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literaryvein-reblogs · 3 months ago

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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

#caffeine #writing notes #writeblr #dark academia #spilled ink #writers on tumblr #writing reference #literature #writing prompt #poets on tumblr #poetry #writing inspiration #writing ideas #coffee #tea #creative writing #fiction #giuseppe de nittis #writing resources

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cardiacreports2 · 1 month ago

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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

#heart attack #male cpr #cpr #resuscitation

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kk095 · 11 months ago

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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.

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dan13579 · 1 year ago

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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.

#cardiophilia #dark cardiophilia #irregular heartbeat #pressure #skips

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jcsmicasereports · 2 months ago

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End-stage renal disease patients developed left ventricular hypertrophy, Gezira State- Sudan by Dr. Nahla Ahmed Mohammed Abdurrahman in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

Background: Left ventricular hypertrophy is the strongest independent predictor of cardiovascular death, and it is worsening in association with SCD. According to studies from the main international registers, cardiac disease is the leading cause of unexpected mortality in dialysis patients. Several studies have found that the prevalence of LVH is high among patients on maintenance haemodialysis, and that numerous risk factors linked with it, such as anaemia, hypertension, and volume overload, are common in these patients. Many clinical and nephrologist researchers are focusing their attention on the processes and factors that are present in these patients in order to prevent and regress the development of LVH.

Aim: The purpose of this study is to investigate the prevalence of left ventricular hypertrophy and associated risk factors among patients receiving routine haemodialysis at Gezira Hospital for Renal Disease and Surgery.

Method: This was a cross-sectional research with 70 patients receiving routine haemodialysis. Personal and clinical information was collected. The measurements included blood pressure, ECG, and echocardiogram. The concentration of haemoglobin was determined.

Result: Patients in the study ranged in age from 20 to 80 years old. Male made up 57 % (n=40). 75% of the individuals had LVH, with 68% undergoing echocardiography and just 7% receiving an ECG diagnosis. LVH affected 30 of the 40 male patients and 15 of the 30 female patients. Anaemia was detected in 44 (88%) of the 48 LVH patients with Hb12 gm/dl. In 74 % of the patients, systemic hypertension (BP>140/90mmHg) was present, and it was identified in 42 of the 48 patients with LVH. According to the evaluation, volume overload was evident in 63 % of the patients (32 out of 48 patients with LVH). The Chi-squire test was performed to determine the frequency and distribution of study participants based on several characteristics (age, gender, anaemia, volume overload, HTN, and dialysis duration) and LVH; the link between age and LVH, HTN and LVH, and DOD and LVH was statistically significant. P-values of 0.001, 0.013, and 0.005 were all significant.

Conclusion: We concluded that LVH is common among haemodialysis patients, and that there is a link between age, HTN, and DOD and LVH in this study.

KEY WORDS: Left Ventricular Hypertrophy, End Stage Renal Disease, Gezira State, Sudan

ABBREVIATION: CKD= Chronic kidney disease, ECG= Electrocardiograph, ESRD=End stage renal disease, Hb=Haemoglobin, HD=Haemodialysis, IVS=Interventricular septum, LVEDD=left ventricular end diastolic diameter, LVH=Left ventricular hypertrophy, LVM=Left ventricular mass, MRI=Magnetic resonance imaging, PW=Posterior wall.

Introduction

When kidney function declines and renal replacement therapy is required, the heart and vascular tree undergo major structural and functional changes, and the prevalence of cardiovascular disease is higher than in the general population (Usrds, 2017), with 40 % of all deaths in patients with end-stage renal disease (ESRD) due to cardiac causes ( Steddon, S, 2014). Left ventricular hypertrophy (LVH) is a typical indication of cardiac structural disease in ESRD patients, defined as an increase in left ventricular mass (LVM) due to increased wall thickness. Anaemia, hypertension, hypervolemia, and mineral metabolism problems are all linked to a loss in renal function, which increases the risk of LVH (McCullough et al., 2016). The researchers discovered that the strongest independent predictor of cardiovascular mortality in patients with chronic kidney disease is LVH (Shlipak et al., 2005), and that worsening of it is associated with SCD in haemodialysis patients (Kim H et al., 2015), which is a major cause of mortality in these patients (Paoletti et al., 2004). In individuals with chronic kidney disease (CKD), the prevalence of LVH is around 40%, and it increases with CKD progression until it reaches 75% in ESRD patients (McCullough et al., 2016).

