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97 Cards in this Set

  • Front
  • Back
delta P / flow (Q) = 8n x Length/pie r^4
n= eta or viscosity

Q = dP/R
S3 - end of rapid ventricular filling - or dilated CHF -
It is caused by the sudden slowing of blood rushing in from the atrium into the ventricle as it is relaxing.
Stiffened and dilated ventricular walls
atrial kick, hypertrophic ventricle
a wave
c wave
v wave
a wave - atrial contraction (S4)
c wave - RV contraction and bulging in of the tricuspid valve
v wave - incr in atria press due to filling against a closed tricuspid
all three are in relation to the jugalar venous pulse (or RA pulse)
calcium induced ca rls
extracell ca++ enters cell during plateau of AP and stim Ca++ rls from cardiac muscle SR
aka - Compliance - the inverse of elastance
C = V/P
Capacitance arteries and age
decreases with age as teh art become stiffer and less distensible.
leads to increased pulse press
Pulse pressure
Systolic P - diastolic P = PP
largest determinant of PP is SV - because diastolic P remains relatively unchanged during ventricular systole.
MAP = 1/3 systolic P + 2/3 diastolic P

MAP = 1/3 PP + 2/3 DP
Pulmonary Wedge Press
LA pressure. Catheter inserted into the smallest branches of the pulm artery which makes almost direct contact with the pulm capillaries. Will be slightly higher than LA pressure.
PR interval
depends on conduction velocity through the AV node.
PR interval decr with incr HR
ST segment
end of S to the beginning of T waves.

Should be isoelectric because the ventricles are depolarized.
T wave
ventricular repol.
Action Potential duration
Long duration in non nodal areas - longest in Purkinje - 300ms
Conduction Velocity
time needed for excitation to spread
Size of inwd current during the upstroke of AP determines conduction velocity (slope of phase 0).
Slowest in AV node
Fastest in Purkinje fibers
Chronotropic vs Dromotropic Effect
Negative chronotropic effect:
decr HR by decr rate of phase 4 by slowing Na If current. SA node
Negative Dromotropic Effect:
decr conduction velocity though AV node increases PR interval.
Decr inwd Ca++ (phase 0), and incr inwd K+ current.
AV node.
Length of PR segment
nl <200msec
nl < 120msec
U wave
occurs after t wave - inverted
caused by hypokalemia
Mobitz type 1
2nd degree heart block
progressive lengthening of PR until a QRS is dropped.
usually AXS
Mobitz type 2
2nd degree block
Dropped beats that are not proceeded by a change in the length of the PR interval.
Abrupt nonconducted P wave is pathological.
Often 2:1 can progress to 3rd degree block
Carotid Massage
Influences carotid baroreceptors (cn 9) by stretching them leading to incr firing leading to incr Psym and decr Sym stimulation.
Chemoreceptors central vs peripheral
Carotid and aortic bodies
Periph - respond to pO2 (<60mmHg), pCO2 and pH.
Central - responds to pCO2 and pH
responsible for cushing rxn.
Cushing Reflex
The increased systemic blood preasure stimulates the carotid baroreceptors, causing a reflex parasympathetic response causing the bradycardia.

The Cushing reflex is usually seen in the terminal stages of an acute head injury. It is a sign of impending brainstem herniation due to raised ICP.
* response to cerebral ischemia and incr intracranial press.
HTN and Bradycardia
Atrial response to decr BP
atrial receptors respond to decr volume or press by causing ADH rls from post pit.
Potent Vasoconstrictor - incr TPR via V1 rec on arterioles
Water reabsorption V2 rec on distal tubules and collecting duct.
atrial response to incr atrial press
relaxes vasc smooth muscle
incr excretion of salt and H20 by kids
inhibits renin secr
Swan Ganz cat
measures pulm wedge press -
basically equals LA press
Net fluid flow in capillaries
Pnet x Kf

net pressure times the filtration constant (cap permeability)
R->L shunt
Early cyanosis
1. Tetrology of Fallot
2. Transposition of great vessels
3. Truncus Arteriosis
Children squat to incr venous return
L->R shunt
Late Cyanosis
1. VSD
2. PDA (loud S1, fixed split S2)
3. PDA

