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Arterial blood gas = the acidity (pH) and amounts of oxygen and carbon dioxide in the blood from an artery are measured in an arterial blood gases (ABG) test.

This test determines how well the lungs can transport oxygen into the bloodstream and eliminate carbon dioxide from the bloodstream.

When blood flows through the lungs, oxygen enters the bloodstream, while carbon dioxide exits the bloodstream and enters the lungs. The oxygen and carbon dioxide levels in blood collected from an artery can be evaluated before they enter body tissues in an ABG test.

For this patient, the ABG is normal meaning that the acidity (pH) and amounts of oxygen and carbon dioxide in the blood are on normal level.

Full blood count (FBC) = complete blood count (CBC) = blood test that is used to assess overall health and diagnose a variety of illnesses such as anaemia, infection, and leukaemia.

A complete blood count test measures several components and features of the blood, including:

red blood cells, which carry oxygen,

white blood cells, which fight infection,

haemoglobin, which carries oxygen in red blood cells,

hematocrit, which is the proportion of red blood cells to the fluid component or plasma in the blood,

platelets, which aid in blood clotting.

This result for the patient’s FBC is also normal or another way to say the result does not show abnormal increases or decreases in cell counts may indicate that the patient has an underlying medical condition that needs to be evaluated further.

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After a thorough discussion, we conclude that the patient is having Myocardial Infarction. Here, Hariz and I will discuss regarding Myocardial Infarction.

- Definition
- Incidence and risk factors
- Clinical features
- Pathogenesis
- Patterns of infarction
- Treatment and post management

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Yes sure Syasya. The renal profile is actually tested to find out how well the kidneys are functioning. It is shown by the parameters tested in the test including the levels of creatinine, sodium, calcium, chloride, blood urea and potassium. Sudden change in renal profile may indicate deterioration in kidney function that needs urgent treatment.

In this case, the patient’s renal profile is normal, which means that the patient has a fully functioning kidney.

Liver function tests also have been done to measure how well the patient’s liver performs its normal functions of producing protein and clearing bilirubin (blood waste product). Elevated levels of bilirubin might indicate liver damage or disease or certain types of anaemia. Normal values of liver function tests are generally around 7 to 20 mg/dL (2.5 to 7.1 mmol/L).

The patient shows a normal liver function test reading, which indicates that the patient's liver is functioning normally.

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Patient came to ED due to chest pain (angina).

Differential diagnosis due to chest pain classified below

1. Cardiac

MI

Myocarditis

Pericarditis

Cardiac tamponade

2. Pulmonary

Pneumonia

PE

Pneumothorax

Empyema

Bronchiectasis

TB

3. Vascular

Dissescting aortic aneurysm

Aortic rupture

However, once the patient rested, the pain subsided. Pt display symptoms of stable angina.

Stable angina is most often due to a fixed stenosis caused by an atheroma.

Since Pt’s age is 63 years old male, it is one of the non-modifiable risk factors for atherosclerosis. Patient also smoked 2 packs of cigarettes a day for the last 40 years, one of the modifiable risk factors for atheroma.

This factors predisposes the pt to have decrease myocardial oxygen supply d/t decreased luminal diameter in the presence of atherosclerostic lesion. There will be decrease in the SPO2 causing hypoxemia. Pt’s SPO2 is 80% whereas the normal range is 95-100%

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Definition : an elevated level of blood glucose in blood, can lead to serious damage to the heart, blood vessels, eyes, kidneys and nerves over time.

Types of diabetes

Type 1 diabetes.

- caused by an autoimmune reaction that stops your body from making insulin.

-5-10% of the people

Type 2 diabetes

- an impairment in the way the body regulates and uses sugar (glucose) as a fuel

- 90-95% of people

Gestational diabetes

-pregnant women

What diabetes is experienced by patients and why?

Patient have type 2 diabetes.

Reason: elderly,smokers as research stated that smokers are 30 to 40 percent more likely to develop type 2 diabetes than nonsmokers.

List antidiabetic drugs

meglitinides

metformin

Sulfonylureas

Thiazolidinediones

dipeptidyl peptidase-4 inhibitors

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In trigger 2, it was stated that the patient smoked 2 packs of cigarettes a day for last 40 years

Cigarettes consist of tobacco as one of its components.

Tobacco contains nicotine which is an addictive drug. Therefore, when someone smokes cigarettes or chewing tobacco, it can lead him or her to become more addicted to it.

Once the nicotine enters the body, it will activate nicotine receptors located in the brain. The more cigarettes smoked, the more access of nicotine into the body, thus it will activate a more addictive effect on the brain.

As for this patient, smoking 2 packs of cigarettes a day can be considered as a heavy smoker.

Smokers can be further divided into 3 main groups which are light, moderate and heavy smokers based on how many cigarettes they smoke per day. Below are the groups and its amount of cigarettes smoking per day:

1. Light smokers: <1-5 cigarettes per day
2. Moderate smokers: 6-10 cigarettes per day
3. Heavy smokers: >11 cigarettes per day

Mr Ahmad can be categorized in the heavy smoker group as 1 pack consists of 20 cigarettes. Hence, it will be counted as 40 cigarettes per day for him.

