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
most common non cardiac cause of chest pain
gastrointestinal
causes of high output cardiac failure
Causesinclude: • •Chronic anemia •Pregnancy •Hyperthyroidism •AV fistulas •Wet beri beri(caused by thiamine [vitaminB1 ]deficiency) •Paget disease of bone •MR •Aortic insufficiency
most common cause of diasystolic function
hypertension
causes of diasystolic failure
HTN leading to myocardial hypertrophy—most common cause of diastolic dysfunction
•Valvular diseases such as aortic stenosis(AS) ,mitralstenosis ,and aortic regurgitation •Restrictive cardiomyopathy (e.g.,amyloidosis,sarcoidosis,hemochromatosis)
NYHA CLASSIFICATION
NYHAclassI:
Symptoms only occur with vigorous activities ,such as playing a sport.Patients are nearly asymptomatic.
•NYHAclassII
:Symptoms occur with prolonged o r moderate exertion ,such as climbing a flight of stairs or carrying heavy packages. Slight limitation of activities
. •NYHAclassIII:
Symptoms occur with usual activities of daily living ,such as walking across the room or getting dressed.Markedly limiting.
•NYHAclassIV:
Symptoms occur at rest. Incapacitating.
symptoms of chf
dyspnea orthopnea PND nocturnal cough confusion memory impaired diaphoresis
signs of left sided heart failure
displaced pmi
S3 follows S2
heard best at apex with bell
S4
precedes S1
heard best at left sternal border with bell
Crackles
dullness on percussion due to pulmonary edema
signs of rht sided heart failure
peripheral edema pitting nocturia inc jvp hepatomegaly ascitis rht ventricular heave
relationship of digoxin and potassium
inverse relationship
more pottasium less digoxin
less pottasium more digoxin
thus bblocker }
ace inhibitor } 》》》 prevent digoxin toxicity by inc
arb} pottasium
spironolactone}
signs and treatment of digoxin toxicity
Toxic Effects of Digitalis • Nausea and vomiting • Gynecomastia • Blurred vision • Yellow halo around objects • Arrhythmias—commonly paroxysmal atrial tachycardia (PAT) with block, PVCs (premature ventricular contractions), and bradycardia
treatment
Treatment for Intoxication
• Stop drug
• Lidocaine and phenytoin (for arrhythmia)
• Digibind only for acute overdose
drug interaction of digoxin
▪Quinidine
Increase
Mechanism Decreases renal clearance of digoxin
▪ Verapamil, diltiazam
increases digoxin level
Decreases renal clearance of digoxin
▪Cholestyramine, colestipol
decreases digoxin level
Binds digoxin in GI tract; interferes with enterohepatic circulation
▪ Spironolactone
increases
Inhibits tubular secretion of digoxin
▪Thiazides, furosemide
increases
Diuretic-induced hypokalemia and/or bumetanide hypomagnesemia potentiates digitalis action
treatment of diasystolic heart failure
avoid digoxin and ace inhibitors
use
diuretics if fluid overload
bblocker
drugs tht increase survival in chf patients ie decrease mortality
bblocker
lesser the ejection fraction more the mortality benefit
vasodilators
isosorbide
hydralazine
spironolactone
intracardiac defibrillatortreatment for systolic heart failure
diuretics
symptomatic relief
does not lower mortality
spironolactone
for advanced stage 3/4 heart failure
eplerenone an alternative does not cause gynaecomastia
ace inhibitor
venous and arterial dilator ⬇️preload and afterload
diuretics +ace should be initial treatment for most chf pt
prolong survival
angiotensin receptor blocker
bblocker
⬇️ mortality in post mi heart failure
should be give to stable pts with mild to moderate chf class1,2,3
all blocker are not equal benefit seen by
metoprolol,bisoprolol,carvedilol
digitalis
for pts with ejection fraction <40%, severe CHF ,severe atrial fibrillation
hydralazine and isosorbide dinitrate
priciples of treatment of heart failure
mild CHF (NyHa Classes i to ii)
•Mild restriction of sodium intake (no-added-salt diet of 4g sodium) and physical activity.