Chronic kidney disease CKD is defined as kidney damage or a GFR of less than 60 mL/min/1.73 m2 for at least 3 months and is divided into five stages ('K/DOQI clinical practice recommendations for chronic kidney disease: evaluation, classification, and stratification, 2002). Left ventricular hypertrophy LVH, reduced LV function, regional wall motion abnormality, pericardial effusion, and valvular calcification are among the anatomical and functional cardiac abnormalities seen in ESRD patients. LVH is a common complication in ESRD patients and is a preventable risk factor (Charytan, 2014). HTN, vascular calcification (Nitta et al., 2004), anaemia, and volume overload (Vaiinien et al., 2017) are all risk factors for LVH in ESRD patients. The prevention or regression of LVH was achieved with early and effective management of these risk factors (Kim et al., 2015; Erdan et al., 2018).

LVH was caused by a variety of pathophysiologic variables in CKD and ESRD patients, who were categorized into three groups (Ritz and Wanner, 2008):

Afterload: an increase in systemic arterial resistance, raised arterial blood pressure, and impaired large-vessel compliance, which necessitates a rise in intra cavity pressure during ventricular contraction (Mominadam et al., 2008).

Preload: a condition caused by intravascular volume expansion (salt and fluid loading), anaemia, and an AV fistula (Di Lullo, et al., 2011; Cuadrado et al., 2004).

Not related to afterload or preload.

Arterial hypertension and poor control of blood pressure is the most common cause of chronic pressure overload of the left ventricle and cardiac adaptation in response to chronic pressure overload is LVH (Sweety et al., 2014).

Renal dysfunction and poor cardiovascular prognosis are linked to the coexistence of anaemia and LVH (Chang et al., 2014). Non-hemodynamic and hemodynamic adaptations are used in anaemic persons to maintain adequate tissue oxygenation. Increases in erythropoietin synthesis and intra-erythrocytic concentrations of 2,3-diphosphoglycerate (2,3-DPG) lower the affinity between oxygen and haemoglobin, resulting in a shift to the right of the oxygen haemoglobin dissociation curve (Oski et al., 1971).

When compared to conventional haemodialysis, short haemodialysis reduces LVH due to proper fluid control (Ayus et al., 2005), and intensive HD (McCullough et al., 2016). While frequent haemodialysis resulted in LVH regression (Trinh and Chan, 2016;Chan et al., 2018). In comparison to traditional haemodialysis, the improved clinical outcomes resulted in a higher frequency of vascular access procedures complications (Slinin et al., 2015).

Despite the numerous research that have been conducted to improve the quality of haemodialysis, it remains a complex procedure that necessitates a coordinated effort from your entire health-care team, including your nephrologist, dialysis nurse, dialysis technician, nutritionist, and social worker.

Diagnosis of LVH is by

ECG: This is the first non-invasive test, although it is less sensitive in diagnosing LVH (Vanezis and Bhopal, 2008), and there are various criteria for diagnosing LVH:

Limb lead voltage criteria: R in a VL > 11 mm, R in a VL > 13 mm if left axis deviation is present, and S in L III > 15 mm if left axis deviation is present. >25 mm R in LI + S in LIIII

Sokolow-Lyon criteria for chest lead: S in V1 + R in V5 or V6 >35 mm (Sokolow and Lyon, 1949).

Romhilt-Estes criteria: deep S in V1/V2 and tall R in V5/V6, with the aggregate of both exceeding 7 large squares or one of them exceeding 5 large squares (Romhilt and Estes, 1968).

Echocardiography: is a more sensitive and specific method of diagnosing LVH than an ECG. ECG criteria must account for ethnicity in people of African descent (Vanezis and Bhopal, 2008), and they must be correct in patients with HTN to rule out LVH (Pewsner et al., 2007). Left ventricular mass (using the Troy formula according to the American Society of Echocardiography ASE recommendation):= 1.05 (LVEDD+IVS +PW)3 LVEDD3.

