#heart block

[mcatmemoranda]

Going through the ACLS online training:

The P wave represents depolarization of the atrial myocardial cells.

The PR interval represents the time from the beginning of atrial depolarization to the beginning of ventricular depolarization. It is measured from the beginning of the P wave to the beginning of the QRS complex. The normal duration of the PR interval is 120 to 200 milliseconds.

The QRS complex represents depolarization of the ventricular myocardial cells. The normal duration of the QRS complex is less than 120 milliseconds.

The J point is the point where the QRS complex ends and the ST segment begins.

The T wave represents repolarization of the ventricular myocardial cells. (Atrial repolarization occurs during ventricular depolarization and is not seen on the ECG; it is overshadowed by the depolarization of the larger ventricles).

The QT interval is measured from the beginning of the QRS complex to the end of the T wave. This encompasses the time from ventricular depolarization to the end of repolarization.

The ST segment represents the time between the end of ventricular depolarization and the beginning of ventricular repolarization. It is measured from the end of the QRS complex to the beginning of the T wave.

Is the amount of time between each P wave the same? What about the amount of time between each QRS complex (i.e., the RR interval)?

To estimate the atrial rate, count the number of P waves over a 6-second period and multiply by 10. To estimate the ventricular rate, do the same with the QRS complexes. Alternatively, if the rhythm is regular, divide 300 by the number of large squares between two P waves (to get the atrial rate) and between two R waves (to get the ventricular rate). If the heart rate is very fast, divide 1500 by the number of small squares between two P waves (to get the atrial rate) and between two R waves (to get the ventricular rate). Are the atrial and ventricular rates the same or different? Are they within normal limits?

Look for the P waves. Are they there? Do all the P waves have the same morphology? Is there one––and only one––P wave associated with each QRS complex? Note that in lead II, the P waves are usually upright but in lead V1, the P waves may be inverted or biphasic.

Measure the QRS complex. Is it within the normal range? (QRS complexes that exceed 120 milliseconds in duration are abnormal.) Do all the QRS complexes have the same morphology?

Look for the T waves. Are they there? If so, do all the T waves have the same morphology? The direction of the T wave should be the same as that of the main vector of the QRS. The T waves should be less than 5 millimeters in amplitude in the limb leads and less than 15 millimeters in amplitude in the precordial leads.

Measure the PR interval. Is it within the normal range? Is it consistent throughout the tracing? If it varies, is the variation predictable?

Measure the QT interval and calculate the corrected QT interval. Because the QT interval varies normally with the heart rate, the corrected QT interval (QTc) is used to give a value that is theoretically independent of rate. The QTc adjusts for heart rate differences by dividing the QT interval by the square root of the RR interval (i.e., one cardiac cycle). In general, a QTc greater than 460 milliseconds is considered to be prolonged. If the heart rate is faster than 120 bpm or slower than 50 bpm, the formula for calculating the QTc is not considered valid and should not be used.

Look at the ST segment. Is it elevated or depressed from the baseline?

Determine the rhythm and its clinical significance. Is the patient showing signs or symptoms? Is the rhythm potentially life-threatening?

In normal sinus rhythm:

Each P wave is linked in a 1:1 fashion to each QRS complex (i.e., atrial depolarization is always linked to ventricular depolarization).

The P waves are uniform in shape, indicating that the SA node is the only pacemaker driving atrial depolarization.

P waves in lead II are normally upright and all the same shape. P waves in lead V1 are normally inverted (or on occasion biphasic) and all the same shape.

The rhythm is regular (but may vary slightly during respirations).

The rate ranges between 60 and 100 bpm.

Causes of sinus bradycardia include:

Vagal stimulation.

Myocardial infarction.

Hypoxia.

Medications (e.g., β-blockers, calcium channel blockers, digoxin).

Coronary artery disease.

Hypothyroidism.

Iatrogenic illness.

Inflammatory conditions.

First-degree AV block is characterized by a prolonged delay in conduction at the AV node or bundle of His. The impulse is conducted normally from the sinus node through the atria, but upon reaching the AV node, it is delayed for longer than the usual 0.2 second. In first-degree AV block, although the impulses are delayed, each atrial impulse is eventually conducted through the AV node to cause ventricular depolarization.

First-degree AV block may be a normal finding in athletes and young patients with high vagal tone. It can also be an early sign of degenerative disease of the conduction system or a transient manifestation of myocarditis or drug toxicity.

In second-degree AV block type I (also called Mobitz type I or Wenckebach block), impulses are delayed and some are not conducted through to the ventricles. After three or four successive impulse delays, the next impulse is blocked. After the blocked impulse, the AV node resets, and the pattern repeats. Second-degree AV block type I usually occurs at the AV node but may be infranodal.