In addition, the patient had been smoking for the last 40 years. It can be considered a very long time thus causing him to have very serious conditions and lead him to have a very serious disease.

Every smoker, no matter what category there is, will be affecting other people’s life and comfort.

This can happen when tobacco smoke, also known as second-hand smoke from cigarettes, is exposed to the environment and makes other people, especially non-smoker breathing in that polluted environment.

These people are known as secondary smokers or having passive smoking.

Tobacco smoke consists of many types of chemicals that can affect a smoker itself such as it can lead to cancer, lung disease, heart disease and many more. As the smoke is also released to the secondary smoker, breathing in this smoke can also affect their health.

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function

To increase glycaemic control in patient diagnosed with type 2 diabetes mellitus

Mechanism of action

Reduce the hepatic glucose output, largely by inhibiting hepatic gluconeogenesis

excess glucose produced by liver is a major source of high blood glucose in type 2 diabetes

slows intestinal absorption of sugars & improves peripheral glucose uptake and utilization.

Drugs property is it able to modestly reduce hyperlipidaemia (reduce LDL, rise HDL)

Pharmacodynamic

It Increase glucose uptake & use by target tissue, decreasing insulin resistance

Pharmacokinetic

Administered & absorbed via oral

Negligibly bound to plasma proteins

Do not metabolized

Excreted in urine

drug group

insulin sensitizer, biguanides

inc

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Hypertension definition

High blood pressure, also called hypertension, is blood pressure that is higher than normal which is above 120/80 mmHg.

Ways to measure blood pressure

1. Sphygmomanometer

A sphygmomanometer is a device used to measure blood pressure with a stethoscope by using the auscultatory technique.

2. Digital blood pressure monitor

Digital blood pressure monitors are often used on the wrist and can be placed on the finger or upper arm and activated simply by pressing a button.

Antihypertensive drugs

Sympathoplegics drugs

Vasodilators drugs

Renin-angiotensin-aldosterone system (RAAS) inhibitors drugs

In this case, the patient stated that he has hypertension, which means that his blood pressure is above 120/80 mmHg.

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force of the blood pushing against the artery walls during contraction and relaxation of the heart

Each time the heart beats, it pumps blood into the arteries, resulting in the highest blood pressure as the heart contracts

When the heart relaxes, the blood pressure falls.

Two numbers are recorded when measuring blood pressure.

The higher number, or systolic pressure, refers to the pressure inside the artery when the heart contracts and pumps blood through the body

The lower number, or diastolic pressure, refers to the pressure inside the artery when the heart is at rest and is filling with blood

Both the systolic and diastolic pressures are recorded as "mm Hg" (millimetres of mercury) by using sphygmomanometer.

From the blood pressure reading in vital sign monitor, it recorded 80/40mmHg of blood pressure which the 80 indicates the systolic pressure, and 40 indicates diastolic pressure.

Blood pressure is categorized as normal when the systolic of less than 120 and diastolic of less than 80. But it can’t be to lower or the patient will be in hypotension condition.

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Okay Syuhada. I would love to explain it to you. We can see the patient’s lab test shows elevated cardiac markers. So, this tells us that we  can rule out other differential diagnosis that is not cardiac related.

Since the atheroma cause blockage of coronary blood flow, irreversible cell death occur due to ischaemia.

Once myocyte membrane damage, cell enzymes/proteins leak into blood.

Cardiac markers elevated such as Troponin I indicates there is cardiac muscle injury.

Troponin I is the cardiac marker in acute coronary syndromes and in heart failure.

Differential diagnosis of elevation would be

MI

CHF

Myocarditis

Acute PE

Having a result higher than 0.40 ng/ml showing the underlying cardiac injury is MI. Since Pt’s troponin I is 12.90 ng/ml. This can confirms that the Pt has MI after seeing his ECG results also shows an ST- segment elevation.

D-dimer normal level is below 0.25 ug/ml. D-Dimer, an expression of ongoing thrombus formation and lysis, is a marker of substantial incremental value for the early diagnosis of acute coronary syndromes presenting with chest pain. This ticks the box since the patient also presents with chest pain. It adds independent information to the traditional assessment for myocardial infarction. D-Dimer can be incorporated into clinical decision models in the ED to find the definitive diagnosis.

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Before we can identify the effected part of the abnormalities, it is important to know the anatomy of the heart.

Location: The human heart is  located within the thoracic cavity, medially between the lungs in the space known as the mediastinum

Chamber of the heart: Consist 4 chambers

Left & Right atrium:  acts as a receiving chamber and contracts to push blood into the lower chambers, the right ventricle and the left ventricle.

Left & Right ventricle: serve as the primary pumping chambers of the heart, propelling blood to the lungs or to the rest of the body.

Heart Valve: Prevent the backflow of the blood through the heart.

Tricuspid valve:  Between the right atrium and the right ventricle

Pulmonary semilunar valve: Emerging from the right ventricle at the base of the pulmonary trunk

Mitral valve: Located at the opening between the left atrium and left ventricle

Aortic semilunar valve: At the base of the aorta

Heart Wall: consist 4 walls

Pericardium: the outermost layer of the heart wall, it is the layer in which arteries supply blood to the heart.

Epicardium: the layer just below the pericardium, between both these layers there is a presence of the cavity; this cavity is known as the pericardial cavity.