•Start a loop diuretic if volume overload or pulmonary congestion is present
. •Use an ACE inhibitor as a first-line agent.
mild to moderate CHF (NyHa Classes ii to iii)
•Start a diuretic (loop diuretic) and an ACE inhibitor. •
Add a b blocker if moderate disease (classIIorIII) is present and the response to standard treatment is suboptimal.
moderate to severe CHF (NyHa Classes iii to iv)
•Add digoxin(to loop diuretic and ACE inhibitor).
•Note that digoxin may be added at any time for the relief of symptoms in patients with systolic dysfunction. (It doesnot improve mortality.)
•In patient with class IV symptoms who are still symptomatic despite the above, adding spironolactone can be helpful.
which medications are contraindicated in chf
Metformin—may cause potentially lethal lactic acidosis •Thiazolidinediones—causes fluid retention
•NSAIDs may increase risk of CHF exacerbation
symptoms of mitral stenosis
Dyspnea
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Fatigue
• Wasting
• Hemoptysis (due to rupture of pulmonary vessels)
• Systemic embolism (due to stagnation of blood in an enlarged left atrium)
• Hoarseness (due to impingement of an enlarged left atrium on the recurrent laryngeal nerve)
• Right-sided heart failure–Hepatomegaly–Ascites–Peripheral edema
signs of mitral stenosis
Physical Signs
• Atrial fibrillation (irregular cardiac rhythm)
• Loud S1
• Opening snap following S2
• Diastolic rumble (low-pitched apical murmur)
• Sternal lift (due to right ventricular enlargement)
signs if enlarged left atrium
straightening of left heart border
double bouble behind the ventricle
pushed up left main br bronchus
surgical treatment for mitral and aortic
ballooning of mitral valve
replacement od aortic valve
best initial test for valvular heart ds
echocardiography
most accurate test for valvular heart ds
cardiac catherisation
criteria for operation in mitral regurgitation
EJECTION FRACTION
presentations of mitral valve prolapse
pain
palpitations
panic attacks
syncope
ausculatatory finding of mitral valve prolapse
mid to late systolic click
effect of valsalva and squatting
valsalva and standing ⬇️ blood to heart
leg raising and squaatimg ⬆️blood to heart
all left sided murmer ⬇️with dec in blood and ⬆️with inc in blood except mitral valve prolapse and hypertrophic obstructive cardiomyopathy
most common cause of aortic steosis
age related calcificatiom
symptoms of mitral stenosis
symptoms
Exertional dyspnea,
orthopnea,
PND
b. Palpitations,
chest pain
Hemoptysis—as the elevated LA pressure ruptures anastomoses of small bronchial veins
d. Thromboembolism—often associated with AFib
e. If RVF occurs, ascites and edema may develop
signs of mitral stenosis
Mitral stenosis murmur. •
The opening snap is followed by a low-pitched diastolic rumble and presystolic accentuation.
This murmur increases in length as the disease worsens. •Heard best with bell lof stethoscope in left lateral decubitus position.
b. S2 is followed by an opening snap. The distance between S2 and the opening snap can give an indication as to the severity of the stenosis. The closer the opening snap follows S2, the worse is the stenosis.
