CVS Flashcards
ANGINA
Chest pain or discomfort caused by a reduced blood flow to the heart muscle, typically due to CAD
This reduction in blood flow leads to an oxygen supply-demand mismatch, often triggered by physical exertion or emotional stress.
ANGINA PATHOPHYSIOLOGY
- Atherosclerosis is the most common cause, where plaque buildup in the coronary arteries narrows the vessels, limiting blood flow.
- When the heart requires more oxygen (e.g., during exercise or stress), the narrowed arteries can’t deliver enough oxygen-rich blood, resulting in ischemia (insufficient blood supply).
- Stable angina occurs with predictable triggers (e.g., exercise), while unstable angina is more unpredictable and can occur at rest or with minimal exertion, often signaling an impending heart attack.
ANGINA PHARMA TREATMENT
- Nitroglycerin: Dilates blood vessels, reducing heart workload and relieving pain.
- Beta-blockers: Lower heart rate and blood pressure, decreasing oxygen demand.
- Calcium channel blockers: Relax blood vessels and reduce heart workload.
- Antiplatelet agents (e.g., aspirin): Prevent blood clot formation, reducing the risk of a heart attack.
ANGINA SURGICAL TREATMENT
- Percutaneous coronary intervention (PCI): Balloon angioplasty or stent placement to open blocked arteries.
- Coronary artery bypass grafting (CABG): Surgical bypass of blocked arteries.
ANGINA MANUAL THERAPY TREATMENT
Can help manage MSK aspects of angina such as referred pain or Tx in the chest, shoulders or upper back
- Soft tissue mobilisation: Helps to alleviate muscle tension, particularly in the chest, shoulders, and upper back, which may reduce discomfort or tightness associated with angina.
- Myofascial release: Addresses fascial restrictions in the upper body to alleviate discomfort.
- Joint mobilisation: Assists in reducing any restriction in thoracic or cervical spine mobility that may contribute to pain or discomfort.
ACUTE CORONARY SYNDROME
Spectrum of conditions that result from a sudden reduction in blood flow to the heart muscle, leading to ischemia (lack of oxygen)
It includes unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI)
ACUTE CORONARY SYNDROME PATHOPHYSIOLOGY
-
Atherosclerotic Plaque Rupture:
ACS typically results from the rupture of an atherosclerotic plaque in a coronary artery. This rupture exposes the inner contents of the plaque to the bloodstream, triggering blood clot formation (thrombosis). -
Ischemia and Myocardial Injury:
The blood clot can partially or completely occlude the affected artery, reducing blood flow to the heart muscle (myocardium). This causes myocardial ischemia and injury. In NSTEMI, there is partial occlusion, whereas in STEMI, the artery is completely occluded, leading to more severe damage. -
Damage to the Heart Muscle:
NSTEMI and unstable angina may result in reversible ischemia, while STEMI leads to irreversible myocardial damage (infarction), which can cause a loss of heart muscle function and electrical disturbances.
ACUTE CORONARY SYNDROME PHARMA TREATMENT
- Antiplatelet drugs (e.g., aspirin, clopidogrel): Reduce clot formation and prevent further blockage.
- Anticoagulants (e.g., heparin): Prevent further blood clotting.
- Nitroglycerin: Relieves pain by dilating coronary arteries and reducing myocardial oxygen demand.
- Beta-blockers: Reduce heart rate and blood pressure to minimise the workload on the heart.
- ACE inhibitors: Help reduce the workload on the heart and prevent further damage.
- Statins: Lower cholesterol to prevent further plaque buildup.
ACUTE CORONARY SYNDROME INTERVENTIONAL TREATMENTS
- Percutaneous Coronary Intervention (PCI): Includes angioplasty and stent placement to open up blocked coronary arteries.
- Coronary Artery Bypass Grafting (CABG): Surgical procedure to bypass blocked coronary arteries and restore adequate blood flow.
ACUTE CORONARY SYNDROME MANUAL THERAPY
Manual therapy doesn’t directly treat the underlying heart condition in ACS, it can help manage symptoms and improve recovery in a post-ACS setting, particularly with musculoskeletal pain and discomfort associated with the condition.
