-
what encloses the heart and roots of the great vessels
a fibroserous sac called the pericardium
-
the inner serosal layer that adheres to the external wall of the heart is known as the what
visceral pericardium
-
what does the pericardium attach to
sternum and mediatstinal portions of the R and L pleura
-
this is shaped by the R atrium and ventricle
anterior surface of the heart (the L atrium and ventricle lie more posterior so contributes only to a small tip of the anterior)
-
this is shaped by both ventricles (mainly the left)
inferior surface of the heart
-
which area of the heart lies on the diaphragm
inferior surface (diaphragmatic surface)
-
what are the 2 basic rules of normal cardiac anatomy
- 1) right sided structures lie mostly anterior to their left sided counterparts
- 2) atrial chambers are located mostly to the right of their corresponding ventricles
-
what lines the heart valves and interior surface of the chambers
a single layer of endothelia cells (endocardium)
-
which parasympathetic nerved innervates the heart and great vessels
vagus nerve
-
explain S1 and where it is best heard
it is best heard at the apex (listening for closure of mitral valve)
S1= systole and the aortic and pulmonic are open and mitral and tricuspid are closed
-
explain S2 and where it is best heard
best heard at the base
S2= diastole and the aortic and pulmonic are closed and the mitral and tricuspid are open
-
why would you have an accentuated S1
- shortened PRI (WPW)
- mild mitral stenosis
- increased cardiac output or tachycardia
- (ie: exercise or anemia)
-
why would you have a diminished S1
- prolonged PRI= 1st degree heart block
- mitral regurgitation
- severe mitral stenosis
- "stiff" left ventricle
-
explain a widened S2 split and what causes it
RBBB or stenotic pulmonic valve
there is a delayed closure of the pulmonic valve
-
what is the common cause of a fixed S2 split
ASD
-
explain a paradoxical S2 spilt and what is the most common cause
it is the delayed closure of the aortic valve, heard best with expiration
LBBB is the main cause
-
when is a physiological S2 split heard
on inspiration
-
explain the pathophys behind an ejection click
presence of aortic or pulmonic valve stenosis or dilation of the pulmonary artery or aorta
the sound occurs as the valve reaches max accent into the great vessels and reaches elastic limit and the decelerates rapidly
-
where is an aortic ejection click heard best and how does it differ from a pulmonic ejection click
heard at both base and apex
DOES NOT VARY WITH INSPIRATION
-
where is a pulmonic ejection click best heard and how does it differ from an aortic click
heard only at base
INTENSITY DIMINISHES DURING INSPIRATION
-
an opening snap is heard with what and what is this usually associated with
mitral or tricuspid stenosis
*rheumatic heart dz
-
explain the "a" wave in the cardiac cycle
it represents transient venous distention caused by back pressure from RA contraction
-
what does the "c" wave represent in the cardiac cycle
a small rise in atrial pressure as the tricuspid and mitral valves close and bulge into their respective atria
-
what does the "v" wave represent in the cardiac cycle
it is a result of passive filling of the RA from the systemic veins during systole, when the tricuspid is closed
-
the faster the heart beat, the shorter the ______ phase
diastolic
-
what is an easily obtainable way to measure the right heart function
JVP
-
what does the "y" mean in the cardiac cycle
a fall in RA pressure due to filling of the ventricle
-
if you see a prominent "a" in the cardiac cycle, what could be the etiologies (pg 31)
RVH, TS
-
if you see a prominent "v" in the cardiac cycle, what could be the etiology (pg 31)
TR
-
if you see a prominent "y" in the cardiac cycle, what could be the etiology
constrictive pericarditis
-
what is a normal JVP measurement
≤ 9cm
-
why wouldn't you use the external jugular vein to measure JVP
because it contains valves that interfere with venous return to the heart
-
why would you hear a split between the closure of the mitral and tricuspid valves, where there is a delay in closure of the tricuspid (pg 32)
RBBB
-