Myocardium: the layer that is responsible for the contraction and relaxation of the atrium and ventricle, thus ensuring the blood supply of the heart.

Endocardium: The innermost layer of the heart wall.

The blood supply of the heart

Coronary arteries: supply blood to the myocardium and other components of the heart.

Classes: left coronary artery (then divides into the left anterior descending (LADA) and circumflex branches) and right coronary artery ( then bifurcate into the right marginal artery and posterior descending artery).

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HEART ATTACK

Myocardial infarction is a death of cardiac muscle due to prolonged severe ischemia.

It's also defined as an area of necrosis of heart muscle resulting from a sudden absolute or relative reduction in the coronary blood supply.

The commonest precipitating cause is thrombosis superimposed on or haemorrhage within an atheromatous plaque in an epicardial coronary artery.

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A coronary angiogram is a special procedure that takes dynamic x-ray pictures of the heart.

Purpose: to see if the coronary arteries are narrowed or blocked & to look for abnormalities of heart muscle or heart valves.

Various tests performed before the angiogram: blood tests, ECG, chest x-ray or cardiac CT

Problems diagnosed by coronary angiogram

Diagnose a range of heart problems

Aneurysm (abnormal ballooning of the heart wall), heart arrhythmias (irregular heart beat) or birth defects, such as a hole in the heart

Medical issues to consider before having an angiogram

medical history; including asthma, allergies or kidney disease

allergic reactions to any drugs

current medications

fasting: 4-6 hours prior to test

other tests prior to angiogram: blood tests, an electrocardiogram and chest x-ray and cardiac CT

Procedure:

1. History taking

2. Prepare for the procedure by putting in an IV cannula and shaving both sides of groin and wrist if necessary.

3. A heart monitor will record the heart beat during the test.

4. The skin on the wrist and both sides of the groin is cleaned with an antiseptic wash and covered with sterile drapes.

5. The doctor injects a small amount of local anaesthetic around the access site (wrist or groin) to numb the area then inserts a small catheter through the skin into the blood vessel.

6. The doctor watches the progress of the catheter via dynamic x-rays transmitted to a television monitor.

7. Once the catheter is in place, a small amount of contrast (x-ray sensitive dye) is injected through it.

8. Further dynamic x-rays are taken as the contrast goes through the blood vessels.

9. The angiogram lasts for around 40 minutes.

Complications of a coronary angiogram

allergic reaction to the contrast dye, including hives and itchy skin

bleeding from the wound

heart arrhythmia

heart attack

stroke

Results

An angiogram shows what's wrong with patients' blood vessels.

Show how many coronary arteries are blocked or narrowed by fatty plaques (atherosclerosis)

Pinpoint where blockages are located in blood vessels

Show how much blood flow is blocked through the blood vessels

Check the results of previous coronary bypass surgery

Check the blood flow through the heart and blood vessels

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To answer Ain's curiosity, here I explained about the risk factor and incidence for myocardial infarction or for easy understanding, heart attack.

1. Approximately 10% of myocardial infarcts occur in people younger than age 40
2. 45% occur in people younger than age 65
3. It frequently rises progressively with increasing age
4. Strongly correlates with genetic and behavioural predisposition to atherosclerosis
4. Male gender increases the relative risk of MI

SINCE PATIENT IS A 65 YEARS OLD MALE AND A SMOKER, HE IS PREDISPOSE TO THIS CONDITION

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Chest tightness  is common sensation and can be a symptom of many different conditions and associated with chest pain that you've explained.

It is the result of diseases that affect internal organs within the thorax (heart, lungs, esophagus, stomach, gallbladder, pancreas, and liver)

It caused by disease of the chest wall (abnormalities of muscle, bone, cartilage, and skin)

Other than that, pain and tightness can also radiate in other areas of the body including arm, upper abdomen, shoulder, back, neck/throat, teeth or jaw

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Patient was sweating and gasping for air on the second episode.

12-16 breath per min is the normal respiratory rate. Since pt’s respiratory rate is high. Patient starts to hyperventilate.

Due to the nature of the symptoms that may arise during hyperventilation, the differential is broad and may include:

Arrhythmia or myocardial infarction

Stroke or seizure

Asthma exacerbation

Pneumothorax

Pulmonary embolism

Ketoacidosis (eg, diabetic ketoacidosis)

Hyperthyroidism

Acute panic attack / panic disorder

Congestive heart failure

Pleural effusion

Pneumonia (bacterial, viral)

Interstitial lung disease

Agonal breathing or gasping for air can occur when someone has gone into cardiac arrest. Unlike a heart attack — which happens when one or more arteries narrow and stop blood from reaching the heart muscle — cardiac arrest is an electrical problem. During cardiac arrest, the heart stops beating effectively. This is known as an arrhythmia, or pattern of irregular heartbeats.

Blood continues to flow briefly in the brain and other organs, which can cause gasps for a few minutes after the heart stops. If cardiac arrest is the cause of agonal breathing, the labored breaths may only last a few minutes. Having had a heart attack due to MI makes it more likely to have cardiac arrest.

