#non shockable rhythms

[whumpy-daydreams]

CPR in hospitals

I did a post on doing cpr as a 'civilian' (i.e. in public with no equipment). But most people who follow me are writers! So here's how it goes down in hospital.

It varies on where someone is in hospital having a cardiac arrest, so this is just for if a patient is in a hospital bed with monitoring on.

The first sign is going to the monitor going crazy and the patient unconscious.

Step 1 - pull the emergency button and start chest compressions (they are still the most important thing!)

Step 2 - someone else will give rescue 'breaths' using an oxygen mask and bag (technically called a bag valve mask or BVM). Two breaths after every 30 compressions

Step 3 - someone else is cutting clothes off and putting defibrillator pads on. An anaesthetist may also intubate the patient and put them on a ventilator (this means you can do compressions continuously)

Step 4 - the defibrillator will scan the heart rhythm. If it's shockable (ventricular tachycardia or fibrillation) then everyone steps away while it shocks. As soon as it's safe, CPR continues (most defibrillators determine the rhythm and calculate voltage automatically)

Step 5 - if it's a non-shockable rhythm, give IV adrenaline ASAP

Step 6 - if it's a shockable rhythm, wait 2 minutes after first shock, check and shock again. Repeat a third time.

Step 7 - if the patient is still in cardiac arrest after 3 shocks, give IV adrenaline and amiodarone

Step 8 - continue CPR and give adrenaline every 5 minutes.

The person giving compressions should switch every 60 compressions (two cycles of 30) - the next person is counted in so there's no time without compressions

There are 10 main causes of cardiac arrest - while all of this is happening a team of doctors will be trying to work out the cause so they can treat it. I won't go into the causes because it's boring and technical.

CPR, defibrillation, and drugs will continue until the cardiac arrest stops or the patient is declared deceased.

If someone is in hospital because of hypothermia, remember! They're not dead until they're warm! (there have been cases of hypothermia patients being successfully resuscitated after over 5 hours of CPR!)

[lonelynpc]

Shockable and Non-Shockable Rhythms

grey's anatomy has been lying to you. flatline is not a shockable rhythm.

automated external defibrillators (AEDs) have a safety feature that can recognise shockable and non-shockable rhythms, this is why they may not authorise a shock.

now, i know that sometimes in fics, people like to describe a flatline before administering a shock but this is incorrect so i'm making this post to show you the different rhythms and whether or not they're shockable. i hope this helps with describing how things look on a monitor.

basically though, a shock acts as a sort of reset button to return the electrical activity to normal. in non-shockable rhythms, there is nothing to be "reset".

here are the shockable rhythms:

a shockable rhythm has the best prognosis with early CPR and defibrillation, we also give epinephrine.

pulselesss ventricular tachycardia (pVT): the ventricles in the heart are contracting too quickly (tachycardia) which decreases ventricular refill, resulting in a reduction in cardiac output. basically, the heart is beating so quickly that the blood can't perfuse anymore and there's no chance for blood to re-enter the heart, meaning that a pulse cannot be palpated.

ventricular fibrillation (VF): uncoordinated contraction of the ventricles causing disorganised electrical activity in the heart, notice that there are no identifiable QRS complexes. this is probably the most common. think erratic, disorganised.

here are the non-shockable rhythms:

these are treated with CPR, epinephrine and correction of the cause. shocks won't do anything.

pulseless electrical activity (PEA): this is when we are unable to palpate a pulse despite the presence of sufficient electrical activity. basically, the electrical activity is not eliciting a ventricular response.

asystole: this is flatlining. this is the cessation of electrical and mechanical activity in the heart. obviously, as a result, cardiac output and perfusion stops.

remember the Hs and Ts for the possible causes of cardiac arrest.

go forth. enjoy. i hope this helps.

[borbology]

WAIT FUCK the emoji didn't copy and that was what was in my clipboard IM SORRY HERE'S YOUR FORK 🍴

NOBODY TOLD ME IT WAS YOUR BIRTHDAY WTF

have cake 🎂

I did msyelf ! Wdym??/lh /j AnwyS TJANK YOUUU!!! ‼️‼️

[cleverwordsandotherstuffilike]

Lazarus phenomenon

Autoresuscitation is a phenomenon of the heart during which it can resume its spontaneous activity and generate circulation. It was described for the first time by K. Linko in 1982 as a recovery after discontinued cardiopulmonary resuscitation (CPR). J.G. Bray named the recovery from death the Lazarus phenomenon in 1993. It is based on a biblical story of Jesus’ resurrection of Lazarus four days after confirmation of his death. Up to the end of 2022, 76 cases (coming from 27 countries) of spontaneous recovery after death were reported; among them, 10 occurred in children. The youngest patient was 9 months old, and the oldest was 97 years old. The longest resuscitation lasted 90 min, but the shortest was 6 min. Cardiac arrest occurred in and out of the hospital. The majority of the patients suffered from many diseases. In most cases of the Lazarus phenomenon, the observed rhythms at cardiac arrest were non-shockable (Asystole, PEA). Survival time after death ranged from minutes to hours, days, and even months. Six patients with the Lazarus phenomenon reached full recovery without neurological impairment. Some of the causes leading to autoresuscitation presented here are hyperventilation and alkalosis, auto-PEEP, delayed drug action, hypothermia, intoxication, metabolic disorders (hyperkalemia), and unobserved minimal vital signs. To avoid Lazarus Syndrome, it is recommended that the patient be monitored for 10 min after discontinuing CPR. Knowledge about this phenomenon should be disseminated in the medical community in order to improve the reporting of such cases. The probability of autoresuscitation among older people is possible.

National Library of Medicine

[anauro]

Self rec time! Rec one of your fluff fics, one angst, one multichaptered, one AU and send this to your favourite writers 💖

Hello Julia my love 💗

Fluff fic:

Snow on the beach

Lily and Pandora take their daughter Luna on holiday, where Luna has her accidental magic incident.

Angst fic:

Non-shockable rhythm

Marlene and Dorcas are both terminally ill. One watches the other one die.

Multichaptered fic (maybe this will give me the motivation to finish it):

Chicks before dicks

Lily needs help getting over her crush on James Potter. Marlene is eager to help.

AU fic:

Drugs and surgical scrubs

James was fairly certain nothing could ever come close to heroin, absolutely nothing, but Regulus Black wasn’t far off.

[amit-vikhe]

ACLS Skills That Save Lives During Myocardial Infarctions

When someone has a heart attack, also called a myocardial infarction, their life hangs in the balance. Advanced Cardiovascular Life Support (ACLS) training gives healthcare teams the exact skills needed to act quickly and save lives in these emergencies. Some of the best courses for ACLS renewal are available online. With ACLS skills sharpened, rapid response can preserve heart muscle and prevent permanent damage or death.

What Are The ACLS Skills That Can Save Lives?

ACLS certification arms its students with a lot of essential skills. Here are the crucial ACLS skills that make all the difference.

Recognizing Heart Attack SignsThe very first ACLS skill is being able to spot the warning signs that someone is having a heart attack or myocardial infarction. The most common signs include:

Chest pain, pressure, squeezing or discomfort

Shortness of breath

Cold sweats

Nausea or vomiting

Dizziness or lightheadedness

However, not everyone has obvious symptoms. Heart attacks can be "silent" with no pain at all, especially in women, the elderly, and those with diabetes. That's why ACLS trains teams to look for any combination of concerning symptoms.

Being able to swiftly identify a probable heart attack allows ACLS protocols to kick in without delay.

