heart Flashcards
DVT CAUSE
inflammation
hypercoagulation
endothelial injury
genetic factor V leiden
prothrombin mutation
acquiredb- antiphospholioid antibody syn
cancer, hypertension, COPD,chronic kidney
long travel
hormone replacement
surgery
trauma
pregnancy
most common cause of thromnoohilia
antiohospholioid antibody syn
?
Increased pulmonary vascular resistance due to vascular obstruction or platelet secretion of vasoconstricting neurohumoral agents such as serotonin. Release of vasoactive mediators can produce ventilation-perfusion mismatching at sites remote from the embolus, thereby accounting for discordance between a small PE and a large alveolar-arterial O2 gradient.
effecet of pulmonary embolism on heart?
Pulmonary artery obstruction causes a rise in pulmonary
artery pressure and in pulmonary vascular resistance. When RV wall tension rises, RV dilation and dysfunction ensue, with release of the PART 10 Disorders of the Cardiovascular System cardiac biomarker, brain natriuretic peptide. The interventricular septum bulges into and compresses an intrinsically normal left ventricle (LV). Diastolic LV dysfunction reduces LV distensibility and impairs LV filling. Increased RV wall tension also compresses the right coronary artery, limits myocardial oxygen supply, and precipitates right coronary artery ischemia and RV microinfarction, with release of cardiac biomarkers such as troponin. Underfilling of the LV may lead to a fall in LV cardiac output and systemic arterial pressure, with consequent circulatory collapse and death.
clinical manifestations of DVT
calf pain tenderness erythema pitting edema collateral nonvaricose veins if PE dyspnea hemopsis syncopw hypotension cyanosis
chest xray finding of PE
Well-established abnormalities include focal oligemia (Westermark’s sign),
a peripheral wedged-shaped density above the diaphragm (Hampton’s hump), and an
enlarged right descending pulmonary artery (Palla’s sign).
decide for imaging
for dvt and pe same
if low risk - then ddimer if normal no dvt / no pe
high imaging
if moderate or high - imaging
in imaging for DVT
venous ultrasound if diagnostic then stop
if non diagnostic then MR/CT/PHLEBOGRAPHY
pe imaging test
PE IMAGING TEST
CHEST CT IF diagnostic stop
if non diagnostic
lung scan ( VQ MISMATCH)
IF DIAGNOSTIC stop
if not diagnostic
venous ultrasound if + then treat for PE
if - then do ECHO transesoppsgeal /MR/inavsive pulmonary angiography
lower extremity occlusive ds classification
fontaine
e Fontaine classification uses four stages: Fontaine I is the stage when patients are asymptomatic; Fontaine II is when they have mild (IIa) or severe (IIb) claudication; Fontaine III is when they have ischemic rest pain; and Fontaine IV is when patients suffer tissue loss, such as ulceration or gangrene (Tab
rutherford
The Rutherford classification has four grades (0–III) and seven categories (0–6). Asymptomatic patients are classified
into category 0; claudicants are stratified into grade I and divided into three categories based on the severity of the symptoms; patients with rest pain belong to grade II and category 4; and patients with tissue loss are classified into grade III and categories 5 and 6 based on the significance of the tissue loss.2 These clinical classifications help to establish uniform standards in evaluating and reporting the results
TASC CLASSIFATION
debakey classification
type 1 ascending + descending
type2 only ascending
type3a descending thoracic
3b descending thoracic + aortal
STANFORD
A Ascending
B Descending
clinical manifestations of peripferal artery ds
symptoms
intermittent claudication
rest pain
signs decreased or absent pulse muscle atrophy hairloss thicked nails smooth shiny skin decreased skin temp pallor cyanosis ulcer gangrene edema if they keep leg in dependant position ischemic neuropathy leading to numbness
wht is intermittent claudication
t. The most common symptom is intermittent claudication, which is defined as a pain, ache, cramp, numbness, or a sense of fatigue in the muscles; it occurs during exercise and is relieved by rest. The site of claudication is distal to the location of the occlusive lesion. For example, buttock, hip, thigh, and calf discomfort occurs in patients with aortoiliac disease, whereas calf claudication develops in patients with femoral-poplite
