Right and left sides of the heart, both atria, ventricles, and major vessels (superior and inferior vena cava, pulmonary artery and vein, and aorta) are visible.
Normal Blood Flow
Follows the path of least resistance.
Deoxygenated blood from the upper body returns via the superior vena cava.
Deoxygenated blood from the lower body returns via the inferior vena cava.
Blood flows from both vena cavae to the right atrium, then through the tricuspid valve into the right ventricle.
The pulmonary valve opens, and blood flows through the pulmonary artery to the lungs for oxygenation.
Oxygenated blood returns to the left atrium via the pulmonary veins and flows through the mitral valve into the left ventricle.
Blood exits the heart through the aortic valve into the aorta and is directed to the systemic circulation.
Cardiac Physiology
Cardiac Output
Amount of blood ejected from the left ventricle in one minute.
Measured in liters or milliliters per minute per kilogram of body weight.
Determined by heart rate and stroke volume.
Good cardiac output = good tissue perfusion.
Pediatric patients: Varies from 200 ml/kg/min in neonates to 100 ml/kg/min in adolescents.
Cardiac Index
Cardiac output divided by body surface area.
Normal range: 3 to 4.2 liters per minute per meter squared.
Accounts for variations in cardiac output due to a child's body size.
Important to know normal cardiac index for the CCRN exam.
Stroke Volume
Volume of blood ejected from the left ventricle with each contraction.
Ejection fraction: 60-75% of ventricular volume.
Affected by preload, afterload, compliance, and contractility.
Preload
Volume of blood in the ventricles at the end of diastole before the next contraction.
Resting force in the myocardium.
Measured directly with intracardiac catheters (right atrial or central venous pressure).
Most accurate assessment: pulmonary artery capillary wedge pressure.
Related to cardiac fiber length, stretch, and blood volume returning from systemic and pulmonary circulation.
Increased preload stretches myocardial muscle fibers, leading to more forceful contraction and increased stroke volume, thus increasing cardiac output.
Frank-Starling Law: Direct relationship between blood volume during diastole and the force of the next contraction.
Excessive stretching of muscle fibers decreases stroke volume.
Increased blood volume in myocardial failure worsens clinical status due to cardiac fiber stretch and contractility issues.
Factors altering preload:
Hypovolemia or hypervolemia.
Systemic or pulmonary hypertension.
High PEEP: Decreases blood return to the heart, decreasing cardiac output.
Dysrhythmias: Affect atrial or ventricular systole.
Vasopressors or inotropes: Increase contractility and heart rate.
Parasympathetic Stimulation: Releases acetylcholine, acting on the vagus nerve to decrease heart rate and conduction.
Adrenergic Receptors
Stimulation causes an intracellular response.
Alpha Receptors: Located in arteries; stimulation causes vasoconstriction.
Beta Receptors:
Beta-1: Located in the heart; stimulation increases heart rate, contractility, and AV conduction time (One heart, Beta 1).
Beta-2: Located in smooth muscles of the lungs; stimulation results in bronchodilation (Two lungs, Beta 2).
Terminology
Agonists: Stimulate receptors to perform their function.
* Example: Neo-synephrine stimulates alpha agonist receptors and increases vascular resistance.
Antagonists: Stimulate receptors to stop performing their function.
Vasoactive: Raises or lowers heart rate or blood pressure.
Vasopressors: Act to raise blood pressure.
Inotropic: Affects contractility through alpha and beta receptors.
Chronotropic: Changes heart rate affecting nerves controlling the heart or by changing the rhythm of the SA node.
Cardiac Failure
Failure of the heart to maintain a cardiac output sufficient to meet the metabolic demands of the body.
Results from problems in the pericardium, myocardium, endocardium, heart valves, or great vessels.
Can result from congenital and acquired forms of heart disease, structural abnormalities in those cardiac defects, or intrinsic myocardial dysfunction like the pediatric cardiomyopathies.
Left-Sided Heart Failure
The left ventricle is unable to empty during systole, leading to a decrease in cardiac output and contractility.
Causes include obstruction to the outflow tract of the left ventricle, ventricular underdevelopment, volume overload, left ventricular infarction, arrhythmias, and systemic hypertension.
Affects many body systems due to decreased cardiac output and perfusion.
Pulmonary venous congestion with pulmonary edema, dyspnea, rails, and frothy sputum are observed.
Heart enlargement, increased heart rate with decreased blood pressure, and potentially an S3 heart sound.
Decreased glomerular filtration rate leads to acidosis, acute kidney injury, and decreased urinary output.
Decreased mentation due to insufficient oxygenated blood to the brain.
Right-Sided Heart Failure
Often occurs as a progression of left heart failure.
Obstruction to forward flow, volume overload from intracardiac shunting, and muscle underdevelopment cause increased myocardial oxygen demand and pulmonary artery pressures.
Increased myocardial oxygen demand and pulmonary artery pressures will lower cardiac output.
Clinical signs include jugular venous distension, hepatojugular reflex, dependent pitting edema, and hepatomegaly.
Weight gain due to fluid overload, increased central venous pressure, and increased pulmonary vascular resistance.
Diagnosis of Heart Failure
Thorough patient history and physical exam are crucial.
Chest X-ray can reveal cardiomegaly, increased pulmonary vascular markings, pulmonary edema, and pleural effusion.
Carefully listen for heart murmurs and abnormal heart sounds.
Assess the patient’s respiratory status and listen to their lungs for indications of fluid overload.
Evaluate peripheral pulses for any decrease.
ECG can reveal any associated conduction disorders or arrhythmias.
Echocardiogram is important for assessing the structures of the heart and measuring systolic and diastolic function.
