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DIT FACTS > CARDIO > Flashcards

CARDIO Flashcards

1
Q

Most common congenital cardiac anomaly.

A

VSD

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2
Q

What are the components of the tetralogy of Fallot, and which is the most important determinant for prognosis?

A

Pulmonary infundibular stenosis * most impt
VSD
RVH
Overriding aorta (overrides VSD.)

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3
Q

How does squatting reduce the symptoms of Tetralogy of Fallot?

A

Although VSD is normally a left-to-right shunt, in tetralogy there is also pulmonary stenosis present. This actually forces the VSD to be a right-to-left shunt instead, causing cyanosis since blood is bypassing the pulmonary system and entering the systemic circuit too soon. When you squat, you constrict blood flow going to the legs and increase peripheral vascular resistance. This increases the “afterload”, decreasing the right-to-left shunt, and allowing blood to reach the pulmonary circuit to be oxygenated.

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4
Q

What 3 congenital defects can lead to Eisenmenger’s syndrome later on?

A

Uncorrected VSD, ASD, or PDA. Since this is a left-to-right shunt, eventually the pulmonary vasculature tries to compensate and becomes hypertrophic to accommodate the new blood flow. Eventually, the pressure gets so high in the right side of the heart that it becomes a right-to-left shunt instead. This blood will now bypass the pulmonary circuit and enter the systemic circuit deoxygenated, causing clubbing, cyanosis, and polycythemia.

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5
Q

Explain why a PDA is so detrimental.

A

A PDA allows a portion of the oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta (which has higher pressure) to the pulmonary artery. If this shunt is substantial, the neonate becomes short of breath: the additional fluid returning to the lungs increases lung pressure to the point that the neonate has greater difficulty inflating the lungs.
In some cases, such as in transposition of the great vessels, a PDA may need to remain open since the PDA is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the DA open.

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6
Q

What is the problem in infantile coarctation of the aorta, and what disease is it associated with?

A

It is associated with Turner Syndrome.
Coarctation is a narrowing of the aorta that lies after the aortic arch but before the PDA (which is necessary for oxygenated blood to mix with deoxygenated blood to be delivered to the lower extremities). It presents as lower extremity cyanosis, because the left ventricle is generating a ton of pressure in order to force blood through the stenotic valve. However, there will be a deficiency of blood able to reach the lower half of the body, other than the mixed blood (from the PDA), which is why this generally presents with these symptoms.

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7
Q

Where is the coarctation in the adult form of Coarctation of the Aorta and how does this present?

A

The coarctation lies after the aortic arch but in this case, there is no PDA. There will be hypertension in the upper extremities due to all of the pressure generated by the hard-working left ventricle against the stenotic valve, and hypotension with weak pulses in the lower extremites. Often, rib notching is seen on xrays since collateral circulation develops across the intercostal arteries in order to compensate.

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8
Q

What 2 congenital cardiac defects are associated with DiGeorge syndrome?

A

Truncus arterosus

Tetralogy of Fallot

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9
Q

What 3 congenital cardiac defects are associated with Congenital Rubella?

A

Septal defects
PDA
Pulmonary artery steosis

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10
Q

What 2 congenital disorders are associated with Aortic dissection?

A

Turners and Marfans

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11
Q

What problems are offspring of diabetic mothers at higher risk for?

A

Transposition of great vessels
Hypoglycemia
Large for gestational age –clavicle fracture, shoulder dystocia, Erb Duchenne palsy, failure to progress during labor and delivery

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12
Q

Describe the murmur of a VSD. How can it be accentuated?

A

Holosystolic, harsh sounding murmur that is loudest the tricuspid area. Accentuated with the hand grip maneuver due to increased afterload, causing increased L – > R shunting.

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13
Q

What is the MAP equation?

A

MAP = 1/3 (systolic) + 2/3 (diastolic)

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14
Q

What is the Fick principle?

A

CO = rate of O2 consumption / (arterial O2-venous O2)

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15
Q

Does decreased extracellular Na+ increase or decrease contractility of the heart?

A

Increases it. By decreasing extracellular Na+, less Na will want to come into the cell via the Na/Ca2+ exchanger, thus less calcium exits the cardiac myocytes – > increasing contraction.

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16
Q

Name one way to increase afterload and 2 drugs that decrease it.

A

Increase: Squatting (increases TPR)
Decrease: Ace inhibitors, hydralazine

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17
Q

Acidosis, hypoxia, and hypercapnea all have what effect on the heart’s contractility?

A

Decrease it.

