1.28 Cardiac Pathophysiology

Cardiac Pathophysiology: The Numbers

• About 702,880 Americans died from heart disease in 2022; this is approximately 1 in every 5 deaths
• Coronary heart disease is the most common type of heart disease, killing more than 375,476 people in 2021
• Approximately 20.1 million adults aged 20 and older have CAD
• Heart disease is the leading cause of death for both men and women in most racial and ethnic groups in the U.S.
• Heart disease costs the United States $252.2 billion each year (2019-2020)
• This total includes the cost of health care services, medications, and lost productivity due to death
• Heart disease is the leading cause of death for people of most racial/ethnic groups in the United States, including African Americans, America Indian, Alaska Native, Hispanic, and White men
• For women of Asian or Pacific Islander, American Indian, Alaska Natives, or Hispanic descent, heart disease is second only to cancer

Medicine Admission Note

• Patient is a 93-year-old male with ischemic cardiomyopathy (ICM) with an ejection fraction (EF) of 30-35%
• The patient has severe pulmonary hypertension (pHTN), 3+ mitral regurgitation (MR), and presents with dyspnea for one day
• Recent admission was for congestive heart failure (CHF) exacerbation with discharge (d/c) to a skilled nursing facility (SAR)
• The patient reports that their daughter sets up their medications
• The patient often forgets to take their Lasix

Objectives of Cardiac Pathophysiology Study

• Explain the basics of Coronary Heart Disease and how atherosclerotic plaques are formed
• Identify the types of angina
• Explain myocardial infarction, including types and zones of infarction
• Identify how MI is diagnosed and the basic treatment
• Explain the difference between cardiac pump dysfunction and failure
• Explain the differences between right and left heart failure, as well as systolic and diastolic heart failure
• Identify the consequences of CHF and ventricular remodeling
• Identify how CHF is diagnosed and basic treatment
• Effectively describe the types of cardiomyopathy
• Accurately describe valvular heart disease, sudden cardiac death, aneurysms, endocarditis, pericarditis, and cardiac tumors

Topics in Cardiac Pathophysiology

• Ischemic Heart Disease, including Atherosclerotic Heart Disease, Coronary Artery Disease, Coronary Heart Disease, Angina, and Myocardial Infarction
• Cardiac Muscle Dysfunction, including Heart Failure and Cardiomyopathy
• Valve Disease
• Sudden Cardiac Death
• Aneurysms that may cause Vascular Disease
• Endocarditis
• Pericarditis
• Tumors

Coronary Heart Disease (CHD) Overview

• CHD involves the buildup of plaque in the heart's arteries, which can cause a heart attack
• CAD is Coronary Artery Disease
• CHD is Coronary Heart Disease
• The terms CAD and CHD are often used interchangeably
• CHD is actually caused by CAD
• Ischemia
• Infarction

Atherosclerotic Heart Disease

• Atherosclerotic Heart Disease is also known as Coronary Artery Disease
• Athero means gruel or soft deposit
• Sclerosis means hardening
• Atherosclerotic Heart Disease is characterized by nodular deposits of fatty material that line the walls of the artery (plaques)
• Vessel walls may lose their elasticity and become sclerotic; This is known as "Hardening of the Arteries"

CAD Risk Factors

• Lifestyles are the modifiable risks
• Tobacco use
• Diet high in saturated fat, cholesterol, and calories
• Excess alcohol consumption
• Physical inactivity
• Biochemical or Physiologic Characteristics are modifiable risks
• Blood lipid abnormalities
• Cholesterol production
• Elevated blood triglycerides
• Hyperglycemia / DM
• Obesity
• Hypertension
• Personal Characteristics are non-modifiable risks
• Gender
• Age
• Family history of CAD
• Personal history of CAD

Cholesterol Fundamentals

• Cholesterol is an essential compound used by the body for cell membrane structure and enzymatic activity
• Cholesterol transports fatty acids and lipids
• The body synthesizes 75% of cholesterol
• Food sources comprise 25% of cholesterol, found only in animal products

LDL Cholesterol

• LDL (Low-Density Lipoprotein) is considered "bad" cholesterol
• A higher LDL number signifies a higher risk
• Desirable LDL: <100
• Near optimal LDL: 100-129
• Borderline high LDL: 130-159
• High LDL: 160-189
• Very high LDL: >190
• An LDL of <70 is recommended for patients with Coronary Heart Disease or vessel disease
• An LDL of <100 is recommended for those with Diabetes Mellitus or other risk factors

