Cardio Flashcards

1
Q

What is Quincy’s sign?

A

Capillary beds in the fingers are pulsating because of aortic regurgitation which causes high sys and low Diastole.

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2
Q

Systolic ejection murmur with widely split second heart sound.

A

Atrial Septal Defect

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3
Q

Highly associated with Turner’s Syndrome.

A

Coarctation of the Aorta (females with only ONE X chromosome).

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5
Q

The pulmonary valve closes during

A

Diastole

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6
Q

“3” sign

A

Coarctation of the Aorta

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7
Q

What area of the ventricular septum is most likely to have a defect in VSD?

A

Membranous region

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8
Q

What causes the snap sound in mitral valve stenosis?

A

Higher pressure in the RA

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9
Q

What might you feel on the patient with pulmonary stenosis?

A

Palpable parasternal lift (because of right ventricular hypertrophy).

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11
Q

What might you see in an ECHO on a patient with Pulmonary Stenosis?

A

Doming or Dysplastic Valve.

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13
Q

Describe what goes on with the valve and blood during stenosis.

A

Pressure builds up, Ejection click, followed by turbulence (which gets louder, then quieter)…the CRESCENDO DE CRESCENDO murmur.

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14
Q

Common. Left to right shunt. Often involves a patent foramen oval.

A

Atrial Septal Defect

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15
Q

Failure of the ductus arteriosus to close after birth

A

Patent Ductus Arteriosus

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16
Q

What happens to the kidneys in coarctation of the aorta?

A

Blood reduced to kidneys>release Renin-Angiotensin-Aldosterone > causes water retention>leads to hypertension.

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17
Q

How does squatting help infants with Tetralogy of Fallot?

A

Increases aortic pressure, back flow to force left to right shunt to get more oxygenated blood and prevent deoxygenated blood to flow into LV.

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18
Q

Consider this when you see a young male with hypertension

A

Coarctation of the Aorta

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19
Q

What happens to blood with mitral valve regurgitation?

A

Blood leaks back into left atrium, pools, creates clots.

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20
Q

Where does the coarctation of the aorta occur in most infants?

A

AFTER the aortic arch ,BEFORE ductus arteriosus.

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21
Q

The only right sided ausculatory event that decreases with inspiration.

A

Pulmonary Stenosis (because of reduced flow of blood to lungs).

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22
Q

Continuous murmur heard superiority and midline in the back over the left anterior chest.

A

Coarctation of the Aorta

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23
Q

Harsh, Holosystolic murmor. Loudest along the left sternal border.

A

VSD

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24
Q

What are some risk factors for pulmonary stenosis?

A

Maternal Congenital Heart Disease. Maternal Gestational Diabetes. Congenital Rubella. Fetal alcohol syndrome. NOONAN SYNDROME. TETRALOGY OF FALLOT.

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25
Q

Boot shaped heart

A

Tetralogy of Fallot

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26
Q

When should you refer patients with pulmonary stenosis?

A

Peak Pulmonary valve gradient is GREATER THAN 60 mmHG.

(Patients w/ peak of 60 mmHg or mean of 40 mmH by echo/Doppelgänger should undergo intervention, regardless of symptoms).

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27
Q

What it’s he heart sound of Mitral Valve Stenosis

A

Snap Sound. Diastolic Rumble

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28
Q

What is an Epstein anomaly?

A

Leaflets are too low and located in the ventricle

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29
Q

Large pulmonary arteries. Increased pulmonary vascularity and enlarged RA and RV..BUT small aortic knob.

A

ASD

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30
Q

What is associated with Coarctation of the Aorta?

A

Turner’s Syndrome and Cerebral Berry Aneurysms.

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31
Q

What does the mitral valve do during diastole?

A

Opens and blood fills ventricle.

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32
Q

90% of ASD cases are due to…..

A

Optium Secundum

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33
Q

What are treatment options for Coarctation of the Aorta?

A

Balloon dilation to widen the aorta.

Surgical Removal of Coarctation.

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34
Q

What is myxomatous degeneration?

A

Weakened connective tissue, chordate tendinae and papillary muscles.

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35
Q

Eisenmenger syndrome

A

Pressure converting from left to right to right to left as left ventricle weakens.

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36
Q

How does Coarctation of the Aorta cause scalloping of the ribs?

A

UPSTREAM INCREASE PRESSURE, UNEVEN PRESSURE, causing REVERSED FLOW and PULSATING POSTERIOR INTERCOSTAL ARTERIES. (Where there is lower pressure). Ribs 3-9, mostly 3 & 4.

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37
Q

When the pulmonary valve doesn’t open all the way

A

Pulmonary stenosis

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38
Q

Most often due to pulmonary hypertension.

A

Tricuspid valve regurgitation

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39
Q

What happens to pressure in upper and lower extremities in coarctation of aorta?

A

Higher-upper extremities.

Lower-Lower extremities

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40
Q

You hear a CONTINUOUS MURMUR SUPERIORLY AND MIDLINE in the BACK and OVER LEFT ANTERIOR CHEST?

A

Coarctation of the Aorta

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41
Q

The pulmonary valve opens during…

A

Systole

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42
Q

Symptoms in spells, squatting.

A

Tet Spell-squatting helps kink the femoral arteries, increases vascular resistance-increases systemic pressure-pressure (Left>Right). Shunt REVERSES

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43
Q

Why is there a delayed pulmonic valve closure in ASD and what does in sound like?

A

Because there is extra blood flowing into the RV. Splitting of the S2

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44
Q

What are cerebral berry aneurysms?

A

When a wall of a cerebral artery becomes weak and balloons out. May enlarge and burst, sending blood into brain.

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45
Q

Severe cases of right-sided heart failure due to pulmonary stenosis may be related to……

A

Congenital rubella.

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46
Q

At risk for embolism

A

Atrial Septal Defect. Clot flows from right to left and end ups in brain.

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47
Q

What is a Holosystolic murmur?

A

Blood flowing back through duration of systole

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48
Q

What is Carvallo’s Sign?

A

A murmur that gets louder with inspiration because there is negative pressure which brings more blood back into the heart.

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49
Q

What condition is the only RIGHT SIDED HEART SOUND that DECREASES with INSPIRATION?

A

Pulmonary Stenosis

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50
Q

Hypertension in arms, but NOT in legs.

A

Coarctation of the Aorta

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51
Q

You see a patient with his head bobbing “pulsatively”

A

Aortic Regurgitation..caused by increased Sys pressure and Decreased Diastolic pressure

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52
Q

Incomplete right bundle branch block present in nearly all cases of

A

ASD

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53
Q

Describe the heart sound in aortic stenosis.