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18
Q

How does heart failure impact the Starling forces of fluid movement through capillaries?

A

Increases capillary pressure causing fluid to leave the capillaries.

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19
Q

How does liver failure impact the Starling forces of fluid movement through capillaries?

A

Decreases oncotic pressure (fluid exits capillaries).

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20
Q

How does renal failure impact the Starling forces of fluid movement through capillaries?

A

Decreases plasma protein, thus decreasing plasma colloid osmotic pressure.

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21
Q

How does lymphatic blockage impact the Starling forces of fluid movement through capillaries?

A

Increases osmotic pressure of interstitium.

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22
Q

How does venous insufficiency impact the Starling forces of fluid movement through capillaries?

A

Increases capillary pressure.

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23
Q

Tree bark appearance of the aorta

A

This is seen in TERTIARY SYPHILIS.
Tree bark appearance refers to the intimal and sub-intimal plaques that encase the mouth of small aortic branches, due to obliterative endarteritis of vasa vasorum with ischemic destruction of the vascular media causing inflammation, neo-vascularization and fibrous scarring, leading to aneurysms and surface irregularities.

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24
Q

What does S3 correspond with in relation to the cardiac cycle? Name 4 pathological causes and 2 normal physiologic causes.

A

S3 is in early diastole after mitral valve opens during rapid ventricular filling phase. It is associated with increasing filling pressures (e.g. mitral regurg, CHF, L–>R shunt, dilated cardiomyopathy) as well as dilated ventricles (children, pregnant women).

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25
Q

What does S4 correspond with in relation to the cardiac cycle? Name 4 pathological causes.

A

This is the atrial kick that can occur in late diastole due to high atrial pressure pushing against a stiff LV wall. It is associated with ventricular hypertrophy, aortic stenosis, post-MI, and chronic HTN.

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26
Q

What does the a wave correspond with in JVP?

A

Atrial contraction.

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27
Q

What does the c wave correspond with in JVP?

A

RV contraction (the closed tricuspid valve is bulging into the RA, causing an increase in JVP).

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28
Q

What does the x descent correspond with in JVP?

A

This is atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction, thus causing a decrease in JVP.

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29
Q

What does the v wave correspond with in JVP?

A

This is an increase in RA pressure due to filling against a closed tricuspid valve that occurs during venous return.

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30
Q

What does the y descent correspond with in JVP?

A

This is diastole, when blood is flowing from RA to RV, decreasing JVP.

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31
Q

Describe normal splitting.

A

This occurs during INSPIRATION. When we inspire, our intrathoracic pressure must drop to allow air into the lungs. This also increases venous return, causing an increasing stroke volume and ejection time in the RV. This delays the closure of the pulmonic valve, thus splitting the aortic and pulmonic valve closure times more than usual.

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32
Q

Describe wide splitting and 2 pathological causes.

A

This is when the RV emptying is delayed, as in the case of pulmonic stenosis and right bundle branch block. It occurs regardless of inspiration and expiration phase, and is an exaggeration of normal splitting. Note that there is still a difference between expiration and inspiration, its just more dramatic.

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33
Q

Describe fixed splitting and 1 pathological cause.

A

This is seen in ASD, where a left to right shunt is present. Thus, there is an increase in RA volume (from the LA), and an increased flow through the pulmonic valve. This increased flow causes more time for the RV to empty, delaying pulmonic closure. There is NO difference between expiration and inspiration.

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34
Q

Describe paradoxical splitting and 2 pathological causes.

A

This is seen in conditions that delay LV emptying such as aortic stenosis and LBBB. The normal order of valve closure is reversed because the LV is going to take much longer to close than the RV, so P2 occurs before A2. In this case, splitting would occur during EXPIRATION, and the normal inspiration split would be eliminated.

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35
Q

Name 2 systolic murmurs heard best in the 2nd right intercostal space.

A

Aortic stenosis/sclerosis

Flow murmur

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36
Q

Name 2 diastolic murmurs heard best at the left sternal border.

A

Aortic regurgitation

Pulmonic regurgitation

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37
Q

Name 1 systolic murmur heard best at the left sternal border.

A

Hypertrophic cardiomyopathy.

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38
Q

Name 2 systolic ejection murmurs heard best at the 2nd left intercostal space.

A 
Pulmonic stenosis
Flow murmur (e.g. ASD, PDA)
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39
Q

Name 2 pansystolic murmurs heard best at the 4th and 5th left intercostal space.

A

Tricuspid regurgitation

VSD

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40
Q

Name 2 diastolic murmurs heard best at the 4th and 5th left intercostal space.