Supporting Breathing and CirculationOnce a heart attack is suspected, ACLS skills focus on quickly restoring oxygen flow to the heart muscle. Key actions include:

Giving oxygen through a face mask or nasal cannula

Starting an IV line to give medications

Hooking up monitoring to check heart rate and rhythm

Preparing to do CPR if needed

This buys critical time while getting ready for definitive treatment to open the blocked artery.

Interpreting ECG Rhythms 

A key ACLS skill is being able to quickly interpret ECG/EKG rhythm strips to diagnose heart conditions like:

ST-elevation myocardial infarction (STEMI)

Non-ST-elevation myocardial infarction (NSTEMI)

Deadly arrhythmias requiring defibrillation

This guides the next treatment steps like activating the cath lab or delivering shocks.

Performing Defibrillation/CardioversionIf the ECG shows a shockable rhythm like ventricular fibrillation, ACLS provides the protocols for immediate defibrillation. This helps to restart the heart. Or if unstable rhythms are present, ACLS covers performing synchronized cardioversion.

Going through the proper sequences of shocks and medications in ACLS has saved countless lives.

Providing Crucial Medications 

ACLS has clear protocols on what medications to give during a heart attack, such as:

Aspirin to help dissolve blood clots

Nitroglycerin is given to relieve chest pain

Anti-clotting drugs are used to prevent any clot forming anymore

Epinephrine or other pressors if blood pressure drops dangerously

ACLS training covers dosages, timing, and how to administer these drugs safely and effectively in an emergency.

Arranging Prompt Procedures A heart attack is treated by returning the flow of blood and removing the clot in the heart. There are two main options:

Cardiac Catheterization:

ACLS stresses preparing the patient for rapid transfer to have a catheter inserted to open the artery with balloons or stents. Goal is under 90 minutes.

Clot-Busting Medications:

ACLS also teaches IV drugs like TNKase or tPA to help dissolve clots, if catheterization can't happen right away.

Having these methods arranged ahead of time through ACLS systems avoids any delay in reopening the artery.

Managing ComplicationsHeart attacks often trigger other life-threatening issues. ACLS equips teams to swiftly recognize and treat problems like:

Dangerous heart rhythms like ventricular fibrillation

Extremely low blood pressure from shock

Acute heart failure as the heart muscle weakens

ACLS protocols cover techniques like defibrillation, CPR, medications, breathing support, and more to stabilize the patient. With these ACLS skills ready, complications can be managed until the patient reaches a higher level of cardiac care.

Who Can Enroll in ACLS Courses?

Healthcare professionals who need to lead or participate in resuscitation for adult cardiovascular emergencies like heart attacks, such as:

Doctors

Nurses

Paramedics

Other prehospital providers

Many hospitals require ACLS certification for staff in high-risk areas:

Emergency departments

Intensive care units

Cardiac care units

Healthcare trainees are strongly encouraged to get ACLS training early on:

Medical students

Nursing students

Resident physicians

Other healthcare students

Some facilities also recommend ACLS for other roles:

Respiratory therapists

Phlebotomists

Clinical staff who may need to provide basic life support

How to Stay ACLS Certified?

ACLS courses are very important for achieving the full potential of a health professional. Full ACLS courses provide:

Classroom lessons on the latest guidelines

Hands-on practice with equipment

Testing to ensure competency

But these crucial skills need ongoing practice. ACLS certification can be updated by enrolling in an ACLS renewal course every two years. The recertification is to:

Review any updates to treatments or steps

Build knowledge through extra learning

Retest skills to ensure they stay sharp

Most hospitals and EMS agencies require an active ACLS card at all times. With online renewal now available, it's easy to recertify ACLS skills on a flexible schedule.

Conclusion

With well-practiced ACLS abilities, myocardial infarction patients have a far better chance. ACLS equips the care team to provide high-quality emergency cardiac care in those first critical moments. You can find some of the best courses online and offline. Having current ACLS means teams can seamlessly use these skills when heart attacks or cardiac arrests happen without warning. The best courses for ACLS renewal can be found online.

[defibrillatoraus09]

How AED Defibrillators Work: A Comprehensive Guide

In times of emergency, knowing how to use an AED defib could mean the difference between life and death.

These portable devices are designed to deliver an electric shock to the heart, restoring its normal rhythm during sudden cardiac arrest. Let's delve into the mechanics of AED defib and understand how they function.

Understanding AED Defibrillators

AED defibs are compact, user-friendly devices commonly found in public spaces, workplaces, and healthcare facilities.

They are specifically designed for individuals with minimal medical training to use in emergencies. The primary function of an AED defib is to analyse the heart rhythm and deliver a shock if necessary to restore normalcy.

Components of an AED Defibrillator

To comprehend how AED defibs operate, it's essential to familiarise yourself with their key components:

Electrode Pads: These adhesive pads are placed on the patient's chest to detect the heart's rhythm and deliver the electrical shock.

Control Panel: The interface through which users operate the AED and defibrillator. It typically includes buttons for power, shock delivery, and audio prompts.

Battery: Powers the device and ensures it remains operational during emergencies.

Internal Circuitry: The brains behind the AED defib are responsible for analysing heart rhythms and determining the need for a shock.

How do AED Defibrillators Function?

The operation of an AED defib can be broken down into simple steps:

Power On: Upon activating the AED defib, it performs a self-check to ensure all components are functioning correctly.

Apply Electrode Pads: The electrode pads are placed on the patient's bare chest. These pads detect the heart's rhythm and relay information to the AED defib.

Analyse Rhythm: The device analyses the heart rhythm to determine whether a shock is necessary. It distinguishes between shockable rhythms like ventricular fibrillation and non-shockable rhythms like asystole.

Shock Delivery: If a shockable rhythm is detected, the AED defib prompts the user to stand clear and delivers a controlled electric shock through the electrode pads.

CPR Guidance: In addition to shock delivery, many AED defibs provide audio and visual prompts to guide users through cardiopulmonary resuscitation (CPR) until emergency medical services arrive.

Continued Monitoring: After delivering a shock or initiating CPR, the AED defib continues to monitor the patient's heart rhythm and provides instructions as needed.

Importance of AED Defibrillators

The widespread availability of AED defibs has significantly improved survival rates for sudden cardiac arrest victims.

Prompt defibrillation within the first few minutes of cardiac arrest can increase the chances of survival by up to 70%. This makes AED defibs invaluable assets in public safety initiatives and healthcare settings.

Training and Accessibility

While AED defibs are designed for ease of use, proper training enhances effectiveness and confidence during emergencies. Many organisations offer basic life support (BLS) courses that include AED defib training, empowering individuals to respond effectively to cardiac emergencies.

Conclusion

AED defibrillators are lifesaving devices that play a crucial role in the chain of survival for sudden cardiac arrest victims. Understanding how they function and being prepared to use them can make a significant difference in saving lives.

With their intuitive design and widespread availability, AED defibs empower individuals to become proactive first responders in emergency situations. By increasing awareness and accessibility to these devices, we can create safer communities where everyone has the opportunity to receive timely lifesaving interventions.

[cardiacreports2]

Paramedic Report

Patient Information:

Name: Gingerbreadhb

Age: 30 years

Gender: Male

Height: 5'8"

Hair: Ginger

Eyes: Brown

Distinguishing Marks: Hairy chest, nipple piercing (right nipple), thick but semi-muscular build

Incident Description:

Location: Iron Forge Gym, 2345 Maple St., [City]

Date and Time of Call: October 8, 2024, 5:25 PM

Nature of Call: Respiratory distress and subsequent cardiac arrest

Initial Assessment:

Upon arrival, patient Gingerbreadhb was found at the gym, sitting on the floor and experiencing an asthma attack. The patient was struggling to breathe, using an inhaler with minimal relief. Skin was flushed, and the patient was conscious but distressed. He reported chest tightness and shortness of breath.

