Heart

Most common type of birth defect

structural heart issues present at birth-congenital heart defects

Acyanotic defects

left to right shunting of blood

• Ventricular septal defect(VSD)

• Atrial septal defect(ASD)

• patent ductus arteriosis(PDA)

• coarctation

Cyanotic defects

right to left

• tetralogy

• transposition

• truncus arteriosus

• total anomalous pulmonary venous return

• hypoplastic left heart syndrome

What are risk factors for CHD?

heredity, genetic disorders (Down’s syndrome), fetal substance exposure(tobacco or meds), maternal health status (diabetes, obesity, etc.)

Manifestations of CHD

heart murmurs, dyspnea, tachypnea, cyanosis, fatigue, chest pain/discomfort, difficulty gaining weight

HEART FAILURE MAY DEVELOP

Alterations Resulting in Decreased Cardiac Output

NERVES AND HORMONES—> HR(BPM)

BV AND VASCULAR RESISTANCE—>STROKE VOLUME(ML/BEAT)

Pericarditis

• causes

Inflammation of pericardium by viral infection, thoracic trauma, myocardial infarction, tuberculosis, malignancy, and autoimmune conditions￭

Pericarditis may cause…

pericardial effusion: Fluid accumulatesIn space between pericardial sac and heart; swollen tissue creates friction

What is a complication of pericarditis?

• manifestations of this

Cardiac tamponade: life-threatening cardiac compression from fluid accumulation (pleural effusion)

• falling arterial pressures, rising venous pressures, narrowing pulse pressure, and muffled heart sounds

Constrictive pericarditis

• manifestations

loss of elasticity from chronic inflammation

• pericardial friction rub (grating sound); sharp, sudden, severe chest pain that increases with deep inspiration and decreases when sitting up/leaning forward; dyspnea; tachycardia; palpitations; edema; flu-like symptoms

Pericarditis acronym

FRICTION

F- friction rub

R- relieved pain when sitting up/ leaning forward

I- increased pain with inspiration

C- chest pain (sharp, stabbing)

T- tachycardia

I- increased pain when lying flat

O- overall malaise and fever

N- not relieved by medication

Infective Endocarditis

• formerly called

• caused by

Infection of endocardium and heart valves

• formerly called bacterial endocarditis

• (commonly caused by streptococcus and staphylococcus)

What can form and travel due to Infective Endocarditis?

Thrombi form that travel(emboli), causing microemboli and microhemorrhage

Infective Endocarditis signs and symptoms

FROM JANE

Fever(flu-like symptoms)

Roth spots(retinal hemorrhages)

Osler nodes(small, painful, raised, red or purple bumps on finger and toe pads)

Murmer(new onset)

Janeway lesions(small, painless, red or purple flat spots on palms or soles of feet)

Anemia

Nail-bed hemorrhages(splinter)

Emboli

also petechiae

Risk factors for Infective endocarditis

IV drug use, valvular disorder, prosthetic heart valves/implanted devices, rheumatic heart disease, aortic coarctation, congenital heart defect, Marfan Syndrome

Life-threatening complications for IE

myocardial infarction, stroke, or pulmonary embolism

Infective Myocarditis

• complications

uncommon and poorly understood inflammation of myocardium

• heart failure, cardiomyopathy, dysrhythmia, thrombus formation

Infective Myocarditis caused by

Manifestations

• infections(viruses, bacteria, parasites)

• drugs and vaccines

• Autoimmune diseases

palpitations, cardiomegaly, pale and cool extremities, syncope, decreased urine output, leg swelling(fluid stays in legs)

Infective Myocarditis acronym

HEARTFAIL

H- Heart murmur

E- Edema (peripheral or pulmonary)

A- Arrhythmias

R- Rapid pulse (tachycardia)

T- Tiredness and weakness

F- Fever(flu-like symptoms)

A- Aching chest (angina-like pain)

I- Increased respiratory rate (dyspnea)

