Flashcards in cardio pathophys Deck (390):
Wall stress = ((pressure x chamber radius)/2x wall thickness)
What factors increase cardiac contractility?
Increased SS tone
What factors decrease contractility?
SS blockade (Beta Blocker)
What is concentric hypertrophy?
Seen w/ high BP
increase in number of sarcomeres laid in parallel -> decreased cavity size and increased wall thickness -> decreased wall stress w/ preserved contractility
What is eccentric hypertrophy?
Occurs w/ chronically elevated preload
Increased sarcomeres in series -> increased chamber size + increased wall stress -> increased sarcomeres in parallel
proportional increases in cavity size and wall thickness
What is concentric remodelling?
Reversible, physiologic LV hypertrophy seen in athletes.
4 ways that IC Ca++ is recovered after cardiomyocyte contraction
1: SERCA - in SR, ATP dependent
2: Na/Ca exchanger - uses Na gradient to move Ca out
3: Plasma membrane Ca++ -ATPase
4: Mitochondrial Ca++ uniporter
What is preload?
Passive tension in cardiac myocyte at rest - length of cell prior to contraction
Greater length -> stronger contraction
What is afterload?
The force that a muscle cell must overcome in order to contract
What is isometric contraction?
Afterload > contraction force
sarcomere does not shorten
What is contractility?
contractility = inotropy
intrinsic ability of cardiac myocyte to alter ability to contract independent of preload and afterload
due to changes in biochemical environment of myocyte
due to increased actin-myosin interractions.
EDV - ESV = SV
EF = SV / EDV
3 phases of ventricular filling
Early rapid filling
Slow mid-diastolic filling
Rapid filling from atrial contraction
2 factors that influence Preload
Venous return (blood volume, venous tone, posture, pericardial constraint, atrial contraction efficacy)
What is normal EF? What EF %s indicate mild, moderate, severe dysfunction?
Mild LV dysfunction: 45-54%
Moderate LV dysfunction: 30-44%
Severe LV dysfunction: <30%
2 methods of measuring CO
Thermodilution: most common - cath inserted, cold saline injected in RA, measured in PA, CO is calculated
Fick method: tedious
equation: CO = O2 consumption / AV O2 difference
What is a Wood Unit (WU)?
Used in calculations of TPR
WU = (dyne . sec . cm^-5) / 80
How is TPR calculated? Normal values?
measure of afterload
Mean pressure difference across vascular bed / mean blood flow
Systemic VR = (MAP - MRAP)/CO. Normal = 13-16 WU
Pulmonary VR = (MPAP - PCWP)/CO. Normal = 0.5-11 WU
What is initial treatment for STEMI?
If not immediately possible - thrombolytics
what anti-ischemic treatments are recommended for early hospital care of ischemic heart disease?
1: oxygen (maintain O2 sat >90%)
2: nitrates (SLx3 or IV for ongoing ischemia, HF, HTN)
3: Oral B-blocker in 1st 24 hrs if no contraindication
4: NDHP Ca++ channel blocker if B-blocker contraindicated
5: ACE inhibitor in 1st 24 hrs for HF or EF <40%
What are contraindications for Nitrate use?
Hypotension (present or likely)
Right ventricular infarct
Severe aortic stenosis
PDEi taken in last 24 hours
What are indications for Beta blocker use in Ischemic heart disease and what are the preferred agents?
Ongoing chest pain, hypertension or tachycardia not caused by HF
Metoprolol or atenolol are preferred
Should a patient w/ MI precipitated by cocaine use be treated with a beta-blocker?
Blockade of B2 mediated vasodilation may precipitate coronary artery spasm
What patients may receive IV beta blocker?
Patients with ischemic heart disease and significant hypertension
Afib with RVR
Contraindications for beta-blocker use
hypotension, bradycardia, heart block, pulmonary edema
MI assoc. w/ cocaine use
What is the recommended statin in treatment of ischemic heart disease?
Atorvastatin, 80mg / day
What studies demonstrated the efficacy of statin treatment in treatment of ischemic heart disease?
PROVEIT-TIMI 22 and MIRACL
What is class III therapy for ischemic heart disease?
-Nitrates if Systolic pressure <90
-Nitrates if Sildenafil or Tadalafil w/in 24 hrs
-Immediate release Ca Channel blockers w/o B-blocker
-IV B-blocker if AHF, low output, long PR, 2nd or 3rd deg heart block, asthma or reactive airway disease
-NSAIDs and COX-2 inhibitors
What is the mechanism of aspirin's anti-platelet activity?
inhibition of Thromboxane A2 (stimulates platelet aggregation)
Aspirin irreversibly inhibits COX inhibiting PGI2 and TxA2 production.
What is the recommended dosing for aspirin?
Initially: 325 mg non-coated, chewed
Prophylaxis: 75-100 mg/day inhibits TXA2 w/o significant impairment of PGI2
Name 4 P2Y12 receptor blockers and differentiate
Ticlopidine: worse side effect profile - not used
Prasugrel: greater anti-platelet activity, increased risk of bleeding
Ticagrelor: reversible blockade. greater anti-platelet activity
What is recommended anti-platelet therapy for a patient w/ ACS?
1 year of dual anti-platelet therapy: aspirin + P2Y12 receptor blocker
Clopidogrel dosing for pt. w/ NSTEMI ACS
300mg loading dose
Prasugrel vs. Clopidogrel
Prasugrel: faster onset, higher degree of platelet inhibition, effective for more patients (20-25% of pts are clopidogrel resistant)
What are contraindications for Prasugrel?
Hx of TIA or stroke
> or = 75 yoa
What are 2 classes of P2Y12 receptor blockers?
Thienopyridine - clopidogrel
Cyclopentyltriaolopyrimidines - ticagrelor
In treatment of ACS what patients are given GIIbIIIa inhibitors?
Those receiving early invasive therapy
examples of GIIaIIIb inhibitors
eptafibatide - preferred
tirofiban - lowest preference
What are the anticoagulants of choice for ACS patients undergoing early invasive treatment? what about conservative treatment?
early invasive: bivalirudin or UFH
conservative: enoxaparin or fondaparinux
What ACS patients should receive fibrinolytic therapy?
STEMI patients w/in 12 hours of onset w/ no contraindications for whom reperfusion therapy cannot be performed w/in recommended timeframe.
Patients presenting after 12 hrs but before 24 hrs of symptom onset for whom reperfusion therapy is not available
3 fibrinolytics and differences
Reteplase (rPA) - sim to tPA, longer half-life
Tenecteplase (TNK-tPA) - sim to tPA, lower incidence of noncerebral bleeding and easier to use, longer half-life
When is Ranolazine used and what is the dose?
Used in patients receiving max-dose of long acting nitrates with persistent symptoms. Decreases frequency of anginal events.
Dose: 500 mg bid (1000 mg bid w/ persistent symptoms)
Contraindications for Ranolazine
pre-existing QT prolongation
use of diltiazem or verapamil
Note: inhibits degradatory path for simvastatin and digoxin - lower doses needed.
What is Cardiac X syndrome? Treatment?
Angina-like chest pain w/ exertion, positive ECG (ST depression during stress test), normal coronary angiography, no inducible vasospasm.
Treatment: reassure stable patients. B-blockers help, Nitro helps. Calcium channel blockers not very helpful.
What is the use of CRP in understanding risk of a CV event?
independently of questionable use, but can be used for stratification w/in risk groups
What inflammatory cells are primarily involved in atheromatous plaque formation?
