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Flashcards in cardio (from HD1) Deck (65):

diastolic murmur

low sound heard with bell, = from mitral stenosis


S1 heart sound

= mitral and tricuspid valves closing (AV valves), normal. before carotid pulse. loudest at apex. * changes w/ leaflet mobility & rate of L ventricular riseAbnormal: short P-R interval, mitral stenosis


Forward heart failure

inability of the heart to pump blood forward sufficiently to meet metabolic demands of the body


Backward heart failure

inability of the heart to pump sufficient blood to body to meet metabolic demands EXCEPT when cardiac filling pressures are abnormally high.



ventricular wall tension at the end of diastole. = end diastolic Pressure-- if high => increased CO



degree of pressure to overcome during systole. = wall stress during systole [= (P x r)/(2 x thickness)]--> measure as systolic pressure


systolic Heart Failure

impaired ventricular contractility--> increased afterload
1. normal filling (but enlarged ventricles),
2. decreased % blood pumped out


diastolic heart failure

impaired ventricular filling;
1. stiff ventricles --> reduced filling (less volume in)
2. ~same % pumped out, but since total volume = less, still less blood out to body


concentric hypertropy

add muscle fibers in parallel, so get thick walls.can be from: - Aortic stenosis (HTN)- pulmonary stenosis (pulm. HTN)


eccentric hypertrophy

add myocyte fibers in series, so dilate chambers (walls not thicker), from: aortic insufficiency, mitral regurgitation, pulmonic insufficiency, tricuspid regurgitation, shunts


calcific aortic stenosis pathogenesis

increased LDL combines with inflammatory cells, and interacts w/ myocytes --> causes smooth muscle cell proliferation and ossification of cardiac tissue (by osteopontin).


3 possible causes of aortic stenosis

1. bicuspid stenosis
2. calcific stenosis
3. rheumatic stenosis


Left to right shunt (a congenital heart defect)

shunt of oxygenated blood into pulmonary flow, => increase pulmonary BF
ie: ventricular septal defect, atrial septal defect, patent ductus arteriosus
Long-term: pulmonary HTN (w/ sm m hypertrophy) --> SWITCH to Right-Left Shunt (BAD!)


Right to Left Shunt (congenital defects)- Problem - Causes

Problem: mix deoxygenated blood in LV, pump to systemic circ.,--> hypoxemia, cyanotic heart disease
Causes = "terrible T's"
- Transposition of the Great Vessels
- Tetralogy of Fallot
- Truncus Arteriosus


Ductus Arteriosus (normal)

in the fetus, connects RV/Pulm. artery to aorta--> shunts blood into systemic circulation bc all blood is oxygenated by mom (enters via placenta), so no need to go to lungs


Ductus-dependent Lesions (congenital)

(when ductus shunt provides most or all oxygenated blood for body) * neonatal emergency, MUST give prostaglandin E until fixed!
- transposition w/ intact septa
- aortic atresia
- interrupted aortic arch
- hypoplastic left heart


Ventricular Septal Defect (congenital)

L to R shunt, (bc LV has higher P)- Large --> heart failure @ birth; => failure to thrive bc can't meet metabolic need (from high work of breathing).- Small --> holosytolic murmur w/ mid-diastolic rumble only after 2-6 wks bc pulm. vascular resistance changes; LA & LV hypertrophy; heart failure @ 3 mo.


Atrial Septal Defect

L to R shunt btwn atria, w/ diastolic flow murmur & fixed wide splitting of S2, classic RSR' on ECG.
* may be asymptomatic in adults,
- secundum: incomplete closure of foramen ovale (gap persists)
- primum: sinus venosus defect
* flow determined by ventricular compliance


Atrioventricular canal (aka atrioventricular septal defect)

failure of endocardial cushions to fuse.
Complete = 3 problems:
- atrial septal defect
- ventricular septal defect/membranous ventricular septum
- AV valve abnormalities
** 50% of Down syndrome (trisomy 21) pts have AV canal**