Pain Management:
- Soft Tissue Mobilisation: Helps alleviate muscle tension and discomfort in the chest, neck, shoulders, and upper back, which are common areas of referred pain following ACS.
- Myofascial Release: Targets fascial restrictions to reduce tightness and discomfort in surrounding musculature.
Post-ACS Rehabilitation:
- Joint Mobilisation: Focuses on improving thoracic and cervical spine mobility, which may be restricted following prolonged bed rest or post-surgical recovery.
- Breathing Techniques: Manual therapy can be used to encourage proper diaphragmatic breathing, aiding in reducing anxiety and improving oxygenation and ventilation during recovery.
Improving Mobility and Function:
- Gentle Mobilisation and Stretching: Encourages return to normal movement and function while addressing any stiffness, particularly in the upper body, after a myocardial event or surgical intervention (e.g., after PCI or CABG).
- Rehabilitation Support: Manual therapy, in combination with physical therapy, may assist in safely increasing physical activity levels in the early stages of recovery, under the supervision of a healthcare provider.
Manual therapy should not be performed during the acute phase of ACS or an active myocardial infarction
HYPERTENSION
High blood pressure
A condition in which the force of blood against the walls of the arteries is consistently too high. It is a significant risk factor for cardiovascular diseases like stroke, heart attack, and kidney failure.
PRIMARY (ESSENTIAL) HYPERTENSION
- The most common form, with no identifiable cause, typically develops over many years. It is often linked to genetic factors, aging, obesity, and lifestyle factors (e.g., diet high in salt, alcohol, lack of exercise).
- The heart has to pump harder to circulate blood, causing the arteries to become stiffer and narrower over time, leading to increased blood pressure.
- Sympathetic nervous system (SNS) activation: The SNS can increase heart rate and constrict blood vessels, leading to higher blood pressure.
- Renin-Angiotensin-Aldosterone System (RAAS): This system regulates blood pressure through fluid balance and vasoconstriction, contributing to increased blood pressure when overactive.
- Endothelial dysfunction: The lining of the blood vessels may lose its ability to dilate effectively, contributing to increased vascular resistance.
SECONDARY HYPERTENSION
This type is caused by an underlying condition, such as kidney disease, hormonal disorders (e.g., hyperthyroidism, Cushing’s syndrome), or medication (e.g., oral contraceptives, corticosteroids).
HYPERTENSION PHARMA TREATMENTS
- Diuretics: Help the kidneys remove excess salt and water, reducing blood volume and lowering blood pressure.
- Beta-blockers: Lower heart rate and decrease the force of contraction, reducing blood pressure.
-
Angiotensin-converting enzyme (ACE) inhibitors: Relax blood vessels by blocking the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor.
Calcium channel blockers: Dilate blood vessels and reduce the force of the heart’s contractions. - Angiotensin II receptor blockers (ARBs): Block the effects of angiotensin II, reducing blood pressure.
HYPERTENSION LIFESTYLE MODIFICATIONS
- Dietary changes: Reducing salt intake, eating a balanced diet rich in fruits and vegetables (DASH diet), and managing weight.
- Exercise: Regular aerobic activity can lower blood pressure.
- Limiting alcohol: Reducing alcohol consumption helps control blood pressure.
- Stress management: Practices like yoga and mindfulness can help manage stress, which can contribute to high blood pressure.
HYPERTENSION MANUAL THERAPY
Stress Reduction:
- Massage Therapy: Helps reduce muscle tension and promotes relaxation, which may lower sympathetic nervous system activity and reduce blood pressure in some individuals.
- Myofascial Release: Targeting areas of tension in the neck, shoulders, and back can reduce overall stress and improve circulation.
- Trigger Point Therapy: Relieving muscle knots and tightness can lead to a reduction in overall body tension, indirectly affecting blood pressure.