c. Murmur is followed by a loud S1. A loud S1 may be the most prominent physical finding
. d. With long-standing disease, will find signs of RVF (e.g., right ventricular heave, JVD, hepatomegaly, ascites) and/or pulmonary HTN (loud P2)
echocardiography finding of mitral valve strnosis
Echocardiogram— most important test in confirming diagnosis a. Left atrial enlargement b. Thick, calcified mitral valve c. Narrow, “fish mouth”-shaped orifice d. Signs of RVF if advanced disease
symptoms of aortic stenosis
Angina(35%)—average survival,3years
•Syncope(15%)—average survival,2years
•Heartfailure(50%)—average survival,1.5years similiar to metastatic ds
signs of aortic stenosis
Signs
a. Murmur
•Harsh crescendo–decrescendo systolic murmur •Heard in second right intercostal space
•Radiates to carotid arteries
b. Soft S2. S2 may also be single since the aortic component may be delayed and merge into P2
c. S4
d. Parvus et tardus—diminished and delayed carotid upstrokes
e. Sustained PM
I f. Precordial thrill
cresendo decresendo murmer heard in
aortic stenosis
pulsus parvus et tardus is present in
aortic stenosis
diminished and delayed carotid upstroke
pulse is weak ( parvus ) and late (tardus)
causes of aortic regurgitation
- Acute
a. Infective endocarditis
b. Trauma
c. Aortic dissection
d. Iatrogenic as during a failed replacement surgery- Chronic
a. Primary valvular:
Rheumatic fever, bicuspid aortic valve, Marfan syndrome, Ehlers–Danlos syndrome, ankylosing spondylitis, SLE
b. Aortic root disease: Syphilitic aortitis, osteogenesis imperfecta, aortic dissection, Behçet syndrome, Reiter syndrome, systemic HTN
- Chronic
examination finding of aortic regurgitation
Physical examination
a. Widened pulse pressure—markedly increased systolic BP, with decreased diastolic BP.
b. Diasystolic decrescendo murmur best heard at left sternal border.
c. Corrigan pulse (water-hammer pulse)—rapidly increasing pulse that collapses suddenly as arterial pressure decreases rapidly in late systole and diastole; can be palpated at wrist or femoral arteries.
d. Austin Flint murmur—low-pitched diastolic rumble due to competing flow anterograde from the LA and retrograde from the aorta. It is similar to the murmur appreciated in mitral stenosis.
e. Displaced PMI (down and to the left) and S3 may also be present.
f. Murmur intensity increases with sustained handgrip. Handgrip increases systemic vascular resistance (SVR), which causes an increased “backflow” through the incompetent aortic valve.
watterhammer pulse seen in
Corrigan pulse (water-hammer pulse)— rapidly increasing pulse that collapses suddenly as arterial pressure decreases rapidly in late systole and diastole; can be palpated at wrist or femoral arteries.
austin flint murmer seen in
Austin Flint murmur—low-pitched diastolic rumble due to competing flow anterograde from the LA and retrograde from the aorta. It is similar to the murmur appreciated in mitral stenosis.
Classically, it is described as being the result ofmitral valveleaftlet displacementandturbulent mixing ofantegrademitralflow and retrogradeaorticflow:[7]
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.
Turbulence of the two columns of blood:Blood fromleft atriumto left ventricle and blood from aorta toleft ventricle.
increases digixin
ebstein anomaly
congential malformation of tricuspid valve in which there is downward displacement of valve into rht ventricle
seen with lithium
most common cause of TR
left ventricular failure
demusset sign
aortic regurgitation
head bobbing rhythmical jerking of head
muller sign
uvula bobs
muller sign
uvula bobs
present in aortic stenosis
duroziez sign
pistol shot sound heard over femoral arteries
present in aortic stenosis
signs and symptoms of tricuspid regurgitation
ususally asymptomatic signs of rht heart failure pulsatile liver prominent v waves and rapid y desecnt blowing holosystolic murmer rht ventricular pulsation along left lower sternal border
mitral valve prolapse cause
MVP is defined as the presence of excessive or redundant mitral leaflet tissue due to myxomatous degeneration of mitral valve leaflets and/or chordae tendineae.
causes of TR
TR is usually secondary to RV dilation
. Any cause of RV dilation can result in enlargement of the tricuspid orifice.
•Left ventricular failure is the most common cause. •Right ventricular infarction. •Inferior wall MI. •Corpulmonale,secondary to pulmonary HTN
. b. Tricuspid endocarditis—seen in IV drug users.
c. May be secondary to rheumatic heart disease; usually accompanied by mitral and aortic valve disease.
d. Epstein anomaly—congenital malformation of tricuspid valve in which there is downward displacement of the valve into the RV.
e. Other causes include carcinoid syndrome, SLE, and myxomatous valve
murmer of TR
holosystolic murmer at left lower sternal border
most common cause of MR IN developed countries
mitral valve prolapse
ausculatatory finding of mitral valve prolapse
mid to late systolic click
mid to late systolic murmer
effect of maneurs on mvp
Standing and the Valsalva maneuver increase murmur and click because these maneuvers reduce LV chamber size, allowing the click and murmur to occur earlier in systole. e.
