Heart Pt. 1 Flashcards
What is hypertrophy?
increase in ventricular thickness
What is heart dilation?
enlarged chanber size
What is cardiomegaly?
increase in cardiac wt
What does Atrial Natriuretic Peptide do?
stimulates renal salt and water elimination (natriuresis and diuresis)
* beneficial in setting with HTN and CHF!
What are the 3 types of cardiac damage mentioned, and give their example
- collagen: mitral prolapse
- nodular calcification: calcific aortic stenosis
- fibrotic thickening: rheumatic heart dz
What starts ventricular diastole?
closing of the aortic valve, leading to blood flow to myocardium thru coronary vessels
What is lipofiscin?
wear and tear on heart leaves yellow/brown lipid deposits in the myocardium
What is the danger with mitral valve calcification?
it can affect electrical signaling
What are Llambl excrescences?
small filliform processes that form on the closure lies of the aortic and mitral valves, most likely resulting from the organization of small thrombi
What is basophilic degeneration?
pathologic blue staining of connective tissue on H&E stain
What is pump failure?
- weak myocardium contraction during systole leads to inadequate CO
- myocardium may relax insufficiently during diastole to permit adequate ventricular filling
What is flow obstruction?
lesions obstructing blood flow through a vessel (atherosclerotic plaque) that prevent valve opening, or cause increased ventricular chamber pressure
What is regurgitant flow?
portion of the output from each contraction flows backward through an incompetent valve, adding volume overload to the affected atria or ventricles
What is shunted flow?
blood can be diverted from one part of the heart to another thru defects that can be congenital or acquired
NOTE: can also occur between blood vessels
What is cardiac exsanguination?
the loss of enough blood to cause cardiac death
When does CHF occur?
when the heart is unable to pump blood at a rate to meet peripheral demand, or can only do so with increased filling pressure
What causes CHF?
may result from
- loss of contractile function (systolic dysfunction)
- loss of ability to fill the ventricles during diastole
What causes cardiac myocytes to become hypertrophic?
- sustained pressure or volume overload (systemic HTN or aortic stenosis)
- sustained trophic signals (beta-adrenergic stimulation)
What does pressure overload hypertrophy lead to?
myocytes become thicker, LV increases in thickness concentrically
What does volume over load hypertrophy lead to?
myocytes elongate and ventricular dilation seen
What is the best way to measure cardiac hypertrophy?
heart weight (rather than wall thickness)
Why the the hypertrophied heart vulnerable to ischemia-related decompensation?
because myocyte hypertrophy is NOT accompanied by a matching increase in blood supply, despite the increase in energy demand
What are the 4 most common causes of left-sided heart failure?
- myocardial ischemia
- HTN
- left-sided valve disease
- primary myocardial disease
What causes clinical effects of left-sided heart failure?
- pulmonary circulation congestion
- decrease in tissue perfusion
What are the symptoms of pulmonary congestion?
- cough
- crackles
- wheezes
- blood-tinged sputum
- tachypnea
What is the histological hallmark of left-sided heart failure?
heart failure cells! aka hemosiderin-laden macrophages
What does left ventricular dysfunction lead to?
left atrial dilation, which can cause atrial fibrillation, stasis, or thrombus
What does decreased ejection fraction lead to?
decreased glomerular perfusion
- stimulates renin release -> increased fluid volume
What is prerenal azotemia?
aka prerenal failure
- when excess nitrogen compounds in the blood due to lack of blood flow to the kidneys
What can advanced CHF lead to?
decreased cerebral perfusion (hypoxic encephalopathy)
What is the most common cause of right-sided heart failure?
LEFT-SIDED HEART FAILURE
What are the 3 main causes of isolated right sided-heart failure?
- parenchymal lung disease
- primary pulmonary HTN
- pulmonary vasoconstriction
What is congested in primary right-sided failure?
the venous system!
- pulmonary congestion is minimal
What is seen in primary right-sided failure?
- nutmeg liver
- splenic congestion -> splenomegaly
- peritoneal, pleural and pericardial effusions
- peripheral edema
- renal congestion
When do you see congestion of venous circulation?
when there is inadequate cardiac output (CHF)
What is the most common cause of left-sided heart failure?
ischemic heart disease, systemic HTN, mitral or aortic valve disease, and primary diseases of the myocardium
What are the symptoms of right heart failure related to?
peripheral edema and visceral congestion
What are the major known causes of congenital heart disease?
sporadic genetic abnormalities!