why is ankle pressure higher thn arm
due to pulse wave amplification
fibromuscular dysplasia
small veselsa
mostly renal , carotid involved
string of beads on angiography
thromboangitis obliteratans
Thromboangiitis obliterans (Buerger’s disease) is an inflammatory occlusive vascular disorder involving small and medium-size arteries and veins in the distal upper and lower extremites
men
cigratter smoking
TRIAD of claudication of the affected extremity, Raynaud’s phenomenon, and migratory superficial vein thrombophlebitis
burger ds
thromboangitis obliteratans
vesels effected in thromboangitis obliteratans
distal radial , ulnar tibial mostly
causes of acute limb ischemia
emboli most common from heart, also from aorta
thrombus plaque rupture
dissection
trauma punctures and placement of catheters
thoracic outlet compression sym
triad of claudication of the affected extremity, Raynaud’s phenomenon, and migratory superficial vein thrombophlebitis
painful
clinical manifestations of av fistula
pulsatile mass
thrill briut continuously for systolic and diastole
increased temp
chronic av fistula leads to venous insufficiency
large av fistula lead to high output cardiac failure
nicoladoni branham sign
Compression of a large arteriovenous fistula may cause reflex slowing of the heart rate (Nicoladoni-Branham sign).
raynauds phenomenon
Raynaud’s phenomenon is characterized by episodic digital ischemia, manifested clinically by the sequential development of digital blanching, cyanosis, and rubor of the fingers or toes after cold exposure and subsequent rewarming
primary cause all sec excluded due to stress / emotions
idiopathic
secondary causes
Collagen vascular diseases: scleroderma, systemic lupus erythematosus,
rheumatoid arthritis
, dermatomyositis, polymyositis, mixed connective tissue disease, Sjögren’s syndrome
Arterial occlusive diseases:
atherosclerosis of the extremities, thromboangiitis obliterans, acute arterial occlusion, t
thoracic outlet syndrome
Pulmonary hypertension
Neurologic disorders: intervertebral disk disease, syringomyelia, spinal cord tumors, stroke, poliomyelitis, carpal tunnel syndrome, complex regional pain syndrome
Blood dyscrasias: cold agglutinins, cryoglobulinemia, cryofibrinogenemia, myeloproliferative disorders, lymphoplasmacytic lymphoma
Trauma: vibration injury, hammer hand syndrome, electric shock, cold injury,
typing, piano playing
Drugs and toxins: ergot derivatives, methysergide, β-adrenergic receptor blockers, bleomycin, vinblastine, cisplatin, gemcita
where does raynauds phenomenon occur
fingers and toes only
colour change in raynauds phenomenon
sequential?
acrocyanosis
this condition, there is arterial vasoconstriction and secondary dilation of the capillaries and venules with resulting persistent cyanosis of the hands and, less frequently, the feet. Cyanosis may be intensified by exposure to a cold environment. Acrocyanosis may be categorized as primary or secondary to an underlying condition. In primary acrocyanosis, women are affected much more frequently than men, and the age of onset is usually <30 years. Generally, patients are asymptomatic but seek medical attention because of the discoloration. The prognosis is favorable, and pain, ulcers, and gangrene do not occur. Examination reveals normal pulses, peripheral cyanosis, and moist p
difference between raynauds phenomenon
no ulcer / gangrene
persistent not episodic
normal pulses
liveido reticularis
In this condition, localized areas of the extremities develop a mottled or rete (netlike) appearance of reddish to blue discolora
pernio
Pernio is a vasculitic disorder associated with exposure to cold; acute forms have been described. Raised erythematous lesions develop on the lower part of the legs and feet in cold weather (Fig. 302-3D). They are associated with pruritus and a burning sensation, and they may blister and ulc
erythromelalgia
burning pain erythema of extremities
feet ?
