​Pathology - Hyperkalemia
Pathophysiology 
The patient had substantially compromised renal function; skipping scheduled dialysis resulted in fluid overload and hyperkalemia. He needs dialysis right away because his body has accumulated fluid and poisons. There may be mild hyperventilation, which is an attempt to make up for the metabolic acidosis brought on by insufficient kidney function.

The patient's hyperkalemia, which might result in deadly dysrhythmia, is the reason why the ECG results are very concerning. Moderate hyperkalemia is indicated by elevated (or "peaked") T waves and decreased P wave amplitude in the ECG. More severe electrolyte imbalances can cause the QRS to broaden and the ECG to start looking like a sine wave. Elevated serum potassium levels cause direct effects on the repolarization of the ventricular cell membrane, which leads to problems in conduction. Intravenous calcium is used in this patient's care to stabilize membrane potentials and lower the chance of an arrhythmia.
Additional short-term tactics include the intravenous (IV) infusion of bicarbonate, insulin (with glucose), or beta-2 agonist drugs to lower serum potassium levels and cause an intracellular potassium shift. However, in order to adequately manage this patient's severe condition, emergency dialysis is necessary.

Pathology - End Stage  Dilated Cardiomyopathy
Pathophysiology 
This patient's condition, which is characterized by a damaged myocardium and accompanying cardiac dysfunction, is most frequently caused by ischemic heart disease, which accounts for about 65% of cases. Additional frequent causes of dilated cardiomyopathy include drug-induced (cancer chemotherapy drugs), genetic metabolic problems, neuromuscular diseases, toxins (alcohol) or viral infections. Patients may eventually experience decompensated states of insufficient perfusion, which often involve fluid retention in the abdomen, pulmonary circulation, and peripheral extremities. A constricted pulse pressure is frequently observed, resulting from an inadequate systolic contraction. 

The greatly inflated left ventricle is the cause of the displaced point of maximum impulse (PMI), and the failing heart's interruption of optimum flow is the cause of the audible murmur. Due to chronic heart ischemia, decreased ventricular compliance causes the S3 gallop that has been observed. Every bodily system is impacted, and the goal of medical treatment is to eliminate extra fluid and lessen the strain on the heart. The best course of action in cases where the myocardium is as severely injured as this one is is cardiac transplantation.

​Clinical Procedures - Barium Follow-Through
Indications
• Investigation of small bowel pathology, particularly suspected Crohn's disease and strictures. Indications include pain, diarrhea, malabsorption, partial obstruction, anemia
• D Always consider alternatives (e.g. MRI, small bowel enema).
Contraindications
• Absolute: lack of informed consent, complete small bowel obstruction, suspected perforation (a water-soluble contrast may be used instead).
Procedure
The patient drinks barium and the small bowel is intermittently imaged until the barium has reached the caecum. Usually performed by a radiologist.
• The patient is given a mixture of barium to drink
• The exact mixture given to the patient varies between centres and between radiologists. Some add Gastrografin® to the barium, which has been shown to reduce transit time. Many add 20mg of metoclopramide to the mixture which enhances gastric emptying
• Once the barium has been consumed, the patient is asked into the fluoroscopy room and images are taken of the small bowel with the patient lying supine
• Real-time fluoroscopy is employed to assess small bowel motility
• Images are taken every 20-30 minutes until the barium has reached the
colon
• The radiologist may use a 'spoon' or similar radiolucent device to press on the patient's abdomen to separate loops of bowel
• Additional images of the terminal ileum are usually obtained, often with the patient supine and many radiologists also acquire an 'overcouch' plain abdominal radiograph with compression applied to the lower abdomen
• The time taken depends on the small bowel transit time and, although usually an hour, patients are advised to allow up to 3 hours
• After the procedure, the patient may eat and drink as usual but is advised to keep their bowel moving to avoid barium impaction.
Risks
• Leakage of barium through an unsuspected perforation:
• Intraperitoneal barium causes hypovolaemic shock and a 50% mortality. Of those that survive, 30% have adhesions
• Barium impaction (causing large bowel obstruction) or barium appendicitis
• Medication effects

Patient Preparation
• Fasting: nil by mouth for 12 hours before the examination
• Bowel preparation: laxative (usually Picolax®) taken 12 hours before.
Other information
• Metoclopramide aids gastric emptying. Extra-pyramidal side effects may occur, especially in young women and there is a risk of acute dystonic reactions such as oculogyric crisis. Contraindicated in patients with Parkinsonism/Parkinson's disease
• D A barium study will prevent a CT examination of the same area for a period of time as intestinal barium creates dense streak artefact.