L- low cardiac output

Valve stenosis

narrowing; less blood can flow through the valve

• decreased cardiac output, increases workload—>hypertrophy

  • atresia: failure to open valve

Valve regurgitation

insufficient closure; bidirectional blood flow

• decreases cardiac output, increases workload on the heart—>hypertrophy and dilation of ventricles

Valvular disorders are caused by

congenital defect, infective endocarditis, rheumatic fever, myocardial infarction, cardiomyopathy, heart failure

• manifestations vary and reflect depending on valve and changed cardiac flow

Cardiomyopathy

acquired or inherited conditions

• weaken and enlarge the myocardium(heart muscle)

• makes it harder for the heart to pump blood to body

• can lead to heart failure

• 3 types…

  • dilated (too big), hypertrophic (too thick) and restrictive (too stiff)cardiomyopathy

Dilated Cardiomyopathy

• who is at high risk

• caused by

most common type: primary myocardial dysfunction —> ventricular dilation and cardiomegaly —>decreased cardiac output and blood stagnation

• high risk: african american men and O.A.

Causes: ￭ chemotherapy, alcoholism, cocaine abuse, pregnancy, infection, thyrotoxicosis, diabetes mellitus, neuromuscular disease, hypertension, coronary artery disease, med hypersensitivity

Dilated Cardiomyopathy manifestations: appear as compensatory mechanisms fail

breathing changes and nonproductivecough ⚬Fatigue⚬ dysrhythmia(s), cardiac pain and abnormalities⚬ dizziness, activity intolerance⚬abnormal lung sounds⚬peripheral edema⚬Ascites, hepatomegaly⚬weak pedal pulse⚬cool/pale extremities⚬poor capillary refill⚬jugular vein distension

Hypertrophic Cardiomyopathy mainly affects who and what?

• what happens to ventricle

systolic function in men and sedentary individuals; ventricle wall becomes thick and unable to relax

Hypertrophic Cardiomyopathy risk factors

hypertension, obstructive valvular disease, thyroid disease, dominant genes

Hypertrophic Cardiomyopathy manifestations

dyspnea/intolerance on exertion, syncope(fainting), orthopnea(dyspnea when lying down), angina, dysrhythmia, left ventricular failure, myocardial infarction, fatigue

Restrictive Cardiomyopathy

rigid ventricles affects diastolic function

• poor prognosis

• common in south and central America, India, Asia, and Africa

caused by amyloidosis, hemochromatosis, sarcoidosis, radiation, connective tissue diseases, myocardial infarction, cardiac neoplasms

Manifestations: if present, fatigue, breathing and lung changes, angina, hepatomegaly, jugular vein distension, ascites, murmurs, peripheral cyanosis, pallor

Cardiomyopathy Acronym

WEAK HEART

W- weakness and fatigue

E- edema (peripheral and pulmonary)

A- Arrythmias

K- keep cough in mind (left-sided HF)

H- Heart murmur

E- Enlarged heart (cardiomegaly)

A- Angina or chest pain

R- respiratory distress (dyspnea, othropnea)

T- tachycardia

DCM

HCM

RCM

• big and stretched ventricle-weak pump

  • decreased contractility

  • systolic dysfunction

  • “cant pump”

• thick ventricle(septum) - crowded chamber

  • decreased ventricular filling

  • diastolic dysfunction

  • “too thick to fill”

• stiff ventricle - won’t relax

  • normal size, but rigid

  • diastolic dysfunction

  • “too stiff to fill”

EKG - 1 small square

.04 seconds

1 large box

.2 sec (5 small squares)

QRS complex

.04 - .12 sec

• 1-3 small boxes

• ventricular depolarization

PR Interval

.12 - .20 sec

• 3-5 small boxes

• pause before the pump; allows time for ventricles to fill

Electrical Alterations

Dysrhythmias - abnormal or irregular heartbeat(rate and rhythm)

• classified by origin and affect on Cardiac output and BP

caused by: acid-base imbalance, electrolyte imbalance(potassium), CHD, anything creating issues with walls of heart can affect beat

• manifestations vary based on dysrhythmia: sometimes asymptomatic, palpitations, fluttering, skipped beats, etc