Another common cause of agonal breathing is cerebral ischemia, or a reduction in blood flow to the brain. This can be caused by a ministroke due to a blood flow blockage within a brain blood vessel. It can also be caused by a hemorrhagic stroke due to a bleeding blood vessel within the brain. Either can lead to a condition called cerebral hypoxia, which is insufficient oxygen supply to the brain regardless of the cause. The brain can have permanent damage if it’s deprived of oxygen for too long.

HOWEVER,

Since our differential diagnosis overlaps with MI, we should run more tests to confirm the diagnosis.

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1. Severe chest pain - often develops suddenly but may build up gradually and generally lasts for several hours

2. Present with prolonged chest pain described as crushing, stabbing and squeezing

3. Pain accompanied by profuse sweating, nausea and vomiting

4. In at least 10% of patients, MI is painless or silent, particularly true in elderly

MOST OF THE FEATURES HAVE BEEN SHOWN AND EXPERIENCED BY THE PATIENT

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Well nurin, I will now explain in detail what intubation is and why this patient needed to be intubated along with its relation to heart diseases. Intubation is a procedure where a tube called an endotracheal tube (ET) is inserted down the patient’s throat and into the trachea making it easier for air to get into and out of the lungs. This is done so that said tube can then be attached to a machine called the ventilator, which pumps air into the lungs by providing extra oxygen as well as helping you to breathe out the air that is full of carbon dioxide. This process is called Mechanical ventilation and it helps to balance our oxygen and carbon dioxide level in a healthy state.

Before moving on, we need to understand the purpose of intubation and when is the appropriate time a patient needs to be intubated. Intubation is given to those who cannot maintain their airway, cannot breathe on their own without assistance. This is common when patients are undergoing general anesthesia which is a drug given prior to surgery or a medical procedure to put them in a sleep-like state and in accordance with Mr Ahmad’s case, a coronary angiogram was performed. Although an angiogram requires one to lie awake on the table they will still need to be mildly sedated. General anesthesia acts as a drug to paralyze the muscle of the body including the diaphragm which makes it impossible for a patient to inhale air without using a ventilator. Hence, general anesthesia can hold down your own breathing, making Mr Ahmad unable to breathe on his own during the procedure and with intubation it lets the machine do the breathing for us.

Besides, intubation is also done to those who have any injury or illness that makes it hard to breathe. As breathing provides oxygen to every cell in our body and if one doesn't get enough it can lead to passing out, brain damage or even death. Ventilation also helps us to breathe out the air accumulated by getting rid of the carbon dioxide so that it does not build up in our blood. This can cause the blood to be more acidic which would result in unwanted health problems such as respiratory acidosis. As Mr Ahmad had arrived the hospital in an unconscious state would also be one of the reasons as to why he might need to be intubated. He could possibly have an injury or illness that can weaken the reflexes in his airway. Furthermore, his vital signs showed low oxygen saturation level which is 80% and this was also an indication for him to be intubated to allow more oxygen to enter the lungs.

To put it simply, patients who require intubation have at least one of the following five indications:

Inability to maintain airway patency

Inability to protect the airway against aspiration

Failure to ventilate

Failure to oxygenate

Anticipation of a deteriorating course that will eventually lead to respiratory failure

Intubation Procedure

1) Typically a patient is sedated or is in an unconscious state due to injuries that relaxes both the mouth and airway. The patient would lie flat on their backs with the person in charge of inserting the tube standing at the head of the bed.

2) The patient's mouth is  opened gently by using a lighted instrument in order to move the tongue out of the way providing a visible opening to the throat, the tube is then guided in the throat furthering into the trachea

3) There is a small balloon around the tube that is inflated to prevent the tube from moving and to keep air from escaping.Once said balloon is inflated, the tube is securely placed by taping it at the mouth.

3) To check whether the placement is correct, it is first listened to the lungs with a stethoscope and verified with a chest X-ray. In comparison in the operating room, a device that measures carbon dioxide is only present if the tube was in the lungs, rather than in the esophagus. This used to confirm that it was rightfully positioned.

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The relation of intubation with heart diseases

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The relation of intubation with heart diseases

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When one is experiencing cardiac arrest, the heart would suddenly stop pumping oxygenated blood from reaching the brain and other organs. This can lead to chest pains and difficulty in breathing. In Mr Ahmad’s case we were informed that after a few hours upon arriving at the emergency department, he was gasping for air meaning that he was experiencing shortness of breath or dyspnea. Dyspnea is one of the common symptoms in patients in cardiac arrest. Certain patients stay unconscious after having a cardiac arrest, hence they are required to be intubated with the assistance of the breathing machine to ensure adequate oxygenation and ventilation to help the air to enter and exit the lungs.

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Thank you najwa for your question and to answer yes there are risks regarding intubations. Though it may be low, there are still some potential issues that can arise when a patient must remain for an extended period of time on the ventilator. Risks such as the scope can cause trauma or cut inside the mouth. The tube can also hurt your throat and voice box making one have a sore throat or find it difficult to talk and breathe for a certain time. This procedure may hurt your lungs by causing one of them to collapse. Infection as well as pneumonia can occur due to aspiration. Accidental intubation in the esophagus instead of the trachea are likely if one just ate as it increases the risk for food to be pulled into the lungs.  Besides, the scope has the possibility to cause trauma to the teeth if they are in poor shape. As Mr Ahmad’s past medical history stated that he was a smoker, it can make intubation and recovery a lot more harder.