Postural Correction:
- Joint Mobilization and Soft Tissue Techniques: Can improve posture and alleviate musculoskeletal discomfort, particularly in individuals who have poor posture or muscle tightness that may exacerbate stress or pain.
Breathing Techniques:
- Diaphragmatic Breathing: Manual therapy can be used to teach deep breathing techniques to improve oxygenation and relaxation. Proper breathing techniques can activate the parasympathetic nervous system, which helps lower blood pressure.
Exercise and Movement:
- Mobilisation of the Spine: Gentle spinal manipulations may help improve mobility, especially for individuals with tension or stiffness, thus aiding overall relaxation and contributing to stress reduction.
- Physical Therapy: Manual therapy can complement an exercise program, ensuring proper movement patterns, addressing muscle imbalances, and promoting physical activity, which helps in controlling hypertension.
DVT
DVT occurs when a blood clot forms in a deep vein, usually in the lower leg or thigh.
DVT PATHOPHYSIOLOGY
Virchow’s Triad: The three key factors that increase the risk of clot formation:
- Stasis of blood flow: Caused by immobility, long periods of sitting (e.g., during surgery or travel), or heart failure.
- Endothelial injury: Damage to the blood vessel wall, often due to trauma, surgery, or inflammation.
- Hypercoagulability: An increased tendency for blood to clot, which can be caused by genetic disorders, medications (e.g., birth control), or conditions like cancer.
Formation of the Clot:
When these factors combine, they can lead to the formation of a clot (thrombus) in the deep veins, obstructing blood flow. The clot may stay localized or grow over time.
PULMONARY EMBOLISM PATHOPHYSIOLOGY
PE occurs when a portion of the thrombus from DVT breaks off and travels through the bloodstream to the lungs, where it blocks a pulmonary artery or one of its branches, obstructing blood flow to the lung tissue.
This blockage leads to impaired oxygen exchange, right heart strain, and can cause severe respiratory and circulatory complications, potentially leading to death if not treated promptly.
DVT AND PE PHARMA TREATMENTS
- Anticoagulants (e.g., heparin, warfarin, direct oral anticoagulants): Prevent further clot formation and allow the body to gradually dissolve the clot.
- Thrombolytics (e.g., tPA): Used in severe cases of PE or extensive DVT, these medications help dissolve large clots.
- Compression stockings: In DVT, these can help improve venous return, reduce swelling, and prevent post-thrombotic syndrome.
DVT AND PE SURGICAL TREATMENTS
- Thrombectomy: In severe cases of PE or large DVT, surgical removal of the clot may be necessary.
- Inferior Vena Cava (IVC) filter: In patients who cannot take anticoagulants, an IVC filter can be placed to prevent clots from traveling to the lungs.
- Embolectomy: In life-threatening PE, removal of the clot directly from the pulmonary arteries may be necessary.
DVT AND PE MANUAL THERAPY TREATMENT
Manual therapy is not recommended during the acute phase of DVT or PE due to the risk of dislodging a clot and causing a PE or exacerbating the condition.
Post-Acute Phase (After Anticoagulation and Stabilisation):
- Gentle Soft Tissue Mobilisation: Once anticoagulation therapy is well-established and the clot has been managed, gentle soft tissue techniques may help improve circulation, reduce swelling, and alleviate discomfort in the affected limb.
Compression and Manual Therapy:
- Manual Lymphatic Drainage (MLD): Can help manage edema (swelling) associated with DVT. MLD is a gentle massage technique that promotes lymphatic fluid circulation and may reduce swelling and discomfort.
- Stretching and Range-of-Motion Exercises: These can help maintain mobility and prevent stiffness in the affected limb, especially after prolonged bed rest or immobilization during treatment.
Post-Thrombotic Syndrome (PTS) Prevention:
- Joint Mobilisation and Stretching: Manual therapy can help reduce the development of PTS, which can occur after DVT, characterized by chronic pain, swelling, and skin changes in the affected limb. Stretching techniques and joint mobilisation can assist in maintaining proper circulation and joint function.
