Heart I Flashcards
Cardiac weight in female vs male
F: 250-320gm
M: 300-360 gm
Avg. size of right and left ventricles
Rt: 0.3-0.5 cm thick
Lt: 1.3-1.5 cm
Greater than these values is hypertrophic
Hypertrophy
Dilation
Cardiomegaly
Hypertrophy: increase in ventricular thickness
Dilation: enlarged chamber size
Cardiomegaly: increased cardiac weight
How do valves generally get their nourishment?
Diffusion
3 types of valve damage and common example of each:
Collagen damage: mitral prolapse
Nodular calcification: calcific aortic stenosis
Fibrotic thickening: Rheumatic heart disease
ANP function
Promotes arterial vasodilation and activate renal salt and water elimination (naturesis and diuresis), which is beneficial in setting of HTN and CHF.
What is the normal rate of spontaneous depolarization of the SA node?
60-100 bpm
Blood supply to the myocardium (3)
LAD (and diagonal branches)
LCX (marginal branches)
RCA
When does blood flow into the myocardium?
During ventricular diastole, once the aortic valve closes.
What stem cells are in the myocardium? (2)
How much is replaces yearly?
Bone marrow derived precursors and cardiac stem cells.
About 1% yearly. Not enough to overcome necrosis.
What changes occur in the myocardium and chambers in aging? (3)
Increased LV size
Increased epicardial fat
Lipofuscin and basophilic degeneration
What changes occur in the heart valves in aging? (4)
Aortic and mitral annular calcification
Fibrous thickening
Mitral leaflets buckle -> increase in left atrium size
Lambl excrescenses
What are Lambl excrescences?
Small filiform processes that form on the closure line of aortic and mitral valves, likely from small thrombi.
What changes occur in the vasculature of the heart in aging? (2)
Coronary atherosclerosis
Stiffening of the aorta
CHF occurs when…
How can the heart meet its needs?
The heart is unable to pump blood at a rate to meet peripheral demand.
It can only meet the demand with increased filling pressure.
What might CHF result from? (2)
Loss of myocardial contractile function
Loss of ability to fill the ventricles during diastole (diastolic dysfunction)
What chamber hypertrophies in CHF?
LV
Cardiac myocytes become hypertrophic when… (2)
Sustained pressure or vol. overload (systemic HTN or aortic stenosis)
Sustained trophic signals (beta-adrenergic stimulation)
What occurs in the setting of pressure overload hypertrophy? (2)
Myocytes become thicker
LV increases in thickness concentrically
What occurs in the setting of volume overload hypertrophy? (2)
Myocytes elongate
Ventricular dilation occurs
How should heart hypertropy by measured in pressure and volume overload?
Pressure: wall thickness
Vol.: weight
Left-sided HF is most commonly a result of: (4)
Myocardial ischemia
HTN
Left-sided valve DZ
Primary myocardial DZ
Clinical effects of LSHF are due to: (2)
Pulmonary circulation congestion
Decreased tissue perfusion
What are common SX of LSHF?
Edema Cyanosis Pulmonary SX Tachycardia DOE Fatigue
What changes occur in the chambers in LSHF?
(1) LV hypertrophy
LV dysfunction leads to (2) LA dilation, which can lead to AFib, stasis and thrombus
What effect does LSHF at the kidneys? (2)
Lower EF can cause decreased glomerular perfusion -> increased renin -> increased BV. Prerenal azotemia (increased nitrogen levels)
What effect does LSHF have at the brain? (1)
Lower cerebral perfusion -> hypoxic encephalopathy
What cells are found in LSHF upon histologic exam?
HF cells = hemosiderin-laden Mo
What is the most common cause of RSHF?
LSHF
Isolated RSHF is from any cause of pulmonary HTN, for example: (3)
Parenchymal lung diseases
Primary pulmonary HTN
Pulmonary vasoconstriction
In primary RSHF, what is the big problem?
The venous system is highly congested.
This kind is much more rare than isolated RSHF.
What are complications of primary RSHF? (5)
Liver congestion (nutmeg liver) Splenic congestion -> splenomegaly Effusions involving peritoneum, pleura and pericardium LE edema Renal congestion
2 key features of CHF
Inadequate CO
Increased congestion of venous circulation
Most common genetic cause of congenital heart disease:
Trisomy 21
What do most defects arise from embryologically?
Arterioventricular spetae -> endocardial cushion
What genetic pathway is responsible for bicuspid aortic valve?
NOTCH1
What genetic pathways are responsible for Tetralogy of Fallot?
JAG1
NOTCH2
What heart defects are left-to-right shunts? (3)
ASD
VSD
PDA
*most common
ASD presention/onset
Usually asympomatic until adulthood
>30 y/o
Most common ASD is:
Where does it occur within the septum?
Secundum ASD (90%)
Center of atrial septum
Which 2 ASDs are less common?
Where do they occur within the septum?
Primum anomalie (5%) - near AV valves and may be associated with valvular abnormalities.
Sinus venosa defects (5%) - near entrance of SCV and may be associated with anomalies in venous return to RA.
Left-to-right shunting causes volume overload on the rigth side, which may lead to: (3)
Pulm HTN
RSHF
Paradoxical embolism
May be closed surgically w/ normal survival.
PFO outlook:
What is a unique problem that can occur in a PFO?
80% close by 2 y/o.
