOST commonly heard breath sounds, and have a much more obvious inspiratory component.
A. Vesicular
B. Tracheal
C. Bronchovesicular
D. Bronchial
6. A 29-year-old woman is experiencing a severe asthma attack. Her husband reports that she was admitted to an intensive care unit about 6 months ago, and had a breathing tube in place. Prior to your arrival, the patient took 3 puffs of her rescue inhaler without effect. She is anxious and restless, tachypneic, and has audible wheezing. You should: Choose one answer. A. attempt to slow her breathing with respiratory coaching, administer a nebulized bronchodilator, and transport. B. start an IV of normal saline, administer methylprednisolone via IV push, and transport as soon as possible. C. apply a CPAP unit, transport immediately, and attempt to establish vascular access en route to the hospital. D. begin assisting her ventilations with a bag-mask device and 100% oxygen and prepare to intubate her trachea.
6.
A 29-year-old woman is experiencing a severe asthma attack. Her husband reports that she was admitted to an intensive care unit about 6 months ago, and had a breathing tube in place. Prior to your arrival, the patient took 3 puffs of her rescue inhaler without effect. She is anxious and restless, tachypneic, and has audible wheezing. You should:
A. attempt to slow her breathing with respiratory coaching, administer a nebulized bronchodilator, and transport.
B. start an IV of normal saline, administer methylprednisolone via IV push, and transport as soon as possible.
C. apply a CPAP unit, transport immediately, and attempt to establish vascular access en route to the hospital.
D. begin assisting her ventilations with a bag-mask device and 100% oxygen and prepare to intubate her trachea.
7. The presence of diffuse rhonchi in the lungs indicates:
A. thick secretions in the large airways.
B. isolated consolidation of secretions.
C. right-sided congestive heart failure.
D. air being forced through narrowed airways.
8. Uncontrollable coughing and hemoptysis in a cigarette smoker are clinical findings MOST consistent with: Choose one answer. A. acute bronchitis. B. lung cancer. C. emphysema. D. pleural effusion.
8. Uncontrollable coughing and hemoptysis in a cigarette smoker are clinical findings MOST consistent with:
A. acute bronchitis.
B. lung cancer.
C. emphysema.
D. pleural effusion.
Copied from the AAP Textbook of Pediatric Care
Shock can be classified by cause and mechanism: hypovolemic, cardiogenic, and distributive. Again, the primary clinician should recall that despite complexities of cause, the early stages of shock are easy to recognize, and the treatments are straightforward.[13]
Shock from loss of blood volume caused by trauma, diarrhea, burns, and 3rd spacing (as in peritonitis) is the most common form of shock in children. Loss of fluid leads to low intravascular volume and preload to the heart is decreased. If such losses (up to 30% of circulating blood volume) occur over days, then patients can compensate by increasing thirst, heart rate, and retention of fluid by concentrating urine. Large volumes of fluid loss that occur acutely lead to decompensation represented by diminished mental status, tachycardia, poorly perfused skin with prolonged capillary refill, oliguria, and, eventually, hypotension.
Nonhemorrhagic shock is seen in diarrhea, vomiting, urinary losses, evaporative losses, 3rd spacing of fluid (peritonitis, edema), and burns. The causes of hypovolemic shock are seen in BOX 358-2.
Physical signs in hypovolemic shock occur as a result of decreased venous return to the heart, which leads to diminished cardiac output. Catecholamines are released, which produces the hallmark vasoconstriction in skin, muscle, and splanchnic blood vessels. The renin-angiotensin system is activated, promoting the retention of salt and water. Fluid resuscitation restores preload, and cardiac output is increased with resolution of symptoms. Physical signs in dehydration reliably indicate the percentage of body fluid compartment losses (Table 358-3). In hemorrhagic shock, physical findings correlate to the amount of blood loss[15] (Table 358-4).
Cardiac shock can be caused by mechanical obstruction or muscle (pump) failure. In obstructive cardiogenic shock, air and fluid in the pericardium or pleural spaces (rarely) can impede venous return to the heart and decrease systolic ejection. Common causes are listed in BOX 358-3. These patients usually exhibit distended neck veins because of increased jugular venous pressure and hypotension. Massive pulmonary embolus, rare in children, can obstruct flow from the right to the left side of the heart. In coarctation of the aorta, hypoplastic left heart syndrome, and left ventricular outflow tract stenosis, cardiac output is compromised.
The heart can fail as a mechanical pump from a variety of causes (BOX 358-4). Patients with cardiac failure have low cardiac output resulting in the clinical signs of altered mental status, tachycardia, decreased capillary refill, and evidence of venous congestion (hepatomegaly, rales). Children with pericardial effusion may have muffled heart tones.
