cardiovascular disruptions

Cardiovascular Disruptions

Objectives

• Describe the normal structure, function and regulatory mechanisms of the cardiac system

• Define the factors that can influence cardiac output and their significance

• State the conditions/situations which can lead to the development of cardiac disruptions.

• Identify the common disruptions to cardiac function and discuss each condition according to definition, pathogenesis, clinical manifestations, and medical/nursing management.

Normal Cardiac System

The heart is the pump of the circulatory system, and sits in the mediastinal space of the intrathoracic cavity, in loose fitting sack called the pericardium.• The heart is suspended by the great vessels and is

positioned with the wide side up, and the apex (narrower side) down and to the left.

• Heart is comprised of 3 layerso Epicardiumo Myocardiumo Smooth Endocardium

Anterior view of heart and great vessels, and their relationship to lungs & skeletal structures of chest cage

Layers of the heart

Atria and Ventricles

The heart is broken up into 2 sets of 2 different chambers. • Atria: Function as a collection chamber for blood returning

to the heart, and as a pump to fill the ventricle.• Ventricle: Main pumping chamber of the heart.

o Right Ventricle: pumps the blood out of the heart and into the lungs through the pulmonary artery

o Left Ventricle: pumps the blood out of the heart and into the body via the aorta

Heart Valves

The atria and ventricles have 2 sets of valves that separate the atria and ventricles from each other, and from the systemic circulation. The closure of these valves allows for the filling of the chambers of the heart and to allow the blood to be pumped out of the heart during systole.

• Atrioventricular valves: control the flow of blood between the atria & the ventricles supported by the cordae tendonaeo Tricuspid Valve (RT)o Bicuspid (Mitral) Valve (LT)

• Semilunar valves: control the flow of blood out of the hearto Pulmonic Valveo Aortic Valve

Valvular structures of the heart.Atrioventricular valves are in an open position, semilunar valves are closed.There are no valves to control blood flow at inflow channels (vena cavae & pulmonary veins) to the heart.

Coronary Arteries

Provide oxygenated blood to the heart muscle.

They are broken down into Right and Left Coronary Arteries and branch directly off the aorta.

• Right Coronary Artery: feeds the right side of the heart

• Left Coronary Artery: breaks into 2 segmentso Left anterior descending arteryo Left circumflex artery

Coronary arteries & some of the coronary sinus veins.

Function/Cardiac Cycle Events

Cardiac cycle is the rhythmic pumping action of the heart, which is broken into 2 events:

• Systole: period during which the ventricles are contracting

• Diastole: period during which the ventricles are relaxing and filling with blood.

Regulation of Cardiac FunctionThe conduction of heart is dependent on the depolarization of the nerve cells in the heart.The initial stimulus for a heartbeat originates in the Sinoatrial Node (P-wave on the EKG)

• P-wave atrial contraction that moves blood ventricles• The AV-valves close (first heart tone S1)• Ventricular pressure rises

semilunar valves open blood is ejected from the hear

• The Semilunar valves close (second heart tone S2)• Ventricular pressure < atrial pressure

AV-valves open blood moves from the atria to the ventricle

Regulation of Cardiac Function:

Cardiac regulation via the Sinoatrial Node (pacemaker of the heart) has some functions that make it unique in terms of regulation of function:• Automaticity• Rhymthic• Speed of spread

The initial depolarization in the Sinoatrial Node, is then spread to the AV node that transmits the electrical impulse to the Bundle of His that transmits it to Left/Right Bundle Branches and ends in the Purkinje fibers

What can affect the regulation of the cardiac cycle?• Autonomic Nervous System:

o Sympathetic Nervous System: increases the HR, speed of conduction through the AV node, and increases the force of atrial and ventricular contractions

o Parasympathetic Nervous System: the vegus nerve innervation of the SA node directly allows for a slowing of SA node depolarization rate, and decrease in AV node conduction

• Baroreceptors: sensitive to stretch or pressure, and when stimulated cause temporary inhibition of the sympathetic nervous system stimulation in the heart.