The LVMI is calculated by dividing the LVH mass by the body surface area. LVH was characterized as an LVMI of greater than 150 g per m2. (from the Framingham Heart Study) (Armstrong and colleagues, 2014).

MRI: is the gold standard for assessing left ventricular mass, cavity volume, and pattern of LVH, whereas M-mode echocardiography (ECHO) overestimates LV mass in haemodialysis patients when compared to CMRI (Ebeid et al., 2017)

ESRD: but they are not commonly utilized due to cost and lack of availability. In practice, echocardiography is a good all-around instrument that is well-suited to long-term research studies.

Sudden cardiac death is the most prevalent cause of mortality in dialysis, accounting for 40% of deaths, most of which occur in the first three months of dialysis due to difficulty adapting to the cardiovascular stress that is characteristic of dialysis. And it could be due to LVH after a period of acclimatization. LVH is becoming more common among ESRD patients, particularly those on haemodialysis. It is also one of the most common causes of mortality among such patients. Many risk factors for LVH in such people could be treated to reduce the prevalence or regress LVH, and thus the risk of death. As it stands, diagnosis is not difficult and can be accomplished using less invasive techniques such as echocardiography and ECG.

MATERIALS AND METHODS

Study area: The study was conducted in Gezira hospital for renal disease and surgery- Gezira State- Wad Madani Central Sudan, which service the Gezira and whole nearby areas.

Study design: In Gezira hospital for renal disease and surgery, a descriptive, cross-sectional study was done among haemodialysis patients.

Study population: The study comprised 70 patients on daily haemodialysis, both male and female, ranging in age from 20 to 80 years. Each of the patients in this study dialyzed twice a week at the Gezira hospital for renal disease and surgery. Time and duration of dialysis, symptoms of volume overload, blood pressure, and lower limb oedema were among the personal, demographic, and clinical data obtained. The concentration of haemoglobin was determined. In patients with patent arterio-venous fistulae, blood pressure was monitored in the contralateral arm with a mercury sphygmomanometer. Standard limb and chest leads were used, with a paper speed of 25mm/s and a gain of 10mm/mV (or 5mm/mV). Sum of S wave in lead V1 and R wave in lead V5 or V6 35mm and/or R wave in lead aVL 11mm was classified as Sokolow-Lyon LVH. A physician performed the ECG interpretations. IVS, LVPW, LVEDD, and LVESD were measured using M-mode echocardiography and 2-dimensional ultrasonography.

Haemodialysis: The blood is filtered and cleaned out of the body, then reintroduced to the body in this operation, three times a week, for 4-5 hours. which has been used to treat advanced and permanent kidney failure.

Inclusion criteria: All patients who receive regular haemodialysis are eligible.

Exclusion criteria: Patients with established congenital heart disease or a history of heart disease, diabetics, and hypertensive patients prior to dialysis are also excluded.

Data analysis: The data were analysed using statistical package of social science (SPSS) version 24 .

Ethical consideration: All participants in this study were fully told about the study's goal and were promised that any personal information regarding their health status would be kept private.

Ethical clearance: Ethical clearance was acquired from the Gezira university faculty of medicine's ethical committee. Permission to conduct research in the Gezira hospital for renal disease and surgery from the director.

RESULTS

This study included 70 patients on regular haemodialysis in Gezira hospital for renal disease and surgery, including 40 males and 30 females ranging in age from 20 to 80 years. The Chi-square test was performed to determine the frequency and distribution of research participants based on various characteristics. At 0.05, the P-value is considered significant.

There is a significant relationship between duration of hemodialysis and LVH P value (0.005 )

DISCUSSION

Many risk factors contribute to the prevalence of left ventricular hypertrophy in CKD and ESRD patients, which has encouraged clinical nephrologists and researchers to focus their attention on processes and factors that are present in these patients for many years. LVH, which worsens with SCD in haemodialysis patients, is the strongest independent predictor of cardiovascular death in patients with chronic renal disease (Shlipak et al., 2005). The goal of this cross-sectional study was to find out how common LVH is and what the risk variables are among haemodialysis patients.

