Alterations of pulmonary function

COPD chart Bronchoconstriction: Three

Obstructive lung diseases mechanisms
•Changes in bronchioles during an
asthma attack
•Airway obstruction that is worse with •sudden contraction of smooth
expiration muscle that causes acute
dyspnea
•Common signs and symptoms •thick, viscous secretions
•Dyspnea and wheezing •edema
•caused by engorgement of
pulmonary blood
Common obstructive disorders vessels
•Asthma
Pathophysiology: Early vs Late
•COPD Response
•Emphysema •Early asthmatic response

•Chronic bronchitis •vasodilation

•increased capillary permeability

COPD •mucosal edema

•bronchial smooth muscle
contraction
•Characterized by persistent airflow limitation (bronchospasm)
•Usually progressive •tenacious mucous secretion
•Most common chronic lung disease in the world ' •Late asthmatic response
•Preventable/treatable •begins 4–8 hours after the early
•Enhanced chronic inflammatory response response.
•chemotactic recruitment of
•Exacerbations/comorbidities contribute to severity lymphocytes, eosinophils,
basophils, neutrophils, and
lymphocytes occurs.
Risk factors •airway scarring
•Tobacco smoke •increased bronchial
hyperresponsiveness
•Occupational dusts and chemicals
•Air pollution indoor and outdoor
•Any factor affecting lung growth during gestation and
childhood
•Treatment- bronchodilators, mucolytics, antioxidants, anti
inflammatory medicine

Pathogenesis
Inhalation of cigarette smoke or other noxious particles
causes chronic inflammation
•Chronic inflammatory response may cause
parenchymal tissue destruction (emphysema), and
disruption of normal repair and defense mechanisms
(small airway fibrosis)
•airways, lung tissue, pulmonary vasculature all affected

•Changes lead to gas trapping and progressive airflow Emphysema

limitation
•structural changes result from repeated injury and
repair
•airflow limitation that is not fully reversible
Asthma
Chronic inflammatory disorder of the
airways
•Inflammation results from hyper-
responsiveness of the airways
•Can lead to obstruction and status
asthmaticus
•Symptoms include expiratory wheezing,
dyspnea, and tachypnea
•Peak flow meters, corticosteroids, beta-
agonists, and anti-inflammatories
used to treat
airways accompanied by destruction of alveolar walls without obvious fibrosis
•Obstruction results from changes in lung tissues rather than mucus production and
inflammation
•Inherited deficit of α1-antitrypsin (1%)
•Destruction of alveoli, production of large air sacs (Bullae) and air spaces (Blebs) not
effective in gas exchange
•Loss of elastic recoil/expiration difficult/ air trapping
•Treatment – smoking cessation, inhaled anticholinergic, bronchodilators, steroids,
phosphodiesterase inhibitors, lung volume reduction surgery
Chronic Bronchitis
Hypersecretion of mucus and chronic productive cough that
lasts for at least 3 months of the year and for at
least 2 consecutive years.
•Inspired irritants increase mucus production and the size
and number of mucous glands
•Causes smooth muscle hypertrophy, fibrosis and narrowing
of airways
•Chronic inflammation causes Bronchial edema
•Mucus is thicker than normal.

