Ulcers that do not heal with unna boot in CVI results in use of
split thickness skin grafts +/- ligation of adjacent perforation veins
Pericardial friction rub sounds = (3)
ECG changes in acute pericarditis = (4)
1. Scratching between atrial systole (pre systole)
2. Ventricular systole post S2
3. Early diastole between S2-->S1
Heard best sitting up and leaning forward
1. ST segment elevatin and PR segment depression
2. ST returns to normal
3. T wave inverts
4. T wave normalizes
WPW syndrome on the EKG will show?
Narrow complex tachycardia
Delta wave (will upward deflect seen before QRS)
RX: Radiofreq ablastion of one arm of reentrant loop; avoid drugs active on AV node that prolongs QT and can accelerate conduction through accessory.
Medication: Type IA (Procainamide) and Type IC good
Complications of acute MI?
1. Pump failure (CHF) - if mild, ACEi; if severe, cardiogenic shock
2. Arrhythmias = PVCs, Afibb, VT, Vfibb, AIR PSVT, STachy, SBrady, Asystole, AVBk
3. Recurrent infarctions
4. Mechanical complication
5. Acute pericarditis
6. Dresslers syndrome
Chest pain differential diagnosis?
1. HEART/pericardium/vascular causes: stable angina, USA, variant angina; MI; pericarditis, aortic dissection
2. Pulmonary: Pulmonary embolism (pain and pulm infarct); pneumothorax; pleuritis (pleural pain); pneumonia/status asthaticus
3. GI: GERD; diffuse esophageal spasms, PUD, esophageal rupture
4. Chest wall
IF not thrombus is found subsequent to performing a TEE in a patient that is in Afibb, what therapy (anti-coag_ should be started if < 48hr since diagnosis?
Start IV heparin and cardiovert within 24 horus. Continue anticoag for 4 weeks post A fibb episode
Causes of Systolic DYS v. Causes of Diastolic DYS
1. Systolic: impaired contractility (post MI, Cardiomyopathy, Myocarditis)
2. Diastolic: imparired ventricular filling during diastole: HTN --> hypertrophy' valvular diseases (AS, MS, AR); restrictive CM
NBTE Marantic Endocarditis refers to?
What types of deposits are often found?
Endocarditis associated with debilitating illnesses like metastatic cancer found in up to 20% of cancer patients.
1. Sterile deposits of fibrin and platelets forming along closure line of valve leaflets.
Embolize to brain/periphery therefore requires the use of heparin.
Treatment of AORTIC dissection
1. IV - BB to decrease HR and decrease force of LV ejection
2. IV - nitroprusside to decrease systolic BP decreased 120 mm Hg
If type A: surgical management = ant chest pain
If type B: medical management = interscapular pain
When superficial thrombophlebitis occurs over different locations over short period of time --> think of migratory superficial thrombophelbitis --> caused by?
Secondary to occult malignancy of pancreatic origin
When is pulses paridoxicus seen?
1. exaggerated decrease in arterial pressure during inspiration (> 10 mm Hg drop). Detected by decrease in amplitude of femoral/carotid pulse during inspiration. Stronger when expiring.
SIgns of HCM
1. SUSTAINED PMI
2. S4 (precedes S1) - loud at the LL border
3. SYSTOLIC ejection murmor (inc with standing, valsalva, leg raise) and decreases with squatting and handgrip)
4. Increase pulse @ carotid with 2 upstrokes with BISFERIOUS pulse
What mechanical complications occur subsequent to MI
1. Free wall rupture
a. Catastrophic, usually fatal event that occursduring the first 2 weeks post MI (905 will occur within 2 weeks, 1-4 days after MI)
b. 90% mortality
c. Leads to hemipericardium and cardiac tamponade
d. Hemodynamic stability; immediate pericardiocentesis; surgical repair
Ventricular septal defect (VSD)
Most common congenital malformation of the heart
1. Blood flows from the LV to the RV (low pressure) causing an increase in pulmonary blood flow.
2. If PVR < SVR, shunt is always L --> R. But if the PVR > SVR, shunt will then be R --> L.
Therefore is patient with VSD has L to R shunt: CHF, dec growth, elevated LRI
Therefore if patient with VSD has a R to L shunt: SOB, chest pain, dyanosis
Multiple focal depolarizations in ventricles that fire rapidly that cause quivering ventricles with little to NO output --> most start as ventricular tachycardia.