A

Ejection click..Loud Murmur that gets quieter…Pressure build up..clicking through..turbulence.A crescendo-Decrescendo murmur.

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54
Q

What are symptoms of Coarctation of the Aorta (generally in adults)?

A

Headache. Epistaxis. Chest pressure. Claudication w/ exercise.

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55
Q

Does the murmur in pulmonary stenosis radiate to the right or left?

A

Left. (Because of the flow pattern)

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56
Q

What is a complication of an ASD?

A

Embolis-Deep Vein Thrombosis moving into brain.

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57
Q

What is a recommended treatment for severe pulmonary stenosis?

A

Percutaneous Balloon Valvulosplasty

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58
Q

What might you see on an ECG for pulmonary stenosis?

A

Right Axis deviation. Peaked P waves (because of right atrial overload).

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59
Q

Babies with clubbing in fingers and toes. Sign of.

A

Tetralogy of Fallot

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60
Q

How does mitral valve regurgitation cause left sided heart failure?

A

Blood pumped back into atrium, which causes an increased preload and causes volume overload, which causes eccentric hypertrophy..or building to left ventricle muscle..which can cause the LV to be exhausted.

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61
Q

Crescendo-Decrrescendo murmur is found in what?

A

Pulmonary Stenosis–pressure build up followed by a click.

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62
Q

Thickening of Pulmonary Valve

A

Pulmonary Stenosis

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63
Q

How does adult coarctation differ from infant?

A

No patent ductus arteriosus. NO MIXING OF DEOXYGENATED BLOOD, JUST A PINCH IN THE AORTA.

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64
Q

What happens to heart sound with patients with mitral valve regurgitation when they are squatting?

A

Click comes later and the murmur is shorter.

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65
Q

Risk of berry aneurysms

A

Coarctation of the Aorta

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66
Q

You hear a LOUD HARSH SYSTOLIC MURMUR. SPLIT S2. It DECREASES with INSPIRATION. What might this suggest?

A

Pulmonary Stenosis

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67
Q

What are the four abnormalities in Tetralogy of Fallot?

A

1) Narrowing of pulmonary valve or infundibulum (de02 blood harder to flow out).
2) Myocardium of RV hypertrophy. (Boot Shaped)
3) Large Ventricular septal defect (VERY CYANOTIC).
4) Aorta overrides septal defect (variable).

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68
Q

What does the mitral valve do during systole?

A

Closes-blood flows out through aorta.

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69
Q

Patient has dyspnea, dysphagia, fatigue, and harder to breath.

A

Mitral valve stenosis

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70
Q

This can create schystocytes

A

Pulmonary stenosis

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71
Q

What happens to blood in ASD?

A

Oxygenated blood is pushed from the Left atrium to Right Atrium.

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72
Q

What causes aortic regurgitation?

A

Aortic Root Dilation-leaflets pulled apart and not able to close all the way.

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73
Q

Mid-systolic click followed by a systolic murmur

A

Mitral valve regurgitation

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74
Q

Characteristic EJECTION click

A

Stenosis

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75
Q

What is associated with a bicuspids aortic valve?

A

Coarctation of the Aorta

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76
Q

What does “optimum secundum mean”?

A

“Second opening”

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77
Q

WEAK FEMORAL PULSATOINS

A

Coarctation of the Aorta

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78
Q

Enlarged liver and spleen

A

Hepatosplenomegaly

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78
Q

The most common cardiac anomaly.

A

Atrial Septal Defect.

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80
Q

Described what can happen during a larger VSD.

A

02 blood initially left to right shunt. LV weakens. De02 blood flows right to left shunt out into AORTA, causing CYANOSIS!

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81
Q

Treatment usually involves balloon valvuloplasty

A

Pulmonary Stenosis (other answers)

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82
Q

Associated with Noonan Syndrome and Congenital Rubella

A

Pulmonary Stenosis

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82
Q

What are common symptoms of severe pulmonary stenosis?

A

Cyanosis. Shortness of breath and fatigue (Can’t get O2 to lungs! Because pulmonary valve is obstructed!)

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83
Q

Most common of all valvular conditions.

A

Mitral Valve Prolapse

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84
Q

Explain what happens to blood flow in mitral valve stenosis.

A

Increased blood volume-increased pressure–blood flows back into hearts–causes pulmonary congestion and edema.-pulmonary hypertension–can make it harder for the right ventricle to pump blood to the lungs…over time right ventricle will hypertrophy…pace maker cells stretch and become more irritable..increasing risk of atrial fibrillation..causing static pools of blood..thrombus formation..which can immediately get into the systemic circulation…if atrium dilates it can compress the esophagus.

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86
Q

What is the most common congenital defect amongst babies?

A

VSD

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87
Q

Associated with Turner’s Syndrome

A

Patent Ductus Arteriosus

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88
Q

What size of commissar all fusion can be found in mitral valve stenosis?

A

2 cm

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88
Q

What is pulmonary stenosis?

A

Increases resistance of the right ventricle outflow because the pulmonary valve does not completely open.

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89
Q

Atrial septal defect is common associated with:

A

Fetal Alcohol Syndrome. Downs Syndrome.

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89
Q

Found in 25% of patients with Down Syndrome.

A

Ostium Primum Atrial Septal Defect

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90
Q

What ribs are particularly effected by rib notching?

A

Ribs 3-9, mostly 3 and 4

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90
Q

What kind of pulse might you find in the femur of adults with Coarctation of the Aorta?

A

Weak

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91
Q

How does coarcatation of the aorta happen in infants?

A

The ductus arteriosus exists during fetal development and usually closes after birth, but doesn’t.

PREDUCTAL COARCTATION

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93
Q

Narrowing of the aortic arch distal to the origin of the left subclavian artery

A

Coarctation of the Aorta

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93
Q

Increased pressure in upper extremities of the head

A

Coarctation of the aorta

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93
Q

When should you definitely consider an intervention for Coarctation of the Aorta?

A

Greater than 20 mm Hg.

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93
Q

What is the most common cause of cyanotic congenital heart defect?

A

Tetralogy of Fallot

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93
Q

What is tetralogy of Fallot associated with?

A

Chromosome 22 deletions and DiGeorge Syndrome

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93
Q

A infant shows cyanosis in his legs, what might cause this?

A

Coarctation of the Aorta.