Breathing Exercises:
- After a PE, manual therapy could include teaching breathing techniques to improve lung function and reduce shortness of breath. Techniques such as diaphragmatic or pursed-lip breathing can assist with improving oxygenation and reducing respiratory strain.
VALVULAR HEART DISEASE
Valvular heart disease (VHD) involves dysfunction of one or more of the heart valves (aortic, mitral, tricuspid, or pulmonary) due to stenosis (narrowing) or regurgitation (leakage), impairing normal blood flow.
VALVULAR HEART DISEASE PATHOPHYSIOLOGY
Valvular Stenosis (Narrowing):
- Occurs when a valve becomes stiff or calcified, restricting blood flow.
- Common causes: Aging (degenerative calcification), rheumatic fever, congenital defects, or infections (endocarditis).
- Leads to increased cardiac workload, left or right ventricular hypertrophy, and eventually heart failure.
- Examples: Aortic stenosis, mitral stenosis.
Valvular Regurgitation (Insufficiency or Leakage):
- The valve does not close properly, allowing backflow of blood, increasing the volume load on the heart.
- Common causes: Valve prolapse, infection, rheumatic disease, ischemic heart disease, or connective tissue disorders (e.g., Marfan syndrome).
- Leads to ventricular dilation, hypertrophy, and heart failure over time.
- Examples: Mitral regurgitation, aortic regurgitation.
VALVULAR HEART DISEASE PHARMA TREATMENT
Diuretics: Reduce fluid overload and relieve symptoms of heart failure.
Beta-blockers: Lower heart rate and reduce myocardial workload.
ACE inhibitors / ARBs: Help manage heart failure and hypertension.
Anticoagulants (e.g., warfarin): Used in cases like mitral stenosis with atrial fibrillation to prevent thromboembolism.
Antibiotics (for infective endocarditis prophylaxis) in high-risk patients.
VALVULAR HEART DISEASE SURGICAL TREATMENT
Valve Repair (e.g., Mitral Valve Repair): Preferred in cases where native valve function can be preserved.
Valve Replacement (Mechanical or Bioprosthetic Valves): Required in severe cases of stenosis or regurgitation.
Balloon Valvuloplasty: A catheter-based procedure to widen stenotic valves, mainly used for mitral or aortic stenosis.
Transcatheter Aortic Valve Replacement (TAVR): A minimally invasive alternative for aortic stenosis in high-risk patients.
VALVULAR HEART DISEASE MANUAL THERAPY
Breathing Techniques and Postural Therapy:
- Diaphragmatic Breathing: Helps reduce cardiac workload by promoting efficient oxygenation and relaxation.
- Postural Correction: Especially in patients with chronic heart failure due to VHD, improving thoracic mobility can enhance lung expansion and reduce dyspnea.
Soft Tissue and Myofascial Release:
- Gentle soft tissue work in the chest, shoulders, and upper back can alleviate tension associated with restricted breathing and reduced mobility from heart-related fatigue.
- Avoid deep pressure over the carotid artery in patients with aortic stenosis, as it may reduce blood flow to the brain.
Circulatory Support (Avoiding Excessive Stimulus):
- Light massage (avoiding deep techniques) can enhance circulation without putting excess demand on the cardiovascular system.
- Avoid vigorous manual therapy or prolonged prone positioning, especially in patients with heart failure symptoms.
Exercise-Based Manual Therapy for Mobility and Function:
- Joint mobilisation (particularly of the thoracic spine) can improve breathing mechanics.
- Gentle stretching and low-impact movement therapy (e.g., assisted range of motion) help maintain flexibility and circulation in patients with reduced physical activity due to VHD symptoms.
Manual therapy should NOT be performed during active decompensated heart failure, severe stenosis, or acute endocarditis.
AORTIC DISSECTION
Aortic dissection is a life-threatening condition in which a tear occurs in the intimal layer of the aorta, allowing blood to flow between the layers of the arterial wall. This leads to the formation of a false lumen, which can extend along the aorta, potentially compromising blood supply to major organs.
AORTIC DISSECTION INITIATION
- The intimal tear exposes the underlying media to high-pressure blood flow, leading to separation of the layers.