"Conotruncal" abnormalities

= defects in arterial outflow tracts; cause cyanotic heart disease.
- transposition of great arteries
- truncus arteriosus
** strong connection w/ Del 22q11 syndrome**


transposition of the great arteries

defect where connections to aorta & pulmonary artery = switched
(R ventricle to aorta, L ventricle to pulmonary artery)
* NEED shunt to survive!
- 40% stable VSD
- 60% UNstable patent foramen ovale OR ductus arteriosus)
Tx: arterial switch surgery


Del 22q11 syndrome

abnormal migration of neural crest cells to neck & upper thorax; can cause conotruncal defects:
- transposition of great vessels
- tetralogy of Fallot
- Interrupted aortic arch
Also: thymic hypoplasia/aplasia, parathyroid defects


Tetralogy of Fallot (4 main features)

*most common cyanotic congenital heart defect*
problems bc displaced "infundibular" (outflow) septum;
4 features: 1. pulmonary outflow tract stenosis
2. overriding aorta
3. Ventricular septal defect (VSD)
4. R ventricular hypertrophy


Aortic Coarctation

= narrowing of the aorta, near ductus arteriosus; => infant heart failure, & BP higher in upper extremities than lower extremities
Often w/: bicuspid aortic valve, VSD (ventricular septal defect), other lesions
** some association w/ Turner's Syndrome (45 XO)


equation for calculating wall tension

wall tension = P*d/h= (systolic LV pressure x LV chamber diameter)/wall thickness


path to angina

1. ischemia
2. ATP loss
3. impaired relaxation (requires O2)
4. systolic dysfunction
5. ST depression
6. angina


variant angina ("prinzmetal")

angina @ rest, = ischemia due to coronary artery spasm;
Dx: ST elevation
Tx: nitroglycerine, beta-blockers, ASA


pathological findings of MI & their molecular causes

1. intracellular edema: low ATP production --> increased intracellular Ca2+ and extracellular K+
2. chromatin clumping: lactic acidosis (low pH)
3. PMN infiltration of tissue (= acute inflammatory response)


time intervals to tissue damage

20 minutes of ischemia: IRReversible damage
18 hrs - 4 days: coagulative --> total necrosis
2-3 weeks: fibrosis
* 3-6 weeks: healing


partial vs. complete occlusion from coronary thrombosis

- Partial: NSTEMI, w/ ST depression & T wave inversion (= subendocardial MI), OR Unstable angina
- Complete: STEMI / Q wave MI = transmural (all layers affected)


stunned myocardium

injured but not necrotic myocardial tissue that remains dysfunctional after blood flow is restored; recovers over time.
Mech: Ca2+ overload from mitochondia, ROS accumulation, or disrupted excitation coupling.


Hibernating myocardium

hypocontractile myocardium due to chronic hypOperfusion (not MI); ~immediately reversed when restore full blood flow.
ie: from severely (& chronically) atherosclerotic coronary artery


Arrhythmias due to damaged conduction

(aka: increased parasympathetic tone)
- sinus bradycardia
- junctional escape rhythm
- atrioventricular block
** these ppl need catheterization IMMEDIATELY & pacemakers**


Normal hemodynamic values (from catheterization)

R atrium: 0-6 mmHg
R ventricle: 15-30/0-6
Pulmonary a: 15-30/6-12
L atrium: 6-12
L ventricle: 100-140/6-12
Aorta: 100-140/60-80


Recommended drug treatment for Congestive Heart Failure

#1: ACE inhibitor & beta blocker * not b-blocker if volume overload
*2nd line: ARB (if can't tolerate ACE I)
3rd: Nitrates & Hydralazine combo (if can't tolerate 1st 2 options, OR esp. if african-american)


Contraindications for ACE inhibitors in CHF

* = 1st line therapy, but can't use if:
- pregnant
- renal stenosis
- asthma
- DM (only if unable to ID drops in glucemia)


causes of Dilated Cardiomyopathy (4 types)

1. familial/genetic (sarcomere proteins)
2. inflammatory (viral, sarcoidosis, peripartum, CT disorders)
3. toxic (EtOH, chemotherapy - ie: adriamycin)
4. neuromuscular


exam findings for diagnosing Hypertrophic cardiomyopathy

S4 w/ systolic murmur. * murmur: LOUDer w/ valsalva (when increase preload)


Restrictive Cardiomyopathy

rare disease of heart muscle => rigid ventricles & atria may be larger than ventricles. Caused by infiltrates into muscle fibers OR muscle tissue fibrosis. => Normal contraction, but poor filling.