by exposure to warm environment
frost bite
In this condition, tissue damage results from severe environmental cold exposure or from direct contact with a very cold object. Tissue injury results from both freezing and vasoconstriction. Frostbite usually affects the distal aspects of the extremities or exposed parts of the face, such as the ears, nose, chin, and cheeks
2 types deep and superficial
varicose veins
dilated bulging torturous primary- superficial system secondary - deep and perforators PRIMARY obesity aging hormonal therapy Obesity
SECONDARY
venous hypertension
dvt
incompetent perforators
clinical manifestations of varicose veins
asymptomatic rupture dull , ache throbbing sensation pressure sensation relived by leg elevation cramping burning pruritis leg swelling skin changes - hyperpigmentation- eczema- lipodermatosclerosis( induration, hemosiderin,inflammation) atrpohie blanche( white patch of scar) phlebectasia corona( fan shaped pattern of intradermal veins)
causes of lymohedema
Primary Sporadic (no identified cause) Genetic disorders Milroy’s disease Meige’s disease Lymphedema-distichiasis syndrome Cholestasis-lymphedema Hypotrichosis-lymphedema-telangiectasi a Turner’s syndrome Klinefelter’s syndrome Trisomy 13, 18, or 21 Noonan’s syndrome Klippel-Trénaunay syndrome Parkes-Weber syndrome Hennekam’s syndrome Yellow nail syndrome Intestinal lymphangiectasia syndrome Lymphangiomyomatosis Neurofibromatosis type 1 Secondary Infection Bacterial lymphangitis (Streptococcus pyogenes, Staphylococcus aureus) Lymphogranuloma venereum (Chlamydia trachomatis) Filariasis (Wucheria bancrofti, Brugia malayi, B. timori) Tuberculosis Neoplastic infiltration of lymph nodes Lymphoma Prostate Others Surgery or irradiation of axillary or inguinal lymph nodes for treatment of cancer Iatrogenic Lymphatic division (during peripheral bypass surgery, varicose vein surgery, or harvesting of saphenous veins) Miscellaneous Contact dermatitis Rheumatoid arthritis Pregnancy Factitious
primary and secondary lymphedema
primary
agenesis , hypoplasia,
secondary
acquired ??
clinical manifestations of lymphedema
painless thickening of skin peud orange woody texture edema stemmer sign
difference bw primary and secondary lymphededema
lymphoscintigraphy
lymangiography
who grp
WHO
GRP 1 PULMONARY ARTERY HYPERTENSION mean
pulmonary artery wedge pressur <15
trans pulmonary gradient elevated
pulmonary vascular resistance elevated
GRP2.PULMONARY HYPERTENSION WITH LEFT HEART DS
mean pulmonary artery wedge pressur increased
trans pulmonary gradient normal
pulmonary vascular resistance normal
GRP3 PULMONARY HYPERTENSION WITH LUNG DISEASE
GRP4 PULMONARY HYPERTENSION WITH CHRONIC THROMBOEMBOLIC EMBOLISM
GRP 5 PULMONARY HYPERTENSION WITH MULTI FACTORIAL CAUSES
characteristics of ischemic pain
•duration
not for seconds nor for days but for mins
•quality
dull sore
•location
diffuse 95% of time cannot be pointed by a finger
substernal 90%
•radiation neck or arm can be nonradiating
not associated with tenderness or does not change with change in posture
• increased by exertion and relieved by rest
response to therapy can be used for diagnosis of
- naloxone and opiates
- fluconazole and esophageal candidiasis
- ?
differnce of more than 20 mmhg in both arms is indiactive of
aortic dissection
differnce of more than 20 mmhg in both arms is indiactive of
aortic dissection
wide split S2 causes
RIGHT BUNDLE BRANCH BLOCK
pulmonary hypertension
pulmonary stenosis
rht ventricular hypertrophy
paradoxical split s2
LBBB
Left ventricular hypertrophy
hypertension
aortic stenosis
fixed split s2 causes
atrial septal defect
cause of s4 gallop
contraction of atrial against a stiff or noncompliant ventricle
pt presenting with history of long term hypertension wht is most likely physical finding
s4 gallop
ck mb start increasing when
3-4 hrs peak by 12hrs
remain elevated for 3- 4 days
biomarker for reinfarction
treatment of choice in STEMI
PCI OR THROMBOLYTICS
how much elevation in ecg of stemi is significant
1 mm or more in 2 leads
pt comes with 7th day post mi with chest pain
which is the initial test
initial test is ekg
next is cardiac biomarker
ckmb if elevated it is reinfarction as it decreases by 3- 4 th day
preferred biomarker for myocardial infarction
troponins greater senstivity and specificity
tropins are elevated in which condition
myocardial infarction
renal ds
polymyositis
dermatomyositis
Patients with a normal CK-MB level but elevated troponin level
signify ?
