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Step Up Medicine > CVS > Flashcards

CVS Flashcards

1
Q

Clinical presentations of CAD

A

Asymptomatic

Stable angina

Unstable angina

MI: NSTEMI/STEMI

Sydden cardiac death

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2
Q

Pain of SA

A

Last less than 10-15 min(not in sec or hrs)

Heaviness,pressure, squeezing( not stabbing,sharp)

Not localised to a point

Substernal i.e. central

Inc by emotion,exhertion

Dec by rest, nitroglycerin

No change with breathing
Position

No tenderness

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3
Q

Normal max heart rate of a person

A

220 - age

Till 85% of above is normal

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4
Q

Most accurate test for CAD

A

Cardiac catheterisation with coronary angiography

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5
Q

Main indications for CABG

A

Left main ds

3 vessel ds

2 vessel ds in diabetics

Left ventricular dysfxn

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6
Q

Types of stress test for SA

A

3 types:stress can be induced by exercise or phamacologoc(adenosine, dipyradimole, dobutamine)

ECG

ECHO

PERFUSIOM STUDY

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7
Q

What has to be see on stress test to call it ishemia in SA

A

ECG:ST depressiom

ECHO: wall motion abnormalities

PERFUSION : dec uptake of nuclear isotope

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8
Q

Best initial test for all forms of chest pain

A

Ecg

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9
Q

When is a stress test considered positive ?

A

St seg depression

Chest pain

Hypotsn

Arrythmia

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10
Q

Dx of SA

A

RESTING ECG
normal

STRESS TEST(Exercise/ pharmacologic)
Ecg
Echo
Perfusion

CARDIAC CATHETERISATION
Most accurate test

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11
Q

Site of action of nitrates

A

Act on smooth muscles of

Arteries: dec afterload

Veins: dec preload

Cornonary arteries: inc myocardial perfusion

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12
Q

Std of care for SA( dec mortality)

A

aspirin

Bblockers

Nitrates

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13
Q

When are CCBs used in SA

A

Secondry rx(because they inc HR)when nitrates and BB are not fully effective

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14
Q

Distinction bw NSTEMI and USA is based on

A

Cardiac enzymes entirely

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15
Q

Acute cornary syndrome includes

A

USA

NSTEMI

STEMI

not stable angina

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16
Q

Medical Rx of SA and USA

A

SA
aspirin,nitates ,BB
CCB (2° if BB and nitrates not eff)

USA
Aspirin, nitrates , BB
Enoxaparin ( to prevent progression, clot development)

Others
Clopidogeral
Glp IIb/IIIa inh

FIBRINOLYSIS HAS NOT BEEN PROVEN TO BE BENEFICIAL IN USA.
IT IS ONLY INDICATED IN STEMI WHEN NO ACCESS TO CARDIAC CATHETERISATION FOR PCI IS POSSIBLE

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17
Q

USA pain features

A

Have Chronic angina ,now has inc in frequency ,duration and intensity

New onset that is severe /worsening

Angina at rest

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18
Q

Dx of prizmetal angina

A

Has ST seg elevation in ECG like STEMI (but there is no infarction)

but on cardiac catheterisation there are normal vessels.
Shows vasospasm on giving ergonovine/actetylcholine

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19
Q

Rx of prinzmetal angina

A

ccb

Nitates

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20
Q

pain of myocardial infarction

A

Similar to angina pectoris in character and distribution but much more severe and lasts longer. Unlike in angina, pain typically does not respond to nitroglycerin.

Other symptoms

a. Dyspnea
b. Diaphoresis
c. Weakness, fatigue
d. Nausea and vomiting
e. Sense of impending doom
f. Syncope

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21
Q

What does ST seg elevation and depression indicates

A

STEMI
transmural injury
Indicates infarction 75%of the time

NSTEMI
Subendocardial injury
Indicates infarction 25% of the time

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22
Q

Which cardiac enzymes has greater specificity and sensitivitu for MI

A

Troponin I and T not CK-MB

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23
Q

Which enzyme is useful to assess recurrent MI

A

Ck-mb

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24
Q

Rise ,peak and fall of cardiac enzymes

A

TROPONIN I/T
Rise 3-5 hrs
Peak 1- 2 days
Fall 10 days

CK-MB
Rise 4-8 hrs
Peak 1 day
Fall 4 days

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25
Q

diagnostic gold standard for myocardial injury

A

Cardiac enzymes

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26
Q

Rx of MI

A 
MEDICAL
1.Nitroglycerin
Bb
Aspirin
(As in SA)
2.oxygen
Morphine
Enoxaparin
(As in USA )
3. Additional ACE-I