Asthma
Asthma VS COPD
Drug therapy : what they do
Used to prevent or treat
reversible airway obstruction
and airway
hyperresponsiveness
Bronchodilators
• muscarinic antagonists
(anticholinergics) • β2-
adrenergic agonists
Anti-inflammatory drugs
• inhaled corticosteroids (ICS) Long-term control drugs
Alterations of pulmonary function
Pneumothorax Pulmonary hypertension
and cor pulmonae
Presence of air or gas in pleural space
• Caused by rupture of visceral pleura (surrounds the
lungs)
• Or parietal pleura and chest wall COPD and right sided
heart failure
• Air separates pleura, loss of negative pressure Cor pulmonae
• Lung recoils toward hilum
• Spontaneous- healthy men 20-40 rupture of bullae and
blebs apex of lung
• 80% emphysemic changes, 10% no hx
• Secondary caused by trauma, rib #,bullet, stabbing, or
mechanical ventilation
• Open/tension (one way valve) accumulating pressure
• Pushes lung to other side , displaces heart, vessels, life
threatening
Pleural abnormalities
Pleural effusion
• Transudative effusion
• Exudative effusion • Hemothorax
• Empyema
• Infected pleural effusion; pus • Chylothorax
•Pulmonary edema
• Excess water in the lungs
Pulmonary embolis
Pulmonary vascular disorders: pulmonary embolus
• Occlusion of a portion of the pulmonary vascular bed
by a thrombus, embolus, tissue fragment, lipids, or an
air bubble
• Pulmonary emboli commonly arise from the deep
veins in the lower leg
Virchow triad
• Venous stasis, hypercoagulability, and injuries to the
endothelial cells that line the vessels
Onset and duration of action Devices used to deliver
respiratory drugs
Quick-relief (fast-acting) drugs
• quick onset • metered dose inhaler
• shorter duration of action • nebulizer with
• tx symptoms of exacerbations attached mask
• rescue therapy
Short-Acting Muscarinic Antagonists (SAMA)
• ipratropium
• Short-Acting ß2-adrenergic Agonists (SABA)
• salbutamol
• slow onset
• longer duration of action
• achieve and maintain control of persistent
symptoms
• maintenance therapy
Long-Acting Muscarinic Antagonists ( LAMA) •
tiotropium
Long-Acting ß2-adrenergic Agonists (LABA) •
salmeterol
Inhaled corticosteroids (ICS)
• fluticasone
• beclomethasone
 normal anatomy and physiology of the cardiovascular system.

The cardiovascular system, also known as the circulatory system, is responsible for the transportation of oxygen, nutrients,
hormones, and waste products throughout the body. It consists of the heart, blood vessels, and blood.

The heart is a muscular organ located in the chest cavity. It is divided into four chambers: two atria and two ventricles. The
right side of the heart receives deoxygenated blood from the body and pumps it to the lungs for oxygenation, while the left
side receives oxygenated blood from the lungs and pumps it to the rest of the body.

The blood vessels are divided into three types: arteries, veins, and capillaries. Arteries carry oxygenated blood away from the
heart to the body's tissues, while veins carry deoxygenated blood back to the heart. Capillaries are tiny, thin-walled vessels
that connect arteries and veins, allowing for the exchange of oxygen, nutrients, and waste products between the blood and
the surrounding tissues.

Blood is a fluid connective tissue that consists of plasma, red blood cells, white blood cells, and platelets. Plasma is a yellowish
liquid that carries nutrients, hormones, and waste products. Red blood cells, or erythrocytes, are responsible for carrying
oxygen to the body's tissues. White blood cells, or leukocytes, are involved in the immune response and help fight off
infections. Platelets are small cell fragments that play a crucial role in blood clotting.

The cardiovascular system functions to maintain homeostasis by ensuring the delivery of oxygen and nutrients to all cells
and removing waste products. The heart pumps blood throughout the body, generating blood pressure that helps propel blood
through the blood vessels. The arteries and veins regulate blood flow and blood pressure through vasoconstriction and
vasodilation. Capillaries allow for the exchange of gases, nutrients, and waste products between the blood and the tissues.

Overall, the normal anatomy and physiology of the cardiovascular system are essential for the proper functioning of the
body, ensuring the delivery of oxygen and nutrients to all cells and the removal of waste products.

mechanisms involved in the regulation of blood pressure

The regulation of blood pressure involves a complex interplay of various mechanisms that work together to maintain a stable blood
pressure within a normal range. These mechanisms include:

1. Autonomic Nervous System: The autonomic nervous system, specifically the sympathetic and parasympathetic divisions, plays a
crucial role in regulating blood pressure. The sympathetic nervous system increases blood pressure by causing vasoconstriction
(narrowing of blood vessels) and increasing heart rate and contractility. On the other hand, the parasympathetic nervous system
decreases blood pressure by causing vasodilation (widening of blood vessels) and decreasing heart rate.

