cardiac Flashcards
Coronary Artery Disease
Coronary arteries branch from the aorta.
Arteries become CLOGGED d/t atherosclerosis.
problems with the heart
- Electrical (conduction)
- Plumbing (ARTERY BLOCKAGE, spasm, or valve issues)
- Pump (heart muscle)
Non-modifiable Risk Factors
Age- advanced
Family history
Gender- men earlier in life, women after menopause at same risk.
Ethnicity- blacks, African Americans, hispanics, native americans, indigenous people.
Genetics
shared environmental exposure.
Modifiable Risk Factors
HTN
Cigarette smoking- & second hand smoking.
Diabetes
Obesity/Inactivity
Diet
Hyperlipidemia
Depression/Stress
Patho: Ischemic Heart Problems
“a plumbing issue”
Etiology: Atherosclerosis develops in the arteries supplying the myocardium = ARTERY BLOCKAGE.
The blockage causes decreased tissue perfusion.
Is ENDOTHELIAL DYSFUNCTION.
The heart must work harder to pump the blood.
Endothelial Dysfunction
Vessels aren’t necessarily blocked but become narrowed when they are supposed to dilate.
causes of endothelial dysfunction
DM, HTN, HPL, smoking
Angina: main symptom of CAD
May be asymptomatic.
Eventually, as coronary arteries continue to narrow, the decreased blood flow may cause chest pain/ANGINA.
COMPLETE OCCLUSION = myocardial infarction.
stable angina
definition: angina- coronary blood flow is diminished but NOT BLOCKED.
There is an imbalance between oxygen supply and demand.
Is brought on by EXERTION and is relieved with REST.
Usually only last 2-5 minutes.
Most often caused by ATHEROSCLEROSIS.
coronary heart disease symptoms
ANGINA
heartburn
irregular HR
dizziness
nausea
burning sensation
cardiac chest pain symptoms
pressure or tightness
diffuse, poorly localized.
associated w/ physical exertion or other stress.
relieved with rest, usually w/in minutes.
prolonged symptoms may represent an acute coronary syndrome (MI).
non-cardiac chest pain symptoms
sharp or stabbing
focal, well localized.
may be positional, spontaneous at rest.
no predictable relation to physical exertion.
may last from seconds to even days at a time.
Atypical Angina in Women
Discomfort: Hot or burning, Tenderness.
Location: Not always the chest.
Other symptoms: Indigestion, Heart burn, Nausea, Fatigue/weakness, Lightheadedness, Dyspnea.
Angina Pectoris and Pain with Myocardial Infarction
Chest pain not brought on by exertion & may radiate to other areas.
Pain not relieved in 2-5 min.
Often accompanied by N/V, SOA, diaphoresis.
Risk for myocardial infarction increased.
what do we do with stable angina?
EDUCATION: remember rest and relaxation; DECREASING DEMAND.
Nitrates.
Prevent/treat further atherosclerosis.
TEACH ABOUT myocardial infarctions: if pain last more than 5 minutes call 911.
Cardiomyopathy: definition, causes, what it leads too
definition: Disease that affect the myocardium.
Causes: Usually idiopathic, can be caused by ischemia, HTN, inherited disorders, infections, toxins, myocarditis, auto-immune condition.
Leads to heart failure
heart failure is a _ problem
pumping problem (heart muscle)
what is heart failure?
myocardium is weakened.
pump is insufficient to pump blood forward & cant meet the body’s demands.
most common cause of hospitalizations.
Heart failure results in _ cardiac output, _ myocardial contractility, _ preload, _ afterload
decreased
decreased
increased
Increased
Etiology: Major causes of HF
REPEATED ISCHEMIC EPISODES – ischemic cardiomyopathy.
Myocardial infarction ± papillary muscle rupture.
Chronic HTN.
COPD (RVF).
Dysrhythmias.
Valve disorders; mitral insufficiency, aortic stenosis.
Pulmonary Embolus (RVF).
HF –PATHOLOGICAL changes that occur
volume OVERLOAD.
IMPAIRED ventricular filling- when does the heart fill? diastole.
WEAKENED ventricular muscle.
DECREASED ventricular contractile function- when does the heart contract? systole.
risk factors for HF
HTN: Greatest RF, DM can also contribute.
Within 6 months of MI.
Men and postmenopausal women have same risk of CV disease.
Higher incidence in Black/African-Americans.
Genetics
Major Risk Factors for HF
Age: increases with age; most common reason for hospitalization in people age 65 years and older.
Ethnicity: Black/African Americans are at higher risk than Caucasians.