• Chemoreceptors: present in the aorta and carotid bodies, and are stimulated by a drop in oxygen and an increase in carbon dioxide levels

Cardiac Output:

Definition: Cardiac Output = Heart Rate x Stroke Volume

The cardiac output can vary from person to person based on:• body size• metabolic needs

o physical activityo rest/sleep

• Ranges from 3.5-8 L/min

Influencing factors on cardiac output

• Preload

• Afterload

• Cardiac contractility

• Heart Rate


Preload:• This represents the

volume workload of the heart

• Determined by the amount of blood that the heart has to pump with each beat.o largely comprised of the

venous return to the heart

o diuretics have an affect on the preload

Afterload:• This represents the

pressure or tension work of the heart to move blood from the left ventricle into the aorta/pulmonary artery.

• Largely determined by the systemic arterial blood pressure for the left ventricle

• Pulmonary arterial pressure determines afterload for the right ventricle


Cardiac Contractility:• This is the ability of the

heart to change the strength of it's contraction without changing it's resting lengtho increased extracellular

contraction can increase contractile strength

o decreased ATP from ischemia can cause decreased contractility

Heart Rate:• this determines the

frequency with which blood is ejected from the heart.o increased heart rate can

increase CO to a point, however, the quicker the heart needs to eject blood, the shorter time it has to fill with blood to eject.

Overview of Alterations in the Cardiac System

1. Lack of Blood Supply

2. Infections of the heart

3. Immune mediated inflammatory conditions

4. Cardiomyopathy

Consequences of decreased blood flow to the myocardium (heart muscle)Lack of blood supply or perfusion to the myocardium can result in ischemia, anginal pain, cardiac arrhythmias, myocardial infarction (heart attack), conduction defects, heart failure and sudden death.

Conditions that cause this "ischemic heart disease" are as follows:

1. Atherosclerosis of the coronary arteries

2. Thrombus within the coronary arteries

3. Vasospasm of the coronary arteries

4. Hypovolemia

Atheroscelrosis of the Coronary ArteriesThis disease process of the coronary arteries is the direct cause of many cases of myocardial ischemia and infarction. The manifestations of atherosclerosis in the coronary arteries include:

1. Angina pectoris (myocardial ischemia)

2. Myocardial ischemia (heart attack)

3. Sudden cardiac death

Stages in development of atherosclerosis

Developing atherosclerosis in the coronary arteries is a slowly progressing process, that occurs over many years. Symptoms often don't occur until the vessel is 75% occluded, which is the point at which collateral circulation or compensatory vasodilation cannot keep up with myocardial muscle oxygen needs.

1. Fatty Streak

2. Fibrous Plaque

3. Complicated lesion

Angina Pectoris

Angina comes from a Latin word meaning: "to choke"

• Symptomatic paroxysmal chest pain or pressure sensation associated with transient myocardial ischemia

• precipitated by situations that increase the work demands of the hearto physical exertiono exposure to coldo emotional stress

• Pain is described at constricting, squeezing, or suffocating sensation located in the precordial or substernal area of the chest

Areas of pain due to angina.

Myocardial Infarct: Heart Attack

An acute myocardial infarct is characterized by ischemic death of the myocardial tissue associated with atherosclerotic disease of the coronary artery.Area of infarction is determined by the coronary artery that is affected:

• 30-40% Right Coronary Artery

• 40-50% Left Anterior Descending Artery

• 15-20% Left Circumflex Artery

Manifestations of an MI

Onset of an MI can be abrupt or it can progress from unstable

angina.• pain, usually severe and crushing• pain substernal radiating to the left arm, neck or jaw• pain prolonged, not relieved by nitroglycerin • associated with a feeling of impending doom• Atypical presentations:

o Women have more atypical ischemic like discomforto Elderly people often have more shortness of breath

• Tachycardia, anxiety, restlessness• pale, cool, moist skin

Diagnosing an MI

• EKG changeso T-wave Inversion o T-wave Elevation o ST segment changes

ST depression (injury confined to the subendothelium) ST elevation (injury to the heart is transmural)

