#ventricular pressure

[er-cryptid]

Ventricular Ejection

-- follows isovolumetric ventricular contraction

-- both ventricles continue to contract

-- the ventricular pressures exceed aortic and pulmonary arterial pressure

-- the aortic valve and pulmonary valve open

-- blood is ejected into aorta and pulmonary artery

[macgyvermedical]

The Difference Between Heart Attack, Heart Failure, and Cardiac Arrest

I think fiction has done us a huge disservice when they conflate the above, but even my nursing students were kind of on the edge of not understanding this, so we're gonna talk about it here.

Heart Attack: A blockage in the coronary arteries

A heart attack, also called a myocardial infarction, is when one of the arteries that supplies the actual muscle of the heart gets blocked by a blood clot. When this happens, the muscle the artery was supplying starts to die. The more muscle impacted, or the longer the heart attack goes untreated, the worse the outcome for the patient.

Symptoms of this are different between men and women:

Treatment for a heart attack usually involves inserting a small tube into the wrist or groin, snaking it up to the blocked artery, and stenting open the blockage, thus returning blood flow to the heart muscle.

Heart Failure: A problem with the heart's ability to pump

Heart failure occurs when the heart is not beating hart enough or well enough to adequately get blood out to the body. This can occur for several reasons. It can be because of damage from a heart attack, because a valve in the heart isn't working right, from poorly functioning electrical system, or from long term exposure to untreated high blood pressure.

The symptoms of heart failure come both from blood collecting "in front" of the heart waiting to get pumped (swelling, shortness of breath, weight gain), and not enough blood getting pumped out to the body (dizziness, fatigue).

Heart failure is treated with medications that make the heart beat more normally and get rid of excess fluid to take workload off the heart. It can also be treated with surgery if the problem is with a valve, or with a pacemaker if the heart is beating too slowly.

Cardiac Arrest: A problem with the heart's electrical system

The heart beats in a synchronized way because it is made of muscle cells that are responsive to electricity. Special cells called pacemaker cells generate small electrical currents, which wash over the heart. When the cells are stimulated with that current, they contract, creating a beat.

Cardiac arrest occurs when that normally organized current becomes disorganized, and lots of cells, not just the pacemaker cells, start making their own currents. This can happen because of a lack of oxygen, too much or too little of particular electrolytes like potassium, an electrical shock, or damage to the muscle from a heart attack.

See below for a comparison between the normal electrical activity of the heart (top) and the disorganized rhythm of ventricular fibrillation:

When the electrical rhythm is disorganized, the heart isn't beating, just quivering, and no blood gets out to the body. This is treated with CPR to keep some blood flowing to vital organs, medications that can stabilize the heart's electrical system, and defibrillation. Defibrillation works by stopping the heart with an overwhelming amount of electricity and letting it restart (hopefully) in a normal rhythm.

If someone has no electrical activity in their heart (known as asystole), defibrillation won't work, but sometimes medication will.

[literaryvein-reblogs]

Writing Notes: Caffeine

Caffeine - A mild alkaloid stimulant made by some plants.

Found in coffee beans, tea leaves, and cocoa beans; added to soft drinks, energy drinks, and energy bars; and sold in capsules and tablets as a dietary supplement.

A mild stimulant. It is used to temporarily relieve fatigue and increase mental alertness. Caffeine is added to some antihistamine drugs to help counteract the sleepiness they may cause. It is also added to over-the-counter headache remedies (e.g., Excedrin) and migraine headache drugs to enhance their painkilling effects. Under medical supervision, citrated caffeine (a prescription drug) is used to treat breathing problems in premature infants.

From the Italian word cafée, meaning "coffee", is naturally made by about 60 plants. The most familiar of these are coffee leaves and beans, tea leaves, kola nuts, yerba mate, guarana berries, and cacao (the source of chocolate). In plants, caffeine is a pesticide. Insects eating plants that contain caffeine become disabled or die.

It has no nutritional value. But there seem to be some benefits to regular caffeine consumption, despite conflicting research.

Effects on the Body

Increases heart rate

Temporarily increases blood pressure

Relaxes smooth muscle cells in the airways

Releases fatty acids and glycerol in the body for energy use

Easily crosses the blood-brain barrier and changes the level of neurotransmitters in the brain

Passes into breast milk

Caffeine is absorbed in the stomach.

Its effects are noticeable in about 15 minutes and usually last several hours.

However, there is a huge variation among people both in their sensitivity to caffeine and in how long it stays in their bodies.

Although the average time it takes half a dose of caffeine to be eliminated from the body is 3-4 hours, this time may extend to 6 hours in women taking oral contraceptives; much longer in pregnant women and in people with liver damage.

Many well-designed, well-documented studies show that caffeine makes people more alert, improves short-term memory, enhances the ability to concentrate, increases the individual’s capacity for physical work, and speeds up reaction time.

In habitual caffeine drinkers, caffeine achieves this by preventing the detrimental effects of withdrawal.

It does not boost functioning to above normal levels.

All of these effects are temporary.

Caffeine does not replace the need for rest or sleep.

Caffeine Withdrawal

Discontinuing caffeine among regular users can cause withdrawal symptoms. These can include:

Headaches (very common)

Irritability

Nausea

Fatigue

Sleepiness

Inability to concentrate

Mild depression

Caffeine withdrawal symptoms begin 12–24 hours after caffeine is stopped.

Withdrawal symptoms peak at around 48 hours, and can last up to 5 days.

Tapering caffeine use, for example cutting down on caffeine by the equivalent of half a cup of coffee (about 50 mg) a day, minimizes or eliminates withdrawal symptoms.

Caffeinism

People who consume more than 500 mg of caffeine a day—equivalent to about five cups of coffee—may develop a condition called caffeinism, though the threshold varies among individuals.

Produces unpleasant sensations, some of which are similar to withdrawal symptoms. Symptoms of Caffeine Overuse include:

Restlessness

Irritability

Nervousness

Anxiety

Muscle twitching

Headaches

Inability to fall asleep

A racing heart

Related Disorders

Severe overuse of caffeine can cause a number of related disorders, including:

Caffeine Intoxication—usually the result of taking caffeine pills (e.g., NoDoz), this condition causes mental changes, rambling thoughts and speech, irregular heartbeat, and other symptoms associated with overuse. In severe cases death can result from ventricular fibrillation (unsynchronized contractions of the ventricle of the heart).

Caffeine-Induced Anxiety Disorder—severe anxiety that interferes with daily social interactions and occurs after caffeine intoxication or heavy long-term use of caffeine.

Caffeine-Induced Sleep Disorder—an inability to sleep that is so great it requires medical/psychiatric attention and occurs after prolonged caffeine consumption.

Non-Specific Caffeine-Induced Disorder—disorders not listed that are attributable to either acute or long-term caffeine consumption.