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94
Q

First heart sound followed by a click then a rough systolic murmur and a single or split S2

A

Pulmonary Stenosis

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95
Q

What happens to blood and heart with a tricuspid valve regurgitation?

A

Blood flows back into atrium, causes a larger volume and back flow, or preload. The right ventricle becomes larger because it is working harder. This can lead to stretching of the annulus, worse regurgitation, and right sided heart failure. (Distended neck veins, swelling of ankles and feet).

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96
Q

What is a decrescendo murmur caused by?

A

Back flow of blood–increases the blood volume–more work of ventricle. Eccentric ventricular hypertrophy.

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97
Q

Loud harsh systolic murmur. Radiates to the left shoulder.

A

Pulmonary Stenosis

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99
Q

Causes scalloping of the ribs.

A

Coarctation of the Aorta-thoracic arteries high pressure wear away ribs.

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99
Q

Increased o2 saturation in right atrium, right ventricle, pulmonary artery…slight delay in pulmonic valve closure

A

ASD

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99
Q

What happens to aortic valve during stenosis?

A

Thickens/stiffens and opens to LESS THAN 1 cm

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99
Q

What happens during systole (or heart contraction) with tricuspid valve regurgitation?

A

Heart flows back into the right atrium

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99
Q

What are the heart sounds of Tricuspid Valve Regurgitation?

A

Holosystolic Murmur

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99
Q

Can present with severe cyanosis.

A

Pulmonary Stenosis (other answers possible)

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103
Q

Is pulmonary stenosis common in children or adults?

A

Adults

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106
Q

What is a common cause of cryptogenic stroke in patients under 55?

A

ASD

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107
Q

Digital clubbing is common with this condition.

A

Pulmonary Stenosis

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108
Q

What happens during Phase 1 of the action potential of ventricular myocytes?

A

The notch.

Efflux of K+ and Cl-, initial rapid repolarization

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109
Q

What happens during Phase 1 of the action potential of ventricular myocytes?

A

The notch.

Efflux of K+ and Cl-, initial rapid repolarization

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110
Q

What size is a Stenosis aortic valve (usually)?

A

<1cm2

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111
Q

Who is at more risk for aortic stenosis?

A

Patients with bicuspid aortic valve (stress on 2 leaflets instead of 3, more calcification).

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112
Q

What is a cause of Aortic Valve Stenosis?

A

Rheumatic Fever-causes increase inflammation of valve—repeated damage and repair.

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113
Q

What causes commissural fusion and where does it usually occur?

A

Rheumatic Fever. Fusion of Aortic Valve.

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114
Q

You see a patient with a bobbing head, bounding pulse, pulsing capillary beds in his fingers….

A

Aortic Regurgitation (LV working really hard to pump blood out during systole, increased stroke volume).

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115
Q

A young person with hyperthyroidism what might you consider?

A

A-fib

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116
Q

“Holiday heart” can be caused by __________

A

A fib

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117
Q

Symptoms are caused by DECREASE CARDIAC OUTPUT.

A

A fib

*Decreased diastolic filling and decreased ventricular contractility

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118
Q

A fib is associated with a ________ fold increase risk of stroke.

A

5

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119
Q

A fib is associated with a ________fold increase in RISK OF HEART FAILURE.

A

3

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120
Q

A fib is associated with a ___________fold RISK OF DEMENTIA.

A

2

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121
Q

How do you diagnose A fib?

A
  • Irregular and often rapid pulse

- MAY find murmur, gallop (S3), JVD (may also be b/c of heart failure), peripheral edema

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122
Q

What might you find on an EKG with A fib?

A

ERRATIC, DISORGANIZED atrial activity between discrete QRS complexes occurring in an irregular pattern.

Rate ranges from slow to extremely rapid, but irregular (ALL OVER THE PLACE), unless there is an underlying heart block or a ventricular pacemaker has taken over control of pacing the heart.

The atrial activity may appear as VERY FINE WAVES or QUITE COARSE (can be confused with ATRIAL FLUTTER).

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123
Q

Besides an ECG what else might you use for A fib?

A

Echocardiogram (know more about what the heart is doing)

Ambulatory rhythm monitoring (paroxysmal a fib, comes and goes, patients may not be experience A fib during a visit, this allows for consistent monitoring to catch events when they occur)

Metabolic profile, thyroid panel (Rule out metabolic and/or thyroid causes)

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124
Q

A patient comes in with A fib, but does not show any symptoms at the clinic, what might you use as a diagnostic study?

A

Ambulatory rhythm monitoring

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125
Q

Define paroxysmal a fib.

A

Spontaneous

Terminates by itself.

Returns to normal after an intervention

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126
Q

Define persistent A fib.

A

Continuous. LASTING > 7DAYS

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127
Q

Define chronic/permanent A fib.

A

No treatment to restore or maintain sinus rhythm.

Lasts forever. Can’t keep them in sinus rhythm.

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128
Q

What do you think about in terms of A fib treatment?

A

Rate vs. Rhythm Control

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129
Q

What are the key points for rate control in A fib treatment?

A

Reduces ventricular rate WITHOUT changing rhythm.

Goal: SYMPTOM MANAGEMENT. PREVENT TACHYCARDIA-MEDIATED CARDIOMYOPATHY.

Target heart rates: Resting: < 80 bpm. Ambulatory: <100 bpm

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130
Q

What do you use to manage rate control in a fib?

A

AV nodal blocking agents: Beta blockers and Calcium channel blockers

DIGOXIN: may add synergistic rate control effect when combined with beta blockers or CCBs. (Needs monitoring)

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131
Q

What are key points for rhythm control in A fib?

A

Preferred when:

  • symptomatic despite rate control
  • difficult to rate control
  • develop tachycardia-mediated cardiomyopathy
  • are younger
  • have a first episode or have AFib triggered by acute illness.
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132
Q

How is rhythm control achieved in AFib?

A

Cardioversion

Anti arrhythmias

Ablation

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133
Q

Electrical cardioversion restores sinus rhythm in _______% of patients.

A

75-90%

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134
Q

For rhythm control, initial shock of _________ Joules is administered in synchrony with the _________wave

A

100-200, R

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135
Q

In cardioversion rhythm control if the conversion does not occur an additional attempt at _____________Joules is indicated.

A

360

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136
Q

Following cardioversion Rhythm Control

AFib recurs in _________of patients at 3 months.
AFib recurs in__________o Patients at 12 months.

A

40-60%

60-80%

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137
Q

In terms of AFib rhythm control:

Antiarrhythmics maintain sinus rhythm in ___________% of patients

A

50

138
Q

What are medications you may use in AFib rhythm control?