2. Baroreceptor Reflex: Baroreceptors are specialized nerve endings located in the walls of certain blood vessels, particularly in the
carotid sinus and aortic arch. They detect changes in blood pressure and send signals to the brain, specifically the medulla oblongata,
which then initiates appropriate responses to regulate blood pressure. If blood pressure increases, the baroreceptors signal the
brain to decrease sympathetic activity and increase parasympathetic activity, resulting in vasodilation and decreased heart rate.
Conversely, if blood pressure decreases, the baroreceptors signal the brain to increase sympathetic activity and decrease
parasympathetic activity, leading to vasoconstriction and increased heart rate.

3. Renin-Angiotensin-Aldosterone System (RAAS): The RAAS is a hormonal system that regulates blood pressure and fluid balance.
When blood pressure decreases or there is a decrease in blood flow to the kidneys, special cells in the kidneys release an enzyme
called renin. Renin acts on a protein called angiotensinogen, converting it into angiotensin I. Angiotensin I is then converted into
angiotensin II by an enzyme called angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor, causing blood
vessels to narrow and increasing blood pressure. It also stimulates the release of aldosterone from the adrenal glands, which
promotes sodium and water retention, further increasing blood volume and blood pressure.

4. Kidneys: The kidneys play a vital role in regulating blood pressure through the control of fluid balance. They help maintain blood
pressure by adjusting the amount of water and sodium excreted in urine. When blood pressure decreases, the kidneys conserve water
and sodium, leading to increased blood volume and blood pressure. Conversely, when blood pressure is high, the kidneys excrete
excess water and sodium, reducing blood volume and blood pressure.

5. Endothelial Function: The endothelium, the inner lining of blood vessels, produces various substances that regulate blood pressure.
Nitric oxide (NO) is a potent vasodilator released by the endothelium, promoting relaxation of blood vessels and lowering blood
pressure. Endothelin, on the other hand, is a vasoconstrictor that can increase blood pressure.

These mechanisms work together to maintain blood pressure within a normal range, ensuring adequate perfusion of organs and
tissues while preventing excessive strain on the cardiovascular system. Dysfunction in any of these mechanisms can lead to
hypertension (high blood pressure) or hypotension (low blood pressure), which can have detrimental effects on health.
 pathophysiological mechanisms associated with primary hypertension.

Primary hypertension, also known as essential or idiopathic hypertension, refers to high blood pressure that has no identifiable cause. While the exact pathophysiological mechanisms
underlying primary hypertension are not fully understood, several factors have been implicated in its development. These include:

1. Increased Peripheral Vascular Resistance: Primary hypertension is often associated with increased resistance to blood flow in the peripheral blood vessels. This can result from
abnormalities in the small arteries and arterioles, leading to vasoconstriction and reduced vessel compliance. The exact mechanisms contributing to increased vascular resistance are
complex and involve dysregulation of various vasoactive substances, such as endothelin, angiotensin II, and nitric oxide.

2. Renin-Angiotensin-Aldosterone System (RAAS) Dysregulation: In primary hypertension, there is often an imbalance in the RAAS, leading to increased levels of angiotensin II.
Angiotensin II is a potent vasoconstrictor and promotes sodium and water retention, leading to increased blood volume and elevated blood pressure. Dysregulation of the RAAS can result
from genetic factors, abnormal renal function, or abnormalities in the production or response to renin.

3. Sodium and Fluid Imbalance: Excessive sodium intake and impaired sodium excretion by the kidneys can contribute to primary hypertension. High sodium levels in the blood can lead to
increased fluid retention, expanding blood volume and raising blood pressure. This can be influenced by dietary factors, genetic predisposition, and abnormalities in renal sodium handling.