Septic shock is the most common and certainly best-studied cause of cardiovascular collapse the primary caregiver will encounter.[9] The causes of bacterial septic shock have changed since vaccination against Haemophilus influenzae type b was instituted in 1988. If sepsis in the (increasingly common) immunocompromised patient is excluded, meningococci and streptococci are then the most frequently encountered bacterial causes of sepsis.
Patients with infections caused by Staphylococcus aureus, Pseudomonas aeruginosa, Candida species, and Streptococcus pyogenes have higher mortality rates compared with patients with infections caused by coagulase-negative Staphylococcus and Acinetobacter species.[16]
Studies of children who have meningococcemia highlight important issues in the care of children in septic shock (see Chapter 353, Meningococcemia). Mortality remains high despite modern advances in critical care.[17] An unfortunate characteristic of meningococcal disease is its rapid progression in fatal cases. Characteristics of cases rapidly progressing to death include young age, absence of meningitis, thrombocytopenia, leukopenia, multiorgan failure, and severity of petechiae.[17] Invasive meningococcal disease is most common in children younger than 4 years. Meningitis and sepsis occurs in 1.3:100,000 in the United States, but incidence in Ireland is 15:100,000.[17] Clinicians who encounter these clinical stigmata in primary care settings should recognize the importance of early stabilization, the need for referral for definitive therapy, and the high mortality despite aggressive intervention.
Children and adults exhibit developmental differences in the hemodynamic response to sepsis. In adults, mortality is caused by a pressor and volume resistant state characterized as vasomotor paralysis. Myocardial dysfunction is common in adults, but cardiac output is maintained by tachycardia and ventricular dilatation.[7] [18]
In pediatric septic shock, low cardiac output, not vasodilatation, is associated with mortality.[19] In children, oxygen delivery is the major determinant of oxygen consumption, whereas in adults, oxygen used by tissues (oxygen extraction) is more important. Survival correlates to the restoration of cardiac output and oxygen delivery.[8] [20]
Some patients with severe septic shock may develop a hypoadrenal response to shock. This scenario is clinically characterized as patients who are in refractory shock (see Table 358-2) who are, by definition, unresponsive to volume resuscitation, the addition of 2 catecholamine drugs, and normalization of acid base, glucose, and calcium homeostasis. Infants and children at risk include those with septic shock and purpura, those with known or suggested adrenal abnormalities, and children who have received a therapeutic course of steroids in the 6 months before the onset of sepsis.[21]
In patients whose shock state is refractory to volume, dopamine or dobutamine, and the addition of epinephrine or norepinephine (catechol resistant shock), empirically initiating stress-dose steroids (hydrocortisone at stress doses of 50 to 100 mg/m[2]/day would be reasonable. If time and condition allow it, a baseline serum cortisol level is drawn, followed by a 250 microgram dose of corticotropin, and a repeat cortisol level is drawn at 30 minutes. The response (or absence of) will determine the presence of a hypoadrenal state and the need for continued steroid administration. A baseline serum cortisol of less than 18 Tg/dL and a poststimulation increment of less than 9 Tg/dL indicate a hypoadrenal state.[9] [21] If a stimulation test cannot be done, then continued steroid therapy for 3 to 5 days should be based on clinical response.
In distributive shock disorders, global disorder in vasomotor control is present, resulting in maldistribution of blood flow and oxygen to tissue. Anaphylaxis and spinal cord injury are the 2 types most likely to be encountered in primary care. Cardiac output may be normal or increased. These patients lose sympathetic control of the vascular system, which reduces peripheral vascular tone. This circumstance produces pooling of blood in the periphery, which, in turn, leads to decreased venous return to the heart.
In anaphylactic shock, the inciting agent should be removed if possible. These patients uniformly respond well to volume administration, epinephrine infusion, antihistamines that include an H2-receptor blocker, and steroid therapy.
John Clappin
Three Qualities
Central Nervous System (CNS)
Peripheral Nervous System (PNS) Central (Nerves and Ganglia)
Types of Nervous Tissues
Saltatory Conduction ( impulses pause at breaks in myelin, draws in sodium)
Neuron
Neural Communication
Synaptic Cleft
Nerves
Cell bodies are frequently grouped together;
Anatomy of the Spinal Cord
The Brain
The Peripheral Nervous System (PNS)
Since the Lumbar and Sacral plexus are interconnected, they are sometimes referred to as the Lumbosacral plexus. The nerves that serve the chest are the only ones that do not originate from a plexus
More on EKGs… Andy Rodriguez
Escape Mechanism – normal pacemaker slows down or fails and a lower pacing site assumes pacemaking responsibility.