late eisenmengers - reversal of shunt due to Pulm HTN
Tet of Fallot
R-> L shunt
boot shaped heart bc of RVH
Caused by anterosuperior discplacement of infundibular septum.
How do you maintain patency?
fetally a nl R->L shunt. In neonatal period pulm vasc resistance decr reversing shunt - L->R --> RVH and failure.
Continuous machinery like murmur
Keep patency via PGE synth and low O2 tension.
Cardiac abnl
Abnl Facies
Thymic Aplasia
Cleft palate
Hypocalcemia - (bc of hypoPTH)
Congenital cardiac abnl
Congenital rubella
Offspring of DM mom
Digeorge - truncus arteriosus, tet of fallot
Downs - ASD, VSD
Rubella - septal defects, ASD
Turners - Coarctation of Aorta
Marfan - aortic insuff
DM - transposition of great art
hyaline thickening of small arteries in essential HTN.
Onions skinning seen in malignant HTN
Monckeberg Arteriosclerosis
calcification of the arteries esp radial or artery. mostly benign
Elastic art and med to large musc art.
Risk: aneurysm, ischemia, infarct, thrombus, emblus.
Location: abdom aorta>coronary art>popliteal art>carotid art.
Red vs pale infarcts
red - organs with collaterals
lungs, intestine, or following reperfusion
pale - solid tiss with single blood supply - brain, heart, kids, spleen.
contraction band necrosis
indicative of MI coagulation necrosis
evident after 4 hours.
a microscopic change in myocardial cells in which excessive contraction, associated with elevated intracellular calcium and serum norepinephrine, causes the formation of transverse amorphous bands in the fibres which are then incapable of contracting again.
5-10 days after MI
hyperemic border, central yellow brown softening, maximally yellow and soft by 10 days.
EKQ changes in MI
ST elevation + pathological Q waves - transmural infarct
ST depression - subendocardial infarct.
Dressler syndrome
several weeks post MI - fibrinous pericarditis.
Dilated Cardiomyopathy (5)
drugs bugs
Acohol toxicity
beri beri
Coxsackie virus
Chagas dz
Hypertrophic Cardiomyopathy
heart sounds
hypertrophic septum - diastolic dysfx
Loud S4, apical impulses, systolic murmur.
Tx with beta blocker
Restrictive /obliterative Cardiomyopathy (5)
Sarcoidosis, amyloidosis, postradiation fibrosis
endocardial fibroelastosis
Endomyocardial fibrosis (Lofflers)
Holosystolic (2)
mitral regurgitation -blowing murmur loudest at apex
Crescendo decrescendo systolic ejection murmur following ejection click
Aortic Stenosis
Radiates to crotids/apex
Pulsus parvus Tardus - pulses weak compared to heart sounds
Late systolic mumur with midsystolic click
mitral prolapse
most frequent valvular lesion
immdediate high pitched diastolic blowing murmur
Wide PP
Aortic regurge
Murmur follows opening snap.
Delayed rumble late diastolic murmur
What if it got louder during inspiration
Mitral stenosis
LA >> LV pressure during diastole
Tricuspid stenosis - would be louder on inspiration because of incr the RA pressure even more.
Continous machine like murmur
loudest at S2
Most common heart tumor
Most common in adults
Most common in children
Myxomas most common primary in adults - LA - ball valve obstruction
Rhabdomyomas most common primary in children
Virchow triad
predisposes to DVT
1. Stasis
2. Hypercoagubility
3. Endothelial Damage
Pulsus Paradoxis
Cardiac Tamponade and Constrictive pericarditis
1. Limitation in increase in inspiratory blood flow to the right ventricle and pulmonary artery
2. Greater than normal pooling of blood in the pulmonary circulation
3. Wide excursions in the intrathoracic pressure during inspiration and expiration
4. Interference with venous return to either atrium especially during inspiration
The LA cannot dilate as much the pulm venous vasc. LV sv is decr on inspiration.
Electrical Alternans
Cardiac tamponade
EKG phenomenon of alternation of QRS complex amplitude or axis between beats. It is seen in cardiac tamponade and is thought to be related to changes in the ventricular electrical axis due to fluid in the pericardium.
Subacute bacterial endocarditis
Group B strep Virdidans
sequela of dental procedures
smaller vegetations
Marantic endocarditis
secondary to metastasis
Acute bacterial Endocarditis
Staph Aureus - large vegetations on previously nl valves
Bacterial Endocarditis
New Murmur
Oslers Nodes
Roth Spots
Janeway Lesions
Splinter hemorrage on nail beds
Mitral valve most freq
Tricuspid in IV drug use
Complications of bact endocarditis (5)
Chordae Tendinae rupture
suppurative pericarditis
valvular damage
Rheumatic Fever
1. Cause
2. Valvular involvement
3. Symptoms
4. Labs
Group A strep pyogenes
after strep throat
Elevated ASO
erythema marginatum
incr ESR
SubQ nodules
St. Vitus dance (sydnehams chorea)
aschoff bodies and anitschkow cells
Aschoff bodies
Anitschow Cells
Aschoff bodies - granuloma with giant cells
Anitschkow cells - activated histiocytes
Found in Rheumatic Heart Dz
Serous Pericarditis(4)
SLE, RA, infection, uremia
Fibrinous Pericarditis (3)
Rheumatic Heart Dz, uremia, MI
Hemorrhagic Pericarditis
TB, malignancy (melanoma),
diffuse ST elevation
pericardial pain, friction rub, pulsus paradoxus, distant Heart Sounds
Can resolve without scarring or -> chronic adhesive or chronic constrictive pericarditis.
Pulsus Parvus Tardus
periph pulse weak compared to heart sounds

