Cardio Flashcards 2
What is shock?
Clinical syndrome resulting from inadequate tissue perfusion and oxygen delivery to meet metabolic demands.
Results in global tissue hypoperfusion and metabolic acidosis
What occurs in cells in response to decreased systemic oxygen delivery?
Switch to anaerobic metabolism, causing systematic acidosis
ATP depletion causes ion pump dysfunction
Cellular edema and hydrolysis of cellular membranes occurs, resulting in cell death
What is the goal of the body in shock?
Maintain cerebral and cardiac perfusion
Vasoconstriction of splanchnic, musculoskeletal and renal blood flow
Can cause mulit-organ failure and death if the underlying abnormalities are not corrected
What is the ultimate outcome of shock, if underlying abnormalities are not corrected?
Multiorgan failure and death - caused by systemic metabolic lacti acidosis that overcomes the body’s compensatory mechanisms
What are useful hemodynamic parameters in shock?
Systemic vascular resistance
Cardiac output
Mixed venous oxygen saturation
Pulmonary capillary wedge pressure
central venous pressure
What is SVR?
Systemic vascular resistance
reflects degree of vasoconstriction/vasodilation in peripheral vasculature
What is CO?
Cardiac output
HR*Stroke volume
What is SvO2?
Mixed venous oxygen saturation
Saturation of systemic venous blood after delivering oxygen to peripheral tissues
What is PCWP?
Pulmonary capillary wedge pressure
surrogate for left arterial pressure
What is CVP?
Central venous pressure
surrogate for right atrial pressure
What hemodynamic measurement is a surrogate for left atrial pressure?
pulmonary capillary wedge pressure
Which hemodynamic measurement is a surrogate for right atrial pressure?
Central venous pressure
What is the normal value of right atrial pressure/central venous pressure?
0-6 mmHg
What is the normal value for systolic pulmonary artery pressure?
15-30 mmHg
What is the normal value for End-diastolic pulmonary artery pressure?
4-12 mmHg
What is the normal value for mean pulmonary artery pressure?
9-19 mmHg
What is the normal value for mean pulmonary capillary wedge pressure (PCWP)
i.e. left atrial pressure
4-12 mmHg
What is the normal value for cardiac output?
4-8 L/min
What is the normal value for mixed venous oxygen saturation (SvO2)?
>70%
What is the normal value for systemic vascular resistance?
800-1200 dynes*sec/cm^5
How is mean arterial pressure calculated?
MAP = CO x SVR
Recall, CO = HR * SV
What defines hypovolemic shock?
Heart pumps well, but not enough blood volume to pump
What causes hypovolemic shock?
decreased intravascular volume (preload) - causes decreased stroke volume
Hemorrhagic (trauma, GI bleed, AAA rupture)
Hypovolemic - burns, GI losses, dehydration, third spacing, diabetic ketoacidosis
What is another name for distributive shock?
Vasodilatory shock
What is distributive (or vasodilatory) shock?
Heart pumps well, but there is peripheral vasodilation due to loss of vessel tone
What caues distributive (vasodilatory) shock?
Loss of vessel tone
Can be caused by overwhelming inflammation (sepsis, toxic shock syndrome, anaphylaxis)
Can be caused by C-spine or thoracic cord injuries - decreased sympathetic tone
Toxins - cellular poisons (Carbon monoxide, methemoglobinema, cyanide)
What is cardiogenic shock?
Heart fails to pump blood out
What are causes of cardiogenic shock?
Decreased contractility (MI, myocarditis, cardiomyopathy)
Mechanical dysfunction (papillary muscle rupture post MI, severe aortic stenosis, rupture of ventricular aneurysms)
Arrhythmia (heart block, ventricular achycardia, supraventricular tachycardia, atrial fibrillation, etc.)
Caridotoxicity (β-blocker or CCB overdose)
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What are the stages of shock?
Insult
Preshock
Shock
End organ dysfunction
What occurs during the insult stage of shock?
Splenic rupture, blood loss, MI, anaphylaxis, etc.
What occurs during the preshock stage of shock?
Hemostatic compensation to maintain MAP within normal ranges
(After insult)
What occurs during the shock stage of shock?
After preshock stage
Compensatory mechanisms fail and MAP declines
What occurs during the end-organ dysfunction stage of shock?
Occurs after shock stage
Cell death and organ failure
What is the definition of cardiogenic shock?
Systemic hypoperfusion secondary to severe depression of cardiac output and sustained systolic arterial hypotension despite elevating filling pressures
What are the three main keys to categorize someone as having cardiogenic shock?
Severe depression of cardiac output
Sustained arterial hypotension
Elevated filling pressures
How do patients with cardiogenic shock present?
Hypotension
Tachycardia/tachypnea
Elevated neck veins
Rales, gallop rhythm (S3)
New murmur
Cool extremities
Will patients in cardiogenic shock present with cool or warm extremities?
Cool extremities - physiological response to maintain perfusion to vital organs
What is the goal of medical treatment of shock?
Try to maintain mean arterial pressure
What agents are useful in the treatment of shock?
Dopamine - α1, β1, β2 and DA agonist
Dobutamine- α1, β1, β2 agonist
Norepinephrine - α1, β1, β2 agonist
Epinephrine - α1, β1, β2 agonist
How does dopamine help patients in shock?
Stimulates D1 receptors (coronary, renal, mesenteric and cerebral beds)
Promotes vasodilation and increased flow
Also direct precursor to norepinephrine
How does dobutamine help patients in shock?
Vascular smooth muscle binding results in β1 adrenergic agonism/antagonism and β2 stimulation with net vasodilation (low doses)
Tolerance can develop though
(not the best agent)
How does norepinephrine help patients in shock?
increases systolic, diastolic, and pulse pressure wtih minimal impact on cardiac output
Coronary flow is increased owing to elevated diastolic blood pressure and indirect stimulation of cardiomyocytes - release vasodilators
What are downfalls of adrenergic inotropes in shock patients?
Can further increase heart rate, afterload, and wall tension
Further exacerbating the problem
What non-pharmacologic treatmetns are available to treat shock?
Left ventricular assist devices (LVAD), which unload the heart, boost coronary and systemic flow, and promotes myocardial and end-organ recovery
What is an intra-aortic balloon pump (IABP)?
Inflates in diastole, deflates in systole
Displaces blood that is upstream towards the heart, increasing diastolic pressure
When deflated - draws blood volume downstream, reducing end-diastolic pressure and left ventricular afterload (creates suction)
Can also decrease LV volume, systolic work and myocardial oxygen consumption
Reduces end-diastolic and peak diastolic aortic pressure
What are the hemodynamic effects of IABP (intraaortic balloon pump)?
Reduce systolic pressure
Increase diastolic pressure
Reduces heart rate
Decreases pulmonary wedge pressure (LA pressure
Elevate cardiac output
Decrease LV wall stress
What is the most common cause of cardiogenic shock?
Acute MI
What two broad categories of pharmacologic treatment is available for the treatment of shock?
Vasopressors and inotropic agents
What are the two aortic valve diseases?
Stenois
Insufficiency
What is the normal aortic valve area?
3-4 cm^2
When do aortic valve stenosis symptoms start presenting?
Shen stenosis makes valve area 1/4 of normal area
What defines aortic stenosis and severe aortic stenosis?
When area becomes less than 2 cm^2 ( less than 1 cm^2 for severe)
Normal is 3-4 cm^2
What are three types of aortic stenosis?
Supravalvular - in ascending aorta
Subvalvular - from hypertrophic caridiomyopathy, for instance
Valvular
What are etiologies of aortic stenosis?
Congenital - leaflet cusps are deformed - can be unicuspid or bicuspid valve; or a fused tricuspid valve
Acquired - degenerative, rehumatic, or other
Congenital will present earlier than acquired or degenerative
What type of aortic stenosis do patients under 70 usually present with?