• Serum Markerso myoglobino Creatinine Kinase MB (CK-MB)o Troponin 1 and Troponin To C-reactive proteino B-cell natriuretic peptide (BNP)

Top:A.Normal ECGB.ST elevation with acute ischemiaC.Q wave with acute MIBottom: current of injury patterns with acute ischemiaA.With predominant subendocardial ischemia, resultant ST segment is directed toward inner layer of the affected ventricle & ventricular cavity. Overlying leads therefore record ST-segment depression.B.With ischemia involving the outer ventricular layer (transmural/epicardial injury), the ST vector is directed outward. Overlying leads record ST-segment elevation.

Acute MI – X-section of ventricles infarct(death few days after onset of severe angina pectoris)

• LV transmural infarct in posterior & septal regions.• Necrotic myocardium is soft, yellowish, and sharply

demarcated.

LV transmural infarct

in posterior & septal regions

Consequences of AMI

• Damage to the muscle wall of the hearto ventricular aneurysms

• Damage to the conduction system of the hearto arrhythmias

• Heart failureo decreased cardiac output

Treatment of AMI

• Administration of Oxygen• Administration of analgesics• Aspirin• Beta-adrenergic blockers• Nitrates• If ECG evidence of infarction, Immediate Reperfusion

therapy should be initiated:o Thrombolytic Therapyo Revascularization Interventions

Sudden Cardiac Death

Unexpected death from cardiac causes, usually within 1 hour of an MI, can occur up to 24 hours post MI.• coronary artery disease accounts for 80% of cases

o decreased blood flow causes an acute ventricular dysrhythmia

o less frequently, the SCD can result from primary left ventricular outflow obstruction issues aortic stenosis hypertrophic cardiomyopathy

• abrupt disruption in cardiac function, that produces an abrupt loss of cardiac output and cerebral blood flow

• Biggest risk factors: left ventricular dysfunction (EF<30%) and ventricular dysrhythmias following MI

Conditions that disrupt blood flow in the heartThrombus within the coronary arteries:• Areas that have complicated lesions of atherosclerosis can

cause the formation of thrombi. • The smooth muscle and foam cells in the lipid core

contribute to the expression of tissue factor in unstable plaques, which leads to the activation of the extrinsic coagulation cascade and formation of thrombin and the deposition of fibrin = Red thrombi

• If a plaque is disrupted, the endothelium is damaged and platelets bind there = white platelet containing thrombi

Vasospasm of the Coronary Arteries

This is a spasm of the coronary arteries causing an acute decrease in coronary blood flow, and ischemia• occurs most often during rest, or with minimal exercise• most frequently between midnight and 8am• can precipitate life threatening arrhythmias, and patient is at

high risk for SCD• Causes (not totally known)

o hyperactive sympathetic nervous systemo defects in the management of Ca influx into vessel

smooth muscle cells o alteration in nitric oxide productiono imbalances between endothelium derived relaxing and

contracting factors

Hypovolemia

Lack of circulating blood flow throughout the whole body can lead to a generalized ischemia in the heart due to the overall decrease in oxygen carrying capacity. Hypovolemia is also associated with electrolyte abnormalities that can cause cardiac problems• Hypokalemia: K+ levels below 3.5 mEq/L• Hyperkalemia: K+ levels >5.5 mEq/L• Hypocalcemia: Ca++ levels <8.5 mg/L• Hypercalcemia: Ca++ levels >12 mg/dL

Infections of the Heart

Infections in the pericardium, epicardium, myocardium, endocardium and the valves• Result in a decrease in the cardiac output• Can also cause a backward flow of blood into the ventricles

(due to diseased valves) that can cause congestion of blood flow

Infective Endocarditis

This was previously known as bacterial endocarditis, but other infectious agents can cause endocarditis. Most common cause is bacterial though:• Staphylococcus aureus (can be MRSA)• Streptococcus viridans