Source ⚜ More: Writing Notes & References ⚜ Describing Food ⚜ Cocktails

[cardiacreports2]

Paramedic Incident Report

Incident Number: 2024-19245 Date: December 6, 2024 Time of Call: 15:23

Incident Location: ClimbX Indoor Gym, 345 Summit Street, Boulder, CO

Patient Information:

Name: Daniel Carson

Age: 20

Gender: Male

Height: 5'11"

Weight: 165 lbs

Physical Description: Lean and muscular build with well-defined arms and torso typical of an experienced climber. Short dark brown hair, light complexion.

Description of Incident: At 15:23, dispatch received a 911 call reporting a young male climber had collapsed while bouldering at an indoor climbing facility. The patient was reportedly scaling a mid-level climb when witnesses described him suddenly clutching his chest, losing his grip, and falling to the mat below. He was unresponsive upon initial assessment by gym staff.

Initial Assessment Upon Arrival (15:30):

Level of Consciousness: Unresponsive

Pulse: Absent

Respiratory Effort: None

Skin Condition: Pale, cool, and clammy

Pupils: Fixed and dilated

Bystanders reported that staff initiated CPR immediately after the collapse and delivered one shock using the facility's automated external defibrillator (AED).

Treatment at Scene (15:30-15:45):

CPR: High-quality chest compressions continued upon paramedics’ arrival.

Airway Management: Airway secured with a bag-valve mask; oxygen at 15 L/min.

AED Analysis: AED advised one additional shock, which was administered at 15:35. Return of spontaneous circulation (ROSC) achieved at 15:37.

Vital Signs Post-ROSC:

Pulse: Weak and irregular at 45 bpm

Blood Pressure: 80/50 mmHg

Respiration: Shallow and labored at 10 breaths/min

Oxygen Saturation: 78%

Transport Summary (15:45-16:00): Patient was loaded into the ambulance for transport to St. Anthony's Hospital. During transport, the patient exhibited further signs of cardiac distress. At 15:50, he experienced ventricular fibrillation (VF).

Intervention: CPR resumed, epinephrine 1 mg administered IV, and defibrillation attempted twice.

Outcome: No ROSC achieved after second cardiac arrest.

Time of Death: 16:00

Remarks: The patient suffered two cardiac arrests within a 30-minute period, likely indicative of a severe underlying cardiac condition. Efforts to stabilize were unsuccessful due to continued arrhythmias and compromised circulation.

Autopsy Report

Case Number: 2024-AU-1245 Date of Examination: December 7, 2024 Time of Examination: 09:00

Name: Daniel Carson Age: 20 Height: 5'11" Weight: 165 lbs Sex: Male Race: Caucasian

External Examination:

General Appearance: Well-developed and muscular young male. No evidence of external trauma except for mild abrasions on the back of hands and forearms, consistent with climbing activities. Skin pale with slight cyanosis around the lips and nail beds.

Scars/Marks: None significant.

Tattoos: None noted.

Clothing: Patient arrived wearing climbing shorts and a tank top.

Internal Examination:

Cardiovascular System:

Heart: Enlarged, weighing 420 grams (average for age/weight: 300-350 grams).

Valves: Mitral valve revealed significant calcification and fibrosis, indicative of a congenital defect. The defective valve exhibited stenosis, which restricted blood flow and created turbulent circulation.

Coronary Arteries: Severe occlusion (95%) of the left anterior descending (LAD) artery due to atherosclerotic plaque.

Myocardium: Evidence of acute ischemic changes and scarring, suggesting prior silent infarctions. The ventricular walls were thickened (hypertrophic cardiomyopathy).

Aorta: Normal caliber and appearance.

Respiratory System:

Lungs congested, with frothy fluid in the trachea and bronchi.

Right lung: 450 grams; Left lung: 430 grams.

Gastrointestinal System:

Stomach contained approximately 200 mL of partially digested food.

No abnormalities in the esophagus, stomach, or intestines.

Central Nervous System:

Brain weight: 1,450 grams. No gross abnormalities.

Other Organs:

Liver: Enlarged (1,600 grams), possibly due to mild congestion.

Kidneys: Unremarkable.

Spleen: Normal size.

Microscopic Examination:

Heart Tissue: Acute myocardial infarction visible in sections of the left ventricle.

Coronary Arteries: Advanced plaque buildup with rupture and thrombus formation.

Mitral Valve: Fibrotic thickening and calcification evident.

Toxicology:

No evidence of drugs or alcohol.

Summary and Cause of Death: Daniel Carson, a 20-year-old male, died from complications of a congenital mitral valve defect and severe coronary artery disease. The primary event was a massive myocardial infarction triggered by the blockage of the LAD artery. A second cardiac arrest during transport proved fatal.

Final Diagnosis:

Acute myocardial infarction secondary to LAD artery occlusion.

Congenital mitral valve stenosis and calcification.

Hypertrophic cardiomyopathy contributing to cardiac instability.

Cause of Death: Cardiac arrest due to a defective valve and blocked artery.

Manner of Death: Natural.

Signed by: Dr. Margaret Li, MD Pathologist

[kk095]

Kiana’s Cardioversion

Kiana was a 25 year old black girl who worked as a personal trainer. She stood at 5’3 with a slim, but fit and toned build. Kiana had dark, medium length, curly, natural hair with a side part. Her eyes were a darker shade of brown, and she had a nose ring and bellybutton ring.

Earlier today, Kiana found herself in our emergency department after developing an array of worrisome symptoms completely out of the blue. She experienced a severe tearing pain in her chest, heart palpitations, and shortness of breath. As a result, she was sitting in the upright position on one of our trauma room tables. She was barefoot, and stripped down to only her sports bra and matching underwear. There were EKG electrodes stuck onto Kiana’s chest, and there were IVs set up in both arms. She was visibly uncomfortable, writhing in pain, squirming around a bit.

The heart monitors were beeping, chirping, and alarming rather loudly, creating a bit of tension and sensory overload in the exam room. The readings on the monitors were a bit concerning as well. Kiana’s heart was racing at 170 beats per minute, and her blood pressure was low at 75/40. The rhythm itself was a tachyarrhythmia of some sort. The EKG showed a narrow QRS complex and possible atrioventricular block. The symptoms and EKG readings pointed Dr Lindsay and in a few very different directions. One possibility was an NSTEMI heart attack, but how likely is that in a 25 year old personal trainer? Next was junctional ectopic tachycardia, which is an uncommon, but potentially deadly arrhythmia that tends to occur in infants or people who recently had open heart surgery. The other possibilities were an electrolyte imbalance, particularly potassium, or her symptoms could be attributed to stimulant use from substances such as cocaine, meth, or molly.

Since the possibilities were all very different, Dr Lindsay had to be thorough and order a whole bunch of tests. First off were blood samples. A CBC, a BMP, a toxicology screening, a cardiac enzyme test, an HCG, and a d-dimer were all drawn and sent off to the lab for stat analysis. Because Kiana was experiencing chest pain, Dr Lindsay decided to order a chest x-ray and an echocardiogram. Unfortunately, both tests didn’t help Lindsay narrow anything down. The chest x-ray came back completely normal, and the echocardiogram showed slight thickening of the ventricular septum, which is a sign of hypertrophic cardiomyopathy. But some of the other symptoms didn’t point in that direction. So what exactly was going on with Kiana? Dr Lindsay was certainly stumped. All she could do was treat Kiana’s symptoms, and hope the lab tests would come back soon and show something noteworthy.