Congenital
What type of aortic stenosis do patients over 70 yo usually present with?
Acquired
What is the most common etiology of aortic stenosis that will be seen in the next 10-20 years?
Degenerative calcification - seen in patients in their 70s-80s, comorbid with risk factors for CAD
(because of aging population)
What is the effect of aortic stenosis on the left ventricle?
Imposes increased afterload
Causes concentric hypertrophy
What type of hypertrophy is seen in aortic stenosis?
Concentric left ventricular hypertrophy
What symptoms do you see in aortic stenosis?
Decreased outflow - dizziness, etc
Left heart failure symptoms - elevated left atrium pressures - backup to lungs - shortness of breath
Angina - increased work load of left ventricle
What type of murmur is heard in aortic stenosis?
Systolic crescendo/decrescendo - diamond shape
Ejection systolic murmur
What can happen to the second heart sound in aortic stenosis?
Can run into pulmonic valve sound - can even run past it and become paradoxical split
What occurs during paradoxical S2 splitting?
Occurs in Aortic Stenosis
Upon inspiration - split decreases. Upon exhalation, split increases
Normally - aortic first, pulmonary second; split on inspiration
What changes in the heart sounds do you see with aortic stenosis?
Systolic ejection murmur (crescendo decrescendo)
S2 sound changes - A2 delays - may even occur after P2 (reversal of splitting/timing)
More noticable upon expiration
What is the difference between the systolic murmur seen in aortic stenosis and in obstructive hypertrophic cardiomyopathy?
Aortic stenosis - there is a delay between S1 and murmur - also crescendo, decrescendo
HCM - starts at S1 and is relatively constant throughout
AS:
HCM:
How do you reduce the hypertrophic cardiomyopathy murmur sounds?
Squat
Opens up LV outflow
How do you increase the murmur from a hypertrophic cardiomyopathy?
Stand up from squating position
Valsalva maneuver to reduce size of LV
How do you exacerbate murmur seen in aortic stenosis?
Make patient run around and then you can hear it better - but does not help to differentiate from HCM
How do patients with aortic stenosis usually present?
Asymptomatic - onset of symptoms is a poor prognostic indicator
How good of a prognostic indicator is symptom onset in aortic stenosis?
Poor
What are the classical symptoms of severe aortic stenosis?
Dyspnea on exertion
Syncope - low forward cardiac output
Angina
Sudden death
What is DOE?
Dypsnea on exertion
What are physical findings of aortic stenosis?
Slow rising carotid pulse (pulsus tardus) and decreased pulse amplitude (pulsus parvus)
Soft and split second heart sound, S4 gallop
Systolic ejection murmur (crescendo-decrescendo
Other manifestations - bleeding, embolic events, CAD)
What are pulse findings in aortic stenosis?
Slow rising carotid pulse (pulsus tardus)
Decreased pulse amplitude (pulsus parvus)
What are heart sound findings in aortic stenosis?
Soft and split second heart sound and reverse split
S4 gallop due to left ventricular hypertrophy
Systolic ejection murmur - diamond shaped crescendo-decrescendo (peaks later as severity of stenosis increases)
What is pulsus tardus?
Slwo rising carotid pulse
What is pulsus parvus?
Decreased pulse amplitud
What is characteristic of the natural history of aortic stenosis after developing symptoms?
Sudden deaths soon after devleopment of symptoms if no valve replacement
What EKG findings do you see on AS?
Left axis deviation from hypertrophy
Conduction blocks from calcification
What can you see on chest x-ray in aortic stenosis?
Calcification
Other non-specific findings (hypertrophy)
What is the most specific diagnostic tool for diagnosing valvular heart disease?
Echocardiogram
Why must you perform cardiac catheterization on aortic stenosis patients?
Must ensure there is no coronary artery disease before undergoing surgery for valvular repair
What defines mild aortic stenosis?
Valve area > 1.5 cm^2
What defines moderate aortic stenosis?
Valve area 1-1.5 cm^2
What defines severe aortic stenosis?
Valve area < 1 cm^2
How do you manage patients with aortic stenosis?
Antibiotic prophylaxis in dental procedures or with prostetic valves or with patients with history of endocarditis
Few mediations - don’t want to give vasodilators because you’ll increase chances of syncope
Aortic valve replacement is definitive treatment
Aortic balloon valvotomy as a bridge to surgery
Why does aortic balloon valvotomy not work for aortic stenosis?
Too much calcium - can reclose or spread to brain
What are indications for surgery in aortic stenosis?
Any symptomatic patient with severe aortic stenosis
Any patient with decreasing ejection fraction
Any patient already undergoing CABG with moderate or severe stenosis
What is the only situation in which patients with moderate aortic stenosis are indicated for replacement surgery?
When they are already undergoing CABG
What is aortic regurgitation?
Leakage of blood back into the LV during diastole
What causes aortic regurgitation?
Ineffective coaptation of the aortic cusps
What is the pathophysiological result of aortic regurgitation?
Combined pressure and volume overload
Causes compensatory LV dilatation and hypertrophy
Progressive dilation leads to heart failure
What can cause acute aortic regurgitation?
Endocarditis - leaflet perforation or rupture from infection
Aortic dissection - can split aortic wall and continue through to the valve
What are avenues for treatment for patients with acute aortic regurgitation?
True surgical emergency
Medicines as a bridge to surgery:
Give positive ionotrope (dopamine, dobutamine)
Give vasodilators (nitroprusside)
Avoid beta blockers
NO balloon pumps
How do vasodilators help in the short-term treatment of aortic regurgitation?
Keeps blood in periphery and reduces amount of blood that flows back into heart
What are balloon pumps contraindicated in aortic regurgitation/aortic insufficiency?
Will only make it worse - make more blood flow backwards
What can cause chronic aortic regurgitation?
Bicuspid aortic valve (normally tricuspid)
Rheumatic
Infective endocarditis
Marfans
What type of murmur will you see in aortic regurgitation?
Early, low pitched diastolic murmur
What is the most common diastolic murmur?
Aortic regurgitation murmur
What changes in heart sounds will you see in aortic regurgitation?
Functional stenosis of aortic valve too - small crescendo-decrescendo systolic murmur
More importantly, low-pitched early diastolic murmur
What are differences in heart sounds between acute and chronic aortic regurgitation murmurs?
In acute - the diastolic murmur is very quick and faint - difficult to pick up
What are cliical features of aortic regurgitation?
Asymptomatic until 30s-40s
Progressive symptoms:
Dyspnea - exertional, orthopnea, PND
Angina
Palpitations - increased contractile force
No syncope
What clinical features of aortic stenosis are absent in aortic regurgitation?
Syncope - instead feel palpitations
Issue is increased volume!
What physical findings do oyu see in patients with aortic regurgitaiton?
Wide pulse pressure -very sensitive
Hyperdynamic and displaced apical impulse - can see chest wall excursion and feel it
Diastolic blowing murmur
Austin flint murmur - at apex - regurgitant jet impinges on anterior mitral valve leaflet causing vibration (resembles mitral valve murmur)
Systolic ejection murmur - increased flow across aortic valve
What is an Austin flint murmur?
Regurgitant jet impinges on anterior mitral valve leaflet causing vibration (resembles mitral valve murmur)
Heard best at apex
What pulse changes do you see in patients with aortic regurgitation?
Wide pulse pressure - very sensitive finding
When do you see Austin flint murmurs?
In aortic regurgitation
Regurgitant jet impinges on anterior mitral valve leaflet causing vibration (resembles mitral valve murmur)
What is Corrigan’s sign?
In aortic regurgitation - dancing carotids
What is Quincke’s pulse?
Exaggerated redennign and blanching of nail beds -pulsatile
seen in Aortic regurgitation
What is the main feature of aortic regurgitation that you can see signs of in almost all organs?
Hyperdynamism of the cardiac system - nail beds, chest excursion, etc
What do you see on chest x-ray in patients wtih aortic regurgitation?