HDL Cholesterol

• HDL (High-Density Lipoprotein) is considered "good" cholesterol
• A higher HDL number signifies a lower risk
• Optimal HDL: >60
• Low HDL: <40 for men and <50 for women
• HDL Cholesterol protects against Coronary Heart Disease by removing LDLs from the blood and preventing their buildup in arteries

Triglycerides Overview

• Triglycerides are part of the lipoprotein profile
• High triglyceride levels equal high risk
• Triglycerides are fats carried in the blood from food
• Normal triglycerides: <150
• Borderline high triglycerides: 150-199
• High triglycerides: 200-499
• Very high triglycerides: >500

Total Cholesterol Insights

• Total Cholesterol is a measure of LDL, HDL, and other lipid components
• Desirable: <200
• Borderline high: 200-239
• High: >240

LDL:HDL Ratio

• This ratio provides a composite risk marker
• A ratio of < or = 3:1 is low risk
• A ratio of > or = 5:1 indicates increased risk

Total Cholesterol (CHOL):HDL Ratio

• Useful as a predictor for development of cholesterol related blockages
• A ratio of >4.5 is increased risk of atherosclerosis

Atherosclerotic Lesions

• Atherosclerotic Lesions can develop because of abnormal lipid metabolism, excessive intake of cholesterol/saturated fats, and/or genetic predisposition

Pathogenic Mechanism of Plaque Formation Basics

• The earliest detectable atherosclerotic lesion is the fatty streak (lipid foam cells)
• Fatty streak becomes fibrous plaque

The Lipid Hypothesis

• Increased plasma LDL levels penetrate the arterial wall, leading to lipids accumulating in smooth muscle cells and macrophages (foam cells)
• LDL increases smooth muscle cell hyperplasia and migration of cells into sub-intimal and intimal regions
• As the fatty streak and fibrous cap enlarge, they tear the endothelium, where platelets aggregate causing thrombus formation

Chronic Endothelial Injury

• Injury to the interior of the cell wall by macrophages causes platelets, monocytes, lipids, and smooth muscle cells to migrate from the media to the intima
• Cells aggregate where they form a fibrous cap
• Platelets form clots and release proteins with tough fibers, hardening the artery
• This can block blood flow or break off and throw a clot

Review of Cardiac Blood Supply

• Coronary Arteries arise from, terminate in vessel that supply the heart
• Left Coronary Artery supplies blood to most of left parts and septum of the heart
• Right Coronary Artery supplies blood to the posterior septum and inferior parts of the heart

Understanding Myocardial Ischemia

• Myocardial Ischemia occurs when myocardial oxygen demand is greater than the supply
• Myocardial Ischemia is reversible
• Myocardial Ischemia can be caused by increased oxygen demand from exercise or stress
• Myocardial Ischemia can be caused by decreased oxygen supply due to decreased coronary blood flow
• Myocardial Ischemia is diagnosed by exercise stress test, arrhythmias and T wave inversion on an EKG that later becomes ST elevation

Angina Pectoris (Angina) Overview

• Is described as pressure or heaviness in the substernal (midchest) area, over the heart (precordial), or in the shoulder, arm, throat or jaw
• Types of angina are Chronic and Unstable

Chronic Stable Angina

• Is generally associated with a set level of O2 demand and usually lasts several minutes
• Chronic Stable Angina is precipitated by exertion, emotional stress, or heavy meals
• Symptoms include pressure and heaviness
• Relief with nitroglycerin (NTG)

Unstable Angina

• Involves angina symptoms without the demands to generate it
• Displays change in typical pattern or symptoms at rest (without O2 demand)
• Evidenced by complex coronary stenosis plaque rupture/ulceration, and Hemorrhage and thrombus formation
• An unstable situation may progress to complete occlusion and infarction

Prinzmetal's Angina

• Occurs almost exclusively at rest due to coronary artery spasm
• Often responds to NTG but not always
• Often severe, awakening patient from sleep
• Usually involves the RCA
• Associated with arrhythmias and conduction defects as well as acute MI
• Silent Ischemia is asymptomatic

Myocardial Infarction (MI) Explained

• Is a COMPLETE interruption of blood supply to an area of the myocardium
• Is caused by sudden arterial or venous insufficiency that produces an area of necrosis
• Develops from ischemia