Of course the lab was taking their sweet ass time with Kiana’s stat labs. And of course Kiana started to get worse. Her heart raced faster and faster, and the arrhythmia became more troublesome. Dr Lindsay wasted no time and started chemical cardioversion, urgently trying to calm Kiana’s heart and relieve her symptoms a bit. But as the next little while unfolded, Kiana’s condition didn’t improve, almost as if the antiarrhythmic medications did absolutely nothing. When chemical cardioversion doesn’t work, the next step is electrical cardioversion.

Dr Lindsay explained to Kiana that her heart was in a dangerous rhythm, and they had to give it a quick shock to make it beat normally again. Kiana was a bit nervous and hesitant, but nodded in response to Dr Lindsay, reluctantly agreeing. The defib pads were then stuck onto Kiana’s chest and charged to a lower setting of 125 joules. Lindsay told Kiana the defibs were ready, then pushed the shock button a few seconds later. “MMMM!” Kiana moaned loudly, squeezing her eyes shut, wincing in pain from the quick jolt of electricity. After the shock, Dr Lindsay studied the monitors for a few moments and listened to Kiana’s heart and lungs with a stethoscope. Lindsay discovered there was no change in the rhythm and informed Kiana she had to be shocked again. The defib pads were recharged to 150 joules, and the next shock was sent into Kiana’s racing heart. Her torso shivered, and she clenched her chest with one hand while her face had a distressed look.

Dr Lindsay repeated the same process as before, studying the heart monitors and listening to Kiana’s heart and lungs. Just like before, Dr Lindsay didn’t see any change whatsoever and needed to shock Kiana again at 175 joules. The pads were charged and readied, and Kiana received the next shock. Her chest propelled forwards, and she let out a grunt, reacting to the electricity racing through her while wide awake. This shock failed to correct the arrhythmia, and Lindsay informed Kiana she had to be shocked again. “NO MORE! NO MORE!” She protested, writhing around on the table, on the verge of tears. Despite Kiana’s protests, Lindsay shocked her again at 200 joules. “AHH!” Kiana yelped. After that shock, she started to breathe heavily and tears started to roll down her face. “PLEASE! NO MORE, NO MORE!” she cried, begging Dr Lindsay to stop. But the arrhythmia was still there, so unfortunately Lindsay was unable to stop the cardioversion. The defibs were recharged to 225, and the next shock was delivered. Kiana gasped and cried out reacting to the shock, but just like all the others, the arrhythmia was still there. “PLEASE… JUST STOP! NO MORE! I DON’T WANNA DIE!” Kiana cried out hysterically, squirming and writhing around on the table wanting the nightmare to end.

The defib pads were recharged to 250 joules- twice the strength of the very first shock, and the next shock was administered. Kiana’s body trembled, and she scrunched her toes at the far end of the table trying to fight the pain, showing off the white nail polish on her toes and the thick, soft, wide wrinkles throughout the soles of her size 6 feet. Immediately after that particular shock, Kiana’s breathing slowed a bit. Her head lolled to the side and her eyes rolled back. Kiana’s body went completely limp, and the heart monitors were practically shouting at Dr Lindsay and the rest of our team.

It didn’t take long to realize that Kiana had gone into v-fib, so the team had to change gears and start running a normal code. The bed was lowered, and Kiana’s sports bra was snipped off, allowing her perky, deceptively large breasts to spill out. CPR was immediately started, causing Kiana’s chest to cave in, and her belly to ripple out. At the head of the bed, her airway was the priority. A 7.0 ET tube was carefully but quickly navigated into her airway, being held in place by a blue tube holder once proper placement was confirmed. Post intubation, CPR was halted, and the team decided to try their luck with the defib paddles, rather than the pads. The paddles were gelled, charged to 250 joules, and pressed up against Kiana’s bare chest. KA-THUNK! Her small body was thrown around effortlessly on the table while her eyes remained half open, almost as if she was still watching the events unfold around her. V-fib was still on the monitors, so the paddles were readied once again, and Kiana received a 300 joule shock. Her chest shot up and her back arched. Her big, perky tits jiggled around while she crashed back down onto the table. Kiana remained in v-fib even after this shock, so she was defibbed again after a cycle of CPR and ambu bagging. Her shoulders shrugged forwards. Kiana’s hands made loose fists from the electric current that ran through her body. Unfortunately, the shock didn’t bring her back.

With a few unsuccessful shocks out of the way, the team decided to resume chest compressions and push meds into Kiana’s IV line. Kiana’s chest was pumped violently but rhythmically for several minutes, but the compressions and 2 doses of meds failed to restart her heart. The team decided to defib Kiana again. The paddles were gelled, charged to 360, and she was shocked again. Kiana’s body twitched sharply in response to the shock, but her heart didn’t start back up. “again! Everyone…CLEAR!” Lindsay shouted, immediately shocking Kiana again. KA-THUMP! Kiana jolted violently on the table while her eyes remained open, staring up above with an expressionless gaze. Kiana was shocked unsuccessfully another 3 times after that and given another dose of meds, but v-fib was the clear winner of the battle up to that point.

Dr Lindsay was reluctant to give up on the beautiful young lady. However, the code became redundant the longer it went on. Kiana would receive a few shocks, then it was back to a few minutes of CPR and meds, rinse and repeat. At the 30 minute mark of the code, it was noted that Kiana’s pupils were fixed and dilated. Dr Lindsay knew she exhausted all possible options in this particular case. At that point, resuscitation efforts were ceased, and Kiana’s time of death was called at 4:48pm. The ambu bag was detached and the chirping, flashing v-fib monitors were turned off. The EKG electrodes were disconnected, and the defib pads were peeled off. The defb gel was wiped off of Kiana’s bruised, battered chest. Her eyes were gently shut for the final time, and her body was covered up. Lastly, a toe tag was filled out and placed on the big toe of her left foot. The tag dangled against the wrinkled soles of Kiana’s feet, signifying a sudden and tragic end for the beautiful young lady.

[dan13579]

My ideas on how pressure works

* Warning: I am not a professional, this is just a speculation based on info found online *

While looking up about commotio cordis, I learned that mechanical stress on cardiac muscle causes it to discharge an electrical signal, disrupting the electrical activity of the heart.

I thought that since pressure is causing mechanical stress on the heart, the reason why pressure causes irregular heartbeats follows a similar principle.

Irregular beats can be divided into two categories, and I will speculate why pressure causes each type of irregular beat.

1. Atrial ectopic beat

These are caused by abnormal electrical signals from the atrium. Pressure disrupts blood flow in the heart. And I think because the walls of the atria are thin, disruptions in blood flow can cause abnormal stretching of the atria walls, causing them to release abnormal electrical signals. These cause atrial ectopic beats, such as PACs, and if you’re lucky, SVT.