what are the 3 factors that determine the intensity of S1
- 1) the distance separating the leaflets of the open valves at the onset of ventricular contraction
- 2) the mobility of the leaflets (normal, or rigid because of stenosis)
- 3) the rate of rise of ventricular pressure
-
this is heard when the PR interval is shorter than normal because the valve leaflets do not have sufficient time to drift back together and are therefore shut from a relatively wide distance
accentuated S1
-
what determines the intensity of S2
it depends on the velocity of blood coursing back toward the valves from the aorta and pulmonary artery after the completion of ventricular contraction, and the suddenness with which that motion is arrested by the closing valves
-
what would cause an accentuated S2
in systemic or pulmonary HTN, the diastolic pressure in the respective artery is higher than normal, such that the velocity of the blood surging toward the valve is elevated
-
what will cause a diminished S2
severe aortic or pulmonic valve stenosis
-
what is the cause of an S3 heart sound in a middle-aged or older adult
it indicated volume overload owing to CHF, or increased transvalvular flow that accompanies advanced mitral or tricuspid regurgitation
-
if there is an S4 heart sound, when does it occur and what does it coincide with
it occurs in late diastole and it coincides with contraction of the atria (atrial kick)
-
what is the etiology behind an S4 heart sound
it specifically indicates a decreased ventricular compliance which typically results from ventricular hypertrophy or myocardial ischemia
-
what is the hallmark sign of constrictive pericarditis (pg 38)
the abrupt cessation of ventricular filling in early diastole which is known as the pericardial knock
-
what grade is a systolic murmur that is barely audible
1/6
-
what grade is a systolic murmur that is faint but immediately audible
2/6
-
what grade is a systolic murmur is easily heard
3/6
-
what grade is a systolic murmur easily heard and associated with a palpable thrill
4/6
-
what grade is a systolic murmur that is very loud; heard with a stethoscope lightly on the chest
5/6
-
what grade is a systolic murmur that is audible without the stethoscope directly on the chest wall
6/6
-
what grade is a diastolic murmur that is barely audible
1/4
-
what grade is a diastolic murmur that is faint but immediately audible
2/4
-
what grade is a diastolic murmur that is easily heard
3/4
-
what grade is a diastolic murmur that is very loud
4/4
-
a systolic ejection murmur is typical of what
aortic or pulmonic valve stenosis
-
what is the "shape" of the systolic ejection murmur
crescendo- decrescendo type
-
what are the causes of pansystolic murmurs
- mitral regurgitation
- tricuspid regurgitation
- VSD
-
what are the reasons for a late systolic murmur
mitral valve prolapse
-
this murmur is heard best at the apex and is a high pitched and "blowing" in quality, it often radiates to the L axilla (pg 41)
pansystolic murmur of advanced mitral regurgitation
-
this murmur is best heard at the fourth to sixth left intercostal spaces, is high pitched, and may be associated with a thrill (pg 41)
VSD
-
which radiological study is performed when greater structural detail is required (pg 50)
transesophageal imaging
-
which type of study evaluates blood flow direction and velocity and turbulence. It also permits estimation of pressure gradients within the heart and great vessels
Doppler imaging
-
this imaging is particularly helpful in the assessment of aortic and atrial abnormalities, conditions that are less well visualized by conventional transthoracic echo imaging
transesophageal echocardiography (TEE)
-
this is the most sensitive noninvasive technique for evaluating perivalvular leaks (pg 54)
transesophageal echocardiography (TEE)
-
this imaging study is highly sensitive for the detection of abnormal intracardiac shunts (pg 55)
contrast echocardiogram
-
to measure pressures in the right atrium, right ventricle, and pulmonary artery, a catheter is usually inserted through which veins
femoral, brachial, or jugular vein
-
