Quiz 2 Flashcards
What is the most significant cause of bradycardia?
Impulse propagation through the AV node/His-Purkinje system
In what situations is sinus bradycardia normal?
What are some extrinsic causes of sinus bradycardia? What are some intrinsic causes?
What is a first degree AV block? What are reversible causes? What are permanent causes?
What is a Mobitz type 1 (Wenckeback) second degree AV block? Which PR interval is the shortest in a rythym strip? What is the site of the block?
What is a second degree AV block?
What is a Mobitz type 2 second degree AV block? How does it differ from Mobitz type I? What is the site of the block? What other pathology is often seen with a Mobitz 2 block?
What is a third degree AV block? What is site is most likely blocked? What part of the heart is assuming pacemaker activity?
How can bradycardia be treated?
What acute treatments may be indicated for bradycardia?
What treatment may be indicated for chronic bradycardia?
What is a major defining factor of an escape rythym?
Lack of a p wave
What is junctional bradycardia? Where can the p wave be found?
Why does junctional rythym not result in an inability to pump blood?
Since the ventricular pressure in systole is so much greater than atrial systole, even if contraction occurs at near the same time, the tricuspid/mitral valves will still be closed while the pulmonic and aortic valves are open
What pathology is visible here?
*The picture is of atrial premature contraction (PAC), ventricular contractions can also occur (PVC)
How are PAC and PVC treated normally?
What can cause an inverted p-wave as pictured here?
An inverted p-wave can be caused by a PAC originating from the AV node
What abnormality is visible in this EKG strip? What is characteristic of the QRS interval in this abnormality?
PVC
Wide QRS complex
Ectopy can be induced by increased automaticity of __________________ or by abnormal automaticiity of cells _______________________
Latent pacemakers
outside the specialized conduction system
Sine waves such as those seen here are a sign of what electrolyte abnormality?
Hyperkalemia
What are 6 potential EKG signs of hyperkalemia?
What is rheumatic fever (RF)?
About how long can RF typically appear in patients after a group A streptococcal infection? About how many patients infected with GAS will contract RF?
10 days to 6 weeks post infection
3% of GAS patients will contract RF
Rheumatic fever is characterized by what specific criteria?
The JONES criteria
Joints
O (pancarditis)
Nodules
Erythema marginatum
Sydenham chorea
What clinical features comprise the JONES criteria?
J- migratory polyarthritis of large joints
O- Pancarditis (myocarditis, pericarditis, or endocarditis)
N- subcutaneous nodules (typically extensor surfaces)
E- Erythema marginatum- irregular circinate skin rash
S- sydenham chorea- neurologic disorder of involuntary movements
Fusion of the chordae tendinae as well as the verrucae visible on this mitral valve are indicative of what likely pathology?
Rheumatic heart disease
In this biopsy from a patient with acute rheumatic myocarditis what distintive lesions are visible here? What are they composed of?
Aschoff bodies
T lymphocytes, occasional plasma cells and Anitschkow cells (plump activated macrophages)
In which layers of the heart may Aschoff bodies be found?
All three; epicardium, myocardium, and endocardium
What are MacCallum plaques?
Irregular thickenings of the valves, usually found in the left atrium caused by subendocardial lesions
What are the cardinal anatomic changes to the mitral valve in chronic RHD?
-Leaflet thickening
-Commissural fusion and shortening
-Thickening and fusion of the chordae tendinae
What is Infective endocarditis (IE)?
Microbial infection of the heart valves OR mural endocardium that leads to vegetations composed or thrombotic debris and organisms
*This is often associated with destruction of underlying cardiac tissues
What has historically been the major antecedent disorder to infective endocarditis? What are more common antecedents currently?
Historically, RHD
More commonly:
-mitral valve prolapse
-bicuspid aortic valve
-prosthetic valves
What organism is responsible for around 55% infective endocarditis? Which organism is responsible for around 25% of IE?
55% -> S. viridans
25% -) S. aureus
What is the classic hallmark of IE visible in this heart?
Vegetations on heart valves- friable, bulky lesions containing fibrin, inflammatory cells, bacteria/other organisms.
What is the Duke criteria? What is it used to diagnose?
Infective endocarditis
How is the Duke criteria used to diagnose IE? How is it used to diagnose possible IE?
What pathology is visible here?
Janeway lesions
What pathology is seen here?