Enlarged cardiac silhouette
Aortic root enlargement
What do you see on echocardiogram in patients with aortic regurgitation?
AV and aortic root measurements
LV dimensions and funciton
Can see flow-back via doppler
What do you do to manage aortic regurgitation in patients?
Prophylaxis for infectious endocarditis in dental procedures
Vasodilators (ACE inhibitors), Nifedipine improve stroke volume and reduce regurgitation (only if patient is symptomatic or hypertensive)
Surgical treatment is definitive
When do you perform surgery on patients with aortic regurgitation?
When there are any symptoms at rest or with exercise
Or in patients who are asymptomatic and whose ejection fraction drops below 50% or LV becomes dilated
What pharmacologic treatments are given to patients with aortic regurgitation?
Vasodilators (ACE inhbitors), Nifedipine to improve stroke volume
Only if patient is symptomatic or hypertensive
What is infectious endocarditis?
Infection of endocardial surface
What are the four classification groups of infective endocarditis?
Native valve endocarditis
Prosthetic valve endocarditis
IV druge abuse endocarditis
Nosocomial endocarditis
What are charactaristics of acute infectious endocarditis?
Fulminant - rapidly destructive
Affects normal heart valves
Metastatic foci
Commonly Staph
Usually fatal within 6 weeks if untreated
What are characteristics of subacute infectious endocarditis?
Often affects damaged heart valves
Indolent in nature - slower
Fatal if untreated, usually by one year
What is the common cause of acute infectious endocarditis?
Staph - staph aureus or coagulase negative
What type of endocarditis is caused by staphylococci?
Acute
What organisms are commonly implicated in subacute infectious endocarditis?
Streptococci species
What kind of endocarditis is seen with stretpococcal infections?
Subacute (viridans, enterococci, bovis, others)
What is IE?
Infectious endocarditis
What is the pathogenesis of IE?
Turbulent blood flow leads to the development of thrombus at site of injury
Bacteria that enters the circulation can adhere and colonize the injured surface
What is the most common non-bacterial thrombotic endocarditis seen?
In SLE - generalized state of inflammation
Libman-Sacks Endocarditis
What are cardiac lesions that predispose to endocarditis?
Rheumatic valvular disease
Acquired valvular lesions (left sided more common - higher shear stress)
Hypertrophic obstructive cardiomyopathy
Congenital heart disease
Surgically implantable intravascular hardware
Which side of the heart are lesions that predispose to endocarditis more commonly seen? Why? What is the exception?
On the left side - higher flow rates - more shear stress
On the right side in IV drug use
What are symptoms of acute IE?
High grade fever, chills
Shortness of breath
Arthralgias/myalgias
Abdominal pain (emboli)
Pleuritic chest pain (emboli)
Back pain (emboli)
What are symptoms of subacute IE?
Low-grade fever (indolent course)
Anorexia
Weight loss
Fatigue
Arthralgias/myalgias
Abdominal pain
N/V
(many non-specific symptoms)
Can be over days to weeks to months
What are signs of IE?
Fever
Clubbing - not specific
Splenomegaly
Neurological manifestations
Heart murmur - NEW
Peripheral manifestations - Osler’s nodes, Subungal hemorrhage, Janeway lesions, Roth Spots, petechiae
Why do you see splenomegaly in IE?
Attempting to clear the infection
What types of murmurs are seen in IE?
NEW murmurs
What are cardiac manifestations of IE?
New murmurs - regurgitations
CHF - valvular damage, myocarditis, intracardiac fistulas
Perivalvular abscesses
Fistula
Pericarditis
Heart block
essentially, all sorts of things
What are non-cardiac signs of IE?
Septic embolization - petechial hemorrhage, Janeway lesions, Oslers nodes
Infarcts in skin, spleen, kidney, meninges, skeletal system
Embolic strokes
Mycotic aneurysms - infetion of vasa vasorium of the blood vessel
Brain microabscesses
Glomerulonephritis
WHereaWhere can you see petechia from IE?
Skin, conjuntiva, palate
Mucous membranes and extremities
What are splinter hemorrhages?
Non-specific, nonblanching, linear reddish-brown lesions found under nail bed
What are Osler’s Nodes?
Extremely painful nodes in fingers
More specific for IE and more common in subacute
Erythematous
What are Janeway lesions?
Specific, erythematous, blanching macules that are not painful
On palms and soles
Seen in IE
What are Roth spots?
Seen on fundoscopic examination
Indicative of IE
What labs are helpful in identifying IE?
CBC showing anemia, leukocytosis
Blood cultures - from 3 different sites at least 1 hour apart
Evidence of brucella, bartonella, legionella, c. burnetti
Signs of inflammation:
Elevated ESR, CRP
Reduction of serum complement
Elevated Rheumatoid factor
What do you see in chest x-ray in IE?
Try to find clear lung fields to rule out pulmonary infections
May see multiple focal infiltrates and calcification
What can you see on EKG in IE?
May see ischemia or arrhythmias, or heart blocks
What can you see on echocardiography in IE?
Can see vegetations
What are major criteria for diagnosis of endocarditis?
Persistently positive blood culture for typical organisms
Vegetations, dehiscence, abscesses on echocardiogram
New valvular regurgitation murmur
Coxiella burnetii infection
What are indications of definite endocarditis?
2 major clinical criteria
1 major and any 3 minor
5 minor critera
Histology findings
+ Gram stain or cultures from surgery or autopsy
What are minor critera for the diagnosis of endocarditis?
Predisposing heart condition or IV drug use
Fever
Emboli to organs/brain, hemorrhages
Glomerulonephritis, Osler’s nodes, Roth spots, Rheumatoid factor
Positive blood cultures that don’t meet specific criteria
When do you treat a patient for infectious endocarditis?
Wait until blood samples come back from microbiology before treating with antibiotics - don’t want to conflate results
You can wait 24 hours
How do you treat IE?
4-6 weeks of IV parenteral antibiotics
When might surgery benefit a patient with IE?
If they are in congestive heart failure
If there is a prosthetic valve endocarditis
If it is caused by fungal or other highly-resistant organisms
If there are perivalvular infections with abscesses or fistula formations
When is prophylaxis indicated for IE?
Patients have:
Prosthetic heart valves
Prior history of IE
Unrepaired cyanotic congenital heart disease (shunts and gradients and non-laminar flow)
When do you give prophylaxis for IE?
To protect in the time frame during which bacteremia will happen - i.e. right before, through, and after a dental procedure
What procedures warrant prophylaxis for endocarditis?
Dental procedures
If there is evidence of infection during:
Upper respiratory tract procedures
GU or GI procedures
Procedures of skin, or MSK
If there is a gradient between the left atrium and left ventricle during diastole, which valve is affected?
Mitral
What type of murmur will be present in mitral valve issues?
Diastolic
What happens to S1 in mitral stenosis?
Fast mitral valve closure - S1 is loud
What happens to S2 in mitral stenosis?
Loud becuase of pulmonary hypertension
During which cardiac phase will you see a murmur in mitral regurgitation?
Systole - it is holosystolic (pansystolic)
What type of murmur do you see during mitral regurgitation?
Holosystolic (pansystolic)
Do you see a diastolic murmur in mitral regurgitation?
Yes - lots of blood that entered the atrium is trying to now enter the ventricle
Flow murmur (relative mitral stenosis, for the amount of blood that is flowing through)
Durign what stage of the cardiac cycle do we see murmurs during mitral valve prolapse?
Systole
What maneuvers can you perform to help diagnose mitral valve prolapse?
Delay the click - make the patient squat - this makes the venous return increase. SVR increases. LV dilates a bit and tightens. Valve has lesser tendency to prolapse and it takes longer in systole for it to prolapse
Accelerate the click - standing will bring it back
How do the murmurs of aortic stenosis and hypertrophic cardiomyopathy differ with valsalva/squatting?