pressures in the aorta and left ventricle are measured via the catheters into which arteries (pg 61)
brachial or femoral
-
the pulmonary capillary wedge is a direct measurement of what
it reflects the left atrial pressure
-
why would you see a cannon "a" wave
- JVP due to tricuspid stenosis
- 3rd degree heart block (AV node dissociation)
-
what are the etiologies of an increased pulmonary artery wedge pressure
- left-sided CHF
- mitral stenosis or regurgitation
- cardiac tamponade
-
what causes a pulmonary artery wedge pressure "a" wave
LVH
-
what causes a pulmonary artery wedge pressure "v" wave
- mitral regurgitation
- ventricular septal defect
-
what is the non-invasive study of choice that gives you the highest precise indirect measurement of the ejection fraction
MUGA
-
what is the leading cause of mortality and morbidity in the developed world
atherosclerosis
-
what are the 3 layers of the arterial wall
- intima- closest to the arterial lumen
- media- middle layer
- adventitia- outer layer
-
what are some key components that contribute to the atherosclerotic inflammatory process (pg 121)
- 1) endothelial dysfunction
- 2) accumulation of lipids within the intima
- 3) recruitment of leukocytes and smooth muscle cells to the vessel wall
- 4) formation of foam cells
- 5) deposition of extracellular matrix
-
what are the 3 pathological states of atherosclerosis
- 1) fatty streak
- 2) plaque progression
- 3) plaque disruption
-
what is the earliest visible lesion of atherosclerosis
fatty streak
-
this is known as an endogenous vasodilator, an inhibitor of platelet aggregation, and anti-inflammatory substance
nitric oxide (NO)
-
what is the key step in atherogenesis
recruitment of leukocytes to the vessel wall
-
what are the modifiable risk factors for atherosclerosis (pg 132)
- aberrant levels of circulating lipids (dyslipidemia)
- tobacco smoking
- HTN
- DM
- lack of physical activity and obesity
-
what are the major nonmodifiable risk factors for atherosclerosis (pg 132)
- advanced age
- male gender
- heredity
-
what are the major groups of lipid altering agents
- HMG-CoA reductase inhibitors (statins)
- niacin
- fibric acid derivatives
- bile-acid binding agents
-
what are the most effective agents to lower LDL
HMG-CoA reductase inhibitors
-
what are the coronary artery dz risk equivalents
-
which 2 disorders are predisposed to increased TG
-
how long does it take for ventricular remodeling in a transmural infarct
7+ days
-
which imaging study can be used to dx the presence of CAD
stress echo (sees ischemia)
-
what is the most common cause of secondary HTN
chronic kidney disease (CKD)
-
why would you have isolated increased diastolic HTN
hypothyroidism
-
what is the most common cause of a compensatory pause
PAC
-
what can be the cause of a bisferiens pulse
aortic regurgitation
-
what is the class drug of choice for isolated TG >500
fibrates
-
what is the most common cause of a SVT
AVNRT (WPW)
-
what has been identified as an independent risk factor for CAD (pg 138)
Lipoprotein (a)
-
what is the leading cause of death in industrialized nations (pg 141)
ischemic heart dz
-
what is the most common manifestation of ischemic heart dz
angina pectoralis
-
the supply of oxygen to the myocardium depends on the ______ content of the blood and the rate of ______ ______ flow
-
when does the predominance of coronary perfusion take place
diastole
-
perfusion pressure of the coronary arteries can be approximated by what
aortic diastolic pressure
-
these issues can decrease the aortic diastolic pressure which can lead to decreased coronary artery perfusion pressure and may impair myocardial oxygen supply
- HoTN
- aortic valve regurgitation
-
what is a reason why the subendocardium is the region most vulnerable to ischemic damage (pg 143)
when the myocardium contracts, the subendocardium, adjacent to the high intravascular pressure, is subjected to greater force than are the outer muscle layers
-
any additional oxygen requirement of the heart must be met by what and what controls this
- an increase in blood
- autoregulation of coronary vascular resistance is the most important mediator
-
this is a potent vasodilator and is thought to be the prime metabolic mediator of vascular tone