2. Ventricular ectopic beat

These are caused by abnormal electrical signals coming from the ventricles. Normally I don’t get much of these with light pressure, so I think that you need heavy pressure to create the sufficient mechanical stress to make the ventricles misfire. This causes PVCs and VT.

I also think that by controlling the amount and location of pressure, you can control what kind of irregular heartbeat you get. With light pressure near the base of the heart, to screw with blood flow, you get PACs and SVT. With heavy pressure on the ventricles(near the apex), you get PVCs and VT.

These are just my thoughts on how pressure works. This may be totally wrong, so don’t take it too seriously.

[fasterthan-jimmyjohns]

Redacted Audio Shifter OC RP blog

Robin Bowey

30

Trans man

5'8

All photos not reblogged are from pintrest

So what had happened was, I was an Olympic Track Hopeful. Unfortunately during trials I took a bad fall and had to get medical attention. Turns out I developed a Ventricular Arrythmia. Sayonara Olympic dreams.

I moved out to Cali to chill out. And it was great. My blood pressure's never BEEN more stable. But my Arrythmia was still concerning my doc and I was bedrotting. So I needed something to get me out of the house. Enter Eden, my service dog.

Anyway, I figure delivery'll be really fulfillin, give me purpose again.

[clanoffelidae]

If you write anything that features characters dying in fights and want to spice things up a bit then incorporate more commotio/contusio cordis, please it’s so cool. It’s where someone is hit in the chest at a very specific point during the cardiac cycle and the energy released by the impact disrupts the cycle and causes the person to go into ventricular fibrillation. (The thing defibs treat)

And if you don’t necessarily want to kill them there is a very slim chance (<5%) that their body will sort out the heart’s electrical fuckup and get things back online; OR, if you write supernaturally powerful characters/non-human characters who wouldn’t necessarily be killed by having their heart stopped, this can be a fun way to knock them out for a moment by stopping their heart, rapidly dropping their blood pressure, and making them pass out. This is especially applicable with supernaturally powerful characters imo since they would be more likely to have the reaction time needed to hit that very precise window to trigger this.

My favorite part is how you don’t even technically need to cause physical trauma to the heart to do it, that’s what commotio cordis is vs contusio cordis. Contusio cordis is when the heart shows signs of physical trauma after the incident, bruising and such, whereas commotio cordis is where the heart actually looks perfectly fine upon physical exam. You don’t even need to be struck hard enough to cause physical trauma to the heart in order to fatally disrupt the heart’s ability to beat which is so cool imo.

But of course for those worried about it irl now don’t be, it’s super fucking rare and especially not in adults who have thicker chest walls due to puberty which protects the heart. It has to be struck in a very specific location and at a very specific time in the cardiac cycle, a window of 40 milliseconds max per heart beat, in order for it to happen, not to mention that you need to be struck with a pretty large amount of force for it to happen since it has to be enough energy to go through all those tissues and still be enough to fuck up the heart. It mostly happens in baseball and mostly boy’s baseball since again, less developed chest wall, and that’s where you’re most likely to find small objects accidentally hitting very specific parts of the chest with a large amount of force. So tl;dr don’t be worried about it irl (unless you’re a young boy playing baseball ig lol), but if you want something to spice up your writing you should totally incorporate it because it’s pretty fucking cool lbr.

[expertacademicassignmenthelp]

The pathophysiology of hypertension

Introduction

Hypertension, or high blood pressure, is a complex medical condition affecting a significant proportion of the global population. Despite its prevalence, there remains uncertainty regarding its pathophysiology, with essential hypertension constituting a substantial portion where no single identifiable cause is found. This comprehensive discussion aims to delve into the physiological mechanisms involved in the development of hypertension, exploring factors such as cardiac output, peripheral resistance, the renin-angiotensin-aldosterone system, the autonomic nervous system, endothelial dysfunction, genetic factors, and intrauterine influences.

Cardiac Output and Peripheral Resistance

Maintaining normal blood pressure relies on the delicate balance between cardiac output and peripheral vascular resistance. Essential hypertension often involves a normal cardiac output but elevated peripheral resistance, primarily determined by small arterioles. The role of smooth muscle cells, calcium concentration, and structural changes in arteriolar vessel walls contribute to the irreversible rise in peripheral resistance.

Renin-Angiotensin System

The renin-angiotensin system plays a crucial role in blood pressure regulation. Renin, released in response to various stimuli, initiates the conversion of angiotensinogen to angiotensin I, which is then converted to the vasoconstrictor angiotensin II. This system also stimulates aldosterone release, promoting sodium and water retention. While the circulating system may not be directly responsible for essential hypertension, local renin-angiotensin systems in organs like the kidney, heart, and arterial tree gain significance in regulating regional blood flow.

Autonomic Nervous System

Sympathetic nervous system stimulation affects arteriolar constriction and dilation, playing a pivotal role in maintaining normal blood pressure. Although the exact role of epinephrine and norepinephrine in hypertension etiology remains unclear, drugs blocking the sympathetic nervous system demonstrate therapeutic efficacy.

Endothelial Dysfunction

Vascular endothelial cells, producing vasoactive agents like nitric oxide and endothelin, play a key role in cardiovascular regulation. Endothelial dysfunction, implicated in essential hypertension, involves impaired production of nitric oxide. This dysfunction, once established, becomes irreversible, highlighting its primary nature in hypertension.

Vasoactive Substances

Various vasoactive substances, such as bradykinin, endothelin, atrial natriuretic peptide, and ouabain, influence sodium transport and vascular tone. These substances contribute to the delicate balance in maintaining normal blood pressure.

Genetic Factors

Genetic predisposition significantly contributes to hypertension, with specific mutations linked to disorders like Liddle’s syndrome, glucocorticoid-remediable aldosteronism, and others. The intricate interplay of multiple genes makes it challenging to pinpoint individual contributions.

Intrauterine Influences

Fetal influences, particularly birth weight, emerge as determinants of adult blood pressure. The Barker hypothesis suggests a link between low birth weight, metabolic abnormalities, and hypertension in later life. However, the role of genetic factors in this relationship requires further exploration.

Diastolic Dysfunction

Hypertensive left ventricular hypertrophy leads to impaired diastolic relaxation, affecting ventricular input during exercise. This dysfunction contributes to increased atrial pressure, pulmonary congestion, atrial fibrillation, and potential complications like pulmonary edema.

Conclusion

In conclusion, understanding the pathophysiology of hypertension involves a multifaceted exploration of various physiological mechanisms. While essential hypertension remains a complex and often multifactorial condition, advancements in research shed light on factors such as cardiac output, peripheral resistance, the renin-angiotensin system, the autonomic nervous system, endothelial dysfunction, genetic influences, and intrauterine factors. A comprehensive understanding of these elements is crucial for developing effective therapeutic strategies and preventive measures against the global burden of hypertension.

We hope this helps in improving our comprehension of the Hypertension condition. All the best in your journey in the medical field.