  • catch dysrhythmias before they cause sudden cardiac death

Preload

volume of blood in ventricles at end of diastole(end diastolic pressure)

• increased in: hypervolemia, regurgitation of cardiac valves, heart failure

Afterload

pressure needed to eject blood/resistance left ventricle must overcome to circulate blood

• increased in: HTN and vasoconstriction

Congestive heart failure(HF)

inadequate pumping that leads to decreased cardiac output (CO) and increased preload/afterload

Causes: congenital defect, myocardial infarction, valvular disease, dysrhythmia, thyroid disease

• Compensatory mechanisms (sympathetic nervous system, renin-angiotensin-aldosterone system, and hypertrophy) help at first, but perpetuate heart failure

• Systolic dysfunction: decreased contractility(ventricles can’t pump hard enough during systole) ￭ Diastolic dysfunction: decreased filling (not enough blood fills ventricles during diastole)

  • Mixed dysfunction: decreased contractility and filling (both systolic and diastolic)

Definition of heart failure

Ejection fraction: measurement of how much blood is pumped by left ventricle every time the heart pumps

• 50-70% is normal ejection fraction

• HF with reduced EF < 40%

• HF with preserved EF >50%

may be acute or chronic depending on underlying cause

• manifestations depend on type and severity (graded I-IV) and appear as compensatory mechanisms fail

Left-sided heart failure

think left→lungs

cardiac output falls; blood backs up to pulmonary circulation—> pulmonary congestion, dyspnea, activity intolerance

• causes: left ventricular infarction, hypertension, aortic or mitral valve stenosis, CAD

manifestations: pulmonary manifestations

• pulmonary congestions: cough, crackles, pink-tinged sputum, tachypnea

  • tachycardia, cyanosis, exertional dyspnea, fatigue

Right-sided Failure

Blood backs up to peripheral circulation, causing edema/weight gain

causes: pulmonary disease, left-sided failure, right MI, pulmonic or tricuspid valve stenosis

Manifestations: systemic

• peripheral edema

• ascites

• enlarged liver and spleen

• JVD

• weight gain

• increased peripheral venous pressure

Alterations resulting in Ineffective Tissue Perfusion

Aneurysms

• caused by weakening of an artery

• commonly: abdominal or thoracic aorta; cerebral, femoral, or popliteal arteries

  • exsanguination(bleeding out) is a possible consequence of rupture

• caused by HTN, build up of plaques(atheroscelrosis), dyslipidemia, DM, tobacco, older age, trauma, infection, congenital defects

True aneurysms affect

all three layers

Saccular aneurysm

bulge on the side (asymmetrical)⚬

Fusiform aneurysm

affects entire circumference(symmetrical)

Dissecting aneurysm

occurs in inner layers, not a true aneurysm

Manifestations of aneurysm

if present, depend on location/size; pulsating mass(esp. with abdominal aneurysm), pain, respiratory difficulty, neurologic

Dyslipidemia

high levels of lipids in the blood, which increases risk for chronic disease

• lipids come from dietary sources and are produced by liver

classified based on density; triglycerides(low density lipoproteins(LDLs): “bad” cholesterol, makes up most serum cholesterol and is more invasive in nature) and protein(high density lipoproteins(HDLs); “good)” cholesterol, helps remove LDL cholesterol from blood)

• manifestations: asymptomatic until it causes other diseases and complications

Atherosclerosis

chronic inflammatory disease TRIGGERED BY A VESSEL WALL INJURY(have to have this occur to develop this disease)

• vessel wall injury can happen from HTN, smoking, high cholesterol(dyslipidemia), diabetes

Characterized by thickening/hardening lesions calcifying on the arterial wall—>obstructs vessel, leads to platelet aggregation, and vasoconstriction

• complications: PVD(symptoms start when vessels become 70% occluded; clients may report pain in distal tissues, or chest pain if coronary artery issue) CAD, thrombi, HTN, stroke

• manifestations: asymptomatic until complications develop

Peripheral Vascular Disease(PVD)

narrowing of the peripheral vessels - (arteries and/or veins)

• commonly atherosclerosis in the arteries

• may also be caused by a thrombus, inflammation, or vasospasm

Examples:

• Thromboangitis Obliterans

• Raynaud Phenomenon

Thromboangitis Obliterans

aka buerger disease

• chronic inflammatory condition of the arteries

• may lead to thrombosis and eventually complete occlusion of the small/medium arteries in extremities

  • bv are occluded so tissue becomes ischemic at first and eventually necrotic

  • pale, cyanotic, necrotic

• MOST COMMONLY AFFECTS MALES 20-40, WHO SMOKE

  • exact cause unknown

Raynaud Phenomenon

vasospams of the arteries related to sympathetic stimulation—> tissues can change color; white, blue, red

• associated with cold temperatures, autoimmune conditions(lupus and scleroderma), and stress

• most commonly affects females between 18-30 years old

  • increased vessel occlusion may lead to ischemia of affected tissue(but less likely than with buerger disease)

Coronary Artery Disease

Narrowing or blockage of the arteries that supply blood to the myocardium(heart) - most commonly caused by atherosclerosis

• also caused by vasospasm, cardiomyopathy, and thrombi occlusion

• most common type of heart disease in the U.S. and leading cause of myocardial infarction

Nonmodifiable risk factors:

￭ age: males > 45 years; females > 55 years or premature menopause￭ family history: premature cad in first-degree male relatives

Modifiable risk factors:￭ tobacco use, stress, obesity, physical inactivity, diabetes mellitus, hyperlipidemia, hypertension

3 main types: obstructive, nonobstructive, and coronary microvascular disease

Obstructive CAD

Plaque accumulates in the large arteries causing narrowing and decreased blood supply to the myocardium

⚬Coronary artery is occluded by more than 50%

⚬Blood flow may become completely occluded—> MI

Nonobstructive CAD:

large arteries occluded less than 50%

⚬ also caused by damage or injury to the lining of the coronary arteries that impact the ability to vasodilate in response to increased myocardial oxygen demand

Coronary Microvascular Disease

Affects the smallest arteries of the myocardium(arteries that branch off of the coronary arteries)

⚬Caused by molecular changes in small vessels aspart of normal age or damage (i.e., inflammation, diabetes, hypertension)

⚬Arteries do not respond to signals to vasodilate with increased oxygen demands on the myocardium

CAD: Angina

Stable Angina: Chest pain caused by ischemia that is initiated by increased oxygen demand(like walking up the stairs) and relieved with decreased demand (at rest)⚬ Decreased blood flow may or may not cause permanent ischemia

Unstable Angina(BAD): ⚬ unpredictable chest pain ⚬ Occurs at rest, or increases in frequency and/or intensity ⚬ Considered a “preinfarction” state (high risk for MI)

Coronary Artery Disease: Clinical Manifestations

• angina that may radiate to neck, jaw, arm, or back

• indigestion-like sensation

• N/V

• cold/clammy extremeties

• diaphoresis

• dyspnea, dizziness, fatigue, weakness, lightheadedness

• sleep distrubances(worse when trying to sleep/lay down)

Coronary Artery Disease: acronym

H- heavy or squeezing chest pain (angina)

E- exertion triggers pain

A- anxiety or fear

R- radiating pain

T- tachycardia

P- pallor and diaphoresis

A- atypical symptoms in women/ older adults

I- indigestion or epigastric discomfort

N- numbness or tingling

S- shortness of breath

Thrombus

• blood clot that forms anywhere in the circulatory system

• 3 conditions promote thrombus formation:

  • endothelial injury(physical trauma, strain, injury), sluggish blood flow,(congenital abnormalities affect venous anatomy-may thurner and paget schroetter) hypercoagulability(estrogen therapy, inflammation, dehydration)

• venous thrombi more common than arterial due to lower pressure against gravity

Emboli

part or all of a thrombus breaks loose, travels through circulatory system, embeds in smaller vessel

• can be air, fat, tissue, bacteria, amniotic fluid, tumor cells, foreign substance

Right side of the heart origin

venous circulation that travels first to pulmonary circulation, creating a pulmonary embolism