Oxygen saturation: 84% on room air

Heart rate: Elevated (130 bpm)

Respirations: Rapid and shallow (28 breaths per minute)

Blood pressure: 150/95 mmHg

Intervention:

Oxygen therapy was immediately initiated via non-rebreather mask (15 L/min).

Patient was assisted with a second dose of albuterol from his inhaler.

Despite interventions, the patient's condition deteriorated. He became cyanotic and unresponsive, and within minutes of arrival, he collapsed into cardiac arrest.

Cardiac Arrest:

Time of Arrest: 5:38 PM

CPR was initiated immediately, with chest compressions administered at a depth of 2 inches, 100-120 compressions per minute.

AED (automated external defibrillator) applied and delivered one shock after detecting ventricular fibrillation.

Advanced airway management provided, and IV access established. Epinephrine administered per protocol.

After 2 rounds of defibrillation and approximately 8 minutes of CPR, return of spontaneous circulation (ROSC) was achieved at 5:46 PM.

Transport:

Patient remained unconscious but with a palpable pulse.

Monitored en route to the hospital. Blood pressure remained low (90/50 mmHg) and oxygen levels unstable despite oxygen therapy.

Approximately 5 minutes into transport, the patient lost pulse again at 5:51 PM. CPR was resumed, and additional defibrillation attempted, but no shockable rhythm was detected.

Outcome:

Despite continued resuscitation efforts, patient Gingerbreadhb was pronounced deceased at 6:03 PM during transport to St. Mary’s Medical Center.

Final Disposition:

Deceased.

Body was handed over to hospital staff upon arrival for further examination.

Hospital Examination:

Upon arrival at St. Mary’s Medical Center, the patient was examined post-mortem. The following assessments were made regarding the condition of the heart and lungs:

Heart:

The patient’s heart displayed signs of significant stress. Evidence of left ventricular hypertrophy (thickened walls) was present, likely secondary to chronic stress and overexertion.

Cardiac tissue showed focal areas of fibrosis, indicative of past cardiac insults, potentially related to untreated or undiagnosed cardiovascular disease.

The coronary arteries showed mild atherosclerotic changes, though no immediate signs of atherosclerosis-induced myocardial infarction were found.

Conclusion: Likely acute cardiac arrest precipitated by an asthma attack and compounded by pre-existing, undiagnosed heart disease.

Lungs:

The lungs were hyperinflated, consistent with the asthma attack noted prior to collapse.

There were widespread bronchial constrictions, with mucosal edema visible in the airways, consistent with severe bronchospasm.

No evidence of infection or pneumonia was found.

Conclusion: The patient’s severe asthma exacerbation likely contributed to hypoxia, which played a role in precipitating cardiac arrest.

Signatures:

Paramedic #1: John Doe

Paramedic #2: Jane Smith

EMS Unit: 52-Alpha

Medical Examiner:

Dr. Sarah Hernandez, MD, St. Mary’s Medical Center

I did some cardio yesterday... Tried to push my heart above 200 bpm, stayed there for a few minutes and the I would slow down to get it back to 160-170 just to start over again.

It is crazy to think that I used to avoid this kind of exercise as my airways would just close as a child due to my athsma. Now it just feels amazing on the heart (plus a little athsma sometimes).

Maybe one day I would just collapse in the middle of the gym hahah

[amaryllisbia]

One of my biggest pet peeves in medical tv dramas, any movies or just about any scene involving a code blue in fiction, there’s a tendency to think you can shock any heart rhythm.

Like NO, you CANNOT.

But, here’s some tips for shockable rhythms if you want to be medically accurate in your piece of fiction. These are tips from a medical student.

There are 2 categories:- SHOCKABLE RHYTHM & NON-SHOCKABLE RHYTHM

Note:- when there’s VT, you can only shock if it’s pulseless VT. Hence, you always check for a pulse if you see this rhythm on the defibrillator monitor.

In cases of non-shockable rhythms, you administer IV drugs and recheck the rhythm. Of course, do continue administering chest compressions via another health professional.

[sodasback]

Overdose

ER Nurse Rafe x ER Nurse Reader

Reposting from my deleted account. 

TW: Mentions of drug overdose, CPR, death, panic attack

One of your guy best friends in high school, Chris, died of a drug overdose. And you were the one who found him. You tried to do CPR, but 1. you didn’t really know how to do CPR when you were 16 and 2. it was too late even if you did know how to do it correctly. This traumatic experience did 2 important things for you. You became a total straight edge, scared to death of drugs. And it made you want to save everyone. It’s probably why you became a nurse. 

Tonight, you and Rafe were working in the ER together. Rafe was off taking care of patients on the other side of the emergency department, when the Charge nurse told you a cardiac arrest was coming in. She assigned roles to you and a couple of other nurses. You were assigned compressions. 

“What’s coming in?” Someone asked. 

“16 year old male, OD’d on unknown substances, found pulseless. ETA is 3 minutes.” 

Your throat went dry. Of course you have dealt with drug overdoses in the ER all the time. But so far, none of them had been teens who were found pulseless. It just hit too close to home. You considered backing out and asking someone else to take your role. But then you realized: this is why you’re here. You’re here to give this kid the best chance at surviving this. You nodded your head to yourself and decided you could do this. 

“Do we know his name?” You asked.

“No, not yet.” 

By this time, Rafe had heard about the call coming in and he transferred and discharge his last couple patients, so he popped over to see if there was anything anyone needed. 

When he saw you getting ready by the empty gurney and setting up the step stool you would stand on to be able to give proper compressions all the dots connected for him. He realized you were about to give compressions to a 16 year old who OD’d, just like your friend in high school. 

“Y/N” he got your attention as a handful of people scurried and danced around each other preparing the area for this resuscitation attempt. 

You looked up at him wondering what he wanted. “Let me do compressions” He said with some authority. 

“It’s fine Rafe. I got it.” You shook your head at him. 

“Y/N” he said more sternly. No one seemed to notice the exchange going on between you two as they busied themselves with their tasks. 

“I said I got it.” You said aggressively. Rafe came over next to you so he could talk to you without anyone else hearing. 

“Y/N you don’t have to do this. You shouldn’t.” He said with a hand on your hip, ready to physically pull you off the stool. You pushed his hand away roughly. 

“I’m fine, Cameron” you said coldly. He recoiled at your tone and the use of his last name in a non-teasing way. 

He backed away silently and stood out of the way to watch the resuscitation and be there as extra hands ...and to be there for you. 

Then, the gurney came crashing through the doors. The medics who brought him in got him transferred onto your gurney. 

“What’s his name?” You asked as soon as you got the chance.

“Michael” The medic replied and you nodded. 

“Good to take over compressions?” the medic asked you. 

“Yep” you stated confidently and he lifted his hands away from the boys chest. You replaced his hands with your’s. With your elbows locked and fingers laced together you used your body weight to push down on the kid’s chest, pumping his heart for him so blood would circulate his body. 

You could feel Rafe standing nearby with his arms crossed, gloves already on in case he needed to jump in. Someone would have to take over compressions for you eventually no matter what. No one is supposed to do compressions for more than 2 minutes, because you get tired and start to not be as effective. 

You knew the chances for this kid were not good. He was already dead. Someone found him dead. Who knows how long he had been that way. Narcan had already been given. His heart didn’t have a shockable rhythm. All you could do was compressions, breaths and give him epinephrine in hopes of starting his heart again. 

“Come on Michael” you whispered over and over again. 