Monocytes and Tcells (CD4)
What are two main causes of endothelial injury precipitating atheromatous plaque formation?
hemodynamic stress: HTN, turbulent flow
chemical / physical agents: hypercholesterolemia, smoking (free-rad and toxins), chronic inflamm, homocysteine
How do foam cells form in atherosclerotic plaques?
endothelial damage -> increased adhesion molecules (VCAM-1) and increased permeability -> increased lipid infiltration, cholesterol deposition and monocyte infiltration
local free radicals -> oxidized LDL -> activated macs phagocytosis of oxidized lipid via SCAVENGER RECEPTOR-> foam cells
How are smooth muscle cells recruited to atherosclerotic plaques?
PDGF from platelets, macs, endothelium, and other sm.m. cells
FGF and TGF-a
What are the most common sites of atherosclerosis?
Large elastic and medium sized muscular arteries
abdominal aorta, coronary aa., popliteal, carotid aa.
What is a fatty streak?
Pre-atherosclerotic lesion. Present in childhood, may not lead to atherosclerosis.
Aggregate of lipid filled macrophages w/in intima.
What is an atheroma and what are its components?
An uncomplicated fibrofatty plaque
inflammation at periphery - Tcells and macs, granulation tissue
What is hypertension?
Elevation of arterial BP that results in adverse health effects
Generally: systolic >140 or diastolic > 90
4 targets of Angiotensin II
1. Vasculature -> vasoconstriction
2. Post. Pituitary -> Vasopressin (ADH) production
3. Kidney -> Na+ and H2O retention
4. Adrenal glands -> Aldosterone release
What are the underlying causes of Primary Hypertension?
1) genetic predisposition - multifactorial, familial hx
2) environmental influences - stress, obesity, Na+ intake
Potential mechanisms of primary HTN
Genetic defects in
1) renal Na excretion -> increased CO
2) vascular sm. muscle Na / Ca transport -> increased peripheral vascular resistance
5 major causes of Secondary HTN
1. Renal disease (renal artery stenosis)
3. Endocrine disorder
4. Aortic coarction
What is the mechanism underlying renovascular HTN?
Reduction in renal perfusion due to atherosclerosis (or other process) -> persistent activation of renin-angiotensin-aldosterone system
What is fibromuscular dysplasia?
Irregular thickening of the intima and most often the media of the renal artery -> renal artery stenosis
Most common in young women (30-40s)
2 types of arteriolosclerosis
1. hyaline: endothelial damage -> leakage of plasma protein and sm. m. matrix synth -> luminal narrowing
2. hyperplastic: malignant HTN. concentric thickening of vessel walls - sm. m w/ thickened reduplicated basement membrane
What defines malignant HTN?
Diastolic pressure >130
What is the pathogenesis of hyperplastic arteriolosclerosis?
endothelial damage -> plasma protein leakage (esp. fibrinogen) and thrombosis -> PDGF -> intimal hyperplasia and luminal narrowing -> deceased renal perfusion -> increased renin production -> vasoconstriction and exacerbation (self-perpetuating cycle)
What kind of necrosis is associated with hyperplastic arteriolosclerosis?
fibrinoid necrosis - vessel walls replaced by smudgy fibrin deposits.
Where is cerebral hemorrhage most likely to occur secondary to HTN?
Putamen, thalamus, pons
What are 2 changes that can occur to the kidney due to HTN
1) benign nephrosclerosis - normal w/ aging, exacerbated w/ HTN, diabetes: fibroelastic hyperplasia of larger aa, hyaline arteriolosclerosis, ischemic changes in parenchyma (fibrosis), mild reduction of GFR
2) malignant nephrosclerosis - malignant HTN: "flea-bitten" kidneys, hyperplastic arteriolosclerosis, infarction, ischemic atrophy, papilledema, encephalopathy, cardiac complications, proteinuria, hematuria, acute RF
What are the differences between flame shaped and dot shaped retinal hemorrhages in the setting of HTN?
flame: closer to the inner limiting membrane (more superficial) - due to nerve fiber lying parallel to membrane
What are cotton wool spots seen on retinal exam?
Cytoid bodies: due to arteriolar occlusion (vascular damage / HTN related) swollen dammaged axons distal to occlusion
What is a macular star and what is it associated with?
Due to intraretinal lipid deposition in plexiform layer due to breakdown or blood-retinal barrier
Seen in malignant HTN +/- increased intracranial pressure
What cardiac cells produce "fast response" action potentials and what is the respective conduction velocity of each?
Regular atrial and ventricular cardiomyocytes: 0.3-1 m/s
Purkinje fibers: 1-4 m/s
What cells produce "slow response" action potentials and what is the respective conduction velocity of each?
Pacemaker cells in the SA and AV nodes: 0.02 - 0.1 m/s
4 phases of fast myocyte AP cycle and ion flow associated w/ each
0: inward Na+ (depolarization)
1: Na+ close, outward K+ open
2: inward Ca++ balance outward K+ (plateau)
3: Ca++ close, outward K+ (repolarization)
4: Na+/K+ ATPase restores normal [ion] (resting membrane potential)
If measuring EKG deflection in terms of voltage, what is the scale?
1mV = 10mm vertically
What is the time scale on EKG paper?
Small square = 1mm = 0.04s
Large square = 5 small squares = 5mm = 0.2s
5 large squares = 25 mm = 1.0s
What is Einthoven's Triangle?
Orientation of EKG leads I - III
I: RA (-), LA (+)
II: RA (-), LL (+)
III: LA (-), LL (+)
What are the lateral leads on 12 lead EKG?
I and aVL
What are inferior leads in 12 lead EKG?
II, III, aVF
What is placement of the precordial leads?
V1: 4th intercostal, R of sternum
V2: 4th intercostal, L of sternum
V3: between V2 and V4
V4: 5th intercostal, mid clavicular line
V5: between V4 and V6
V6: 5th intercostal, mid axillary line
What areas of heart do the precordial leads look at?
V1 and V2: Right
V3 and V4: septal
V5 and V6: Left
What does a biphasic deflection on EKG indicate?
Wave of depolarization is moving perpendicularly to (+) electrode
What is the normal rate of sinus rhythm?
60 - 100 bpm (sinus rhythm - set by SA node)
What is the normal amplitude of a P wave on EKG?
What leads record a biphasic Pwave?
III and V1
What leads record positive and negative P waves?
Positive: I, II, V6
What structures insulate the ventricles from electrical activity of the atria?
Atrio-ventricular valves (tricuspid and mitral)
What does the PR interval represent?
Delay between the onset of atrial depolarization and ventricular depolarization.
Beginning of P wave -> beginning of QRS
Normal: <0.2 s
What structures are composed of Purkinje fibers?
Bundle of His
L and R bundle branches
Terminal Purkinke filaments
What is a QS wave?
Depression missing an R wave. R wave divides and defines Q and S waves, so minus the R it appears as a single depression. Generally considered a Q wave.
What do the components of the QRS complex represent?
Q: Septal depolarization
R: Apical ventricular depolarization
S: Basal (near valves) ventricular depolarization
What is the directionality of septal depolarization?
Right, Forward, and Down
What is the directionality of early ventricular depolarization?
Left, down, forward
How is early ventricular depolarization seen on EKG in each lead?
Frontal: positive R wave in I and II, negative QS in aVR
Horizontal: positive R wave w/ progressive intensity from V1-6
What is the directionality of late ventricular depolarization?
Left and upward
How is late ventricular depolarization seen on EKG?