The main conclusion is that, 68 % of patients had LVH, accords with Foley et al, 2010 who found that LVH was present in 62 % of the study group, implying that the prevalence of LVH is dependent on the degree of renal impairment (Amoako et al., 2017). The current study found no statistically significant link between gender and LVH (p= 0.141), in contrast to the study of Amoako et al. and Paoletti et al., 2016. The link between age and LVH was confirmed in this investigation, with a substantial rise in patient age (P-value 0.001), which was constant with previous findings of (Paoletti et al., 2016).

The drop in haemoglobin concentration begins at levels of creatinine clearance of around 70 ml/min in men and 50 ml/min in women (Hsu, et al., 2002). As a result, the majority of ESRD patients suffer anaemia. In the current study, 88 % of patients have anaemia, defined as Hb 12 mg/dl, with a P-value of 0.512. Many studies have found that a haemoglobin level of 12-13 mg/dl in ESRD patients is related with a better outcome (Regidor, 2006), while a higher haemoglobin level is associated with a higher risk of mortality and arteriovenous access thrombosis (Phrommintikul et al., 2007). The goal haemoglobin level was not reached in the majority of patients due to poor management, blood loss in the dialyzer, and repeated blood sampling, however the basic underlying issue is erythropoietin insufficiency. Sweety et al. (2014) found an association between anaemia and LVH. Anaemic patients have insufficient tissue oxygenation, which is compensated for by increasing blood volume, resulting in an increase in left ventricular mass and assuming an eccentric geometry LVH (Metivier et al., 2000). This finding was consistent with our finding of blood volume in 42 of LVH patients, which was confirmed also by Nasri and Baradaran, 2005. Moreover, their study was confirmed our findings that 40 participants with hypertension had a significant connection between HTN and LVH with P-value of 0.013. Because volume overload is the most common cause of hypertension in ESRD patients (Bellizzi et al., 2006), insufficient clearance of this excess fluid leads to resistant hypertension (Fishbane, et al.,1996). The target blood pressure for adults with CKD is 130/80 mmHg, and for hypertensive individuals without target organ damage is 140/90 mmHg (Chobanian et al., 2003). However, this aim is not met in most patients, resulting in chronic pressure overload of the left ventricle and LVH.

When it comes to volume overload, 15% extracellular volume overload equates to around 2.5 litres of extra fluid in an HD patient (Wabel and colleagues, 2008). As a result, total fluid evacuation during dialysis may not be completed, and normal fluid status may not be achieved even immediately after dialysis. We discovered that 62% of patients were overloaded based on clinical assessment and the presence of lower limb oedema, and that 32 out of 48 patients had LVH (presence of lower limb oedema and shortness of breath does not indicate haemodialysis patients have LVH), but there was no significant relationship between volume overload and LVH P-value 0.238. While Unver et al. found a substantial positive link between hypervolemia and LVH in a study of 97 patients on regular haemodialysis (Unver et al., 2015), and that the presence of lower limb odema and shortness of breath does not mean that haemodialysis patients had LVH. Observational studies have shown that more frequent or longer haemodialysis sessions are associated with proper fluid management and a lower prevalence of LVH (Ly and Chan, 2006). However, another study found that more frequency and longer dialysis did not improve clinical outcome (Slinin et al., 2015).

Significant connection between haemodialysis duration and LVH was found in this study, with P-value of 0.005. Because all patients in this trial have just two- four hrs. sessions per week, they will not achieve their dry weight and will stay hypovolemic even after dialysis, as their Intera-dialytic weight gain will be more than 3 kg between sessions. Foley et al. (2010) investigated whether the incidence of LVH correlates with the length of dialysis in 596 incident haemodialysis patients with no prior history of heart disease. According to the study, 62% of the patients had an elevated LV mass volume index, and 49% of them developed overt LV failure.

Conclusion

We concluded that LVH is common among haemodialysis patients, and that there is a link between age, HTN, and DOD and LVH in this study.

RECOMMENDATION: • Follow up with a nephrologist and a nutritionist on a regular basis to ensure adequate anaemia management during the pre-dialysis phase and after the start of haemodialysis, as well as blood pressure control and prober volume management.