​Clinical Procedures - Barium Enema
• The following refers to the standard 'double contrast' barium enema.
Indications
• Investigation of colonic pathology. Indications include pain, melaena, anaemia, palpable mass, change in bowel habit, failed colonoscopy, investigation of remaining colon in the case of a known colonic tumour
• • Always consider alternatives (e.g. colonoscopy, CT colonography).
Contraindications
• Absolute: lack of informed consent, possible perforation, pseudomembranous colitis, toxic megacolon, biopsy via rigid sigmoidoscope within 5 days, biopsy via flexible endoscope within 1 day
•Relative: barium meal within 7-14 days, patient frailty or immobility:
• • The procedure requires a large amount of patient cooperation.
The patient must be able to lie flat and to turn over easily
•  The patient must be able to retain rectal barium and air.
Procedure
The colon is coated with barium, then inflated with air and images are taken from several different angles. Performed by a radiographer or radiologist.
• The patient lies in the left lateral position on the fluoroscopy table
• The operator may perform a digital rectal examination before beginning
• A rectal tube is placed, attached to a bag of barium sulphate. The barium is run into the colon under x-ray guidance until it reaches the right colon
• The barium is drained
• IV buscopan or, if contraindicated, glucagon is given
• The colon is inflated with air (or with CO, in some centres)
• The patient is instructed to roll and is tilted as images are acquired
• Once the images are obtained, the colon is deflated and the patient can go to the bathroom to empty their bowel and shower if necessary
• The examination may last 15-30 minutes
• The patient should be kept in the department until any medication side effects (e.g. blurred vision) have worn off.
Risks
• Perforation (increased risk in elderly, ulcerating lesions, systemic steroids, hypothyroidism, large bowel obstruction):
• Intraperitoneal barium causes hypovolaemic shock and a 50% mortality. Of those that survive, 30% have adhesions
• Cardiac arrhythmia (secondary to the large bowel distension)
• Medication effects
 
Patient Preparation
• Iron tablets: stop 5 days before
• Constipating agents: stop 2 days before
• Fasting: low residue diet 2 days before, fluids only on the day before
• Bowel preparation: laxative (usually Picolax® taken at 08:00 and
18:00 on the day before.
Other Information
• Buscopan is given to inhibit intestinal motility. Side effects include blurred vision, dry mouth, and tachycardia:
Contraindicated in angina, untreated closed-angle glaucoma, prostatic hypertrophy, myasthenia gravis, paralytic ileus, and pyloric stenosis
• Glucagon is given if buscopan cannot. Risk of hypersensitivity and is contraindicated in phaeochromocytoma, insulinoma, and glucagonoma
• After the procedure, the patient may eat and drink as usual but is advised to keep their bowel moving to avoid barium impaction
• A barium study will prevent a CT examination of the same area for a period of time as intestinal barium creates dense streak artefact.
Water-Soluble Contrast Examinations
• In the case of recent surgery, suspected perforation, or investigation of a leak, water-based iodinated contrast is used instead of barium.
Examples include Gastrografin®, Urografin®, Niopam®, Omnipaque®
• A single-contrast examination is performed (i.e. the colon is not inflated with air) and many of the standard' views are not included
• No bowel preparation or fasting is needed.

Pathology - Myocardial infarction with ST segment elevation (STEMI)
Pathophysiology 
This is an instance of ST elevation myocardial infarction, or acute coronary syndrome (ACS). Stable angina and ST and non-ST segment elevation myocardial infarctions (STEMI and NSTEMI, respectively) are included in this category of illnesses. A classic presentation is pain, heaviness, or pressure in the substernal chest that may radiate to the patient's left arm or left jaw. Although the illness usually progresses over time and may eventually lead to symptoms at rest, the discomfort is most frequently triggered by effort and eased by rest. Both pain and sympathetic nervous system (SNS) activation have raised this patient's blood pressure and pulse. Relatively low blood pressure in this context would be concerning as it would probably imply substantial ischemic left ventricular (LV) damage. Another sign of the SNS's reaction to pain and injury is diaphoresis.

​The S3 sound is a sign of decreased ventricular compliance, most likely as a result of myocardial ischemia-induced transient alterations. This patient has a clean lung field, a normal JVP, and no signs of heart failure because the event is acute and not yet decompensating. Normal perfusion in the extremities suggests sufficient ventricular function, but the anteroseptal distribution of the ECG (V1–V4) is crucial for myocardial damage. To restore heart circulation as soon as possible, this patient requires intravascular stent implantation or fibrinolysis in addition to oxygen, nitrate, aspirin, and morphine therapy.

Pathology - Myocardial infarction with non-ST segment elevation (NSTEMI) 
Pathophysiology 
This is an Acute Coronary Syndrome (ACS) episode; NSTEMI or unstable angina are the most likely causes. Both NSTEMI and STMI, as well as unstable angina, fall within this category of conditions. Biochemical indicators and the presence or absence of ECG abnormalities are used to differentiate the illnesses. Substernal chest pain, heaviness, or pressure that may spread to the patient's left arm or left jaw region is the classic presentation of acute coronary syndrome (ACS). Though the illness usually progresses over time and may eventually lead to symptoms at rest, the discomfort is most frequently triggered by effort and relieved by rest. This patient's pulse and blood pressure have increased due to SNS activation and discomfort. Relatively low blood pressure in this context would be concerning as it would probably imply substantial ischemia left ventricular injury.

