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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
diagnostic gold standard for myocardial injury
Cardiac enzymes
26
Rx of MI
``` 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 2. thrombolytic :if came late , PCI c/i 3. CABG
27
absolute Contraindications to thrombolytic therapy in MI
Trauma:Recent head trauma or traumatic CPR * Previous stroke * Recent invasive procedure or surgery * Dissecting aortic aneurysm * Active bleeding or bleeding diathesis
28
Time limit for PCI in MI
door to balloon time less than 90minutes
29
Time limit for thrombolytic therapy for MI
.Administer as soon as possible upto 24 hours after the onset of chest pain .Outcome is best if given within the first 6hours.
30
Use of heparin in angina
Heparin is used for USA and MI (both NSTEMI and STEMI) .It is NOT used for stable angina.
31
Sinus bradycardia in MI is seen in
Especially right sided / inferior MI
32
Mc cause of death in first few days after MI is
Ventricular arrythmia | Either VT or VFib
33
Nitroglycerin reduces pain in
STABLE ANGINA ESOPHAGEAL SPASM
34
Thrill and heave
THRILL It is a tactile equivalent of murmer and is a palpable vibration Palpated with flat of hand HEAVE Heave has 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
35
Heat sounds in left sided heart failure
S3 S4 Increased intensity of pulmonic component of second heart sound indicates pulmonary HTN
36
High output heart failure
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 ```
37
Kerley b lines
Short horizontal lines near periphery of lung Near costophrenic angle Prependicular to surface of pleura Represent edema of interlobular septa Seen in CHF
38
BNP
Released from ventricles in response to pressure overload Differentiaties bw dyspnoea caused by CHF and COPD
39
Standard Rx for CHF
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
40
Most common cause of death from CHF
Ventricular arrythmia due to ischemia
41
Drugs CI in CHF
Metformin: lactic acidosis Thiazolidenediones: fluid retention NSAIDs
42
Signs of DIGOXIN toxicity
GIT: n/v, anorexia CARDIAC: arrythmia CNS:visual disturbances, disorrientation
43
Medications that lower mortality in CHF
ACE/ARB Bb Aldosterone antagonist Hydralazine plus nitrate Do not dec mortality: loop diuretic, digoxin
44
Maneuovers inc or dec the intensity of murmer of HCM and MVP
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
45
Pericarditis caused by MI
first 24 hr after MI Dressler syn: usually weeks to months after MI, immunological basis
46
Causes of restrictive CMP
``` Amylodoisis Sarcoidosis Hemochromatosis Scleroderma Carcinoid syn Chemotherapy Radiation Idiopathic ```
47
Causes of HCMP
Inherited mostly AD Spontaneous mutation also
48
Causes of dilated CMP
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
49
Type of pain of acute pericarditis
PLEURITIC Ass with breathing,inc on deep insp POSITIONAL Inc on lying supine, coughing, swallowing Dec on sitting up, leaning forward
50
Which type of pain dec on leaning forwards
Pericatditis Pancreatitis
51
Pericardial friction rub
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
Cardinal manifestation of acute pericarditis
Chest pain:pleuritic, positional Pericardial friction rub ECG changes:diffuse ST elevation and PR depression
53
ECG changes in acute pericarditis
Diffuse ST elevation PR depression
54
Squre root sign seen in
Constrictive pericarditis Ventricular pressure tracings Dip amd a plateau (normal early diastolic filling but later diastole restricted by pericardium)
55
Difference in diastolic dysfxn of constrictive pericarditis and cardiac tamponade
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
Diffuse ST elevation and PR depression seen in
Acute pericarditis
57
Prominent x and y descent seen in
Constrictive pericarditis
58
X descent and normal y descent/y ascent seen in
Cardiac tamponade
59
Kussmaul sign
JVD fails to decrease during inspiration
60
Feature of pericardial effusion
auscultation:Muffled heart sound ECG:Electical alternans Xray: water bottle appearance
61
CXR of pericardial effusion
Enlargement of cardiac siloutte which change with position Water bottle appearance Without pulmonary congestion
62
Mechanism of pulsus paradoxus
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
Causes of pulsus paradoxus
CARDIAC Pericarditis Pericardial effusion Cardiac tamponade ``` RESPIRATORY Pul embolism Asthma Copd Tension pneumothorax ```
64
Becks triad
Cardiac tamponade Hypotension Muffled heart sound JVD
65
Murmer of mitral stenosis
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
Murmer of aortic stenosis
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
Parvus et tardus
Dimished and delayed carotis upstokes In aortic stenosis
68
Pulsus bisferiens
Single pulse with 2 peaks in systole Seen in: Severe AR AS with AR HOCM
69
Austin flint murmer
Finding in AR Heard at apex Classically, it is described as being the result of mitral valve leaftlet displacement and turbulent mixing of antegrade mitral flow and retrograde aortic flow. Displacement: The blood jets from the aortic regurgitation strike the anterior leaflet of the mitral valve, which often results in premature closure of the mitral leaflets. This can be mistaken for mitral stenosis.