REVASCULARISATION
1. PCI: better than thrombolytic therapy

  1. thrombolytic :if came late , PCI c/i
  2. CABG
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27
Q

absolute Contraindications to thrombolytic therapy in MI

A

Trauma:Recent head trauma or traumatic CPR

  • Previous stroke
  • Recent invasive procedure or surgery
  • Dissecting aortic aneurysm
  • Active bleeding or bleeding diathesis
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28
Q

Time limit for PCI in MI

A

door to balloon time less than 90minutes

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29
Q

Time limit for thrombolytic therapy for MI

A

.Administer as soon as possible upto 24 hours after the onset of chest pain .Outcome is best if given within the first 6hours.

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30
Q

Use of heparin in angina

A

Heparin is used for USA and MI (both NSTEMI and STEMI) .It is NOT used for stable angina.

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31
Q

Sinus bradycardia in MI is seen in

A

Especially right sided / inferior MI

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32
Q

Mc cause of death in first few days after MI is

A

Ventricular arrythmia

Either VT or VFib

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33
Q

Nitroglycerin reduces pain in

A

STABLE ANGINA

ESOPHAGEAL SPASM

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34
Q

Thrill and heave

A

THRILL
It is a tactile equivalent of murmer and is a palpable vibration

Palpated with flat of hand

HEAVE
Heavehas to do with the upward push on your hand when you palpate the precordium, suggesting the presence of hypertrophy.

Felt with the heel of hand

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35
Q

Heat sounds in left sided heart failure

A

S3

S4

Increased intensity of pulmonic component of second heart sound indicates pulmonary HTN

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36
Q

High output heart failure

A

Cause: inc in peripheral O2 demand results in high cardiac output

Chronic anemia  
•Pregnancy
 •Hyperthyroidism
 •AVfistulas •Wetberiberi(causedbythiamine[vitaminB1]deficiency)
 •Paget disease of bone
 •MR
 •Aorticinsufficiency
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37
Q

Kerley b lines

A

Short horizontal lines near periphery of lung

Near costophrenic angle

Prependicular to surface of pleura

Represent edema of interlobular septa

Seen in CHF

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38
Q

BNP

A

Released from ventricles in response to pressure overload

Differentiaties bw dyspnoea caused by CHF and COPD

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39
Q

Standard Rx for CHF

A

Combination of ACE-I and loop diuretic is the initial Rx

B blocker (only in mild to moderate/stable )

Spironolactone

Digoxin(if EF<40% despite above drugs)

Hydralazine,nitrates

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40
Q

Most common cause of death from CHF

A

Ventricular arrythmia due to ischemia

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41
Q

Drugs CI in CHF

A

Metformin: lactic acidosis

Thiazolidenediones: fluid retention

NSAIDs

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42
Q

Signs of DIGOXIN toxicity

A

GIT: n/v, anorexia

CARDIAC: arrythmia

CNS:visual disturbances, disorrientation

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43
Q

Medications that lower mortality in CHF

A

ACE/ARB

Bb

Aldosterone antagonist

Hydralazine plus nitrate

Do not dec mortality: loop diuretic, digoxin

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44
Q

Maneuovers inc or dec the intensity of murmer of HCM and MVP

A

INCREASING THE MURMER
Standing
Valsalva
*dec in blood in LV -dec in size of LV- incresing the obstruction caused by thickened walls

DECREASING THE MURMER
Squatting
Hand grip
*increase in PVR 
Lying down
Leg raise
*increase venous return

Rest in all the the murmers opposite occurs

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45
Q

Pericarditis caused by MI

A

first 24 hr after MI

Dressler syn: usually weeks to months after MI, immunological basis

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46
Q

Causes of restrictive CMP

A 
Amylodoisis
Sarcoidosis
Hemochromatosis
Scleroderma
Carcinoid syn
Chemotherapy
Radiation
Idiopathic
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47
Q

Causes of HCMP

A

Inherited mostly
AD

Spontaneous mutation also

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48
Q

Causes of dilated CMP

A

MI

Toxic:alcohol, doxorubicin, adriamycin

Metabolic: beri beri, Se def., uremia

Infection

Thyroid:hyper/hypo

Peripartum cardiomyopathy

Collagen vascular ds: SLE

Catecholamine induced: pheochromocytoma, cocaine

Genetic

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49
Q

Type of pain of acute pericarditis

A

PLEURITIC
Ass with breathing,inc on deep insp

POSITIONAL
Inc on lying supine, coughing, swallowing
Dec on sitting up, leaning forward