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Primary hyperhidrosis

If excessive sweating has no underlying medical cause

It happens when excess sweating is not triggered by a rise in temperature or physical activity.

Secondary hyperhidrosis

If the excess sweating is due to an underlying medical condition

It could be an early warning sign of heart problems.

Pumping blood through clogged arteries takes more effort from the heart, so the body sweats more to try to keep our body temperature down during the extra exertion.

Underlying health conditions:

diabetes

Infection (tuberculosis, endocarditis, osteomyelitis)

hormonal changes (menopause)

side effects of medication (antidepressants, diabetes medication)

anxiety

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Ofcourse Ain. When we talk about a disease we should actually know how it develop on someones body and whats the progression from one to one steps. Before I explain further about MI, here is a diagram to help you understand the  overview of progression of myocardial infarction.

Coronial Artery Occlusion

A coronary artery atheromatous plaque undergoes an acute change consisting of intraplaque hemorrhage, erosion or ulceration or rupture of fissuring

When exposed to subendothelial collagen and necrotic plaque contents, platelet adhere become activated release their granule contents and aggregate to form microthrombi

Vasospasm is stimulated by mediator released from platelets

Tissue factor activates the coagulation pathway adding to the bulk of the thrombus

Within minutes, the thrombus can expand to completely occlude the vessel lumen

The progression of ischemic necrosis in the myocardium:

Due to the myocardial perfusion pattern from epicardium to endocardium, ischemia is most pronounced in the subendocardium; thus, irreversible injury of ischemic myocytes occurs first in the subendocardial zone

The progression of ischemic necrosis in the myocardium after coronary artery occlusion:

Necrosis begins in a small zone of the myocardium beneath the endocardial surface in the center of the ischemic zone.

The area that depends on the occluded vessel for perfusion is the “at risk” myocardium.

Note that a very narrow zone of myocardium immediately beneath the endocardium is spared from necrosis because it can be oxygenated by diffusion from the ventricle.

Necrosis involves approximately half of the thickness of the myocardium in 2 to 3 hours of the onset of severe myocardial ischemia, and is usually transmural within 6 hours.

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For a better understanding on the pathogenesis of MI, I provide you a brief video explained about it from Youtube. Have a look!

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Heart attack (myocardial infarction) pathophysiology | NCLEX-RN | Khan Academy

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In general, heparin is an antithrombotic drug which lies under anticoagulant medication.

Anticoagulant can be described as a substance that can avoid coagulation from happening. Therefore, it will prevent blood from clotting either in a patient who has a medical condition or medical procedures that can increase the probability for clot to be formed.

To be more specific, heparin can be divided into 3 types which are:

- Unfractionated heparin (UFH)
- Low molecular weight heparin (LMWH)
- Synthetic heparin

LMWH is a chemical, enzymatic degradation of UFH. It can be further divided into some groups such as dalteparin, enoxaparin  and tinzaparin

LMW heparin is indicated for patient who hass deep vein thrombosis (DVT) and myocardial infarction.

As in trigger 5, the ECG showed that the patient was having anterolateral STEMI. Therefore, it was the best choice for the patient by giving him a LMWH.

It was administered by a parenteral route which is subcutaneous. It means that this drug is injected into the tissue or fat underlying the dermis. This route will provide the slow absorption of heparin since there is less blood flow happening underlying the skin. Therefore, the drug will flow slowly at a good rate of absorption.

By administering LMWH subcutaneously, this slow absorption gives more time for subcutaneous tissue to fit in with the volume injected to the patient. As a result, this will reduce the pressure, the pain and reduce damage to other sites.

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Left coronary angiogram showing tight stenosis of proximal left anterior descending (LAD) coronary artery

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The Catheter angiography confirms critical stenosis in the proximal LADA

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The Catheter angiography confirms critical stenosis in the proximal LADA

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Left Anterior Descending Artery (LADA)

Location: The left anterior descending (LAD, interventricular) artery appears to be a direct continuation of the left coronary artery which descends into the anterior interventricular groove. Branches of this artery, anterior septal perforating arteries, enter the septal myocardium to supply the anterior two-thirds of the interventricular septum (in ~90% of hearts).

Function: In general, the LAD artery and its branches supply most of the interventricular septum; the anterior, lateral, and apical wall of the left ventricle, most of the right and left bundle branches, and the anterior papillary muscle of the bicuspid valve (left ventricle). It also provides collateral circulation to the anterior right ventricle, the posterior part of the interventricular septum, and the posterior descending artery.

What does stenosis mean?

Stenosis it self means narrowing.

Hence, we can define that stenosis in proximal Left Anterior Descending Artery (LADA) is narrowing of the proximal LADA or the blockage of the LADA that can interfere the supplies of the blood to the front of the left side of the heart.

Hence, blockage of this artery due to coronary artery disease can lead to impairment or death (infarction) of the conducting system. The result is a "block" of impulse conduction between the atria and the ventricles known as "right/left bundle branch block."

