CV Patho Flashcards
examples of ischemic heart disease
–coronary artery disease
–stable angina
–unstable angina
role of coronary arteries
they feed the heart
what causes coronary artery disease?
atherosclerosis of coronary arteries
name for issue with left anterior descending artery
widow maker
what is the powerhouse of the heart?
left ventricle
where are the coronary arteries situated?
branch from the aorta
problems with the heart
- electrical (conduction)
- plumbing (artery blockage, spasm, or valve issues)
- pump (heart muscle)
non-modifiable risk factors of CAD
–increased age
–family history
–gender (males early, women after menopause)
–ethnicity (POC)
–genetics
modifiable risk factors of CAD
–HTN
–smoking
–diabetes
–obesity/inactivity (android)
–diet (DASH = protective)
–HLD (HDL not high enough)
–depression/stress (inflammation)
etiology of ischemic heart problems
–atherosclerosis develops in arteries supplying the heart muscle –> artery blockage
–blockage = decreased tissue perfusion
–endothelial dysfunction
–heart has to work harder to pump
endothelial dysfunction
vessels aren’t necessarily blocked but become narrowed when they are supposed to dilate
causes of endothelial dysfunction
–DM
–HTN
–HDL
–smoking
inappropriate hormones
main symptom of CAD
angina
what does a complete artery occlusion result in?
myocardial infarction
symptoms of CAD
–dizziness
–chest pain
–heartburn
–irregular heart rate
–weakness
–anxiety
–nausea
–cold sweat
–burning sensation
stable angina
coronary blood flow is diminished but not blocked
specifics about stable angina
–imbalance between oxygen supply and demand
–brought on by exertion
–relieved with rest
–usually only lasts 2-5 minutes
what is stable angina usually caused by?
atherosclerosis
determining cause of chest pain
important to rule out heart being the cause of CP before exploring non-cardiac causes
cardiac chest pain
–pressure or tightness
–diffuse, poorly localized
–physical exertion, stress
–relieved with rest
–prolonged = MI
non-cardiac chest pain
–sharp or stabbing
–focal, well localized
–may be positional, spontaneous at rest
–no relation to physical exertion
–may last from seconds to even days at a time
common non-cardiac causes of CP
–esophageal reflux disease
–muscle problems
–ulcer
–lung disorders
–bone disorders
–deep breath
–emotional disorder
–esophageal rupture
angina in women
–discomfort: hot/burning, tenderness
–location: not always in chest
–indigestion
–heart burn
–nausea
–fatigue/weakness
–lightheadedness
–dyspnea
possible areas of radiating pain with MI
–neck
–jaw
–upper abdomen
–shoulders
–arm
chest pain with MI
–not brought on by exertion
–may radiate
–pain not relieved in 2-5 min
–N/V, SOA, diaphoresis
how do we handle stable angina?
–education: rest and relaxation (rest for 5 minutes and, if pain persists, call 911)
–nitrates
–prevent/treat further atherosclerosis
–teach about MIs
cardiomyopathy
disease that affects the myocardium
causes of cardiomyopathy
–idiopathic
–ischemia
–HTN
–inherited disorders
–infections
–toxins
–myocarditis
–autoimmune
types of cardiomyopathy
–normal
–dilated
–hypertrophic
–restrictive
heart failure
chronic, progressive condition in which the heart muscle is unable to pump enough blood to meet the body’s needs for blood and oxygen
most common cause of hospitalization with heart disease
myocardium is weakened
–pump is insufficient to pump blood forward
–can’t meet body’s demands
what are the factors that determine cardiac output?
–stroke volume
–heart rate
preload
fluid volume
what is afterload associated with?
BP
what does heart failure result in?