Before starting haemodialysis, all ESRD patients must have an echocardiogram to see if they have LVH and be treated as high-risk patients.

ACKNOWLEDGMENTS: Our best regards and thanks to the staff member of Gezira Hospital for Renal Disease and Surgery , and our appreciate is extend to the patients who participate in this study.

#cardiovascular death #cross-sectional research #Gezira State #Sudan #Left Ventricular Hypertrophy #End Stage Renal Disease #jcrmhs #Clinical Images submissions #Clinical decision making

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clanoffelidae · 9 months ago

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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.

#writing #whump #idk how else to tag this tbh lol #fanfiction #original writing #fantasy #ig??? idk

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expertacademicassignmenthelp · 1 year ago

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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;

[email protected]

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sandhyamedicity · 8 months ago

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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.

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usascripthelpersofficial · 10 months ago

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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.

#usascriphelpersofficial #heart failure #heart disease #heart disease prevention #heart disease risk #health care #medical care #public health

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killed-by-choice · 11 months ago

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“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

#tw abortion #pro life #unsafe yet legal #unidentified victim #tw coercion #tw ab*rtion #tw murder #abortion #abortion debate #death from legal abortion #victims of roe

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nursingscience · 2 years ago

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Medical Abbreviations on Pharmacy Prescriptions

Here are some common medical abbreviations you may see on pharmacy prescriptions:

qd - once a day

bid - twice a day

tid - three times a day

qid - four times a day

qh - every hour

prn - as needed

pc - after meals

ac - before meals

hs - at bedtime

po - by mouth

IV - intravenous

IM - intramuscular

subQ - subcutaneous

mL - milliliter

mg - milligram

g - gram

mcg - microgram

stat - immediately, right away

NPO - nothing by mouth

cap - capsule

tab - tablet

susp - suspension

sol - solution

amp - ampule

inj - injection

Rx - prescription

C - Celsius

F - Fahrenheit

BP - blood pressure

HR - heart rate

RR - respiratory rate

WBC - white blood cell

RBC - red blood cell

Hgb - hemoglobin

Hct - hematocrit

PT - prothrombin time

INR - international normalized ratio

BUN - blood urea nitrogen

Cr - creatinine

Ca - calcium

K - potassium

Na - sodium

Cl - chloride

Mg - magnesium

PO2 - partial pressure of oxygen

PCO2 - partial pressure of carbon dioxide

ABG - arterial blood gas

CBC - complete blood count

BMP - basic metabolic panel

CMP - comprehensive metabolic panel.

ECG - electrocardiogram

EEG - electroencephalogram

MRI - magnetic resonance imaging

CT - computed tomography

PET - positron emission tomography

CXR - chest x-ray

CTX - chemotherapy

NSAID - nonsteroidal anti-inflammatory drug

DMARD - disease-modifying antirheumatic drug

ACE - angiotensin-converting enzyme

ARB - angiotensin receptor blocker

SSRI - selective serotonin reuptake inhibitor

TCA - tricyclic antidepressant

ADHD - attention deficit hyperactivity disorder

COPD - chronic obstructive pulmonary disease

CAD - coronary artery disease

CHF - congestive heart failure

DVT - deep vein thrombosis

GI - gastrointestinal

UTI - urinary tract infection

OTC - over-the-counter

Rx - prescription

OD - right eye

OS - left eye

OU - both eyes.

TID - thrombosis in dementia

TDS - ter die sumendum (three times a day)

BOM - bilaterally otitis media (infection in both ears)

BT - body temperature

C&S - culture and sensitivity

D/C - discontinue or discharge

D/W - dextrose in water

ETOH - ethyl alcohol

FUO - fever of unknown origin

H&P - history and physical examination

I&D - incision and drainage

I&O - intake and output

KVO - keep vein open

N&V - nausea and vomiting

PERRLA - pupils equal, round, reactive to light and accommodation

PR - per rectum

QAM - every morning

QHS - every bedtime

QOD - every other day

S/P - status post (after)

TPN - total parenteral nutrition

UA - urinalysis

URI - upper respiratory infection

UTI - urinary tract infection

VO - verbal order.