A

Tricuspid stenosis

ASD

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41
Q

Name 1 systolic and 1 diastolic murmur heard best at the apex along the mid clavicular line.

A

Systolic: MR
Diastolic: MS

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42
Q

Inspiration causes what effect on heart sounds?

A

Increases intensity of the right heart sounds since it increases the afterload for the RV.

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43
Q

Expiration causes what effect on heart sounds?

A

Increases intensity of left heart sounds

44
Q

Name 4 murmurs accentuated by hand grip maneuver.

A

This increases afterload, thus increasing the intensity of MR, AR, VSD, and MVP.

45
Q

Name 2 murmurs decreased by hand grip maneuver.

A

This decreases the intensity of AS and hypertrophic cardiomyopathic murmurs, since this decreases preload.

46
Q

Name 2 murmurs that are the only ones increased by the valsalva maneuver.

A

This decreases preload, and increases the intensity of MVP and hypertrophic cardiomyopathy murmurs.

47
Q

Name 2 murmurs decreased by rapid squatting.

A

This increases venous return and preload. If prolonged, it also increases afterload. The murmurs of MVP and hypertrophic cardiomyopathy are decreased.

48
Q

Name 5 causes of a crescendo-decrescendo systolic murmur best heard in the 2nd-3rd right interspace close to the sternum.

A 
This is aortic stenosis, due to:
Bicuspid aortic valve
Senile/degenerative calcification
Syphilis
Chronic rheumatic valve disease
Unicuspid valve
49
Q

This is an early diastolic decrescendo murmur heard best along the left side of the sternum.

A

Pulmonic regurgitation.

50
Q

This is a late diastolic decrescendo murmur heard best along the left side of the sternum.

A

Tricuspid stenosis.

51
Q

Name 3 causes of a pansystolic murmur heard best at the apex and radiates to the left axilla.

A

This is MR due to ischemic heart disease, mitral valve prolapse, or LV dilation.

52
Q

Name 3 causes of a late systolic murmur usually preceded by a mid-systolic click. Best heard at the apex.

A

MVP – the mid systolic click is due to the abrupt tensing of chordae tendinae.
Can be due to myxomatous degeneration, rheumatic fever, or chordae rupture.

53
Q

This is a crescendo-decrescendo systolic murmur best heard in the 2nd-3rd left interspaces close to teh sternum.

A

Pulmonci stenosis.

54
Q

This is a pansystolic murmur heard best along the left lower sternal border and generally radiates to the right lower sternal border. There are 2 possible causes that can be determined by the history. What are they?

A

Tricuspid regurg OR VSD.
Drug user = TR
Baby = VSD

55
Q

Name the most common cause of a rumbling late diastolic murmur with an opening snap.

A

Rheumatic fever that has led to mitral stenosis.

56
Q

Describe the murmur that usually presents with bounding pulses and head bobbing. Name 4 possible causes.

A

This is aortic regurg! A high pitched diastolic murmur associated with a widened oulse pressure. It is often due to aortic root dilation (Marfans), bicuspid aortic valve, endocarditis, or rheumatic fever.

57
Q

Murmurs heard best in left lateral decubitus position.

A

MR
MS
Left sided S3 or S4.

58
Q

What physiology accounts for the automaticity of the AV and SA nodes?

A

Phase 4 gradual Na+ conductance.

59
Q

Name 3 substances that act on smooth muscle myosin light chain kinase and the effect they have on BP.

A

Dihydropyridine CCBs, Epinephrine (on beta 2 receptors), PGE2. These relax BP.
CCBs inhibit calmodulin-Ca, which is responsible for phosphorylating myosin via myosin light chain kinase causing smooth muscle contraction.
Both beta 2 receptors and PGE2 receptors act on cAMP, which inhibits myosin light chain kinase.

60
Q

Which organ has the largest blood flow?

A

Lung

61
Q

Which organ receives the largest share of systemic CO?

A

Liver

62
Q

Which organ has the largest arteriovenous O2 difference?

A

Heart

63
Q

Describe the Cushing reaction.

A

This is a triad of HTN + bradycardia + respiratory depression. Increased intracranial pressure constricts arterioles, causing cerebral ischemia. The body responds to this ischemia but increasing sympathetic stimulation. This increases the stretch detected by your baroreceptors, so now your body thinks you have HTN and slows the heart rate.

64
Q

Describe the chain of events in which hypotension causes a reflex tachycardia.