Family history and genetics
Diabetes
Ischemic heart disease
Obesity
HTN
Lifestyle factors: Smoking and sedentary lifestyle.
COPD
Severe anemia
Congenital heart defects
Alcohol abuse/Drug Abuse
Viruses
Kidney conditions: Excess blood volume, edema, HTN, and accumulation of nitrogenous waste, which can weaken the heart.
What symptoms are going to be apparent with left sided HF?
Blood backs up in pulmonary circulation.
Congestion in LEFT chambers.
LV increases in size (LVH).
Back flow into pulmonary veins.
Congestion in LUNGS
Findings: Cough, crackles, wheezes, Frothy sputum, may be blood tinged, Paroxysmal nocturnal dyspnea (PND), Orthopnea.
With right sided HF?
Blood backs up in systemic circulation.
Often due to COPD with cor pulmonale.
Congestion in RIGHT chambers.
RV increases in size (RVH).
Back flow into vena cava, decreased to the lungs.
Congestion in jugular veins, liver, lower extremities.
Findings: JVD, Dependent edema, Weight gain, Hepatosplenomegaly.
Heart failure: Reduced Ejection Fraction (HFrEF) [Systolic HF].
Determined by patient’s ejection fraction: EF < 40%.
Caused by IMPAIRED contractile function, increased afterload, cardiomyopathy, and mechanical problems.
Left ventricle loses ability to generate pressure to eject blood.
Weakened muscle cannot generate SV & lowers CO.
LV fails, blood backs up, causes fluid backup and accumulation.
Heart failure: Preserved Ejection Fraction (HFpEF) [Diastolic HF]
Inability of the ventricles to relax and fill during diastole.
HTN is the primary cause.
RF: Being female, older age, diabetes, and obesity.
LV is stiff & noncompliant leading to high filling pressures leads to decreased SV & decreased CO.
Reduced CO leads to fluid congestion.
EF is normal or only moderately decreased (40-49%)
Chronic versus Acute HF
Progressive
Chronic
+ Episodes of “decompensated” HF: New or worsening S/S, Frequent visits to the ER, Hospitalization, Less common- new onset HF (20%).
Ventricular REMODELING in HF
A weakened heart muscle: Secretion of molecular substances; Angiotensin II, aldosterone, endothelin, TNF-alpha, catecholamines, insulin-like growth factor, and growth hormone; Provoke genetic changes, apoptosis, and hypertrophy of cardiac myocytes, as well as collagen deposits and myocardial fibrosis.
These molecules cause changes that lead to ENLARGEMENT AND DILATION OF THE LEFT VENTRICLE: Worsens HF.
S3 Gallop in HF
Low-pitched sound heard after S2.
During rapid filling of the ventricle in the early part of diastole.
High ventricular end-diastolic volume.
Increased pressure within ventricles.
In adults older than age 40 years an S3 is abnormal and indicative of heart failure.
automaticity
ability to generate an electrical impulse
conductivity
ability to receive an electrical impulse and conduct it
excitability
ability to respond to an outside impulse (chemical, mechanical, or electrical)
contractility
ability of myocardial cells to shorten in response to an impulse
“Pump part”
atrial depolarization
atrial squeeze
=P wave
ventricular depolarization
ventricle squeeze
= QRS complex
ventricular repolarization
ventricles recharge
= T wave
Normal Electrical Conductivity of Heart
(SINUS RHYTHM)
Rate: 60-100
Rhythm: Regular
P waves: Upright & rounded, One before every QRS, Regular rhythm.
PR interval: 0.12-0.20 sec
QRS: < 0.12 sec
Sinus arrhythmia
ANOTHER NORMAL
A degree of variability in the HR.
Common in young people.
HR fluctuates with respiration or autonomic nervous system.
STILL HAS NORMAL HR, RHYTHM, P WAVES, PR INTERVAL 0.12-0.20, QRS <0.12.
What is a dysrhythmia?
Abnormality of the cardiac rhythm.
Problem with impulse generation or conduction.
What causes dysrhythmias?
- Inappropriate automaticity: A cell initiates action potentials when it isn’t supposed to
- Triggered activity: An extra impulse is generated during or just after repolarization.
- re-entry: Cardiac impulse in one part of the heart continues to depolarize after the main impulse has finished.
Sinus BRADYCARDIA
Originates in SA node
Regular, rate < 60 bpm
Rhythm normal
Normal PR interval and QRS.
Causes of Sinus Brady
Hyperkalemia (slows depolarization)
Vagal response
Digoxin toxicity
Late hypoxia
Medications-beta blockers, CCB.