“Let’s do a pulse check.” The code leader called out. “Pause compressions”

“Stopping compressions” you confirmed as you pulled your hands away from his chest. Rafe was already by your side, pushing you out of the way with his body. 

“I’ll take over compressions” he announced to the entire room, so you couldn’t argue with him. You rolled your eyes and stepped out of the way. Even though you were mad at him for being overprotective, you knew someone would have had to take over for you soon, because you were getting tired, so you let it go. 

Because it was a 16 year old kid on the table the team tried for almost 2 hours to resuscitate him. Rafe and one of the techs took turns doing compressions.

 Finally, the team leader said, “One more round of epi and then we need to call it.” Rafe was the last one to give compressions.

The last round of epi was given and then there was a final pulse check. 

“Still no pulse.” The nurse who was checking stated solemnly. 

“Time of death 2347″ the doctor announced. 

Rafe instantly looked at you. You were staring at Michael laying on the table as everyone started to back away from the gurney and clean up the area for when his family came in. Your stare was blank, your body was numb. Rafe was helping pick up all the discarded supplies and position Michael in a way that was appropriate, but he kept looking up at you. And you just kept staring at the gurney. 

You felt your eyes get wetter. Finally, the room cleared out almost completely. One nurse stayed with Michael’s body. Rafe came over to you. 

“Let’s go outside.” He said to you, trying to be gentle and firm at the same time. You finally broke out of your trance. 

“What? No. I’m fine. I have other patients.” You said sniffling and shrugging off Rafe’s arm that he was trying to wrap around you.

“No, we have plenty of coverage. There’s no admits. We’re fine. Come on.” He said a little more sternly. 

Before you could reply and before Rafe could get you to move from the trauma bay where Michael’s body was still laying in a gurney, his parents rushed in already in tears. Already grieving the loss of their son.

That’s when you felt your chest explode. Your legs felt weak, but something was holding you up. All of a sudden you were outside and everything was blurry, but you didn’t know how you got there. You were sobbing for a while before you realized Rafe was holding you against his chest. 

“Breathe” Rafe was telling you calmly but you could hear concern in his voice. He was stroking your hair. “Y/N I need you to breathe.” You heard him again. 

“Here, were gonna sit” Rafe guided you down to the ground to sit, he sat behind you with a leg on either side of you. Another nurse came outside, “Is she okay?” He asked. 

“Yeah man, can you just grab a paper bag for her? She’s just hyperventilating a little. She needs to hold on to her CO2″ Rafe told him. 

He placed his fingers on your shoulders, “Open up your chest, baby.” He told you gently, pulling your shoulders back. “Breathe ... slower ... breathe with me. Breathe in... good, hold it for a sec. 1, 2, 3, 4. Okay exhale. Slow slow. Good love. Again, slow.” 

“Here ya go man.” The nurse handed Rafe a paper bag and went back inside. But you were breathing better now. Rafe moved so he could see your face. You took a deep breath and looked at his worried expression. 

“It was just like Chris, Rafe. I just wanted to save him.” You cried and you weren’t sure if you meant save Chris or Michael or both.

“I know baby.” He said. “We can’t save everyone though.” 

“And see?! I know that. We frickin watch people die all the time! I shouldn’t be out here crying on the sidewalk. There’s patients in there that need stuff and I’m out here crying.” 

“You’re allowed to cry over it. There is no one inside who needs you right now. The census is low, they’re probably going to send someone home anyway because were overstaffed right now. ...And you’re allowed to get upset over it sometimes. This is a tough job, babe. And we all have patients that hit us a little harder sometimes. You don’t need to be a robot. Part of what makes us good at our jobs is that were human, ya know? You care, you have a huge heart. The world is a better place with a nurse like you who treats every patient like someone you care about. That was a tough loss on everyone, love, but we tried everything we could.”

You nodded, really soaking in his words, knowing Rafe was right. Everyone has especially hard days when a patient hits a little too close to home or it’s a patient you’ve bonded with and things don’t go the way you want. 

“Yeah, I know” You gave Rafe the tiniest smile and sniffled. “Thanks Rafe”

“Of course, baby.” He leaned forward and used his thumbs to wipe the mascara stained tears from your face. Then he stood up and pulled you up. 

“Do you wanna see if you can be the one sent home?” He asked. 

“No, I’d rather stay and be distracted.” You said. 

Just then, an ambulance pulled up and medics jumped out with a patient who had a table saw accident. You and Rafe looked at each other. “I’ll apply pressure.” You said already stepping towards the patient. 

“I’m paging the blood bank and surgery.” Rafe said putting his phone between his shoulder and ear helping push the gurney into the trauma bay while you held pressure.

Taglist: @moniamaybank @abbyj1822 @october-cameron @hernameisnoell @railmerafe

[holliano]

Today’s infomercial:

A defibrillator will not shock a stable heart rhythm. Or a non-existent heart rhythm. When the pads are attached the computer inside analyses the heart rhythm and will only shock if it detects a shockable rhythm.

That means: if you come across an unconscious person and attach an AED to them and they’re having a seizure for example, not a cardiac event, you will not do them any harm and you have ruled that option out for paramedics.

You cannot make an AED shock if there isn’t a shockable heart rhythm.

AEDs also record this rhythm and it can be checked back after the fact if you have the equipment to do so.

[didanawisgi]

2020 Yale-G’s Monthly Clinical Updates According to www.uptodate.com

(As of 2020-11-12, updated in Yale-G’s 6th-Ed Kindle Version; will be emailed to buyers of Ed6 paper books)

       Chapter 1: Infectious Diseases

Special Viruses: Coronaviruses

     Coronaviruses are important human and animal pathogens, accounting for 5-10% community-acquired URIs in adults and probably also playing a role in severe LRIs, particularly in immunocompromised patients and primarily in the winter. Virology: Medium-sized enveloped positive-stranded RNA viruses as a family within the Nidovirales order, further classified into four genera (alpha, beta, gamma, delta), encoding 4-5 structural proteins, S, M, N, HE, and E; severe types: severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV), and novel coronavirus (2019-nCoV, which causes COVID-19). Routes of transmission: Similar to that of rhinoviruses, via direct contact with infected secretions or large aerosol droplets. Immunity develops soon after infection but wanes gradually over time. Reinfection is common. Clinical manifestations: 1. Coronaviruses mostly cause respiratory symptoms (nasal congestion, rhinorrhea, and cough) and influenza-like symptoms (fever, headache). 2. Severe types (2019-nCoV, MERS-CoV, and SARS-CoV): Typically with pneumonia–fever, cough, dyspnea, and bilateral infiltrates on chest imaging, and sometimes enterocolitis (diarrhea), particularly in immunocompromised hosts (HIV+, elders, children). 3. Most community-acquired coronavirus infections are diagnosed clinically, although RT-PCR applied to respiratory secretions is the diagnostic test of choice.              

Treatment: 1. Mainly consists of ensuring appropriate infection control and supportive care for sepsis and acute respiratory distress syndrome. 2. In study: Chloroquine showed activity against the SARS-CoV, HCoV-229E, and HCoV-OC43 and remdesivir against 2019-nCoV. Dexamethasone may have clinical benefit.

Prevention: 1. For most coronaviruses: The same as for rhinovirus infections, which consist of handwashing and the careful disposal of materials infected with nasal sec retions. 2. For novel coronavirus (2019-nCoV), MERS-CoV, and SARS-CoV: (1) Preventing exposure by diligent hand washing, respiratory hygiene, and avoiding close contact with live or dead animals and ill individuals. (2) Infection control for suspected or confirmed cases: Wear a medical mask to contain their respiratory secretions and seek medical attention; standard contact and airborne precautions, with eye protection.