Causes of Myocardial Infarction

• Prolonged myocardial ischemia, usually due to plaque rupture/thrombus formation
• Prolonged vasospasm, inadequate myocardial blood flow or excessive metabolic demand
• Embolic occlusion, aortitis, vasculitis or coronary artery dissection
• Cocaine and other stimulants may cause severe vasoconstriction resulting in MI
• Leads to focal death of myocardial tissue in the area supplied by the involved coronary artery, in the left ventricle

Response to Myocardial Infarction

• Cells die, and necrotic tissue is referred to as the zone of infarct
• Between 18 – 24 hours post MI is an inflammatory response to necrosis
• Visible necrosis is present, and myocardial recovery begins in 2-4 days after MI
• From 4 – 10 days after MI, debris is cleared, and matrix is laid down
• Between 10 and 14 days after MI, there is formation of a weak fibrotic scar and Revascularization is present
• Scar tissue is inelastic and cannot contract and relax like healthy myocardial tissue

Zones Affected by an Infarction

• Zone of Infarct
• Zone of Injury
• Zone of Ischemia

MI Classification with EKG

• Subendocardial MI is partial thickness and defined by non-ST segment elevation (NSTEMI)
• NSTEMI stems from an acute injury to the myocardium that does not extend through the full thickness of the wall with ST-segment depression on EKG
• Transmural MI is full thickness and defined by elevated ST segment (STEMI)
• STEMI stems from full thickness extending through the entire wall muscle with ST-segment elevation, significant Q wave indicates acute infarction
• Note: ST returns to baseline in 24-48 hours with a STEMI

Newer Classification of Myocardial Infarctions

• Type 1 MI stems from acute coronary atherothrombotic myocardial injury with plaque rupture or erosion. It can be STEMI or NSTEMI
• Type 2 MI occurs when Evidence of myocardial ischemia caused by oxygen supply-demand imbalance for other reasons than atherothrombotic injury

MI Location Depends On

• Anatomic distribution of occluded vessel
• More proximal a lesion – greater area of infarction
• Presence of additional stenotic lesions
• Collateral circulation
• Anterior Wall MI involves the Left Anterior Descending artery (LAD)
• Lateral wall MI involves the Left Circumflex artery (LCX)
• Inferior wall MI involves the Right Coronary Artery (RCA)

Myocardial Infarction Diagnosis Criteria (2/3 Must Occur)

• Anginal Symptoms such as chest pressure, heaviness, pain in the arm or jaw, DOE, fatigue, syncope, and belching
• EKG Changes such as peaked T waves and ST elevation
• Rise of Cardiac Enzymes such as troponin

Variations in Women's Myocardial Infarctions

• Women are slightly more likely than men to report unusual symptoms for MIs
• 78% of women in a multi-center study of 515 women reported at least one symptom for more than one month before their heart attack
• Frequently reported symptoms were unusual fatigue, sleep disturbances, shortness of breath, indigestion and anxiety

Silent Myocardial Infarction

• Involves no symptoms of angina
• Can occur in any patient but more common in those with Diabetes Mellitus and/or chronic alcohol abuse
• May be related to the presence of peripheral neuropathies
• Ruled in by EKG changes and Cardiac Enzymes

MI Diagnosis & EKG Changes

• EKG Changes are almost always present
• Peaked T Waves
• ST Elevation
• Q Wave Present
• T Wave Inversion

Troponin Use in MI

• Troponin is the preferred marker for myocardial infarctions as of 2004
• It is highly cardiac specific and is released into the blood
• Troponin I and Troponin T are types of troponins, specifically the high sensitivity troponins
• Troponin is elevated between 4-6 hours post MI, remain elevated for several days, and peaks at 24 hours after MI

Role of CK-MB and Myoglobin in MI

• Creatine Kinase is released when cells die
• Elevated CK-MB band is specific for myocardial cell necrosis
• Creatine Kinase is elevated 4 – 8 hours post MI, returns to normal in 2- 3 days, peak elevations occur during the first 24 hours, and produces many false results
• Myoglobin is a protein released with injury to the myocardium
• Elevated in 1-4 hours
• Useful in patients that get to ER quickly