Myocardial infarction
Clinical Manifestations of Sinus Bradycardia
lightheaded or dizziness, easy fatiguability, syncope or near syncope, dyspnea (SOB), chest pain or discomfort, confusion.
Treatment of symptomatic bradycardia
atropine: anticholinergic
If drug not effective: PACEMAKER
sinus tachycardia
Originates in SA node
Heart Rate 100 -150 BPM
Rhythm = regular
P waves similar (may be partially hidden)
Normal PR interval and QRS
Sinus Tachycardia Causes
Catecholamines: exercise, pain, strong emotions
Fever- increased metabolic rate.
Fluid volume deficit
Medications- epinephrine, albuterol, beta agonist.
Substances- caffeine, nicotine, cocaine
Hypoxia
Treatment for Sinus Tachycardia
BASED ON CAUSE.
Hypovolemia=fluids
Fever=antipyretics
Pain=Analgesics
Beta blockers to reduce HR and myocardial oxygen consumption.
Paroxysmal Supraventricular Tachycardia (PSVT)
HR 150-250 bpm.
Originates in AV node.
Usually no ”P” wave, If present they look abnormal.
QRS normal.
Usually caused by a re-entry phenomenon.
Typically begins and ends suddenly.
Often described as “feeling like my heart is racing”.
PSVT Causes
Over exertion
Emotional stress
Stimulants
Digitalis toxicity
Rheumatic heart disease
CAD
WPW (Wolff-Parkinson-White)
Right sided heart failure (cor pulmonale)
PSVTClinical Signs and Symptoms
Palpitations
Chest pain
Fatigue
Lightheadedness or dizziness
Dyspnea
Premature Atrial Contractions (PACs)
Early p waves that usually look a little different (morphological changes).
Normal PR interval.
QRS does follow the PAC.
Usually has no consequences, but if frequent indicates that patient at high risk for other dysrhythmia (usually afib).
CHECK ELECTROLYTES.
May need O2.- can be a sign for hypoxia.
Atrial flutter
Originates in the AV node overrides the SA node.
Reentry impulse that is repetitive & cyclic.
Regular atrial rhythm with an ATRIAL rate of >250 bpm.
Ventricular rate is slower.
P wave classical “sawtooth” appearance.
QRS usual narrow.
May be 2:1, 3:1, or 4:1.
Causes of Atrial Flutter
Coronary heart disease
cardiomyopathy
heart valve disease
congenital heart disease
inflammation of the heart (myocarditis)
High BP
lung disease or overactive thyroid
electrolytes
atrial fibrillation (AF)
Multiple irritable spots in the atria.
IRREGULARLY IRREGULAR (both atrial and ventricular).
HR 100-175 bpm.
No identifiable ”P” wave.
“fibrillation” waves.
A Fib: Clinical Manifestations
Palpitations
Heart Racing
Fatigue
Dizziness
Chest discomfort
Shortness of breath
May be asymptomatic
Atrial Fibrillation Causes and Complications
Causes: Electrolytes, Hypoxia, CV disease (all)
complications: Decreased CO, HF, EMBOLUS -> stroke
Treatment of A Fib
The most common type of treated dysrhythmia.
Pharmacological: Rate control- Beta blockers, CCB, digitalis, amiodarone; Stroke Prevention- anticoagulants, antiplatelets.
Non-pharmacological: Abalation, cardioversion.
Premature Ventricular Contractions:PVCs
Contraction coming from an ectopic focus in the VENTRICLES.
It comes EARLIER than the QRS should come and doesn’t follow a normal rhythm or p-wave.
Wide and distorted in shape compared to normal QRS .
cause & treatment of PVCs
Causes: stimulants, ELECTROLYTES, hypoxia, fever, exercise, emotional stress and CVD
Treat the CAUSE
Ventricular Tachycardia (V-TACH)
Consists of 3 or more PVCs together.
Ectopic focus within the ventricles takes controls and fires repeatedly, no atrial contractions occurring.
SERIOUSLY decreases CO.
Rate usually 150-200BPMs, usually regular
No p-wave evident, PR not measurable
what is V-tach associated with?
MI, CAD, significant electrolyte abnormalities, heart failure, drug toxicity and other bad things
treatment for V-Tach.
ACLS, depend on pulse, patient will be symptomatic very quickly unless converts back to other rhythm.
May need an anti-dysrhythmic medication like beta blocker or CCB
Electrolyte replacement
DO THEY HAVE A PULSE???
Ventricular Fibrillation: VFIB
Irregular waveforms of varying shapes and sizes.
The ventricles are just ‘quivering’.
No effective contractions = NO CARDIAC OUTPUT