Do dihydropyridines have more of a vasodilating or cardiac depressan effect?
Vasodilating
Decrease myocardial oxygen demand (venodilation and arterial dilation)
These are CCBs
How do dihydropyridines work?
Vasodilate more than cardiac depressant
Decreased myocardial O2 demand by venodilating and dilating arteries
how do nondihydropyridines work?
Cardiac depressants more than vasodilating
Reduce HR, contractility to lower O2 demand
Careful with β-blockers
Do nondihydropyridines have more of a vasodilating or cardiac depressant effect?
Cardiac depressant
Reduce HR, contractility
(Calcium channel blocker)
What is the effect of ranolazine on stable CAD?
Decreases anginal frequency
Improves exercise tolerane
Unclear how
What drug can be given to CAD patients to decrease anginal frequency and improve exercise tolerance?
Ranolazine
What is a benefit of a drug-eluting stent?
Reduces risk for restenosis and subsequent revascularization
May result in higher thrombotic risk
What is a potential risk in drug-eluting stents?
Higher thrombotic risk
What are indications for percutaneous coronary intervention?
Refractory symptoms despite optimizing medical therapy
Intolerance to medical hterapy
Always attempt medical therapy first!!
What is a benefit from arterial vs venous grafts for coronary revascularization?
Higher patency at 10 years, but used for most critical epicardial stenoses
typically use saphenous veins from leg
What is PCI?
Percutaneous coronary intervention (i.e. stent)
What is CABG?
Coronary artery bypass graft
What are advantages of PCI vs CABG?
Lower procedural risk
Minimal recuperation (more and more done on outpatient basis)
What are advantages of CABG vs PCI?
Complete revascularization
No need for long term dual antiplatelet therapy (causing bleeding risk)
Has a proven mortality benefit
What is antithrombin?
Plasma protein that inactivates thrombin (Factor IIa)
Heparan increases its efficacy 1000 fold
What is the effect of heparan on antithrombin?
Increases efficacy 1000 fold
antithrombin inactivates thrombin (factor IIa)
What is thrombomodulin/proteinC/protein S?
Trombin receptor present on endothelial cells
Bound thrombin is unable to convert fibrinogen to fibrin
The thrombin/thrombomodulin complex activates protein C which degrades Factors Va and VIIa
What is tissue factor pathway inhibitor (TFPI?
Factor VIIa + TFPI initiate the extrinsic pathway of coagulation
This is inhibited by factor Xa (negative feedback)
What is tissue plasminogen activator (TPA)?
Cleaves plasminogen to plasmin, which degrades fibrin clots
Is secreted by endothelial cells in response to clot formation
Important in clot lysis
What are the components of a clot?
Platelets + fibrin
What are clotting factors important in preventing thrombosis?
Antithrombin
Protein C/Protein S/Thrombomodulin
Tissue Factor Pathway Inhibitor (TFPI)
What are endothelial anti-thrombotic mechanisms?
Platelet inhibition - prostacyclin and NO; ADP->adenosine conversion
Vasodilation
What is the effect of prostacycin on thrombosis?
Prostacyclin released by endothelial cells inhibits platelet activation
Prostacyclin is also vasodilatory (minimizes contact between procoagulant factors (reducing propensity of thrombus formation)
What is the effect of NO on thrombus formation?
NO inhibits platelet activation
NO is a vasodilator - minimizes contact between procoagulant factors, reducing propensity to form thrombus
What is the major cause of coronary thrombosis?
Plaque rupture
What can cause plaque rupture that leads to coronary thrombosis?
Chemical factors that destabilize fibrous cap (cytokines inhibit collagen synthesis, a key component; MMPs within plaques degrade matrix)
Physical stresses (shoulder region prone to rupture due to high stress; high BP; torsion from myocardial contraction)
Triggers (strenuous activity or emotional upset; early morning with high BP, viscosity, sympathetic tone)
What are chemical factors that can estabilize a fibrous cap and cause plaque rupture?
T lymphocytes secrete cytokines that inhibit collagen synthesis
Enzymes in plaques degrade matrix - matrix metalloproteinases
What are physical stresses that can cause plaque rupture and cause coronary thrombosis?
High stress on the shoulder region of the cap (most prone)
Intraluminal blood pressure
Torsion from myocardial contraction
What are triggers of plaque rupture that can cause coronary thrombosis?
Strenuous physical activity or emotional upset
MIs usually occur in the early morning hours when physiologic stress is highest (BP, blood viscosity, sympathetic tone)
What time of day is more likely for an MI to occur? Why?
Early mornin hours
Physiologic stress is highest - BP, blood viscosity, sympathetic tone
What role does endothelium dysfunction play in the pathogenesis of coronary thrombosis?
Reduced secretion of NO and prostacyclin by endothelial cells results in a state where vasoconstriction is favored over vasodilation
Platelet products (thromboxane, 5-HT) and thrombin promote vasoconstriciton while ADP (vasodilatory) is attenuated in endothelial cell dysfunction
This increases hemodynamic stress on plaque and reduces coronary flow and normal clearance of procoagulant factors
What are some triggers of acute plaque rupture?
Exertion
Sexual activity
Anger, mental stress
Cocaine use
Tobacco, marijuana use
Exposure to air pollution
Fever, specific infections (e.g. influenza)
What are functional sequellae of MIs?
Impaired contractility (systolic dysfunction) - due to necrosis of functional myocytes (hypo-,a-, or dys-kinesis)
Impaired relaxation (diastolic dysfunction) - this is an energy-dependent process, thus impaired duringMI; Reduces compliance and increases filling pressures
Stunned myocardium - prolonged, but reversible period of contractile dysfunction; restored days-weeks later; adjacent to MI
Ischemic preconditioning - episodes of ischemia render tissue resistant to subsequent; seen in stable angina - increases ischemic threshold
What is hypokinesis of the myocardium?
reduced contraction
What is akinesis of the myocardium?
Loss of contraction
What is dyskinesis of the myocardium?
Outward bulging during contraction
Why is diastole dysfunctional after MI?
Diastole is energy dependent - thus MI causes problems (Oxygen, ATP, etc)
If compliance is reduced, filling pressures increase
What is stunned myocardium?
Prolonged, but reversible period of contractile dysfunction seen after MI
Function is restored days to weeks after episode
Commonly seen in areas adjacent to region of MI
What is ischemic preconditioning?
Episodes of ischemia render tissue resistant to subsequent episodes (sometimes)
Observed in the setting of stable angina, which causes an increase in the ischemic threshold with continued exercise
What is ventricular remodeling?
Changes in cardiac size, shape, structure and physiology
May be physiological and adaptive during normal growth
Or pathological in the setting of MI, cardiomyopathy, HTN, or valvular heart disease
What cardiac remodeling occurs initially, post-MI?
Fibrotic repair of necrotic area and scar formation and elongation
Thinning of the infarcted zone
LV volumes increase in the adaptive response - associated with increased stroke volume to maintain normal cardiac output
What is the significance of infarct expansion in the context of MI?
Associated with higher mortality, incidence of non-fatal complications such as heart failure or ventricular aneurysm
Seen on echo
Can be severe and lead to systolic function deterioration, new/louder gallops, or new/worsening pulmonary congestion
What remodeling occurs late, post-MI?
Hypertrophy
Myocytes hypertrophy due to neurohormonal activation, myocardial stretch, activation of local tissue RAS, an para-/autocrine factors
Ang II production locally, likely stimulates hypertrophy in non-infacted myocardium
What is acute coronary syndrome?
Acute MI, unstable angina or sudden cardiac death
What are non-atherosclerotic causes of acute coronary syndroem?
In young patients or in pts with no coronary risk factors:
- Mechanical valves or infectious endocarditis (emboli resultin gin coronary occlusion)
- Inflammatory disorders (vasculitis)
- peripartum female (spontaneous coronary dissection)
Cocaine abuse - causes vasospasm (decreasing O2 supply), increases HR (increased O2 demand), and associated with increased atherosclerosis
What is type 1 MI?