Remaining 20% have flap that can open if right sided pressure is great enough (even temporary pressure hikes can cause shunting)
Paradoxical embolus
What is the most common form of congenital heart disease?
What are the 2 subtypes?
VSD (50% of small VSDs close spontaneously)
Membranous VSD (90%) in membranous IV septum Infundibular VSD: below pulmonary valve or within muscular septum
Large VSDs can cause significant shunting which can lead to (2)
RV hypertrophy
Pulm HTN
Unclosed large VSD will ultimately lead to:
Shunt reversal, leading to cyanosis and death.
Why does a PDA remain open?
If infants are hypoxic and/or have increased pulmonary vascular pressure.
What sort of murmur accompanies PDA?
Harsh, machinery-like murmur (PDA)
Presentation of PDA
Usually ASX at birth
Isolated PDA should be:
When should it stay open? How is it done?
Closed ASAP
Should stay open in patients w/ obstruction of pulmonary or systemic outflow. Via PGE, the PDA stays open.
What shunt causes cyanosis?
R-to-L
4 cardinal features of Tetralogy of Fallot
VSD
Obstruction of RV outflow
Aorta overrides the VSD
RV hypertrophy
What malformation looks like a “boot”? Why?
ToF because of right ventricular hypertrophy
What does the clinical severity of ToF depend on?
Mild vs. classic
Subpulmonary stenosis
Mild: L to R shunt
Classic: R to L shunting w/ cyanosis
*most infants are cyanotic from birth.
Transposition of the great vessels results in:
Common features of the malformation (4)
2 separate systemic and pulmonary circulations -> incompatible w/ life.
Approx 1/3 have VSD
2/3 have PFO or PDA
RV becomes hypertrophic and LV atrophies
W/O surgery, pts. die within a few mo.
Coarctation of the Aorta w/ PDA
Infantile form
Cyanosis in lower half of body
Associated w/ Turner syndrome (XO)
Coarctation of the Aorta w/o PDA
Adult form
ASX
Claudication and cold LE
May eventually see LV hypertrophy
SX of Aortic Coarctation (3)
Murmurs throughout systole
Vibratory thrill
Concentric LVH
3 obstructive lesions
Coarctation of the Aorta
Pulmonary stenosis/atresia
Aortic stenosis/atresia
When does Eisenmenger syndrome occur?
When pressure in the pulmonary arteries becomes so high that it causes oxygen-poor blood to flow from the right to left ventricle and then to the body, leading to cyanosis.
This damages the walls of the pulmonary aa. and leads to RV hypertrophy.
Stable angina
Where is the occlusion?
SX? Relieved by?
What induces it?
Stenotic occlusion of coronary a.
Squeezing, burning sensation relieved by rest/vasodilators.
Induced by physical activity, stress.
Prinzmental variant angina is…
Relieved by:
What is it unrelated to?
Episodic coronary a. spasm.
Relieved by vasodilators.
Unrelated to activity, HR or BP.
Unstable (Crescendo) angina definition
What causes it?
What might be imminent/
Transient, often recurrent chest pain induced by myocardial ischemia insufficient to cause MI. Increases in freq., duration, and severity.
Usually rupture of atherosclerotic plaque w/ patrial thrombus.
Acute MI, as 50% have evidence of myocardial necrosis.
Classic presentation of MI
Prolonged CP (>30 min)
Diaphoresis
Dyspnea
Nausea-vomiting
25% are ASX
Times for:
Onset of ATP depletion Loss of contractility ATP reduced to 50%, 10% Irreversible cell injury Microvascular injury
Onset of ATP depletion: secs. Loss of contractility: <2 min ATP reduced to 50%: 10 min, 10%: 40 min Irreversible cell injury: 20-40 min Microvascular injury: >1 hr
Areas of infarct: LAD (40-50%) (3)
Apex
LV anterior wall
Anterior 2/3 of septum
Areas of infarct: RCA (30-40%) (3)
RV free wall
LV posterior wall
Posterior 1/3 of septum
Areas of infarct: LCX (15-20%) (1)
LV lateral wall
Ac. MI after 24 hrs (3)
Coagulative necrosis
Pyknotic nuclei
Loss of cross striation
MI after 1-3 days (2)
Loss of striations
Neutrophilic infiltration
What comes into the heart 3-4 days after MI?
What comes into the heart 7-10 days after an MI?
What comes into the heart 10 days after an MI?
PMNs: Neutrophils, eosinophils, and basophils.
Mo.
Granulation tissue
4 ways to treat an MI
Thrombolysis
Angioplasty
Stent placement
CABG
Most sensitive and specific biomarkers of myocardial damage (2)
Why?
When do each peak?
cTnT: 12-48 hrs
cTnI: max at 24 hrs
*both elevate 3-12 hrs
They are specific because they are not normally in circulation.
Where does CK exist?
Why is it less specific?
Brain, heart, skeletal muscle.
Because it is found elsewhere.
What markers peak at 24 hrs? (2)
CK-MB
cTnI
When does CK-MB return to normal?
cTnI?
cTnT?
CK-MB: 48-72 hrs
cTnI: 5-10 days
cTnT: 5-14 days
What is the most common COD of pts. w/ MI?
Arrythmias
6 major complications of MI
- Arrhythmia
- Contractile dysfunction
- Fibrinous pericarditis
- Myocardial rupture (2-4 days post MI)
- Infarct expansion
- Ventricular aneurysm