XRT - radiation therapy

YOB - year of birth

BRBPR - bright red blood per rectum

CX - cervix

DVT - deep vein thrombosis

GB - gallbladder

GU - genitourinary

HCV - hepatitis C virus

HPI - history of present illness

ICP - intracranial pressure

IVP - intravenous pyelogram

LMP - last menstrual period

MRSA - methicillin-resistant Staphylococcus aureus

MVA - motor vehicle accident

NKA - no known allergies

PEG - percutaneous endoscopic gastrostomy

PRN - pro re nata (as needed)

ROS - review of systems

SOB - shortness of breath

TAH - total abdominal hysterectomy.

TIA - transient ischemic attack

Tx - treatment

UC - ulcerative colitis

URI - upper respiratory infection

VSD - ventricular septal defect

VTE - venous thromboembolism

XR - x-ray

w/c - wheelchair

XRT - radiation therapy

ASD - atrial septal defect

Bx - biopsy

CAD - coronary artery disease

CKD - chronic kidney disease

CPAP - continuous positive airway pressure

DKA - diabetic ketoacidosis

DNR - do not resuscitate

ED - emergency department

ESRD - end-stage renal disease

FFP - fresh frozen plasma

FSH - follicle-stimulating hormone.

GCS - Glasgow Coma Scale

Hct - hematocrit

Hgb - hemoglobin

ICU - intensive care unit

IV - intravenous

JVD - jugular venous distension

K - potassium

L - liter

MCH - mean corpuscular hemoglobin

MI - myocardial infarction

Na - sodium

NGT - nasogastric tube

NPO - nothing by mouth

OR - operating room

PCN - penicillin

PRBC - packed red blood cells

PTT - partial thromboplastin time

RBC - red blood cells

RT - respiratory therapy

SOA - short of air.

SCD - sequential compression device

SIRS - systemic inflammatory response syndrome

STAT - immediately

T - temperature

TPN - total parenteral nutrition

WBC - white blood cells

ABG - arterial blood gas

A fib - atrial fibrillation

BPH - benign prostatic hypertrophy

CBC - complete blood count

CO2 - carbon dioxide

COPD - chronic obstructive pulmonary disease

CPR - cardiopulmonary resuscitation

CT - computed tomography

CXR - chest x-ray

D5W - dextrose 5% in water

Dx - diagnosis

ECG or EKG - electrocardiogram

EEG - electroencephalogram

ETO - early termination of pregnancy.

FHR - fetal heart rate

GSW - gunshot wound

H&P - history and physical exam

HCG - human chorionic gonadotropin

I&D - incision and drainage

IBS - irritable bowel syndrome

ICP - intracranial pressure

IM - intramuscular

INR - international normalized ratio

IOP - intraocular pressure

LFT - liver function test

LOC - level of consciousness

LP - lumbar puncture

NG - nasogastric

OA - osteoarthritis

OCD - obsessive-compulsive disorder

OTC - over-the-counter

P - pulse

PCA - patient-controlled analgesia

PERRLA - pupils equal, round, reactive to light and accommodation.

PFT - pulmonary function test

PICC - peripherally inserted central catheter

PO - by mouth

PRN - as needed

PT - physical therapy

PT - prothrombin time

PTSD - post-traumatic stress disorder

PVC - premature ventricular contraction

QD - once a day

QID - four times a day

RA - rheumatoid arthritis

RICE - rest, ice, compression, elevation

RSI - rapid sequence intubation

RSV - respiratory syncytial virus

SBP - systolic blood pressure

SLE - systemic lupus erythematosus

SSRI - selective serotonin reuptake inhibitor

STAT - immediately

TB - tuberculosis

TIA - transient ischemic attack.

TID - three times a day

TKO - to keep open

TNTC - too numerous to count

TPN - total parenteral nutrition

URI - upper respiratory infection

UTI - urinary tract infection

V-fib - ventricular fibrillation

V-tach - ventricular tachycardia

VA - visual acuity

WNL - within normal limits

AED - automated external defibrillator

ARDS - acute respiratory distress syndrome

BID - twice a day

BP - blood pressure

BUN - blood urea nitrogen

CAD - coronary artery disease

CHF - congestive heart failure

CVA - cerebrovascular accident

D/C - discontinue

DKA - diabetic ketoacidosis.