- The false lumen may continue to expand, reducing flow in the true lumen and causing ischemia to vital organs.
AORTIC DISSECTION COMPLICATIONS
- Rupture: If the dissection extends through the outer layer (adventitia), it can lead to massive hemorrhage and death.
- End-organ ischemia: The false lumen may obstruct branches of the aorta, leading to stroke, myocardial infarction, kidney failure, or mesenteric ischemia.
- Aortic regurgitation: If the dissection involves the aortic valve, it can cause backflow of blood into the heart, leading to heart failure.
AORTIC DISSECTION CLASSIFICATION
- Stanford Type A: Involves the ascending aorta (requires immediate surgery).
- Stanford Type B: Involves the descending aorta (may be managed medically or surgically, depending on severity).
AORTIC DISSECTION MEDICAL TREATMENT
Emergency Medical Treatment (Acute Dissection)
- Strict blood pressure control:
- Beta-blockers (e.g., labetalol, esmolol) reduce heart rate and blood pressure, preventing further progression.
- Vasodilators (e.g., nitroprusside) may be added to lower blood pressure further.
- Pain management: Morphine is often used to relieve severe pain and reduce sympathetic stress.
AORTIC DISSECTION SURGERY
Surgical & Interventional Treatment
- Type A Dissection: Requires emergency open-heart surgery to replace the affected aorta with a graft.
- Type B Dissection: If stable, it may be managed medically with strict blood pressure control.
- If complicated (e.g., organ ischemia, rupture), endovascular aortic repair (TEVAR) or open surgery is required.
AORTIC DISSECTION MANUAL THERAPY
Manual therapy is strictly contraindicated in the acute phase of aortic dissection.
Breathing and Relaxation Techniques
- Diaphragmatic breathing exercises can help regulate blood pressure and reduce stress-related sympathetic activation.
- Gentle manual therapy for stress reduction (light craniosacral or relaxation-focused touch) may aid in lowering systemic tension.
Postural and Mobility Support (After Surgery or Recovery)
- Post-surgical patients often experience thoracic stiffness and muscular tightness due to prolonged immobility.
- Gentle thoracic mobilisation (NOT manipulation) can assist with improving breathing mechanics post-surgery.
- Scar mobilisation techniques (once healed) can help reduce post-surgical adhesions and discomfort.
Soft Tissue and Myofascial Release (Caution Required)
- Focused soft tissue work in the upper back, shoulders, and neck can help with musculoskeletal tension from prolonged bed rest.
- Avoid deep pressure on the chest or abdomen, as excessive mechanical force may affect blood pressure and vascular integrity.
AORTIC DISSECTION KEY PRECAUTIONS TO MANUAL THERAPY
- Strict avoidance of deep tissue techniques, high-velocity manipulations, or aggressive mobilisation.
- Monitor for dizziness, shortness of breath, or fatigue, as blood flow dynamics may still be compromised.
- Always work in collaboration with the medical team, particularly for post-surgical cases.
ANEURYSM
An aneurysm is a localized dilation or bulging of an artery due to weakening of the arterial wall. It can occur in various arteries, with the most common locations being the aorta (aortic aneurysm), brain (cerebral aneurysm), and peripheral arteries.
ANEURYSM PATHOPHYSIOLOGY
Arterial Wall Weakening:
- Chronic hypertension, atherosclerosis, genetic disorders (Marfan syndrome, Ehlers-Danlos syndrome), or infections can lead to progressive wall degeneration.
- The vessel wall loses structural integrity, causing it to balloon outward under arterial pressure.
Risk of Rupture and Complications:
- Large aneurysms (>5 cm in the aorta) are at high risk of rupture, leading to life-threatening hemorrhage.
- Cerebral aneurysm rupture causes subarachnoid hemorrhage, potentially leading to stroke, coma, or death.
- Aortic dissection can occur if the aneurysm weakens the arterial layers, creating a tear.
ANEURYSM TYPES
True Aneurysm: Involves all three layers of the artery (e.g., fusiform, saccular).
