MUST KNOWS Flashcards
Stage I Hypovolemic Shock
Stage II Hypovolemic Shock
Stage III Hypovolemic Shock
Stage IV Hypovolemic Shock
Most important things to focus on with shock
Blood loss
BP
HR
Mental status
Urine output
- Wallace rule of 9’s: answer was 36%
Just remember for adults
ALL 18s and all 9s
For Kids
18s
14s
9s
ABG disorders Chart
pH in ABG disorders
pH is inversely proportional to the actual hydrogen ion concentration of blood. So, as the hydrogen ion concentration decreases, the pH goes up. A pH of 7.35-7.45 is a normal value; greater than 7.45 is considered alkalosis and less than 7.35 is acidosis.
PCO2 in ABG disorders
PCO₂ is a measure of the partial pressure of CO₂ in the blood. This is the respiratory component in acid-base determination because it is primarily controlled by the lungs. As the CO₂ level increases, pH decreases and vice versa. The faster and more deeply the patient breathes, the more CO₂ is blown off causing PCO₂ levels to drop. This can be used as a compensatory mechanism for respiratory acidosis. Alternatively, in metabolic acidosis, the respiratory rate may decrease to retain CO2 and decrease pH.
HCO3 in ABG disorders
HCO₃- (bicarbonate ion) is regulated by the kidneys and used as a measure of the metabolic component of acid-base equilibrium. As HCO₃- increases, the pH also increases- HCO₃- is elevated in metabolic alkalosis and decreased in metabolic acidosis. The kidneys are also used to compensate for respiratory acid-base imbalances. In respiratory acidosis, the kidneys attempt to compensate by retaining excess amounts of HCO₃- and in respiratory alkalosis, the kidneys excrete more HCO₃- out of the body in an attempt to lower the pH.
PO2 in ABG disorders
PO₂ is an indirect measure of the O₂ content of the arterial blood. The normal value for PO₂ is 80-100 mmHg. This measure is useful in determining the effectiveness of O₂ therapy.
Acidosis or Alkalosis
Determine the PCo2 and respiratory effect
If the PCO₂ is high in a patient who has acidosis, the patient has respiratory acidosis and if their PCO₂ is low with a high pH, the patient has respiratory alkalosis. If the PCO₂ is low in a patient who has been said to have acidosis, the patient has metabolic acidosis and is compensating by blowing off CO₂. If their PCO₂ is high with a high pH, the patient has metabolic alkalosis and is compensating by retaining CO₂. If that lost you (I got lost a bit just writing it), the chart below simplifies the thought process and is right most of the time.
Assume metabolic cause when respiratory is ruled out.
Use the HCO₃- to verify metabolic effect (normal is 21-28 mmHg).
PATIENT SAFETY NOTE: After an ABG draw, pressure should be held or applied to the site for 3-5 minutes. The draw puts a patient at risk for excessive bleeding and hematoma formation.
WILKES Classification for TMJ
First Degree Heart Block
In first-degree heart block, the heart’s electrical signals are slowed as they move from the atria to the ventricles (the heart’s upper and lower chambers, respectively). Longer P-R interval.
Second-Degree Heart Block
Mobitz Type I
In this type (also known as Wenckebach’s block), the electrical signals are delayed more and more with each heartbeat, until the heart skips a beat. On the EKG, the delay is shown as a line (called the PR interval) between the P and QRS waves. The line gets longer and longer until the QRS waves don’t follow the next P wave.
Second-Degree Heart Block
Mobitz Type II
Mobitz Type II
In second-degree Mobitz type II heart block, some of the electrical signals don’t reach the ventricles. However, the pattern is less regular than it is in Mobitz type I. Some signals move between the atria and ventricles normally, while others are blocked.
On an EKG, the QRS wave follows the P wave at a normal speed. Sometimes, though, the QRS wave is missing (when a signal is blocked).
Ventribular Fibrillation/Pulseless ventricular tachycardia
Ventricles consist of areas of normal myocardium alternating with areas of ischemic, injured, or infarcted myocardium, leading to chaotic pattern of ventricular depolarization
■ Rate/QRS complex: unable to determine; no recognizable P, QRS, or T waves
■ Rhythm: indeterminate; pattern of sharp up (peak) and down (trough) deflections
Causes of vFib (6) & recommended treatment
■ Acute coronary syndromes leading to ischemic areas of myocardium
■ Stable-to-unstable VT, untreated
■ PVCs with R-on-T phenomenon
■ Multiple drug, electrolyte, or acid-base abnormalities that prolong the relative refractory period ■ Primary or secondary QT prolongation
■ Electrocution, hypoxia, many others
Recommended Therapy
■ Early defibrillation is essential
■ Agents given to prolong period of reversible death (oxygen, CPR, intubation, epinephrine,
vasopressin)
■ Agents given to prevent refibrillation after a shock causes defibrillation (lidocaine, amiodarone,
procainamide, β-blockers)
■ Agents given to adjust metabolic milieu (sodium bicarbonate, magnesium)
With no pulse
PEA
Cardiac conduction impulses occur in organized pattern, but this fails to produce myocardial contraction (former “electromechanical dissociation”); or insufficient ventricular filling during diastole; or ineffective contractions
■ Rhythm displays organized electrical activity (not VF/pulseless VT)
■ Seldom as organized as normal sinus rhythm
■ Can be narrow (QRS <0.10 mm) or wide (QRS >0.12 mm); fast (>100 beats/min) or slow
(<60 beats/min)
■ Most frequently: fast and narrow (noncardiac etiology) or slow and wide (cardiac etiology)
PEA etiology 5 Hs & 5 Ts
■ Hypovolemia
■ Hypoxia
■ Hydrogen ion—acidosis
■ Hyperkalemia/Hypokalemia
■ Hypothermia
■ “Tablets” (drug OD, ingestions)
■ Tamponade, cardiac
■ Tension pneumothorax
■ Thrombosis, coronary (ACS)
■ Thrombosis, pulmonary (embolism)
Treatment for PeA
■ Secondary AB (advanced airway and ventilation);
C (IV, epinephrine, atropine if electrical activity <60 complexes per minute); D (identify and treat reversible causes)
■ Key: identify and treat a reversible cause of the PEA
Asystole
■ Rate: no ventricular activity seen or ≤6/min; so-called “P-wave asystole” occurs with only atrial impulses present to form P waves
■ Rhythm: no ventricular activity seen; or ≤6/min
■ PR: cannot be determined; occasionally P wave seen, but by definition R wave must be absent
■ QRS complex: no deflections seen that are consistent with a QRS complex