Because the block usually occurs above the bundle of His, conditions or medications that affect the AV node (such as myocarditis, electrolyte abnormalities, inferior wall myocardial infarction or digoxin) can cause second-degree AV block type I. This type of arrhythmia can also be physiologic.

Second-degree AV block type I rarely produces symptoms. Some patients may have signs and symptoms similar to sinus bradycardia.

In second-degree AV block type II (Mobitz type II), the block occurs below the AV node, in the bundle of His. As with second-degree AV block type I, some atrial impulses are conducted through to the ventricles, and others are not. However, there are no progressive delays. The blocked impulses may be chaotic or occur in a pattern (e.g., 2:1, 3:1 or 4:1). In high-grade second-degree AV block type II, the ratio is greater than 2:1 (i.e., 3:1, 4:1, or variable).

Second-degree AV block type II is always pathologic. It is usually caused by fibrotic disease of the conduction system or anterior myocardial infarction.

Patients may present with light-headedness or syncope, or they may be asymptomatic. The clinical presentation varies, depending on the ratio of conducted to blocked impulses.

In third-degree (complete) AV block, no impulses are conducted through to the ventricles. The block can occur at the level of the AV node but is usually infranodal. Pacemaker cells in the AV junction, bundle of His or the ventricles stimulate the ventricles to contract, usually at a rate of 30 to 45 bpm. This means that the atria and ventricles are being driven by independent pacemakers and are contracting at their own intrinsic rates (i.e., 60 to 100 bpm for the atria and 30 to 45 bpm for the ventricles), a situation known as AV dissociation.

Degenerative disease of the conduction system is the leading cause of third-degree AV block. This arrhythmia may also result from damage caused by myocardial infarction, Lyme disease or antiarrhythmic drugs.

If ventricular contraction is stimulated by pacemaker cells above the bifurcation of the bundle of His, the ventricular rate is relatively fast (40 to 60 bpm) and reliable, and symptoms may be mild (such as fatigue, orthostatic hypotension and effort intolerance). However, if ventricular contraction is stimulated by pacemaker cells in the ventricles, the ventricular rate will be slower (20 to 40 bpm) and less reliable, and symptoms of decreased cardiac output may be more severe.

First-Degree AV Block

In first-degree AV block, normal P waves are followed by QRS complexes, but because the impulse is delayed at the AV node or bundle of His, the PR interval is longer than normal (i.e., it exceeds 200 milliseconds). Each P wave is linked in a 1:1 fashion to each QRS complex. QRS complexes of normal duration suggest that the delay is occurring at the level of the AV node, whereas wide QRS complexes suggest that the delay is infranodal.

Regularity: regular Rate: variable, can occur with normal rate, bradycardia or tachycardia P wave: upright and uniform, one for every QRS complex QRS complex: < 0.12 second PR interval: > 0.20 second

Second-Degree AV Block Type I

Because some impulses are not conducted through to the ventricles, the ratio of P waves to QRS complexes is greater than 1:1. Because each impulse is delayed a little more than the last until eventually one impulse is completely blocked, the ECG shows progressive lengthening of the PR interval with each beat, then a P wave that is not followed by a QRS complex (a “dropped beat”). In most cases, the RR interval decreases before each dropped beat. After the dropped beat, impulse conduction through the AV node resumes and the sequence repeats.

Regularity: irregular in a pattern Rate: variable, usually < 100 bpm P wave: upright and uniform; more P waves than QRS complexes QRS complex: < 0.12 second PR interval: becomes progressively longer until a P wave is not conducted, then cycle repeats.

Second-Degree AV Block Type II

Second-degree AV block type II is characterized by a constant PR interval. Because impulses are intermittently blocked, there are more P waves than QRS complexes.

Regularity: regular (2:1), unless conduction ratio varies Rate: usually < 100 bpm (atrial and ventricular), tendency for bradycardia P wave: upright and uniform; more P waves than QRS complexes (2:1, 3:1, 4:1 or variable) QRS complex: < 0.12 second PR interval: < 0.20 second or prolonged; constant for every QRS complex.

Third-Degree AV Block

In third-degree AV block, there is no electrical communication between the atria and ventricles, so there is no relationship between P waves and QRS complexes. The RR interval is constant. The PP interval is constant or slightly irregular. If pacemaker cells in the AV junction stimulate ventricular contraction, the QRS complexes will be narrow (less than 120 milliseconds in duration). Impulses that originate in the ventricles produce wide, bizarre QRS complexes.