- Turner syndrome, trisomies 13, 18, 21
What is the single most common genetic cause of congenital heart disease?
trisomy 21**- 40% of Down syndrome pts have at least one heart defect
What are the most common heart defects in Trisomy 21?
defects of the endocardial cushion
- ostium primum, ASDs, AV valve malformations, VSDs
What is the Notch pathway associated with?
a variety of congenital heart defects, including bicuspid aortic valve (NOTCH1) and tetralogy of Fallot (JAG1 and NOTCH2)
What are Fibrillin mutations associated with?
valvular defects and aortic aneurysms
What is the most common congenital cardiac malformation?
ventricular septal defect (90%)
What causes CHARGE syndrome? What are the effects?
helicase-binding protein defect (CHD7 gene)
- ASD, VSD, PDA, hypoplastic right side of the heart
What causes DiGeorge syndrome? What are the effects?
transcription factor defect (TBX1 gene)
- ASD, VSD, or outflow tract obstruction
What are the common congenital left-to-right shunts?
ASD: increases RV and pulmonary outflow volumes
VSD, PDA: increase pulmonary blood flow and pressure
Which type of heart defect can go unnoticed until adulthood?
atrial septal defect
What is secundum ASD?
90% of all ASDs, center of atrial septum, may be multiple or fenestrated
What is primum anomalie?
5% of all ASDs, near entrance of SVD (single ventricle defect), can be associated with anomalous pulmonary venous return to the R atrium
What is TAPVR?
total anomalous pulmonary venous return
- rare congenital malformation in which all four pulmonary veins do not connect normally to the left atrium
- instead the four pulmonary veins drain abnormally to the right atrium
What does left-to-right shunting cause? What does it lead to?
volume overload on the right side, which may lead to
- pulmonary HTN
- right heart failure
- paradoxical embolization (patent foramen ovale)
What will an increase in right sided pressure do to a PFO?
the flap can open, producing brief periods of R-L shunting, which can lead to a paradoxical embolus
What is an infundibular VSD?
below the pulmonary valve, within muscular septum
What can large VSDs lead to?
- right ventricular hypertrophy
- pulmonary HTN
- unclosed large VSD can ultimately result in shunt reversal, leading to cyanosis and death
What kind of murmur does a PDA produce?
harsh, machinery-like murmur
- usually asymptomatic at birth
- initially left-to-right, so NO CYANOSIS
What can saving in infants with obstruction of pulmonary or systemic outflow?
Prostaglandin E
What is the most common Right-to-Left shunt? Other examples?
- *Tetralogy of Fallot**
- transposition of the great arteries
- persistent truncus arteriosus
- tricuspid atresia
- total anomalous pulmonary venous connection
NOTE: q’s often mention third world country, because these shunts are repaired very early in US
What type of shunt causes cyanosis in early postnatal life?
right-to-left shunts
What are the four cardinal features of Tetralogy of Fallot?
- VSD
- obstruction of RV outflow tract
- aorta overrides VSD
- RV hypertrophy
When would you see an enlarged, “boot-shaped” heart?
Tetralogy of Fallot
- because RV hypertrophy
What is the classic presentation of Tetralogy of Fallot?
right-to-left shunting with cyanosis***
- most infants cyanotic from birth
What does Transposition of the great vessels (TGA) result in?
two separate systemic and pulmonary circulations
- incompatible with life after birth unless a shunt is present (mixing blood from the two circulations)
- 1/3 have a VSD
- 2/3 have PDA or PFO
- RV becomes hypertrophic, LV atrophies
What does Coarctation of the Aorta cause?
narrowing of the aorta, generally seen with a PDA (infantile) or without (adult form)
When do you see coarctation of the aorta?
2x males > females, TURNER SYNDROME**
What causes cyanosis in the lower half of the body?
coarctation of the aorta with PDA, manifests at birth
What are the symptoms of coarctation without PDA?
usually asymptomatic at brith…
- HTN in upper extremities, hypotension in lower extremities
- claudication and cold LE***
- may eventually see concentric LV hypertrophy
- enlarged mammary arteries “notching” on undersurface of ribs
What is Eisenmenger syndrome?
VSD causes increased blood flow to pulmonary arteries
- eventually pressure in pulmonary arteries becomes so high that it causes oxygen-poor blood to flow from right to left ventricles
What does ischemic heart disease result from?
insufficient perfusion to meet metabolic demands of the myocardium
What can ischemic heart disease lead to?
- MI
- angina pectoris
- chronic ischemic heart disease, with heart failure
- sudden cardiac death
What is the leading cause of death in the US? What are 90% of cases secondary to?
ischemic heart disease
- atherosclerosis (chronic vascular occlusion, thrombus)
What is angina pectoris?
transient, often recurrent chest pain induced by myocardial ischemia
What are the 3 clinical variants of angina?