Frontal: positive in I and aVL -> increased R wave amplitude, negative in aVF -> S wave
Horizontal: negative in V1 and 2 (S) and positive in V5 and 6 (+R)
What is the R wave Transition Zone?
in precordial leads, the point at which the positive R amplitude = negative S amplitude.
Usually in V3 or 4
In what leads should the Q wave be most apparent?
aVL and I
What is a normal QRS duration?
0.06 - 0.1 s
What is the direction of the ventricular repolarization vector?
Right and up
How is the T wave seen on EKG?
Frontal: positive in I, II, aVF; negative in aVR
Horizontal: positive V6, negative V1
What is a normal QT interval? What is it used for clinically?
0.30 - 0.44s (0.45 in women): at normal HR, < 1/2 of R-R interval.
Majority of QT is ventricular repolarization - clinical indicator of this.
What is QTc?
QT corrected for HR. > 0.44 is considered prolonged.
QTc = QT/sq. rt (R-R)
What are the rates of 3 ectopic pacemakers?
junctional (w/in AV node): 40-60
What is a normal mean QRS vector?
0 - +90 degrees
Right deviation: > 90
Left deviation: < 0
In what settings are vertical and horizontal mean electrical axi seen?
Vertical: axis is vertically downward - heart is shifted toward right - variant of normal seen in tall, slender, healthy people
Horizontal: axis is leftward horizontally - apex of heart is pressed up by diaphragm in obese individual
What two settings could a deviated MEA be seen on EKG?
1. Ventricular hypertrophy: increased electrical activity of hypertrophied ventricle dominates
2. MI: infarcted area is dead. Deviation away from infarcted region.
What leads are used for evaluation of atrial enlargement?
V1: perpendicular to wave -> biphasic EKG tracing
LII: parallel -> positive deflection
What is normal P wave amplitude?
What are signs of RV hypertrophy seen on EKG?
Precordial: Large R wave on V1, rightward movement of transitional point, shrinking R wave from V1-6 w/ persistence of S wave in 5 and 6.
Limb: Right MEA axis deviation.
What signs of LV hypertrophy can be seen on EKG?
Precordial: V1: deep S, V5: tall R
Sokolow Index: depth of S in V1 (mm) + height of R in V5 > 35mm - diagnosis of LVH
Limb: Lewis Index: LI R (mm) + LIII S (mm) > 25mm - diagnosis of LVH
What is an indication of ventricular strain seen on EKG?
Usually coupled w/ LVH:
Inverted T wave in V5 and V6 w/ gradual down slope and rapid upslope.
3 Stages of EKG changes seen in STEMI
1: Large T wave peaks followed by symmetrical inversion
2: ST elevation
3: Q wave emergence (pathological Q waves longer than 0.04s and at least 1/3 the amplitude of R wave of same complex)
ST and T wave changes may disappear w/ time, but Q wave will remain and is a marker of previous MI
What is seen on EKG in acute anterior infarction?
ST elevation and Q waves in V1-4
What is seen on EKG in lateral infarction?
ST elevation and Q waves in LI and aVL
What is seen on EKG in inferior infarction?
ST elevation and Q waves in LII, LIII, and aVF
What is seen on EKG in acute posterior infarction?
Large R waves and ST depression in V1, 2, and sometimes 3
What are 2 methods of EKG evaluation to assist in cases of suspected posterior infarction?
Transillumination: flip EKG paper and hold in front of a strong light - if what originally looked like ST depression looks like ST elevation, supports posterior MI.
Mirror test: look at tracing in a mirror.
Is EKG diagnosis of infarction valid in a patient w/ left bundle branch block?
What modifiable risk factors have a causal relationship to CAD?
What effect does raising HDL levels have on CAD risk?
Does not reduce risk
What is positive remodeling in CAD?
Expansion of vessel wall outward to accommodate growing plaque and maintain vessel integrity.
After this process exhausts -> luminal narrowing
At what point does a fixed coronary obstruction become critical? What happens at this point?
70% diameter stenosis
90% reduction in cross-sectional area
1. resistance vessels are maximally dilated at rest
2. O2 supply threshold reached - if demand exceeds -> symptoms
3 factors that determine myocardial O2 demand:
Wall stress (preload, LV hypertrophy)
Formula for approximating myocardial O2 demand
Rate Pressure Product
HR x SBP
2 factors determining myocardial O2 supply
O2 carrying capacity (Hgb)
How is pre-test probability for Angina determined?
Other tests to confirm or refute (ECG, Stress test +/- imaging, coronary angiography)
How is a stress test w/ imaging performed?
Thalium or Technetium injected at peak exercise and hours later at rest.
Isotope concentrates in metabolically active cells.
Cells that are ischemic w/ exercise do not concentrate isotope.
***Perfusion defect w/ exercise compared to rest.***
Gold standard for diagnosis of CAD
Treatments for chronic stable Angina
Pharm: TNG, B-blocker, Ca++ channel blocker
Mechanical: PCI, CABG
Most important components of chronic stable angina treatment
HMG-CoA reductase inhibitor (statin) - treats causal factor
BP control - treats causal factor
Diet and exercise - lower LDL
What is the pathophysiology of ACS?
Thrombus overlying disrupted plaque obstructs blood flow
-transient or persistent
What are the clinical symptoms of ACS?
Prolonged chest discomfort at rest, radiation
-variable between pts.
Dyspnea, diaphoresis, N/V, HTN, hypotension
Who is more likely to have atypical symptoms of ACS?
Elderly, diabetic, females, history of CABG
Symptoms of proximal LAD occlusion
hypotension, reciprocal tachycardia
S3 - increased LVEDP
S4 and rales - pulmonary congestion (decreased diastolic compliance)
Exam findings suggestive of RCA occlusion
No pulmonary congestion, no S4
bradycardia, variable heart block
murmur of mitral valve regurgitation
Primary diagnosis of STEMI
Persistence of ST elevation - indicates occluded epicardial artery or distal embolization obstructing microvascular perfusion
What is seen on NSTEMI EKG? How is NSTEMI diagnosed?
No ST elevation - may be ST depression (ischemia). Chest pain persists at rest.
Diagnosis: biochemical markers - elevated Troponins
What are the two main causes of cardiovascular disease related deaths?
Coronary Heart Disease: >50%
According to the Framingham study, what are the major risk factors for cardiovascular disease?
Elevated total or LDL cholesterol
Family history (male: 1st deg <65 yoa)
Age (men 45, women 55)
What BMI is considered obese? What is abdominal obesity?
25-29 = overweight
Abdominal obesity: men: waist 40+; women: waist 35+
What patients should have a 10-year risk assessment for CHD?
Those with 2+ major risk factor.
Not required for those with fewer than 2, most have 10 year risk of <10%.
What factors are considered in Framingham CHD risk assessment?
After 10 points (men), risk grows rapidly from 6%
After 18 points (women), risk grows rapidly from 6%
What are primary, primordial, and secondary disease prevention?
Primary: prevention of disease onset in asymptomatic
Primordial: prevention of causative risk factors to prevent disease
Secondary: preventing recurrence or death in symptomatic pts.
How do gerontologists define "old"?
Young old: 60-74
very old: >85
How do the WHO and US Task Force define old?
US Task Force: >65
What is the leading cause of death in the elderly?
What is the most frequent hosiptal discharge diagnosis in older adults?
Usually diastolic dysfunction w/ preserved EF
More common in women
What are the 4 most common chronic medical conditions seen in addition to CVD in older adults?