A

Class I Fast Sodium Channel Blockers

Class II Beta Blockers

Class III Potassium Channel Blockers

Class IV Slow Calcium Channel Blockers

Class V Variable Mechanism

139
Q

When is ablation indicated in Afib rhythm control?

A

In patients who have failed greater than or equal to 1 antiarrhythmic.

140
Q

What is ablation (in terms of Afib rhythm control)?

A

Left atrial radio frequency catheter ablation.

(Cryogenic (freezing) ablation can also be done).

Cauterized the “short circuits” that are causing the AF

Electrical impulses cannot pass the ablation lines

141
Q

Who is a good candidate for ablation?

A

Patient who has failed greater than or equal to 1 antiarrhythmic, possibly a younger patient who you don’t want to put through rate control.

142
Q

What should you think about when considering antiarrhythmics in terms of Afib rhythm control?

A

Comorbidities.

Proarrythmic potential

Toxicity potential

143
Q

Strokes related to Afib are _______ as likely to be fatal.

A

Twice

144
Q

What is a PRIMARY goal in Afib management?

A

Prevent STROKES

145
Q

What do you use to calculate emboli risk in a patient with Afib?

A

CHADS Vasc score

146
Q

What should the antithrombotic therapy be based on?

A

EMBOLIC RISK SCORE (regardless of A fib type)

147
Q

A CHADS VASc Score of > or equal to 2=

A

High risk-anticoagulation recommended

148
Q

A CHADS VASc score of 1=

A

Moderate risk-anticoagulation, ASA, or no therapy

149
Q

A CHADS VASc Score of 0=

A

Low risk-no anticoagulation recommended

150
Q

Multifocal atrial tachycardia is most commonly seen in patients with_____________

A

Severe COPD

151
Q

What might you see on an ECG with patients with MAT?

A

Varying P wave morphology and irregular P-P intervals

152
Q

What is a medication that may be helpful for MAT?

A

Verapamil (may be helpful, but MAT is difficult to manage)

153
Q

Atrial flutter most often appear in patients with _______

A

COPD

154
Q

In terms of Atrial Flutter, a reentrant circuit generate atrial rates of ____________bpm with transmission every second, third, or fourth impulse through the _______node to the ventricles.

A

250-350

AV

155
Q

What might you see on an EKG in atrial flutter?

A

A “sawtooth” pattern of atrial activity in the INFERIOR leads (II, III, aVF).

156
Q

You hear an early decrescendo diastolic murmur.

A

Aortic Regurgitation (blood flowing back into LV).

157
Q

Generally, how long is one heartbeat?

A

0.75-1 second

158
Q

How much of a cardiac cycle is spent in systole? Diastole?

A

Systole = 1/3

Diastole =2/3

159
Q

What are the phases of the cardiac cycle?

A
  • Ventricular filling
  • Atrial contraction
  • Isovolumic contraction
  • Ventricular ejection
  • Isovolumic relaxation

Repeat

160
Q

What happens during ventricular filling?

A

The ventricle is relaxed and mitral valve is open.

This phase begins when the ventricle pressure is less than atrial pressure.

161
Q

What happens during atrial contraction?

A

The atrium forces additional blood into the ventricles and the Mitral valve closes, producing the first heart sound (S1)

162
Q

What happens during Isovolumic contraction?

A

The ventricles begin to contract, but both valves are still closed. Brief phase.

163
Q

What happens during Ventricular ejection?

A

The aortic valve opens, blood flows from ventricles to aorta. This phase begins when left ventricle pressure equals aortic pressure, and systole ends when ventricular pressure is less than aortic pressure. The aortic valve closes, producing the second heart sound (S2)

164
Q

What happens during isovolumic relaxation?

A

First phase of diastole. Both valves are closed, and the ventricle relaxes, leading to a decrease in ventricular pressure. When ventricular pressure is less than atrial pressure, the Mitral valve opens and ventricular filling will begin.

165
Q

What is the amount of blood ejected from the heart is one contraction called?

A

Stroke volume

166
Q

Stroke volume x heart rate =

A

Cardiac output

-expressed in L per minute

167
Q

What is Ejection Fraction?

A

The percentage of blood ejected from the ventricle in one contraction

168
Q

How is ejection fraction usually measured?

A

Echocardiography

169
Q

Why is ejection fraction important?

A

Used to clinically assess ventricular function.

170
Q

What is a normal ejection fraction percentage?

A

55-60%

171
Q

In what phase does ventricular filling happen?

A

Relaxation phase of diastole

172
Q

What is the Frank-Starling relationship?

A

It states that the more a myocyte is stretched, the more it can contract. So..increased ventricular filling increases stroke volume.

173
Q

What is Preload?

A

The filling pressure of the heart. i.e. the initial stretching of myocytes prior to contraction

174
Q

What increases Preload? Decreases?

A

Increases-> anything that increases the volume of the blood delivered to the ventricle (increased blood volume, increased force of atrial contraction)

Decreases-> stiffness of the ventricle, or a decrease in blood volume

175
Q

What is Afterload?

A

The pressure against which the ventricle contracts; or, as the aortic pressure for the left ventricle.

176
Q

What is the overall goal of antihypertensives?

A

Decrease systemic blood pressure, therefore decreasing the work of the heart.

177
Q

How do ACE inhibitors work?

A

They work on the renin-angiotensin-aldosterone system to decrease afterload.

178
Q

How do diuretics help HTN?

A

They decrease blood volume, thereby decreasing preload.

179
Q

True or false: standard treatments for systolic CHF are effective in diastolic CHF

A

False.

Treatment of diastolic dysfunction is difficult

180
Q

What are the 2 main lipids in the blood?

A

Cholesterol & Trigylceride

181
Q

What are the subgroups of Lipoproteins? (a protein-lipid complex which transports lipids in the blood)

A
  • HDL (high-density lipoprotein)
  • LDL (low-density lipoprotein)
  • VLDL (very low-density lipoprotein)
  • Chylomicrons
  • LpA (lipoprotein A)
182
Q

A protein contained on the surface of a lipoprotein

A

Apolipoprotein

183
Q

Role of LDL

A
  • Carry most of the cholesterol in the blood

- heterogeneous in size

184
Q

Role of HDL

A
  • Carries cholesterol from peripheral tissue to liver
  • smaller and denser
  • consists primarily of apoproteins & cholesterol
185
Q

What constitutes TOTAL cholesterol?

A

HDL + LDL + VLDL

186
Q

What is atherosclerosis?