False Aneurysm (Pseudoaneurysm): A contained rupture where blood leaks outside the arterial wall but is held by surrounding tissue.
ANEURYSM MEDICAL TREATMENT
Blood Pressure Control:
- Beta-blockers (e.g., propranolol, labetalol) lower stress on the arterial wall.
- ACE inhibitors/ARBs may also be used.
Cholesterol Management: Statins help reduce atherosclerosis progression.
Lifestyle Modifications: Smoking cessation, weight control, and stress reduction.
Regular Monitoring: Ultrasound or CT scans track aneurysm growth.
ANEURYSM SURGICAL TREATMENT
- Endovascular Aneurysm Repair (EVAR): A minimally invasive procedure using a stent graft to reinforce the arterial wall, commonly for abdominal aortic aneurysms (AAA).
- Open Surgical Repair: Required for large or ruptured aneurysms, involving direct graft placement.
- Coiling or Clipping (For Cerebral Aneurysms): Prevents rupture by blocking blood flow into the aneurysm.
ANEURYSM MANUAL THERAPY TREATMENT
Stress Reduction & Blood Pressure Management
- Gentle soft tissue techniques may help regulate the nervous system and lower sympathetic activity, indirectly assisting with blood pressure control.
- Diaphragmatic breathing exercises can reduce cardiovascular strain.
Postural & Musculoskeletal Support
- Upper Back and Thoracic Mobility: Aortic aneurysm patients, especially post-surgery, may experience chest tightness and restricted mobility. Gentle joint mobilization (avoiding aggressive techniques) can help.
- Post-surgical scar mobilisation (only after full healing) can prevent adhesions and improve movement.
Soft Tissue and Myofascial Release (Caution Required)
- Avoid direct pressure over the aneurysm site.
- Avoid deep massage or high-velocity spinal manipulations, especially near the neck (cervical aneurysm risk).
STROKE/TIA
Stroke and transient ischemic attack (TIA) occur due to an interruption of blood flow to the brain, leading to neurological deficits. The key difference is that a stroke causes permanent brain damage, while a TIA is temporary, with symptoms resolving within 24 hours without lasting injury.
STROKE TYPES AND PATHOPHYSIOLOGY
Ischemic Stroke (87% of strokes)
- Caused by an arterial blockage, often due to:
- Atherosclerosis (plaque buildup narrowing cerebral arteries).
Thrombus formation (clot forms in a cerebral artery).
- Embolism (clot or debris traveling from the heart or other arteries, e.g., in atrial fibrillation).
- Leads to neuronal ischemia, triggering energy failure, excitotoxicity, and eventual cell death if blood flow is not restored quickly.
Hemorrhagic Stroke (13% of strokes)
- Caused by the rupture of a weakened blood vessel, leading to bleeding into the brain.
- Common causes: Hypertension, aneurysm rupture, arteriovenous malformation (AVM), or trauma.
- The bleeding increases intracranial pressure (ICP), damaging brain tissue.
TIA PATHOPHYSIOLOGY
- A temporary blockage of cerebral blood flow, often a warning sign of future stroke.
- Symptoms resolve within minutes to hours, but underlying vascular disease or embolic sources must be addressed.
STROKE AND TIA ACUTE MANAGEMENT (EMERGENCY PHASE)
Ischemic Stroke
- Thrombolysis with tPA (Tissue Plasminogen Activator): Must be given within 4.5 hours of symptom onset.
- Mechanical Thrombectomy: Catheter-based clot removal for large-vessel occlusions.
Hemorrhagic Stroke
- Blood Pressure Control: Avoiding excessive hypotension or hypertension.
- Surgical Intervention: Hematoma evacuation, aneurysm clipping, or coiling if needed.
STROKE AND TIA LONG-TERM MANAGEMENT
- Antiplatelet Therapy: Aspirin, clopidogrel to reduce clot formation.
- Anticoagulation (e.g., warfarin, DOACs) for atrial fibrillation-related stroke prevention.
- Blood Pressure & Cholesterol Management (ACE inhibitors, statins).