4. Sympathetic Nervous System Overactivity: Increased sympathetic nervous system activity has been observed in individuals with primary hypertension. This can lead to
vasoconstriction, increased heart rate, and elevated blood pressure. The exact mechanisms underlying sympathetic overactivity in primary hypertension are not fully understood but may
involve abnormalities in baroreceptor reflexes, central nervous system dysfunction, or dysregulation of neurotransmitters.

5. Endothelial Dysfunction: Dysfunction of the endothelium, the inner lining of blood vessels, is commonly observed in primary hypertension. Endothelial dysfunction is characterized by
impaired production and release of nitric oxide, a potent vasodilator. This results in reduced vasodilation and increased vasoconstriction, contributing to elevated blood pressure.

6. Genetic Factors: There is evidence to suggest a genetic predisposition to primary hypertension. Multiple genes have been identified that may influence blood pressure regulation,
including those involved in the RAAS, sodium transport, and vascular function. However, the specific genetic mechanisms and their interactions with environmental factors are still being
investigated.

It is important to note that primary hypertension is a multifactorial condition, and the interplay of these mechanisms can vary among individuals. Lifestyle factors, such as diet, physical
activity, and stress, also play a significant role in the development and progression of primary hypertension.

treatment strategies for the prevention and management of hypertension.

The treatment strategies for the prevention and management of hypertension aim to lower blood pressure and reduce the risk of complications. These strategies typically involve a
combination of lifestyle modifications and medication. Here are some common approaches:

1. Lifestyle Modifications:
- Dietary Changes: Adopting a healthy eating plan, such as the DASH (Dietary Approaches to Stop Hypertension) diet, which emphasizes fruits, vegetables, whole grains, lean
proteins, and low-fat dairy products while limiting sodium, saturated fats, and added sugars.
- Sodium Restriction: Limiting sodium intake to less than 2,300 milligrams per day (or even lower for certain individuals, such as those with diabetes or kidney disease).
- Weight Management: Achieving and maintaining a healthy weight through a combination of regular physical activity and a balanced diet.
- Regular Exercise: Engaging in aerobic exercise for at least 150 minutes per week, or 75 minutes of vigorous exercise, along with muscle-strengthening activities at least twice a
week.
- Limiting Alcohol Consumption: Moderating alcohol intake to no more than one drink per day for women and two drinks per day for men.
- Smoking Cessation: Quitting smoking, as smoking can raise blood pressure and increase the risk of heart disease.

2. Medications:
- Antihypertensive Medications: Various classes of medications are available to lower blood pressure, including diuretics, beta-blockers, ACE inhibitors, angiotensin II receptor
blockers (ARBs), calcium channel blockers, and others. The choice of medication depends on factors such as the individual's age, ethnicity, comorbidities, and potential side effects.
- Combination Therapy: In some cases, multiple medications may be prescribed to achieve blood pressure control.
- Medications for Underlying Conditions: If hypertension is secondary to another medical condition, such as kidney disease or hormonal disorders, treating the underlying condition
may help manage blood pressure.

3. Regular Blood Pressure Monitoring: Regular monitoring of blood pressure at home or in a healthcare setting is important to track progress and ensure that blood pressure remains
within the target range.

4. Stress Management: Adopting stress-reducing techniques, such as relaxation exercises, meditation, or engaging in hobbies and activities that promote relaxation.

5. Regular Medical Check-ups: Regular visits to a healthcare provider to monitor blood pressure, assess overall health, and adjust treatment as needed.

It is important to note that treatment strategies may vary depending on individual factors, such as age, overall health, and the presence of other medical conditions. It is
recommended to work closely with a healthcare provider to develop a personalized treatment plan for hypertension management.
 Week 6 Cardiovascular System; Hypertension and Coronary Artery Disease; Acute Coronary Syndrome
Hypertension
Coronary artery disease
Increase in peripheral resistance (arteriolar vasoconstriction) an increase in • any vascular disorder that
circulating blood volume or both narrows or occludes the
coronary arteries leading to
• consistent elevation of systemic arterial blood pressure myocardial ischemia
• SBP of 140 or higher or DBP of 90 or higher • atherosclerosis (thickening
and hardening caused by
Malignant HTN accumulation of lipid-laden
• rapidly progressive hypertension microphages in the arterial
• DBP is usually 140 wall)
• life threatening organ damage • form plaques

primary hypertension
is the most common
> essential or idiopathic
• leading cause of CAD and CVA
hypertension
> genetic & environmental
factors
> Risk factors, age - high sodium
intake- natriuretic peptide
abnormalities - inflammation -
obesity - insulin resistance

