Persius/hicric huggingface dataset:
The EKG in the patient treated with adenosine

# Electrocardiographic Findings:
- Decreases the automaticity of the sinus node and AV nodal conduction
- Caused by an increase in the AH interval and not by an increase in the HV interval
- Blocks occur within 20 seconds of i.v. administration
- The incidence of transient second degree AV block is high
The EKG in the patient treated with lidocaine

# Electrocardiographic Findings
- Like all type 1B agents, this shortens the action potential duration
- May slow the rate or cause sinus arrest in high doses, the automaticity of ectopic atrial pacemakers may be reduced.
- In usual doses, it is not associated with any noticeable changes in the P wave, the PR interval, the QRS complex, The QT interval, or the T wave.
The EKG in the patient treated with phenytoin

# Electrocardiographic Findings
- QTc may be decreased
- In patients with heart disease, IV phenytoin may produce bradycardia, AV block, asystole, or ventricular fibrillation.

# Additional resources
- ECGpedia: Course for interpretation of ECG
- The whole ECG - A basic ECG primer
- 12-lead ECG library
- Simulation tool to demonstrate and study the relation between the electric activity of the heart and the ECG
- ECG information from Children's Hospital Heart Center, Seattle
- ECG Challenge from the ACC D2B Initiative
- National Heart, Lung, and Blood Institute, Diseases and Conditions Index
- A history of electrocardiography
- EKG Interpretations in infants and children
The EKG in the patient treated with quinidine

# Electrophysiologic Mechanisms
- Direct effect is to reduce the automaticity, excitability and conductivity, but this is counterbalanced by the indirect vagolytic effect of the drug which tends to increase the rate.
- With higher toxic doses, the automaticity of the SA node may be depressed resulting in sinus bradycardia or sinus arrest. SA and AV conduction may be impaired and intraventricular conduction time markedly prolonged. The automaticity of ventricular tissue may be paradoxically increased with the appearance of ventricular arrhythmias.

### EKG Findings
- Decrease in the amplitude of the T wave or T wave inversion
- ST depression
- Prominent U waves (an early finding)
- Prolongation of the QTC
- Notching and widening of the P waves

### EKG Findings with Toxic Effects
- Widening of the QRS
- Various degrees of AV block
- Ventricular arrhythmias, syncope and sudden death
- Marked sinus bradycardia, sinus arrest or SA block
The Patient History in Cardiovascular Disease

# The cardinal symptoms of cardiac disease are shown below.  Click on the link in blue to read about a component of the patient history in detail.

# Chest Pain:
Discomfort in the chest which can be squeezing, a heaviness, a tightness, a burning or an aching.

# Claudication:
Recurring burning, aching, fatigue, or heaviness in the leg muscles with predictable level of walking, that resolves with a predictable duration of rest.

# Cough:
- Cough is defined as being a reflex explosive expiration that promotes the removal of secretions and foreign particles from the lungs, while preventing aspiration
- Coughing can take on two forms:
Nonproductive
Productive
- Nonproductive
- Productive
- A cough can either be chronic or acute (coughing lasting less than three weeks)
- The production of sputum is important when assessing a cough
- The quality, quantity and circumstances of the sputum production surrounding the coughing episodes are also important

# Dyspnea:
Dyspnea is an uncomfortable awareness of breathing, shortness of breath, or difficulty or distress in breathing. It is often associated with cardiac or pulmonary disease.

# Orthopnea:
Orthopnea is dyspnea which occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair. Orthopnea is generally a symptom of heart failure. It can also occur in those with asthma and chronic bronchitis, as well as those with sleep apnea or panic disorder. The condition is often due to left ventricular failure and/or pulmonary edema.  It is also associated with Polycystic Liver Disease. Patients with orthopnea often complain of waking up suddenly during the night 'unable to breathe' if they have slipped down from their pillows into the supine position. They may run to the window to 'get some air'. It is commonly measured according to the number of pillows needed to prop the patient up to enable breathing (Example: "3 pillow orthopnea"). See also: Paroxysmal Nocturnal Dyspnea which means that a patient wakes up short of breath.