A

Plaques lining the arterial walls contain larges amounts of cholesterol.

High levels of LDL = greater risk of atherosclerotic disease

High levels of HDL = lower risk of atherosclerotic disease

187
Q

Extremely high levels of chylomicrons or VLDL particles (triglycerides) result in the formation of…

High LDL concentrations result in…

A
  • Eruptive xanthomas

- Tendinous xanthomas on certain tendons

188
Q

Abnormal lipids are technically _____ disorders

A

Endocrine

189
Q

True or false: HDL is considered normal at any level

A

False: low levels are abnormal, are a form of dyslipidemia, and is associated with metabolic syndrome

190
Q

What numbers are high and low levels for LDL?

A

Very high: over 190

Low: under 70

191
Q

At what number is HDL considered cardioprotective?

A

Over 60.

Under 40 is considered low.

192
Q

For triglycerides, what number is considered normal?

A

Under 150
150-200 = borderline
200-500 = high
Over 500 = very high

193
Q

Which lipoprotein complexes are high in Triglycerides?

A

Chylomicrons & VLDL

194
Q

Why do we need cholesterol?

A
  • Stabilize cell membranes & helps membrane transport.
  • Required for adrenal and sex hormones
  • Required for bile acids which helps with absorption of dietary fats
195
Q

Why do we need triglycerides?

A
  • Energy storage in adipose tissue
  • Lighter than glycogen stores
  • It gets converted to fatty acids and then produces ATP which is the major source of energy for muscle cells
  • Can be converted into glucose via gluconeogenesis
196
Q

Important enzymes in lipid metabolism…

A

HMG-CoA-reductase

PCSK-9

197
Q

Steps in the development of cholesterol-rich plaque in arteries:

Macrophages ingest LDL particles and become _______. These cells invade arterial walls, forming ________ and then extracellular lipid cores. A reaction ensues that causes fibrous thickening, forming a ________. With time, this becomes unstable and can rupture. Plaque material is released, causing a _______ and blockage of the artery.

A
  • Foam cells
  • Fatty streaks
  • Fibroatheroma
  • Thrombosis
198
Q

Primary causes of hyperlipidemia…(born with it)

A

-Familial hypercholesterolemia
- Familial hypertriglyceridemias
-Familial combined forms
(Rare in severe forms)

199
Q

Secondary causes of hyperlipidemia…(developed it)

A
  • Diabetes
  • Obesity
  • Chronic kidney disease
  • Hypothyroidism
  • HIV
  • Alcoholism
  • Many meds, including estrogen, retinoids, B-blockers
200
Q

What are common Sx of elevated cholesterol?

A

Usually asymptomatic, although can present with vascular disease. Very high triglycerides can present with Xanthomas

201
Q

A constellation of metabolic abnormalities which increase risk for atherosclerotic disease is called?

A

Metabolic Syndrome

202
Q

Tx of metabolic syndrome?

A

optimal management of BP, blood sugars, and lipids. Weight management

203
Q

Diseases that put you at risk for Metabolic Syndrome

A
DM2
HTN
Elevated uric acid/gout
abdominal obesity
elevated triglycerides
Low HDL
Small, dense LDL
204
Q

Recommendations for lipid screening for children

A
  • Screen once between 9-11, and again between 17-21

- Review risk factors at every visit & screen if high risk

205
Q

Recommendations for lipid screening in Adults

A

ACC/AHA = all adults over 21 & stop at 75 for those without CV disease

USPSTF (more conservative) = begin at 20 for those with CV risk factors, begin at 35 for men without other risk factors, begin at 45 for women without other risk factors

206
Q

Best screening for lipid disorders?

A

In low risk = measure total and HDL w/out fasting

For most pts = fasting lipid panel w/ total, LDL, HDL & triglycerides

207
Q

What lipid disorders should be referred to specialty care?

A
  • Familial hyperlipidemia
  • CV disease at very young age
  • Extremely high triglycerides that do not improve with care
208
Q

Does a low fat diet work to lower cholesterol?

A

No.

Will often lower HDL. Decreasing fat intake will reduce satiety and people end up consuming more calories.

209
Q

What type of diet has shown to be heart-healthy and contains fruits, vegetables, lean protein, dairy with the use of monounsaturated fats?

A

Mediterranean diet

210
Q

How does the parasympathetic ANS affect the heart?

A

Slows heart rate, decreases force of atrial contraction. Comes from the vagus nerve and affects the SA and AV nodes

211
Q

True or false: If someone is treated with medication for high cholesterol, then they don’t have to work out.

A

False.

Meds in addition to 2.5 hours of moderate or 75 min of vigorous activity per week is recommended, plus a BMI <25

212
Q

What 4 groups of people should receive lipid management medication?

A
  • previously dx atherosclerotic CVD
  • LDL over 190
  • Diabetes + LDL over 70 +age 40-75
  • Calculated 10 year CV risk of 7.5% or greater + age 40-75
213
Q

Treatment of elevated triglycerides is of uncertain benefit, so why would we treat someone whose levels are >500?

A

To prevent pancreatitis

214
Q

What is first line Tx to lower lipids?

A

Statins

  • inhibit rate limiting enzyme in cholesterol formation
  • reduce MI, stroke & total mortality
215
Q

Common adverse effects of Statins?

A

Muscle aches, mild GI upset, increased risk of DM

Rare: liver failure, rhabdomyolysis (muscle breakdown). more likely with high doses or drug interactions

216
Q

Statin Tx divided into Moderate and High intensity based on risk and prior CVD history:

Moderate Intensity dosing lowers LDL by __%

High Intensity dosing lowers LDL by __%

A

30-50%

50%

217
Q

Other possible Medications to lower lipids:

A
Niacin
Bile-acid binding resins
Fibrates
Ezetimibe
PCSK-9
218
Q

What lipid lowering medication reduces production of VLDL particles with secondary decrease in LDL, causes flushing, and is currently not recommended for use?

A

Niacin

219
Q

What lipid lowering medication binds bile acids in the intestine to decrease LDL levels, reduces absorption of fat soluble vitamins, causes GI effects and is generally not well tolerate?

A

Bile-acid binding resins

220
Q

What lipid lowering medication is used primarily for triglyceride lowering, and shouldn’t be used with statins?

A

Fibrates

221
Q

What lipid lowering medication blocks absorption across intestinal wall to lower LDL, is often used with a statin, and may or may not reduce CVD risk?

A

Ezetimibe

222
Q

What lipid lowering medication is monoclonal antibodies given by subcutaneous injection, lowers LDL, and is extremely expensive?

