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97 Cards in this Set
- Front
- Back
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Resistance
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delta P / flow (Q) = 8n x Length/pie r^4
CO=MAP-RAP / TPR n= eta or viscosity Q = dP/R |
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S3
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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 |
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S4
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atrial kick, hypertrophic ventricle
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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) |
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calcium induced ca rls
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extracell ca++ enters cell during plateau of AP and stim Ca++ rls from cardiac muscle SR
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Capacitance
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aka - Compliance - the inverse of elastance
C = V/P |
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Capacitance arteries and age
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decreases with age as teh art become stiffer and less distensible.
leads to increased pulse press |
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Pulse pressure
determinant |
Systolic P - diastolic P = PP
largest determinant of PP is SV - because diastolic P remains relatively unchanged during ventricular systole. |
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MAP
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MAP = 1/3 systolic P + 2/3 diastolic P
MAP = 1/3 PP + 2/3 DP |
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Pulmonary Wedge Press
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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.
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PR interval
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depends on conduction velocity through the AV node.
PR interval decr with incr HR |
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ST segment
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end of S to the beginning of T waves.
Should be isoelectric because the ventricles are depolarized. |
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T wave
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ventricular repol.
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Action Potential duration
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Long duration in non nodal areas - longest in Purkinje - 300ms
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Conduction Velocity
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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 |
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Chronotropic vs Dromotropic Effect
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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. |
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Length of PR segment
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nl <200msec
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QRS
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nl < 120msec
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U wave
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occurs after t wave - inverted
caused by hypokalemia |
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Mobitz type 1
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2nd degree heart block
progressive lengthening of PR until a QRS is dropped. usually AXS |
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Mobitz type 2
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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 |
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Carotid Massage
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Influences carotid baroreceptors (cn 9) by stretching them leading to incr firing leading to incr Psym and decr Sym stimulation.
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Chemoreceptors central vs peripheral
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Carotid and aortic bodies
Periph - respond to pO2 (<60mmHg), pCO2 and pH. Central - responds to pCO2 and pH responsible for cushing rxn. |
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Cushing Reflex
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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 |
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Atrial response to decr BP
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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. |
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ANP
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atrial response to incr atrial press
relaxes vasc smooth muscle incr excretion of salt and H20 by kids inhibits renin secr |
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Swan Ganz cat
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measures pulm wedge press -
basically equals LA press |
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Net fluid flow in capillaries
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Pnet x Kf
net pressure times the filtration constant (cap permeability) |
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R->L shunt
Early cyanosis |
1. Tetrology of Fallot
2. Transposition of great vessels 3. Truncus Arteriosis Children squat to incr venous return |
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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 |
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Tet of Fallot
cause |
R-> L shunt
boot shaped heart bc of RVH Caused by anterosuperior discplacement of infundibular septum. |
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PDA
Murmur? 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. |
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DiGeorge
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CATCH 22
Cardiac abnl Abnl Facies Thymic Aplasia Cleft palate Hypocalcemia - (bc of hypoPTH) |
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Congenital cardiac abnl
Digeorge Downs Congenital rubella Turners Marfan 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 |
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Arteriolosclerosis
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hyaline thickening of small arteries in essential HTN.
Onions skinning seen in malignant HTN |
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Monckeberg Arteriosclerosis
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calcification of the arteries esp radial or artery. mostly benign
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Atherosclerosis
locale |
Elastic art and med to large musc art.
Risk: aneurysm, ischemia, infarct, thrombus, emblus. Location: abdom aorta>coronary art>popliteal art>carotid art. |
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Red vs pale infarcts
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red - organs with collaterals
lungs, intestine, or following reperfusion pale - solid tiss with single blood supply - brain, heart, kids, spleen. |
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contraction band necrosis
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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. |
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5-10 days after MI
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hyperemic border, central yellow brown softening, maximally yellow and soft by 10 days.
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EKQ changes in MI
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ST elevation + pathological Q waves - transmural infarct
ST depression - subendocardial infarct. |
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Dressler syndrome
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several weeks post MI - fibrinous pericarditis.