# Paroxysmal Nocturnal Dyspnea:
Paroxysmal nocturnal dyspnea (PND) is a medical symptom wherein people with congestive heart failure develop difficulties breathing after lying flat. PND commonly occurs several hours after a person with heart failure has fallen asleep. PND resolves quickly once a person awakens and sits upright.
PND is caused by increasing amounts of fluid entering the lung during sleep and filling the small, air-filled sacs (alveoli) in the lung responsible for absorbing oxygen from the atmosphere. This fluid typically rests in the legs during the day when the individual is walking around and redistributes throughout the body (including the lungs) when recumbent. PND is a sign of severe heart failure

# Pedal Edema:

# Syncope:
Ticarcillin clavulanate clinical pharmacology

# Clinical Pharmacology
- Absorption:
After an intravenous infusion (30 minutes) of 3.1 grams of TIMENTIN, peak serum concentrations of both ticarcillin and clavulanic acid were attained immediately after completion of the infusion. Ticarcillin serum levels were similar to those produced by the administration of equivalent amounts of ticarcillin alone with a mean peak serum level of 324 mcg/mL. The corresponding mean peak serum level for clavulanic acid was 8 mcg/mL. (See Table 2.)
The mean area under the serum concentration curve was 485 mcghr/mL for ticarcillin and 8.2 mcghr/mL for clavulanic acid.
- Distribution:
Ticarcillin has been found to be approximately 45% bound to human serum protein and clavulanic acid approximately 25% bound. Ticarcillin can be detected in tissues and interstitial fluid following parenteral administration.
Distribution of ticarcillin into bile and pleural fluid has been demonstrated. The results of experiments involving the administration of clavulanic acid to animals suggest that this compound, like ticarcillin, is well distributed in body tissues.
- Elimination:
Approximately 60% to 70% of ticarcillin and approximately 35% to 45% of clavulanic acid are excreted unchanged in urine during the first 6 hours after administration of a single dose of TIMENTIN to normal volunteers with normal renal function. Two hours after an intravenous injection of 3.1 grams of TIMENTIN, concentrations of ticarcillin in urine generally exceed 1,500 mcg/mL. The corresponding concentrations of clavulanic acid in urine generally exceed 40 mcg/mL. By 4 to 6 hours after injection, the urine concentrations of ticarcillin and clavulanic acid usually decline to approximately 190 mcg/mL and 2 mcg/mL, respectively.
The mean serum halflife of both ticarcillin and clavulanic acid in healthy volunteers was 1.1 hours.
- Pediatrics:
In pediatric patients receiving approximately 50 mg/kg of TIMENTIN (30:1 ratio ticarcillin to clavulanate), mean ticarcillin serum halflives were 4.4 hours in neonates (n = 18) and 1.0 hour in infants and children (n = 41). The corresponding clavulanate serum halflives averaged 1.9 hours in neonates (n = 14) and 0.9 hour in infants and children (n = 40). Area under the serum concentration time curves averaged 339 mcghr/mL in infants and children (n = 41), whereas the corresponding mean clavulanate area under the serum concentration time curves was approximately 7 mcghr/mL in the same population (n = 40).
- Renal Impairment:
An inverse relationship exists between the serum halflife of ticarcillin and creatinine clearance. The halflife of ticarcillin in patients with renal failure is approximately 13 hours. The dosage of TIMENTIN need only be adjusted in cases of severe renal impairment .
Ticarcillin may be removed from patients undergoing dialysis; the actual amount removed depends on the duration and type of dialysis.
Ticarcillin clavulanate indications and usage

