conditions

long QT syndrome

cardiac conduction system abnormality that prolongs QT interval on ECG

• inherited in autosomal-dominant manner

syncope conditions for assuming life threatening

• exercise induced syncope

• syncope associated with chest pain

• history of syncope in close family member

• syncope associated with startle

cardiomyopathy

diseases of the myocardium (heart muscle) that progress to heart failure, AMI, or death

• make heart muscle thin, flabby, dilated, or enlarged

hypertrophic cardiomyopathy

excessive thickening of heart muscle

• symptoms are SOB, chest pain, palpitations, syncope, sudden cardiac death

• autosomal dominant

• beta blockers can be effective, otherwise surgery or automatic implantable cardiac defibrillator

mitral valve prolapse

mitral valve leaflets balloon into left atrium during systole

• usually benign and symptomless

• when symptomatic chest pain, fatigue, dizziness, dyspnea, palpitations

• clicking sound heard during cardiac auscultation

• cardiac arrhythmia is rare

• can lead to mitral regurgitation

mitral regurgitation

caused by mitral valve prolapse, large amount of blood leaks backward through defective valve

• can lead to thickening of heart wall bc of extra pumping needed to make up for the backflow

• can cause SOB and tiredness

• treated with medication and sometimes surgery

coronary heart disease

caused by impaired circulation to heart

• typically patients have critical narrowing or occluded coronary arteries from atherosclerotic plaque buildup

• effects range from ischemia to infarction and necrosis of myocardium

risk factors: father who had AMI or died suddenly before 55, mother who experienced AMI or died suddenly before 65, hyperchlosterolemia, cigarette smoking, hypertension, age, diabetes

hypercholesterolemia

elevation of the blood cholesterol level

BCL is divided into high and low density lipoproteins

• HDL: good cholesterol

• LDL: bad cholesterol

low levels of HDL and/or high levels of LDL are at increased risk for coronary heart disease

thromboembolic disease

includes deep vein thrombosis and pulmonary embolism

• significant cause of death following musculoskeletal injuries, especially to pelvis and lower extremities that lead to prolonged immobilization

• treatment is maintaining airway; adequate oxygenation and intravascular volume; and rapid transport

deep vein thrombosis

type of thromboembolic disease where a clot forms in a deep vein, usually legs

• symptoms are disproportionate swelling of extremity, discomfort in extremity that worsens with use, and warmth and erythema (reddening) of the extremity

• when portion of DVT dislodges, may cause pulmonary embolism

• caused by injury, inflammation, stasis, sepsis, pregnancy, birth control, malignancy, couagilopathies, smoking, varicose veins, high altitude

prevention:

pulmonary embolism

a blood clot that travels to, and occludes, a pulmonary artery

• symptoms are sudden onset dyspnea; pleuritic chest pain (either side); syncope; tachypnea; tachycardia; low fever; right side heart failure; shock; cardiac arrest

• large volume boluses should be avoided when suspected massive pulmonary embolism bc they can cause the intraventricular septum into the left ventriclar outflow tract which worsens shock (may receive order for trial of inotropic therapy)

fat embolism

fat droplets from bone marrow enter circulation and become lodges in arteries (most common are lungs, brain, skin)

• usually occurs in patients with long bone or pelvic fractures

• symptoms begin 12-72 hours of injury

• when lodged in pulmonary artery symptoms are similar to pulmonary embolism

• when other organ systems involved, altered LOC ranging from agitation to coma; skin petechiae (small red spots on skin), fever

pulmonary edema

swelling of the lungs when fluid from blood plasma migrates into lung parenchyma (tissue of capillaries and alveoli)

• compromises gas exchange long before fluid spills into alveoli and becomes noticeable

• common cause is heart failure resulting from left side acute myocardial infarction

• inhaled toxins can damage alveolar tissue causing fluid to seep into lungs

• trauma or altitude changes can lead to acute respiratory distress syndrome or high altitude pulmonary edema

signs and symptoms:

• early on crackles in the base of the lungs at the end of inspiration can be heard

• as it worsens, crackles can be heard from higher up

• as fluid moves to larger airways and mixes with mucus, coarse crackles are heard during inspiration and expiration

• tactile fremitus may be felt (vibration on chest wall when speaking)