• Interaction genetics/
environment/neurohormonal
• SNS, RAAS, inflammation,
obesity, insulin resistance ,
increase blood volume all
contribute
• Decreased excretion of salt
(pressure naturesis
relationship)
• Structural changes in blood
vessels

secondary hypertension
> caused by a systemic disease process that Relationship between CAD, chronic stable angina, and
raises peripheral vascular resistance or cardiac ACS
output
> Renal vascular or parenchymal disease,
adrenocortical tumours, adrenomedullary
tumours, and medication

Dyslipidemia
• abnormal concentration of serum
lipoproteins Markers of inflammation and thrombosis
• absorbed by GI tract delivered to liver and • c-reactive protein
cells • marker of inflammation
• chylomicrons made of cholesterol taken up in • synthesized in liver uses an indirect marker of atherosclerotic plaque related
liver, converted to LDL inflammation
• LDL delivers cholesterol to tissues • Troponin 1-highly sensitive reflection of myocardial Ischemia
• LDL accumulates in artery wall
• too high of an amount increases coronary
risk
Myocardial infarction (mi)
• result of sustained ischemia more than 20 minutes, causing irreversible myocardial cell death (necrosis)
• necrosis of entire thickness of myocardium takes 4-6 hrs Clinical manifestations of ACS
• cellular injury Pain
• cellular death • total occlusion → anaerobic metabolism and lactic
Structural & functional changes acid accumulation → severe, immobilizing chest
• myocardial stunning pain not relieved by rest, position change or
• hibernating myocardium nitrate administration
• myocardial remodelling • described as heaviness, constriction, tightness,
Manifestations burning, pressure, or crushing
• sudden severe chest pain; may radiate
• nausea, vomiting Common locations:
• diaphoresis • substernal
• Dyspnea • retrosternal
Complications • epigastric areas;pain can radiare to neck,jaw,arms
• sudden cardiac arrest due to ischemia, left ventricular dysfunction and electrical instability Simulation of SNS (sympathetic nervous system)
results in
Myocardial ischemia • release of glycogen
• diaphoresis
Pathophysiology • vasoconstriction of peripheral blood vessels
• skin : ashy, cool, clammy
• coronary arteries supply blood to the myocardium
under varying workloads (healthy arteries can dilate
under strenuous conditions
• ischemia happens if vessel narrows by 50%
• plaque

Reversible myocardial ischemia

Stable angina pectoris

• gradual narrowing of lumen
• narrowing and hardening with inflammation and ↓ vasodilation
• rest bloodflow restored
• transient substernal chest pain/heaviness/pressure Within 24 hours, leukocytes infiltrate the area
• pain caused by anaerobic metabolism and build up of lactic acid & stretching of of cell death.
ischemic myocardium • Enzymes are released from the dead cardiac
cells (important indicators of MI).
Variant (prinzmetal) angina • Proteolytic enzymes of neutrophils and
• occurs unpredictable often at rest macrophages remove all necrotic tissue by
• pain caused by vasospasm often without atherosclerosis second or third day.
• occurs at night mostly • Development of collateral circulation
improves areas of poor perfusion
Silent ischemia • Necrotic zone identifiable by ECG changes and
• complaints of fatigue nuclear scanning
• unease • 10 to 14 days after MI, scar tissue is still weak
• dyspnea and vulnerable to stress
• chronic stress can contribute • By 6 weeks after MI, scar tissue has replaced
necrotic tissue.
➢ Area is said to be healed, but less compliant.
• Ventricular remodeling
➢ Normal myocardium will hypertrophy and
dilate in an attempt to compensate for the
infarcted muscle.
What is the most common Complication of Myocardial Dysrhythmias Infarction?
Collaborative Care: Acute Coronary Syndrome
➢ Most common complication
➢ Present in 80% of MI patients
Emergency management
➢ Most common cause of death in the prehospital period
➢ Initial interventions
➢ Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock
➢ Ongoing monitoring
• Heart failure
Emergent PCI
➢ A complication that occurs when the pumping power of the heart has diminished
➢ Treatment of choice for confirmed MI
➢ Balloon angioplasty + drug-eluting stent(s)