decreased CO
decreased contractility
increased preload
increased afterload
development of HF
–volume overload
–impaired ventricular filling (diastole)
–weakened ventricular muscle
–decreased ventricular contractile function (systole)
major causes of HF
–repeated ischemic episodes
–MI, papillary muscle rupture
–chronic HTN
–COPD
–dysrhythmias
–valve disorders/mitral insufficiency/aortic stenosis
–pulmonary embolus
risk factors of HF
–HTN (greatest risk factor)
–DM
–men and postmenopausal women
–Black/AA
–Genetics
–obesity
–smoking and sedentary lifestyles
–COPD
–severe anemia
–congenital heart defects
–viruses
–alcohol/drug abuse
–kidney conditions
left sided heart failure
blood backs up in pulmonary circulation
right sided heart failure
blood backs up in systemic circulation
etiology of left sided HF
–congestion in left chambers
–LV increases in size
–backflow into pulmonary veins
–congestion in lungs
findings in left sided HF
–cough, crackles, wheezes
–frothy sputum, pink
–paroxysmal nocturnal dyspnea
–orthopnea
etiology of right sided HF
–COPD
–congestion in right chambers
–RV increases in size
–backflow into vena cava, decreased to lungs
–congestion in jugular veins, liver, lower extremities
findings in right sided HF
–JVD
–dependent edema
–weight gain
–hepatosplenomegaly
symptoms of left sided HF
–cough
–crackles
–wheezes
–tachypnea
–confusion
–restlessness
–orthopnea
–tachycardia
–exertional dyspnea
–fatigue
–cyanosis
most common cause of left sided HF
poorly controlled HTN
symptoms of right sided HF
–fatigue
–increased peripheral venous pressure
–ascites
–enlarged liver and spleen
–distended JV
–anorexia
–complaints of GI distress
–weight gain
–dependent edema
most common cause of right sided HF
COPD
deoxygenated blood is on what side of heart?
vena cavea to lungs (right)
oxygenated blood on what side of the heart?
lungs to aorta (left)
normal ejection fraction
55-65%
ejection fraction
amount of blood pumped from left ventricle with each squeeze
Reduced Ejection Fraction
HFrEF, systolic HF
how is HFrEF/systolic HF determined?
by patient’s EF < 40%
cause of HFrEF/systolic HF
–impaired contractile function
–increased afterload
–cardiomyopathy
–mechanical problems
patho of HFrEF/systolic HF
–left ventricle loses ability to generate pressure to eject blood
–weakened muscle cannot generate SV and then lowers CO
–LV fails, blood backs up, causes fluid backup and accumulation
preserved ejection fraction
HFpEF/diastolic HF
patho of HFpEF/diastolic HF
–LV is stiff and noncompliant leading to high filling pressures –> leads to decreased SV and decreased CO
–reduced CO leads to fluid congestion
HFpEF/diastolic HF
inability of ventricles to relax and fill during diastole
cause of HFpEF/diastolic HF
HTN
risk factors for HFpEF/diastolic HF
–female
–older age
–diabetes
–obesity
–alcohol use
–potassium levels
EF in HFpEF/diastolic HF
normal or moderately decreased (40-49%)
risk factors for HFrEF/systolic HF
–younger age
–male
–CAD
–DM
–valve disease
heart muscle in HFrEF
round ventricle muscle
heart muscle in HFpEF
thickened ventricle muscle
chronic HF
–progressive
–chronic
–episodes of decompensated HF
ventricular remodeling
weakened heart muscle
molecular substances involved in ventricular remodeling
–angiotensin II
–aldosterone
–endothelin
–TNF-alpha
–catecholamines
–insulin-like growth factor
–growth hormone
what does ventricular remodeling provoke?
–genetic changes
–apoptosis
–hypertrophy of cardiac myocytes
–collagen deposits
–myocardial fibrosis
what do the molecules in ventricular remodeling cause?
changes 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
high ventricular end-diastolic volume
fluid left in ventricle after pump
S3 and age
in adults > 40, S3 is abnormal and indicative of heart failure
automaticity
ability to generate electrical impulses
excitability
ability to respond to an outside impulse
conductivity
ability to receive electrical impulse and conduct it
contractility
ability of myocardial cells to shorten in response to impulse
electrical components of cardiac muscle cells
–automaticity
–excitability
–conductivity
mechanical component of cardiac muscle cells
contractility
depolarization
contraction in atria and ventricles
–systole
–squeeze
repolarization
ventricles; recharging
what controls action potentials?
sodium-potassium pump
what causes a P wave?
atrial depolarization/atrial squeeze
what causes the QRS complex?
ventricular depolarization/ventricular squeeze
what causes the T wave?
ventricular repolarization
what does the SA node preced?
atrial depolarization
what does the AV node precede?
ventricular depolarization
what triggers left ventricular contractions?