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50
Q

Which type of pain dec on leaning forwards

A

Pericatditis

Pancreatitis

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51
Q

Pericardial friction rub

A

Heard in acute pericarditis

Not always present

Very specific

Friction bw visceral and parietal peritoneum

Scratching ,high pitched

Heard best at expiration with sitting up

52
Q

Cardinal manifestation of acute pericarditis

A

Chest pain:pleuritic, positional

Pericardial friction rub

ECG changes:diffuse ST elevation and PR depression

53
Q

ECG changes in acute pericarditis

A

Diffuse ST elevation

PR depression

54
Q

Squre root sign seen in

A

Constrictive pericarditis

Ventricular pressure tracings

Dip amd a plateau (normal early diastolic filling but later diastole restricted by pericardium)

55
Q

Difference in diastolic dysfxn of constrictive pericarditis and cardiac tamponade

A

CONSTRICTIVE PERICARDITIS
Venticular filling is unimpeded during early diastole beacause intrathoracic vol has not yet reached the limit of stiff pericardium

Late diastolic dysfxn when the limit defined by stiff pericardium is reached

CARDIAC TAMPONADE
Ventricular filling is impeded throughout diastole

56
Q

Diffuse ST elevation and PR depression seen in

A

Acute pericarditis

57
Q

Prominent x and y descent seen in

A

Constrictive pericarditis

58
Q

X descent and normal y descent/y ascent seen in

A

Cardiac tamponade

59
Q

Kussmaul sign

A

JVD fails to decrease during inspiration

60
Q

Feature of pericardial effusion

A

auscultation:Muffled heart sound

ECG:Electical alternans

Xray: water bottle appearance

61
Q

CXR of pericardial effusion

A

Enlargement of cardiac siloutte which change with position

Water bottle appearance

Without pulmonary congestion

62
Q

Mechanism of pulsus paradoxus

A

Fall in BP> 10 mmhg during inspiration

  1. inc in venous return leads to rt ventricle enlargement such that septum pushes into left ventricle decreasing the blood vol in it
  2. during insp- lung expands-pulmonary vasculature expands - pooling of blood in lungs
63
Q

Causes of pulsus paradoxus

A

CARDIAC
Pericarditis
Pericardial effusion
Cardiac tamponade

RESPIRATORY
Pul embolism
Asthma
Copd
Tension pneumothorax
64
Q

Becks triad

A

Cardiac tamponade

Hypotension
Muffled heart sound
JVD

65
Q

Murmer of mitral stenosis

A

1.S2 followed by Openeing snap
(Closer the opening snap to S2 worse is the stenosis)

2.Low pitched diastolic rumble with presystolic accentuation (due to atrial contraction)
Longer the murmer , worse the stensis

3.Loud S1

Heard at rt 5 ICS midclavicular line

66
Q

Murmer of aortic stenosis

A

Crescendo- decrescendo systolic murmer

Radiates to carotid

Soft S2

S2 may be single since the A2 may merge with P2

Heard at right 2 ICS

67
Q

Parvus et tardus

A

Dimished and delayed carotis upstokes

In aortic stenosis

68
Q

Pulsus bisferiens

A

Single pulse with 2 peaks in systole

Seen in:
Severe AR
AS with AR
HOCM

69
Q

Austin flint murmer

A

Finding in AR

Heard at apex

Classically, it is described as being the result ofmitral valveleaftlet displacementand turbulent mixing ofantegrademitralflow and retrogradeaorticflow.

Displacement:Thebloodjets from the aortic regurgitation strike the anterior leaflet of themitral valve, which often results in premature closure of the mitral leaflets. This can be mistaken for mitral stenosis.

70
Q

Widened pulse pressure seen in

A

AR

71
Q

Murmer in AR

A

Diastolic

Decrescendo(left sternal border)

Austin flint murmer(apex)