Classic case of plaque rupture with thrombus
What is type 2 MI?
Supply/demand imbalance without a plaque rupture
What is type 3 MI?
Sudden cardiac death - fixed atherosclerosis and supply/demand imbalance
What is type 4/5 MI?
MI in the setting of revascularization procedures
What is a transmural infarction?
(Q wave MI)
Necrosis spans the entire thickness of the myocardium
Caused by a total, prolonged occlusion of a coronary artery
What is a subendocardial infarction?
(non-Q wave MI)
Subendocardium susceptible to ischemia, exposed to the highest pressures from the ventricles with few collaterals.
Vessels that supply O2 must pass through the contracting myocardium
What is the most common cause of ACS (acute coronary syndrome)?
Rupture of an atherosclerotic plaque leading to superimposed thrombus
Plaque erosion may lead to thrombus
More common in younger women, smokers
What demographics are more likely to have plaque erosion leading to thrombus as a cause of ACS?
Younger women
Smokers
What is the result of a non-occlusive thrombus in the coronary vasculature?
Unstable angina
NSTEMI (non-ST-elevation MI)
Transient occlusion or distal imbolization may cause necrosis
What is the result of an occlusive thrombus in the coronary vasculature?
ST-elevation MI (STEMI)
What is the least severe on the spectrum of ACS?
unstable angina
What is the most severe on the spectrum of ACS?
STEMI
What is the spectrum of ACS?
Unstable angina -> NSTEMI -> STEMI
What are the three classifications of unstable angina?
Rest angina - at rest and prolonged (>20 mins)
New-onset angina - <2 months
Increasing (crescendo) angina - previously diagnosed angina has become more frequent, longer, or worse in severity
What is the effect of nitroglycerin on MI?
No improvement and minimal releif
What are clinical symptoms in myocardial infarction?
More severe, longer, and more radiating chest pain, compared to stable angina
No improvement with rest and minimal releif with nitroglycerin
Sympathetic response (diaphoresis, nausea, tachycardia, cool skin)
25% may have no symptoms (diabetes)
Shortness of breath
In what population of patients might you not see symptoms of MI?
Diabetics
What are physical findings of MI?
S4 - atrial contraction into non-compliant LV (atrial kick)
S3 - volume overload (blood sloshing in)
Systolic murmur due to papillary muscle dysfunction causing MR or ventricular septal defect from rupture
Fever (low grade), as inflammatory response
How is ACS (acute coronary syndrome) diagnosed?
Clinical symptoms, ECG findings, biomarkers of necrosis
Unstable angina/NSTEMI = T wave inversion; ST depression or normal :: elevated biomarkers in NSTEMI; normal in USA
STEMI = ST elevation, elevated biomarkers
What ECG findings do you find in NSTEMI or unstable angina?
T wave inversion
ST depression or normal
What ECG findings do you see in STEMI?
ST elevation
What EKG findings do you find within minutes to hours after STEMI?
ST elevation and perhaps hyperacute T
What EKG findings do you see hours-1 day after STEMI?
T wave inversion, elevated ST, depressed Q wave
What EKG findings do you see ~1 week after STEMI?
Pronounced Q, ST elevation, T wave inversion
What findings do you see months after STEMI?
Pronounced Q, ST elevation, marked T wave
How is STEMI defined?
Angina unreleived by nitroglycerin with ST elevation on EKG and rise in biomarkers
How is NSTEMi defined?
Angina at rest >20 minutes without ST elevation but with rise in cardiac biomarkers
What is the pathophysiology of STEMI?
Total or near-total thrombotic occlusion of coronary artery
What is the pathophysiology of NSTEMI?
Abrupt decrease in myocardial oxygen supply
Thrombus formation on an atherosclerotic plaque
What are biomarkers of myocardial necrosis?
Troponin core complex (TnT, TnI, TnC)
Creatinine kinase myocardial band (CK-MB)
What is the value of using troponin as a biomarker for MI?
They are generally not detected in blood of healthy individuals
Levels rise within 3-4 hours, peak between 18-36 hours and decline slowly (~2 weeks)
What is the time course of troponin as a biomarker for MI?
Rises within 3-4 hours, peaks between 18-36, and declines slowly (up to 2 weeks)
What is the value of creatinine kinase myocardial band (CK-MB) as a biomarker for MI?
Has sharper kinetics than troponin (peaks faster and returns to normal faster)
Good for identifying subsequent MIs after initial event
What are the kinetics of CK-MB as a biomarker for MI?
Peak wtihin 24 hours and decline quickly (couple of days)
What are the narrow complex tachycardias?
Sinus tachycardia
AVNRT/AVRT
Atrial fibrillation
Atrial flutter
Atrial tachycardia
Multi-focal atrial tachycardia
How do you approach an EKG with narrow complex supraventricular tachycardia?
Regular or irregular R-R intervals?
P waves or no P waves
Long RP or Short RP? - transect R-R segment (P on left or right side?)
Response to adenosine -AV nodal blocker
What is the classic irregular narrow complex tachycardia?
Atrial fibrillation
What does an irregular narrow complex tachycardia tell you?
atrial fibrillation
What does a regular narrow complex tachycardia tell you?
It’s NOT atrial fibrillation - check for long or short RP segments
What does a short RP, regular narrow complex tachycardia tell oyu?
AVNRT/AVRT
What does a long RP, regular, narrow complex tachycardia tell you?
Sinus tachycardia or atrial tachycardia - check nodal block effects
What does a regular, narrow complex tachycardia with multiple p waves tell you?
atrial flutter
What is AVNRT?
Narrow complex tachycardia seen in all ages
Manifests as palpitations “racing heart”
Re-entrant arrhythmia dependent on having dual AV nodal physiology
Psuedo R’ in V1
Pseudo S in II, III, aVF
no P wave (short RP) - P and QRS often on top of each other
In AVNRT, the […] pathway has slower conduction and faster recovery
In AVNRT, the slow pathway has slower conduction and faster recovery
Fast pathway has faster conduction, slower recovery
If you walk a mile, you only need short rest
If you run a mile, you have to rest for a long time
In AVNRT the […] pathway has faster conduction and slower recovery
In AVNRT the fast pathway has faster conduction and slower recovery
Slow pathway has slower conduction and faster recovery
If you walk a mile, you only need short rest
If you run a mile, you have to rest for a long time
How do you treat AVNRT acutely?
Adenosine, Vagal maneuvers, AVN blocking agent
How do you treat AVNRT chronically?
AVN blockers
Single dose during episodes, daily dosing
Class I and Class III anti-arrhythmics are effective
ABLATION of slow pathway is most efficacious (low risk)
Which pathway (slow or fast) do you attempt to ablate to resolve an AVNRT?
slow!
What is AVRT?
AV reciprocal tachycardia
Re-entrant arrhythmia
Dependent upon accessory pathway
Can be manifest on EKG = Wolff-parkinson-white (WPW)
Risk for sudden death
What is WPW?
Wolff-Parkinson-White
Type of AVRT - re-entrant arrhythmia with accessory pathway
Characteristic Δ-wave on EKG and short PR interval
What is atrial flutter?
Common arrhythmia in patients with heart disease
Can present with palpitations, dyspnea, heart failure, stroke
Re-entrant arrhythmia involving atria
Atria beating at 250-300 bpm, with ventricles at 2:1, or 3:1 or slower rate
Saw-tooth pattern P waves
What is atrial fibrillation?
Highly prevalent arrhythmia
Risk factors are numerous (age, HTN, DM, etc)
Can be paroxysmal (in and out) or persistent
Variable symptomaticity
EKG is Irregularly irregular
Atria at >300bpm but uncoordinated
Originate from impulses from the pulmonary veins
Tx with AV nodal blockade, anti-arrhythmics, catheter ablation
What are you thinking?