sustained minor myocardial damage, or microinfarction,
patients with elevations of both CK-MB and troponins are ____
considered to have had acute myocardial infarction.
late biomarker for infarction
troponins
Differential Diagnosis of Conditions Causing Chest Pain
••NON CARDIOVASCULAR
Costochondritis
Pain exacerbated with inspiration; reproduced with chest wall palpitation
Hiatal hernia Reflux of food; relief with antacids
GERD Acid reflux; relief with antacids
Peptic ulcer Epigastric pain worse 3 h after eating Gallbladder disease Right upper quadrant abdominal pain and tenderness
••CARDIOVASCULAR Disorders
Differentiating Features Myocardial infarction Pain more severe, usually >20 min in duration
Aortic stenosis Typical systolic ejection murmur
Myocarditis Pain is usually vague and mild if present Pericarditis Pain is sharper, pain worse with lying down and relieved by sitting up
Dissecting aortic aneurysm Pain is sharp, tearing, often occurs in back
Mitral valve prolapse Transient pain, midsystolic click murmur, and young female with no risk factors
••PULMONARY DISORDERS Differentiating Features
Pulmonary embolus-infarction Tachypnea, dyspnea, cough, pleuritic pain, hemoptysis
Pulmonary hypertension Signs of right ventricle (RV) failure Pneumothorax Sudden onset of pain and dyspnea
test of choice for pulmonary embolism in pregnant women
VQ scanning
a guy comes with pleuritic chest pain which improves on leaning forward there is ST segment depression without q waves is given naproxen but does not improve wht next treatment
give steroids
most specific sign for pericarditis iS
PR SEGMENT DEPRESSION
which of following improves most with excesise triglycerides HDL LDL total cholesterol
HDL
life style modification like wt loss
excersise quit smoking dec HDL MOST
how to diagnose stable angina
history of chest pain increased on excertion relieved on taking rest
ekg - ve
stress test +ve
by excersise or those who cannot excersise dobutamine
exercise treadmill test (exercise stress test) is the most useful test for evaluating the cause of chronic chest pain when there is concern about IHD (stable angina).
Exercise stress testing provides a controlled environment for observing the effects of increases in the myocardial demand for oxygen.
In order to do an appropriate analysis, a target heart rate must be reached
. • Target heart rate is 85% of predicted maximum heart rate: 85% × (220 – patient’s age)
positive stress test means
An exercise stress test is considered positive for myocardial ischemia when large (>2 mm) ST-segment depressions or hypotension (a drop of >10 mm Hg in systolic pressure) occur either alone or in combination.
criteria for positive stress test
An exercise stress test is considered positive for
myocardial ischemia when large (>2 mm) ST-segment depressions or
hypotension (a drop of >10 mm Hg in systolic pressure) occur either alone or in combination
contraindications for stress test
Exercise stress testing is contraindicated when it may place the patient at increased risk of cardiac instability, as in the following settings: • Aortic dissection • Acute myocardial infarction • Unstable angina • Severe CHF • Uncontrolled sustained ventricular arrhythmias • Symptomatic supraventricular arrhythmia • Significant aortic stenosis • Hypertrophic cardiomyopathy • Severe uncontrolled hypertension
stress test for those who cannot excersise or those whose ekg cannot be read ( LBBB , on digoxin, pacemaker , lvh )
▪dipyradomole thallium uptake
shows decreased thallium uptake
▪dobutamine echo
decreased wall motion
difficulty reading ekg
lbbb
on digoxin
lvh
ekg changes by digoxin
downsloping st segment
stess + ve wht next
stress test +ve 》angiography
↙️ ↘️
3 vsel ds or left main a 1/2 vessel
and 2 vsel in diabetic ⬇️
⬇️ ⬇️
CABG ANGIOPLASTY ie balloon
dilation and stenting
if both st depression or st elevation present on mi which to consider?