The causes of LADA stenosis:

smoking

High LDL cholesterol, high triglycerides levels, and low HDL cholesterol

hypertension

obesity

diabetes

The symptoms of having LADA stenosis:

tightness of the chest (angina)

shortness of breath (dyspnea)

Weakness and fatigue

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Sure Afrina! Thank you for your question.

The mechanism of action of LMWH is similar as UFH

Both of them inactivate the coagulation cascade by activating antithrombin (AT) III.

As ATIII is an inhibitor enzyme, its activation will then eventually inhibit thrombin and other serine proteases by binding covalently to factor IIa (thrombin) and factor Xa.

LMWH selectively inhibits factor Xa meanwhile UFH predominantly accelerates inhibition of both factor IIa and Xa.

For this patient, as he was taking LMWH, once factor Xa is inhibited, the cleavage of prothrombin to thrombin will also be inhibited.

Therefore it will slow down or prevent clot formation as inhibition of thrombin will make no conversion of fibrinogen to fibrin. Thus, clotting is prevented and this will irreversibly inhibiting their procoagulant activities

UFH or LMWH will dissociate from AT and can be reutilized.

As for additional informations, there are some differences between UFH and LMWH

LMWH is cleared renally

LMWH has longer elimination  half life compared to UFH

LMWH is less likely to cause heparin-induced thrombocytopenia (HIT)

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Infarction may be

Transmural

Nontransmural (Subendocardial)

Multifocal microinfarction

Transmural infarction

Transmural infarcts involve the whole thickness of myocardium from epicardium to endocardium and are usually characterized by abnormal Q waves on ECG

Usually associated with a combination of chronic coronary atherosclerosis, acute plaque change, and superimposed thrombosis.

Nontransmural infarction

Nontransmural (including subendocardial) infarcts do not extend through the ventricular wall and cause only ST-segment and T-wave (ST-T) abnormalities.

Subendocardial infarcts usually involve the inner one third of myocardium, where wall tension is highest and myocardial blood flow is most vulnerable to circulatory changes.

Multifocal microinfarction

Involving only SMALLER INTRAMURAL VESSELS.

May occur in the setting of microembolization, vasculitis, or vascular spasm, for example, due to endogenous catechols (epinephrine) or drugs (cocaine or ephedrine).

Elevated levels of catechols also increase heart rate and myocardial contractility, exacerbating ischemia caused by the vasospasms

Because the transmural depth of necrosis cannot be precisely determined clinically, infarcts are usually classified as STEMI or NSTEMI by the presence or absence of ST-segment elevation or Q waves on the ECG.

Non–ST-segment elevation myocardial infarction (NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by cardiac markers in blood; troponin I or troponin T and CK will be elevated) without acute ST-segment elevation. ECG changes such as ST-segment depression, T-wave inversion, or both may be present.

ST-segment elevation myocardial infarction (STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed by nitroglycerin. Troponin I or troponin T and CK are elevated.

PATIENT HAVE STEMI OR TRANSMURAL MYOCARDIAL INFARCTION DUE TO ST ELEVATION THAT CAN BE SEEN ON THE ECG RESULTS

As for treatment and post management, Hariz will help me to give a brief discussion about it.

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ASPIRIN
For the treatment of myocardial infarction, the patient can be given the aspirin. Aspirin known as acetylsalicylate is a commonly drug that is used for the treatment of pain and fever as it has both antipyretic, anti-inflammatory (NSAID), and anti-coagulant effects. Using as anti-coagulant drug in low dose, aspirin inhibit platelet aggregation and is used in the blood clots prevention which will further causing infarction or necrosis in different organs such as stroke, coronary artery disease and myocardial infarction. Besides that, acetylsalicylate in high dose works as anti-inflammatory (NSAID) by blocking both cyclooxygenase (COX-1 and COX-2) which responsible for converting arachidonate into prostaglandin thus decrease the response toward injury or trauma. Aspirin is non-selective NSAID that blocks both COX-1 and COX-2 which also responsible for platelet aggregation inhibition as it inhibits thromboxane A2 (TXA2) and capable for blood clotting up to 7-10 days due to average platelet lifespan. This drug will help in patient from getting infarction or necrosis diseases.

The adverse drug reaction of aspirin is severe bleeding as it blocks the platelet aggregation and might cause blood loss for the body. Furthermore, aspirin also can cause rapid breathing because it blocks production of prostaglandin-E2 (PGE2) which responsible for smooth muscle relaxation. Low amount of PGE2 cause muscle contraction in bronchus thus trigger bronchoconstriction which resulting in low inhaled oxygen volume. This further causing body lacks oxygen, then further trigger the respiratory mechanism to increase respiratory rate which finally increase the respiratory rate and hyperventilation (rapid breathing) occur. Besides that, ADR of aspirin can cause stomach pain due to inhibiting the prostaglandin-I2 (PGI2). PGI2 function to increase the gastric mucous secretion in the stomach. If the PGI2 production is inhibited, gastric mucous production will be inhibited thus causing no protection of stomach lining then causing inflammation which finally gastritis occurs.

People at age more than 60 or with history of gastrointestinal (GI) disease or infection has higher risk for serious GI bleed. It is due to anti-coagulant reaction of aspirin that cause blood leakage cannot be blocked in the GI if any bleeding occurs either from infection or hard stool. In people with asthma, taking aspirin can cause acute asthma attack or can aggravate asthma symptom due to COX inhibition. It is because over amount of arachidonic acid will enter the 5-lipoxygenase pathway and finally produce leukotriene C4 which will increase the hyperresponsiveness in asthma patient.