Laboratory Findings in Heart Failure
Possible anemia.
Electrolyte changes (hypocalcemia and hypoglycemia).
End-organ dysfunction (protein in the urine, increased serum lactate levels, and acidosis).
Increased white blood cell and platelet counts related to the patient’s inflammatory response.
Brain natriuretic peptide (BNP) levels are monitored to assess prognosis and response to therapy.
Treatment Goals for Heart Failure
Preserve ventricular function.
Reduce symptoms.
Improve cardiac output.
improve oxygen delivery.
Medication Treatment Strategies for Heart Failure
Medication management strategies for heart failure focus on maximizing cardiac performance, optimizing preload, and then decreasing afterload.
Cardiac performance can be enhanced by inotropic agents and phosphodiesterase inhibitors such as milrinone.
Optimize preload using diuretics and sodium and fluid restriction.
Decrease afterload using vasodilator nitroprusside or with ACE inhibitors.
Pulmonary vasodilation with nitric oxide helps with right sided heart failure and pulmonary hypertension.
Enhance contractility using Digoxin and monitoring the patient's response.
Avoid dobutamine, because it can actually increase myocardial oxygen demands.
Medications used to improve contractility include calcium chloride and milrinone.
Mechanical Cardiac Support and Supportive Tratement
Mechanical cardiac support (ventricular assist device, ECMO) may be needed as a bridge to recovery or heart transplantation.
Supportive treatment strategies focus on decreasing myocardial oxygen demand.
Bed rest, pain, and anxiety management alongside respiratory support is needed, and family support.
Cardiomyopathies
Dilated Cardiomyopathy
The heart is very large with left ventricular dilation.
Congestive heart failure signs along with decreased stroke volume and decreased ejection fraction.
Hypertrophic Cardiomyopathy
Thickening of the heart muscle may interfere with the normal functioning of the heart.
Narrows the outflow of the left ventricle and reduces the ability of the heart to relax and fill with blood during diastole.
Can worsen with increases in contractility or heart rate.
Most common cause of sudden cardiac death in people who are younger than the age of 35.
Restrictive Cardiomyopathy
A defect of the anatomy and the endocardium that's related to fibrosis and scarring.
Minimal contractile movement from the heart.
There is normal systolic function and a decrease in diastolic function.
Has the poorest prognosis.
Clinical Manifestations of Cardiomyopathies
Related to heart failure.
Patients may be asymptomatic initially, but once the patient gets into heart failure they can experience poor perfusion.
Decreased level of consciousness, and they may experience syncope.
Symptoms includes decreased urine output, thromboembolic events, arrthymias, and shock.
Diagnosis and Management of Cardiomyopathies
Familial and is genetically inherited.
Common cardiac diagnostic tests are listed here on the screen, and they're similar to what we already reviewed with heart failure,Genetic testing.
Management involves decreasing the cardiac workload while we do things to improve cardiac output along with DVT prophylaxis.
Patients with severe conditions may require mechanical cardiac support and an implantable cardioverter defibrillator and transplantation,
Calcium channel blockers can be used to provide afterload reduction, decreased myocardial contractility, and improved left ventricular diastolic function.
Cardiogenic Shock
Inability of the cardiac muscle to pump adequately enough to meet the metabolic needs of the tissues.
Decreased stroke volume results inadequate blood flow to the tissues, inadequate oxygen and nutrients for the body’s cells.
Management of Cardiogenic Shock
Principles for managing this type of shock include improving oxygenation and minimizing oxygen demands on the body while we maximize the myocardial performance.
Oxygenation should be improved by intubation and mechanical ventilation along with pain/sedation management.
Patients should be maintained at a normal temperature and the patient can't be anemic.
Myocardial performance may be maximized with positive inotropic agents and implementations to reduce afterload as needed.
Work the patient up for congenital heart disease or traumatic injury to the heart.
Obstructive Shock
Occurs when cardiac output is impaired by a physical obstruction to blood flow leaving the heart.
A small valvular will impede blood flow.
Etiology symptoms of obstructive shock improve.
Hypertensive Crisis
Acute life-threatening elevation in systolic and diastolic blood pressure, resulting in death.
Causes and Management of Hypertensive Crisis
Things like tumors and neurologic causes can be symptoms of hypertensive crisis.
Management should consist of lowering the blood pressure safely, treating and minimizing end organ damage while we identify the underlying etiology. We may use beta blockers such as labetalol and esmolol.
Changes in diet and exercise may be necessary.
Inflammatory Heart Disease (Itises)
Inflammation of cardiac or vascular tissues from bacteria, viruses or systemic autoimmune disorders.
May manifest as general malaise, fever, cardiac murmurs or rubs, chest pain, tachycardia, or signs of heart failure.
Treatment includes antibiotics, anti-inflammatory agents, removal of infected prosthetic material, and heart failure interventions.
Vascular Occlusions
Venous Thromboembolism
This consist of deep vein thrombosis, or DVT, and pulmonary embolism.
DVTs are a condition that happens when a blood clot forms in a deep vein. They are painful and include swelling in the area affected, possibly redness in the legs. Nursing care should consist of DVT Prevention by applying a sequential compression device.
We should watch for worsening symptoms of poor perfusion such as things like delayed a diminished perfusion from the vessel.
Superior Vena Cava Syndrome
Obstruction of blood flow through the superior vena cava leads to reduced cardiac output and blood pooling.
Often caused by a central venous catheter, thromboembolism or is associated by malignancy.
Symptoms: Facial swelling, dyspnea, cough, and arm edema
Diagnose is done on base of signs described. Treatment needs supportive care to alleviate symptoms and is done by giving chemotherapy.