Diagnosis of Acute MI: Additional Tests

• CXR that is not very specific for myocardial infarctions
• TEE (Transesophageal Echocardiogram)
• Coronary Angiography (Angiogram)
• Cardiac Catheterization that can rule in for myocardial infarctions if uncertain and/or used as a treatment option

Medical Treatment of MIs

• Utilize Pharmacological Agents that reduce myocardial oxygen demand, increase myocardial oxygen supply, or improve myocardial muscle function
• Decrease myocardial oxygen demand with Beta Blockers and Calcium Channel Blockers
• Increase myocardial oxygen supply with Vasodilators (Nitroglycerin)
• Improve myocardial muscle function with Digitalis Glycosides

Surgical Treatment of MIs

• Thrombolysis is an option
• Intra-aorta Balloon Pump (IABP) can be used
• Percutaneous Transluminal Coronary Angioplasty/Percutaneous Coronary Intervention (PTCA/PCI) with or without Stent Placement can be leveraged
• Coronary Artery Bypass Graft (CABG) is another option
• Left Ventricular Assist Device (LVAD) can be used
• Cardiac Transplantation is the most extreme option

Post-MI Protocol

• Patients should stay within 20-25 bpm of baseline (resting heart rate) in the first 6-8 weeks post MI
• Perform light warm-up exercises in sitting
• Undertake a walking program

Cardiac Muscle Pump Dysfunction vs Failure Explained

• Cardiac Muscle Pump Dysfunction causes small cardiac impairment and leads to small decreases in SV, CO, EF with less marked functional effects
• Cardiac Muscle Pump Failure causes a failure of muscle to contract and results in significant decreases in SV, CO, EF
• Both will increase pressures in the Heart Chambers, Pulmonary artery, and throughout the peripheral & pulmonary vasculature

Cardiac Muscle Dysfunction Overview

• Impairs the heart's ability to pump or accept blood
• May cause Congestive Heart Failure or Cardiomyopathy

Congestive Heart Failure (CHF) Basics

• CHF is a syndrome where the heart is unable to pump enough output to meet the body's metabolic demands
• It may result from structural or functional cardiac disorder that impairs the filling or pumping ability of the ventricles
• CHF is affected by: CAD, HTN, DM, Valvular and congenital heart disease, Arrhythmias, or ETOH/drug abuse

Characteristics of Congestive Heart Failure

• Dyspnea
• Tachypnea
• Paroxysmal Nocturnal Dyspnea
• Orthopnea
• Fatigue
• Peripheral edema
• Cyanosis
• Weight gain
• Hepatomegaly
• Jugular Vein Distension
• Rales/crackles (especially wet)
• S3 heart sound
• Sinus tachycardia
• Poor exercise tolerance

CHF Classification

• Systolic versus Diastolic Heart Failure
• Left Sided versus Right Sided Ventricular Failure
• Heart Failure with Reduced Ejection Fraction (HFrEF) versus Heart Failure with Preserved Ejection Fraction (HFpEF)

Systolic Heart Function

• Is measured by the time for ventricular contraction
• Relies on Preload, Afterload, Contractility of the myocardium, and Rate of contraction

Diastolic Heart Function

• Is measured by the time for filling of the ventricles
• Relies on the Frank-Starling mechanism, namely Left ventricular end-diastolic pressure (LVEDP) and amount of muscle fiber stretch at end of diastole, as it impacts the strength of the ventricular contraction

Systolic Heart Failure

• Decreased CONTRACTILITY leads to pump failure
• Is the most common problem with heart failure
• Leads to increased PRELOAD, resulting in pump failure
• Leads to increased PRELOAD, resulting in pump failure
• Affects CHRONOTROPY, resulting in a heart rate that is too slow or too rapid and leads to pump failure

Diastolic Heart Failure

• Is caused by impaired Diastole dueto excessive hypertrophy of ventricles and changes in composition of myocardium
• Reduced End Diastolic Volume(EDV) may be caused by decreased filling of the left ventricle from increased stiffness
• Can have an increase in ventricular pressure because of decreased compliance of the left ventricle
• Overall see elevated diastolic pressures that may cause decreased cardiac output

Edema and CHF

• Edema may be caused by increased EDV which leads to increased pulmonary capillary pressure, which will lead to transudation of fluid
• Pulmonary edema develops with Pressure in pulmonary vasculature at 25 mmHg

