Cardiac Flashcards
Phases of cardiac cycle
…see study guide
QT interval
electrical systole of the ventricles
-varies inversely w/HR; approximates time of ventricular contraction
ST interval
ventricular myocardium depolarized
P wave
atrial depolarization
PR interval
time from onset of atrial activation to the onset of ventricular activation
QRS
sum all of ventricular depolarization
right ventricle preload =
CVP central venous pressure - estimate of R atrial pressure
left ventricle preload =
pulmonary artery occlusion or wedge pressure - measures L atrial pressure
decreased afterload causes the heart to contract at what pace?
more rapidly
*think about decreased afterload causing increase in the amount of blood ejected (increase in CO) bc there is less resistance - so decreased vascular resistance causes an increase in cardiac output
increased afterload causes the heart to
slows contractions and increases heart workload - increase in vascular resistance = decreased CO
right ventricle afterload =
PVR (pulmonary vascular resistance)
left ventricle afterload =
SVR - systemic vascular resistance
frank starling law
More stretch means what?
related to the volume of blood at the end of diastole/preload and stretch placed on the ventricle
myocardial stretch determines the force of myocardial contraction
More stretch = increased force of contraction. Greater stretch during diastole = greater force of contraction = greater amount of blood pumped out
Laplace law
smaller champers and thicker chamber walls equal increased contraction force
*in ventricular dilation, the force needed to maintain ventricular pressure lessens available contractile force
negative inotropes and examples
acetylcholine (vagus nerve)
hypoxia _____ contractility
DECREASED
EF is what? what is it normally?
amounts of blood ejected per heartbeat by the ventricles
Stroke volume/end-diastolic volume
normally is 55% or higher
Decreased cardiac input caused by?
anything that causes decreased contractility or decreased blood flow to the heart
*increased vascular resistance, MI, shock, bradycardia, decreased SV, negative inotropes, cardiac tamponade, hypovolemia, valvular heart disease, HIGH PEEP
Poiseuille’s law
greater resistance, the lower the blood flow
- think when vessel wall injured it constricts to prevent excess flow
- question: if pt receives a medication that causes vasoconstriction the student knows that according to Poiseuille’s law, what will happen to blood flow? Blood flow will decrease
the semilunar valves are?
pulmonic and aortic
excess K+ does what to heart contractility?
decreases contractility
- hyperpolarization occurs - cannot initiate AP
- with hyperkalemia, it’s easier to initiate AP initially, however, w/myocytes initial increase in K+ increases excitability, but further rise of K+ has the opposite effect
- think lethal injection
excess Ca++ causes what in the heart?
spastic contraction
*opposite of hypercalcemia in skeletal muscle which causes decreased neuromuscular excitability + muscle weakness
low ca++ causes what in the heart?
cardiac dilation
*calcium abnormalities are not as big of a concern – blood levels are more regulated
electrical pathway of the heart
SA node – internodal pathway – AV node – AV bundles – left and right bundles of Purkinje fibers
SA node - causes what? HR?
pacemaker of the heart - spontaneously depolarizes and impulse spreads rapidly from SA node along individual atrial muscle cells to depolarize the right and left atria
causes atrial contraction
60-100bpm
AV node - what does it do? HR beginning from here rate?
delays cardiac impulse – allows atria to empty blood into the ventricles before ventricular contraction
AV bundles transmission time…
transmission time b/w AV bundles and last of the ventricular fibers is the QRS time (0.06 sec)
Purkinje fibers bpm and where are they
from AV node through AB bundle into ventricles
fast conduction – large fibers transmit AP quickly – gap junctions enhance velocity
20-40 bpm
Norepinephrine what does it do? what receptors does it interact with?
vasoconstrictive by interacting with blood vessel alpha 1 receptors
Does not act on beta 2 receptors
Epinephrine what does it do? what receptors does it work on?
vasoconstrictor (alphas 1) and vasodilator (beta 2)
beta 2 - vasodilation of bronchioles and skeletal muscle tissue
Adrenergic (adrenaline - SNS) receptor function
Beta 1, beta 2, alpha 1
beta 1 and b2 both do what? chronotrophy is what? inotropy?
increase HR (chronotrophy) and force of contraction (inotropy)
beta 1 - activation leads to, which hormones act on these receptors?
normal heart
- activation leads to increase in contractile force and HR
- norepinephrine and epinephrine
- renin release - aldosterone - vasoconstriction - increase in BP
beta 2 - located where, and does what? which hormones act on?
vascular and non-vascular smooth muscle
-located on: smooth muscle, GI tract, bladder, skeletal muscle, arteries, bronchial tree, some coronary arteries (increased coronary blood flow)
- epinephrine only
- and activation leads to vascular and non-vascular smooth muscle relaxation
-vasodilation of bronchioles and skeletal muscle tissue
alpha 1 - direct response. Does what and what hormones act on?
activity or muscle tone is increased
located on all vascular smooth muscle, GI and urinary sphincters, dilator muscle of the iris, arrestor pilli muscles in hair follicles (goosebumps)
norepinephrine and epi bind
norepinephrine binds with alpha 1 receptors causing smooth muscle contraction and vasoconstriction of the coronary arteries
acetylcholine receptors
PSNS - muscarinic (slows HR, decreases contractility, bronchial constriction)
nicotinic (only involved in muscle contraction, neuromuscular junction)
left circumflex artery
supplies left atrium and left ventricle
left anterior descending artery
supplies the right ventricle, left ventricle, and interventricular septum
left marginal artery
supplies the left ventricle
right marginal artery
supplies the right ventricle and the apex
right coronary artery
supplies the right atrium and the right ventricle
troponin is the most specific marker and elevates in what amount of time?