Regularity: usually regular RR interval, regular PP interval Rate: varies depending on escape focus; junctional (40–60 bpm) and ventricular (< 40 bpm) P wave: upright and uniform, more P waves than QRS complexes QRS complex: < 0.12 second if junctional escape, ≥ 0.12 second if ventricular escape PR interval: total dissociation from QRS complexes

Tachyarrhythmias can be categorized as narrow complex or wide complex.

Narrow-complex tachyarrhythmias include sinus tachycardia, atrial flutter, atrial fibrillation and supraventricular tachycardia. These tachyarrhythmias usually originate in the atria or AV node and run normally through the bundle branches, producing a normal QRS complex.

Wide-complex tachyarrhythmias originate in the ventricles and include ventricular tachycardia (monomorphic and polymorphic) and ventricular fibrillation. Supraventricular tachycardia with aberrant conduction can also produce a wide-complex tachyarrhythmia.

Sinus tachycardia is the most common tachyarrhythmia. It is identical to normal sinus rhythm, except the rate is between 100 and 150 bpm.

Atrial flutter is caused by an ectopic focus in the atria that causes the atria to contract at a rate of 250 to 350 bpm. The underlying mechanism of atrial flutter is most often a re-entrant circuit that encircles the tricuspid valve annulus.

Supraventricular tachycardia (SVT) is an arrhythmia originating above the ventricles. In general, the rate is greater than 150 bpm, which helps to differentiate SVT from sinus tachycardia. SVT can be classified as AV nodal re-entrant tachycardia (AVNRT), AV-reciprocating tachycardia (AVRT) and atrial tachycardia.

This rhythm is seen in patients with:

Low potassium and magnesium levels.

Family history of tachycardia.

Structural abnormalities of the heart.

Adverse reactions from certain pharmacologic agents (e.g., antihistamines, theophylline, cough and cold preparations, appetite suppressants).

Certain medical conditions (e.g., cardiovascular disease, long-term respiratory disease, diabetes, anemia, cancer).

Illicit drug use.

Atrial fibrillation is caused by multiple ectopic foci in the atria that cause the atria to contract at a rate of 350 to 600 bpm. Rarely, the atrial rate may be as high as 700 bpm. The AV node only allows some of the impulses to pass through to the ventricles, generating an irregularly irregular rhythm that is completely chaotic and unpredictable.

Atrial fibrillation can occur in young patients with no history of cardiac disease. Acute alcohol toxicity can precipitate an episode of atrial fibrillation in otherwise healthy patients. However, atrial fibrillation commonly occurs in the presence of underlying heart disease, lung disease, hyperthyroidism or myocardial infarction.

Ventricular tachycardia occurs when a ventricular focus below the bundle of His becomes the new pacemaker. The ventricles contract rapidly (usually at a rate faster than 100 bpm) and usually with a regular rhythm. The rapid ventricular rate significantly diminishes cardiac output and can only be sustained for a short period before the patient becomes hemodynamically compromised. Ventricular tachycardia can quickly turn into ventricular fibrillation, leading to cardiac arrest.

In atrial flutter, atrial contraction occurs at such a rapid rate that discrete P waves separated by a flat baseline cannot be seen. Instead, the baseline continually rises and falls, producing the “flutter” waves. In leads II and III, the flutter waves may be quite prominent, creating a “sawtooth” pattern. Because of the volume of atrial impulses, the AV node allows only some of the impulses to pass through to the ventricles. In atrial flutter, a 2:1 ratio is the most common (i.e., for every two flutter waves, only one impulse passes through the AV node to generate a QRS complex). Ratios of 3:1 and 4:1 are also frequently seen.

Regularity: usually regular (could be irregular with variable conduction) Rate: varies with conduction; < 100 bpm is controlled; > 100 bpm is uncontrolled (rapid ventricular response); usually has ventricular rates of 75 bpm (4:1), 100 bpm (3:1) or 150 bpm (2:1), depending on conduction ratio P wave: none; flutter (F) waves; characteristic “sawtooth” baseline QRS complex: < 0.12 second PR interval: not discernible

Supraventricular Tachycardia

In supraventricular tachycardia (SVT), the P waves may be absent or abnormal. There is minimal to no beat-to-beat variability and the heart rate is usually greater than or equal to 150 bpm.

Regularity: regular; minimal beat-to-beat variability Rate: > 150 bpm P wave: absent or not clearly identifiable QRS complex: < 0.12 second PR interval: if P waves are visible, PR interval may be shortened or lengthened depending on mechanism

Atrial Fibrillation

The two key features of atrial fibrillation on ECG are the absence of discrete P waves and the presence of irregularly irregular QRS complexes. The baseline appears flat or undulates slightly, producing fibrillatory waves.