Arise from infections somewhere else in the body, that allows the infectious organism into the blood stream.• blood flow turbulence in the heart allows the infective agent

to infect previously damaged heart valves or other endothelial surfaces

• the infectious agents attach the heart surfaces and form vegetations of infectious agent, platelets, fibrin, and leukocytes


• The vegetations are very friable, they can break apart easily and "embolize"o 22-50% of patients with IE will experience systemic

emboli from the vegetations left side heart vegetations cause emboli to the brain,

kidneys, spleen, or the limbs right side of heart vegetations cause emboli to the lung

• The infective vegetations can also cause damage to the valves and supporting structures


Acute Bacterial Endocarditis:• Usually affects those with

healthy valves• presents as an acute,

rapidly progressing illness

Subacute Bacterial Endocarditis:• Affects those who have

preexisting valve disease• Clinical course may extend

over months

Although this classification system was in historical use, now clinicians classify IE based on the cause, or the site of involvement

What does endocarditis look like?

Immune Mediated Inflammatory ConditionsThese conditions primarily infect the valves, which results in congestion within the ventricles and in the lung and viseral circulation • Rheumatic heart disease is a prime example of this

o sequela to group A (beta hemolytic) streptococcal (GAS) throat infection

o decreased incidence in the US because of antimicrobial treatment of GAS infection

• Thought that the untreated GAS leads to antibody formation, which can affect the heart, joints, CNS and skin.

• the myocardium develops Aschoff Bodies that are nodules with swelling and fragmentation of the collagen fibers that become more fibrous as we age

Rheumatic Heart Disease

Type III hypersensitivity: antibodies against the strep are formed, and there is a complex of strep and strep antibodies that are deposited in the heart, activates complement.

• These complexes can also be deposited into the joints, but the effects on the joints are reversible

• effects on the myocardium are permanent

Cardiomyopathy

A group of disorders that affect the heart muscle, which can develop as primary or secondary disorders. Often lead to cardiomegaly and heart failure (dilitation of the heart muscle, hypertrophy of the the heart, or stiffening of the ventricles).

Primary: Result of disease in the heart muscle itself, but usually an unknown cause

Secondary: from a secondary disease, like a myocardial infarction

Types of Cardiomyopathy

1. Dilated2. Hypertrophic3. Restrictive

Each of these types of cardiomyopathy have their own etiology, presentation, pathophysiology and treatments.

General Causes of Cardiomyopathy: Toxins such as alcohol, cocaine, chemotherapy agents, excess thyroid hormone, uremic disorders, metabolic abnormalities and familial tendencies

Dilated Cardiomyopathy

Characterized by progressive cardiac hypertrophy and dilation and impaired pumping ability by one or both ventricles. Atria are also enlarged.• because of wall thinning that occurs, the hypertrophied

ventricles are thinner than one would expect.• mural thrombi are common and may be source of

microemboli• Stasis of blood in the left ventricle • Causes:

o Alcoholismo familial conditiono toxic agents (chemotherapy)

Most common form of cardiomyopathy.

Hypertrophic Cardiomyopathy

Abnormality that causes excessive ventricular growth or hypertrophy. Involvement of the interventricular septum tends to be disproportionate, which produces intermittent left ventricular outflow obstruction and impaired relaxation of the heart.• Genetic disorder identified in many of the cases

o mutation in one of the 10 genes coding for the cardiac sarcomeres

o found to have myofibril disarray on microscopic evaluation of the heart

• most common cause of SCD in the young• need to screen 1st degree relatives once discovered in an

individual

Restrictive Cardiomyopathy

Ventricular filling is restricted because of excessive rigidity of the ventricular walls, although the contractile properties of the heart remain relatively normal.

• Endemic in parts of Africa, India, South and Central America, and Asia

• In the U.S., the number 1 cause is amyloidosis, or amyloid infiltrations of the heart

• Symptoms include: dyspnea, PND, orthopnea, peripheral edema, ascites, fatigue and weakness.

Least common cardiomyopathy in the U.S.

cardiovascular disruptions

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