Atrial fibrillation
Irregularly irregular
Atria at >300 bpm
What do you see here?
Atrial Flutter
Saw-tooth appearance
What are clinical manifestations of lower extremity atherosclerosis?
Intermittent claudication
Critical limb ischemia
What is intermittent claudication?
Pain, ache, or fatigue in the calf, thigh, hip, buttock, or low back that occurs on walking and is releived with rest
Location of symptoms correlates with level of obstruction
What is critical limb ischemia?
Pain or paresthesia in the toes, foot, or leg at rest
Exacerbated by leg elevation or when supine
Releived with dependency
Persistent pain +/- ulceration with severe ischemia
What is the Leriche triad?
Bilateral high claudication
Impotence
Global Atrophy
What is aorto-iliac disease?
Peripheral artery disease characterized by the Leriche triad (bilateral high claudication, impotence, global atrophy)
Collaterals are typically well develope
There are multiple revascularization options with high patency
What is Femoropopliteal disease?
Most frequent peripheral artery disease
Collaterals determine course of disease
Intermediate graft patency
What is tibeal-peroneal disease?
Peripheral artery disease commonly seen in diabetes
Low graft patency without in-situ vein techniques
What are trophic signs of acute limb ischemia on examination?
Ulceration
Petichae
Calf tenderness
Dependent edema
What are trophic signs of chronic arterial obstructive disease?
Hair loss
Subcutaneous atrophy
Thickened nails
Dependent rubor
How do you treat limb obstructive arterial disease pharmacologically?
Platelet inhibitors (aspirin, clopidogrel)
Lipid-lowering agents (statins)
ACE inhibitors
NO role for vasodilators
What are etiologies of acute arterial occlusion?
In-situ thrombosis (ruptured atherosclerotic plaque)
Embolism from a proximal source
Arterial trauma
Vasculitis
Hypercoagulable state
Severe venous thrombosis
What are sources of arterial emboli?
Atrial fibrillation
Valvular heart disease (rheumatic mitral stenosis, prosthetic valves, endocarditis)
Thrombus in cardiac chambers (left atrial appendage, LV mural thrombus)
Proximal arterial disease (AAA, atherosclerosis)
What is a true aneurysm?
Intima, media and adventitia are in tact, but balloon out
What is a false aneurysm?
Hole in intima and media that allows for hematoma to balloon the adventitia out and give the appearance of an aneurysm
What are etiologies of aortic aneurysmal diseases?
Atherosclerosis
Cystic medial necrosis (primary, Marfan, Ehlers-Danlos)
Vasculitis
Dissection
Post-stenotic
Infections
Trauma
Congenital
What are risk factors for abdominal aortic aneurysms?
Age
HTN
Tobacco smoking
Family history (males)
Hyperlipidemia
Atherosclerosis
What is the natural history of an abdominal aortic aneurysm (AAA)?
Expand at 1-4 mm/ year
Predictors of expansion include initial size, active smoking, HTN)
What are risk factors for aortic dissection?
HTN
Tobacco smoking
Cocaine use or stimulant use
Connective tissue disease (Marfans, Ehlers-Danlos)
Congenital structural abnormalities (bicuspid aortic valve, coarctation of aorta)
Inflammatory disease of aorta
Pregnancy
Weight lifting
Trauma
What is Raynaud’s Phenomenon??
“asphyxiation of digits”
What is primary raynaud’s disease?
most cutaneous vasospasm
Females more than males
15-40 year old onset
Symmetrical involvement of digits, earlobes, tip of nose, elbows, knees
Spontaneous improvement in 15%; progression in 30%
Ulceration is rare
What is Buerger’s Disease??
Medium vessel vasculitis associated wtih tobacco smoking
Cessation of smoking is theapy
What is Virchow’s Triad?
Stasis of blood flow
Endothelial injury
Hypercoagulable state
Describes factors that contribute to thrombosis
Where are DVTs more common?
Calf > popliteal > femoral > iliac (more distal = more common)
What sites of DVTs are more dangerous?
Proximal
Iliac > femoral > popliteal > calf
Deep > superficial veins
What symptoms are seen in massive pulmonary embolism?
Syncope, profound dyspnea, cardiogenic shock, cardiac arrest
sub-massive = chest pain, dyspnea
What symptoms are seen in sub-massive pulmonary embolism?
chest pain, dyspnea
massive = Syncope, profound dyspnea, cardiogenic shock, cardiac arrest
What symptoms are seen in pulmonary infarction?
Hemoptysis (coughing blood), chest pain, dyspnea
What are signs of chronic venous insufficiency?
Edema and induration
Hemosiderin pigmentation
Ulceration
What are clinical syndromes associated with chronic venous insufficiency?
Superficial varicose veins
Deep venous incompetence
Postphlebitic syndrome
What are symptoms of lymphedema?
limb swelling
heaviness
recurrent lymphanigitis or erysipelas
Skin changes
fungal infestation
What are physical findings of lymphedema?
Non-pitting edema
Dorsal pedal hump
Elephantine distribution
Chronic induration without pigmentation
Lichenification
What are causes of primary lymphedema?
Aplasia, hypoplasia or hyperplasia of lymphatic channels
Obstruction
Incompetence of lymphatic valves
What can cause secondary lymphedema?
Malignancy
Radiation
Infection - pyogenic lymphangitis, filariasis
Surgery
trauma
Where is the most common location for atherosclerotic aneurysms in the aorta?
Below renal arteries and above bifurcation of iliac artery
How do β-blockers help in treating MIs?
Releive ischemic pain
Reduce infarct size and life-threatening arrhythmias
Presumed to decrease cardiac work and myocardial oxygen demand
How do nitrates help treat MI?
They enhance coronary blood flow by coronary vasodilation
Decrease ventricular preload by increasing venous capacitance (reduce wall stress)
Contraindicated in pts with hypotension
How do calcium channel blockers help MIs?
Symptom improvement
Nondihydropyridines reduce heart rate and contractility
Useful in pts with contraindications to β-blockers or ischemia refractory to β-blockade or nitrates
What is the risk with antithrombotic therapies?
Can go too far, and thin blood, causing a bleeding risk
What is the effect of Aspirin on MI?
Effective across all ACS categories
Give as soon as possible
Produces rapid antiplatelet effect
Reduces oronary occlusion and recurrent ischemic events after fibrinolytic therapy
What is a drawback/issue with using clopidogrel?
There is substantial interindividual variability in the response
How do glycoprotein IIb/IIIa receptor antagonists work/help in MIs?
Potent inhibitors of the final common pathway of platelet aggregation
Use has declined with advent of more potent antiplatelet drugs
Beneficial in highest risk patients undergoing PCI
What is the goal of STEMI treatment?
To achieve reperfusion.
Restores flow in the infarct-related artery, limits infarct size and translates into early mortality benefit.
What are treatment avenues for STEMI patients?
Fibrinolysis and invasive strategies are essentially equal in efficacy unless there are reasons not to do one (occupied cath lab, no access, delay to invasive, etc)
What are complications of MIs?
Arrhythmias - signiicantly V. fib = sudden cardiac death;also supraventricular arrhythmias and conduction blocks
Pump failure
Free wall rupture/pseudoaneurysm
Papillary muscle rupture
Pericarditis
What are left sided heart failure signs/symptoms?
Dyspnea, pulmonary rales, third heart sound
Diuretics can relieve volume overload
Standard heart failure meds indicated
What are right sided heart failure signs/symptoms?
Elevations in JVD and hypotension (LV is underfilled)
Treat with volume expansion
Usually due to MI of RCA
During what time scale does a free wall rupture typically occur after MI?
Within first 2 weeks
This is a surgical emergency, and usually fatal
What is a psuedoaneurysm?
Caused by a contained myocardial rupture, still at risk for rupture
What is a LV aneurysm?
