CVS Flashcards
Clinical presentations of CAD
Asymptomatic
Stable angina
Unstable angina
MI: NSTEMI/STEMI
Sydden cardiac death
Pain of SA
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
Normal max heart rate of a person
220 - age
Till 85% of above is normal
Most accurate test for CAD
Cardiac catheterisation with coronary angiography
Main indications for CABG
Left main ds
3 vessel ds
2 vessel ds in diabetics
Left ventricular dysfxn
Types of stress test for SA
3 types:stress can be induced by exercise or phamacologoc(adenosine, dipyradimole, dobutamine)
ECG
ECHO
PERFUSIOM STUDY
What has to be see on stress test to call it ishemia in SA
ECG:ST depressiom
ECHO: wall motion abnormalities
PERFUSION : dec uptake of nuclear isotope
Best initial test for all forms of chest pain
Ecg
When is a stress test considered positive ?
St seg depression
Chest pain
Hypotsn
Arrythmia
Dx of SA
RESTING ECG
normal
STRESS TEST(Exercise/ pharmacologic)
Ecg
Echo
Perfusion
CARDIAC CATHETERISATION
Most accurate test
Site of action of nitrates
Act on smooth muscles of
Arteries: dec afterload
Veins: dec preload
Cornonary arteries: inc myocardial perfusion
Std of care for SA( dec mortality)
aspirin
Bblockers
Nitrates
When are CCBs used in SA
Secondry rx(because they inc HR)when nitrates and BB are not fully effective
Distinction bw NSTEMI and USA is based on
Cardiac enzymes entirely
Acute cornary syndrome includes
USA
NSTEMI
STEMI
not stable angina
Medical Rx of SA and USA
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
USA pain features
Have Chronic angina ,now has inc in frequency ,duration and intensity
New onset that is severe /worsening
Angina at rest
Dx of prizmetal angina
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
Rx of prinzmetal angina
ccb
Nitates
pain of myocardial infarction
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
What does ST seg elevation and depression indicates
STEMI
transmural injury
Indicates infarction 75%of the time
NSTEMI
Subendocardial injury
Indicates infarction 25% of the time
Which cardiac enzymes has greater specificity and sensitivitu for MI
Troponin I and T not CK-MB
Which enzyme is useful to assess recurrent MI
Ck-mb
Rise ,peak and fall of cardiac enzymes
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
diagnostic gold standard for myocardial injury
Cardiac enzymes
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
- thrombolytic :if came late , PCI c/i
- CABG
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
Time limit for PCI in MI
door to balloon time less than 90minutes
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.
Use of heparin in angina
Heparin is used for USA and MI (both NSTEMI and STEMI) .It is NOT used for stable angina.
Sinus bradycardia in MI is seen in
Especially right sided / inferior MI
Mc cause of death in first few days after MI is
Ventricular arrythmia
Either VT or VFib
Nitroglycerin reduces pain in
STABLE ANGINA
ESOPHAGEAL SPASM
Thrill and heave
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
Heat sounds in left sided heart failure
S3
S4
Increased intensity of pulmonic component of second heart sound indicates pulmonary HTN
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
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
BNP
Released from ventricles in response to pressure overload
Differentiaties bw dyspnoea caused by CHF and COPD
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
Most common cause of death from CHF
Ventricular arrythmia due to ischemia
Drugs CI in CHF
Metformin: lactic acidosis
Thiazolidenediones: fluid retention
NSAIDs
Signs of DIGOXIN toxicity
GIT: n/v, anorexia
CARDIAC: arrythmia
CNS:visual disturbances, disorrientation
Medications that lower mortality in CHF
ACE/ARB
Bb
Aldosterone antagonist
Hydralazine plus nitrate
Do not dec mortality: loop diuretic, digoxin
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
Pericarditis caused by MI
first 24 hr after MI
Dressler syn: usually weeks to months after MI, immunological basis
Causes of restrictive CMP
Amylodoisis Sarcoidosis Hemochromatosis Scleroderma Carcinoid syn Chemotherapy Radiation Idiopathic
Causes of HCMP
Inherited mostly
AD
Spontaneous mutation also
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
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
Which type of pain dec on leaning forwards
Pericatditis
Pancreatitis
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
Cardinal manifestation of acute pericarditis
Chest pain:pleuritic, positional
Pericardial friction rub
ECG changes:diffuse ST elevation and PR depression
ECG changes in acute pericarditis
Diffuse ST elevation
PR depression
Squre root sign seen in
Constrictive pericarditis
Ventricular pressure tracings
Dip amd a plateau (normal early diastolic filling but later diastole restricted by pericardium)
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
Diffuse ST elevation and PR depression seen in
Acute pericarditis
Prominent x and y descent seen in
Constrictive pericarditis
X descent and normal y descent/y ascent seen in
Cardiac tamponade
Kussmaul sign
JVD fails to decrease during inspiration
Feature of pericardial effusion
auscultation:Muffled heart sound
ECG:Electical alternans
Xray: water bottle appearance
CXR of pericardial effusion
Enlargement of cardiac siloutte which change with position
Water bottle appearance
Without pulmonary congestion
Mechanism of pulsus paradoxus
Fall in BP> 10 mmhg during inspiration
- inc in venous return leads to rt ventricle enlargement such that septum pushes into left ventricle decreasing the blood vol in it
- during insp- lung expands-pulmonary vasculature expands - pooling of blood in lungs
Causes of pulsus paradoxus
CARDIAC
Pericarditis
Pericardial effusion
Cardiac tamponade
RESPIRATORY Pul embolism Asthma Copd Tension pneumothorax
Becks triad
Cardiac tamponade
Hypotension
Muffled heart sound
JVD
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
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
Parvus et tardus
Dimished and delayed carotis upstokes
In aortic stenosis
Pulsus bisferiens
Single pulse with 2 peaks in systole
Seen in:
Severe AR
AS with AR
HOCM
Austin flint murmer
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.