Fibrinolytic therapy
Complications of Myocardial Infarction ➢ Indications and contraindications
• Cardiogenic shock ➢ Best marker of reperfusion: return of ST segment to
➢ Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure baseline
➢ Requires aggressive management ➢ Rescue PCI if thrombolysis fails
• Papillary muscle dysfunction ➢ Major complication: bleeding
➢ Causes mitral valve regurgitation
➢ Condition aggravates an already compromised LV Coronary surgical revascularization
• Ventricular aneurysm ➢ Coronary artery bypass graft (CABG) surgery
➢ Results when the infarcted myocardial wall becomes thinned and bulges out during contraction • Requires sternotomy and cardiopulmonary bypass (CPB)
Dressler syndrome • Uses arteries and veins for grafts
➢ Minimally invasive direct coronary artery bypass
(MIDCAB)
Complications of Myocardial Infarction
• Alternative to traditional CABG
• Acute pericarditis
• An inflammation of visceral and/or parietal pericardium
Drug therapy
• May result in cardiac compression, ↓ LV filling and emptying, heart failure
➢ IV nitroglycerin
• Pericardial friction rub may be heard on auscultation
➢ Morphine sulphate
• Chest pain different from MI pain
➢ β-Adrenergic blockers
➢ Angiotensin-converting enzyme inhibitors
Dressler syndrome
➢ Antidysrhythmia drugs
➢ Cholesterol-lowering drugs
• Characterized by pericarditis with effusion and fever that develop 4 to 6
➢ Stool softeners
weeks after MI
• Pericardial (chest) pain
Pericardial friction rub may be heard on auscultation
➢ Arthralgia
 Systolic heart failure

Pathophysiology
Pathophysiology of Systolic Heart Failure:
In systolic heart failure, the heart muscle becomes weakened and is unable to
contract forcefully enough to pump blood effectively. This leads to a reduced
ejection fraction, which is the percentage of blood pumped out of the heart with
each beat. The weakened heart muscle results in decreased cardiac output, causing
inadequate blood supply to the body's organs and tissues.
As a compensatory mechanism, the sympathetic nervous system is activated,
leading to increased heart rate and vasoconstriction. This helps maintain blood
pressure and perfusion to vital organs in the short term but can be detrimental in
the long term, leading to further damage to the heart muscle.
Etiology
Etiology of Systolic Heart Failure:
Systolic heart failure can have various causes, including:
1. Coronary artery disease: Blockage or narrowing of the coronary arteries can lead
to reduced blood flow to the heart muscle, causing damage and weakening of the
heart.
2. Myocardial infarction (heart attack): A heart attack occurs when there is a
sudden blockage of blood flow to a part of the heart, leading to damage and impaired
heart function.
3. Cardiomyopathy: This refers to diseases of the heart muscle, which can be
inherited or acquired. Cardiomyopathy can weaken the heart muscle and impair its
ability to pump effectively.

4. Hypertension: Chronic high blood pressure can cause the heart muscle to thicken
and become stiff, leading to reduced pumping ability.

5. Valvular heart disease: Conditions such as aortic stenosis or mitral regurgitation

can cause the heart to work harder to pump blood, eventually leading to heart
failure.