Dementia (13% @65, 40% @80)
**50% of pts >80 have at least 2 other chronic conditions
What CV parameters increase w/ aging?
incidences of CAD and afib
What CV parameters decrease w/ age?
early diastolic filling (EF more dependent on atrial contraction)
max exercise HR
max aerobic capacity and O2 consumption
HR response to B agonist
Vasodilator response to endothelium dependent vasodilators
What causes changes in PWV changes w/ age and what is the end effect?
Arterial stiffening -> increased PWV (from 5m/s in youth - 12 m/s in elderly)
young: reflected wave augments diastolic pressure -> increased coronary perfusion
Old: reflected wave augments systolic pressure -> high systolic BP and pulse pressure
What changes in cardiac Ca++ handling occur w/ aging?
L-type receptor: reduced and delayed inactivation
Decreased and delayed SERCA reuptake
Reduced and delayed outward K+ rectifier current
-> prolonged AP, prolonged contraction, prolonged relaxation
What 3 factors are considered in the Unifying Hypothesis of Age Related Changes in CV Function?
Cumulative oxidative stress from increased superoxide anions
Inflammatory cell response to stress / infection
Programmed cell death
What type of HTN is particularly prevalent in the elderly population and what medication is it most responsive to?
Isolated systolic HTN
Responds to diuretics
In an older patient w/ diabetes, what HTN med is recommended?
ACE inhibitor to delay nephropathy
What causes post-prandial hypotension?
Shunting of blood to digestive tract. Occurs 30-120 min after meal.
May be symptomatic in elderly pop.
What % of elderly population may have silent cardiac ischemia and why?
25-50% due to decreased pain perception, dementia, memory impairment.
How do PCI and CABG compare in elderly?
PCI: better procedure survival rate, lower post-procedure stroke rate
CABG: better survival after 6mos.
What effect does revascularization have in the setting of stable angina in an elderly population?
No survival benefit over optimized medical therapy - symptomatic treatment
What is the link between influenza vaccination and cardiac death in the elderly?
Flu vaccine decreases risk of cardiac death in elderly
Also prevents CHF hospitalizations
What defines systolic CHF? What are common causes in the elderly? How are elderly treated?
EF improved survival
What causes diastolic HF and what are effective treatments for elderly pts?
Diastolic HF (preserved EF) caused by stiff ventricles - abnormal relaxation
No treatment improves survival in elderly
HF w/ PEF has better survival in younger pop, same as systolic CHF in elderly.
How do BNP levels compare in older and younger patients w/ CHF?
4x higher in older population
Examples of medications that may require weight based dosing in elderly
Are drugs metabolized by glucuronidation, sulfation, and methylation affected by age?
ex: methyldopa, diazepam, procainamide
Is the P450 pathway affected by aging?
Yes - slows down
drugs affected: a-blockers, B-blockers (meto, propan), CCB, statins
may increase side effects.
3 factors affecting Warfarin activity
CYP2C9 polymorphisms may increase effect (12% of dose variations)
Vitamin K epoxide reductase complex polymorphism may increase or decrease sensitivity (25% of dose variation)
Increased age (40% of dose variation)
What happens in cocaine induced MI?
Do not give B-blocker - may worsen.
In the course of MI, how long from time of onset to irreversible myocyte injury? How long until total infarct size determination?
30 minutes of ischemia -> irreversible damage
6 hours - total infarct size determination
Sequence of morphological changes in MI
12-24 hrs: Dark red, mottled
1-3 days: pale, tan region
3-10: well defined, soft, tan, red hyperemic border
10 days - 2 mos: red - gray -> gray - white, changes from periphery to center
2+ mos: rubbery white scar
What is myocytolysis?
reversible ischemic injury - hydropic change - swelling of cells
Sequence of microscopic changes post MI
4-24 hours: coagulative necrosis - ghost cells, hypereosinophilia, pinknotic nuclei
2-3 days: invasion of inflammatory cells (macs and neutrophils), interstitial edema
3-7 days: tissue disintegration by phagocytosis
1-2 weeks: gradual replacement by granulation tissue (capillaries and fibroblasts
2 weeks - 2 mos: increased collagen, decreased fibroblasts and capillaries with ensuing aggregate of dense collagen
What is myocardial stunning?
Temporary decrease in contractility following reperfusion therapy
3 features of reperfusion injury
1) myocyte death (free-radicals)
2) microvascular injury (endothelial cell swelling
2 labs evaluated in MI timing of changes
Troponin (I and T): elevation 2-4 hrs, peak in 48 hrs, remain elevated 7-10 days
Creatine Kinase MB (CK-MB): elevation 2-4 hrs, peak in 24, return to normal in ~3 days
At what point is fibrinous pericarditis seen in MI patients?
2-3 days after a transmural MI
When is the greatest risk for myocardial rupture after MI?
4-5 days post MI (maximal tissue disintigration)
* usually older women
* -> hemopericardium and tamponade, rarely -> false aneurism
What is the pathological characterization of chronic ischemic heart disease?
LVH + dilation
Severe coronary atherosclerosis
Multiple areas of myocardial fibrosis
3 causes of serous pericarditis
Etiology of fibrinous pericarditis
Early bacterial infection
Characteristic finding in fibrinous pericarditis
pericardial friction rub
Causes of hemorrhagic pericarditis
metastatic malignancy (cancer -> angiogenesis)
status post cardiac surgery
What is adhesive pericarditis?
Sequela of serous or fibrinous pericarditis
Strands of fibrinous CT between visceral and pericardial surfaces
What are soldiers plaques?
Chronic pericardial disease
Pericardial thickenings that may become calcified.
4 forms of chronic pericarditis
Adhesive (sequela of serous / fibrinous)
Soldier's Plaques - benign thickening
Constrictive - sequela of purulent or caseous
Adhesive mediastinopericarditis - complication of radiation, surgery, purulent, or caseous
What is Carney Syndrom?
Autosomal Dominant condition characterized by multiple myxomas
What condition is rhabdomyoma occasionally associated with?
What kind of tumor is rhabdomyoma?
Most common cardiac tumor in children
What tumors spread to the heart?
carcinomas (lung, breast)
WBC malignancies (leukemia, lymphoma)
Three complications resulting from tumor derived mediators
1. Non Bacterial Thrombotic Endocarditis - assoc. w/ mucinous adenocarcinomas
2. Carcinoid heart disease (serotonin secreting neuroendocrine tumor of GI w/ hepatic metastasis)
3. Amyloidosis: excessive Ig production
Drug toxicity linked to decreased myocardial contractility and CHF
3 Etiological causes of CHF
1. decreased contractility
2. increased resistance to ventricular filling or ejection
3. systemic disease (severe anemia, hyperthyroidism)
What are "heart failure cells"?
Intra-alveolar macrophages filled w/ hemosiderin - indication of CHF chronicity
pulmonary congestion -> microhemorrhage -> phagocytosis of RBCs
Role of the kidney in CHF
decreased renal perfusion -> activation of renin - angiotensin - aldosterone system -> retention of Na+ and H2O -> worsening pulmonary edema
How much pericardial fluid is typically present?
What EKG changes are seen in acute pericarditis?
Stage 1: elevated, concave ST, and early PR depression in all leads except aVR
Stage 2: J point normalizes and decrease in T wave amplitude
Stage 3: T wave inversion
Stage 4: EKG resolution
3 components of pericardial friction rub as heard in acute pericarditis
1. Mid-systolic: V. contraction
2. Mid-diastolic: Rapid V. filling
3. Late-diastolic: A. contraction
What lab abnormalities are seen in acute pericarditis?
elevated WBC (11-13,000) w/ mild lymphocytosis (viral / idiopathic)
elevated CK, CK-MB, Troponin (inflamm of neighboring myocardium)
What infections are associated with pericarditis?