Widened pulse pressure seen in
AR
Murmer in AR
Diastolic
Decrescendo(left sternal border)
Austin flint murmer(apex)
Holosystolic murmer heard in
Tricuspid and mitral regurgitation
Murmer of TR
Holosystolic murmer
At mitral area
Intensified with inspiration
Reduced with expiration, valsalva
Pulsatile liver seen in __ valvular heart ds
MR
Murmer of MVP
Midsystolic/ late systolic click
Mid-to -late systolic murmer
Increase: standing, valsalva
Decrease: squatting
MCC of infective endocarditis in IV drug use
S. Aureus
Right sided heart ds
MC org for IE of native valve
S.viridans
Mc org for IE of prosthetic valve
Less than 60 days
Staph
More than 60 days
Strepto
Jones and dukes criteria
JONES
Rheumatic heart ds
2major/ 1 major +2 minor
DUKE
Infective endocarditis
2 major/ 1major + 3 minor/ 5 minor
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
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
Does abs for IE prophylaxis required in routine GI(colonoscopy/EGD)
Or GU(cystoscopy)
No
Marantic endocarditis
Nonbacterial thrombotic endocarditis
Dibilitating illness
Sterile deposits of fibrin and platelets
Along closure line of valves
Libmman sacks endocarditis
Nonbacterial vereucous endocarditis
SLE
Small warty vegetations on both sides of valve
Diastolic plop
In atrial myxoma
Due to tumor prolapsing in ventricle during diastole
Low pitched murmer
Changes with position of person
Saw toothed ECG
Atrial flutter
Most common arrythmia associated with digoxin toxicity
Paroxysmal atrial tachcardia with 2:1 block
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
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
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
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
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
TORSADES DE POINTES
Rapid polymorphic ventricular tachycardia
Caused by factor that prolong QT interval
IV Mg for stabalisation
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
Cannon A waves seen in
Ventricular tachycardia
Ventricular fibrillation ECG
No atrial P waves
No QRS complex can be indentified
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
Mc types of ASD
Ostium secundum
Central portion of septum
Fixed split S2 seen in
ASD
Eisenmenger syndrome
Irreversible pul HTN leads to reversal of shunt and cyanosis
Murmer of VSD
Harsh blowing Holosystolic murmer with thrill
4th left ICS
The smaller the defect , louder the holosystolic murmer
CXR of coarctation of aorta
Notching of ribs
Figure 3 appearance (indentationnof aorta at the site of stenosis with dilation before and after stensosis)
Continous machinery murmer
PDA
Both systoleand diastole
Differential cyanosis
Coarctation of aorta
In women coarctataion of aorta may be ass with
Turner syn
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.
Murmer of TOF
Due to VSD
pul stenosis
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 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
Hypertensive emergency
SBP >180 , DBP>120 in addition to end organ damage
Hypertensive urgency: no evidence of end organ damage
rate of lowering of BP in hypertensive emergency
25% in 1- 2 hrs
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)
Rx of aortic dissection
Stanford
Type a:ascending, asc+ desc
SURGICAL
Type b
descending
MEDICAL
Rupture of AAA
Abdominal pain
Hypotension
Palpable pulsatile abdominal mass
Emergent laprotomy indicated
Initial Test of choice for AAA
USG
CT SCAN if haemodynamically stable
Intsermittent claudication
Crampy lef pain
Reproducible by walking same distance
Relieved completely by rest
Rest pain in chronic arterial insufficiency
Continous
Prominent at night
Relieved ny hanging foot, standing
Felt over siatal metatarsel
Gold std for PVD
Arteriography
Nornal ABI
0.9-1 3
ABI
Ratio of SBP at ankle to the SBP at the arm
What does ABI of > 1.3 indicates
Noncompressible vessels and indicates severe ds
Higher pressure is required to compress the cough due to artheroscleosis
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)
Skeletal mUscles can tolerate___ hrs of ischemia
6 hrs
Sphypillitic aortitis
Complication
Aneurysm of aortic arch with retrograde extension exyends backwards to cause AR and stenosis of aortic branches
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.
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
Trousdeaus syndrome
Migratory superficial thrombophlebitis
Secondry to occult Malignancy:mostly pancreatic