      Hepatitis A: HAV vaccine is newly recommended to adults at increased risk for HAV infection (substance use treatment centers, group homes, and day care facilities for disabled persons), and to all children and adolescents aged 2 to 18 years who have not previously received HAV vaccine.

      Hepatitis C: 8-week glecaprevir-pibrentasvir is recommended for chronic HCV infection in treatment-naive patients. In addition to the new broad one-time HCV screening (17-79 y/a), a repeated screening in individuals with ongoing risk factors is suggested.

      New: Lefamulin is active against many common community-acquired pneumonia pathogens, including S. pneumoniae, Hib, M. catarrhalis, S. aureus, and atypical pathogens.  

      New: Cefiderocol is a novel parenteral cephalosporin that has activity against multidrug-resistant gram-negative bacteria, including carbapenemase-producing organisms and Pseudomonas aeruginosa resistant to other beta-lactams. It’s reserved for infections for which there are no alternative options.

      New: Novel macrolide fidaxomicin is reserved for treating the second or greater recurrence of C. difficile infection in children.       Vitamin C is not beneficial in adults with sepsis and ARDS.    

      Chapter 2: CVD

      AF: Catheter ablation is recommended to some drug-refractory, paroxysmal AF to decrease symptom burden. In study: Renal nerve denervation has been proposed as an adjunctive therapy to catheter ablation in hypertensive patients with AF. Alcohol abstinence lowers the risk of recurrent atrial fibrillation among regular drinkers.

VF: For nonshockable rhythms, epinephrine is given as soon as feasible during CPR, while for shockable rhythms epinephrine is given after initial defibrillation attempts are unsuccessful. Avoid vasopressin use.

All patients with an acute coronary syndrome (ACS) should receive a P2Y12 inhibitor. For patients undergoing an invasive approach, either prasugrel or ticagrelor has been preferred to clopidogrel. Long-term antithrombotic therapy in patients with stable CAD and AF has newly been modified as either anticoagulant (AC) monotherapy or AC plus a single antiplatelet agent.

      Long-term antithrombotic therapy (rivaroxaban +/- aspirin) is recommended for patients with AF and stable CAD. Ticagrelor plus aspirin is recommended for some patients with CAD and diabetes.

VTE (venous thromboembolism): LMW heparin or oral anticoagulant edoxaban is the first-line anticoagulants in patients with cancer-associated VTE.

Dosing of warfarin for VTE prophylaxis in patients undergoing total hip or total knee arthroplasty should continue to target an INR of 2.5.

     Chapter 3: Resp. Disorders

Asthma: Benralizumab is an IL-5 receptor antibody that is used as add-on therapy for patients with severe asthma and high blood eosinophil counts.

Recombinant GM-CSF is still reserved for patients who cannot undergo, or who have failed, whole lung lavage.

Pulmonary embolism (PE): PE response teams (PERT, with specialists from vascular surgery, critical care, interventional radiology, emergency medicine, cardiac surgery, and cardiology) are being increasingly used in management of patients with intermediate and high-risk PE.

Although high-sensitivity D-dimer testing is preferred, protocols that use D-dimer levels adjusted for pretest probability may be an alternative to unadjusted D-dimer in patients with a low pretest probability for PE.

     Non-small cell lung cancer (NSCLC): Newly approved capmatinib is for advanced NSCLC associated with a MET mutation, and selpercatinib for those with advanced RET fusion-positive. Atezolizumab was newly approved for PD-L1 high NSCLC.

Circulating tumor DNA tests for cancers such as NSCLC are increasingly used as “liquid biopsy”. Due to its limited sensitivity, NSCLC patients who test (-) for the biomarkers should undergo tissue biopsy.

Cystic Fibrosis (CF): Tx: CFTR modulator therapy (elexacaftor-tezacaftor-ivacaftor) is recommended for patients ≥12 years with the F508del variant.

Vitamin E acetate has been implicated in the development of electronic-cigarette, or vaping, product use associated lung injury.

     Chapter 4: Digestive and Nutritional Disorders

     Comparison of Primary Biliary Cholangitis (PBC) and Primary Sclerosing Cholangitis (PSC):

     Common: They are two major types of chronic cholestatic liver disease, with fatigue, pruritus, obstructive jaundice, similar biochemical tests of copper metabolism, overlapped histology (which is not diagnostic), destructive cholangitis, and both ultimately result in cirrhosis and hepatic failure. (1) PBC: Mainly in middle-aged women, with keratoconjunctivitis sicca, hyperpigmentation, and high titer of antimitochondrial Ab (which is negative for PSC). (2) PSC: Primarily in middle-aged men, with chronic ulcerative colitis (80%), irregular intra- and extra-hepatic bile ducts, and anti-centromere Ab (+).

      CRC: Patients with colorectal adenomas at high risk for subsequent colorectal cancer (CRC) (≥3 adenomas, villous type with high-grade dysplasia, or ≥10 mm in diameter) are advised short follow-up intervals for CRC surveillance. Pembrolizumab was approved for the first-line treatment of patients with unresectable or metastatic DNA mismatch repair (dMMR) CRC.

      UC and CRC: Patients with extensive colitis (not proctitis or left-sided colitis) have increased CRC risk.

      Eradication of H. pylori: adding bismuth to clarithromycin-based triple therapy for patients with risk factors for macrolide resistance.

      Thromboelastography and rotational thromboelastometry are bedside tests recommended for patients with cirrhosis and bleeding.

      Pancreatic cancer: Screening for patients at risk for hereditary pancreatic cancer (PC): Individuals with mutations in the ataxia-telangiectasia mutated gene and one first-degree relative with PC can be screened with endoscopic ultrasound and/or MRI/magnetic retrograde cholangiopancreatography.

      Olaparib is recommended for BRCA-mutated advanced pancreatic cancer after 16 weeks of initial platinum-containing therapy.

      HCC (unresectable): New first-line therapy is a TKI (sorafenib or sunitinib) or immune checkpoint inhibitor atezolizumab plus bevacizumab, +/- doxorubicin. Monitor kidney toxicity for these drugs.

      UC: Ustekinumab (-umab) anti-interleukin 12/23 antibody, is newly approved for the treatment of UC.

      Crohn disease: The combination of partial enteral nutrition with the specific Crohn disease exclusion diet is a valuable alternative to exclusive enteral nutrition for induction of remission.

      Obesity: Lorcaserin, a 5HT2C agonist that can reduce food intake, has been discontinued in the treatment of obesity due to increased malignancies (including colorectal, pancreatic, and lung cancers).

      Diet and cancer deaths: A low-fat diet rich in vegetables, fruits, and grains experienced fewer deaths resulted from many types of cancer.

      Note that H2-blockers (-tidines) are no longer recommended due to the associated carcinogenic N-nitrosodimethylamine.

      Gastrointestinal Stromal Tumors (GIST):

      GIST is a rare type of tumor that occurs in the GI tract, mostly in the stomach (50%) or small intestine. As a sarcoma, it’s the #1 common in the GI tract. It is considered to grow from specialized cells in the GI tract called interstitial cells of Cajal, associated with high rates of malignant transformation.

Clinical features and diagnosis: Most GISTs are asymptomatic. Nausea, early satiety, bloating, weight loss, and signs of anemia may develop, depending on the location, size, and pattern of growth of the tumor. They are best diagnosed by CT scan and mostly positive staining for CD117 (C-Kit), CD34, and/or DOG-1.