Left-Sided Ventricular Failure Characteristics

• Left ventricle is not working efficiently, leading to Decreased SV and CO, Increased LVEDV, Decreased LV compliance, Increased left atrial dilatation, Increased pressure in pulmonary vessels and Transudation of fluid from pulmonary capillaries
• Increased LVEDP can occur
• Mitral valve regurgitation can occur if LV dilatation may stretch mitral valve annulus.
• Caused by myocardial diseases, cardiomyopathy, hypertension, dysrhythmia/arrhythmia, or medication toxicity

Right Sided Ventricular Failure Characteristics

• Right ventricle not working effectively: Prolonged pulm HTN, Increased right ventricle afterload, and Anatomical changes to right ventricle
• Right ventricular end-diastolic pressure (EDP) increases and Reflects back up to right atrium and venous system May can be caused by Jugular vein distension (JVD), liver engorgement, ascites, and peripheral edema or pulmonary vasoconstriction
• It can result from Pulmonary HTN, Mitral Valve regurgitation, Chronic/acute pulmonary dz (ex: PE, COPD), Left HF, Cardiomyopathy

Heart Failure with Reduced Ejection Fraction

• Heart failure with reduced ejection fraction (HFrEF) is most frequently associated with heart failure and is caused by low CO at rest/with exertion

Heart Failure with Preserved Ejection Fraction

• Heart failure with preserved ejection fraction (HFpEF) often indicates a volume overload
• Total cardiac output is lower than "normal" but is considered "preserved"

Cardiac Ventricular Remodeling

• Refers to changes in size, shape, structure and physiology of the heart after injury to the myocardium from MI or chronic HTN
• Includes Physiologic or Pathologic changes
• Occurs structurally and functionally in the zones of infarction, injury, ischemia
• Begins minutes post MI and continues over time
• The Left ventricle may change from elliptical to spherical
• Apoptosis, or programmed death of cells, may occur

Ventricular Remodeling

• This is an Increase ventricular (usually left) size
• The Heart becomes more spherical
• Functional mitral regurgitation occurs
• Systolic performance worsens

Physiologic Consequences of Chronic Heart Failure

• Decreased myocardial performance. There will be an increased venous return and a contraction of vasculature due to increased peripheral vascular resistance.
• The sympathetic stimulation also desensitizes the heart to β1-adrenergic receptor stimulation and increases heart’s force.
• Pulmonary edema can occur in severe cases due to increased filling pressures
• CO decreases renal blood flow, which causes a change to the glomerular filtration rate. This causes the sodium and retaining of fluids in the kidney. Heart failure is associated to circulating levels of arginine vasopressin with the vasoconstrictor function and inhibitor of water in extraction.

Consequences of Heart Failure

• Muscle wasting & possible muscles skeletal disorders and osteoporosis are possible as a result to activities and co-morbidities. Due to the vascular and impared ability to lead to sedentary results with Inability to increase HR. Diastolic causes exercise intolerant with low ejection fracture.
• Anemia and abnormal red white blood cells and hemostatic.
• Cardiac cirrhosis happens due to hepatic results such as: hypoperfusion to decreased in the venous congestions. With also increasing the factor to myocardial as pressant.
• See anorexia that result to malnutrition

Summary of Body's Compensation Mechanisms for CHG

• Sympathetic NS (SNS)
• Renin-angiotensin-aldosterone system (RAAS)
• Natiuretic peptide counter-regulatory system

The SNS Compensation for Congestive Heart Failure

• Compensation starts with decreased Cardiac Output sensed by the baroreceptors
• The body's sympathetic nervous system increases to improve Cardiac Output. This results to increase systemic with the vasoconstrictor stimulate the releasing of renal function in the kidneys.
• Leads to increased Release of norepinephrine with increases HR and SV myocardial to help improved cardiac output.

The RAAS Compensation for Congestive Heart Failure

• Compensation starts to help cardiac and balance pressure to the setting of what cause that to being depletion. Increases with venous and atrial contractions. Increasing the retaining on salts and water to help triggered norepinephrine to be balanced.
• With the Angiotensin factor will help powerful blood that can effect the functions with the reduced renal perfusion or lead to causes that will promote aldosterone. Which can results in the releasing of red blood cells, the process that can help kidneys with actions of kidneys.
• Maintaings BP and CO with balances

Hormones Involved in Congestive Heart Failure

• Norepinephrine
• Renin
• Angiotensinogen
• Aldosterone
• All contribute to further the disease process, and their concentration correlates with severity and prognosis

Counter-regulatory Hormones in Congestive Heart Failure

• Natriuretic peptides (NP): ANP, atrial NP (atria). C type NP (endothelial)—contributes to vasodilation
• Release of ANP, BNP stimulates the ventricles and high fillings in pressure. Have systemic that relates to kidneys with water diuretics. Also, relax the lusitropic with myocardium functions.
• Can help reflect the amount of water through the acute and chronic overload.