VFIBB + MI post 48 hours (low recurrence)
VFIBB (-) MI; increase in recurrence of VFIBB episode
Cholesterol embolization syndrome
Syndrome due to "showers" of cholesterol crystals originating from proximal source (most common the abdomial aorta, iliacs, femorals) - triggered by surgical/radiographic intervention (arteriogram) or thrombolytic therapy
"Blue toe syndrome"
A myocardial infarction is due to the necrosis of ______ as a result of an interruption of blood supply.
Number one cause:
Acute coronary thrombosis = atheromatous plaque ruptures into the vessel lumen and thrombus formed ontop of lesion. Occlusion of vessel results.
What is the diastolic dysfunction seen in CONSTRICTIVE PERICARDITIS
Early diastole will be unimpeded because volume during filling threshold has not yet been impeded
early diastole - unimpeded
late diastole - halted filling
Treatment of DVT
a. Prevents further propagation of thrombus
b. IV heparin at constant to maintain PTT of 1.5-2 times aPTT
c. Start warfarin once aPTT theraptuc and continue 3-6 mo. INR 2-3
2. Thrombolytic therapy (streptoK; uroK; tPA (alteplase))
3. IVC filter placement (Greenfield filter in patients) if other prophylaxis isnt working. PE prevention, NOT DVT prevention
What are the side effects of nitrates?
NITRATES get HOTS
Rheumatic heart disease: Characteristics
Occurs as a complication of streptococcal pharyngitis (GAS)
-acute RF immunologically mediated systemic process (RHD)
-most common valvular abnormality 2ndary to ARF is MV stenosis; AV or TV can be affected too.
Chronic venous insufficiency (venous stasis DZ)
1. Postphlebitic syndrome (superficial, deep, both)
2. Anatomy = lower extremity venous system consists of deep, superfiial and perforating which connects valves allow super --> deep
3. Pathophysiology = hisotry of dvt is the underlying cause
How is cardiac tamponade treated?
1. Nonhemorrhagic tamponade = if stable, monitor with ECHO, EXR, EKG (dialysis > pericentesis if renal failure present)
2. Hemorrhagic tamponade = emergent surgery pericardiocenttesis only temporizing measure is not definitive treatment
What is the treatment for VFIBB?
1. Unsynchronized cardioversion - start CPR
2. Give 3 sequential shocks (120, 150, 180); assess rhythm
3. IF VF persists --> do CPR and intubate
4. Admin 2 doses amiodarone 2-4 min. Admin 1 mg IV bolus epi every 3-5 minutes (will increase myo and dec cerebral blood flow and dec defib threshold)
Substernal chest pain ("crushing") lasting > 30 minutes + diaphoresis strongly suggests ______ _______
myocardial infarction (ACUTE)
LMWH versus UF Heparin
Longer 1/2 life than UF heparin - 1 dose daily (lovenox).
1. Admin outpt basis
2. No need to follow aPTT
3. More $$ than UF Hep
Orthodromic AV reentrant tachycardia as a PVST
Accessory pathway between the atria/ventricles that conducts regradly (concealed bypass tract) common cause of SVTs
Treatment of Rheumatic Heart Disease
1. Penicillin/erythromycin to prevent RF - by GAS
2. Acute RF treat with NSAIDS. Look at CRP for monitoring treatment (patients with a history of HD by RF should get prophylactic treatment of erythro/amoxacillin for dental/GI/GU procedures
____ ______ IS IMPORTANT clinically when it develops rapidly because it can become cardiac tamponade
Pericardial effusion (if >250mL fluid accumulates, can see on CXR as "water bottle" silhouette)
Second degree AV heart block
Mobitz type I v. type II
Mobitz type I - Wenchbach - progressive prolongation of PR interval until the p wave fails to conduct suddenly. Site of block is at the AV node - no treatment needed but will have a dropped QRS complex.
Mobitz type II - Pacement implant for Rx - P waves fails to conduct suddenly, without a preceding PR interval prolong therefore QRS is dropped randomly. Site of block is @ the BUNDLE OF HIS
Sustained handgrip increases the intensity of a ____ murmor while _____ the intensity of HCM murmor. WHY?
Handgrip increases the MVP murmur and decreases the HCM murmor.
This is due to tht of increase in systemic vascular resistance
Clinical features of Vtachycardia
1. Palpitations SOB, lightheadedness
2. Sudden cardiac death
3. Cardiogenic shock
4. Canon "a" waves in neck (secondary) to AV dissociation resulting in atrial contraction during ventricular contraction and an S1 that varies in intensity.
Signs of serum digitoxin toxicity
GI: N/V, anorexia
CARDIAC: Ectopic ventricular beats, AV block, Afibb
CNS: disorientation (visually)
What is a hypertensive emergency? What is hypertensive urgency?