Squatting decreases murmur and click because it increases LV chamber size, thus delaying the onset of the click and murmur.
effect of valsalva standing leg raising squatting hand grip
valsalva squatting Handgrip(inc
standing leg raising afterload)
MR MS ⬇️ ⬆️
AR,AS ⬇️ ⬆️ ,⬆️AR
all left sided murmer decreased with decreased blood
and increased with increase blood
except
HOCM ⬆️
MVP ⬆️
most common cause of dilated cardiomyopathy
ischemia
most common cause of cardiac transplantation
dilated cardiomyopathy
clinical manifestations of cardiac tamponade
- Pulsus paradoxus, characterized by a decrease in systolic blood pressure >10 mm Hg with normal inspiration, frequently is present. The paradoxical pulse often can be noted by marked weakening or disappearance of a peripheral pulse during inspiration. Paradoxical pulse is not diagnostic of cardial tamponade and can occur in chronic lung disease, acute asthma, severe CHF, and in some cases of hypovolemic shock.
- Neck vein distension with clear lung
- Shock (hypotension)
- Decreased heart sounds
- Beck’s triad is associated with acute tamponade; it includes low blood pressure, distended neck veins, and decreased heart sounds
cause of distended neck veins
cardiac tamponade
pulmonary edema
differenciated by clear lung fields on chest xray of cardiac tamponade
ekg finding of cardiac tamponade
electric alternans small and big compkexes alternatively
echocardiography finding of pericardial effusion
dancing heart
chest xray of pericardial effusion
water bottle sign
ekg finding of pericarditis
EKG may be diagnostic and reveals a diffuse ST-segment elevation with upright T waves at the onset of chest pain. PR segment depression is VERY SPECIFIC
diffrential of ekg of pericarditis and MI
The diffuseness of the ST-segment elevation, absence of reciprocal leads, and absence of the development of Q waves distinguish the characteristic pattern of acute pericarditis from the pattern seen in acute MI.
treatment of pericarditis
NSAIDS
CORTICOSTEROID if not responding to NSAIDS
causes of restrictive cardiomyopathy
amylodossis sarcodosis hemochromatosis cancer fibrosis
drugs to be avoided with HOCM
Digitalis
• Diuretics
• Vasodilators
• Exercise
effects of various maneures on heart
Effect of Various Maneuvers on Systolic Murmurs
Valsalva Handgrip Squatting Amyl Nitrite Leg Raising
phenylpherine
AS ⬇️ ⬇️ ⬆️ ⬆️ ⬆️
HOCM⬆️ ⬇️ ⬇️ ⬆️ ⬇️
VSD ⬇️ ⬆️ ↔️ ⬇️ ⬆️
MR ⬇️ ⬆️ ⬆️ ⬇️ ⬆️
causes of dilated cardiomyopathy
Idiopathic: most common
•CAD
Alcoholic
• Peripartum
• Postmyocarditis due to infectious agents (viral, parasitic, mycobacterial, Rickettsiae)
• Toxins (cobalt, lead, arsenic)
• Doxorubicin hydrochloride, cyclophosphamide, vincristine• Metabolic: chronic hypophosphatemia, hypokalemia, hypocalcemia, uremia
signs of HOCM
Signs
a. Sustained PMI
b. Loud S4
c. Systolic ejection murmur
•Decreases with squatting, lying down,or straight leg raise(due to decreased outflow obstruction)
•Intensity increases with Valsalva and standing(decreases LV size and thus increases the outflow obstruction) •Decreases with sustained handgrip(increased systemic resistance leads to decreased gradient across aortic valve) •Best heard at left lowersternal border(LLSB)
d. Rapidly increasing carotid pulse with two upstrokes (bisferious pulse)
bisferious pulse
HOCM
Rapidly increasing carotid pulse with two upstrokes (bisferious pulse)
treatment of HOCM
Symptomatic patients a.
