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
Causes of Asystole
■ End of life (death)
■ Ischemia/hypoxia from many causes
■ Acute respiratory failure (no oxygen; apnea; asphyxiation) ■ Massive electrical shock: electrocution; lightning strike
■ Postdefibrillatory shocks
Sinus Tachycardia
Pathophysiology
■ None—more a physical sign than an arrhythmia or pathologic condition ■ Normal impulse formation and conduction
Defining Criteria and ECG Features
■ Rate: >100 beats/min ■ Rhythm: sinus
■ PR: ≤0.20 sec
■ QRS complex: normal
Atrial Fibrillation
Atrial Fibrillation Key: A classic clinical axiom: “Irregularly irregu- lar rhythm—with variation in both interval and amplitude from R wave to R wave—is always atrial fibrillation.” This one is depend- able.
■ Atrial impulses faster than SA node impulses
■ Atrial fibrillation ➔ impulses take multiple, chaotic, random pathways through the atria
■ Atrial flutter ➔ impulses take a circular course around the atria, setting up the flutter waves ■ Mechanism of impulse formation: reentry
Wide-ranging ventricular response to atrial rate of 300-400 beats/min
Atrial Flutter
Flutter waves seen in classic “sawtooth pattern
■ No true P waves seen
■ Flutter waves in “sawtooth pattern” is classic
Afib and Aflutter caused by
■ Acute coronary syndromes; CAD; CHF
■ Disease at mitral or tricuspid valve
■ Hypoxia; acute pulmonary embolism
■ Drug-induced: digoxin or quinidine most common ■ Hyperthyroidism
Atrial Fibrillation
Atrial Flutter
Wolfe Parkinson White Syndrome
normal sinus rhythm with delta wave (arrow) notching of positive upstroke of QRS complex
■ The prototypical pre-excitation syndrome: congenital mal- formation; strands of conducting myocardial tissue between atria and ventricles
■ When persistent after birth strands can form an accessory pathway (eg, bundle of Kent)
■ QRS complex: classically distorted by delta wave (upwards deflection of QRS is slurred)
Supraventricular tachycardia versus Junctional tachycardia
Aortic Stenosis: Systolic or Diastolic?
Systolic
Crescendo,decrescendo systolic murmur, ejection click may be present
Mitral/tricuspid regurgitation: Systolic or Diastolic
Systolic,
Holosystolic, high pitched blowing murmur
Mitral Valve Prolapse: Systolic or Diastolic?
Systolic
Late systolic crescendo murmur with mid systolic click
Best heard over apex
-Caused by chordae rupture
-Rheumatic Fever
-Marfan or Ehlers Danlos syndrome
Ventricular septal Defect: Systolic or diastolic?
Systolic
Holosystolic, harsh soudning murmur.
Loudest in the tricuspid area
Name the 4 systolic murmurs?
1-Aortic stenosis
2-Mitravel/tricuspid regurgitation
3-Mitral Valve Prolapse
4-Ventricular septal defect
Which 2 systolic murmurs are described as holosystolic
1-Ventricular septal Defect-describd as harsh sounding, located within the tricuspid area
2-Mitral/tricuspid regurgitation-described as high-pitched, blowing
Aortic regurgitation: Systolic or Diastolic?
Diastolic
High pitched blowing early diastolic decrescendo murmur
-Head bobbing
-Wide pulse pressure
-Hyperdyanmic Pulse
Caused by-
-Rheumatic Fever
-Endocarditis
-Aoritc root dilitation
-Bicuspid aortic valve
Mitral stenosis: Systolic or Diastolic?
Diastolic
Follows opening snap, delayed late rumbling disastolic murmur
Patent ductus arteriosus: Systolic or Diastolic?
Niether: continuous
Continuous machine-like murmur loudest at S2
Which of the following murmurs has an opening snap?
It is a diastolic murmur and it is mitral stenosis
What are the 2 diastolic murmurs?
1-Aortic regurgitation
2-Mitral stenosis
What does S1 and S2 stand for?