Acetylsalicylate also can cause nephrotoxicity. It is due to decrease PGE2 that function vasodilator. Decreasing in PGE2 will cause vasoconstriction. In kidney, vasoconstriction of glomerular capillary at afferent artery can cause decrease in glomerular filtration rate (GFR) which will resulting in less filtration and secretion of waste product form body. This can cause azotaemia (creatinine and blood urea in blood) due to low filtration of glomeruli. Moreover, aspirin can lead to gout as it can inhibit the tubular uric acid secretion. This will lead to increase uric acid in blood (hyperuricemia) which further causing gout. Lastly for children, aspirin can cause Reye’s syndrome in children if aspirin is used to treat the children.

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Next, the patient is also given clopidogrel. Clopidogrel can reduce the risk of myocardial infarction as it is a prodrug of platelet inhibitor. It is also known as antiplatelet drug. Clopidogrel works only if it is in active form. Its active form can be triggered when the clopidogrel is metabolized by carboxylesterase-1. It active form function as platelet inhibitor that will bind irreversibly to P2Y ADP receptors on platelet. When the active form binds to the P2Y receptor, it will inhibit the binding of ADP and P2Y. Thus, preventing the blood to clots so the blood flow will become smoother.

Clopidogrel also have its adverse effects. If the symptom of the side effect are severe, the patient must immediately contact the doctor. The effects can be varied such as fatigue, headache, nausea, vomiting and stomach pain. For some cases, it will also develop hives, fever, and rash.

For some patients, clopidogrel is contraindicated to them because they have hypersensitivity to clopidogrel. Other than that, patient with severe bleeding such as GI tract bleeding, intracranial bleeding and bleeding form surgery are not recommended to consume clopidogrel as it functions to inhibit platelet aggregation. It will make the other disease become worsen.

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amlodipine was prescribed by a doctor because En. Ahmad has a medical history of hypertension.

amlodipine has a vasodilator effect, it is therapeutically uses in hypertensive patient, asthma, diabetes, angina & peripheral vascular disease.

mechanism of action

Intracellular calcium plays a role in maintaining tone of smooth muscle & in the contraction of myocardium

Calcium enter muscle cell through voltage calcium channels

Triggers release of calcium from sarcoplasmic reticulum. Increase the cytosolic level of calcium.

Calcium-channel antagonist (blocker) will block the inward movement of calcium by binding to L-type calcium channel in heart & smooth muscle of coronary & peripheral arteriolar vasculature.

Cause vascular smooth muscle to relax, dilating mainly arterioles.

pharmacodynamic

strong affinity for cell membranes, modulating calcium influx by inhibiting selected membrane calcium channels.

This drug's unique binding properties allow for its long-acting action and less frequent dosing regimen.

pharmacokinetic

Administered via oral

Absorbed slowly & completely in gastrointestinal tract

Distributed throughout the body by plasma

Metabolised in liver

Excreted in urine

drug group

Dihydropyridines, Calcium-channel blockers

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First of all,it is important to understand the normal ECG, in order to identify the abnormalities of patient’s  ECG result.

A normal ECG contains waves, intervals, segments and one complex.

It can be seen in the figure above and each phase is determined by the electrical signal in cardiac cycles.

The main parts of an ECG are P wave, QRS complex and T waves.

The electrical signal in the cardiac cycle is shown in ECG by P wave,QRS complex,T wave and U wave.

P wave : atrial depolarization

QRS complex :ventricular depolarization

T wave :ventricular repolarization

U wave :Purkinje repolarization

ECG is used to determine or detect:

Abnormal heart rhythm (arrhythmias)

blocked or narrowed arteries in your heart (coronary artery disease) are causing chest pain or a heart attack.

previous heart attack

Monitoring heart disease treatments, such as a pacemaker

Heart beat

Heart rhythm

Heart structure abnormalities

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STEMI results from complete and prolonged occlusion of an epicardial coronary blood vessel.

NSTEMI usually results from severe coronary artery narrowing, transient occlusion, or microembolization of thrombus and/or atheromatous material. NSTEMI is defined by an elevation of cardiac biomarkers in the absence of ST elevation.

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Thus, Patients have STEMI because of elevation in the ST segment shown in his ECG result.The ST elevation because of  myocardial ischaemia or infarction.

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Is a measurement of the number of times the heart beats per minute.

As the heart pump blood through the arteries, the arteries expand and contract with the flow of the blood

The normal pulse for healthy adults ranges from 60 to 100 beats per minute. The pulse rate may fluctuate and increase with exercise, illness, injury, and emotions.

The changes in heart rate can be life threatening

When the heart does not operate as it is supposed to & develops an abnormally slow heart rate that is less than 60 beats per minute, the condition is known as bradycardia

Whereas when the heart develops abnormally fast heart rate that is higher than 100 beats per minute, the condition is known as tachycardia.

The patient’s heart rate recorded was 110bpm, therefore the patient has tachycardia.