- Diabetes Control & Lifestyle Modifications (exercise, diet, smoking cessation).
- Carotid Endarterectomy or Stenting if severe carotid artery stenosis is present.
STROKE AND TIA MANUAL THERAPY
Manual therapy does not reverse neurological damage but can play a key role in rehabilitation, helping to restore mobility, reduce spasticity, and manage pain.
Improving Circulation & Reducing Spasticity
- Gentle soft tissue mobilization: Can help reduce muscle stiffness and spasticity, particularly in affected limbs.
- Myofascial release: Addresses post-stroke muscle tightness and compensatory movement patterns.
- Passive stretching: Helps maintain range of motion and prevent contractures.
Postural & Gait Support
- Joint mobilization (gentle, NOT aggressive): Assists in improving scapular, shoulder, and hip mobility, often restricted after stroke.
- Balance and proprioceptive training: Enhances postural stability, particularly for hemiparetic patients.
Pain Management & Sensory Rehabilitation
- Neuromuscular techniques can address post-stroke shoulder pain (due to subluxation).
- Sensory re-education techniques may help with numbness or hypersensitivity in affected areas.
Breathing and Autonomic Regulation
- Diaphragmatic breathing training: Can assist in reducing sympathetic overactivity and improving respiratory function, especially in brainstem strokes.
NON-CARDIAC CAUSES OF CHEST PAIN - MSK CAUSES
Costochondritis: Inflammation of the costosternal joints causes sharp, localized pain that worsens with movement or palpation.
Rib Dysfunction: Subluxations or joint restrictions in the thoracic spine and ribs may cause referred pain mimicking cardiac symptoms.
Myofascial Pain Syndrome: Trigger points in pectoralis major, serratus anterior, or intercostal muscles can cause chest tightness.
Postural Strain: Prolonged poor posture (e.g., forward head, rounded shoulders) leads to chronic tension and discomfort in the chest and upper back.
NON-CARDIAC CAUSES OF CHEST PAIN - GI CAUSES
Gastroesophageal Reflux Disease (GERD): Acid reflux irritates the esophagus, leading to burning, retrosternal pain that may mimic angina.
Esophageal Spasm: Uncoordinated contractions cause sharp, squeezing pain, often relieved by swallowing warm liquids.
Hiatal Hernia: Protrusion of the stomach into the thorax can cause pressure-like chest discomfort and reflux symptoms.
NON-CARDIAC CAUSES OF CHEST PAIN - RESP CAUSES
Pleuritis (Pleurisy): Inflammation of the pleura causes sharp pain, worsened by deep breathing or coughing.
Pneumothorax: Air in the pleural space leads to sudden, sharp chest pain and respiratory distress.
Pulmonary Embolism (PE): Blockage of a pulmonary artery causes pleuritic pain, shortness of breath, and possible hypoxia.
NON-CARDIAC CAUSES OF CHEST PAIN - NEURO AND PSYCH CAUSES
Intercostal Neuralgia: Compression or irritation of intercostal nerves leads to sharp, burning pain along the ribcage.
Panic Attacks / Anxiety: Hyperventilation and muscle tension cause tightness, breathlessness, and chest pain that mimics cardiac issues.
NON-CARDIAC CAUSES OF CHEST PAIN - MEDICAL MANAGEMENT
GERD: Proton pump inhibitors (PPIs), lifestyle modifications, and avoiding trigger foods.
Pleuritis: NSAIDs or corticosteroids for inflammation.
Intercostal Neuralgia: Neuropathic pain medications (e.g., gabapentin) if severe.
Panic Attacks: Cognitive behavioral therapy (CBT), breathing exercises, or anxiolytic medication.
NON-CARDIAC CAUSES OF CHEST PAIN - MANUAL THERAPY
Manual therapy can be highly effective for musculoskeletal causes of chest pain, particularly those involving rib dysfunction, myofascial tension, and postural imbalances.
Soft Tissue and Myofascial Release
- Pectoralis Major & Minor Release: Reduces anterior chest tightness from postural strain.