A

PCSK-9

223
Q

What Rx is commonly used when a patient can’t tolerate a high-dose statin?

A

Combination of Statin + ezetimibe

224
Q

What is shown to be effective at raising HDL?

A
  • Several methods have been tried including medication, alcohol
  • Even if HDL increases, cardiac risk does not seem affected
  • HDL may be more of a marker than a mediator of low risk
  • Regular vigorous exercise may increase HDL and is essentially risk-free
225
Q

True or false: Statins work as well for Primary hyperlipidemia as it does for Secondary hyperlipidemia

A

False

Benefits less clear in primary

226
Q

What are the major controversies regarding hyperlipidemia prevention?

A
  • Testing for risk factors (homocysteine, hs-CRP, cardiac CT for calcium scoring)
  • At what percentage of calculated risk should statins be started
  • What is a goal number for LDL
227
Q

Myxomatous Degeneration

A

Weakening of connective tissue in valves.

228
Q

What is myxomatous degeneration sometimes associated with?

A

Marfan Syndrome. Ehlers Danlos Syndrome

229
Q

Mid-systolic click followed by a systolic murmur

A

Prolapsed Mitral Valve.

230
Q

What is cardiac excitation-contraction coupling?

A

The action potential depolarizes the cell membrane. Intracellular Ca++ binds troponin.
Actin and myosin bind, producing cardiac muscle tension.
Relaxation occurs when intracellular Ca++ returns to resting levels.

231
Q

What makes mitral valve regurgitation heart sound unique?

A

When squatting, click later, murmur shorter. (b/c squatting increases venous return..more bload in the atrium.)

232
Q

What causes a holosystolic murmur?

A

Mitral valve staying open, blood flowing back into atrium during systole.

233
Q

What is Carvallo’s sign?

A

Heart sounds get louder with inspiration, because there is negative pressure and more blood going back into the heart. (tricuspid valve regurgitation.

234
Q

What are signs of right sided heart failure?

A

Distended neck and veins. Swelling of ankles and feet. Hepatosplenomegaly. (Hypertrophy of RV because of tricuspid valve regurgitation).

235
Q

What happens during Phase 2 of the action potential of ventricular myocytes?

A

Plateau phase.

Balanced inward Ca++ and outward K+ currents

236
Q

What happens during Phase 3 of the action potential of ventricular myocytes?

A

Rapid repolarization.

Inactivation of Ca++ current and increased outward K+ current

237
Q

What happens during Phase 4 of the action potential of ventricular myocytes?

A

Slow diastolic depolarization.

Na+ efflux and K+ influx

238
Q

What is cardiac excitation-contraction coupling?

A

The action potential depolarizes the cell membrane. Intracellular Ca++ binds troponin.
Actin and myosin bind, producing cardiac muscle tension.
Relaxation occurs when intracellular Ca++ returns to resting levels.

239
Q

How are pacemaker cells different from myocytes?

A

Fast sodium channels are absent in pacemaker cells; therefore, there is no rapid Phase 0 depolarization.
Pacemaker cells have increased automaticity (can spontaneously fire) because of relatively rapid spontaneous Phase 4 depolarization

240
Q

Generally, the QRS axis is considered indeterminate or no man’s land when it falls between ______ and _____ degrees (or extreme RAD or extreme LAD).

A

-90 and 180 degrees

241
Q

How does the sympathetic ANS affect the heart?

A

It causes peripheral vasoconstriction, and increases heart rate

242
Q

Leading cause of death in the United States

A

Coronary artery disease

243
Q

Definition of Myocardial Infarction

A

irreversible death (necrosis) of heart muscle secondary to prolonged lack of oxygen supply (ischemia). So basically a thrombosis in an artery blocks O2 delivery to the cardiac muscle.

244
Q

How is MI diagnosed?

A

characteristic history, ECG, and serum cardiac markers (e.g. Troponin)

245
Q

What are common MI symptoms in women?

A

Nausea, vomiting, epigastric pain

246
Q

What is the goal time for reperfusion therapy with a STEMI once a patient comes in the door to fibrinolytic therapy (clot buster meds)?

A

30 minutes

247
Q

What is the goal time for reperfusion therapy with a STEMI once a patient comes in the door to primary percutaneous coronary intervention -device therapy (stent)?

A

90 minutes

248
Q

Risk factors for STEMI

A

LOTS of stuff!
family history, male gender, hypercholesterolemia, low LDL, DM, HTN, abdominal obesity, Metabolic syndrome, being African American, smoking, alcohol, Lupus, psychosocial factors

249
Q

Sx of MI

A
  • Substernal chest pain that is intense and persistent
  • Pain radiates up to the neck, shoulder, and jaw, and down the left arm
  • Chest pain not fully relieved by rest or nitroglycerin
  • Nausea
  • Sweating
  • Apprehension
250
Q

What percentage of MIs are clinically silent (no symptoms)?

A

25%

251
Q

Exam findings of MI?

A
  • Pallor
  • Diaphoresis
  • Tachycardia
  • S4
  • Dyskinetic cardiac impulse
  • Jugular venous distention if right ventricular infarction present
  • Rales and S3 are present if patient has CHF
  • Elevated blood pressure, however may have hypotension if in cardiogenic shock
  • Increased respiratory rate
252
Q

What is the diagnostic tests for MI?

A

ECG, labs (Troponin, CK-MB, CBC, CMP, lipids), maybe Echo, maybe coronary angiography

253
Q

What would you commonly see on ECG for a pt with a STEMI?

A

ST- segment elevation, followed by T-wave inversion, then Q-wave development over several hours

254
Q

Prehospital care for STEMI

A
  • Intravenous access
  • Supplemental oxygen (if <90% via pulse oximetry)
  • Aspirin stat!
  • Nitroglycerin for active chest pain
  • Telemetry and prehospital ECG, if available
255
Q

ER treatment for a STEMI

A
  • 12-lead ECG
  • aspirin if not already given
  • continuous ECG monitoring
  • sublingual nitro & IV morphine for pain
  • O2 if needed
  • CXR
  • Echo
  • Oral B-Blockers
  • anticoagulant
256
Q

In what timeframe are patients considered for reperfusion?

A

12-24 hours of symptom onset

257
Q

What is the preferred treatment for chest pain patients after 3 hours of symptom onset?

A

PCI (stenting), within 1-3 hours of Sx onset -> fibrinolysis

258
Q

Following reperfusion, what Tx do all patients benefit from?