Clinical Manifestations of Congestive Heart Failure

• Progressive Dyspnea that exertion results from pulmonary edema, pallor, cyanosis, diaphoresis, tachypnea, anxiety, agitation, and cerebral hypoxia
• Dependent edema, hepatomegaly, ascites and fatigue
• Anorexia, rales and bloating can be caused by right sided of the heart such as weight gains and pain with the level of the amount of urinating.

Diagnosis of Congestive Heart Failure

• Use an Echocardiogram, Blood test with high/low counts to see if the threshold is to affect that level
• Use Hematology/Lab, Electrolytes,Renin , and Liver test to to test levels

Radiologic Findings in Imaging

• Find if Cardiac area can show an Interstitial region around to alveolars or Perivascular
• Show more fluids and atelectasis on the lungs.

NYHA: Classification of Congestive Heart Failure

• The classification for it the way that can depend on functions by placing the patients to see if their on to be limit or to be physical for certain activity. It also depend on how much objective they are into to see how much function
• Uses functional classification to place patients in one of four categories in terms of limits placed during physical activity
• Uses objective assessment

NYHA Disease

• Is when the cardiac muscle isn’t to allow to carry any activities without being discomfort. For I-no is when the limit in physical. And II as slight then III as markets

Treatment is directed at the underlying cause in Congestive Heart Failure

• Goals of treatment include ability to pump, work to reduce the extra load, and balancing the intake of sodium and water tension
• This can be done with medical and non-medical ways

Non-Medication Management of CHF

• Education on how to maintain a cardio to rehabilitate any other complications that is related. Such, Symptoms education. Maintaining with good exercise with less salt in it. Check the scale and weight.

Medication Management of Congestive Heart Failure

• The goals are the work load.
• Work and maintain with diuretics, beta blocker, ACE antiol, inotopes
• Also use check dialysis

Surgical Management of Congestive Heart Failure

• Includes Cardiac resynchronization therapy with athrectomy
• Angioplasty with rotational of removing the stenting material to create the bypass
• Laser treatments can be use to help promote the heart.
• Use mechanical device such as balloon , a-v,and a implant

Compensated vs Decompensated Congestive Heart Failure

• Chronic HF patients are generally on a cocktail of medications
• Displays mild to moderate symptoms with degree of volume overload
• Decompensation may occur, resulting in worsening of baseline abnormalities

Causes of Cardiomyopathy (CM)

• Cause a variety of issues associated myocardial that cause effect to contracts or muscles around the the chambers of CM
• Includes dilated, hypertrophic or restrictive.

Dilated Cardiomyopathy (DCM)

• Can be caused by large amount mass and Dilation with all the 4 chambers. With little of thichening then has systolic from no working properly when that is damage to the to work with the heart.
• Can lead for issues when breathing it gets and lead for more symptoms of heart failure by causing dyspnea and fatigue. As with this that that can occur to cause more symptomatic to ventricles with increase oxygen
• As with is, the reasons is for many as the heart to disease. Can lead to infections. Also other things with chemicals by toxin then there the hereditaries factor on it.

Results and Risk for Dilated Cardiomyopathy

-Decreases the process to working properly -Can damage your ability with exercising properly -Can damage left and right Ventricle -Can leads to clinical to heart and failure.

Hypertrophic Cardiomyopathy (HCM)

• Is caused by hypertrophic and masses for the heart. With an limited on cavity
• There are two classifications and May lead with a rapid ventricular.
• Is found through routine for patient that have S that may have a heart problem

Restrictive Cardiomyopathy (RCM)

• Is very rare because of infection the in the ventricular and endocardial and also the myocardial issue.
• As result you can have fluid, cause the heart to enlarge and heart failure with increase in the ventricular problems.

Treatment for Cardiopulmonary

• The goal to cause is to help manage what ever conditions were a side cause. Help control any warning to be for heart or any sudden infection. and reduce by complication