# Indications and Usage
TIMENTIN is indicated in the treatment of infections caused by susceptible isolates of the designated bacteria in the conditions listed below:
1.1 Septicemia
Septicemia (including bacteremia) caused by lactamaseproducing isolates of Klebsiella spp.*, Escherichia coli*, Staphylococcus aureus*, or Pseudomonas aeruginosa- (or other Pseudomonas species*)
- Lower Respiratory Infections
Lower respiratory infections caused by lactamaseproducing isolates of S. aureus, Haemophilus influenzae*, or Klebsiella spp.*
- Bone and Joint Infections
Bone and joint infections caused by lactamaseproducing isolates of S. aureus
- Skin and Skin Structure Infections
Skin and skin structure infections caused by lactamaseproducing isolates of S. aureus, Klebsiella spp.*, or E. coli*
- Urinary Tract Infections
Urinary tract infections (complicated and uncomplicated) caused by lactamaseproducing isolates of E. coli, Klebsiella spp., P. aeruginosa- (or other Pseudomonas spp.*), Citrobacter spp.*, Enterobacter cloacae*, Serratia marcescens*, or S. aureus*
- Gynecologic Infections
Endometritis caused by lactamaseproducing isolates of Prevotella melaninogenicus*, Enterobacter spp. (including E. cloacae*), E. coli, Klebsiella pneumoniae*, S. aureus, or Staphylococcus epidermidis
- Intra-abdominal Infections
Peritonitis caused by lactamaseproducing isolates of E. coli, K. pneumoniae, or Bacteroides fragilis- group
To reduce the development of drugresistant bacteria and maintain the effectiveness of TIMENTIN and other antibacterial drugs, TIMENTIN should be used only to treat infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.
Topotecan Hydrochloride (patient information)

# IMPORTANT WARNING:
Topotecan can cause a decrease in the number of blood cells in your bone marrow. Your doctor will order tests before, during, and after your treatment to see if your blood cells are affected by this drug.

# About your treatment
Your doctor has ordered the drug topotecan to help treat your illness. The drug is given by injection into your vein.
This medication is used to treat:
- ovarian cancer
This medication is sometimes prescribed for other uses; ask your doctor or pharmacist for more information.
Topotecan is in a class of drugs known as topoisomerase inhibitors; it slows or stops the growth of cancer cells. The length of treatment depends on the types of drugs you are taking, how well your body responds to them, and the type of cancer you have.

# Precautions
Before taking topotecan
- tell your doctor and pharmacist if you are allergic to topotecan or any other drugs.
- tell your doctor and pharmacist what prescription and nonprescription medications you are taking, especially aspirin and vitamins.
- tell your doctor if you have or have ever had kidney disease.
- you should know that topotecan may interfere with the normal menstrual cycle (period) in women and may stop sperm production in men. However, you should not assume that you cannot get pregnant or that you cannot get someone else pregnant. Women who are pregnant or breast-feeding should tell their doctors before they begin taking this drug. You should not plan to have children while receiving chemotherapy or for a while after treatments. (Talk to your doctor for further details.) Use a reliable method of birth control to prevent pregnancy. Topotecan may harm the fetus.
- do not have any vaccinations (e.g., measles or flu shots) without talking to your doctor.

# Side effects

## Minor Side Effects
Side effects from topotecan are common and include:
- headache
- loss of appetite
- thinned or brittle hair
- diarrhea
- constipation
- nausea
- abdominal pain
Tell your doctor if either of these symptoms is severe or lasts for several hours:
- mouth blistering
- fatigue

## Severe Side Effects
If you experience any of the following symptoms, call your doctor immediately:
- unusual bruising or bleeding
- red, itchy rash
- fever
- chills
- cough
- sore throat
- difficulty swallowing
- change in normal bowel habits for more than 2 days
- severe vomiting
- dizziness
- shortness of breath
If you experience a serious side effect, you or your doctor may send a report to the Food and Drug Administration's (FDA) MedWatch Adverse Event Reporting program online  or by phone .

# In case of emergency/overdose
In case of overdose, call your local poison control center at 1-800-222-1222. If the victim has collapsed or is not breathing, call local emergency services at 911.

# Brand names
- Hycamtin
Transcription initiation protein SPT3 homolog
Transcription initiation protein SPT3 homolog is a protein that in humans is encoded by the SUPT3H gene.

# Interactions
Transcription initiation protein SPT3 homolog has been shown to interact with GCN5L2, TAF6L, TADA3L, TAF5L, SF3B3, SUPT7L, Myc, TAF9, Transformation/transcription domain-associated protein, TAF12, TAF10, TAF4 and DDB1.