Viral: Echo, Coxsackie, Adeno, CMV (HIV pts)
Bacterial: Pneumococcus, Strep, Staph
Mycobacterial: TB, Avium intracellulare
What is the most common precursor to bacterial pericarditis?
Surgery (often w/ endocarditis and bacteremia)
Used to be pneumonia
What is Dressler's Syndrome?
Acute pericarditis weeks or months after MI
Autoimmune etiology - sensitization following necrosis
Treat w/ NSAIDS or steroids
Prognosis in pericarditis secondary to malignancy. Treatments?
Poor - limited survival. Marker for extensive disease.
Percutaneous drainage or surgical "window" in pericardium
What kind of pericarditis can radiation produce?
Constrictive or Restrictive - drainage may not relieve symptoms
4 drugs associated with pericarditis
What is treatment for endocarditis?
No standard treatment
Symptomatic: NSAIDS (2 weeks of indomethacin or ibuprofen)
Steroids - second line following NSAID failure
Colchicine - alternative to steroids
What is Ewart's sign and what is it indicative of?
Dullness, decreased breath sounds, egophony over posterior left lung
Due to lung compression by large pericardial sac
Suggests large pericardial effusion
How does pulsus paradoxus affect stroke voume?
increased right sided filling shifts interventricular septum left -> compression of LV -> decreased SV
PE findings in case of cardiac tamponade
Most common cause of constrictive pericarditis?
Post cardiac Sx
What is Kussmaul's sign and what does it indicate?
Increase in venous pressure during inspiration.
Seen in constrictive pericarditis - not tamponade
What is treatment for constrictive pericarditis?
Palliative - diuretics and salt restriction
Surgery - only definitive treatment - difficult procedure
What heart sound is heard in constrictive pericarditis?
Diastolic knock following S2 (higher pitch than S3)
Sudden cessation of filling due to constriction
Differentiate an Ejection Click and Opening Snap.
Ejection click: follows S1: bicuspid aortic valve/ aortic stenosis
Opening snap: follows S2: mitral stenosis
Differences between S3 and S4
S3: systolic HF
S4: diastolic HF
What are the components of the cardiovascular physical exam?
Inspect: JVP, precordium
Palpate: Pulses, precordium
Where is the usual point of maximal impulse (PMI) on cardiac exam?
4th or 5th IC space, mid clavicular line
What causes palpable "thrills" on cardiac exam?
Obstruction to LV outflow
Assoc. with loud murmurs
usually felt over L sternal border
Where is S1 splitting audible and considered normal?
Lower left sternal border: Tricuspid closes after mitral valve
What is paradoxical splitting?
splitting of S2 heard during expiration - delay in closure of aortic valve so P2 precedes A2
What are the histologic layers of a cardiac valve?
Valvular fibrosa: faces outflow chamber
Valvular spongiosa: central core of loose CT w/ proteoglycans
Elastin-rich layer: inflow surface (atrialis or ventricularis)
2 categories of valvular insufficiency
Primary: abnormality of valve cusps (myxomatous degeneration, infective endocarditis, rheumatic heart disease)
Secondary: abnormality of surrounding structures (chordae tendineae, papillary muscle, ventricular enlargement)
Clinical manifestations of calcific aortic stenosis and who is affected.
CHF, syncope, angina
Presents in older adults in 70-80s w/ previously normal valves
50s and 60s w/ bicuspid valve
What are some complications of Mitral Annular Calcification?
Usually benign, but can -> regurgitation, stenosis, arrhythmia (irritation of underlying ventricle),
What is another name for mitral valve prolapse and how is it usually detected?
Myxomatous Degeneration of the Mitral Valve
Usually detected as mid-systolic click in young woman
What genetic disorder is Mitral Valve Prolapse associated with?
What is seen microscopically in mitral valve prolapse?
Expansion of spongiosa layer and loss of collagen in fibrosa layer of valve
What is the pathogenesis of Rheumatic Heart Disease?
Cross-reacting antibodies induced by B-hemolytic GAS (S.pyogenes) pharyngitis
What is a microscopic indicator of Rheumatic Heart Disease?
Aschoff Bodies: (granulomas) areas of fibrinoid necrosis within heart muscle. Degenerating collagen, lymphocytes, plasma cells, activated macs (Caterpillar cells: nuclear chromatin is disposed into central wavy ribbon)
What pericardial disorder is assoc. with rheumatic heart disease?
What are indicators of chronic rheumatic heart disease?
Neovascularization and fibrotic valvular deformities - fusion of cusps and chordae tendineae, fishmouth stenosis
usually left sided
What antibodies can be found in a patient with acute rheumatic fever?
anti- streptolysin O and DNAase B
Major criteria of Acute Rheumatic Fever
Acute pancarditis (friction rub, arrhythmia, weakening, dilation)
Migratory polyarthritis of large joints (adult)
What are the primary organisms associated with infective endocarditis?
Strep viridans (other oral flora) (50-60% of cases, requires prev. valve damage)
Staph aureus (IV drug use)
Coagulase neg. staph (S. epidermidis) (prosthetic valves)
What is Marantic Endocarditis?
Nonbacterial Thrombotic Endocarditis (NBTE)
2 pathologies that can -> NBTE
1) Hypercoagulability assoc w/ debilitating illness (mucinous adenocarcinoma of the spleen, sepsis)
2) Endocardial injury (IC cath)
What areas of the heart are affected by carcinoid syndrome?
Right side valves - lungs break down serotonin to inactive byproduct.
Usually caused by hepatic metastasis of carcinoid tumor
Which ventricle better tolerates volume overload?
When does congenital valve stenosis typically?
May see symptoms w/ closure of ductus arteriosus.
Mostly seen in pediatrics
What is the equation for estimation of pressure gradient?
P2-P1 = 4(V2^2 - V1^2) where V=velocity
What mitral valve area is considered stenotic?
What differentiates moderate and severe mitral valve stenosis?
Moderate: AV pressure gradient is 6-12 mmHg (normal 13
CO: subnormal at rest, may fall w/ exertion
Sounds heard in mitral valve stenosis
Loud S1 (valve closing - high LV pressure needed to overcome AV pressure gradient -> sharp closing)
Opening Snap (after S2)
What is the most common EKG finding with mitral stenosis?
wide, notched p-wave (2 side by side p waves) - reflective of increased time required for depolarization of enlarged LA
What are indications for mitral valvotomy?
Symptoms w/ moderate stenosis
Asymptomatic female desiring pregnancy (Hx of symptoms)
Key PE findings in case of aortic stenosis
Narrow pulse pressure
Pulsus tardus and parvus (slow and weak)
Systolic Ejection click (can disappear w/ worsening stenosis)
Paradoxical S2 splitting
Ejection murmur / thrill
Physical exam findings with mitral valve prolapse
Midsystolic click, late systolic murmur if regurgitant.
Click moves away from S1 w/ increased preload (increase LV volume), and nearer w/ decreased preload.