β-Blockers should be the initial drug used in symptomatic patients; they reduce symptoms by improving diastolic filling (as HR decreases, duration in diastole increases), and also reduce myocardial contractility and thus oxygen consumption
b. Calcium channel blockers verapamil •Can be used if patientis not responding to β-blocker. •Reduce symptoms by similar mechanism as β-blockers.
c. Diuretics can be used if fluid retention occurs.
d. If AFib is present, treat accordingly (see Atrial Fibrillation). e. Surgery
•Myomectomy
symptoms of acute pericarditis
Chest pain (most common finding)
a. Often severe and pleuritic (can differentiate from pain of MI because of association with breathing)
. b. Often localized to the retrosternal and left precordial regions and radiates to the trapezius ridge and neck.
c. Pain is positional: It is aggravated by lying supine, coughing, swallowing, and deep inspiration. Pain is relieved by sitting up and leaning forward.
d. Pain is not always present, depending on the cause (e.g., usually absent in rheumatoid pericarditis).
- Fever and leukocytosis may be present
- Patient may give symptoms of preceding viral illness such as a nonproductive cough or diarrhea
in which case pain is absent in pericarditis
rheumatoid percarditis
examination finding of pericarditis
Pericardial friction rub
a. Not always present, but it is very specific for pericarditis
b. Caused by friction between visceral and parietal pericardial surfaces
c. Scratching, high-pitched sound with up to three components.
: •Atrial systole(presystolic)
•Ventricular systole(loudest and most frequently heard)
•Early diastole
difference between diasystolic dysfunction of constrictive pericarditis and cardiac tamponade
in constrictive pericarditis
Early diastole:Rapid filling
Late diastole:Halted filling
in cardiac tamponade
impeded filling throughout diastolesigns of constrictive pericarditis
JVD—most prominent physical finding; central venous pressure (CVP) is elevated and displays prominent x and y descents
b. Kussmaul sign—JVD (venous pressure) fails to decrease during inspiration
c. Pericardial knock—corresponding to the abrupt cessation of ventricular filling
d. Ascites
e. Dependent edema
square root sign
in constrictive pericarditis
Ventricular pressure tracing shows a rapid y descent, which has been described as a dip and plateau or a
“square root sign.”
complications of acute pericarditis
pericardial effusion
cardiac tamponade
procedure of choice to diagnose pericardial effusion
Echocardiogram
a. Imaging procedure of choice: Confirms the presence or absence of a significant effusion
b. Most sensitive and specific method of determining whether pericardial fluid is present; can show as little as 20 mL of fluid
c. Should be performed in all patients with acute pericarditis to rule out an effusion
- CXR
a. CXR shows enlargement of cardiac silhouette when >250 mL of fluid has accumulated
b. Cardiac silhouette may have prototypical “water bottle” appearance
c. An enlarged heart without pulmonary vascular congestion suggests pericardial effusion - ECG
electrical alrernans
clinical signs of cardiac tamponade
elevated juglar venous pressure most common finding
PROMINENT X DECENT AND ABSENT Y DECENT
decreased pulse pressure
pulsus paradoxus
ecg - electrical alternans not diagnostic of tamponade also in effusion
diagnostic of cardiac tamponade
•echocardiography most sensitive and non invasive test
•cxr enlargement of cardiac silhouette when >250ml collected
•ecg
electrical alternans not diagnostic of cardiac tamponade
•cardiac catherisation
inc rht heart pressure
ABSENT Y DESCENT
treatment of cardiac tamponade
- Nonhemorrhagic tamponade
a. If patient is hemodynamically stable
•Monitor closely with echocardiogram, CXR, ECG
•If patient has known renal failure ,dialysis is more helpfu lthan pericardiocentesis
b. If patient is not hemodynamically stable •Pericardiocentesis is indicated
•If no improvement is noted, fluid challenge may improve symptoms
- Hemorrhagic tamponade secondary to trauma
a. If the bleeding is unlikely to stop on its own, emergent surgery is indicated to repair the injury b. Pericardiocentesis is only a temporizing measure and is not definitive treatment. Surgery should not be delayed to perform pericardiocentesis
test to differentiate dyspnea of heart failure from COPD
brain natriuretic peptide
released from the ventricles in response to ventricular volume expansion and pressure overload.