Seen in aortic stenosis
Nl pulsus
systolic changes on inspiration
Under normal conditions, arterial blood pressure fluctuates throughout the respiratory cycle, falling with inspiration and rising with expiration. The changes in the intrathoracic pressures during breathing are transmitted to the heart and great vessels. During inspiration, the right ventricle distends due to increased venous return, the interventricular septum bulges into the left ventricle reducing its size (reversed Bernheim effect), and increased pooling on blood in the expanded lungs decreases return to the left ventricle, decreasing the stroke volume of the left ventricle. Additionally, negative intrathoracic pressure during inspiration is transmitted to the aorta. The relatively higher negative pressure in the pulmonary circulation compared to the left atrium in patients with pericardial pathology causes back flow of blood from the left atrium into the pulmonary veins during inspiration.2

Therefore, during inspiration the fall in the left ventricular stroke volume is reflected as a fall in the systolic blood pressure. The converse is true for expiration. During quiet respiration, the changes in the intrathoracic pressures and blood pressure are minor. The accepted upper limit for fall in systolic blood pressure with inspiration is 10 mmHg.
Heart transplant complications
Most serious complicatoin is graft vascular dz - Graft Arteriosclerosis.
Develops years after transplant- intimal thickening of the coronaries without associated atheroma formation or significant inflammation. Prolif of fibroblasts and myocytes leading to a progressive stenosis of the lumen.
*heart transplants are denervated so no ischemic angina
Cannot be prevented with immunosuppressants.
Hyaline arteriosclerosis vs Hyperplastic
Hyaline is from benign HTN - thickening of the media caused by deposition of altered proteins.
Hyperplastic as - follows untreated malignant HTN, thickening of the arteriolar wall media from hyperplasia of myocytes onion skinning.
Loeffler endocarditis
eosinophillic infiltrate but no incr in elastic tiss.
Endomyocardial fibrosis - can be rapidly faal.
Cystic medial necrosis
a disorder of large arteries, in particular the aorta, where there is a focal degeneration of the elastic tissue and the muscle in the tunica media (the middle layer of the artery), with the presence of mucoid material in the media. It is more frequent after 40 years of age and is twice as common in males as in females.

In the aorta, this condition may lead to weakening of the artery, resulting in the formation of a fusiform aneurysm. There is also increased risk of aortic dissection.