- stable angina
- prinzmetal “variant” angina
- unstable “crescendo” angina
What is stable angina?
stenotic occlusion of coronary artery
- “squeezing” or burning sensation, releived by rest of vasodilators
- induced by physical activity, stress
What is prinzmetal “variant” angina?
episodic coronary artery spasm, relieved with vasodilators
- unrelated to physical activity, HR or BP
What is unstable “crescendo” angina?
pain that increases in frequency, duration and severity, at progressively lower levels of physical activity, eventually even at rest
- usually caused by a rupture of atherosclerotic plaque, with partial thrombus
- 50% may have evidence of myocardial necrosis, acute MI may be imminent**
What causes 90% of myocardial infarctions? What are other causes?
atheromatous plaques**
- embolus
- vasospasm
- ischemia secondary to vasculitis, shock, hematologic abnormalities
What is the classic presentation of an MI?
in men: prolonged chest pain (>30mins)
- crushing, stabbing, squeezing, tightness
- radiating down left arm or left jaw
- diaphoresis*
- dyspnea
- nausea, vomiting
What is the timeline of irreversible cell injury following MI?
20-40 mins
What is the timeline of microvascular injury following MI?
> 1 hr
What are the major coronary arteries affected by MI?
- LAD (40-50%)
- RCA (30-40%)
- L circumflex (15-20%)
What areas of the heart would an occlusion of LAD affect?
apex, LV anterior wall, anterior two thirds of septum
What areas of the heart would an occlusion of RCA affect?
RV free wall, LV posterior wall, posterior two thirds of septum
What area of the heart would an occlusion of L circumflex artery affect?
LV lateral wall
What do you see 4-12 hours after irreversible cardiac injury?
early coagulation necrosis, edema, hemorrhage
What do you see 12-24 hours after irreversible cardiac injury?
- dark mottling
- myocyte hypereosinophilia**
- contraction band necrosis
- early neutrophilic infiltrate**
What do you see 7-10 days after irreversible cardiac injury?
maximally yellow-tan and soft tissue, with depressed red-tan margins
- well developed phagocytosis of dead cells
- granulation tissue at margins
What do you see 3-7 days after irreversible cardiac injury?
hyperemic border, central yellow-tan softening
- dying neutrophils, early phagocytosis of dead cells by macrophages** at infarct border
What do you see 10-14 days after irreversible cardiac injury?
red-gray depressed infarct borders
- well-established granulation tissue with new blood vessels and collagen deposition
What do you see 24 hours after acute MI?
- coagulative necrosis
- pyknotic nuclei
- loss of cross striations
What do you see 1-3 days post MI?
- loss of striations
- neutrophilic infiltration
What is granulation tissue considered?
part of the healing process
What is reperfusion?
restoring blood flow to an area of ischemia and impending infarction
- an attempt to limit the infarct size by rescuing at risk myocardium
What is seen histologically in a reperfusion injury?
- contraction bands
- loss of striations
- different coloration
What is the first mycoyte protein to peak following MI?
myoglobin (peaks 4-6 hours after injury)
- levels drop quickly after peak
What is the second myocyte protein to peak following MI?
CK-MB (peaks 16-20 hours after injury)
- not as specific
When do Troponin levels peak following MI?
approx 24 hours post MI
What are the most useful myocyte proteins to measure post MI?
Troponin T and Troponin I (cTnT, cTnI)
What are the most sensitive and specific biomarkers of myocardial damage? Why
cTnT and cTnI
- because they are not normally detectable in circulation
When do troponin levels begin to rise post MI?
3-12 hours
When do cTnT and cTnI levels peak?
cTnT: 12-48 hours
cTnI: maximal at 24 hours
Why is creatine kinase-MB (CK-MB) sensitive, but not specific to MIs?
MB heterodimers are found in skeletal muscle as well as cardiac muscle, so they can be elevated after skeletal muscle injury
When do CK-MB levels rise?
they begin to rise within 3-12 hours post MI, peak at 24 hours, and return to normal within 48-72 hours
What is the most common complication from an MI?
arrhythmias
- half of all MI deaths occur within 1 hour of onset, usually secondary to an arrhythmia
What causes an arrhythmia?
they can result from permanent damage to the conducting system, or from myocardial “irritability”
What are other complications of an MI?
- contractile dysfunction (depends on size of infarct and associated loss of function)
- fibrinous pericarditis (bread and butter pericarditis)
What is myocardial rupture? What are the risk factors?
- typically required a transmural infarct
- 2-4 days post MI, when inflammation and necrosis have weakened the wall
Risk factors: age, large transmural anterior MI, absence of LV hypertrophy
What is a ventricular aneurysm?
- late complication of large transmural infarct with early expansion
- composed of thinned/scarred myocardium
- also associated with mural thrombus (that attach to wall of chamber)