Discrete dyskinetic area of LV wall with broad neck
Develops weeks to months after MI
No communication between LV cavity and pericardium
Complications include thrombus, arrhythmias, heart failure
Tissue bulges with cardiac contractions
LV aneurysm can be associated with ST elevation
What are some issues with a papillary muscle rupture?
Complete rupture may result in severe mitral regurgitation -> heart failure or death
Partial rupture may cause moderate MR and symptoms of heart failure
Which aspect of the papillary muscle is more susceptible to rupture?
Posteromedial papillary more susceptible than anterolateral
What is acute pericarditis?
Inflammation that occurs early in the post-MI period taht extends from myocardium to pericardium
What is Dressler syndrome?
Pericarditis that occurs several weeks after MI
autoimmune process may be contributory
What is ischemic injury?
Injury resulting from reduced blood flow
What are the effects of impaired blood inflow?
Inadequate oxygen supply
Insufficient availability of nutrients
What are the effects of impaired blood outflow?
Insufficient removal of metabolites
What is the etiology of most myocardial ischemia cases?
Obstructive coronary artery disease (CAD)
What is myocardial infarction?
The irreversible myocardial muscle damage caused by prolonged ischemia resulting from a sustained imbalance of perfusion and demand
Discrete focus of ischemic muscle necrosis
What cardiac areas does the right coronary arery supply?
Right atrium
Right ventricle
Bottom portion of left ventricle
Back of septum
What cardiac areas does the left anterior descending artery supply?
Front and bottom of left ventricle
Front of the septum
What cardiac areas does the circumflex artery supply?
Left atrium
Side and back of the left ventricle
You find ischemia on the anterior wall of the LV and down to the apex of the heart. Where do you suspect a coronary artery occlusion?
Left anterior descending (LAD) branch of the left coronary artery
You find necrosis on the posterior wall of the LV. Where do you suspect an occlusion of the coronary arteries?
Right coronary artery
You find necrosis on the lateral wall of the left ventricle. Where do you suspect a coronary artery occlusion?
Circumflex artery - a branch of the left coronary artery
Whhat is a transmural infarct?
ischemic necrosis that involves full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery
What is a subendocardial infarct?
Ischemic necrosis limited to inner 1/3 or 1/2 of the ventricular wall
Zone is least perfused and most vulnerable to any reduction in flow
Regional: transient obstructoin which is releived before necrosis extends across thickness
Circumferential: Prolonged, severe hypotension even without coronary stenosis
What type of infarct can lead to pericarditis or ventricular rupture?
Transmural infarcts
Subendocardial infarts do not
What do you see on pathology of an MI within 4 hours?
Nothing!
What do you see on pathology of an MI after 1-3 days?
Mottling with yellow-tan infarct center
Seen maximally at 7-10 days
When do you see yellow-tan areas in the myocardium following an MI?
After about 3-10 days
What do you see on pathology of an MI after over 2 months?
Complete scarring
How old is this MI?
~ 7 days
Note the yellow-tan zone of necrosis with the surrounding red granulation tissue.
What are clinical findings in Giant Cell Arteritis?
Diminished temporal pulses/headache
Facial pain/jaw claudication
Impaired vision
Elevated inflammatory markers
Treat with high dose steroids before confirming diagnosis to save vision
What is thrombangiitis obliterans?
Buerger disease
Smoking-related vasculitis that presents with triad of symptoms:
Distal arterial occlusion (corkscrew collaterals)
Raynaud’s phenomenon
Superficial vein thrombophlebitis
Smoking cessation is critical treatment
You see corkscrew collaterals in a patient’s angiogram. What are you thinking?
Thrombangiitis obliterans (Buerger disease)
Stop smoking!
What sex is affected more commonly by giant cell/Takayasu arteritis?
Females
Males are affected more by thrombangiitis obliterans (Buerger’s)
What is the diagnosis?
A fibrillation
What is the diagnosis?
Atrial flutter
Which arrhythmia is dependent on having dual AV nodal physiology?
AVNRT
What is the most likely diagnosis?
3rd degree heart block (complete heart block)
What is the most likely diagnosis?
2nd Degree AVB - Mobitz I
What do you see in this EKG?
Atrial fibrillation
Right Bundle Branch Block (RBBB)
3rd Degree AV Block (complete heart block) - no correlation b/w p waves and qrs complexes
What are characteristics of WPW on EKG?
Short PR (less than 120ms)
Slurred QRS upstroke (delta wave)
Broad QRS
Secondary ST and T wave changes
What is the diagnosis?
WPW
What is an orthodromic AVRT?
Electrical activity occurs in a circle but proceeds down septum and around free walls and up to atria
What is an antidromic AVRT?
Re-entrant arrhythmia where the electrical impulse passes from atria down free wall of ventricle and up through septum (backwards)
What is the effect of hyperkalemia on the membrane resting potential of a myocyte?
Decreases it from -90 to -80 mV
What changes are present on EKG in hyperkalemia?
Slowed conduction - fewer cells recruited
Everything delayed until it stops
What is a clear EKG finding of hyperkalemia?
Pointy T waves
Prolonged QRS
Prolonged PR
What is the diagnosis?
Hyperkalemia!
pointy T waves, prolonged QRS, PR
Give IV Ca
What are the congenital long QT syndromes?
LQTS1 - Triggered by exercise, swimming
LQTS2 - triggered by auditory ques (doorbell)
LQTS3 - triggered by sleep
What is the finding?
Long QT Syndrome
LQTS3 - found while sleeping
What is this?
Torsades de Pointes
Causes sudden deaths in Long QT Syndromes when sustained
Can be OK if occurs briefly
What is Brugada Syndrome?
Inherited syndrome that is most common cause of sudden death in southeast asian countries
EKG shows RBBB with downslowing ST segment elevation in the right precordial leads
Pts die from Torsades de Pointes
What are you thinking?
Brugada Syndrome - downsloping ST segment elevation in right precordial leads
What is the shared defining feature of all categories of vasculitis?
Inflammation of blood vessel walls at least at some time during the course of the disease
What are the two broad etiologic categories of vasculitis?
Infectious (direct invasion and proliferation in vessel walls by pathogens)
Non-infectious (not known to be caused by pathogenic invasion)
What are the vessels most frequently involved in polyarteritis nodosa (PAN)?
Renal vessels
Leads to arterial hypertension and ischemic nephropathy with renal failure
No glomerulonephritis
What is Mucocutaneous Lymph Node Syndrome?
Sequellae associated with Kawasaki disease (medium vessel vasculitis)
Seen in infants and young children
What is levocardia?
Heart to the left
What is dextrocardia?
Heart to the right
What is mesocardia?
Heart not left nor right
What defines the right atrium?
The atrium with the broad triangular-shaped appendage (right atrium appendage)
Usually recieves connection from hepatic segment of IVC
Coronary sinus always opens into the morphologically right atrium
What defines the left atrium?
The atrium that is not the right atrium
Flap valve of the foramen ovale is attached to its septal surface
Has a smaller finger-like appendage
What defines the tricuspid valve?
Valve that serves the morphologically right ventricle, regardless of its leaflet morphology
Typically tri-leaflet valve with attachments of septal leaflet to septum via chordae
What defines a mitral valve?
Defined as the valve that serves the morphologically left ventricle, regardless of its leaflet morphology (can be cleft and appear tricuspid)
Typically has two leaflets, connected by chordae to two free wall papillary muscle groups
What defines a right ventricle?
Heavy trabeculations
Septal band
Prominent septal attachments of the tricuspid valve
Pyramidal shape
Moderator band
What defines a left ventricle?
Fine trabeculation
Smooth septal surface
Absent septal connections to mitral valve (generally)
Prolate ellipsoidal shape
What defines the pulmonary artery?
Great vessel that usually gives rise to branch pulmonary arteries (if present)
What defines the aorta?