There is an association between cystic medial necrosis and Marfan syndrome.
Rhabdomyoma ass dz
Tuberous Sclerosis
coronary vasculitis
kawasaki dz
Unstable angina
- coronary

Stable angina- angina with exertion
a developing thrombus in coronaries - with or without atherosclerosis.
- stable angina usually ass with an atherosclerosis
Physiology of AV fistula
due to trauma
Like a direct flow from aorta to pulm vein. Leads to high systolic press and decr diastolic.
Affects of AT2
1. direct stim of Na reabsorption in PCT and distal tubes
2. stim of aldo secr
3. Constriction of efferent arterioles in the kids. (which incr peritubular colloid osmotic press thereby enhancing reabosorption of salt and water from PCT.
indapamide and metolazone
thiazide diuretics - (Na and Cl excretion)
Nitroprusside toxicity and antidote
Cyanide toxicity

treat with thiosulfate.
Ca channel blocker names (5)
nifedipine, nicardipine, amlodipine

verapamil, dilatiazem (also class 4 anti arrhythmics)
Loop Diuretics
Furosemide, Ethacrynic acid, bumetanide, torsemide

hyperuricemia, hypomagnesia, OTOTOXICITY,
osmotic diuretic used in ICP is high and when intraocular pressure is high

Contraindicated in CHF
Cardiac enzymes
Troponin T and I aren't nl in blood but can incr 20X after MI. Is very specific for cardiac isoforms.
Best marker for MI in first 8 hours. Remains elevated for 7-10 days.
CK-MB - most useful 8-24 hrs after MI, peaks in 12-18hrs
LDH1 good for 2-7 days after suspected MI
Trypanosoma cruzi
Chagas Dz - Kissing bug
Intracell protozoan
Heart and nerve cells of myenteric plexus
Myocarditis and dismotility of the hollow organs
HF bc myocyte necrosis and fibrosis, achalasia, megacolon, megaureter
Coxsackie B
myocarditis and pleuritis
Post MI healing phases post ischemia
1hr - no change
12hrs - necrosis
1day- N/T and peak 2-3 days
5 days - resoprtion of necrotic myofibers by histiocytes, and prolif of small blood vessels -early granulation tissues
10days- advanced granulation of fibros, small bv, and residual chronic inflamm cells within matrix of young collagen
Pharyngeal arches and arteries
arch 1 maxillary
arch 2 stapedal
arc 3: internal carotids bilat
arch4: arch of the aorta and subclavian arts
arch6: pulm art and ductus arteriosus
Pericarditis vs dissecting aortic aneurysm
breathing and pain
Pain with pericarditis is ass with breathing while not with a dissection
Cervical rib associations
Above the 1st rib - cervical 7
Compression of Brachial plexus and subclavian
Thoracic outlet syndrome
Heart Septum embryo
septation begins at 26days
Atrial - SEPTUM PRIMUM dwnwd twd endocardial cushions and fuse.
2nd opening OSTIUM SECUNDUM grows dnwd together with flap of ostium primum form foramen ovale.
Ventricular: MUSCULAR IV SEPTUMP starts in floor of vent and grows twd endocardial cushions. MEMBRANOUS IV SEPTUM then forms the fusion of the right bulbar ridge, left bulbar ridge and endocardial cushions. Either failure leads to VSD
great saphenous vein
found in superficial fascia
extends along lower limb - as it ascends the lower limb it passes ANTERIOR TO THE MEDIAL MALLEOLUS
and post to the medial side of the knee. passes through the saphenous hiatus of the fascia lata to empty in to the femoral vein sightly below the inguinal ligament.
How is RA and cardiac complications related
Restrictive cardiomyopathy due to AA amyloid build up.
Fragile X sequela
Common as downs
Large head
perinatal comlication
CT d/o - lax joint, flat feet large ears.
Long narrow face, prominent jaw and nasal bridge. Macro orchidism after puberty,
most common cause of sudden cardiac death
ischemic heart dz
First detectable fetal heart beat
4 weeks
Most common complication post MI 2 day
Time post MI for ventricular rupture
5-8days. During the granulation phase.