In this article, we will discuss the Classification of Myocardial Infarction (MI). So, let’s get started.
Classification
Type 1 – Spontaneous MI – It is related to ischemia due to a primary coronary event such as plaque rupture, ulceration, fissuring, erosion or dissection resulting in coronary thrombosis
Type 2 – Supply/Demand mismatch – MI secondary to ischemia due to either increased oxygen demand or decreased oxygen supply e.g. coronary artery spasm, coronary embolism, anemia, arrhythmia, hypertension or hypotension.
Type 3 – Suspected MI-related death – Sudden unexpected cardiac death often with symptoms suggestive of myocardial infarction.
Type 4a – PCI related MI (percutaneous coronary intervention) – Rise in cardiac biomarkers accompanied by symptoms along with electrographic, angiographic or imaging evidence of ischemia after PCI (MI associated with PCI).
Type 4b – Stent thrombosis – Confirmed stent thrombosis in the context of ischemia and dynamic cardiac biomarkers changes (MI associated with stent thrombosis).
Type 5 – CABG related MI (coronary artery bypass graft) – Rise in cardiac biomarkers accompanied by electrographic, angiographic or imaging evidence of ischemia after CABG (MI associated with CABG).
In this article, we will discuss about Tension Pneumothorax. So, let’s gets started
Tension Pneumothorax
In tension pneumothorax, the mean pleural pressure is positive which means that air in the pleural cavity is under tension which causes compression collapse of the lung. It develops due to persistent air leak (air entry) inside the pleural cavity by the communication which opens during inspiration and closes during expiration preventing the air to escape. In this way, with each successive breath, the intrapleural pressure increases which eventually causes the mediastinum to shift to the opposite side and increased intrapleural pressure also puts pressure on the surrounding blood vessels.
There is decreased venous return to the heart and along with decreased cardiac output causing hypotension (cardiac tamponade) and cyanosis.
Clinical Features
Dyspnea, cough and acute exacerbation of pneumothorax symptoms
Trachea and mediastinum shifts to the opposite side
Decreased or absent breath sounds, there may be amphoric breathing present at a localized place.
Hyperinflated chest with decreased or absent chest wall movement of the involved side
Tachypnea, tachycardia, hypotension, cyanosis, and paradoxical pulse.
In this article, we will discuss about the Clinical features of Pneumothorax. So, let’s get started.
Clinical features
Chest pain ( Pain is sharp, pleuritic, and is localized to the same side of pneumothorax)
Dyspnea
Fullness of intercoastal spaces
Decreased chest wall movement
Hyper-resonant percussion note
Decreased breath sounds, vocal fremitus, and vocal resonance in closed and tension pneumothorax. s
Increased vocal fremitus, vocal resonance, presence of whispering pectoriloquy (on development of large bronchopleural fistula), and amphoric bronchial breathing.
Accumulation of fluid or pus in the pleural cavity in case ocharacterized by f an associated infection (open pneumothorax or pneumothorax due to tuberculosis) along with physical signs of horizontal shifting level of dullness and succussion splash, and additionally there is signs of toxemia
Recurrent spontaneous pneumothorax occurs with emphysema due to the rupture of bullae occurring on the same side.