A

Carotid sinus senses low BP so there is less stimulation of baroreceptors and glossopharyngeal nerve.
Glossopharyngeal afferents send signals to the solitary tact of the medulla causing a decrease in the inhibition of sympathetic output. Thus the decreased parasympathetic and increased sympathetic causes tachycardia.
Remember, the aortic arch is not responsible for any of this since it only acts under high blood pressure states.

65
Q

What CXR finding is a possible sign of aortic dissection?

A

Widening mediastinum.

66
Q

Where is Type A aortic dissection located and what is the management?

A

Type A: ascending aorta, aortic arch

Surgical management

67
Q

Where is Type B aortic dissection located and what is the management?

A

Type B: descending aorta

Medical management

68
Q

What is the most likely cause of chest pain in a patient with ST segment elevation only during brief episodes of chest pain?

A

Prinzmetals

69
Q

During a HS football game, a young athlete collapses and dies immediately. What type of cardiac disease did he have?

A

Hypertrophic cardiomyopathy.

70
Q

Describe pathological changes seen 4-12 hours after an MI.

A 
Early coagulative necrosis
Edema
Hemorrhage
Wavy fibers
Dark mottling
71
Q

Describe pathological changes seen 12-24 hours after an MI

A

Contraction bands due to reperfusion injury
Release of necrotic cell content into blood
Beginning of neutrophil migration

72
Q

Describe pathological changes seen 1-3 days after an MI. What is the patient at greatest risk for during this stage?

A

Extensive coagulative necrosis
Tissue surrounding infarct shows acute inflammation
Neutrophil migration
RISK: Fibrinous pericarditis.

73
Q

Describe pathological changes seen 3-14 days after an MI. What is the patient at greatest risk for during this stage?

A

Macrophage infiltration followed by granulation tissue at the margins.
Hyperemia
Yellow-tan softening
RISK: Free wall rupture, papillary msucle rupture, IV septal rupture due to macrophages that have degraded important cell components.

74
Q

4 classic EKG changes seen with MI

A

ST segment elevation of at least 1 mm in 2 contiguous leads
T wave inversion
New LBBB
New Q waves (at least 1 block wide or 1/3 height of total QRS complex)

75
Q

ST elevation is seen in EKG leads VI-V4, V5. Where is the MI and what artery is affected?

A

Anterior wall MI –LAD

76
Q

ST elevation is seen in EKG leads V4-V6 Where is the MI and what artery is affected?

A

Anterolateral wall

Left circumflex a.

77
Q

ST elevation is seen in leads II, III, aVF. Where is the MI and what artery is affected? What is your next step?

A

Inferior wall MI –Right coronary artery.
You should obtain a right sided EKG (V1-V6 on right chest) –if ST segment elevation is seen in V4, then posterior right ventricle also affected. This indicates a right sided MI.

78
Q

ST elevation is seen in leads I and aVL. Where is the MI and what artery is affected?

A

Lateral wall

Left circumflex

79
Q

What are the two most common complications after an MI?

A

Arrhythmia

LV failure

80
Q

A patient suffers an MI. 4 days later he presents with muffled heart sounds, hypotension, and JVD. What happened?

A

This is cardiac tamponade due to rupture of the ventricular free wall. This allowed fluid to enter the pericardial space, and as it accumulates, the pressure increases and the ventricles begin to fail with a lower and lower SV.

81
Q

A patient suffers an MI. 3 days later he presents with severe mitral regurgitation. What happened?

A

Rupture of papillary muscle.

82
Q

A patient suffers an MI. 7 days later he presents with a holosystolic murmur heard along the left lower sternal border. What happened?

A

This patient now has a VSD because his interventricular septum ruptured.

83
Q

What is Dressler syndrome?

A

Pericarditis that occurs 2-4 weeks after an MI. Presents with chest pain, fever, and increased ESR.
It is an autoimmune process.

84
Q

Patient presents with an S3 heart sound and balloon appearance on CXR. Name 6 etiologies of this disease.

A 
This is dilated cardiomyopathy.
ABCCCD
chronic Alcohol abuse
wet Beri-beri
Coxsackie B virus myocarditis
chronic Cocaine use
Chaga's disease
Doxorubicin toxicity

Hemochromatosis, peripartum cardiomyopathy, etc.
Eccentric hypertrophy occrs.

85
Q

17 y.o. patient presents for his sports physical. You note an S4 heart sound and a systolic murmur. What other disease does he most likely suffer from, and how does this appear histologically?

A

This is hypertrophic cardiomyopathy associated with Friedrich’s ataxia.
Disoriented, tangled, hypertrophied myocardial fibers are seen on histology.