•BNP levels>150pg/mL correlate strongly with the presence of decompensated CHF.
most common cause of CHF
hypertension
premature atrial complexes
early beat arises within atria firing onits own
ECG look for early P waves that differ in morphology from the normal sinus P wave (because these P waves originate within the atria and not the sinus node).
QRS complex is normal because conduction below the atria is normal. There is usually a pause before the next sinus P wave.
TREATMENT
if asymptomatic no treatment
if symptomatic bblockers
premature ventricular complexes
This early beat fires on its own from a focus in the ventricle and then spreads to the other ventricle
. 2. PVCs can occur in patients with or without structural heart disease
ECG
Since conduction is not through normal conduction pathways, but rather through ventricular muscle, it is slower than normal, causing a wide QRS. 4. Wide, bizarre QRS complexes followed by a compensatory pause are seen; a P wave is not usually seen because it is “buried” within the wide QRS complex
PVCs •
•Couplet:Two successive PVCs
•Bigeminy :Sinus beat followed by a PVC
•Trigeminy:Two sinus beats followed by a PVC
wht is cardioversion
Delivery of a shock that is in synchrony with the QRS complex
:Purpose is to terminate certain dysrhythmias such as PSVT or VT; an electric
shock during Twave can cause Vfib, so the shock is timed not to hit the Twave.
•Indications:
AFib
,atrialflutter,
VT with a pulse,
SVT
wht is defibrillation
Delivery of a shock that is NOT in synchrony with the QRScomplex :Purpose is to convert a dysrhythmia normal sinus rhythm Indications \:VFib ,VT without a pulse.
atrial fibrillation
Multiple foci in the atria fire continuously in a chaotic pattern, causing a totally irregular, rapid ventricular rate. Instead of intermittently contracting, the atria quiver continuously. 2. Atrial rate is over 400 bpm, but most impulses are blocked at the AV node so ventricular rate ranges between 75 and175.
clinical manifestations of atrial fibrillation
Fatigue and exertional dyspnea
- Palpitations, dizziness, angina, or syncope may be seen
- An irregularly irregular pulse
- Blood stasis (secondary to ineffective contraction) leads to formation of intramural thrombi, which can embolize to the brain.
ECG FINDING
Irregularly irregular rhythm (irregular RR intervals and excessively rapid series of tiny, erratic spikes on ECG with a wavy baseline and no identifiable P waves)
treatment of acute atrial fibrillation
- Acute AFib in a hemodynamically unstable patient:
Immediate electrical cardioversion to sinus rhythm
2 Acute AFib in a hemodynamically stable patient
a. Rate control
•Determine the pulse in a patien twith AFib
.If it is too rapid,it must be treated.
Target rate is 60 to 100 bpm.
•β-Blockers are preferred. Calcium channel blockers alternative.If left ventricular systolic dysfunction is present,consider digoxin o ramiodarone (useful for rhythm control).
b. Cardioversion to sinus rhythm (after rate control is achieved)
•Candidates for cardioversion include those who are hemodynamically unstable, those with worsening symptoms, and those who are having their first ever case of AFib.
•Electrical cardioversion is preferred over pharmacologic cardioversion. Attempts should be made to control ventricular rate before attempting DC cardioversion.