adenosine
-
when adenosine binds to receptors on vascular smooth muscle, what occurs
it decreases calcium entry into cells which leads to relaxation, vasodilation, and increased coronary blood flow
-
what are the 3 major determinants of myocardial oxygen demand
- 1) ventricular wall stress
- 2) heart rate
- 3) contractility (also known as inotropic state)
-
in Laplace's law, the ventricle wall stress is directly proportional to what
systolic ventricular pressure
-
in Laplace's law, ventricle wall stress is inversely proportional to what
ventricular wall thickness because the force is spread over a greater muscle mass
-
this refers to tissue that, after suffering a period of severe ischemia (but not necrosis), demonstrates prolonged systolic dysfunction even after the return of normal myocardial blood flow
stunned myocardium
-
this refers to the tissue that manifests chronic ventricular contractile dysfunction in the face of a persistently reduced blood supply, usually because of multivessel CAD
hibernating myocardium
-
what refers to pts with typical symptoms of angina pectoralis who have no evidence of significant atherosclerotic coronary stenosis on coronary angiograms
syndrome X
-
what is the sign called for when a pt puts a clenched fist over his/her sternum as if defining the constriction discomfort by that tight group
Levine sign
-
when is a stress test considered markedly positive for severe ischemic heart disease
- 1) ischemic ECG changes develop in the first 3 minutes of exercise or persist 5 minutes after exercise has stopped
- 2) the magnitude of the ST segment depressions in >2mm
- 3) SBP decreases during exercise
- 4) high grade ventricular arrhythmias develop
- 5) pt cant exercise for at least 2 minutes because of cardiopulmonary limitations
-
what pharmacologic agents are used in a stress test for pts who can not exercise
- dobutamine
- dipyridamile
- adenosine
-
what medicatinos are used to decrease the cardiac workload and increase myocardial perfusion
- organic nitrates
- B-blockers
- CCB
-
which CCBs are potent vasodilators
nifedipine and amlodipine
-
which medication has been shown to decrease the frequency of angina episodes and improve exercise capacity in pts with CAD but differs from other anti-ischemic drugs in that it does NOT affect the HR or BP
ranolazine
-
what is the typical cause of unstable angina and NSTEMI
partially occlusive thrombus
-
this causes more severe ischemia and a larger amount of necrosis, manifesting as a STEMI
thrombus completely obstructing the coronary artery
-
this type of infarct spans the entire thickness of the myocardium and result from total, prolonged occlusion of an epicardial coronary artery
transmural infarct
-
this type of infarct exclusively involves the innermost layers of the myocardium
subendocardial infarct
-
how long does it take for irreversible cell injury in a transmural infarct
20-24 min
-
how long does it take for wavy myofibers to form in a transmural infarct
1-3 hrs
-
how long does it take for coagulation necrosis, edema in a transmural infarct
18-24 hrs
-
how long does it take for tissue necrosis in a transmural infarct
12-18 hrs
-
when does ventricular remodeling start to occur
7+ days
-
when is fibrosis and scarring complete in a transmural infarct
7 weeks
-
how long do troponin levels stay elevated
10-14 days
-
what are the preferred serum markers to detect myocardial necrosis
troponins
-
when do troponin markers peak after the onset of the MI
18-36 hours
-
when do CK-MB markers peak after the onset of the MI
24 hrs
-
how long do CK-MB markers stay elevated
48-72 hrs
-
what is the management for a STEMI (reperfusion approach, pg 184)
- ASA
- Heparin (UFH or LMWH)
- clopidogrel
- reperfusion method:
- - fibrinolytic drug (tnk/tpa)
- - primary PCI (with GPIIb/IIIa inhibitor)
-
what is the management for a STEMI in all pts
- 1) anti-ischemic medications
- - B-blockers
- - nitrates
- - +/- CCB
- 2) general measures
- - oxygen (<95%)
- - pain control (morphine)
- 3) additional therapies
- - ACE inhibitors
- - statin
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