• coughing up pink and foamy blood-tinged sputum

arterial blockage symptoms

cold and blue extremity

atherosclerosis

the achilles heel of all cardiac problems

abnormal thickening and hardening of aorta, cerebral, and coronary blood vessel walls which greatly reduces their elasticity

caused by soft deposits of intra-arterial fat and fibrin which harden over time providing location for formation of blood clot

risk factors: hypertension; smoking; diabetes; sigh serum cholesterol levels; lack of exercise, obesity, family history of heart disease or stroke, male sex

effects:

• ischemia (lack of oxygenated blood flow)

• infarction, necrosis (complete obstruction)

• thrombosis

• embolism (obstruction, infarction)

• aneurysm (rupture of vessel)

• vessel calcification (causes rigidity and rupture)

co morbid factors

obesity,

aneurysm

dilation of a vessel

AAA (acute abdominal aneurysm): palpable masses in abdomen, abdominal pain, pulsating mass

thoracic aneurysm: variation of BP in arms

S/S for non ruptured: pain, low BP, shock, palpable pulsating mass

ruptured: shock, stabbing pain, difference in BP between arms, absent radial or femoral pulses (shock), mottling of extremities below aneurysm (lack of circulation), unconsciousness

treatment: large bore IV, fast to operating room, keep patient calm and still

hypertension

known as the silent disease

consistent elevate of systemic arterial BP. resting BP consistently >140/90

risk factors: family history, age, gender (m<55, w>74), black race, high sodium intake, glucose intolerance, cigarette smoking, obesity, alcohol consumption, low intake of K, Ca, Mg

effects:

• damages walls of systemic blood vessels

• prolonged vasoconstriction and high pressures in arteries causes vessels to thicken and strengthen

• vessels lose elasticity

• stimulates biochemical mediators of inflammation which causes increase in vascular endothelium (end result is permanently narrowed blood vessel)

endocarditis

inflammation of the inner lining of the heart, and/or heart valves

caused by either bacteria or virus, usually bacteria

risk factors:

• acquired valvular heart disease (mitral valve prolapse)

• implantation of prosthetic heart valves (because they cannot fight at the cellular level)

• congenital legions

• previous attack

• male

• intravenous drug use

• long term indwelling catheterization

S/S: multiple organ systems (infection spreads), fever, cardiac murmur, petechial lesions of skin, conjunctiva, and oral mucosa

myocarditis

inflammation of the heart muscle (myocardium)

caused by infection or toxic inflammation (drugs or toxins from infectious agents)

S/S: flulike, pain in epigastric region or under sternum, dyspnea, cardiac arrhythmia

pericarditis

inflammation of the pericardium

S/S: flulike symptoms, fever, chest pain, diffuse ST elevation (everywhere)

acute coronary syndrome (ACS)

all of the problems that happen in the heart

• unstable angina UA

• Non-ST-segment elevation myocardial infarction NSTEMI

• ST-segment elevation myocardial infarction STEMI

ischemic heart disease

myocardial ischemia is lack of blood flow to the myocardium and is usually caused by narrowing of coronary arteries

narrowing of blockage of coronary vein disrupts the oxygen supply

if cause of ischemia is not reversed and blood flow is not restored, ischemia may lead to cellular death (infarction)

lack of oxygen causes aerobic metabolism which creates lactic acid in the heart which stimulates the nerve endings causing chest pain which means that chest pain is usually an oxygen supply and demand issue

ischemia » cellular injury » infarction

S/S:

• retrosternal chest pain, pressure, heaviness, or squeezing lasting 10 minutes or longer at rest

• increased extensional dyspnea (SOB when exerted)

• unexplained fatigue

• diaphoresis (sweating)

• N/V

• syncope (fainting)

atypical presentations are common and may include pleuritic chest pain, epigastric pain, acute-onset indigestion, increasing SOB without chest pain

• most often observed in younger and older patients, women, and patients with diabetes mellitus, chronic renal insufficiency, or demential

ischemia » injury » infarction

ischemia

• lack of oxygenation

• ST depression or T inversion

Injury

• prolonged ischemia

• ST elevation

Infarction

• death of tissue

• may or may not show in Q wave

• deep Q wave after some time

ischemia

inadequate oxygen to tissue

• subendocardial

• represented by ST depression or T inversion

• may or may not result in infarct

injury

prolonged ischemia

• represented by ST elevation

• transmural (entire myocardium)