Key physical exam findings in mitral regurgitation
High frequency systolic regurgitation murmur
Differential in Mitral regurgitation
Acute: Endocarditis, papillary muscle/ chordal rupture, trauma
Chronic: Congenital heart disease, mitral prolapse, rheumatic fever, hx of endocarditis, annular calcification, hypertrophic / dilated cardiomyopathy, hx of MI, radiation
Indication for surgery in Mitral regurgitation
Recent onset afib and pulmonary HTN
Asymptomatic: significant LV dilation / dysfunction
Differential Diagnosis in aortic regurgitation
Valve leaflet disease
Aortic root / surrounding apparatus disease: fibromuscular aortic ridge, prolapsed aortic leaflet, syphillis, hypertrophic cardiomyopathy, aortic root dilation, HTN, retrograde aortic dissection
Mechanical vs. Bioprosthetic replacement valves
Mechanical: durable, but req. chronic anticoag therapy and may -> endocarditis
Bioprosthetic: anticoag not needed, but less durable: tears and calcification
When is rheumatic fever's onset?
2-3 weeks post Strep A pharyngitis
stenotic valve disease 10-30 years later
what organs are affected by rheumatic fever?
brain, heart, skin, joints
Rheumatic fever diagnosis according to Jones criteria
Evidence of prior GAS infection and either 2 major ot 1 major and 2 minor of:
Major: Polyarthritis, erythema marginatum, carditis, chorea, subcutaneous nodules
Minor: Fever, acute phase proteins (ESR, CRP), arthralgia, prolonged PR interval
3 exceptions to Jones criteria
1. Chorea may be the only sign
2. Carditis may be the only sign if detected late
3. Lower threshold for diagnosis of current rheumatic fever
Differential Diagnosis in Rheumatic disease
connective tissue disease
What is the prognosis in acute rheumatic disease?
Dependent on severity of cardiac involvement at presentation
Valvular disease resolves in 25%
Worse cardiac disease w/ recurrent disease
Prophylaxis (penicillin) aids in resolution
What are the most common causes of native valve infective endocarditis?
Strep species and S. aureus
What is the organism most frequently seen in prosthetic valve infective endocarditis?
What is a mycotic aneurysm?
Aneurysm caused by bacterial infection of arterial wall. Septic embolus from infective endocarditis may cause.
How do streptococcus organisms adhere to thrombi?
Dextran in cell wall adheres to thrombus -> vegetation
What are Janeway lesions and what organism is most often associated?
Non-tender lesions on palms and soles caused by septic emboli embedded in dermis.
Most often S. aureus
What are Roth Spots?
Retinal hemorrhages caused by emboli - seen in infective endocarditis, but also DM, leukemia, pernicious anemia
What is the cause of petechiae in infective endocarditis?
Immune complex deposition in small vessels.
Painful raised bumps, usually on pads of fingers and toes, associated with bacterial endocarditis.
Caused by immune complex deposition w/ acute inflammation
What lab abnormalities are seen in infective endocarditis?
Anemia: normochromic, normocytic
Elevated CRP and ESR
Elevated Rheumatoid Factor (50%)
How is endocarditis treated?
High dose, long duration ABX (6-8 wks, often 2 abx)
Removal of prosthetic material
Indications for surgery in native valve endocarditis?
Persistent infection despite 7-10 days of abx treatment
-persisting fevers, + blood culture, elevated WBCs
Annular or aortic abscess
Refractory CHF due to valvular dysfunction
What are Duke Criteria?
For diagnosis of infective endocarditis
Major: 2 positive blood cultures (typical organisms)
1 positive culture for Coxiella burneti or antiphase I IgG Ab
Evidence of endocardial involvement (+ echo, new regurg
According to Duke criteria, what is needed for definite diagnosis of infective endocarditis?
2 major criteria
1 major + 3 minor
At what point is a widened QRS considered a danger?
Widened by 20-25%
Class I antiarrhythmic: adjust meds if this occurrs
Primary uses for 1A antiarrhythmics
SVT, AF, VT
What drug is "a pill in the pocket" for afib?
Flecainide: For afib patients who have exacerbations a few times / year, taking flecainide PRN rather than daily dosing is useful
What is the most potent agent for Afib and Vtach?
nota FDA approved for afib
Amiodarone drug interactions
Warfarin (cut in half if amio added), Digoxin, Quinidine, Procainamide, Flecainide
What are the characteristics of a syphilitic aortic aneurism?
Fusiform dilation of aortic arch and thoracic aorta
White, folded intima
Adventitia: narrowed vasa vasorum w/ lymphocytes and plasma cells
Media: patchy loss of sm. muscle cells w/ inflammation and fibrosis
What is a double-barreled aorta?
Aortic dissection that re-ruptures into the lumen
What is seen microscopically in aortic dissection?
"Cystic" degeneration of the media: Fragmentation and loss of elastic tissue replacement by pale, amorphous ECM
2 classifications of aortic dissection
Type A: more severe - requires immediate surgery: proximal +/- descending aorta
Type B: descending only
What is ANCA? 2 examples
Anti-neutrophil cytoplasmic antibody
c-ANCA (cytoplasmic) anti-proteinase 3
p-ANCA (perinuclear) anti-myeloperoxidase
What antibody is present in Kawasaki disease?
Anti-endothelial cell Ab
What antibody complex has been associated with polyarteritis nodosa?
Hep B surface Ag
What Ab-Ag complex is associated with Henoch-Schonlein purpura?
Anti-IgA immune complex
How are ANCAs pathogenic?
initial insult -> immune activation (neutrophil expression of antigens such as PR3 and MPO) -> production of ANCA -> binding of ANCA to neutrophil and degranulation -> vascular injury
What is seen in temporal arteritis?
intimal thickening, granulomatous inflammation, focal destruction of internal elastic lamina in temporal artery -> painful, palpable, nodular temporal artery
treat w/ steroids
What is Takayasu arteritis?
Mononuclear inflammation of aorta and major branches
Young women w/ neurologic or visual defects, HTN, weak or absent pulses of extremities.
involves c-ANCA, affects middle-aged men, responds to immunosuppressive therapy
1) necrotizing granulomatous inflammation of respiratory tract
2) necrotizing granulomatous inflammation of small vessels (esp. of respiratory tract)
3) necrotizing proliferative glomerulonephritis -> hematuria, proteinuria, renal failure
What organs are effected by polyarteritis nodosa?
Small- medium vessels of kidney, GI, heart (NOT lung)
Features of polyarteritis nodosa
Regions of fibrosis, necrosis, thrombosis, aneurism -> tissue ischemia
Young adults w/ fever, malaise, myalgia
Assoc. w/ HTN, GI bleeds, GI infarct
Responds to immunosuppresives
Features of Kawasaki disease
fever, mucosal erythema, desquamating rash, edema, cervical lymphadenopathy, cardiovascular complications (coronary aa involvement)
Features of microscopic polyantiitis
p-ANCA, no granulomas - usually onset after exposure to new antigen: Drug, malignancy
hemorrhagic skin lesions
Effects small vessels - capillaries, arterioles, venules
Similarly aged lesions
Childhood systemic vasculitits, usually follows URI
Necrotizing vasculitis w/ IgA immune complexes and C3
Effects skin, GI, kidneys (hypercellular mesangium)
What is Buerger's Disease?
Seen in heavy smokers >40 yoa
Distal ulcers and gangrene
Medium sized and small arteries - thrombosis, acute and chronic inflammation (stenotic corkscrew vessels)
What is Churg-Strauss Syndrome?
p-ANCA, middle-aged adults
1) allergic rhinitis, sinusitis, asthma
2) peripheral hypereosinophilia
3) extravascular and vascular necrotizing granulomas involving lungs, skin, PNS, CNS, heart, GI, kidney, musculoskeletal ss.
Do varicose veins predispose to thromboembolism?
Thrombosis - yes, but not embolism
What is nevus flammeus?