autoimmune |
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Dilated Cardiomyopathy (5)
drugs bugs |
Acohol toxicity
beri beri Coxsackie virus Chagas dz Cocaine Doxorubicin |
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Hypertrophic Cardiomyopathy
heart sounds treatment |
hypertrophic septum - diastolic dysfx
AD Loud S4, apical impulses, systolic murmur. Tx with beta blocker |
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Restrictive /obliterative Cardiomyopathy (5)
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Sarcoidosis, amyloidosis, postradiation fibrosis
endocardial fibroelastosis Endomyocardial fibrosis (Lofflers) |
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Holosystolic (2)
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mitral regurgitation -blowing murmur loudest at apex
VSD |
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Crescendo decrescendo systolic ejection murmur following ejection click
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Aortic Stenosis
Radiates to crotids/apex Pulsus parvus Tardus - pulses weak compared to heart sounds |
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Late systolic mumur with midsystolic click
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mitral prolapse
most frequent valvular lesion |
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immdediate high pitched diastolic blowing murmur
Wide PP |
Aortic regurge
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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. |
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Continous machine like murmur
loudest at S2 |
PDA
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Most common heart tumor
Most common in adults Most common in children |
Metastasis
Myxomas most common primary in adults - LA - ball valve obstruction Rhabdomyomas most common primary in children |
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Virchow triad
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predisposes to DVT
1. Stasis 2. Hypercoagubility 3. Endothelial Damage |
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Pulsus Paradoxis
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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. |
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Electrical Alternans
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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. |
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Subacute bacterial endocarditis
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Group B strep Virdidans
sequela of dental procedures smaller vegetations |
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Marantic endocarditis
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secondary to metastasis
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Acute bacterial Endocarditis
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Staph Aureus - large vegetations on previously nl valves
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Bacterial Endocarditis
valve? |
New Murmur
Anermia Oslers Nodes Roth Spots Janeway Lesions Splinter hemorrage on nail beds Mitral valve most freq Tricuspid in IV drug use |
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Complications of bact endocarditis (5)
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Chordae Tendinae rupture
Glomerulonephritis suppurative pericarditis emboli valvular damage |
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Rheumatic Fever
1. Cause 2. Valvular involvement 3. Symptoms 4. Labs |
Group A strep pyogenes
after strep throat mitral>aorta>>tricuspid Elevated ASO erythema marginatum incr ESR polyarthritis SubQ nodules St. Vitus dance (sydnehams chorea) aschoff bodies and anitschkow cells |
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Aschoff bodies
Anitschow Cells |
Aschoff bodies - granuloma with giant cells
Anitschkow cells - activated histiocytes Found in Rheumatic Heart Dz |
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Serous Pericarditis(4)
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SLE, RA, infection, uremia
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Fibrinous Pericarditis (3)
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Rheumatic Heart Dz, uremia, MI
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Hemorrhagic Pericarditis
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TB, malignancy (melanoma),
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Pericarditis
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diffuse ST elevation
pericardial pain, friction rub, pulsus paradoxus, distant Heart Sounds Can resolve without scarring or -> chronic adhesive or chronic constrictive pericarditis. |
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Pulsus Parvus Tardus
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periph pulse weak compared to heart sounds
Seen in aortic stenosis |
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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. |
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Heart transplant complications
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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. |
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Hyaline arteriosclerosis vs Hyperplastic
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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. |
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Loeffler endocarditis
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eosinophillic infiltrate but no incr in elastic tiss.
Endomyocardial fibrosis - can be rapidly faal. |
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Cystic medial necrosis
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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. |
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Rhabdomyoma ass dz
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Tuberous Sclerosis
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coronary vasculitis
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kawasaki dz
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Unstable angina
- coronary Stable angina- angina with exertion |
a developing thrombus in coronaries - with or without atherosclerosis.
- stable angina usually ass with an atherosclerosis |
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Physiology of AV fistula
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due to trauma
Like a direct flow from aorta to pulm vein. Leads to high systolic press and decr diastolic. |
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Affects of AT2
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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. |
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indapamide and metolazone
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thiazide diuretics - (Na and Cl excretion)
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Nitroprusside toxicity and antidote
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Cyanide toxicity
treat with thiosulfate. |
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Ca channel blocker names (5)
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nifedipine, nicardipine, amlodipine
verapamil, dilatiazem (also class 4 anti arrhythmics) |
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Loop Diuretics
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Furosemide, Ethacrynic acid, bumetanide, torsemide
hyperuricemia, hypomagnesia, OTOTOXICITY, |
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Mannitol
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osmotic diuretic used in ICP is high and when intraocular pressure is high
Contraindicated in CHF |
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Cardiac enzymes
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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 |
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Trypanosoma cruzi
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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 |
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Coxsackie B
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myocarditis and pleuritis
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Post MI healing phases post ischemia
1hr 12hr 1day 5day 10day |
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 |
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Pharyngeal arches and arteries
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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 |
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Pericarditis vs dissecting aortic aneurysm
breathing and pain |
Pain with pericarditis is ass with breathing while not with a dissection
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Cervical rib associations
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Above the 1st rib - cervical 7
Compression of Brachial plexus and subclavian Thoracic outlet syndrome |
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Heart Septum embryo
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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 |
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great saphenous vein
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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. |
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How is RA and cardiac complications related
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Restrictive cardiomyopathy due to AA amyloid build up.
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Fragile X sequela
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Common as downs
Large head perinatal comlication MR CT d/o - lax joint, flat feet large ears. Long narrow face, prominent jaw and nasal bridge. Macro orchidism after puberty, MITRAL VALVE PROLAPSE AORTIC ROOT DILATION |
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most common cause of sudden cardiac death
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ischemic heart dz
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First detectable fetal heart beat
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4 weeks
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Most common complication post MI 2 day
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arrhythmias
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Time post MI for ventricular rupture
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5-8days. During the granulation phase.
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