A

P2Y12 inhibitor + aspirin

259
Q

There is a high (20-30%) mortality rate from PCI for STEMI in what demographic?

A

The elderly.

Otherwise, potency rate with primary PCI is 90%, with positive long term outcomes. Risks and benefits must be weighed

260
Q

What is the key ingredient in Fibrinolytics, and how does it work?

A

Plasmin.

It degrades fibrin, fibrinogen, prothrombin, and a variety of other factors in the clotting and complement systems. Concomitant use of antithrombotic agents is needed.

Contraindicated in its at high risk for life threatening bleeding. Most serious complication is intracranial hemorrhage.

261
Q

Type of fibrinolytics

A
  • Tissue plasminogen activator (t-PA)
  • Streptokinase
  • Urokinase
  • Reteplase
  • Tenecteplase
262
Q

In hospital management of STEMI

A
  • Admission for continuous cardiac monitoring
  • bed rest for 12-24 hours
  • cardiac diet
  • ACE inhibitors on day one
  • Continuation of B-blockers
  • 81 mg aspirin for life
  • P2Y12 inhibitor for 12 months
  • Statin therapy long term at high doses
263
Q

Follow up care for STEMI

A
  • Lifestyle education
  • cardiac rehab
  • monitor mental health status
  • Meds: B-blocker, statin, aspirin, ACE inhibitor
264
Q

Patients have a higher risk for _______ or _______ in the 6 months following infarction if they have:

  • Advanced age (> 65 years)
  • Prior MI
  • Anterior location of infarction
  • Postinfarction angina
  • NSTEMI
  • Mechanical complications of infarction
  • CHF
  • Diabetes
A

Reinfarction or death

265
Q

Substernal chest pain is a symptom of a STEMI, where does pain often radiate?

A

left shoulder, arm, back or jaw

266
Q

The current generated by the depolarization or repolarization of the atria and ventricles at any given moment is called…

A

Electrical axis or vector

267
Q

What determines the direction of the waveforms in the limb leads?

A

When current travels toward the positive electrode, an upward (+) deflection occurs.
When current travels toward the negative electrode, a downward (-) deflection occurs
When current is perpendicular to the lead axis, no deflection occurs.

268
Q

How is the mean QRS axis determined?

A

The axis may be normal (NA), right axis deviation (RAD), or left axis deviation (LAD).

There are inconsistencies in the definitions of axis deviations, but the normal QRS axis is commonly considered to fall between –30 and +90 (clockwise).

269
Q

When the QRS axis falls between ____ & _____ degrees, LAD is indicated.

A

-30 to -90 degrees

270
Q

When the QRS axis falls between ____ to ____ degrees, RAD is indicated.

A

90 to 180 degrees

271
Q

What can cause hypotension in pregnancy?

A

Pressure on the vena cava. Need to lie on left or right side.

272
Q

What is a common symptom of supine hypotension?

A

Dizziness

273
Q

What are the most effective way of lowering LDL levels?

A

Statins

274
Q

What are some side effects of statins?

A

Mildly raise HDL and decrease TAGs

275
Q

What is the MOA of statins?

A

Inhibit enzyme HMG CoA reductase w/in the cholesterol formation pathway.

276
Q

What should you do before putting a patient on a statin?

A

Check liver enzymes! Can cause hepatic damage.

277
Q

When should statins be discontinued?

A

When liver enzymes are elevated 3 x the normal values.

278
Q

Who is most at risk for primary hypertension?

A

Advanced age (also men, African Americans)

279
Q

Does niacin benefit morbidity or mortality?

A

Recent research says NO

280
Q

Niacin MOA

A

Inhibits hormone sensitive lipase. inc. HDL/ dec LDL

281
Q

For otherwise healthy people, when should they start getting screened for hyperlipidemia?

A

Women >45. Men > 35 (w/other risk factors, earlier)

282
Q

Clinical presentation of HF

A
Early HF:  SBP may be normal or high
Late HF:  SBP decreased 
Tachypnea
Cheyne-Stokes Respiration (periodic respiration or cyclic respiration)
Pulmonary crackles or rales
Pulmonary edema
Pleural effusions
Displaced and sustained PMI 
S3
S4
Murmurs (mitral and tricuspid regurgitation) 
Tachycardia 
JVD 
Hepatomegaly 
Ascites
Jaundice
Peripheral edema
Dependent pitting edema
Indurated and pigmented skin
Decreased pulse pressure 
Cool peripheral extremities
Cyanosis of the lips and nail beds
Weight loss and cachexia.
283
Q

What is the target BP for <60/healthy?

A

140/90 (also patients w/ diabetes or CKD).

284
Q

Describe HR in supine hypo patient.

A

Tachycaria

285
Q

What might you see on a chest Xray of a patient with HF?

A

Kerley B lines and/or enlarged heart

286
Q

To properly diagnose hypertension a patient needs to have…..or more BP readings on different visits.

A

2

287
Q

For really high risk hypercholesterolemia patients what is the LDL goal?

A

<100 mg/dL

288
Q

How might you treat a patient with Stage 1 hypertension?

A

single agent: thiazide diuretic, calcium channel blocker, ACE inhibitor or ARB. (160/100)

289
Q

Patients with reduced nephron numbers are susceptible to what? Why?

A

Kidneys undergoing subtle damage via vasoconstriction while regulating acute changes in BP, leads to renal ischemia. Patients with reduced nephron numbers are more susceptible to this ischemic damage. As more nephrons become dysfunctional hypertension may develop

290
Q

What happens to the blood flowing to the placenta in supine hypotension?

A

Reduced b/c of pressure on vena cava reducing BP.

291
Q

First line of Tx for hypertension (ideally).

A

Lifestyle changes

292
Q

What is the most effect way to decrease TAGs?

A

Fibrates

293
Q

What is the most effective Rx for patients w/ hypertension AND chronic kidney disease?

A

ARB or ACE-I (not together).

294
Q

At what age do women have a higher risk for developing hypercholesterolemia?

A

55 or older

295
Q

What are the ideal HDL values for men and women?

A

> 40 and >50

296
Q

1st line Tx. for African American patients w/ hypertension

A

Thiazide diuretic or calcium channel blocker (often more effective than ACE and ARBs in this population.

297
Q

What causes secondary hypertension?

A

Disease or medication

298
Q

At what BP are we thinking “end-organ damage”!

A

> 180/110

299
Q

Another name for systolic heart failure

A

Heart failure with Reduced Ejection Fraction HFrEF

300
Q

Another name for diastolic heart failure

A

Heart failure with preserved ejection ejection fraction HFpEF

301
Q

What is the Frank Starling Curve?