Incase of any challenges' and in need of professional guidance, contact;

Expert Academic Assignment Help at;

williamsassignmenthelpfredrick@gmail.com

[sandhyamedicity]

Understanding Heart Disease: What is Heart Disease

What is Heart Disease?

Heart disease, also known as cardiovascular disease (CVD), encompasses a range of conditions affecting the heart and blood vessels. It is the leading cause of death worldwide, causing significant morbidity and mortality. The term "heart disease" is often used interchangeably with "cardiovascular disease," although technically, cardiovascular disease includes all diseases of the heart and blood vessels, while heart disease specifically refers to conditions affecting the heart itself.

Types of Heart Disease

Coronary Artery Disease (CAD): CAD is the most common type of heart disease and occurs when the coronary arteries, which supply blood to the heart muscle, become narrowed or blocked due to plaque buildup (atherosclerosis). This can lead to chest pain (angina), heart attacks, and other complications.

Heart Failure: Heart failure, or congestive heart failure, happens when the heart muscle is unable to pump blood efficiently, leading to a buildup of fluid in the lungs and other tissues. Causes include CAD, hypertension, and cardiomyopathy.

Arrhythmias: These are disorders of the heart's rhythm, which can be too fast (tachycardia), too slow (bradycardia), or irregular. Common arrhythmias include atrial fibrillation and ventricular fibrillation, which can significantly impact heart function.

Heart Valve Disease: Heart valve disease involves damage to one or more of the heart's valves, affecting blood flow within the heart. Conditions include stenosis (narrowing of the valve), regurgitation (leakage of the valve), and prolapse (improper closure of the valve).

Congenital Heart Defects: These are heart abnormalities present at birth, ranging from simple defects like a hole in the heart's walls (septal defects) to more complex malformations. They can affect how blood flows through the heart and to the rest of the body.

Cardiomyopathy: Cardiomyopathy refers to diseases of the heart muscle. The heart muscle becomes enlarged, thickened, or rigid, which can lead to heart failure or arrhythmias. Types include dilated, hypertrophic, and restrictive cardiomyopathy.

Pericarditis: Pericarditis is inflammation of the pericardium, the thin sac surrounding the heart. It can cause chest pain and fluid buildup around the heart, affecting its function.

Causes and Risk Factors

Heart disease is influenced by a combination of genetic, environmental, and lifestyle factors. Major risk factors include:

High Blood Pressure (Hypertension): Hypertension forces the heart to work harder to pump blood, leading to the thickening of the heart muscle and potential heart failure.

High Cholesterol: Elevated levels of cholesterol, particularly low-density lipoprotein (LDL), contribute to the formation of plaque in the arteries, leading to atherosclerosis.

Smoking: Smoking damages the lining of blood vessels, increases blood pressure, reduces oxygen to the heart, and raises the risk of heart disease.

Diabetes: Diabetes significantly increases the risk of heart disease. High blood sugar levels can damage blood vessels and the nerves that control the heart.

Obesity: Excess body weight strains the heart, raises blood pressure, and increases the likelihood of diabetes and cholesterol problems.

Physical Inactivity: A sedentary lifestyle contributes to obesity, hypertension, and other heart disease risk factors.

Unhealthy Diet: Diets high in saturated fats, trans fats, cholesterol, sodium, and sugar can lead to heart disease by raising cholesterol levels, blood pressure, and weight.

Family History: A family history of heart disease increases one's risk, suggesting a genetic predisposition.

Age and Gender: Risk increases with age, and men are generally at higher risk earlier in life than women, although women's risk increases and can surpass men's post-menopause.

Symptoms

Symptoms of heart disease vary by condition but may include:

Chest pain or discomfort (angina)

Shortness of breath

Pain, numbness, or coldness in the legs or arms

Fatigue

Lightheadedness or dizziness

Palpitations (irregular heartbeats)

Swelling in the legs, ankles, and feet

Diagnosis and Treatment

Diagnosing heart disease often involves a combination of medical history review, physical examination, and diagnostic tests such as:

Electrocardiogram (ECG or EKG)

Echocardiogram

Stress tests

Blood tests

Cardiac catheterization

CT or MRI scans

Treatment strategies vary based on the specific type of heart disease and its severity and may include:

Lifestyle Modifications: Healthy diet, regular exercise, smoking cessation, and weight management are crucial for preventing and managing heart disease.

Medications: Medications can control risk factors such as hypertension, high cholesterol, and diabetes, or treat specific heart conditions like arrhythmias and heart failure.

Procedures and Surgeries: Angioplasty, stent placement, bypass surgery, valve repair or replacement, and implantable devices like pacemakers or defibrillators may be necessary for severe cases.

Prevention

Preventing heart disease involves managing risk factors through:

Maintaining a healthy diet rich in fruits, vegetables, whole grains, lean proteins, and healthy fats

Regular physical activity

Avoiding tobacco use

Controlling blood pressure, cholesterol, and blood sugar levels

Regular health screenings

Stress management techniques

Understanding and addressing heart disease through lifestyle changes, medical management, and preventive measures is crucial in reducing its impact and improving overall heart health.

[usascripthelpersofficial]

TYPES OF HEART DISEASE

Heart disease encompasses a wide range of cardiovascular problems. Various conditions fall under the heart disease umbrella, each affecting the heart or blood vessels in distinct ways. Understanding these types can help in recognizing symptoms early and seeking appropriate treatment. This article explores the primary types of heart disease, their causes, and potential treatments.

1. Coronary Artery Disease (CAD)

Overview:

Coronary Artery Disease is the most common type of heart disease. CAD occurs when the coronary arteries, responsible for supplying blood to the heart muscle, become hardened and narrowed due to the buildup of cholesterol and other materials, known as plaque, on their inner walls. This process is called atherosclerosis.

Symptoms:

Chest pain (angina)

Shortness of breath

Fatigue

Treatment:

Treatments include lifestyle changes, medication, and possibly procedures like angioplasty or coronary artery bypass grafting (CABG).

2. Heart Arrhythmias

Overview:

Arrhythmias are irregular heartbeats. The heart can beat too fast (tachycardia), too slow (bradycardia), or irregularly. This can be due to a fault in the heart’s electrical system.

Symptoms:

Palpitations

Dizziness

Fainting

Treatment:

Treatment might involve medications, lifestyle adjustments, and in some cases, implantable devices like pacemakers or procedures like catheter ablation.

3. Heart Valve Disease

Overview:

The heart contains four valves: the tricuspid, pulmonary, mitral, and aortic valves. These valves open and close to direct blood flow through the heart. Valve disease occurs when one or more of these valves do not function properly.

Symptoms:

Fatigue

Swollen ankles or feet

Shortness of breath

Treatment:

Treatment may include medication, surgical repair, or valve replacement depending on the severity and specific type of valve disease.

4. Congestive Heart Failure (CHF)

Overview:

Heart failure, sometimes known as congestive heart failure, occurs when the heart can’t pump blood as well as it should. This can result from any condition that damages the heart muscle, including CAD, high blood pressure, and heart valve disease.