Sympathetic – both Atria & ventricles Parasympathic – Only Atria
Analyzing the rhythm
Sinus Rhythms
Normal Sinus Rhythm – Regular, 60-100 BPM, P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12 Sinus Bradycardia - Regular, Rate <60 BPM, P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12 Sinus Tachyardia - Regular, Rate >100 BPM (usually 100-160), P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12 Sinus Arrhythmia – sinus node fires faster during inspiration and slower during expiration. rate is still normal, and still normal QRS – Irregular, 60-100 BPM, P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12
Normal Sinus Rhythm – Regular, 60-100 BPM, P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12
Sinus Bradycardia - Regular, Rate <60 BPM, P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12
Sinus Tachyardia - Regular, Rate >100 BPM (usually 100-160), P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12
Sinus Arrhythmia – sinus node fires faster during inspiration and slower during expiration. rate is still normal, and still normal QRS – Irregular, 60-100 BPM, P waves normal and upright, one before every QRS, PRI 0.12-0.20 and QRS <0.12
Atrial Rhythms
Wandering Pacemaker – pacemaker site wanders between SA node, atria and AV node. rate is usually normal and will conduct normally to ventricles Slightly Irregular, 60-100 BPM, P wave morphology changes from beat to beat, one before every QRS, PRI 0.12-0.20 but may vary, and QRS <0.12 Premature Atrial Contraction (PAC) – irritable focus within atrium that fires prematurely and produces a single ectopic beat. impulses are conducted normally. Usually regular (depending on underlying rhythm) except for PAC, 60-100 BPM, P wave changes – one that comes early looks different than normal sinus P waves, one before every QRS, PRI 0.12-0.20 but may be longer, and QRS <0.12 Atrial Tachycardia (or SVT)– Single atrial site fires repetitively at a very high rate. impulses conducted normally Regular 150-250 BPM, P wave looks different than sinus p wave if visible at all, one before every QRS, PRI not measurable, QRS <0.12 Atrial Flutter - single focus initiates rapid repetitive impulses, AV node protects ventricles by blocking conduction of some impulses. Atrial Rhythm- regular, several flutter waves (saw tooth)before each QRS (F waves), PRI unable to determine, atrial rate 250-350 bpm Atrial Fibrillation – multiple foci initiate rapid repetitive impulses, AV node protects ventricles by blocking conduction of some impulses. Grossly irregular, atrial rate >350 bpm, ventricular rate varies greatly, no discernable P waves, no PRI, QRS <.12
Wandering Pacemaker – pacemaker site wanders between SA node, atria and AV node. rate is usually normal and will conduct normally to ventricles Slightly Irregular, 60-100 BPM, P wave morphology changes from beat to beat, one before every QRS, PRI 0.12-0.20 but may vary, and QRS <0.12
Premature Atrial Contraction (PAC) – irritable focus within atrium that fires prematurely and produces a single ectopic beat. impulses are conducted normally. Usually regular (depending on underlying rhythm) except for PAC, 60-100 BPM, P wave changes – one that comes early looks different than normal sinus P waves, one before every QRS, PRI 0.12-0.20 but may be longer, and QRS <0.12
Atrial Tachycardia (or SVT)– Single atrial site fires repetitively at a very high rate. impulses conducted normally Regular 150-250 BPM, P wave looks different than sinus p wave if visible at all, one before every QRS, PRI not measurable, QRS <0.12
Atrial Flutter - single focus initiates rapid repetitive impulses, AV node protects ventricles by blocking conduction of some impulses. Atrial Rhythm- regular, several flutter waves (saw tooth)before each QRS (F waves), PRI unable to determine, atrial rate 250-350 bpm
Atrial Fibrillation – multiple foci initiate rapid repetitive impulses, AV node protects ventricles by blocking conduction of some impulses. Grossly irregular, atrial rate >350 bpm, ventricular rate varies greatly, no discernable P waves, no PRI, QRS <.12
Steve Kanarian
Some cardiology review:
Depolarization causes contraction.(Na+ rushes in) Repolarization is the refractory state. (K+ left in the cell)
Cardiac Physiology
(Bundle of Kent – Wolf Parkinson’s White –WPW)
EKG Lead Placement
Electrical Conductivity and the EKG
‘Monitoring’ leads are not diagnostic, 12 Lead EKG Machines are diagnostic quality
ECG Paper
Normal Electrocardiogram
5 points to look for