Left side of the heart origin:

arterial circulation and travel to other organs such as brain and heart, causing an infarction

Manifestations depend on

location of the body and whether they are venous or arterial

Indications of deep vein thrombosis(DVT)

calf swelling, erythema(swelling), and leg warmth

Pulmonary Embolism-

thrombus originates elsewhere and disrupts blood flow in the pulmonary artery or branches

Varicose veins

dilated, engorged veins r/t improper valve formation

• most common in legs; may also see in esophagus, rectum, and testicles

• increased venous pressure and pooling

risk factors: genetics, pregnancy, obesity, prolonged sitting or standing, alcohol use(esophagus), constipation(hemorrhoids)

manifestations: purple bulging veins, pedal edema, aching in legs, shiny, hairless pigmented skin on legs and feet, skin ulcer, possible necrosis

Lymph Edema

unusual swelling in the extremeties r/t obstruction

• may be unilater or bilateral

primary caused by: rare; congenital absence or decreased lymphatics

secondary caused by: mastectomy, scarring by radiation, occlusion r/t tumors, obstructions r/t infection, injury/trauma

• staging system 1-4(4 most severe)

manifests: edema and skin changes, hyperpigmentation, ulcer, thick and rough(elephant skin)

Myocardial Infarction

heart attack and acute coronary syndrome

• death of the myocardium from sudden blockage of coronary blood flow

• Myocardial oxygen supply cannot meet body’s oxygen demand⚬ Myocardial cells die as oxygen supply dwindles, leading to tissue necrosis

Leading cause of death in the U.S.

cardiovascular disease(usually caused by cardiac damage post MI)

Myocardial infarction risk factors

dyslipidemia, DM, HTN, stress, tobacco use

Myocardial Infarction manifestation

• very similar to CAD

CRUSHING

Chest pain(intense, crushing, pressure)

Radiating pain

Unrelieved by rest or nitroglycerin(meds)

Sweating(diaphoresis)

Hard to breathe(dyspnea)

Increased hr and BP initially

N/V

Going to be anxious and fearful, dizzy

unstable angina, coughing, indigestion, elevation in cardiac biomarkers, can’t sleep

Alterations Resulting in Decreased Cardiac Output and Ineffective Tissue Perfusion

Hypertension

One of the most prevalent chronic health conditions in U.S.

Prolonged elevation in blood pressure creates excessive cardiac workload due to vasoconstriction, increasing afterload

• decreased renal blood flow inappropriately activated renin-angiotensin-aldosterone system(RAAS)

risk factors: age(females increase risk after menopause), African Americans, family history, obesity, inactivity, tobacco use, high-sodium diet, low potassium/calcium/magnesium diet, high vitamin D intake(RAAS), alcohol, stress

Primary (essential) hypertension:

most common, develops gradually over time￭ No identifiable cause; 95% of adult cases

Secondary hypertension:

more sudden and severe

• caused by renal disease, diabetes, adrenal tumors, meds, and cocaine, and amphetamines(illicit drug use)

Pregnancy-induced hypertension:

Preeclampsia that may lead to eclampsia (increased BP may lead to seizures)

Malignant hypertension (hypertensive crisis):

intense and nonresponsive to interventions ￭ BP is at least 180/120 & symptomatic

HTN can lead to

severe health complications if uncontrolled

• cardiovascular disease

  • MI, heart failure, Left Ventricular Hypertrophy

• Stroke and Brain complications

  • ischemic and hemorrhagic stroke

  • cognitive impairment and dementia

• Kidney damage

  • chronic kidney disease

  • kidney failure

• vision loss and retinal hemorrhages

• aneurysms and Peripheral artery disease

Orthostatic (postural) Hypotension

decrease in both systolic and diastolic BP upon standing(at least 20mmHg and 10 mmHg within 3 minutes of standing up)

• lack of normal BP compensation in response to gravitational changes on the circulation

• acute OH or chronic OH

Symptoms of Low BP

dizzy, lightheaded, fainting or passing out, upset stomach, blurred vision, fast/shallow breathing, fatigue, weakness, tired, confusion, agitation