Symptoms:

Shortness of breath

Persistent coughing or wheezing

Swelling in legs, ankles, and feet

Treatment:

Managing heart failure involves a combination of lifestyle changes, medications, and possibly surgery or devices like ventricular assist devices (VADs) or implantable cardioverter-defibrillators (ICDs).

5. Cardiomyopathy

Overview:

Cardiomyopathy refers to diseases of the heart muscle. These diseases enlarge or make the heart muscle rigid and more prone to arrhythmias.

Symptoms:

Breathlessness

Swelling of the legs

Fatigue

Treatment:

Treatment focuses on controlling symptoms and may include medications, lifestyle modifications, or devices to help the heart pump more effectively.

6. Congenital Heart Defects

Overview:

Congenital heart defects are structural problems with the heart present from birth. They can involve the walls of the heart, the valves of the heart, and the arteries and veins near the heart.

Symptoms:

Symptoms vary widely and can include cyanosis (a bluish tint to the skin, lips, and fingernails), breathing difficulties, and fatigue.

Treatment:

Treatment depends on the type and severity of the defect and may involve medication, catheter procedures, or surgery.

Conclusion

Heart disease is a broad term that covers various conditions affecting the heart’s structure and function. Recognizing the signs and symptoms of these different types can lead to early diagnosis and treatment, significantly improving quality of life and outcomes for those affected. Regular check-ups and conversations with healthcare providers about heart health can help individuals understand their risks and take proactive steps towards heart disease prevention.

[killed-by-choice]

“Gloria Roe,” 35 (USA 1976)

This tragic case of a mother killed by a “safe and legal” abortion was preventable every step of the way. “Gloria Roe” should never have been pushed into the unwanted, unnecessary and unsafe abortion that took her baby’s life and her own.

Gloria had 6 surviving children and had suffered 2 previous miscarriages. Sometime in 1976, she went to the doctor with abdominal pain and nausea. Her doctor diagnosed her with either gastritis or a peptic ulcer and gave her antacids. X-rays of her gall bladder and upper gastrointestinal tract were run 3 days later, with nothing abnormal detected. Gloria’s doctor apparently didn’t notice that his patient was pregnant. She herself didn’t know because her last period had been only two weeks before.

Two months later, Gloria went back to the doctor with what was recognized as morning sickness. The unidentified doctor informed her that she was 10 weeks pregnant and allegedly “counseled on the potential risk of her previous x-ray exposure to the fetus.” Only after this did Gloria agree to an abortion. There is no record of any tests ever being run to see if her child had actually been harmed.

Gloria was referred to an abortionist, but she was likely conflicted because she didn’t actually go for another month. When she eventually did, the abortion was scheduled for 10 days later.

At 15 weeks pregnant, Gloria underwent the abortion. The abortionist used the prostaglandin instillation method that was routine for him, even though this was in an outpatient facility and even the prostaglandin manufacturers warned that the chemical should only be administered in hospitals due to the danger.

About 5 minutes after the prostaglandin was injected, Gloria vomited. Then she collapsed with no pulse. CPR was attempted, but the abortion facility was not equipped to deal with emergencies like this.

Gloria was brought to the ER comatose and had no palpable pulse or blood pressure. She was immediately intubated, and full resuscitation measures were taken. An electrocardiogram detected ventricular fibrillation. Resuscitation was continued for 90 minutes, and her rhythm eventually converted to sinus tachycardia. The serum potassium level, drawn after resuscitation, was 3.A mEq/1.

On the second day in the hospital, Gloria expelled her dead child. Gloria herself was not far from dying. She was in terrible condition with permanent and severe brain damage that never improved. She was unable to move her legs at all, but still felt and responded to her pain.

5 months after the abortion, she died from her injuries. The autopsy identified her cause of death as a pulmonary embolism, along with severe anoxic brain damage suffered during a cardiorespiratory arrest occurring after intrauterine instillation of PGF2a.

The CDC identified several preventable aspects in Gloria’s case.

Gloria was pressured into an abortion she didn’t want. She died without ever knowing that (according to modern research from the American College of Radiology) no single diagnostic x-ray has a radiation dose significant enough to cause adverse effects in a developing embryo or fetus. Her baby was likely fine.

Centers For Disease Control, Abortion Surveillance, Annual Summary 1976, Issued August 1978

[cardiacreports2]

Paramedic Report

Incident Number: 2024-07-08-DK-0562 Patient Name: Darren Kozlowski Age: 31 Sex: Male Height: 6’1” Weight: Approx. 185 lbs Date of Incident: July 8, 2024 Time of Call Received: 10:12 AM

Incident Description: Emergency services were dispatched to a trail located in Riverbend Park following an alert from the patient’s smartwatch, which detected a suspected cardiac event. Bystanders reported finding the patient collapsed approximately 1.3 miles into the trail. The patient was unresponsive and pulseless upon paramedic arrival at 10:22 AM.

Initial Assessment:

Airway: Clear

Breathing: Apneic

Circulation: No palpable pulse; asystole confirmed on ECG

Skin Condition: Cool, pale, diaphoretic

Interventions (On-Site):

CPR initiated: High-quality chest compressions performed immediately upon arrival.

Defibrillation: Delivered one shock (200J) following identification of ventricular fibrillation (VF) on ECG. VF converted to sinus rhythm; ROSC (Return of Spontaneous Circulation) achieved at 10:27 AM.

Medications Administered:

1 mg Epinephrine IV every 3–5 minutes during CPR (3 doses given).

300 mg Amiodarone IV push following initial shock.

Transport to Hospital:

Time En Route: 15 minutes

Condition During Transport: Patient deteriorated en route, suffering a second cardiac arrest at 10:33 AM. Aggressive CPR was resumed with defibrillation (2 shocks, 200J each) and ROSC achieved at 10:38 AM.

Vital Signs Pre-Hospital Arrival:

Heart Rate: 48 bpm (weak, irregular)

Blood Pressure: 72/50 mmHg

SpO2: 82% (on 100% O2 via BVM)

Hospital Arrival:

Time of Arrival: 10:44 AM

Patient presented with recurrent arrhythmia, hypotension, and altered mental status. Handoff provided to ER staff for advanced resuscitation.

Autopsy Report

Patient Name: Darren Kozlowski Case Number: ME-2024-894 Age: 31 Sex: Male Date of Death: July 8, 2024 Time of Death: 11:03 AM Performed By: Dr. Laura Mendelson, MD, Forensic Pathologist Location: County Medical Examiner’s Office

External Examination:

Height: 6’1”

Weight: 185 lbs

Build: Lean and fit; well-developed musculature.

Hair: Short blonde hair and beard.

Eyes: Blue.

Distinguishing Features: None noted.

External Trauma:

Rib fractures (bilateral, 3rd–6th ribs) consistent with CPR.

Bruising along the sternum.

Minor abrasions on knees and hands from collapse.

No other injuries identified.

Internal Examination:

Heart:

Weight: 375 grams (normal range: 280–340 grams).

Severe coronary artery disease identified:

95% occlusion of the left anterior descending artery (LAD).

80% occlusion of the right coronary artery (RCA).