72
Q

Holosystolic murmer heard in

A

Tricuspid and mitral regurgitation

73
Q

Murmer of TR

A

Holosystolic murmer

At mitral area

Intensified with inspiration
Reduced with expiration, valsalva

74
Q

Pulsatile liver seen in __ valvular heart ds

A

MR

75
Q

Murmer of MVP

A

Midsystolic/ late systolic click

Mid-to -late systolic murmer

Increase: standing, valsalva

Decrease: squatting

76
Q

MCC of infective endocarditis in IV drug use

A

S. Aureus

Right sided heart ds

77
Q

MC org for IE of native valve

A

S.viridans

78
Q

Mc org for IE of prosthetic valve

A

Less than 60 days
Staph

More than 60 days
Strepto

79
Q

Jones and dukes criteria

A

JONES
Rheumatic heart ds
2major/ 1 major +2 minor

DUKE
Infective endocarditis
2 major/ 1major + 3 minor/ 5 minor

80
Q

Jones criteria

A

MAJOR

Carditis
Polyarthritis
Chorea
Erythema marginatum
Subcutaneous Nodules

MINOR

Fever
Elevated erythrocyte sedimentation rate Polyarthralgias
Prior history of rheumatic fever
Prolonged PR interval
Evidence of preceding streptococcal infection

81
Q

Modified Dukes criteria

A

MAJOR
Sustained bacteremia by org known to cause IE

endocardial involvement:documented by
either
echocardiogram (vegetation, abscess,valve perforation ,prosthetic dehiscence) or clearly established new valvular regurgitation

MINOR

  • Predisposing condition (abnormal valve or abnormal risk of bacteremia)
  • Fever
  • vascular phenomena :septic arterialor pulmonary emboli, mycotic aneurysms ,intracranial hemorrhage ,Janeway lesions
  • immunephenomena :Glomerulonephritis,Oslernodes, Rothspots,crheumatoidfactor
  • Positive blood cultures not meeting major criteria
82
Q

Does abs for IE prophylaxis required in routine GI(colonoscopy/EGD)

Or GU(cystoscopy)

A

No

83
Q

Marantic endocarditis

A

Nonbacterial thrombotic endocarditis

Dibilitating illness

Sterile deposits of fibrin and platelets

Along closure line of valves

84
Q

Libmman sacks endocarditis

A

Nonbacterial vereucous endocarditis

SLE

Small warty vegetations on both sides of valve

85
Q

Diastolic plop

A

In atrial myxoma

Due to tumor prolapsing in ventricle during diastole

Low pitched murmer

Changes with position of person

86
Q

Saw toothed ECG

A

Atrial flutter

87
Q

Most common arrythmia associated with digoxin toxicity

A

Paroxysmal atrial tachcardia with 2:1 block

88
Q

Atrial fibrillation

A

Atria: quiver ,chaotic pattern, no P waves seen

Ventricles: most of the impulses are blocked by AV node producing a rate of 75- 175. Rapid ,irregular rate

Irregular irregular pulse

89
Q

Cardioversion and defebrillatiom

A

CARDIOVERSION
delivery of shock that is synchrony with QRS complex.
Purpose is to terminate dysrythmia.
Do not hit T wave

DEFEBRILLATION
Shock is not in synchrony with QRS complex.
Convert dysrhthmia to normal sinus rhythm
FOR VFib and VT without a pulse

90
Q

Atrial flutter

A

Atria: regular rapid atrial contractions from one focus

Ventricles: due to refractoriness of AV node ,few impulses pass

SAW TOOTHED BASELINE with QRS complexcappearing after every 2 or 3 rd tooth

91
Q

WPW synd

A

Accessory conduction pathway

This pathway leads to premature ventricular excitation because it lacks delay seen in av node , causing DELTA wave in QRS complex

Can cause paroxysmal tachycardia

92
Q

Ventricular tachycardia

A

Focus in ventricles

Rate of 100-250 bpm

ECG:AV DISSOCIATION
Sinu
s P waves continue their cycle, unaggected by tachycardia

CANNON A WAVES:atrial contraction during ventricular contraction

S1 :varies in intensity

Unlike , PSVT , VT does not respond to vagal manuevers or adenosine

93
Q

TORSADES DE POINTES

A

Rapid polymorphic ventricular tachycardia

Caused by factor that prolong QT interval

IV Mg for stabalisation

94
Q

2 types of QRS complex

A

NARROW QRS COMPLEX
Arrythmia originate at or above the AV node

WIDE QRS COMPLEX
Originate outside the normal conduction system OR SV arrythmia with coexistant abnormality in his- purkunje

95
Q

Cannon A waves seen in

A

Ventricular tachycardia

96
Q

Ventricular fibrillation ECG

A

No atrial P waves

No QRS complex can be indentified

97
Q

Parts of heart tube

A

Above down

TRUNCUS ARTERIOSUS
Aorta
Pulmonary trunk

BULBUS CORDIS
Smooth part of left and right ventricle

PRIMITIVE VENTRICLE
Rough part of right and left ventricle

PRIMITIVE ATRIUM
Rough part of right amd left atria

SINUS VENOSUS
Smooth part of right atrium(left: from absorption of pul veins)
Cornonary sinus