It refers to the pain and weakness of rotator cuff musculature Rotator cuff comprises of four main muscles viz. Subscapularis, Supraspinatus, Infraspinatus, Teres Minor responsible for abduction and rotation movement of shoulder
EPIDEMIOLOGY
Commonly affects athletes involved in sporting activities like Cricket, Swimming, Throwers etc and it can be age related problem affecting old aged patients their is an incidence of 11.2 cases per 1000 patients per year
CLININCAL PRESENTATION AND PATHOPHYSIOLOGY
Their is a difference between tendinitis and tendinopathy. Tendinitis is an inflammation of tendons whereas tendinopathy is deterioration of tendons. Rotator Cuff tendinopathy is clinically presented with
Pain, Weakness, Loss of strength to bear load aur lift weight on shoulders along with tenderness around shoulder joint painfull overhead movement localised swelling may also be present
MECHANISM
PHYSICAL EXAMINATION AND DIAGNOSIS
For Physical examination two clinical tests are performed namely
Empty can test and Hawkins test
Other tests include Modified Belly press test, Palpation, ROM testing the latter two are not so significant In order to see how the tests are performed visit
Other diagnostic tools include ultrasound, radiographs, radionucleotide isotope scan, magnetic resonance imaging (MRI), computed axial tomography (CT), electromyography
Ultrasound reveal partial tear of tendon fibres partial thickened tears and thickened subacromial bursa MRI also reveals rotator cuff tears
DIFFERENTIALDIAGNOSIS
Osteoarthritis
Biceps tendinopathy
Frozen Shoulder
Cervical Disc Disease
Cervical Spondylosis
MEASUREMENT
For measuring extent of rotator cuff tendinopathy VAS score, SPADI (Shoulder pain and disability index) have be adopted extensively by physiotherapist
PHYSIOTHERAPY MANAGEMENT
Physiotherapy is the gold standard treatment for rotator cuff tendinopathy along with Medical Management in majority cases and rarely require surgical intervention if Conservative treatment doesn’t work Medical Management includes NSAIDS, Shoulder immobilisation etc Surgery involves Arthroscopic intervention Physiotherapy treatment includes step wise procedure firstly Stretching, ROM exercises and then Muscle Strengthening exercises for pain management Ultrasound, TENS etc Modalities can be applied Kinesiotaping have shown better result in patients with Rotator Cuff Tendinopathy. Other techniques include
In this article, we will discuss in brief the Management of Cor Pulmonale. So, let’s get started.
Management
The patient is rested in a supine comfortable position.
Treatment of the basic cause.
The patient is advised to avoid smoking.
O2 therapy: O2 therapy to be given intermittently.
Salt restriction and diuretics: Salt restriction is advised to avoid fluid retention and RV volume overload. Intravenous diuretics such as furosemide, etc are given to relieve fluid overload.
Bronchodilators: They are given intravenously to relieve bronchospasm (due to acute exacerbation) and to improve oxygenation.
Carbonic-anhydrase inhibitor, e.g. acetazolamide to be given in order to relieve hypercapnia.
Antibiotics are given to treat superadded infection causing acute exacerbation.
Reduction of afterload by angiotensin-converting enzyme inhibitor (ACE inhibitors) in patients with left heart failure causing right heart failure.
In this article, we will discuss the Clinical Consequences of Vomiting. So, let’s get started.
Clinical Consequences (Complications)
Repeated vomiting, if forceful may lead to pressure rupture of the esophagus (Boerhaave’s syndrome).
It may cause a linear mucosal tear at or near the cardioesophageal junction leading to hematemesis (Mallory-Weiss syndrome).
Prolonged vomiting may lead to fluid loss (dehydration), loss of HCL (metabolic alkalosis), loss of potassium ions K+ (hypokalemia), and loss of nutrients (malnutrition).
Vomiting in an unconscious patient or in patient with depressed consciousness may result in aspiration pneumonia.
In this article, we will discuss the Clinical Features of Cor Pulmonale. So, let’s get started.
Clinical Features
Productive cough
Dyspnea
Chest discomfort
Headache
Abdominal pain
Lower extremity swelling
Ascites
Physical Signs include:
Orthopnea
The patient sits with elbows supported on a table and legs dangling by the side of the chest
Pursed lip breathing and cyanosis (presents in patients with COPD with acute exacerbation)
Periorbital edema
Jugular venous distention (raised JVP) and ‘VY’ (wave) collapse due to tricuspid regurgitation
Peripheral edema
Systemic Signs
Respiratory system may show signs of COPD (barrel-shaped chest, restricted chest movements and expansion, hyper-resonant note and vesicular breathing with prolonged expiration, muffled breath sounds)
Signs of RV hypertrophy or failure e.g. parasternal heave, loud P2, midsystolic and early diastolic (Graham-steel) murmur and pansystolic or holosystolic murmur of tricuspid regurgitation (Carvallo’s sign) may be present.
Abdominal distention may be present along with tender hepatomegaly. Hepatojugular reflex may be present.