Bundle of His and Purkinje fibers
regular heart rate
60-100
normal P wave characteristics
–upright and rounded
–one before every QRS
–regular rhythm
PR interval normal time
0.12-0.20 seconds
QRS normal time
< 0.12 seconds
measurement of P wave
–from beginning to end of wave
–each box = 0.4 seconds
length of time rhythm is measured in
measured in at least 6 beats
sinus arrythmia
–normal rhythm
–degree of variability in the heart rate
–common in young people
–HR fluctuates with respiration or autonomic nervous system
dysrhythmia
–abnormality of cardiac rhythm
–problem with impulse generation or conduction
biggest influence on CO
heart rate
inappropriate automaticity
a cell initiates action potentials when it isn’t supposed to
where does inappropriate automaticity occur?
in the atria
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 main impulse has finished
what triggers sinus rhythms?
SA node
sinus brady
–originates in SA node
–regular, rate < 60 bpm
–normal PR and QRS
causes of sinus brady
–hyperkalemia
–vagal response
–digoxin toxicity
–late hypoxia
–meds
–MI
symptoms of bradycardia
–lightheadedness or dizziness
–easy fatigue
–syncope
–dyspnea
–chest pain or discomfort
–confusion
treatment of sinus brady
atropine (anticholinergic)
–pacemaker if drug not effective
sinus tachycardia
–SA node
–rate 100-150 bpm
–P waves similar
–normal PR and QRS
causes of sinus tach
–catecholamines (exercise, pain, strong emotions)
–fever
–FVD
–meds
–substances
–hypoxia
treatment for sinus tach
based on cause
fix for hypovolemia in sinus tach
fluids
fix for fever in sinus tach
antipyretics
fix for pain in sinus tach
analgesics
meds for sinus tach
beta blockers to decrease HR and myocardial oxygen consumption
paroxysmal supraventricular tachycardia
–HR 150-250 bpm
–AV node
–usually no P wave
–QRS normal
what is PSVT caused by?
re-entry phenomenon
origin location of PSVT
originates above ventricles
causes of PSVT
–overexertion
–emotional stress
–stimulants
–digitalis toxicity
–rheumatic heart disease
–CAD
–WPW
–right sided heart failure
symptoms of PSVT
–palpitations
–chest pain
–fatigue
–lightheadedness or dizziness
–dyspnea
PACs
early P waves that usually look a little different
–normal PR interval
–QRS does not follow the PAC
what to do if your patient is having PACs?
–check electrolytes
–may need O2
–may be at risk for other dysrhythmias
atrial flutter
–AV node overrides SA node
–reentry impulse that is repetitive and cyclic
–sawtooth appearance
–QRS narrow
rate in atrial flutter
–atrial rate > 250 bpm
–ventricular rate is slower
causes of atrial flutter
–coronary heart disease
–cardiomyopathy
–heart valve disease
–congenital heart disease
–inflammation of heart
–high BP
–lung disease, overactive thyroid
–electrolytes
a fib
–multiple irritable spots in the atria
–irregularly irregular
–HR: 100-175 bpm
–no identifiable P wave
symptoms of a fib
–palpitations
–heart racing
–fatigue
–dizziness
–chest discomfort
–SOB
–asymptomatic
causes of a fib
–electrolytes
–hypoxia
–CV disease
complications of a fib
–decreased CO
–heart failure
–embolus = stroke
pharm treatment of a fib and a flutter
–rate control: beta blockers, CCB, digitalis, amiodarone
–stroke prevention: anticoags, antiplatelets
nonpharm treatment of a fib and a flutter
–ablation
–cardioversion
PVCs
–contraction coming from an ectopic focus in the ventricles
–comes earlier than the QRS should come and doesn’t follow a normal rhythm or P-wave
causes of PVCs
–stimulants
–electrolytes
–hypoxia
–fever
–exercise
–emotional stress
–CVD
treatment for PVCs
treat the cause
ventricular tachycardia
–consists of 3 or more PVCs together
–ectopic focus within the ventricles takes control and fires repeatedly –> no atrial contractions occurring
–seriously decreased CO
what is VTACH associated with?
–MI
–CAD
–significant electrolyte abnormalities
–heart failure
–drug toxicity
rate in VTACH
150-200 bpm
morphology of VTACH
–no p-wave evident
–PR not measurable
treatment of VTACH
–ACLS
–depends on pulse
–anti-dysrhythmic meds (BB or CCB)
–electrolyte replacement
ventricular fibrillation
irregular waveforms of varying shapes and sizes
CO and v fib
no effective contractions = no CO