1. Systolic BP > 220 +/- diastolic BP > 120 in addition to end organ damage whereas urgency is only elevated BP alone.
2. End organ damage assessment
a. EYES (papilledema)
b. CNS (altered mental status; intracranial hemorrhage; HTN encephalopathy can develop)
c. KIDNEY (renal failure/hematuria)
d. HEART = USA; CHF with pulm edema; aortic dissection
Clinical features of hypertrophic cardiomyopathy?
SOB on exertion
Chest pain (angina)
Syncope (dizziness) post valsava
Arryhymias (Afibb/V arrhythmia)
Cardiac failure d/t stiffness during diastole - do not fill - hypoxemia - cor pul
For treatment in hypovolemic shock
AIRWAY BREATHING CIRCULATION
Circulation: Iv hydration --> class I no fluid II benefits with fluid III/IV requires it
Causes of HIGH output heart failure
Increased cardiac output needed for req of peripheral tissue for O2
1. Chronic anemia
4. AV fistula
5. Wet beriberi
6. Paget's disease of the bone
8. Aortic insufficiency (stenosis too)
Asystole post MI
VERY HIGH MORTALITY RATE. Treatment should begin with electrical defibrillation for Vfib which is more common in cardiac arrest and may be difficult to clearly differ from asystole
Which Rx options for psvt
Manevers that stimulate vagus to delay AV condunction and block re-entry
1. Valsalva maneuver
2. Carotid sinus massage
3. Breath holding
4. Head immersion in H2O (cold)
ACutely: IV adenosine (short duration of action and effective at dec SA and AV node); IV verapamil/esmolol
Diagnosis of the PVD
ABI = ratio of systolic BP at ankle to the systolic BP @ arm. Normal ABI >/= 1.0
1. Claudication ABI < 0.7
2. Rest pain ABI < 0.4
Pulse volume recordings
1. Assessment of segmental limb perfusion
2. Pulse wave form represents volume of blood/B @ sequential sites down leg.
Arteriography = GOLD STANDARD
Causes of TVR
1. Secondary to RV dilitation resulting in enlargment of TV orifice
-LVF is number 1 cause
-Inferior wall MI
-COR pulmonale; secondary pulm HTN
2. Tricuspid endocarditis due to IV drug users
3. Secondary to RHD; accompanied by mitral and AV disease
4. EPSTEINS anomaly = congenital malformations
5. Carcinoid syndrome, SLE, myxematous valve
What can cause atrial fibrillation?
1. Heart DZ (CAD, MI, HTN, MV dysfunction)
2. Pericarditis/Pericardial trauma
3. Pulmonary disease (PE)
8. Sick sinus syndrome (sinus node dysfunction -SND)
What is the treatment for MV stenosis
1. Medical: diuretics if (CHF); infective endocarditis prophylaxis; anti-coag therpy
2. Surgical: percutaneous ballooning valculoplasty usually producing excellent results and open commissurotomy and MV replacement
3. Management: no therapy if asymptomatic; diuretics can be used if mild symptoms of edema show (pulmonary)
DVT = causes (VIRCHOWS)
DVT Risk factors:
Virchows: 1. hypercoaguability 2. stasis 3. trauma
Risk factors: >60YO, malignancy, prior DVT/PE/Varicose veins, factor v leiden, PC or S def, AT3 def, prolonged immobilization, cardiac disease, estrogen use, obesity, pelvic surgery
Evaluation of patient with PVD or chronic arterial insufficiency
PVD is an occlusive, atherosclerotic disease of the lower extremities.
1. CAD, CHF, Hx of MI
2. DM, Lung Dz
Sites of occlusion/stenosis is after the superficial femoral artery (Hunter's canal) - most common site
Popliteal artery/aortoiliac occlusive disease
Hypovolemia shock = decreases circulatory BV --- decrease preload, decrease CO
The slower the loss the better the compensatory mechanisms. These fall when > 20%-25% of blood volume lost. If CVP low, hypovolemic shock is present
How is AVR diagnosed? How is it treated for?
1. CXR should should LVH, dilated aorta
2. ECG should show LVH
3. ECHO should be performed serially in stable patients with needs to assess surgery.
4. Cardiac cath = assess severity
1. Conservative if stable
2. Definitive Rx = AV valve replacement
3. Acute AR post MI = do immediate replacement
Acute pericarditis causes:
1. Postviral preceded by recent flu like illness; URI; UGI
2. Infectious = viral (coxsackie, ECHO, HIV); bacterial (TB)
3. 1st 24 hours or in dresslers syndrome (wks - mo) post MI
5. Drug-induced lupus (SHIPP)
What is the treatent for patients with chronic A fibb?