98
Q

Mc types of ASD

A

Ostium secundum

Central portion of septum

99
Q

Fixed split S2 seen in

A

ASD

100
Q

Eisenmenger syndrome

A

Irreversible pul HTN leads to reversal of shunt and cyanosis

101
Q

Murmer of VSD

A

Harsh blowing Holosystolic murmer with thrill

4th left ICS

The smaller the defect , louder the holosystolic murmer

102
Q

CXR of coarctation of aorta

A

Notching of ribs

Figure 3 appearance (indentationnof aorta at the site of stenosis with dilation before and after stensosis)

103
Q

Continous machinery murmer

A

PDA

Both systoleand diastole

104
Q

Differential cyanosis

A

Coarctation of aorta

105
Q

In women coarctataion of aorta may be ass with

A

Turner syn

106
Q

Cause of boot shaped heart in TOF

A

It describes the appearances of an upturned cardiac apex due to right ventricular hypertrophy and a concave pulmonary arterial segment.

107
Q

Murmer of TOF

A

Due to VSD

pul stenosis

108
Q

Tet spells

A

Children with tetralogy of Fallot may develop “tet spells”. These are acute hypoxia spells, characterized by shortness of breath, cyanosis, agitation, and loss of consciousness. This may be initiated by any event leading to decreased oxygen saturation (feeding, crying)or that causes decreased systemic vascular resistance, which in turn leads to increased shunting through the ventricular septal defect.

Older children will oftensquatduring a tet spell. This increasessystemic vascular resistanceand allows for a temporary reversal of theshunt. It increases pressure on the left side of the heart, decreasing the right to left shunt thus decreasing the amount of deoxygenated blood entering the systemic circulation

109
Q

Hypertensive emergency

A

SBP >180 , DBP>120 in addition to end organ damage

Hypertensive urgency: no evidence of end organ damage

110
Q

rate of lowering of BP in hypertensive emergency

A

25% in 1- 2 hrs

111
Q

Pain in aortic dissection

A

Severe tearing ,ripping,stabbing pain,typically abrupt in onset , either in the anterior or back of the chest (often the interscapular region)

112
Q

Rx of aortic dissection

A

Stanford

Type a:ascending, asc+ desc
SURGICAL

Type b
descending
MEDICAL

113
Q

Rupture of AAA

A

Abdominal pain

Hypotension

Palpable pulsatile abdominal mass

Emergent laprotomy indicated

114
Q

Initial Test of choice for AAA

A

USG

CT SCAN if haemodynamically stable

115
Q

Intsermittent claudication

A

Crampy lef pain
Reproducible by walking same distance
Relieved completely by rest

116
Q

Rest pain in chronic arterial insufficiency

A

Continous

Prominent at night

Relieved ny hanging foot, standing

Felt over siatal metatarsel

117
Q

Gold std for PVD

A

Arteriography

118
Q

Nornal ABI

A

0.9-1 3

119
Q

ABI

A

Ratio of SBP at ankle to the SBP at the arm

120
Q

What does ABI of > 1.3 indicates

A

Noncompressible vessels and indicates severe ds

Higher pressure is required to compress the cough due to artheroscleosis

121
Q

Diff in clinical presentation of chronic arterial insufficiency and acut arterial occlusion

A 
CHRONIC ARTERIAL INSUFFICIENY/PVD
Intermittent claudication
Rest pain
Dec pulses
Iachemic ulcers
Skn changes
ACUTE ARTERIAL OCCLUSION
Six Ps
Pallor
Pain
Pulselessness
Paresthesia
Paralysis
Polar(cold)
122
Q

Skeletal mUscles can tolerate___ hrs of ischemia

A

6 hrs

123
Q

Sphypillitic aortitis

A

Complication

Aneurysm of aortic arch with retrograde extension exyends backwards to cause AR and stenosis of aortic branches

124
Q

When does classic findings of Dvt occur?

A

If superficial venous system is patent , classic findings(erythema, pain, cords) will not occur because blood drains from these patent veins.

That is only half of all the patients with DVT have classic findings.

125
Q

Phlegmasia cerulae dolen

A

Painful, blue ,swollen leg

Occurs in exreme cases oc DVT

Svere leg edema compromises arterial supply to the limb resulting in impaired sensory and motor fxns

126
Q

Trousdeaus syndrome

A

Migratory superficial thrombophlebitis

Secondry to occult Malignancy:mostly pancreatic

Step Up Medicine (3 decks)

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