Osler nodes
What pathology is seen here?
Roth spots
T/F: Heart failure is a disease
False, it is a syndrome
What are the main differences between technical and operational heart failure?
What are the qualifications for Stage A Heart failure? Stage B? Stage C? Stage D?
What are the qualifications for Class I Heart failure? Class II? Class III? Class IV?
How is the classification of HFrEF made in Left-sided HF?
How is the classification of HFmrEF made in Left-sided HF?
How is the classification of HFpEF made in Left-sided HF?
What are 5 significant causes of dilated cardiomyopathy (there are many diverse causes)?
1) Familial cardiomyopathies
2) Infective (mostly viral)
3) Giant cell myocarditis
4) Chemotherapeutic agents (anthracyclines)
5) Peripartum cardiomyopathy
What is the inheritance pattern of genetic dilated cardiomyopathy (DCM)? What is the most common mutation?
Autosomal dominant w/ variable penetrance
Titin truncating mutation is most common (25%)
*significant overlap with genetic hypertrophic CM
What are two types of inflammatory myocarditis than can lead to DCM?
Giant cell myocarditis (rare and rapidly progressive form of inflammatory myocarditis)
Post-viral inflammatory myocarditis
What is giant cell myocarditis? Why is diagnosis so important? How is it treated?
What pathology is visible in this heart tissue?
Giant cell myocarditis (multinucleated giant cells visible)
What is post-viral inflammatory myocarditis?
What is the typical presentation for DCM brought on by chemotherapy agents?
When does peripartum DCM tend to occur? What are some risk factors?
Old maternal age, multiple pregnancies, pre-eclampsia/eclampsia
How is DCM diagnosed? How is it treated?
What is the inheritance pattern of hypertrophic cardiomyopathy (HCM)? What differentiates it from typical ventricular hypertrophy?
What heart sound is often associated with a HCM? Where is the murmur most prominant? How can it be differentiated from an aortic stenosis murmur?
How can HCM be diagnosed? What would be the expected ECG finding?
What treatments are beneficial for a patient with HCM? What medication types may require cautious use? Why might rythym control be needed?
What are 5 kinds of infiltrative cardiomyopathies?
What is the most common cause of restrictive cardiomyopathy? What are the two types? Which type is the “wild type, familial”?
Which type of amyloidosis requires a tissue biopsy for diagnosis? Which can be detected with non-invasive testing? Which can be detected with a Technetium pyrophosphate scan?
What is the treatment for amyloidosis? How is treatment different for AL amyloidosis vs TTR amyloidosis?
What type of cardiomyopathy is characterized by impaired systolic contraction?
What type of cardiomyopathy is characterized by impaired diastolic relaxation, often with vigorous LV systolic function?
What type of cardiomyopathy is characterized by a stiff LV with impaired diastolic relaxation, usually with normal systolic function?
A physical exam of a patient with dilated cardiomyopathy would be most likely to include what findings? What might be found on an echocardiogram?
A physical exam of a patient with hypertrophic cardiomyopathy would be most likely to include what findings? What might be found on an echocardiogram?
A physical exam of a patient with restrictive cardiomyopathy would be most likely to include what findings? What might be found on an echocardiogram?
Which type of cardiomyopathy is most likely to be due to genetic causes? Which is most likely due to acquired causes?
What finding in this cardiomyopathy biopsy differentiates it from the other two types?
Myocyte disarray (hypertrophied cardiac myocytes occurs in all forms of cardiomyopathy)
The featuers seen in this biopsy are indicative of what kind of cardiomyopathy?
Restrictive cardiomyopathy (specifically amyloidosis)
Coxsackie A or B (most common cause of lymphocytic myocarditis) or other enterovirus
*This is lymphocytic myocarditis, and has likely caused the secondary DCM seen on the left
What other pathology commonly occurs with a bicuspid aortic valve?
How does the Frank-Starling mechanism account for compensation of heart failure?
As the LVEDV increases (due to reduced CO) the stroke volume increases
What are the three principle hormonal systems that are involved in neurohormonal activation as a compensatory mechanism for heart failure?
How does the sympathetic nervous system work to increase the CO (SV x HR) and TPR in heart failure?
What are the short-term effects of these physiological responses to HF?
What are the long term effects of these physiological responses to HF?
Where are ANP and BNP synthesized?
What are the functions of ANP and BNP?