Great vessel which gives rise to at least one coronary artery and the aortic arch and its brachiocephalic vessels (though this may be interrupted)
What is atrial situs solitus?
RA on the right and receives the hepatic IVC connection
LA on the left, as are attachments of septum primum - flap valve of foramen ovale
What is atrial situs inversus?
RA on the left and receives the left-sided hepatic IVC connection
LA on the right, as well as attachments of septum primum
What is atrial situs ambiguus?
Unclear - typically includes common atrium with multiple venous connection anomalies
What is a d-looped ventricular loop?
Normal (Dextro-looping), but only for solitus atrial position in which the RV has developed to the right of the LV
What is a L-looped ventricular loop?
Inverted ventricular loop, wherein the morphologically right ventrile is to the left of the morphologically left ventricle. Normal only for situs inversus of the atria
(left handed)
What is x-looped ventricular looping?
For cases where there is a single ventricle, it is impossible to figure out the ventricular situs or loop (catch-all)
What are the characteristics of normally related great arteries?
Aorta arises in fibrous continuity with the anterior mitral leaflet (no conus separating aortic valve from mitral)
Pulmonary valve is separated from tricuspid by subpulmonary muslce (conus)
LV with aorta; RV with pulmonic
Solitus: aortic valve to right and posterior of pulmonary valve
Inversus: aorta is leftward and posterior to pulmonary
What does D mean with respect to the position of the great arteries?
Aortic valve is rightward of the pulmonary valve
What does A mean with regards to the malpositions of the great arteries?
Aortic valve is anterior to the pulmonary valve
What does L mean with regards to the malpositions of the great arteries?
Aortic valve is leftward and anterior to the pulmonary
What does P mean with respect to the malpositions of the great arteries?
Aortic valve is posterior to the pulmonary valve, irrespective of right-left position
What is AV discordance?
Morphologically right atrium connects abnormally with the morphologically left ventricle
Can be caused by solitus atria and L-looped ventricles or by inversus atria and d-looped ventricles
What is V-A discordance?
When the morphologically left ventricle is aligned with the pulmonary valve
Refers to the great arterial malpositions (Transposition of great arteries, TGA; double outlet right ventricle, DORV; double outlet left ventricle, DOLV, anatomically corrected malposition of the great arteries, ACM, aortic atresia
What does atresia mean?
“without an opening”
Refers to valves that do not form well - have no opening
What is the conotruncus?
Segment which joins the ventricle to the great artery
Why are ventral septal defects not diagnosed until a few days after birth?
Pulmonary resistance takes a while to decrease to “adult” levels. Once this happens, though, blood will flow to least resistance (pulmonary)
What is the tetralogy of Fallot?
Pulmonary stenosis
Right Ventricular Hypertrophy
Overriding Aorta
Ventricular Septal Defect
PROVe
Cyanotic heart disease - Right to left shunting
What is Rheumatic Fever?
Immunologic response to acute streptococcal pharyngitis (Group A strept)
Cross-reactivity b/w antigen and structural glycoprotein found in heart, joints, connective tissues)
Leads to chronic rheumatic valvular heart disease
What are the Jones Critera useful for?
Diagnosis of Rheumatic Fever
2 major or 1 major and 2 minor; PLUS evidence of infection
How do you treat Rheumatic Fever??
Penicillin
Anti-inflammatories (ASA, corticosteroids)
Treat complications
What is Mitral Stenosis?
Obstruction of LV inflow that prevents proper filling during diastole
Normal MV area is 4-6 cm^2
Severe disease is <2cm^2
What is the normal mitral valve area?
4-6 cm^2
What is severe mitral stenosis valve area?
<2 cm^2
What are etiologies of mitral stenosis?
Rheumatic heart disease - most common
Infective endocarditis
Mitral annular calcification
Congenital
What would you hear on auscultation of mitral stenosis?
Loud S1
Opening snap after S2, with diastolic murmur with pre-systolic accentuation
What are clinical manifestations of mitral stenosis?
Can be asymptomatic, but depends on degree of reduction of valve area
Dyspnea, reduced exercise tolerance, fatigue
Pulmonary congestion (orthopnea, paroxysmal nocturnal dyspnea)
RV failure
What does a shorter S2 to opening snap time indicate about mitral stenosis?
More severe disease
Snap represents reachign maximally open aperture
What are complications of mitral stenosis?
Pulmonary edema
Pulmonary HTN
Right heart failure
A fibrillation
Infective endocarditis
Systemic thromboembolism
What can you see on EKG in a patient with mitral stenosis?
Maybe A. Fibrillation
Maybe LA enlargement and RV hypertrophy
What do you see on chest x-ray in patients with mitral stenosis?
LA enlargement
Signs of pulmonary congestion
What do you see on echo in a patient with mitral stenosis?
Can assess mitral valve mobility, and area
Can identify gradients and severity of disease
How do you treat mitral stenosis?
Medicines do not prevent progression - useful for symptoms
β-blockers, CCBs, digoxin control HR and prolong diastole
Diuretics for fluid overload
Surgery is definitive treatment for patients with symptoms or pulmonary HTN
What are causes of mitral regurgitation?
Abnormalities of valve leaflets (Rheumatic heart disease, infective endocarditis, myxomatous degeneration)
Abnormalities of mitral annulus (dilatation, calcification)
Abnormalities of chordae tendinae (congenital, infective, trauma)
Involvement of papillary muscles (CAD)
What happens to LV/LA pressures in mitral regurgitation?
How does the murmur in mitral regurgitation differ in acute vs chronic cases?
Acute - may not be holosystolic; is shorter and softer
Chronic - holosystolic
What are differences between acute mitral regurgitation and chronic mitral regurgitation?
Acute - normal LA size and compliance, increased LA pressure causes backup into pulmonary system (edema)
Chronic - dilated LA, increased compliance; normal LA and pulmonary pressures with decreased CO
What are symptoms of mitral regurgitation?
Can be asymptomatic
Palpitations
Fatigue
Dyspnea
Paroxysmal Nocturnal Dyspnea
Signs of RV failure
What are clinical signs of mitral regurgitation?
Low, collapsing pulse
Heaving apex
Soft S1, loud P2 (pulmonary HTN)
S3 sound
Holosystolic murmur at apex that radiates to left axilla
Increased murmor on expiration, handgrip, squatting (increase resistance)
How do you treat actue mitral regurgitatioN?
Diuretics, nitroprusside (reduce afterload to increase cardiac output that goes forward)
Balloon pump
Surgery (this is an emergency)
How do you treat chronic mitral regurgitation?
Vasodilators for HTN, LV systolic dysfunction
MItral valve repair
What can you see on EKG for a patient with mitral regurgitation?
LA enlargement, LV hypertrophy, A. Fib
What can you see on chest x-ray of mitral regurgitation?
Chronic - cardiomegaly (LV, LA)
Acute - interstitial edema
What can you see on echocardiogram for a patient with mitral regurgitation?
Estimate LA, LV size and function
Assess valve structure - Definitive for diagnosis
What is mitral valve prolapse?
Autosomal dominant inherited disease that is associated with Marfan Syndrome, Ehler-Danlos syndrome
Pathophysiology includes enlarged valvular leaflets that prolapse into left atrium during systole
Can be asymptomatic, have chest pain or palpitations
Midsystolic click, late systolic murmur
Decreased murmur by squatting, increased by valsalva, standing, handgrip
What are clinical signs of mitral valve prolapse?
Midsystolic click, late murmur
Heard best at apex
Decreased murmur with squatting.
Increased murmur with valsalva, standing, handgrip
What can you see on echo for mitral valve prolapse?
Confirm the diagnosis
How do you treat mitral valve prolapse?
Usually benign
Monitor to ensure no development of mitral regurgitation
What are complications associated with mitral valve prolapse?
Rupture of choardae can cause mitral regurgitaiton, pulmonary edema
Infective endocarditis
Thromboembolism
Arrhythmias