•Use pharmacologic cardioversion only if electrical cardioversion fails or is not feasible: Parenteral ibutilide, procainamide, flecainide, sotalol, or amiodarone
C.ANTICOAGULANT
anticoagulate 3wks before and 4 wks after cardioversion
inr of 2-3 is goal
to avoid waiting for 3wks for cardioversion do trans esophageal echocardiography and see if thrombus present ornt ↙️ ↘️
present absent
⬇️ ⬇️
anticoagulate for do cardioversion
3wks and give anticoagulant after it
treatment of chronic atrial fibrillation
rate control + anticoagulant
with bblocker if low risk of embolism then aspirin
or ccb rest all warfarin
atrial flutter
atrial rate around 300 beats /min
diagnosis
ECG
ECG provides a saw-tooth baseline, with a QRS complex appearing after every second or third “tooth” (P wave).
Saw-tooth flutter waves are best seen in the inferior leads (II, III, aVF).
saw tooth waves seen in
atrial flutter
multi focal tachycardia
Usually occurs in patients with severe pulmonary disease (e.g.,COPD)
. •ECG finding
:Variable
P-wave morphology and variable PR and RR intervals
. At least 3 DIFFERENT P-wave morphologies are required to make an accurate diagnosis
. •The diagnosis of wandering atrial pacemaker is identical except that the heart rate is between 60 and 100 bpm (i.e., not tachycardic).
most common arrhythmia due to digoxin toxicity
paroxymal supraventricular tachycardia
treatment of PSVT
•manuvers tht stimualte vegus delay av conduction and block reentrant pathway
acute treatment
a pharmacological
IV ADENOSINE DOC works by dec sinoatrial and av nodal activity
IV verapamil or IV BBLOCKER
DC cardioversion
adenosine is DOC FOR
PSVT
pathology in WPW
An accessory conduction pathway from atria to ventricles through the bundle of Kent causes premature ventricular excitation because it lacks the delay seen in the AV node.
ECG FINDING and treatment of WPW
ECG
Narrow complex tachycardia, a short PR interval, and
a DELTA WAVE (upward deflection seen before the QRS complex)
TREATMENT
•Radiofrequency catheter ablation of one arm of the reentrant loop (i.e., of the accessory pathway) is an effective treatment. Medical options include procainamide or quinidine.
- Avoid drugs active on the AV node (e.g., digoxin, verapamil, β-blockers) because they may accelerate conduction through the accessory pathway
rheumatic hear ds cause
complication of streptococcus pharyngitis
most common abnornality is mitral stenosis
diagnostis of acute rheumatic fever
MAJOR CRITERIA MINOR CRITERIA
migratiory polyarthiritis fever
subcutaneous nodules inc ESR
cardiac involvement history of strep pharyngitis
chorea h/o of rhematic fever
erythema marginatum polyarthralgia
classification of infective endocarditis
Acute endocarditis
•Most vcommonly caused by S. aureus (virulent) •Occur s on anormal heartvalve
•If untreated ,fatal in less than 6weeks
b. Subacute endocarditis
•Caused by less virulent organisms,such as Streptococcus viridans and Enterococcus
•Occurs on damaged heartvalves •If untreated,takes much longer than 6weeks to cause death
most common organism causing of native valve endocarditis
strep viridans
most common cause of prosthetic valve endocarditis
early onset staphylococcus
late onset streptococcus
most commnon cause of endocarditis in iv drug use
STAPH aureus
janeway lesion
in infective endocarditis
Janeway lesions are painless erythematous lesions on palms and soles.
osler nodes
Osler nodes are painful, raised lesions of fingers,toes,or feet.
roth spots
Roth spots are oval,retinal hemorrhages with a clear ,pale center.