# Model organisms
Model organisms have been used in the study of SUPT3H function. A conditional knockout mouse line called Supt3tm1a(EUCOMM)Hmgu was generated at the Wellcome Trust Sanger Institute. Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Additional screens performed:  - In-depth immunological phenotyping
Venlafaxine how supplied storage and handling

# How Supplied Storage And Handling
Effexor XR (venlafaxine hydrochloride) extended-release capsules are available as follows:
37.5 mg, grey cap/peach body with W and "Effexor XR" on the cap and "37.5" on the body.
NDC 0008-0837-20, bottle of 15 capsules in unit of use package.
NDC 0008-0837-21, bottle of 30 capsules in unit of use package.
NDC 0008-0837-22, bottle of 90 capsules in unit of use package.
NDC 0008-0837-03, carton of 10 Redipak blister strips of 10 capsules each.
75 mg, peach cap and body with W and "Effexor XR" on the cap and "75" on the body.
NDC 0008-0833-20, bottle of 15 capsules in unit of use package.
NDC 0008-0833-21, bottle of 30 capsules in unit of use package.
NDC 0008-0833-22, bottle of 90 capsules in unit of use package.
NDC 0008-0833-03, carton of 10 Redipak blister strips of 10 capsules each.
150 mg, dark orange cap and body with W and "Effexor XR" on the cap and "150" on the body.
NDC 0008-0836-20, bottle of 15 capsules in unit of use package.
NDC 0008-0836-21, bottle of 30 capsules in unit of use package.
NDC 0008-0836-22, bottle of 90 capsules in unit of use package.
NDC 0008-0836-03, carton of 10 Redipak blister strips of 10 capsules each.
Store at controlled room temperature, 20 to 25C (68 to 77F).
The unit of use package is intended to be dispensed as a unit.
The appearance of these capsules is a trademark of Wyeth Pharmaceuticals.
2',3'-Cyclic-nucleotide 3'-phosphodiesterase
2',3'-Cyclic-nucleotide 3'-phosphodiesterase also known as CNPase is an enzyme that in humans is encoded by the CNP gene.

# Reaction
CNPase catalyzes the following reaction:
Thus, the two substrates of this enzyme are nucleoside 2',3'-cyclic phosphate and H2O, whereas its product is nucleoside 2'-phosphate.

# Function
CNPase is a myelin-associated enzyme that makes up 4% of total CNS myelin protein, and is thought to undergo significant age-associated changes. It is named for its ability to catalyze the phosphodiester hydrolysis of 2',3'-cyclic nucleotides to 2'-nucleotides, though a cohesive understanding of its specific physiologic functions are still ambiguous.
Structural studies have revealed that four classes of CNPases belong to one protein superfamily. CNPase's catalytic core consists of three alpha-helices and nine beta-strands. The proposed mechanism of CNPases phosphodiesterase catalytic activity is similar to the second step of the reaction mechanism for RNase A.
CNPase is expressed exclusively by oligodendrocytes in the CNS, and the appearance of CNPase seems to be one of the earliest events of oligodendrocyte differentiation. CNPase is thought to play a critical role in the events leading up to myelination.
CNPase also associates with microtubules in brain tissue and FRTL-5 thyroid cells, and is reported to have microtubule-associated protein-like activity (MAP; see MAP2), being able to catalyze microtubule formation at low molar ratios. Deletion of the C-terminus of CNPase or phosphorylation abolish the catalytic activity of microtubule formation. CNPase can link tubulin to cellular membranes, and might be involved in the regulation cytoplasmic microtubule distribution.
CNNPase has also been demonstrated to inhibit the replication of HIV-1 and other primate lentiviruses by binding the retroviral Gag protein and inhibiting the genesis of nascent viral particles.  Whether this is a biological function of CNPase or a coincidental activity remains unclear.
Tension pneumothorax resident survival guide

# Overview
Tension pneumothorax is a life threatening condition that results from the accumulation of air in the pleural cavity.  Air enters the intrapleural space through an injured parietal pleura, visceral pleura or tracheobronchial tree that forms a one way valve.  The one way valve allows the air to enter in the pleural cavity (during inspiration) but prevents its escape (during expiration).  Subsequently, the intrapleural pressure rises and results in respiratory and cardiovascular failure.  Tension pneumothorax can occur as a result of trauma, ventilation or resuscitation.  The cardinal symptoms and signs of tension pneumothorax are severe dyspnea, chest pain, hypotension, hypoxia, tachycardia and jugular vein distention.  Tension pneumothorax should be managed immediately with emergency needle decompression followed by insertion of a chest tube.