1. Rate control (BB or CCB)
2. Anticoagulation therapy: patients with LONE Afib, no hemodialysis or cardiovascular risks < age 60 do not require antigoags due to low risk for embolism. Thus use of ASA is warranted. Pateints who have risk should continue on lifelong WARFARIN post bridging of enoxaparin
Revascularization: Percutaneous tranluminal coronary angioplasty (PTCA) v. CABG
PTCA: 1 or 2 vessel dx if proximal lesion; restenosis significant issue up to 40% in 6 months (if cannot/doesnt happen then likely not to) - stent placement dec rate of stenosis
CABG: Treatment of choice with HIGH RISK DZ; if L main coronary (CCA); 3 vessel disease with decreased EF or proximal LAD stenosis --> SEVERE STENOSIS
Surgical treatment in patients diagnosed with PVD and have severe claudication?
Surgical bypass grafting (most common procedure with 5 year patency rate of 70%)
1. Angioplasty - ballooning
MVP is most common in which patients?
Patients with a genetic tissue disorder:
1. Marfans syndrome (fibrillin)
2. Ehlers danlos syndrome (collagen III)
3. Osteogenesis imperfection (collage I)
Longterm treatment of USA
Decrease risk factors = smoking cessation/wt loss; treat DM and HTN; hyperlipidemia (use statins); folic acid
Three classic symptoms of AV stenosis and survival rates
1. Angina (35%) - avg = 3 years
2. Syncopy (15%) - avg = 2 years
3. Heart failure (50%) - avg = 1.5 years
How is a DVT diagnosed (next step if suspected)
Step 1: Doppler analysis and duplex US; operater-dependent (good for proximal) veins like popliteal and femoral
Step 2: Venography = most accurate dx in DVT in CALF. Invasive
Step 3: Impedence plethsmography noninvasive alt to doppler
Step 4: D-dimer testing (95% sensitive) RULE OUT; 50% specific
CAUSES of hypertensive emergency
1. Noncompliance with antiHYP therapy
2. Cushings syndrome (inc cortisol)
3. Drugs: cocain/LSD/methamphetamine
4. Hyperaldosteronism (Conn's disease)
5. Ecclampsia: gestational HTN and serizures
7. Alcohol withdrawal
9. Noncompliance with dialysis
Features of chronic venous insufficiency
1. Swelling of lower leg (leg elevation relieves it)
2. Skin change (skin thin, atrophic, shiny, cyanotic, browny induration develops with chronicity)
3. Venous ulcers (above medial malleolus; rapidly occuring)
Two major complications associated with acute pericarditis:
1. Pericardial effusion
2. Cardiac tamponade
Clinical features of PDA
Normal pulmonary pressures
Signs of HF
Loud P2 = pulm HTN bc is a L-R shunt through DA.
Will have LVH secondary to L-R shunt
RVD secondary to pulm HTN
Machinery murmor at L intercostal (2nd) space
Lower extremity clubbing
What are the causes of chest wall pain?
Thoracic outlet syndrome
Cardioversion versus defibrillation
Cardioversion: delivery of shock synchronous with QRS complex to terminate dysarrythmias like PSVT or VT so shock timed NOT to hit T wave because would otherwise cause Vfib. Use with Afibb, A fluttle, VT with pulse, SVT
Defibrillation: delivery of shock not synchronous with QRS. Converts the dysrhythmia to normal sinus rhythm (Vfibb, VT without pulse)
What is cardiac heart failure
Hearts inability to meet the bodys demand under normal physiological conditions.
1. Dec cardiac output, activates (RAAS at kidneys) and SYMP nervous system, activates (vasoconstricts) the peripheral vessels by release of EPI and NE causing volume retention, this increase vascular resistance and maintains CO but will INCREASE preload without increasing CO, thus --> will have an elevated LVEDV --> inc LVEDP --> transmitted to the pulmonary veins --> leads to pulmonary congestions and effusions/"CARDIO FLASH PULMONARY EDEMA)
NBVE Endocarditis "Libmann Sacks"
Involves AV in patients with SLE. Small warty vegetations bilaterally causing AVR or AVS. Rarely infective but CAN lead to embolization
Rx: SLE and anti-coag therapy
Symptoms of stable angina and diagnosis
1. Chest pain.substernal
2. <10-15 minutes
3. Heaviness, pressure, squeezing
4. Can be induced by emotion/exertion
5. Relieved with rest or nitroglycerin
Dx: resting ECG - normal in pts with stable angina; Q waves consistant with prior MI if ST depression, treat for USA
Exercise stress test (stress ECG or echo)
Signs and symptoms of SHOCK
1. Hypotension (dec CO dec SVR)
4. Altered mental status
What are the causes of cardiac tamponade?