86
Q

Most common cause of myocarditis in US and histological appearance

A

Coxsackievirus –diffuse interstitial infiltrate of lymphocytes with myocyte necrosis

87
Q

On PE, you note a patient that has decreased SBP by more than 10 mmHg with inspiration. Name 5 common etiologies.

A 
Cardiac tamponade
Asthma
Croup
Obstructive sleep apnea
COPD

This is pulsus paradoxus representative of a decreased LV capacity.

88
Q

On post-mortem histological examination, you note focal myocardial inflammation with multinucleate giant cells. What do you suspect the patient died from?

A

These are Aschoff bodies seen in rheumatic heart disease. This patient died of myocarditis. Other finddings include anitschkow cells (activated histiocytes) and antibodies to M protein.

89
Q

Characteristic EKG finding of cardiac tamponade

A

Electrical alternans

90
Q

Scandinavian patient presents with skin discoloration, joint pain, weakness and fatigue, as well as diabetes. What cardiac condition are you concerned about?

A

This patient has hemochromatosis which is associated with restrictive cardiomyopathy. However, dilated cardiomyopathy could also occur.

91
Q

Which 4 disorders are commonly discovered in patients with Raynaud phenomenon?

A

SLE
Scleroderma
Buerger disease
Atherosclerosis

92
Q

What local skin problems may arise from venous insufficiency resulting in varicose veins?

A

Edema
Stasis dermatitis
Ulcerations
Poor wound healing

93
Q

Elderly patient presents with jaw claudication and unilateral headache. What non-specific lab test would you like to perform first?

A

ESR.

If elevated, cannot R/O temporal arteritis.

94
Q

36 y.o. Asian female presents with fever, night sweats, skin nodules, and weak UE pulses. What would your pathology show?

A

This is takayasu’s arteritis – granulomatous thickening of the aortic arch and proximal great vessels.

95
Q

27 y.o. female presents with fever, weight loss, melena, hypertension, and seizures. What other disease is often seen in these patients?

A

This is polyarteritis nodosa, an immune-complex mediated vasculitis causing transmural inflammation of the arterial wall with fibrinoid necrosis. It does NOT involve the pulmonary arteries.
Hepatitis B seropositivity is seen in 30% of patients.

96
Q

A concerned parent brings in her asian 4 y.o. child whose fingertips are peeling, has a fever and cervical lymphadenitis. What complication are you most concerned about?

A

This is Kawasaki’s disease or mucocutaneous LN syndrome. You’re concerned about coronary aneurysms causing MI or ruptures.

97
Q

36 y.o. male smoker presents with intermittent claudication and Raynaud’s phenomenon. What is the diagnosis, what can this led to, and how should you treat it?

A

This is Buerger’s disease, or thromboangiitis obliterans. Intermittent claudication may lead to gangrene, autoamputation of the digits, and superficial nodular phlebitis. Tell the patient to stop smoking and this disease goes away.

98
Q

Patient presents with dark skin lesions and hematuria. Labs show + p-ANCA and + mpo-ANCA. What is the dx?

A

Microscopic polyangiitis

99
Q

Patient presents with hemoptysis, hematuria, and chronic sinusitis. What is the most likely lab findings and CXR appearance?

A

This is Wegener’s granulomatosis or granulomatosis with polyangiitis. It is c-ANCA positive and CXR displays large nodular densities.

100
Q

Patient presents with multiple dark skin lesions and foot drop. What other disease is most likely present in their history?

A

This is Churg-STrauss associated with asthma and sinusitis that goes on to involve peripheral nerves, heart, GI, kidneys. It is a necrotizing vasculitis with eosinophilia. Thus, it has a positive p-ANCA and elevated IgE levels.

101
Q

Woman presents with her 5 year old daughter 8 days following URI because she noticed blood in her urine. What is the pathogenesis of this disease?

A

Vasculitis secondary to IgA complex deposition in the kidneys – > Henoch Schonlein purpura. It usually presents with palpable purpura on buttocks/legs, arthralgia, and GI issues such as abdominal pain and melena.

102
Q

Physiological parameters seen in cardiogenic shock

A

High preload
Low CO
Adequate intravascular volume

103
Q

Physiological parameters seen in hypovolemic shcok

A

Low pre-load
Low CO
Low intravascular volume

104
Q

Physiological parameters seen in distributive shock

A

Normal/low preload
High CO
Decreased vascular resistance

105
Q

Physiological parameters seen in obstructive shock

A

Low preload
Low CO
Increased vascular resistance

DIT FACTS (16 decks)

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