DM - diabetes mellitus

DVT - deep vein thrombosis

EGD - esophagogastroduodenoscopy

ER - emergency room

F - Fahrenheit

Fx - fracture

GI - gastrointestinal

GTT - glucose tolerance test

HCT - hematocrit

Hgb - hemoglobin

HRT - hormone replacement therapy

ICP - intracranial pressure

IDDM - insulin-dependent diabetes mellitus

IBS - irritable bowel syndrome

IM - intramuscular

IV - intravenous

K - potassium

KVO - keep vein open

L&D - labor and delivery

LASIK - laser-assisted in situ keratomileusis.

ROM - range of motion

RT - radiation therapy

Rx - prescription

SCD - sequential compression device

SOB - shortness of breath

STD - sexually transmitted disease

TENS - transcutaneous electrical nerve stimulation

TIA - transient ischemic attack

TSH - thyroid-stimulating hormone

UA - urinalysis

US - ultrasound

UTI - urinary tract infection

VD - venereal disease

VF - ventricular fibrillation

VT - ventricular tachycardia

WBC - white blood cell

XRT - radiation therapy

XR - x-ray

Zn - zinc

Z-pak - azithromycin (antibiotic).

AAA - abdominal aortic aneurysm

ABG - arterial blood gas

ACS - acute coronary syndrome

ADL - activities of daily living

AED - automated external defibrillator

AIDS - acquired immunodeficiency syndrome

ALS - amyotrophic lateral sclerosis

AMA - against medical advice

AML - acute myeloid leukemia

APAP - acetaminophen

ARDS - acute respiratory distress syndrome

ASCVD - atherosclerotic cardiovascular disease

BPH - benign prostatic hyperplasia

BUN - blood urea nitrogen

CABG - coronary artery bypass graft

CBC - complete blood count

CHF - congestive heart failure

COPD - chronic obstructive pulmonary disease

CPAP - continuous positive airway pressure

CRF - chronic renal failure.

CT - computed tomography

CVA - cerebrovascular accident

D&C - dilation and curettage

DVT - deep vein thrombosis

ECG/EKG - electrocardiogram

EEG - electroencephalogram

ESRD - end-stage renal disease

FSH - follicle-stimulating hormone

GERD - gastroesophageal reflux disease

GFR - glomerular filtration rate

HbA1c - glycated hemoglobin

Hct - hematocrit

HIV - human immunodeficiency virus

HPV - human papillomavirus

HTN - hypertension

IBD - inflammatory bowel disease

IBS - irritable bowel syndrome

ICU - intensive care unit

IDDM - insulin-dependent diabetes mellitus

IM - intramuscular.

IV - intravenous

LFT - liver function test

MI - myocardial infarction

MRI - magnetic resonance imaging

MS - multiple sclerosis

NPO - nothing by mouth

NS - normal saline

OCD - obsessive-compulsive disorder

OSA - obstructive sleep apnea

PCOS - polycystic ovary syndrome

PMS - premenstrual syndrome

PPD - purified protein derivative

PSA - prostate-specific antigen

PT - prothrombin time

PTT - partial thromboplastin time

RA - rheumatoid arthritis

RBC - red blood cell

RSV - respiratory syncytial virus

SLE - systemic lupus erythematosus

TB - tuberculosis.

It is important to remember that medical abbreviations can vary based on location and specialty.

Healthcare professionals should use medical abbreviations with caution and only when they are familiar with their meanings.

Patients should always communicate any questions or concerns they have about their medications or medical care to their healthcare provider or pharmacist to ensure they receive safe and accurate medical care.

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cardiacreports2 · 2 months ago

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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.

#cpr #male cpr #heart attack #cpr resus #defib #resuscitation #dark resus #cpr and aed

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taimoorkhan · 2 years ago

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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.

#emergency medicine #acute care #emergency #health & fitness #biology #emergency physician #foamed #myocarditis

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science-lover33 · 2 years ago

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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.

#atomic heart #science #biology #college #education #school #student #medicine #doctors #health #healthcare #nursing #physiology #pathology

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