- Intercostal Muscle Release: Helps relieve pain from muscular tension and rib dysfunction.
- Thoracic Spine & Upper Back Mobilization: Improves rib mobility and reduces compensatory tension in surrounding structures.
Joint Mobilization & Rib Adjustments
- Thoracic Joint Mobilization: Addresses rib and vertebral restrictions that contribute to referred pain.
- Costosternal & Costovertebral Mobilization: Beneficial for costochondritis and rib dysfunctions.
Postural & Breathing Techniques
- Diaphragmatic Breathing: Reduces hypertonicity in chest and neck muscles, particularly in anxiety-related cases.
- Postural Re-Education: Correcting forward head posture and rounded shoulders helps offload chronic strain on the thoracic region.
ATRIAL FIBRILLATION
Atrial fibrillation (AFib) is a supraventricular arrhythmia characterized by disorganized electrical activity in the atria, leading to irregular and often rapid heartbeats.
ATRIAL FIBRILLATION PATHOPHYSIOLOGY
Electrical Dysfunction:
- Normally, the sinoatrial (SA) node initiates electrical impulses, coordinating atrial contraction.
- In AFib, multiple ectopic electrical impulses originate from the pulmonary veins and atrial myocardium, leading to chaotic atrial activity.
Loss of Atrial Contraction & Irregular Ventricular Response:
- The atria quiver instead of contracting effectively, reducing atrial kick (contribution to ventricular filling).
- The atrioventricular (AV) node filters these impulses, but the ventricular response remains irregular and rapid (often 100-175 bpm).
Complications of AFib:
- Thromboembolism (Stroke Risk): Blood stasis in the fibrillating atria can form clots, which may embolize to the brain.
- Heart Failure: Rapid, irregular heartbeats impair ventricular filling, reducing cardiac output over time.
- Tachycardia-Induced Cardiomyopathy: Prolonged high heart rates can weaken the heart muscle.
ATRIAL FIBRILLATION MEDICAL MANAGEMENT
Rate Control (Slowing Heart Rate):
- Beta-blockers (e.g., metoprolol, atenolol)
- Calcium channel blockers (e.g., diltiazem, verapamil)
- Digoxin (less common, used in heart failure cases)
Rhythm Control (Restoring Normal Sinus Rhythm):
- Antiarrhythmics (e.g., amiodarone, flecainide, sotalol)
- Electrical Cardioversion (shock therapy to reset heart rhythm)
- Catheter Ablation (destroying abnormal atrial foci)
Anticoagulation (Stroke Prevention):
- Warfarin or Direct Oral Anticoagulants (DOACs) (e.g., apixaban, rivaroxaban) to prevent clot formation.
ATRIAL FIBRILLATION SURGICAL MANAGEMENTS
- Pulmonary Vein Isolation (Ablation Therapy): Targets ectopic foci to reduce AFib recurrence.
- Pacemaker Implantation: For AFib with slow ventricular response or after AV node ablation.
ATRIAL FIBRILLATION MANUAL THERAPY
Manual therapy does not treat AFib directly, but it can help manage musculoskeletal tension, stress, and circulation issues associated with the condition.
Stress Reduction & Parasympathetic Activation
- Diaphragmatic breathing & relaxation techniques can help reduce sympathetic nervous system overactivity, which may contribute to AFib episodes.
- Gentle craniosacral therapy or soft tissue mobilization can promote relaxation and support autonomic balance.
Thoracic & Postural Support
- Thoracic spine and rib mobilization may improve breathing efficiency and vagal tone, which can indirectly support cardiovascular function.
- Postural correction techniques (especially for forward head posture) help offload strain on the vagus nerve and autonomic system.
Avoiding Circulatory Overstimulation
- Avoid deep pressure techniques or aggressive soft tissue work in individuals with anticoagulation therapy (risk of bruising or bleeding).
- Avoid strong stimulation of the carotid sinus (e.g., deep neck massage) due to its impact on heart rate.
- Monitor for dizziness, fatigue, or palpitations during treatment.