S1-Usually a single sound and represents the closure of the mitral and tricuspid valves.
S2-Closure of the aortic and pulmonary valves
What is an S3 sound?
The S3 heart sound is a low-pitched sound that doctors can hear when blood rushes rapidly from the heart’s atrium into the ventricle. Sometimes, particularly in children and athletes, it is a typical sound. However, in other cases, it may also indicate that an individual has congestive heart failure.
Staging of Tumor
Size T1, T2, T3 and T4
Staging of tumor - Nodes
N1, N2, N3
Staging of tumor - Metastasis
Stage I
Stage II
Stage III
Stage IV
Survival Rate based upon staging
GCS Score-Eye Opening
GSC Score-Verbal Response
VOICE
GCS Score-Motor Response
My Old Ben
Shock Chart
Arterial Supply to temporals muscle
deep temporal artery
Arterial supply to temporoparietal fascia
Superficail temporal artery
Arterial supply to medial forhead
Supratrochlear (Primary)
-supraorbital and dorsal nasal (secondary)
Arterial supply to platysma
Subdermal plexus (random pattern flap mainly, also supplied by submental artery
Arterial supply to SCM
occipital artery (primary)
Superior thyroid (secondary)
Arterial supply to Deltopectoral skin flap
- Random pattern flap with perforators from internal mammary a
Arterial supply to latissimus dorsi
- Thoracodorsal a & v
Arterial supply to trapezius
- Main pedicle is transverse cervical artery, dorsal scapular artery is sacrificed to increase rotation
Arterial supply to scapula
Circumflex scapular artery
Arterial supply to pectorals major
- Thoracoacromial a. (1o), lat & sup thoracic (2o)
- Lateral pectoral n
Arterial supply to radial foremrm
- Radial a & v
- Lateral antebrachial cutaneous nerve (with cephalic vein)
Arterial supply to iliac crest free flap
deep circumflex artery
Arterial supply to anterolateral thigh flap
- Lateral circumflex femoral a
Maxillary Artery Branch 1st division
MAAID
1-Middle Miningeal
2-Anterior Tympanic
3-Accessory Miningeal
4-Inferior Alveolar
5-Deep Auricular
Maxillary Artery Branch 2nd division
Make Dinner Before Party
M-Masseteric
D-Deep Temporal
B-Buccal
P-Pterygoid
Maxillary Artery Branch 3rd division
PeppA PIGS
P-Posterior Superior Alveolar
A-Artery of pterygoid canal
P-Pharyngeal
I-Infraorbital
G-Greater Palatine
S-Sphenopalatine
Branches of external Carotid ARtery
Some Angry Lady Figured Out Post Menopausal Syndrome
S-Superior Thyroid
A-Ascending Pharyngeal
L-Lingual
F-Facial
O-Occipital
P-Posterior Auricular
M-Maxillary
S-Superficial Temporal
Branches of Maxillary Artery Pneumonic
DAM I AM Piss Drunk, But Stupid Drunk I Pefer, Must Phone Alcoholics Anonymous
Deep auricular
Anterior tympanic
Middle meningeal
IAN
Accessory meningeal
Masseteric
Pterygoids
Deep temporals
Buccinator
Sphenopalatine
Descending palatine
Infraorbital
PSA
MSA
Pharyngeal
ASA
Artery to the pterygoid canal
-Brachial plexus what innervates what?
- C4-pec/deltoid
- C5-bicep
- C6-brachioradialis
- C7-tricep
Plasma cells of a plastmocytoma
Ameloblastoma cells
Intraosseous Mucoep
Histology of a schwannoma
Histology of pyogenic granuloma
chronotropic
Chronotropic effects (from chrono-, meaning time) are those that change the heart rate. Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node.
Alpha vs Beta receptors
They are adrenergic receptors
Ionotropies
Positive inotropes make your heart muscle contractions stronger, raising your cardiac output to a normal level and increasing the amount of blood your heart can pump out. This helps your organs get the blood and oxygen they need to keep working.