Treatment: Approaches include resection of primary low-risk tumors, resection of high-risk primary or metastatic tumors with a tyrosine kinase inhibitor (TKI) imatinib for 12 months, or if the tumor is unresectable, neoadjuvant imatinib followed by resection. Radiofrequency ablation has shown to be effective when surgery is not suitable. Newer therapies of ipilimumab, nivolumab, and endoscopic ultrasound alcohol ablation have shown promising results. Avapritinib or ripretinib (new TKI) is recommended for advanced unresectable or metastatic GIST with PDGFRA mutations.

      Anal Cancer:

Anal cancer is uncommon and more similar to a genital cancer than it is to a GI malignancy by etiology. By histology, it is divided into SCC (#1 common) and adenocarcinoma. Anal cancer (particularly SCC among women) has increased fast over the last 30 years and may surpass cervical cancer to become the leading HPV-linked cancer in older women. A higher incidence has been associated with HPV/HIV infection, multiple sexual partners, genital warts, receptive anal intercourse, and cigarette smoking. SCCs that arise in the rectum are treated as anal canal SCCs.

Clinical features and diagnosis: 1. Bleeding (#1) and itching (often mistaken as hemorrhoids). Later on, patients may develop focal pain or pressure, unusual discharges, and lump near the anus, and changes in bowel habits. 2. Diagnosis is made by a routine digital rectal exam, anoscopy/proctoscopy plus biopsy, +/- endorectal ultrasound.

Treatment: Anal cancer is primarily treated with a combination of radiation, chemotherapy, and surgery—especially for patients failing the above therapy or for true perianal skin cancers.

     Chapter 5: Endocrinology

      Diabetes (DM):       Liraglutide can be added as a second agent for type-2 DM patients who fail monotherapy with metformin or as a third agent for those who fail combination therapy with metformin and insulin.       Metformin is suggested to prevent type 2 DM in high-risk patients in whom lifestyle interventions fail to improve glycemic indices.       Metabolic (bariatric) surgery improves glucose control in obese patients with type 2 DM and also reduce diabetes-related complications, such as CVD.       Teprotumumab, an insulin-like growth factor 1 receptor inhibitor, can be used for Graves’ orbitopathy if corticosteroids are not effective. Subclinical hypothyroidism should not be routinely treated (with T4) in older adults with TSH <10 mU/L.

        Chapter 6: Hematology & Immunology

       Anticoagulants: Apixaban is preferred to warfarin for atrial fibrillation with osteoporosis because it lowers the risk of fracture. Rivaroxaban is inferior to warfarin for antiphospholipid syndrome.

      Cancer-associated VTE: LMW heparin or oral edoxaban is the first-line anticoagulant prophylaxis.

      NH-Lymphoma Tx: New suggestion is four cycles of R(rituximab)-CHOP for limited stage (stage I or II) diffuse large B cell non-Hodgkin lymphoma (DLBCL) without adverse features. New suggestions: selinexor is for patients with ≥2 relapses of DLBCL, and tafasitamab plus lenalidomide is for patients with r/r DLBCL who are not eligible for autologous HCT.

      Chimeric antigen receptor (CAR)-T (NK) immunotherapy is newly suggested for refractory lymphoid malignancies, with less toxicity than CAR-T therapy. Polatuzumab + bendamustine + rituximab (PBR) is an alternative to CAR-T, allogeneic HCT, etc. for multiply relapsed diffuse large B-C NHL.

      Refractory classic Hodgkin lymphoma (r/r cHL) is responsive to immune checkpoint inhibition with pembrolizumab or nivolumab, including those previously treated with brentuximab vedotin or autologous transplantation.

      Mantle cell lymphoma: Induction therapy is bendamustine + rituximab or other conventional chemoimmunotherapy rather than more intensive approaches. CAR-T cell therapy is for refractory mantle cell lymphoma.

      AML: Gilteritinib is a new alternative to intensive chemotherapy for patients with FLT3-mutated r/r AML.

      Oral decitabine plus cedazuridine is suggested for MDS and chronic myelomonocytic leukemia.  

      Multiple myeloma (MM): Levofloxacin prophylaxis is suggested for patients with newly diagnosed MM during the first three months of treatment. For relapsed MM: Three-drug regimens (daratumumab, carfilzomib, and dexamethasone) are newly recommended.

      Transplantation: As the transplant waitlist continues to grow, there may be an increasing need of HIV-positive to HIV-positive transplants.

      Porphyria:       Porphyria is a group of disorders (mostly inherited) caused by an overaccumulation of porphyrin, which results in hemoglobin and neurovisceral dysfunctions, and skin lesions.       Clinical types, features, and diagnosis:  I. Acute porphyrias: 1. Acute intermittent porphyria: Increased porphobilinogen (PBG) causes attacks of abdominal pain (90%), neurologic dysfunction (tetraparesis, limb pain and weakness), psychosis, and constipation, but no rash. Discolored urine is common. 2. ALA (aminolevulinic acid) dehydratase deficiency porphyria (Doss porphyria): Sensorimotor neuropathy and cutaneous photosensitivity. 3. Hereditary coproporphyria: Abdominal pain, constipation, neuropathies, and skin rash. 4. Variegate porphyria: Cutaneous photosensitivity and neuropathies.  II. Chronic porphyrias: 1. Erythropoietic porphyria: Deficient uroporphyrinogen III synthase leads to cutaneous photosensitivity characterized by blisters, erosions, and scarring of light-exposed skin. Hemolytic anemia, splenomegaly, and osseous fragility may occur. 2. Cutaneous porphyrias–porphyria cutanea tarda: Skin fragility, photosensitivity, and blistering; the liver and nervous system may or may not be involved.  III. Lab diagnosis: Significantly increased ALA and PBG levels in urine have 100% specificity for most acute porphyrias. Normal PBG levels in urine can exclude acute porphyria.       Treatment: 1. Acute episodes: Parenteral narcotics are indicated for pain relief. Hemin (plasma-derived intravenous heme) is the definitive treatment and mainstay of management. 2. Avoidance of sunlight is the key in treating cutaneous porphyrias. Afamelanotide may permit increased duration of sun exposure in patients with erythropoietic protoporphyria.

 Chapter 7: Renal & UG

Membranous nephropathy (MN): Rituximab is a first-line therapy in patients with high or moderate risk of progressive disease and requiring immunosuppressive therapy.

      Diabetes Insipidus (DI): Arginine-stimulated plasma copeptin assays are newly used to diagnose central DI and primary polydipsia, often alleviating the need for water restriction, hypertonic saline, and exogenous desmopressin.

      Prostate cancer: Enzalutamide (new androgen blocker) is available for metastatic castration-sensitive prostate cancer. Cabazitaxel, despite its great toxicity, is suggested as third-line agent for metastatic prostate cancer. Either early salvage RT or adjuvant RT is acceptable after radical prostatectomy for high-risk disease.

      UG cancers: Nivolumab plus ipilimumab is suggested in metastatic renal cell carcinoma for long-term survival.

      Enfortumab vedotin is suggested in locally advanced or metastatic urothelial carcinoma. Maintenance avelumab is recommended with other chemotherapy in advanced urothelial bladder cancer. Pyelocalyceal mitomycin is suggested for low-grade upper tract urothelial carcinomas.

Chapter 8: Rheumatology

Janus kinase (JAK) inhibitors (upadacitinib, filgotinib) are new options for active, resistant RA and ankylosing spondylitis.

Graves’ orbitopathy: new therapy–teprotumumab, an insulin-like growth factor 1 receptor inhibitor.

Chapter 9: Neurology & Special Senses

Epilepsy: Cenobamate, a novel tetrazole alkyl carbamate derivative that inhibits Na-channels, provides a new treatment option for patients with drug-resistant focal epilepsy. A benzodiazepine plus either fosphenytoin, valproate, or levetiracetam is recommended as the initial treatment of generalized convulsive status epilepticus.