st elevation as it is worst thing
st depression means ischemia
st elevation means infarction
ventricular tachycardia treatment
wide complex tachycardia qrs greater than 120 msec
if pt is stable➡️amiodarine / lidocaine
if pt is not stable ➡️shock therapy
worst risk factor for cad
diabetes mellitus
most common risk factor for cornonary artery ds
hypertension
presentations of coronary artery disease
CAD can have the following clinical presentations: •Asymptomatic •Stable angina pectoris • unstable angina pectoris •MI—eitherNSTEMIor STEMI •Suddencardiacdeath
types of stress test
Types of Stress Tests test
•Exercise ECG Exercise – STsegment depression
•dobutamine echocardiogram— Wall motion abnormalities
• Exercise or dipyridamole perfusion study (thallium/ technetium) — Decreased uptake of the nuclear isotope during exercise
when a stress test is comsidered +ve
A stress test is generally considered positive if the patient develops any of the following duringexercise: • ST segment depression, •chest pain, • hypotension, or • significant arrhythmias
most accurate method of determining specific cardiac diagnoais
coronary angiography
indiactions for cardiac catherisation
Aftera positive stress test.
•Acute MI with intent of performing angiogram and PCI. •patient with angina in any of the following situations:When noninvasive tests are non diagnostic,
•angina that occurs despite medical therapy, angina that occurs soon afterMI ,and any angina that is a diagnostic dilemma.
•If patient is severely symptomatic and urgent diagnosis and management are necessary.
•For evaluation of valvular disease ,and to determine the need for surgical intervention.
management of stable angina
▪Mild disease (normal EF, mild angina, single-vessel disease) •Nitrates (for symptoms and as prophylaxis)and a β-blocker are appropriate
•Consider calcium channel blockers if symptoms continue despite nitrates and β-blockers
▪. Moderate disease (normal EF, moderate angina, two-vessel disease) •If the above regimen does not contro l symptoms,consider coronary angiography to assess suitability for revascularization (either PCI or CABG)
▪. Severe disease (decreased EF, severe angina, and three-vessel/left main or left anterior descending disease)
Coronary angiography and consider for CABG
treatment of unstable angina
goal is to prevent the expansion of clot
▪medical treatment
aspirin
clopidogeral
bblocker
nitrates
low molecular wht heparin
oxygen
gp2b3a inhibitors
▪ cardiac catherisation
ecg changes in mi and there inference
ST segment elevation – transmural ischemia
ST SEGMENT DEPRESSION— subendocardial injury
duration of time within which thromobolytics can be given
12 hrs
categories of infarcts
•ST segment elevation infarct:
Transmural (involves entire thickness of wall); tends to be larger
•Non-ST segment elevation infarct:
Subendocardial (involves inner one-third to one-half of the wall); tends to be smaller, and presentation is similar to USA—cardiac enzymes differentiate the two
gold standard for myocardial injury
cardiac enzymes
rise , peak and fall of cardiac enzymes
start of increase peak remain elevated l
TROPONINS 3-5 hrs 24-48hrs 5-14days
CKMB 4-8hrs 24hrs 2- 3 days
indication of thrombolytic therapy
Indications
•st segment elevation in two contiguous ECG leads in patients with pain on set within 6hours
•who have been refractory to nitroglycerin.
within wht time thrombolytic can be given
12 hrs of onset of pain upto 24 hrs
best if given within 6hrs
treatment of heart block as a complication of mi
1st and 2nd degree ( type 1) does not require treatment
2nd degree ( type2 ) and third degree
↙️ ↘️
if ant wall mi if inf wall mi
⬇️ ⬇️
•emergent •iv atropine initially
placement of if conduction not restored then
pacemaker pacemaker
• bad prognosis • gud prognosis
dresslar syndrome
postmyocardial infarction syndrome”
a. Immunologically based syndrome consisting of fever, malaise, pericarditis, leukocytosis, and pleuritis, occurring weeks to months after an MI
b. Aspirin is the most effective therapy. Ibuprofen is a second option