Evidence of acute myocardial infarction (MI) involving 40% of the left ventricle, with microscopic examination confirming recent myocardial necrosis and hemorrhage.

Mild left ventricular hypertrophy noted (wall thickness: 1.5 cm).

Lungs:

Pulmonary congestion and edema (weight: 750 grams per lung).

No evidence of pulmonary embolism.

Other Organs:

Liver: Mild steatosis.

Kidneys: Acute tubular necrosis, likely secondary to hypoperfusion during cardiac arrest events.

Brain: Mild cerebral edema, no gross signs of anoxic injury.

Toxicology Results:

Negative for alcohol, illicit drugs, and prescribed medications.

Positive for mild caffeine levels consistent with normal consumption.

Cause of Death: Acute myocardial infarction due to severe coronary artery disease, complicated by multiple cardiac arrests.

Manner of Death: Natural.

Pathologist’s Summary: The decedent, a 31-year-old male, succumbed to complications from a severe heart attack while running. Advanced resuscitation efforts successfully restored circulation twice; however, irreversible cardiac damage and circulatory collapse led to his death. Contributing factors include undiagnosed atherosclerosis and left ventricular hypertrophy, suggesting a predisposition to cardiac events under physical exertion.

[taimoorkhan]

Myocarditis in Emergency Practice

Myocarditis, an inflammatory condition affecting the heart's myocardial tissues, is a significant cause of sudden cardiac death and dilated cardiomyopathy. With diverse etiologies ranging from viral and immune-mediated causes to toxic exposures, diagnosing and managing myocarditis can be challenging. In this blog post, we will explore the important points regarding the etiology, pathophysiology, presentation, diagnostic testing, and treatment options for myocarditis, with a focus on the perspective of emergency physicians.

Myocarditis can be caused by infectious agents (bacterial, parasitic, viral), immune-mediated conditions, and toxic exposures. Viral causes include enteroviruses, influenza, hepatitis viruses, HIV, herpes viruses, and Parvo B-19. Immune-mediated causes include systemic lupus erythematosus (SLE), scleroderma, and giant cell types. Toxic agents such as doxorubicin, antiretroviral medications, clozapine, and cocaine can also trigger myocarditis.

Myocarditis follows a three-step process. In the acute phase, infectious, autoimmune, or toxic agents directly damage cardiac myocytes. Subsequent myocyte destruction triggers immune system activation and secondary inflammation. In the later stages, the immune system mistakenly attacks the myocytes themselves, leading to progressive myocardial damage.

Myocarditis presents with a wide range of symptoms, necessitating a high index of suspicion for timely diagnosis. Symptoms may include dyspnea, palpitations, orthopnea, and chest pain. Dyspnea is the most common presenting symptom, while chest pain can vary from pleuritic to anginal. Patients may exhibit symptoms of congestive heart failure, ranging from fatigue and peripheral edema to cardiovascular collapse. Skin manifestations can be present in cases triggered by medication exposure.

Diagnostic testing for myocarditis overlaps with other cardiopulmonary evaluations. Electrocardiogram (ECG) abnormalities, such as sinus tachycardia, ST-segment elevations, T-wave inversions, AV blocks, widened QRS durations, or prolonged QT intervals, may be observed. Troponin assays may be elevated, but their absence does not rule out myocarditis. Additional blood tests, including CBC, CRP, and ESR, are often abnormal but nonspecific. Imaging studies like chest radiography and echocardiography can provide valuable information.

TThe treatment of myocarditis primarily focuses on supportive care to prevent further damage to the heart. Stabilizing the patient's ABCs (airway, breathing, circulation) is the priority. Supplemental oxygen and non-invasive positive pressure ventilation may be required for hypoxia or pulmonary edema. Heart failure therapy, including diuretics and nitroglycerin, can be administered if systemic perfusion allows. Cardiac dysrhythmias may necessitate treatment with antidysrhythmic medications. Antimicrobial therapy is required for cases associated with bacterial or parasitic infections. In severe cases, advanced interventions such as intra-aortic balloon pumps, extracorporeal membrane oxygenation (ECMO), or ventricular assist devices (VADs) may be necessary.

Myocarditis presents a complex diagnostic and management challenge for emergency physicians. The diverse etiologies, varied clinical presentations, and overlapping diagnostic tests make timely diagnosis crucial. Supportive care, stabilization, and targeted interventions are key elements of treatment. While further research is needed to refine diagnostic and therapeutic approaches, understanding the etiology, pathophysiology, presentation, and treatment options can aid emergency physicians in effectively managing myocarditis cases.

[science-lover33]

Heart Defects

Heart Defects

One very common form of interatrial septum pathology is patent foramen ovale, which occurs when the septum primum does not close at birth, and the fossa ovalis is unable to fuse. The word patent is from the Latin root patens for “open.” It may be benign or asymptomatic, perhaps never being diagnosed, or in extreme cases, it may require surgical repair to close the opening permanently. As much as 20–25 percent of the general population may have a patent foramen ovale, but fortunately, most have the benign, asymptomatic version. Patent foramen ovale is normally detected by auscultation of a heart murmur (an abnormal heart sound) and confirmed by imaging with an echocardiogram. Despite its prevalence in the general population, the causes of patent ovale are unknown, and there are no known risk factors. In nonlife-threatening cases, it is better to monitor the condition than to risk heart surgery to repair and seal the opening.

Coarctation of the aorta is a congenital abnormal narrowing of the aorta that is normally located at the insertion of the ligamentum arteriosum, the remnant of the fetal shunt called the ductus arteriosus. If severe, this condition drastically restricts blood flow through the primary systemic artery, which is life threatening. In some individuals, the condition may be fairly benign and not detected until later in life. Detectable symptoms in an infant include difficulty breathing, poor appetite, trouble feeding, or failure to thrive. In older individuals, symptoms include dizziness, fainting, shortness of breath, chest pain, fatigue, headache, and nosebleeds. Treatment involves surgery to resect (remove) the affected region or angioplasty to open the abnormally narrow passageway. Studies have shown that the earlier the surgery is performed, the better the chance of survival.

A patent ductus arteriosus is a congenital condition in which the ductus arteriosus fails to close. The condition may range from severe to benign. Failure of the ductus arteriosus to close results in blood flowing from the higher pressure aorta into the lower pressure pulmonary trunk. This additional fluid moving toward the lungs increases pulmonary pressure and makes respiration difficult. Symptoms include shortness of breath (dyspnea), tachycardia, enlarged heart, a widened pulse pressure, and poor weight gain in infants. Treatments include surgical closure (ligation), manual closure using platinum coils or specialized mesh inserted via the femoral artery or vein, or nonsteroidal anti-inflammatory drugs to block the synthesis of prostaglandin E2, which maintains the vessel in an open position. If untreated, the condition can result in congestive heart failure.