Regularity: irregularly irregular Rate: varies with conduction; < 100 bpm is controlled; > 100 bpm is uncontrolled (rapid ventricular response) P wave: none; fibrillation (f) waves; chaotic baseline QRS complex: < 0.12 second PR interval: not discernible

Monomorphic Ventricular Tachycardia

In ventricular tachycardia, the QRS complexes are wide (lasting longer than 120 milliseconds) and bizarre in shape. When there is only one ectopic focus in the ventricles, monomorphic ventricular tachycardia is seen on the ECG (i.e., the QRS complexes are generally the same bizarre shape). Monomorphic ventricular tachycardia may also be seen with reentrant rhythms.

Regularity: regular Rate: > 100 bpm P wave: not discernible QRS complex: ≥ 0.12 second, uniform in shape PR interval: not discernible

Polymorphic Ventricular Tachycardia

In polymorphic ventricular tachycardia, which occurs when there are two or more ectopic foci, the QRS complexes vary in shape and rate.

Regularity: irregular (can appear regular due to fast rate) Rate: > 100 bpm P wave: not discernible QRS complex: ≥ 0.12 second, variable in shape PR interval: not discernible

[bevanne46]

Scrappy Heart Block by Corey Download the Scrappy Heart Block PDF Pattern here HTTPS://CORIANDERQUILTS.COM/WP-CONTENT/UPLOADS/2023/05/SCRAPPY-HEART-BLOCK.PDF

[hinamie]

mwah

[divinehearthospital]

Angioplasty is a type of cardiac surgery procedure to improve blood flow in coronary arteries that have become narrow or blocked. People who have had a heart attack or with coronary artery disease may require coronary angioplasty.

[cryptidclownz]

them and their shit❤️

[shilohhastings]

I got the beautiful RadioApple print signed by Jeremy Jordan and Amir Talia as a birthday present from my husband.

I’m obsessed.

[cicada-heart]

hand printed muslin & felt patches 🌿

etsy

[thiccsys]

can i be cured of art block?!!

[anetherealpoetess]

Neil Gaiman, let’s be realistic. A 21-year-old working in the home of a man four decades her senior cannot truly give meaningful consent to any type of sexual encounter, let alone within mere hours of meeting him. Even though you are denying it was not consensual, the fact you have conceded the sexual encounter did happen at all is a full confession. You are, by your own admission, a predator.

[mcatmemoranda]

This is a helpful chart.

[xamnade]

lonely dog

[piedpip3rrr]

MORE VOLLEYBOYS AU

[1000sunnygo]

Law is a lovable character. But I think it blinds people to his flaws.

If Kidd's defeat is considered karma for his bad decisions and bad leadership, the same applies to Law. In fact, in some ways, Law did worse than Kidd. Heart pirates were the least prepared for the race to claim One Piece.

Without Law, Heart pirates had no name and no face. It wasn't because they worked as a team, I think there was an intention to keep them under a veil of protection. Law's appearance contrasted the rest of his crew mates. He pulled the world's attention towards solely himself, perhaps so his friends could mix within the crowd as civilians when he's gone..

Similar to Luffy, Law wasn't particularly looking for strong people. Now take Usopp as an example. He was a regular village boy with great sharpshooting skills. Roughly, he had the same starting point as Penguin and Shachi, but now he's leagues above them bounty and achievement-wise. Straw hats' journey had a clear aim to be the very best, each of them faced the worst adversaries and grew as the crews of the future Pirate king. Penguin and Sachi, on the other hand, spent over a decade with a Captain who they believed was aiming for a great treasure, when in reality, the Captain was stuck in his own world. He was fighting a lone battle with his friends completely left in the dark.

The lack of transparent communication weakened the crew's foundation. They were sheltered by an overprotective captain, it stunted their growth. In fact, it was simply dishonest of Law to lie about his ambition.

Law's detailed background wasn't decided back then, I think we can overlook this one. When Oda drew the panel above, I'm pretty sure Law in his mind was a much more grey character.

Kidd pirates knew what Kidd wanted. They joined their Captain's reckless adventures willingly and gleefully, Kidd never let them feel like a burden. Zoro and Killer could fight beside their captains on the rooftop, but Bepo - a polar bear mink with a great potential - wasn't ready to be there.

Law realized his goal to claim One Piece only a few days prior to leaving wano, and instead of taking time to grow as a team, he marched ahead to join the flow. I don't think he had many options, but it doesn't hurt to acknowledge his shortcomings.

At the end of day, Blackbeard can't be blamed for playing the game like a pirate. The fault was Law's. His crew was trained to tame the depth of the northern sea, not to find their place in a titan's battle royale.

[zephyo]

hot siren summer🧛‍♀️