Birth mark, type of vascular ectasia
Regresses w/ time
Port wine stain - subtype that enlarges w/ growth
What is spider telangiectasia associated with?
Elevated estrogen (pregnancy, cirrhosis)
What is Kaposi's Sarcoma?
STI: HHV-8 or KSHV -> vascular proliferation
Classic: distal extremities of older, eastern-euro and mediterranean men
Endemic: aggressive - involves lymph nodes. Africa.
Immunosuppression assoc: AIDS and post-transplant. multi-organ
What is angiosarcoma and what are risk factors?
Aggressive malignancy of endothelial cells - often breast, liver
mass often contains multiple hemorrhages
Risk: radiation exposure, chronic lymphedema, vinyl chloride, thorotrast, arsenic
What are normal O2 saturations in the heart?
Left side: 100%
Right side: 75%
Coronary sinus: lowest sat in the heart - drains myocardium
What are causes of CHF in the newborn?
Severe valvular insufficiency (usually AV valve)
Myocarditis, arrhythmia, asphyxia
What is the main cause of CHF in the first 3-7 days of post natal life?
PDA dependent circulation:
Systemic (shock): Severe AS, Severe CoA, HLHS
Pulmonary (cyanosis): Pulmonary atresia, Severe PS
What are causes of CHF in the first 1-4 months of life?
Anomalous origin of L coronary artery from pulmonary artery
When does cyanosis become apparent?
5g/dL desaturated hemoglobin (normal is 2 g/dL)
What is a hyperoxia test?
Usually done on an infant to determine whether cyanosis is due to lung disease or circulation
Failure to elevate pO2 to 150 mmHg after 15 mins breathing 100% O2 suggests cyanotic congenital heart disease
In the case of a mixing lesion what is "ideal" saturation?
Higher that 85% indicates excess pulmonary blood flow.
What is the most common risk factor for stroke in an infant w/ cyanotic heart disease?
Iron deficiency anemia -> RBCs that do not deform when passing through vessels
What is the most common cyanotic congenital heart disease?
Tetralogy of Fallot
What is the most common congenital shunt lesion?
What CHD is associated with trisomy 21?
What CHD is associated with Turner's (XO)?
Coarctation of aorta
What CHD is associated with Trisomies 13 and 18?
What CHD is associated with Di George?
Tetralogy of Fallot
How is ASD usually detected? When are most ASDs repaired? What is a consequence of not reparing?
Usually found as an asymptomatic murmur.
Repaired at 2-5 years of age.
w/o repair: pulmonary vascular disease may develop in 4th decade or later.
Two most common locations of ASD
Why does ASD produce a L-> R shunt?
Low pulmonary resistance and high RV compliance.
In VSD, when does shunting develop, what causes the shunting, and when do CHF symptoms appear?
Shunting develops w/ drop in pulmonary resistance below systemic (with first breaths)
CHF symptoms appear in 1st 6 mos.
What are systemic responses to VSD?
Inadequate systemic flow:
Increased SNS activity -> tachycardia
Aldosterone -> fluid retention
RAS -> vasoconstriction
How does the size of a VSD relate to the intensity of a murmur sound?
What is Eisenmenger Syndrome?
L->R shunt -> elevated pulmonary flow and pressure -> pulmonary vascular disease and increase in pulmonary resistance.
If pulmonary resistance exceeds systemic, shunt reverses to R->L
Usually occurs in 2nd decade.
In what patient population is AV Septal Defect most common?
Trisomy 21: 40% w/ CHD, 40% of those w/ AVSD
50-60% of all AVSD have Trisomy 21
What extent of narrowing is considered significant in aortic coarctation?
50% or greater narrowing of lumen
Where does aortic coarctation occur?
distal to L Subclavian branch, opposite ductus arteriosus
What is the clinical effect of aortic coarction and how is it treated?
Closing of ductus arteriosus -> proximal HTN and decreased flow to lower limbs.
Give prostaglandin to maintain patency of ductus until surgery.
What genetic syndromes are associated with Tetralogy of Falot?
Trisomies 13,18, 21
Alagille syndrome w/ associated biliary atresia (Jagged-1 deletion, 20q: Notch ligand)
Components of ToF
Tetralogy of Fallot (PROVe)
Pulmonary Stenosis (RVOTO)
Right Ventricular Hypertrophy (RVOTO)
Ventricular Septal Defect
What is blue TET vs pink TET
Determined by degree of pulmonary stenosis
Pink TET: equal flow to lungs (minor pulmonary stenosis)
Blue TET: decreased flow to lungs -> cyanosis
When are Tet spells typically first observed in a child with Tetralogy of Fallot?
What is a typical murmur heard in a patient with Tetralogy of Fallot? What happens to the murmur during a Tet spell?
Murmur: 1) RVOT systolic murmur (pulmonary stenosis) 2) Holosystolic murmur from VSD (R->L shunt)
PS murmur fades due to increased systemic BF
Management of Tet spell
Knees to chest
When is ToF typically repaired?
Complicated patients may be 1-3 years
What does ToF repair consist of ?
VSD patch repair
Relief of RVOTO
What is the most common cyanotic lesion that presents in the neonate?
Dextro-Transposition of the Great Arteries
What secondary heart defect is essential to survival in cases of TGA?
Septal defect allows mixing of oxygenated and desaturated blood.
Otherwise, 2 circulations in parallel -> death
3 procedures for correction of TGA
1. Atrial switch (Mustard, Senning): largely abandoned
2. Rastelli: sometimes used: repair of VSD (graft connects Aorta to LV); closure of PA and implant of shunt to RV
3. Arterial switch (Jatene): switch arteries, connect coronaries to new aorta.
4 types of Persistant Truncus Arteriosus
I: one pulmonary artery branches from main trunk -> 2 lateral pulmonary aa.
II: two posterior / posterolateral pulmonary aa from main trunk
III: two lateral pulmonary aa. from main trunk
IV: pulmonary aa. do not arise from main trunk, but distal to L. subclavian a. no longer considered a form of TA.
What occurs in tricuspid atresia?
Unequal division of the AV canal -> complete occlusion of tricuspid valve and underdevelopment of RV.
Systemic venous return must pass through PFO
VSD allows communication from LV -> PA
High mortality in first weeks of life
What is a Blalock-Taussig shunt?
Create communication between R. subclavian and R. pulmonary arteries.
Increases pulmonary ciruclation.
What are the steps in correction of Hypoplastic Left Heart Syndrome?
1. Norwood: supply systemic cicrulation: Pulmonary aa. disconnected from Pulmonary Trunk, and Trunk connected to ascending aorta providing systemic circulation. BT or Sano shunt to provided circulation to Pulmonary aa.
2. Hemi-Fontan / Bi-directional Glenn: Pulmonary artery shunt removed and SVC re-routed through pulmonary arteries (reduces load on RH while maintaining pulmonary circulation under venous pressure).
3. Total Caval Pulmonary Anastamosis: IVC connected to pulmonary circulation (further reduces load on right heart, all systemic return routed through pulmonary circulation)
What is the timeline for correction of Hypoplastic Left Heart Syndrome?
Step 1: Ensure pulmonary and systemic ciruclation, protect pulmonary aa: Neonatal
Step 2: Connect SVC -> pulmonary: 6 mos
Step 3: Connect IVC -> pulmonary: 18-24 mos
Degrees of hypothermia
Profound: 18-24 (at 18C, up to 45 min circulatory arrest safe)
What are the effects of hypothermia?