Migraine: Lasmiditan is a selective 5H1F receptor agonist that lacks vasoconstrictor activity, new therapy for patients with relative contraindications to triptans due to cardiovascular risk factors.

      Stroke: New recommendation for cerebellar hemorrhages >3 cm in diameter is surgical evacuation.       TBI: Antifibrolytic agent tranexamic acid is newly recommended for moderate and severe acute traumatic brain injury (TBI).

      Ofatumumab is a new agent that may delay progression of MS.

 Chapter 10: Dermatology

 Minocycline foam is a new topical drug option for moderate to severe acne vulgaris.

       Melanloma: Nivolumab plus ipilimumab in metastatic melanoma has confirmed long-term survival. With sun-protective behavior, melanoma incidence is decreasing.

       New: Tazemetostat is suggested in patients with locally advanced or metastatic epithelioid sarcoma (rare and aggressive) ineligible for complete surgical resection.

       Psoriasis: New therapies for severe psoriasis and psoriatic arthritis: a TNF-alpha inhibitor (infliximab or adalimumab, golimumab) or IL-inhibitor (etanercept or ustekinumab) is effective. Ixekizumab is a newly approved monoclonal antibody against IL-17A. Clinical data support vigilance for signs of symptoms of malignancy in patients with psoriasis.

     Chapter 11: GYH

      Breast cancer:        Although combined CDK 4/6 and aromatase inhibition is an effective strategy in older adults with advanced receptor-positive, HER2-negative breast cancer, toxicities (myelosuppression, diarrhea, and increased creatinine) should be carefully monitored. SC trastuzumab and pertuzumab is newly recommended for HER2-positive breast cancer.

      Whole breast irradiation is suggested for most early-stage breast cancers treated with lumpectomy. Accelerated partial breast irradiation can be an alternative for women ≥50 years old with small (≤2 cm), hormone receptor-positive, node-negative tumors.

      Endocrine therapy is recommended for breast cancer prevention in high-risk postmenopausal women.

      Uterine fibroids: Elagolix (oral gonadotropin-releasing hormone antagonist) in combination with estradiol and norethindrone is for treatment of heavy menstrual bleeding (HMB) due to uterine fibroids.

      Chapter 12: OB

      Table 12-6: Active labor can start after OS > 4cm, and 6cm is relatively more acceptable but not a strict number.

      Table 12-7: Preeclampsia is a multisystem progressive disorder characterized by the new onset of hypertension and proteinuria, or of hypertension and significant end-organ dysfunction with or without proteinuria, in the last half of pregnancy or postpartum. Once a diagnosis of preeclampsia is established, testing for proteinuria is no longerdiagnostic or prognostic. “proteinuria>5g/24hours” may only indicate the severity.

      Mole: For partial moles, obtain a confirmatory hCG level one month after normalization; for complete moles, reduce monitoring from 6 to 3 months post-normalization.

      Chapter 14: EM

SHOCK RESUSCITATION

Emergency treatment—critical care!

“A-B-C”: Breathing: …In mechanically ventilated adults with critical illness in ICU, intermittent sedative-analgesic medications (morphine, propofol, midazolam) are recommended.

 Chapter 15: Surgery

      Surgery and Geriatrics: Hemiarthroplasty is a suitable option for patients who sustain a displaced femoral neck fracture.

    Chapter 16: Psychiatry

     Depression: Both short-term and maintenance therapies with esketamine are beneficial for treatment-resistant depression.

Schizophrenia: Long-term antipsychotics may decrease long-term suicide mortality.

Narcolepsy: Pitolisant is a novel oral histamine H3 receptor inverse agonist used in narcolepsy patients with poor response or tolerate to other medications. Oxybate salts, a lower sodium mixed-salt formulation of gamma hydroxybutyrate is for treatment of narcolepsy with cataplexy.

     Chapter 17: Last Chapter

PEARLS—Table 17-9:  Important Immunization Schedules for All (2020, USA)

Vaccine                 Birth       2M          4M          6M          12-15M                 2Y          4-6Y       11-12Y       Sum

HAV                                                                                       1st                          2nd (2-18Y)                            2 doses

HBV                      1st           2nd                        3rd (6-12M)                                                                             3 doses

DTaP                                    1st            2nd         3rd          4th (15-18M)                        5th                             + Td per 10Y

IPV                                       1st           2nd         3rd (6-18M)                                         4th                             4 doses

Rotavirus                            1st           2nd                                                                                                         2 doses

Hib                                       1st           2nd         (3rd)       (3-4th)                                                                    3-4 doses

MMR                                                                                    1st                                         2nd                              2 doses

Varicella                                                                              1st                                         2nd                        + Shingles at 60Y

Influenza                                                            1st (IIV: 6-12Y; LAIV: >2Y                (2nd dose)               1-2 doses annually

PCV                                     1st           2nd         3rd          4th                                                                        PCV13+PPSV at 65Y

MCV (Men A, B)                                                                                                                                1st         Booster at 16Y

HPV                      9-12Y starting: <15Y: 2 doses (0, 6-12M); >15Y or immunosuppression: 3 doses (0, 2, 6M).

Chapter 17 HYQ answer 22: No routine prostate cancer screening (including PSA) is recommended and answer “G” is still correct–PSA

screening among healthy men is not routinely done but should be indicated in a patient with two risk factors.

[defibrillatoraus]

5 Major Defibrillator Mistakes To Avoid

Imagine a person having a heart attack and want to help them, but you don’t know what to do. That’s why we suggest our customers buy Defibrillator Accessories that will help them to take quick action and save a life.

However, many people who have one make numerous mistakes and end up with a non-reliable defibrillator.

Following are the major mistakes that you must avoid.

Not Storing AED Properly

You have to make sure that your AED is easy to access. It should take no more than 3 minutes to recover the device; that’s almost 90sec each way.

Storing items in front or top of the defibrillator can slow you when retrieving them.

Even a single second can lead to tragedy.

It’s a good start to place AED in a high traffic area. You can also choose an easy-to-access cabinet for reaching the defibrillator.

AED Instructions

In case you are setting an AED, if someone has collapsed, there will be higher chances of adrenaline rushing through you.

It is crucial to stay calm and emphasis instruction.

An average person with no proper medical training can also use an AED as it has audio and visual instructions, which helps you save lives.

From basic instructions such as ‘emergency call’ to specifics such as ‘remove the shirt and jeweler of the patient.

You are not expected to be an AED expert, but you have to follow its instructions properly.

AED Or CPR

Knowing the right time to use an AED versus a CPR can be confusing for anyone.

Successful defibrillation must be supported with top-quality CPR practices. The first analysis of AED is quite critical. If it’s showing no shock, only quality CPR can direct to a shockable rhythm on the next heart examination. In case the first analysis calls for a shock, once you have delivered it, the stunned heart greatly needs blood as it recognizes and regains its natural heartbeat.

Numerous products have featured CPR help. This method gives you real-time feedback on the depth and rate of your compression.

This indicates that you can focus on saving a life and not panicking.

Placement Of Pad

If the pads are not placed in the right position, the AED will not send any electric shock to the victim.  As technology enhances, it is becoming easier to avoid mistakes.

With today’s innovative products such as Heartsine Defibrillator , these come with advanced technology that addresses this issue with CPR-D pads for their AED Plus unit.

The one-piece pad if fast and accurate to place. It also involves a chest goal that you can use for supplying the most effectual CPR.

AED Maintenance

Do you know the upkeep schedule for your AED?

If not, it’s better to consult the seller before making your purchase because they will make you familiar with all the crucial maintenance tips that will make your defibrillator durable and better functioning.