# Causes

## Life Threatening Causes
Tension pneumothorax is a life-threatening condition and must be treated as such irrespective of the underlying cause.

## Common Causes
- Asthma
- Central venous catheter
- Cardiopulmonary resuscitation
- Chronic obstructive pulmonary disease
- Emphysema
- Mechanical ventilation
- Trauma

# FIRE: Focused Initial Rapid Evaluation
A Focused Initial Rapid Evaluation (FIRE) as shown below should be performed to identify patients in need of immediate intervention.
Boxes in red signify that an urgent management is needed.

# Complete Diagnostic Approach
A complete diagnostic approach should be carried out after a focused initial rapid evaluation is conducted and following initiation of any urgent intervention.

# Treatment

# Do's
- Suspect tension pneumothorax in the case of blunt and penetrating trauma to the chest.
- Immediately cover penetrating chest wounds with an occlusive or pressure bandage in trauma patients with suspected tension pneumothorax.
- Suspect tension pneumothorax among patients on mechanical ventilation who develop a rapid onset of hemodynamic instability or cardiac arrest and require an increase in the peak inspiratory pressure.
- Order serial chest radiographs every 6 hours on the first day following chest trauma to rule out pneumothorax.
- Refer the patient to a respiratory specialist within 24 hours of admission.
- Order a chest X-ray before chest tube removal to confirm the re-expansion of the affected lung.

# Don'ts
- Don't remove the catheter from the 2nd intercostal space unless a chest tube is appropriately placed.
- Don't use large bore chest tubes.
- Don't leave the chest tube more than 7 days, as it will increase the risk of infection.
Amoxicillin-clavulanate potassium overdosage

# Overdosage
In case of overdosage, discontinue medication, treat symptomatically, and institute supportive measures as required.  A prospective study of 51 pediatric patients at a poison-control center suggested that overdosages of less than 250 mg/kg of amoxicillin are not associated with significant clinical symptoms1.
Interstitial nephritis resulting in oliguric renal failure has been reported in patients after overdosage with amoxicillin/clavulanate potassium.
Crystalluria, in some cases leading to renal failure, has also been reported after amoxicillin/clavulanate potassium overdosage in adult and pediatric patients. In case of overdosage, adequate fluid intake and diuresis should be maintained to reduce the risk of amoxicillin/clavulanate potassium crystalluria.
Renal impairment appears to be reversible with cessation of drug administration. High blood levels may occur more readily in patients with impaired renal function because of decreased renal clearance of amoxicillin/clavulanate potassium. Amoxicillin/clavulanate potassium may be removed from circulation by hemodialysis.
Antiarrhythmic agent resident survival guide
c

# Overview

# Causes

## Life Threatening Causes

## Common Causes

## Prognosis

# Vaughan-Williams classification of antiarrhythmic agents

# Do's
- Class IA agents are proarrhythmogenic and are associated with increased incidences of Torsade de Pointes, ventricular tachycardia or ventricular fibrillation. If arrhythmia are observed with one class 1A agent all other class 1A agents should be avoided. Due to risk of proarrhythmia all class 1A drugs should be initiated in hospital. If QTC > 500 msec the drug should be stopped.
- Disopyramide side-effects include anticholinergic effects (30%) including dry mouth, blurred vision, constipation, and urinary retention. Pyridostigmine (90 mg twelve hourly to 180 mg every eight hours) prevents or diminishes the anticholinergic effect of disopyramide and allows high tolerated doses of the drug.
- Disopyramide-induced hypoglycemia has been noted. Other reported side effects includes nausea, vomiting, rash, cholestatic jaundice, and agranulocytosis. It prolongs repolarization and may cause proarrhythmia (VF, Torsade de Pointes)
- Procainamide has side-effects similar to Quinidine.

# Don'ts
- Do not start with low dose Dopamine dose to perfuse the kidney.