However, tachycardia has many different types where they’re grouped according to the part of the heart responsible for the fast heart rate & cause of the abnormally fast heartbeat.

Atrial fibrillation = rapid heart rate caused by chaotic, irregular electrical impulses in atria

Atrial flutter = heart's atria beat very fast but at a regular rate. The fast rate results in weak contractions of the atria. Atrial flutter is caused by irregular circuitry within the atria.

Supraventricular tachycardia = abnormally fast heartbeat that starts somewhere above ventricle

Ventricular tachycardia = rapid heart rate that starts with abnormal electrical signals in ventricle

Ventricular fibrillation = rapid, chaotic electrical impulses cause the ventricles to quiver instead of pumping necessary blood to the body

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The number of breaths a person takes per minute.

Usually measure when a person is at rest.

May increase with fever, illness & other medical condition

The normal respiration rate for an adult person at rest range from 12 to 20 breath per minute. While for elderly it range from 15-25 breath per minute

It is because lung capacity decrease over time due to some changes of the lungs as people age such as;

airways get smaller,

air sacs (alveoli) lose their shape,

diaphragm get weaker which preventing from fully inhale & exhale,

muscle near airway may lose their ability to keep the airways completely open in order to fill

rib cage and posture related changes can leave less room for lungs to expand

nerves in airways for coughing may become less sensitive & cause lung to collect particle.

The patient’s respiratory rate recorded was 27 breath per minute, therefore the patient has tachypnea.

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Lastly, the patient is also given nitroglycerin. It can be used to treat acute heart failure in patients with myocardial infarction. The mechanism of action of nitroglycerin is that the nitroglycerin need to be metabolized to its active form. Nitroglycerin is converted to nitric oxide by mitochondrial aldehyde dehydrogenase. The active state of nitroglycerin will be used to activates the enzyme guanylate cyclase. When the enzyme is activated, the synthesis of cylic guanosine 3’, 5’-monophosphate will occur. This event will trigger the activation of cascade of protein kinase dependent phosphorylation in smooth muscle causing the dephosphorylation of myosin light chain of smooth muscle. This will lead to increase blood flow in body. Thus the blood flow to the myocardium increased.

However, nitroglycerin also have its side effect. It is because this medication is a foreign substance to the body so the body need to adjust for the drug. The side effects are headache, dizziness, lightheadedness, nausea . Nitroglycerin did not have very serious adverse effect so many doctor recommend the patient to use the drug.

Nitroglycerin is contraindicated to a patient with anemia, methemoglobinemia, hemorrhage in the brain and low blood pressure. Nitroglycerin also can be used for many purposes. One of them is to hinder and cure angina or chest pain due to cardiovascular disease, then to treat peri-operative hypertension or induce intra-operative hypotension. Nitroglycerin is indicated to treat pain caused by anal fissures when converted into ointment. The transdermal form is applied directly to the skin to prevent acute anginal attacks.

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Temperature of the Body

The onset of an infection is indicated by a rise in body temperature.

Even if patient feel fine, check the vitals to make sure the patient keeping a healthy body temperature. Body temperature swings that are out of the ordinary are grounds for concern.

A normal body temperature is 37 degrees Celsius, however anything between 36.1 and 37.2 degrees Celsius is normal.

Body temperature is influenced by age, gender, weight, ambient temperature, and overall health. The hypothalamus is a brain area that controls body temperature.

When your immune system detects a virus in your body, it sends signals to the hypothalamus to raise body temperature and weaken the infection.

Sweating, clamminess, and other temperature changes are early indicators that your body is fighting a virus. Checking your body temperature allows you to discover problems early and limit the risk of illness to others.

the patient body temperature is 36.5 which is in the normal range.

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SpO2 = oxygen saturation

measurement of the proportion of oxygen-carrying haemoglobin in the blood compared to non-oxygen-carrying haemoglobin.

The body cannot function properly unless there is a particular amount of oxygen in the blood. In fact, extremely low levels of SpO2 might cause life-threatening symptoms.

Hypoxemia is the medical term for this disorder. Because of the blue (cyan) colour it takes on, there is a visible effect on the skin known as cyanosis.

Hypoxia (low oxygen levels in the blood) can develop from hypoxemia (low levels of oxygen in the tissue). This process, as well as the distinction between the two circumstances, must be understood.

The patient SPO2 is 80% which is hypoxemia.

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1. Assess patients Wellbeing
The basic functioning of the patient's body are measured by their vital signs. Vitals show what's going on within your body in real time. They give vital information about inside organs.

A doctor may order additional tests, identify a disease, or recommend lifestyle adjustments based on the results.

Body temperature, blood pressure, heart rate, respiration, and height and weight are the most typical vitals tested.

2. Avoiding Misdiagnosis
Patients should inform their doctor how they're feeling and discuss your symptoms when they're not feeling well. Many medical conditions, however, have overlapping or identical symptoms. As a result, medical practitioners rely on vital signs to provide medical experts with a better understanding of the condition.

Medical practitioners can use patients vital signs to analyse patients health and provide an accurate diagnosis if they keep track of them. Misdiagnosis and inappropriate therapy are possible without vital signs.

3. Encourage people to make changes in lifestyle.
Keeping track of your patients vital signs can provide the motivation they need to start living a healthy lifestyle.