dukes criteria
MAJOR
•sustained bacteremia by a organism known to cause endocarditis
•endocardial involvement documented by either echocardiogram (vegetation, abscess,valve perforation,prosthetic dehiscence)orclearly established new valvular regurgitation
MINOR
•Predisposing condition(abnormalvalveorabnormalrisk ofbacteremia)
•Fever
•vascular phenomena:septic arteria o r pulmonary emboli, mycotic aneurysms,intracranialhemorrhage,Janeway lesionsa
•immune phenomena
:Glomerulonephritis
,Oslernodes
,b Rothspots,
crheumatoidfacto
r •Positive blood cultures not meeting major criteria
•Positive echocardiogram not meeting major criteria
marantic endocarditis
non bacterial thrombotic endocarditis
due to some metastatic ds sterile deposits of fibrin and platelets on valve leaflet
libman sac endocarditis
endoacarditits involving aortic valve in SLE
ventricular septal defect signs
Signs a
. Harsh, blowing holosystolic murmur with thrill
•At fourth left intercostal space
•Murmur decreases with Valsalva and handgrip •The smaller the defect,the louder the holosystolic murmur
b. Sternal lift (RV enlargement)
c. As PVR increases, the pulmonary component of S2 increases in intensity
defect in coarctation of aorta
Narrowing/constriction of aorta, usually at origin of left subclavian artery near ligamentum arteriosum, which leads to obstruction between the proximal and distal aorta, and thus to increased left ventricular afterload.
clinical features of coarctation of aorta
HTN in upper extremities with hypotension in lower extremities
2. Well-developed upper body with underdeveloped lower half
Midsystolic murmur heard best over the back
4. Symptoms include headache, cold extremities, claudication with exercise, and leg fatigue
5. Delayed femoral pulses when compared to radial pulses 6. Prevalence of coarctation of the aorta is increased in patients with Turner syn
murmer of coarctation of aorta
midsystolic murmer best heard over back
CXR
a. Notching of the ribs
b. “Figure 3” appearance due to indentation of the aorta at site of coarctation, with dilation before and after the stenosis
figure of 3 appearence on chest xray in
Figure 3” appearance due to indentation of the aorta at site of coarctation, with dilation before and after the stenosis
signs of PDA
Loud P2 (sign of pulmonary HTN)
- LVH: Secondary to left-to-right shunt
- Right ventricular hypertrophy: Secondary to pulmonary HTN
- Continuous “machinery murmur” at left second intercostal space (both systolic and diastolic components) 7.Wide pulse pressure and bounding peripheral pulses
- Lower-extremity clubbing: Toes more likely than fingers to be cyanotic (differential cyanosis)
machinery murmer heard in
PDA continous murmer best heard at left 2nd intercoastal space
TRIAD OF TETROLOGY OF FALLOT
Characterized by a triad of cardiac abnormalities: Ventricular septal defect, right ventricular hypertrophy, pulmonary artery stenosis, and overriding aorta.
clinical features of tetrology of fallots
Patients experience Tet spells—
they will squat after exertion such as exercise or crying spell in an infant.
This maneuver increases SVR, which helps shunt blood from the RV to the lungs instead of the aorta
. Oxygen, morphine, and β-blockers may also be needed if the patient continues to be cyanotic.
4. Murmur is typically crescendo–decrescendo in nature and heard best at the left upper sternal border.
murmer of tetrology of fallots
Murmur is typically crescendo–decrescendo in nature and heard best at the left upper sternal border
most common artery of occlusion
femoral artery
clinical features of acute arterial occlusion
6ps pallor pain parasesthis polar(cold) pulselessnes paralysis
treatment of acute arterial occlusion
anticoagulate with IV heparin
thrombolytics
emergent surgical embolectomy
fogarty balloon cathetetomy—the catheter is inserted,theballoon is inflated,and the catheter is pulled out—the balloon brings the embolus with it.
wht is mycotic aneurysm
Ananeurysm resulting from damage to the aortic wall secondary to infection
•Blood cultures are positive in most cases
•Treatment:IV antibiotics andsurgical excision
leutic heart
due to complication of syphlic aortits
e. Aneurysm of the aortic arch with retrograde extension extends backward to cause aortic regurgitation and stenosis of aortic branches, most commonly the coronary arteries. •Treatment
:IVpenicillin and surgical repair.
most common primary cardiac neoplasm
atrial myxoma
diastolic plop
Prototypically present with fatigue,fever,syncope,palpitations,malaise,and a low pitched diastolic murmur that changes character with changing body positions
( diastolic plop).
homans sign
calf pain on ankle dorsiflexion
phlegmasia cerulea dolens
painful blue swollwn legs indicating major venous obstruction
impaired sensory and motor function