Septal defects are not uncommon in individuals and may be congenital or caused by various disease processes. Tetralogy of Fallot is a congenital condition that may also occur from exposure to unknown environmental factors; it occurs when there is an opening in the interventricular septum caused by blockage of the pulmonary trunk, normally at the pulmonary semilunar valve. This allows blood that is relatively low in oxygen from the right ventricle to flow into the left ventricle and mix with the blood that is relatively high in oxygen. Symptoms include a distinct heart murmur, low blood oxygen percent saturation, dyspnea or difficulty in breathing, polycythemia, broadening (clubbing) of the fingers and toes, and in children, difficulty in feeding or failure to grow and develop. It is the most common cause of cyanosis following birth. The term “tetralogy” is derived from the four components of the condition, although only three may be present in an individual patient: pulmonary infundibular stenosis (rigidity of the pulmonary valve), overriding aorta (the aorta is shifted above both ventricles), ventricular septal defect (opening), and right ventricular hypertrophy (enlargement of the right ventricle). Other heart defects may also accompany this condition, which is typically confirmed by echocardiography imaging. Tetralogy of Fallot occurs in approximately 400 out of one million live births. Normal treatment involves extensive surgical repair, including the use of stents to redirect blood flow and replacement of valves and patches to repair the septal defect, but the condition has a relatively high mortality. Survival rates are currently 75 percent during the first year of life; 60 percent by 4 years of age; 30 percent by 10 years; and 5 percent by 40 years.

In the case of severe septal defects, including both tetralogy of Fallot and patent foramen ovale, failure of the heart to develop properly can lead to a condition commonly known as a “blue baby.” Regardless of normal skin pigmentation, individuals with this condition have an insufficient supply of oxygenated blood, which leads to cyanosis, a blue or purple coloration of the skin, especially when active.

Septal defects are commonly first detected through auscultation, listening to the chest using a stethoscope. In this case, instead of hearing normal heart sounds attributed to the flow of blood and closing of heart valves, unusual heart sounds may be detected. This is often followed by medical imaging to confirm or rule out a diagnosis. In many cases, treatment may not be needed.

[takeeachdayonebookatatime]

Why did you elbow me? 114

Achilles Castle part 19

Chief Brady: pov I get off the phone with their parents who are very angry. Their parents finally arrive to pick them up, I tell them your sons are very lucky because Kate is not pressing charges. But they will have to pick up trash from the beach for a week as a punishment. Lanie says she is going to take her to the ER as a precaution. Castle calls ahead to let them know Lanie is bringing Kate in. Esposito offers to drive them there Jim is going with them. After talking with Kate for a few minutes the boys apologize. After the boys leave Lanie says to Bronson she will keep him updated.

Kate: pov Alexis runs upstairs and gets me some clothes i can change into Lanie helps me change into the shirt and pants and out of my bathing suit. Esposito is carrying me out to the car. He is driving us there, the ride to the hospital is short since there is not much traffic. Esposito finds a parking spot in the ER parking lot. Lanie helps me out of the car, Esposito is carrying me inside the hospital since I don't feel good. At the front desk my dad is handed forms to fill out. Dr Crane and nurse Suzanne are waiting for us. I'm taken into an exam room, the walls are a pretty yellow color. They mention the scans I had last time I was here looked good concussion wise, so they are not worried about that.

Dr Crane: pov Lanie fills me in on what happened, Esposito puts Kate on the exam table, nurse Suzanne grabs a blood pressure cuff to check her blood pressure. She then checks Kate's temperature, Suzanne hooks Kate up to the heart and pulse ox-meter and checks her other vitals. Lanie mentions she gave her a dose of her meds at the house. I listen to her heart and lungs, I suggest we take Kate for some scan to see how everything is looking.

Nurse Suzanne: pov Kate is taken to the scan room on the cardiac ward. Once she is settled on the exam bed/table. I start the EKG and put the wires/leads on her chest and start the machine. Dr Crane says It is slightly elevated but not too bad. Next Is the Echocardiogram, the ultrasound machine is brought over. Dr Crane squirts the cold gel on Kate's chest and moves the wand around over her heart. So far so good, he pages for a specialist to come look Kate over.

Dr Wendy Blair: pov Dr Crane asked if I could look at his heart patient. In the exam room I'm introduced to Kate, her father Jim, and her friends Lanie and Esposito. Before I examine Kate I ask some general health questions. I've been informed that Kate has a heart condition. Lanie says yes Kate has a form of ventricular tachycardia in her left ventricle. I ask how long she has had it Lanie mentions a few years. I ask if anyone else in her family has heart problems, Lanie tells me Kate has previous chest trauma from a shooting years ago it was at her Captain's funeral she was giving the eulogy when it happened. Requiring her to have emergency heart surgery.

Kate: pov The Dr is concerned because I may have swallowed some water at the beach and he wants me to make sure my lungs are clear. Dr Wendy Blair asks if I have any lung or breathing problems. Lanie is telling the Dr. How i have an issue with my left pulmonary vein and have had a collapsed lung before on the left side. Lanie mentions that my immune system is not that great. Dr Wendy Blair listens to my lungs which sound fine, she orders a chest x-ray for me just to make sure my lungs are clear. And IV is inserted into my arm.

Lanie: pov they are taking her for a chest x-ray I follow the gurney to the scan room. I'm waiting with the technician in the booth, Kate did so amazing. Dr Crane mentions for the time being Kate is being admitted for monitoring until he gets the scan results. The specialist Dr Wendy Blair has to look at them, in her room Kate is getting comfortable. The specialist and Dr Crane walk in Kate's room to go over the scans with us. They say everything looks good, they just want to monitor her until lunch, because of her cardiac history. Dr Burkett is being updated by Dr Crane on how she is doing. Esposito updates Castle and the rest of the group, I mention our group had plans for after lunch. We were going to the mall so Sarah Grace, our co-workers daughter, could go to build a bear workshop. Both Doctors said depending on how it goes with Kate it should be fine as long as Kate takes it easy.

Jim: pov Dr Wendy Blair wants to give Katie some preventive meds since she has a weak immune system. Once the meds are in Katie is asleep, Esposito is going to get us food while Katie sleeps. Dr Wendy mentions walking will help Katie but keep it short. Esposito arrives back at the hospital with tacos for us 3. The food is amazing.

Martha: pov Ryan is making sandwiches for lunch with chips on the side. Castle says Katherine should be back after lunch from what Esposito said. The Dr's said everything looks good but we will have to keep a close eye on Kate.

Ryan: pov I grab stuff out of the fridge to make sandwiches for the group, Alexis and Sarah Grace are filling the cups up with peach tea. All of us sit down at the dining room table to eat, we chat while we eat. Sarah Grace is saying how much fun she is having at the beach.

Esposito: pov Kate is now up Dr Wendy Blair and Dr Crane are saying Kate's vitals look great. A nurse brings in some oatmeal for her to eat. Both Dr's mention keeping a close eye on Kate in case she develops symptoms. If you feel like she needs it you can always ask the mall for a wheelchair or she can use Castle's if he is using his crutches. Lanie and the Dr's go over possible things Kate could get from her swallowing the water. Lanie mentions the possible symptoms she might have if she gets sick. To be continued. ……….