Is the football or basketball shape preferred for the LV?
Will an increase in systolic wall stress (exercise, aortic stenosis) create concentric or eccentric hypertrophy for the heart? Is this good or bad?
Adaptations are mostly good (dysregulation associated with aortic stenosis progresses to be bad)
Will an increase in diastolic wall stress (LV HF) create concentric or eccentric hypertrophy for the heart? Is this good or bad?
It will be bad; fibers are layed down in parallel, and are hypertrophied in a way that reduces contractility, unlike parallel, concentrically hypertrophied fibers
What are the five sections of the primitive heart tube in a developing fetus from top to bottom (before heart looping)?
Describe the process of heart looping using the diagram
Good job!
What structure separates the two AV canals in the initial stages of partitioning of the atria in fetal heart development?
The endocardial cushion
What structure in the intial stages of the partitioning of the atria in fetal development grows towards the endocardial cushion? What is the name of the foramen between these two structures?
What is the name of the second foramen to appear in partitioning of the atria? Where does it appear?
The foramen secundum
It appears in the middle of the septum primum
Where does the septum secundum form in the partitioning of the atria in fetal heart development? What foramen forms in its walls?
What notable four processes/structures do they endocardial cushions contribute to?
As the muscular IV septum grows up towards the endocardial cushions, what is the foramen between these two structures named?
What structure forms the membranous portion of the IV septum
________ cells migrate to the primitive heart tube outflow tract and form bulbar ridges which become the _____________.
Neural crest
Spiral septum
T/F: The bulbar ridges grow down towards the IV septum AND the ventricular septum grows toward the AV canal and outflow tract (bulbar ridges)
True
When is ventricular septation as occuring in the fetal developing heart complete?
Which portion of the IV septum meets the aorticopulmonary septum?
The sinus venosus becomes what structures in the adult heart?
What is the round ligament of the liver?
What congenital heart defect is shown here?
Atrial septal defect (ASD)
What congenital heart defect is shown here?
Ventricular septal defect (VSD)
What congenital heart defect is shown here?
Patent ductus arteriosus (PDA)
What type of ASD is most common? Which type is associated with AV valve abnormalities? Which with anomalous pulmonary venous return to RA?
What percentage of patient foramen ovales will close by 2 years of age? Wat can occur if right-sided pressures remain elevated due to patent foramen ovale?
What percentage of VSD can be classified as membranous VSD? Infundibular VSD?
What 3 pairs of veins come off the primitive heart tube (sinus venosus)?
Which part(s) of the primitive heart tube become the atria?
Which part(s) of the primitive heart tube become the ventricles?
Which part(s) of the primitive heart tube become the outflow tract (aortic/pulm)?
What type of heart shunts (RtL or LtR) will result in acyanotic blood flow?
What type of heart shunts (RtL or LtR) will result in cyanotic blood flow?
What are the 5 T’s of cyanotic heart disease?
*Important for boards, clinically there is more complexity
What pathology is visible on this CXR?
Tetrology of Fallot
*Notice the boot shaped heart with a widened mediastinum
What are the two kinds of blue heart babies?
*Happy and sick refer to presentation of infant with cyanosis
What are examples of causes of “happy” cyanosis?
What is the best treatment for happy cyanosis that is ductal dependent (PDA)?
What is a hypercyanotic “tet” spell? What can bring on a tet spell?
How can a tet spell be managed?
What are two examples of sick cyanosis?
What treatments are typical for sick cyanosis?
What are the main four types of lesions that can cause Acyanotic CHD?
VAPO
What are common comorbidities for HFpEF? How is it diagnosed?
What are four major lifestyle modifications for HF patients?
What are some medical considerations for HF patients?
What is the congestion and perfusion status of a warm and dry patient?
What is the congestion and perfusion status of a warm and wet patient?
What is the congestion and perfusion status of a cold and dry patient?
What is the congestion and perfusion status of a cold and wet patient?
Why are ACEi sometimes inefficient for supression of Angiotensin II?
How is vasculitis classified?
What are the two main types of vasculitis?
What characterizes granulomatous vasculitis?
What characterizes acute necrotizing vasculitis?
In what vessel types is granulomatous vasculitis most common? In what vessel types if acute necrotizing vasculitis most likely?
What type of specific scarring is associated with large vessel vasculitis? What are the feared outcomes (especially in aorta and branches)?