​Another sign of the SNS's reaction to damage and pain is diaphoresis. This patient does not now exhibit any symptoms of ventricular ischemia, as evidenced by normal perfusion to the limbs, no abnormalities in the ECG, and no S3 or S4 heart sounds. Acute and without decompensation at this point, the patient shows no signs of heart failure (normal JVP and clean lung fields). Apart from the treatment with oxygen, nitrate, aspirin, and morphine, this patient requires additional assessment and constant observation to ensure that there is no progression to NSTEMI or STEMI. It is also recommended to evaluate biochemical markers, such as cardiac troponin and creatine kinase MB.

​Pathology - Atrial  Fibrillation
Pathophysiology 
As seen in the following example, this rather typical arrhythmia frequently begins with a subacute episode. This disruption of rhythm might be continuous or sporadic (paroxysmal). Breathlessness and palpitations are commonly observed. Laminar flow throughout the heart is disrupted by ineffective atrial contraction, which has multiple effects.
An inefficient flow can result in "stagnant" cardiac circulation, which puts the patient at risk for stroke and pulmonary embolus as well as atrial blood clots. The erratic and frequently quick ventricular response to erratic atrial activity results in dyspnea. An inadequate forward flow of blood to the systemic circulation results from ineffective ventricular pumping. Although various cardiac or pulmonary diseases might cause this illness, hypertension or valvular heart disease are the most common risk factors. The atrioventricular (AV) node is stimulated rapidly and randomly, leading to an abnormally irregular pattern of QRS complexes and the absence of P waves that make the diagnosis of atrial fibrillation easy to make.

​Pathology - Premature Atrial Contractions (PACs). 
Pathophysiology 
Common cardiac arrhythmias known as PACs are typically regarded as benign, rarely resulting in hemodynamic instability or other severe clinical signs. Premature ventricular contractions, or PVCs, can, however, frequently cause palpitations, anxiety, or psychosomatic chest discomfort, which can be distressing to patients. Although the exact cause of this disorder is unknown, high levels of stress, excessive coffee consumption, or insufficient sleep are frequently linked to the premature beats. It's interesting to note that both the irregular beats and the symptoms they produce usually go away with activity. The "fate" of a PAC is ultimately decided by intrinsic heart rate and the refractory time of the AV node or bundle branch fascicles. PACs are typically not routed through the AV node to the ventricles. A right bundle branch block may result from a PAC's ability to cross the AV node and reach the fascicular bundles because normal conduction pathways are slowed down.
Because PACs have an ectopic origin and follow a different conduction channel through the atria than typical sinoatrial (SA) nodal stimulation, their ECG waveforms may appear abnormal.

​Pathology - Multifocal Atrial Tachycardia 
Pathophysiology 
 This disorder develops when the right atrium contracts at several locations other than the SA node. Many of these atrial beats, in contrast to PACs, are routed through the AV node, which raises the ventricular rate by as much as 200 beats per minute at times. If insufficient ventricular filling is caused by the tachycardia, symptoms and hemodynamic instability may arise. Cardiomyopathy can also result from the heart's increasing strain, particularly in patients who also have other long-term medical conditions. Patients with medical illnesses including COPD, lung cancer, bacterial pneumonia, or pulmonary embolism that diminish blood oxygen content are more likely to have MAT than individuals who are younger than 50. The best way to treat MAT is to assess and address any underlying medical issues. Forceful atrial contraction against a noncompliant left ventricle is the cause of the S4 heart sound heard in this patient, which is a common finding in COPD patients. The patient's prolonged systemic hypertension contributes to increasing afterload on the left ventricle, which eventually becomes hypertrophied and noncompliant.

Pathology -Accelerated Idioventricular Rhythm
Pathophysiology 
The ventricles cause this arrhythmia, which happens when a typically suppressed ventricular "pacemaker" takes over as the primary heart rate regulator rather than the SA or AV nodes. When the intrinsic ventricular rate (IVR) reaches more than 40 beats per minute, the idioventricular rhythm is deemed to be "accelerated." As in the case vignette, the most frequent situation for this to happen is following coronary reperfusion, or the restoration of flow to ischemic heart tissue. Treatment is not necessary for this benign illness, which is typically invisible to the patient. After receiving reperfusion treatment, normal SA node function usually restores in 24 to 48 hours. ECG monitoring is essential because the illness must be distinguished from ventricular tachycardia, which can develop into the potentially fatal arrhythmia ventricular fibrillation. Idioventricular rhythm occurs at a rate of less than 120 beats per minute, more frequently at a rate of less than 100. Ventricular tachycardia typically occurs at a rate much higher than 120 beats per minute.