Decreased metabolic rate
Reduced O2 consumption
Allows flow reduction
What is Atrioventricular septal defect and how is it repaired?
Combination of ASD and VSD with single atrioventricular valve.
Correction includes patching the septal defects and making the single valve into two - will never be normal, will always leak, and almost always requires future 2nd surgery.
What is increased in AVSD (flow, volume, resistance)?
All chamber volumes
pulmonary vascular resistance
When is ASVD surgery usually done and why?
Valve leaflets are too thin at neonatal stage - will not hold a suture.
What is a hybrid stage 1 procedure in treatment of hypoplastic left heart syndrome?
Branch pulmonary artery bands
Stenting of PDA
Balloon atrial septostomy (separate procedure)
**avoids heart and lung machine**
Formula to determine Qp/Qs and normal ratio.
Qp/Qs = (Arterial sat - mixed venous sat) / (pulmonary vein sat - pulmonary artery sat)
Normal 2.5 : 1
What happens to Qp/Qs in a single ventricle setting?
Qp/Qs = (Arterial sat - mixed venous sat) / (pulmonary vein sat - pulmonary artery sat)
Single ventricle: Sa = 82; Smv = 65; Spv = 100; Spa = 82
***Ideal value reduced to 1 : 1***
Should a patient with a single ventricle and 80% arterial sat be given O2?
Will unbalance Qp/Qs (normal is 1, will increase vastly) -> critical decrease in systemic blood flow
How can Pulmonary blood flow be increased?
Decrease pulmonary vascular resistance: O2, decrease pCO2, sedate, lower MAP, Milrinone, Nipride, NO
Increase Systemic vascular resistance: alpha agents: neosynepherine, NEpi, Epi
How can pulmonary blood flow be decreased?
Increase pulmonary vascular resistance: increase pCO2, decrease FiO2, PEEP
Decrease systemic vascular resistance: Morphine, Nipride, Milrinone
Causes of dilated cardiomyopathy
Genetic (1/3 of cases): usually AD (cytoskeleton, mitochondria, nuclear membrane, sarcomere)
Toxicity: ETOH, drug tox
Thiamine deficiency: wet beriberi
Post myocarditis (due to enteroviruses)
Pregnancy-related (peripartum): hemodynamic changes
What is Arrhythmogenic Right Ventricular Cardiomyopathy?
Form of dilated cardiomyopathy in which Right Ventricular myocardium is replaced by fat and fibrous tissue -> Right HF and arrhythmias
Inherited - AD
Another name for hypertrophic cardiomyopathy
Idiopathic Hypertrophic Subaortic Stenosis
What percent of hypertrophic cardiomyopathy cases have an underlying genetic cause?
Causes of myocarditis
a) enterovirus (coxsackie A and B, echovirus), CMV, HIV
b) bacteria (Borellia Burgdorferi - Lyme)
c) fungi (Candida)
d) parasites (T.cruzi (Chagas), T.gondii)
Immunologic disorder: drug hypersensitivity, autoimmune (acute rheumatic fever, SLE)
Name 2 drugs known for cardiotoxicity
Cyclophosphamide (alkylating agent): vascular toxicity -> cardiac hemorrhage
Doxorubicin (DNA binding): myocyte toxicity -> myocyte vacuolation and lysis -> dilated cardiomyopathy
What is a cause of contraction band necrosis?
pheochromocytoma, cocaine abuse
What is present in senile cardiac amyloidosis?
2 forms of systemic amyloidosis that can effect the heart
primary (AL): Ig light chain
secndary (AA): serum amyloid associated protein
What is isolated atrial amyloidosis?
What stain is used in diagnosis of amyloidosis?
Congo red -> yellow / green birefringence
What is the most common cause of CHF?
Ischemic heart disease secondary to coronary artery atherosclerosis
What is the 1 year mortality for patients with NYHA class IV heart failure?
3 gene mutations associated with dilated cardiomyopathy
Sarcomeric contractile machinery
When does peripartum cardiomyopathy usually occur?
last month of pregnancy up to 6 mos post partum
What is seen microscopically in peripartum cardiomyopathy?
Lymphocytic infiltrate in myocardium
What is Takotsubo Cardiomyopathy?
Broken Heart Syndrome
Stress related increase in catecholamines -> acute dilated cariomyopathy
Contraction band necrosis is visible
Reversible w/ proper support
EKG: may look like MI
What is high output heart failure and what are some causes?
Normal heart under excessive burden -> failure
A-V fistula: decreased systemic resistance, shunt from A->V, inadequate perfusion
Renal retention of Na and H2O -> expanded volume + elevated R and L pressures
Thyrotoxicosis, severe Paget's of bone, severe anemia
What are the functions of BNP?
Opposes Renin-Angiotensin-Aldosterone system
Renal Na excretion
Inhibits renin secretion
How does Digoxin work?
Inhibits Na/K ATPase -> decreased intracellular Na++ -> decreased activity of Na/Ca exchanger -> elevated IC Ca++
slowed AV conduction
increased filling time
decreased myocardial O2 demand
What defines chronic kidney disease?
GFR 300 mg/d
200 mg/g spot urine
What pressures are diagnostic for HTN?
140 systolic or 90 diastolic
If diabetic or renal insufficiency: 130/80
What are stage 1 and stage 2 HTN?
Stage 1: 140-159 systolic or 90-99 diastolic
Stage 2: 160+ or 100+
What race has lowest BP control rates?
What is resistant HTN?
BP above goal when taking 3 meds of different classes, one being a diuretic
BP below goal when taking 4 meds of different classes, one being a diuretic
What is the most frequently used drug in treatment of HTN emergency?
How quickly should BP be reduced in the setting of hypertensive emergency?
10-15% in the first few hours
25% in first 24 hrs
If aortic dissection must lower more quickly and to greater extent
3 causes of secondary HTN
1) primary aldosteronism
How does HTN caused by unilateral and bilateral renal artery stenosis compare?
Unilateral: renin dependent - very responsive to ACEi and ARB
Bilateral: plasma volume expansion - little response to ACEi and ARB - diuretic responsive
What is the best screening test for pheochromocytoma?
What percent of patients with pheochromocytoma present with HTN and what are other symptoms?
50% have HTN
Other symptoms: Headache, sweating, anxiety, tachycardia
Pallor, orthostatic hypotension, nervousness, weight loss
On average, what is the difference in systolic BP between blacks and whites w/ HTN? What is the impact of equalization?
Equalizing: decrease stroke deaths: 2,190 ; Heart disease deaths: 5,480
How to calculate MAP
MAP = [2(DBP) + SBP] / 3
MAP = SV * HR * PVR
What are EKG criteria for RBBB?
QRS prolongation of 0.12s +
Slurred S wave in I and V6
RSR' in V1
What is EKG criteria for LBBB?
1: QRS wide: 0.12 +
2: I and V6: wide monomorphic R waves w/ no Q
3: V1: broad monomorphic S, may have small r.
How does SBP and PP differ between the aorta and brachial artery?
Increased by 10-15 mmHg in brachial due to reflected wave. Diastolic is same (thus widened PP)
In a normal person, how does BP differ between day and night?
Night is 10-20% lower
What strategy eliminates racial differences in BP lowering effects of drugs?
Addition of a diuretic or CCB to ACEi/ ARB therapy.
* ACE/ARB less effective than diuretics or CCB in African American
* ACE/ARB less effective in African American than in white
How does the effectiveness of hydrochlorothiazide compare to clorthalidone?
Clorthalidone lowers BP more effectively than HCTZ (and requires lower dosing)