2-4 hours
zone of infection/necrosis ECG
wide QRS
zone of injury ECG
ST elevation
zone of ischemia ECG
inverted T wave
Dresseler syndrome
post infarction syndrome - delayed form of acute pericarditis; r/t antigen/antibody complexes in response to necrotic myocardium
Causes of pericarditis
viruses (coxsackie B, echovirus), bacteria, non-infectious: autoimmune, drugs, malignancy, radiation; post MI: Dressler syndrome
s/s of pericarditis
pleuritic CP, better when the pt leans forward and worse with inspiration and lying down; fever, pericardial rub with auscultation
Constrictive pericarditis (pericardium rigid and impairs filling of heart chambers) similar s/s to, and remember what sign?
heart failure
Kussmaul’s sign: increased JVP during inspiration - heart can’t stretch like it normally does during inspiration
pericardial effusion can cause what + s/s of this? what is it?
accumulation of fluid in pericardial sac
- can cause tamponade: severe restriction of cardiac motion
- fatal if not resolved
- s/s of tamponade are hypotension, increased JVP, distant heart sounds
most common valvular abnormality
aortic stenosis
aortic stenosis murmur?
systolic ejection murmur heard b/w s1 and s2 - crescendo-decrescendo murmur (softer s2)
s/s of aortic stenosis
angina, syncope, faint pulses, heart failure, carotid upstroke (less force - weakened and delayed)
causes of aortic stenosis
congenital bicuspid aortic valve, degeneration with aging, inflammatory damage caused by rheumatic heart disease; same risk factors as CAD
mitral stenosis causes what to happen to the atrium? most common cause?
results in dilation of the atrium since blood has trouble getting into the ventricle - back of blood into the lungs. Untreated will cause pulmonary HTN, Right HF
most common cause is rheumatic fever
mitral stenosis murmur
opening snap heard b/w s2 and s1 - increased atrial pressure on narrowed valve
aortic regurgitation
inability of the aortic valve to close properly during diastole
aortic regurgitation murmur & s/s
diastolic murmur b/w s2 and s1
s/s: widened pulse pressure as a result of increased stroke volume and diastolic back flow
If a murmur is diastolic it will be heart b/w
s2 and s1
mitral regurgitation - what is it and what does it cause?
permits backflow from the left ventricle into the left atrium - results in left ventricular hypertrophy because of increased volume in the left atrium entering the ventricle
mitral regurgitation murmur
systolic murmur - presence of s3 (splashing sound)
most common cause of mitral regurgitation
mitral valve prolapse and rheumatic heart disease
mitral valve prolapse - what is it? what can it cause? affected valves at increased r/f? s/s?
anterior and posterior cusps of the mitral valve billow upward (prolapse) into the atrium during systole
can cause mitral valve regurgitation
affected valves at increased r/f infective endocarditis
s/s: asymptomatic
rheumatic fever causes what kind of deposits? what is rheumatic fever
fibrinoid necrotic deposits: Aschoff bodies
RF is abnormal immune response to the M protein that cross react w/normal tissues
s/s of rheumatic fever - causes what?
carditis - murmur; polyarthritis (large joints); chorea - sudden aimless irregular involuntary movements; erythema marginatum - truncal rash
can cause STENOSIS, and is the most common cause of this (especially mitral)
Systolic heart failure results in a LVEF of what? what happens to ventricle?
LVEF <40% and ventricular remodeling/hypertrophy HFrEF
-also under left heart failure in the notes
s/s and PE findings with LHF
dyspnea, orthopnea, cough w/froth, fatigue, decreased urine output, edema, paroxysmal nocturnal dyspnea
PE: pulmonary edema (cyanosis, inspiratory crackles, pleural effusion), HYPOTENSION OR HYPERTENSION, s3 gallop d/t fluid overload (slapping), evidence of underlying CAD or HTN
Diastolic heart failure LVEF?
LVEF > 40% HFpEF
filling problem
also listed under left heart failure
- pulmonary congestion despite normal stroke volume and cardiac output or ejection fraction
- decreased compliance of left ventricle and abnormal diastolic relaxation which leads to increase in end diastolic pressure – transmitted to pulmonary circulation – causes pulmonary congestion
Right heart failure seen with? normally due to?
seen with pulmonary disease = cor pulmonale
normally due to left-sided heart failure
s/s of RHF?
pedal edema, ascites, hepatosplenomegaly, elevated JVP-JVD, sacral edema, nocturia, jaundice, coagulopathy
classes of heart failure
- Class I - no limitation of physical activity (PA)
- Class II - slight and leads to fatigue, palpitation, dyspnea, or anginal pain but person is comfortable at rest
- Class III - marked limitation of PA in which less-than-ordinary activity results in same s/s as II. Pt ok at rest.
- Class IV - inability to carry out any PA w/o symptoms of HF or the anginal syndrome even at rest, with increased discomfort if any physical activity is undertaken
staging of HF
A - high risk for HF but without structural heart disease or symptoms of HF
B- structural heart disease but w/o s/s of HF (LVH, LV dysfunction)
C- structural heart disease w/current or past symptoms of heart failure
D- refractory heart failure requiring specialized interventions (pacemaker, LVAD, tranplant)