70
Widened pulse pressure seen in
AR
71
Murmer in AR
Diastolic Decrescendo(left sternal border) Austin flint murmer(apex)
72
Holosystolic murmer heard in
Tricuspid and mitral regurgitation
73
Murmer of TR
Holosystolic murmer At mitral area Intensified with inspiration Reduced with expiration, valsalva
74
Pulsatile liver seen in __ valvular heart ds
MR
75
Murmer of MVP
Midsystolic/ late systolic click Mid-to -late systolic murmer Increase: standing, valsalva Decrease: squatting
76
MCC of infective endocarditis in IV drug use
S. Aureus Right sided heart ds
77
MC org for IE of native valve
S.viridans
78
Mc org for IE of prosthetic valve
Less than 60 days Staph More than 60 days Strepto
79
Jones and dukes criteria
JONES Rheumatic heart ds 2major/ 1 major +2 minor DUKE Infective endocarditis 2 major/ 1major + 3 minor/ 5 minor
80
Jones criteria
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
Modified Dukes criteria
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
Does abs for IE prophylaxis required in routine GI(colonoscopy/EGD) Or GU(cystoscopy)
No
83
Marantic endocarditis
Nonbacterial thrombotic endocarditis Dibilitating illness Sterile deposits of fibrin and platelets Along closure line of valves
84
Libmman sacks endocarditis
Nonbacterial vereucous endocarditis SLE Small warty vegetations on both sides of valve
85
Diastolic plop
In atrial myxoma Due to tumor prolapsing in ventricle during diastole Low pitched murmer Changes with position of person
86
Saw toothed ECG
Atrial flutter
87
Most common arrythmia associated with digoxin toxicity
Paroxysmal atrial tachcardia with 2:1 block
88
Atrial fibrillation
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
Cardioversion and defebrillatiom
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
Atrial flutter
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
WPW synd
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
Ventricular tachycardia
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
TORSADES DE POINTES
Rapid polymorphic ventricular tachycardia Caused by factor that prolong QT interval IV Mg for stabalisation
94
2 types of QRS complex
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
Cannon A waves seen in
Ventricular tachycardia
96
Ventricular fibrillation ECG
No atrial P waves No QRS complex can be indentified
97
Parts of heart tube
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
Mc types of ASD
Ostium secundum Central portion of septum
99
Fixed split S2 seen in
ASD
100
Eisenmenger syndrome
Irreversible pul HTN leads to reversal of shunt and cyanosis
101
Murmer of VSD
Harsh blowing Holosystolic murmer with thrill 4th left ICS The smaller the defect , louder the holosystolic murmer
102
CXR of coarctation of aorta
Notching of ribs Figure 3 appearance (indentationnof aorta at the site of stenosis with dilation before and after stensosis)
103
Continous machinery murmer
PDA Both systoleand diastole
104
Differential cyanosis
Coarctation of aorta
105
In women coarctataion of aorta may be ass with
Turner syn
106
Cause of boot shaped heart in TOF
It describes the appearances of an upturned cardiac apex due to right ventricular hypertrophy and a concave pulmonary arterial segment. 
107
Murmer of TOF
Due to VSD pul stenosis
108
Tet spells
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 often squat during a tet spell. This increases systemic vascular resistance and allows for a temporary reversal of the shunt. 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
Hypertensive emergency
SBP >180 , DBP>120 in addition to end organ damage Hypertensive urgency: no evidence of end organ damage
110
rate of lowering of BP in hypertensive emergency
25% in 1- 2 hrs
111
Pain in aortic dissection
Severe tearing ,ripping,stabbing pain,typically abrupt in onset , either in the anterior or back of the chest (often the interscapular region)
112
Rx of aortic dissection
Stanford Type a:ascending, asc+ desc SURGICAL Type b descending MEDICAL
113
Rupture of AAA
Abdominal pain Hypotension Palpable pulsatile abdominal mass Emergent laprotomy indicated
114
Initial Test of choice for AAA
USG CT SCAN if haemodynamically stable
115
Intsermittent claudication
Crampy lef pain Reproducible by walking same distance Relieved completely by rest
116
Rest pain in chronic arterial insufficiency
Continous Prominent at night Relieved ny hanging foot, standing Felt over siatal metatarsel
117
Gold std for PVD
Arteriography
118
Nornal ABI
0.9-1 3
119
ABI
Ratio of SBP at ankle to the SBP at the arm
120
What does ABI of > 1.3 indicates
Noncompressible vessels and indicates severe ds Higher pressure is required to compress the cough due to artheroscleosis
121
Diff in clinical presentation of chronic arterial insufficiency and acut arterial occlusion
``` 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
Skeletal mUscles can tolerate___ hrs of ischemia
6 hrs
123
Sphypillitic aortitis
Complication Aneurysm of aortic arch with retrograde extension exyends backwards to cause AR and stenosis of aortic branches
124
When does classic findings of Dvt occur?
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
Phlegmasia cerulae dolen
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
Trousdeaus syndrome
Migratory superficial thrombophlebitis Secondry to occult Malignancy:mostly pancreatic

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