Causes of Restrictive Cardiomyopathy

Infiltrates (4): amyloidosis, sarcoidosis, hemochromatosis, glycogen storage disease.
Fibrosis (3): metastatic tumors, hypereosinophilic syndrome, radiation therapy.


True Anuerysm

bulging of vessel wall involving all 3 vessel wall layers, > 50% increase in diameter.
2 types: fusiform (symmetrical) or saccular (localized)


causes of aneurysm in ascending aorta

due to cystic medial necrosis, from:
- bicuspid aortic valve
- Connective tissue disease (Marfans, Ehlers-Danlos)


False Aneurysm

Bulging of vessel wall only lined by adventitial layer--> high risk of rupture!
causes: infection, trauma


Key observation to Dx ductal-dependent coarctation of the aorta

systolic BP in legs LOWER than in arms (when supine)[should be same or higher if healthy]


transposition of great vessels vs. Tetralogy of Fallot

Transposition: cyanotic RIGHT AWAY at birth, no murmur usually, "Big blue, happy tachypnic newborn," w/ cardiomegaly.
Tetralogy: cyanotic 1 month AFTER birth,


Leads showing INFERIOR MI

ST-elevation: II, III, aVFreciprocal: aVL


Leads showing LATERAL MI

St elevation: I, aVL (also V5, V6)reciprocal: II, III, aVF


leads showing SEPTAL MI

ST elevation: V1, V2


leads showing ANTERIOR MI

ST elevation: V4, V5* often w/ V-fib (common complication)


leads showing POSTERIOR MI

reciprocal change (ST depression): V1-V4* "carousel" shaped pattern


possible causes of S2 splitting

- Variable splitting, w/ inspiration: physiologic, RBBB, pulmonary stenosis
- Fixed wide splitting: atrial septal defect
- Variable reversed splitting ("paradoxical"): LBBB, LV failure, HTN


midsystolic click indicates

systolic mitral valve prolapse,
* later w/ increased LV volume.


causes of S3 & S4

S3 = early rapid filling
S4 = vigorous atrial contraction


cause of opening snap

rheumatic mitral stenosis.


innocent flow murmur

twangy, crescendo-decrescendo systolic murmur; from high flow through normal valves.


P wave > 2.5 in lead II

Right atrial enlargement


prolonged P wave on ECG (> 1 mm, negative @ end)

Left atrial enlargement, P wave changes = in lead I, changes = early and negative


typical ABG results for pneumonia

Low V/Q --> hypoxemia due to focal shunt. * may have increased PaCO2 if severe lung damage.


obstructive disease PFT

FEV1/FVC < LLN = obstructive disease
* high RV & often high TLC (bc air trapping)!
= slow emptying (bc decreased elastic recoil)
ie: asthma, COPD, upper airway obstruction


PFT for restrictive disease

TLC < 80% predicted w/ symmetrically low RV (not if just poor effort)
(also often low FVC and high FEV1/FVC).
ie: interstitial lung disease, pulmonary fibrosis


Variable Extrathoracic Upper airway obstruction

when tracheal P < atmospheric P w/ Inspiration (only, not expiration) --> trachea narrows. ==> reduced INspiratory limb (bottom) on Flow volume loop
ie: laryngeal tumor


Obstructive vs. Restrictive Flow Volume Loops

Obstructive: scooped out expiratory limb, otherwise normal shape
Restrictive: small, squished loop (shorter & earlier on horizontal axis)


Variable Intrathoracic Upper Airway obstruction

when pleural P > tracheal P => trachea narrows. ==> reduced EXpiratory limb (top) on Flow Volume Loop


Fixed Upper Airway obstruction

BOTH INspiratory & EXpiratory limbs reduced on flow volume loop(could be intrathoracic or extrathoracic)


measuring RV (residual volume) of lung

* cannot measure directly bc RV = volume left after maximal expiration!
==> RV = FRC - ERV(ERV = expiratory reserve volume)