So make sure to avoid the above mistakes with your Defibrillator Accessories.

For more information, consult your seller and ask him certain questions to clear your doubts.

Related: WHY IS IT IMPORTANT TO LOOK OUT FOR REGULAR DEFIBRILLATOR MAINTENANCE?

[aedauthorityau]

All You Need To Know About Defibrillators.

Your life is precious and it's your responsibility to save it from the unwanted circumstances but some situational events occur unexpectedly and unfortunately, you can't control them sometimes, Sudden Cardiac Arrest is one of them. Cardiac Arrest can affect anyone at any time. More than 30,000 cases occur every year outside the hospital premises and it is very unfortunate to hear. With a speedy emergency treatment, chances of survival whooping up by 80%.

CPR and AED can increase the chances of survival if it is given on time that is within 4 minutes. Yet, terrifyingly, the normal ambulance arrival time in an urban area is a full eleven minutes. If we see previous studies then more than 20% of cases occur outside the hospital premises. If you experience an arrest out and about, you would be reliant on the public’s capacity to deliver CPR and indeed the availability of a defibrillator. 

If you use CPR alone it can double the chances of survival but when you aid CPR with AED then the rate of survival increases up to 6% to74% - an incredible difference. 

Here is a brief about AEDs.

What Are AEDs?

Defibrillators are the brightly colored boxes you can see in the supermarkets, churches, schools, tube, in buses, airports, railway stations, and other high traffic areas and other public places.

How does a defibrillator work? 

An AED is an Automated External Defibrillator so it's clear that it automatically detects if someone is in a shockable rhythm and it speaks to you, to tell you what to do. When you give a defibrillator to a person in the state of sudden Cardiac Arrest defibrillators do not jump start the heart like a jump start a car they stop it like rebooting a computer. When sudden cardiac arrest occurs so definitely it doesn't shut your heart completely but it disturbs your heart rhythm and with the help of a defibrillator this enables the individual heart cells to restore concurrently and conceivably start it in a normal rhythm. 

A defibrillator is a powerful kit and with the help of the outstanding device, you can save the lives of your loved ones. The defibrillator delivers a shock to stop the heart if it is an irregular rhythm but a shockable rhythm. It enables the heart's system to reboot and hopefully starts the normal sinus rhythm. 

Different reports have shown that deploying a defibrillator within 3-5 minutes of collapse can increase the chances of survival as high as 50-70%.

Where can you find them? 

Nowadays with the advancement of technology defibrillators are easily accessible. AEDs are easily accessible at several locations which include shopping centers, railway and tube stations, airports, sports grounds, and available for the general public use as well. 

The defibrillator comes in two categories, the first one is Semi-Automatic and the second one is fully automatic. In semi-automatic, you have to press a shock switch when symbolized and in fully automated the machine shocks automatically when a shock is suggested. 

Why are defibrillators important? 

As I said earlier defibrillators are life-saving devices, the AED is necessary to deliver the shock hopefully returning the heart to a viable rhythm.

Most sudden cardiac arrests result from ventricular fibrillation. Ventricular Fibrillation is a fast erratic heart rhythm originating in the heart ventricles. 

AED is only indicated when a person falls unconscious and doesn't breathe normally. An AED will only enable a shock to be given if someone is in a shockable rhythm – Ventricular Fibrillation or Ventricular Tachycardia, the machine will recognize the rhythm and tell whether or not a shock is recommended.

The Chain Of Survival.

The faster you recognize there is a problem, get help on the way, start CPR, use a defibrillator, and transfer the casualty to advanced medical care, the better the outcome.

How to use an AED? 

AED is very simple to use but it's with advised instruction. When you find that a person is suffering from Sudden Cardiac Arrest you just have to activate AED and it will talk to you and tell you what to do.

If you are looking for authenticated Defibrillator Suppliers in Australia then AED Authority is your one-stop destination. We provide several suitable options to tackle your AEDs needs.

AED Authority Heartsine Samaritan Defibrillator is available. Heartsine Samaritan Defibrillator designed specifically for public, non-medically-trained personnel use, the HeartSine AED is absolutely suited for all common gathering place, including institutions, fitness clubs, gyms, fitness centers, work places, home complexes, airports, and homes, because you never know when a heart attack or SCA caused by an arrhythmia can happen. With manageable, easy-to-use commands and a crystal display, the HeartSine AED defibrillator can be employed by nearly anyone.

Like Heartsine Samaritan Defibrillator there are n number of brands offered by AED Authority and if you are in need don't hesitate to visit our website. 

These are the important things you should know about AEDs. We wish you a magnificent and healthy life ahead. 

[confused-scientist]

Things I learned in Med School - Weeks 133 - 134

So started my first two week in the emergency department.

Started my first week doing afternoon shifts - which was a pretty chill way to start the block. Basically got to go to the gym, do a bit of study, before grabbing lunch and attending our (almost) daily ED tutorials, and then starting around about 2ish and hanging around until like 6pm and then heading home.

I also had my practice long case presentation during this week in front of two consultants + an audience. I was kind of lucky in that I went in the morning, so the crowd was minimal (where as those in the afternoon always have close to full houses). I was pretty nervous about it, its always hard doing these sort of things, esp in FRONT of other people, but it went really well and I kind of crushed the Qs tbh. So I’m feeling slightly more comfortable about the long case... but I also not getting too cocky b/c you never know what sort of patient or examiners you are going to get on the actual day.

We also got to attend STAR training - which is mainly for after hour residents - on hypotension. It was quite fun as they got both me and T (the fellow med student attending) part of the team, but my resident made me do all the phone calls but hadn’t really told me all the relevant information needed so all the “consultants” kept yelling and hanging up on me... which tbh fair.

We also had ICU sim training for ALS stuff the week after. This was pretty fun - but our sim was hit by technical issues. Our “patient”/dummy was in VT, so we defib’d and then they transitioned into asystole - so we went into the non-shockable algorithm and kept dumping charges and giving adrenaline... but it was actually just that the defib stopped reading the rhythm... so our instructor was like “omg why are these idiots dumping the charge for an VT?!?!”... took them like 5 min to realise that we were just getting a flat line... and as we all know you don’t shock in asystole.

Last week in ED was quite good - got to do some suturing which was fun and something I can actually do, and failed a bunch load of cannulas which I’m discovering that I really suck at.

One like my first day in ED one of the consultants said to me “Look, I know all med students think they are amazing at bloods and cannulas, but let me tell you now you’ll be rubbish when you start here.”

My response: “Oh no don’t worry, I already know I’m terrible”

Honestly, I’m starting to get a complex lol.

Two more week of ED to finish up crit care!

Anyway, here are some things I learned in Med School this week:

1. Sepsis is from the greek word ‘to putrefy’

2. In sepsis, administering antibiotics within 4 - 8 hours reduced mortality.

3. Studies have shown that putting your dominant hand down on someones check (aka your right hand if you are right-handed) give more effect chest compressions in CPR.

Quotes of the Week:

“No one here is really allowed to die without steroids” - ICU consultant on the usage of steroid in the ICU

“My rule of thumb - if you lay the patient down and their stomach is higher than their nose... you intubate them because gravity is not on your side” - Anaesthetics consultant

‘til next time

[thehouseofthebrave]

Basic and advanced first aid. I know you can’t do proper CPR form but you could at least do the speed and STOP SHOCKING NON SHOCKABLE RHYTHMS.

what skills do yall have that make you annoying abt seeing people do it in media. i’ll go first i ran track for 6 years (first distance then sprinting) and i am physically incapable of not commenting on people’s running form