• usually results in infarct

infarct

death of tissue

• represented by Q wave half the height of the QRS

• not all infarcts develop Q waves

angina

choking pain In the chest caused by imbalance between myocardial O2 supply and demand

stable angina (exertional angina)

• goes away after exertion

unstable angina (pre infarction angina)

• comes on while at rest

prinzmetal’s angina

• result of intense spasm of segment of a coronary artery

• may occur in health individuals

• generally younger with fewer risk factors

spams is result of:

• cold weather

• stress

• medicines - antimigranes, chemo, antibiotics

• smoking

• cocaine use

myocardial infarction

sudden and total occlusion or near occlusion of blood flowing through an affected coronary artery to an area of heart muscle

results in ischemia, injury, and necrosis of the area of myocardium distal to the occlusion

ischemia occurs immediately in the area supplied by affected artery

diastolic and systolic dysfunction appear within 30-45 seconds of blood flow deprivation. ischemia also contributes to dysrhythmias by causing electrical instability of ischemic areas of the heart

if blood flow is not restored to affected artery, myocardial cells within the sub-endocardial area begin signs of injury within 20-40 minutes

ACS management

• reduce physical activity, calm reassurance

• O2 if WOB increased and SPO2 less than 94%

• 3 lead followed by 12 lead ECG (do 3 12 leads, scene, route, arrival)

• notify receiving hospital if ST elevation

• IV

• if clinically indicated ASA 160-325mg PO

• if clinically indicated, Nitro 0.4mg SL, titrate (decreases BP so BE CAREFUL)

• consider calling ALS

cardiomyopathies

diverse group of diseases that effect myocardium

• result from underlying disorders

• in response to injury, the heart may undergo dilation or hypertrophy

when the heart is not an effective pump

dilated: fat floppy left ventricle

hypertrophic:

restrictive: poor contractility and dilation of muscle

incurable diseases only hope is transplantation

pulmonary edema

when fluid from the blood plasma migrates into the lung parenchyma compromising gas exchange in the alveoli’s

• most common cause is left ventricular failure from acute MI (when LV is weak it poorly pumps to the body causing backup to the lungs)

• other causes are inhaled toxins, infections, trauma, altitude changes

S/S:

• hear late inspiratory crackles at lung apices (top)

  • caused by rapid expansion of collapsed alveoli as they reach maximum inflation

• as it worsens, more proximal crackles in lung fields

• as fluid migrates into larger more central airways and mix with mucus the crackles become more coarse sounding

• as lungs fill up, frothy punk sputum may appear, which is an ominous sign

CPAP drives fluid back into the circulatory system and allow for gas exchange

cariogenic shock

shock of a cardiac nature, when the heart fails so badly that hit causes shock

• heart is so damaged it cannot maintain tissue perfusion

• when 25% of left ventricular myocardium is involved

• when 40% or more of left ventricle has been infarcted

• high mortality rate

S/S:

• confusion due to reduce cerebral perfusion (leads to comatose)

• restlessness and anxiety

• pale cold skin

• poor renal perfusion causes less urine output

• rapid shallow respirations

• pulse is racing and weak

• as compensatory mechanisms begin to fail BP will fall (increased HR and vasoconstriction fail)

treatment:

• improve oxygenation and peripheral perfusion

• secure airway and administer 100% supplemental oxygen

• advanced airway necessary if comatose (ALS)

• place patient supine

• IV with normal saline

heart failure

• heart is unable empty chambers

• blood backs up into systemic circuit, pulmonary circuit, or both

• left sided heart failure is most commonly caused by acute myocardial infarction and chronically by continued hypertension

• right ventricle failure is usually caused by left ventricle failure

S/S (left)

• extreme restlessness, anxiety, confusion, agitation (low brain O2)

• severy dyspnea, tachypnea, tachycardia

• hypertension or hypotension

• crackles and wheezes (in lungs)

• frothy pink sputum in severe cases

S/S (right)

• jugular vein distension

• pedal/pitting edema

• left sided heart failure

treatment:

• comfortable position, high fowlers

• administer O2

• administer nebulizer sympathomimetric/anticholinergic

• administer SL nitroglycerin

• initiate continuous positive airway pressure CPAP

• consider ALS intercept

may present acutely as a result of acute pump dysfunction from an myocardial infarction

mechanical loss of critical mass of myocardium resulting in immediate symptoms

if symptomatic hypotension with inadequate perfusion, cardiogenic shock is present