A

The normal relationship between left ventricular pressure generation and ejection can be expressed as a plot of left ventricular pressure versus left ventricular volume

302
Q

Which is more common, systolic or diastolic dysfunction with HF?

A

Systolic

303
Q

Risk factors for Heart Failure

A
  • Coronary heart disease
  • Cigarette smoking
  • Hypertension
  • Obesity
  • Diabetes
  • Valvular heart disease

Plus, age, sleep disorders, and kidney disease

304
Q

What is the diagnostic test for Heart Failure?

A

Not one specific test, but many ways to assess cardiac function. Diagnosis made largely through history and physical examination.

305
Q

As the left heart fails, fluid backs up in the _____ causing _______ _______

A

Lungs

Pulmonary congestion

306
Q

As the right heart fails, fluid backs up in the body causing ______ _______ congestion

A

peripheral tissue

307
Q

The most common cause of left sided heart failure is…

A

Right sided heart failure

308
Q

Patient presents with fatigue and weakness, shortness of breath, progressive exertional dyspnea, orthopnea,paroxysmal nocturnal dyspnea (PND), non-productive cough, and exercise intolerance…what is the most likely diagnosis?

A

Left heart failure (pulmonary congestion)

309
Q

Patient presents with anorexia, nausea, early satiety, abdominal fullness and RUQ pain.
Confusion, disorientation, and sleep and mood disturbances, nocturia, what is the most likely diagnosis?

A

Right sided heart failure (peripheral congestion)

310
Q

Clinical presentation of HF

A
Early HF:  SBP may be normal or high
Late HF:  SBP decreased 
Tachypnea
Cheyne-Stokes Respiration (periodic respiration or cyclic respiration)
Pulmonary crackles or rales
Pulmonary edema
Pleural effusions
Displaced and sustained PMI 
S3
S4
Murmurs (mitral and tricuspid regurgitation) 
Tachycardia 
JVD 
Hepatomegaly 
Ascites
Jaundice
Peripheral edema
Dependent pitting edema
Indurated and pigmented skin
Decreased pulse pressure 
Cool peripheral extremities
Cyanosis of the lips and nail beds
Weight loss and cachexia.
311
Q

What criteria for the diagnosis of heart failure consist of the presence of 2 major or 1 major and 2 minor criteria?

A

Framingham Criteria

312
Q

What labs would you order to evaluate for HF?

A
  • CBC
  • CMP
  • Lipid profile
  • TSH
  • BNP and N-terminal pro-BNP
313
Q

What might you see on a chest Xray of a patient with HF?

A

Kerley B lines and/or enlarged heart

314
Q

What are the Tx options for stable angina (besides nitro)?

A

Angioplasty. Antiplatelets. Rest. CABG.

315
Q

What is another term for angioplasty?

A

PCI (percutaneous coronary intervention)

316
Q

Recommended doses for nitro?

A

3 doses q 5 min.

317
Q

What is most commonly used to treat stable angina?

A

Antiplatelet drugs (aspirin)

318
Q

Time frame for stable angina relief?

A

Usually 15 min

319
Q

What is a more invasive option of treating stable angina?

A

CABG. Coronary artery bypass graft (Internal mammary artery used).

320
Q

What would you see on an ECG in patient w/ stable angina?

A

Depressed ST segment..indicative of myocardial ischemia…ECG returns to baseline when pain is relieved.

321
Q

Precursor to MI

A

Unstable angina

322
Q

Chest pain with rest! Usually >15 min

A

Unstable Angina

323
Q

What should a patient with unstable angina be given?

A

Ck-MB and troponins (may have NSTEMI).

324
Q

Which side of the heart leads to pulmonary congestion?

A

Left sided heart failure

325
Q

Which side of the heart leads to peripheral edema?

A

Right side

326
Q

Signs of Right Heart Failure.

A

JVD. Peripheral Edema. Hepatosplenomegaly. Nocturia. Weight gain. Ascites

327
Q

What type of testing would you order to assess for HF?

A

EKG, Echo, Exercise/stress testing, coronary angiography

328
Q

What condition is very hard on the heart and shouldn’t be forgotten when conducting testing for HF

A

Sleep apnea

329
Q

What meds are effective in treatment of HFrEF

A

B-blockers, ACEI, ARBs, as well as cardiac resynchronization
+ diuretics, ARNI, MRA, nitrates, Vasoslective CCB, Hydralazine, Digoxin, statins, calcium channel blockers,

Not shown to decrease morbidity or mortality in HFpEF

330
Q

The two main causes of death in patients with HF are…

A

sudden or arrhythmic death, and progressive pump failure

331
Q

What essentially happens in HF?

A

The heart can’t supply enough blood to meet the bodies demands

332
Q

Systolic heart failure is essentially…

A

The heart can’t pump hard enough

333
Q

Diastolic heart failure is essentially….

A

The heart can’t fill enough

334
Q

JVD (jugular veinous distention) is a sign of what?

A

Right sided heart failure.

335
Q

Treatment for end stage heart failure

A

Heart transplant

336
Q

Mid-systolic click with late systolic murmur. Heard at Apex.

A

Mitral Valve Prolapse

337
Q

S1 ejection click. S1 crescendo-decrescendo murmur. Radiates to neck. Heard in right 2nd intercostal space.

A

Aortic stenosis

338
Q

Holo/Pan Systolic murmur heard THROUGH ALL OF SYSTOLE. Heard in APEX. Radiates to AXILLA

A

Mitral Regurgitation

339
Q

Listen along LEFT STERNAL BORDER.

Early Diastolic Decrescendo Murmur

A

Aortic Regurgitation

340
Q

Heard in UPPER LEFT SIDE OF STERNUM.

Early Diastolic Decrescendo Murmur

A

Pulmonic Regurgitation

341
Q

Describe Mitral Stenosis Heart sound.

A

S2 opening SNAP followed by MID DIASTOLIC RUMBLE

Heard: APEX

342
Q

ACYANOTIC

A

Atrial Septal Defect

344
Q

What are risks of coarctation of the aorta in adults?

A

Berry Aneurysms (increased pressure in blood going to brain).

Aortic dissection (walls of aorta tearing in upper extremity region, due to high pressure).

377
Q

A patient comes in with palpitations, dyspnea, weakness/fatigue, and decreased exercise tolerance. What might you suspect?

A

A fib

378
Q

Sleep apnea is often caused by ___________.

A

A fib