Compensatory Mechanisms in Heart Failure:

In response to reduced cardiac output, the body activates compensatory mechanisms to maintain blood pressure and perfusion to vital organs.
These mechanisms include:

1. Activation of the sympathetic nervous system: This leads to increased release of adrenaline and noradrenaline, which increase heart rate and
contractility, as well as vasoconstriction to maintain blood pressure.
2. Activation of the renin-angiotensin-aldosterone system (RAAS): This system is activated to increase fluid retention and vasoconstriction,
helping to maintain blood pressure.
3. Ventricular remodeling: The heart undergoes structural changes, including enlargement and thickening of the ventricles, in an attempt to
compensate for reduced pumping ability.

Clinical manifestations Treatment

Clinical Manifestations of Systolic Heart
Failure:
The clinical manifestations of systolic
heart failure can vary but commonly
include:
1. Shortness of breath (dyspnea),
especially during physical activity or when
lying flat (orthopnea).
2. Fatigue and weakness.
3. Fluid retention, leading to swelling in
the legs, ankles, and abdomen (edema).
4. Persistent cough or wheezing.
5. Reduced exercise tolerance.
6. Rapid or irregular heartbeat
(arrhythmias).
7. Weight gain due to fluid retention.
Diagnostic Tests for Systolic Heart Failure:
Complications of Systolic Heart Failure: To diagnose systolic heart failure, healthcare providers may perform the following tests:
Systolic heart failure can lead to various complications,
including: 1. Physical examination: This includes listening to the heart and lungs, checking for signs of fluid
retention, and assessing overall health status.
1. Pulmonary edema: Fluid can accumulate in the lungs, causing 2. Blood tests: These may include measuring B-type natriuretic peptide (BNP) levels, which can be
severe shortness of breath and respiratory distress. elevated in heart failure.
2. Arrhythmias: Irregular heart rhythms can occur, increasing 3. Electrocardiogram (ECG): This test records the electrical activity of the heart and can help
the risk of stroke or sudden cardiac arrest. identify abnormal rhythms or signs of heart damage.
3. Kidney dysfunction: Reduced blood flow to the kidneys can 4. Echocardiogram: This ultrasound test provides detailed images of the heart's structure and
impair their function, leading to fluid and electrolyte function, including the ejection fraction.
imbalances. 5. Stress test: This test evaluates the heart's response to physical activity and can help assess
4. Liver dysfunction: Congestion in the liver can lead to exercise tolerance and detect any abnormalities.
impaired liver function and fluid retention. 6. Cardiac catheterization: This invasive procedure involves inserting a catheter into the heart to
5. Cardiogenic shock: In severe cases, the heart's pumping measure pressures and assess blood flow.
ability can become severely compromised, leading to 7. Imaging tests: Additional imaging tests such as MRI or CT scan may be performed to further
inadequate blood supply to the body's organs and tissues. evaluate the heart's structure and function.
Management of Systolic Heart Failure:
The management of systolic heart failure aims to improve symptoms, slow disease progression, and reduce
the risk of complications. It typically involves the following approaches:
1. Lifestyle modifications: These include dietary changes (such as reducing sodium intake), regular exercise,
weight management, smoking cessation, and limiting alcohol consumption.
2. Medications: Various medications may be prescribed, including diuretics (to reduce fluid retention), ACE
inhibitors or ARBs (to dilate blood vessels and reduce workload on the heart), beta-blockers (to slow heart
rate and reduce workload), and aldosterone antagonists (to reduce fluid retention).
3. Cardiac rehabilitation: This program involves supervised exercise, education, and counseling to help
improve physical fitness and manage heart failure.
4. Device therapy: In some cases, devices such as implantable cardioverter-defibrillators (ICDs) or cardiac
resynchronization therapy (CRT) devices may be implanted to help regulate heart rhythm and improve
pumping efficiency.
5. Surgical interventions: In certain situations, surgical procedures such as coronary artery bypass grafting
(CABG) or valve repair/replacement may be necessary to improve heart function.
6. Heart transplant: For severe cases of heart failure that do not respond to other treatments, a heart
transplant may be considered.