1. Penetrating trauma to the thorax such as a gunshot and stab wound
2. Iatrogenic - central line placement; pacemaker insertion; pericardiocentesis
3. Pericardition - idiopathy, neoplastic, uremic
4. Post MI - free wall rupture
Post MI: Rupture of IV septum versus Papillary muscle rupture
Rupture of IV: greater potential for successful therapy than with a free wall rupture, although state of critical event --> occurs within 10 days after MI.
Mitrial valve REGURGITATION will be heard. Get an echocardiogram, perform surgery with MV replacement. Administer intr-aortic balloon pump (IABP)
Harsh blowing holosystolic murmor at the 4th L intercostal space with sternal lift (d/t RV enlargment) and as the PVR increase, S2 increases with intensity
VSD - murmur will decrease with valsalva and decrease with handgrip
What causes VFIBB?
1. Ischemic heart disease
2. Antiarrhythmics (esp those causing torsades that PROLONG QT)
3. A fibb with rapid ventricular rate due to accessory reeentrant pathways (WFW is a good example)
How does ventricular filling in costrictive pericarditis differ from that of cardiac tamponade?
Constrictive pericarditis: inflammation and thickening of the pericardium that results in decreased volume filling and decreased cardiac output during systole. Early fills rapid and late fills slowly
Cardiac tamponade: ventricular filling is impeded throughout diastole
Variant (prinzmetal's) angina
ST segment elevation on ECG during chest pain representing transmural ischemia
-this is a coronary vasospasms that is accompanied by a fixed, sclerotic lesion in 75% of cases but can occur in a normal coronary artery
Which cardiac enzymes is most important in MI dx?
Troponin I and T
1. Increases within 5-14 days and peaks 1-2 days
2. Greater sensitivity/specificity than CKMB for MI
3. Obtain on admission and again in cycles of 8 hours for 24 hours
4. Can be falsly elevated in renal F patients (thus isnt specific to heart)
Sustained VT versus NONsustained VT
Sustained VT = persists in absense of intervention
->30 seconds, hypotension or MI, life threatening, progress to VFIBB
NONsustained VT = breif and self-limited runs of asymptomatic VTACH
-if CAD or LVF present can cause sudden cardiac death
Interpretation of diagnositic tests for DVT:
Pretest probability = Intermediate --> HIGH
Low --> intermediate
Doppler (+) - begin anticoag
Doppler not diagnostic then repeat the US in 2-3 days
Doppler (-); no need for anticoag; observe repease US 2 days
Cardiac arrest versus SCD
Dx of Vfibb (leads to cardiac arrest)
Cardiac arrest: loss of CO; reversible with ABCs promptly restored
SCD: unexpected death within 1 hour of symptom onset secondary to cardiac etiology
Rx: No atrial p waves, no QRS waves identified
Diagnosis of restrictive CM?
1. Echocardiogram will show thickened mycardium and SYS ventricular dysfunction (both LV and RV)
a. Increased RA and LA size with normal LV and RV size
b. If amyloid, myocardium bright
2. ECG shows low voltages, arrhythmias, afibb, endomyocardial biopsy is DIAGNOSTIC
Multifocal atrial tachycardia
Most common to COPD patients!
-Variable p waves morphology (PR segment and RR interval)
-Vagal maneuvers and adenosine shows AV block without a change in atrial tachycardia
-Treatment is to improve O2 and CO2 ventilation. If LV good, use CCB/BB, digotoxin, amiodarone, IV fluconide and IV propafenone
Leutic heart v. Mycotic Aneurysm
Complication of syphilitic aortitis affecting men in 40-50s. Aneurysm of aortic arch with retrograde extention backwards to cause AVR and stenosis of aortic branches (coronary) Rx: IV penicillin and surgical repair
Mycotic aneurysm (secondary to infection)
benign gelatinous growth arising from intratrial septum of heart in region of fossa ovalis - primary cause of cardiac neoplasm that can embolize leading to metastatic disease or can cause relative valve dysfunction
Treatment: surgical excision
What is the diagnosis of constrictive pericarditis? Treatment?
ECG: Low QRS voltages, generalized Twave flattening and inversion, atrial fibrillation.
ECHO: Thickened pericardium
CT Scan/MRI = better accuracy than an ECHO
Cardiac cath = elevated and equal diastolic pressures in all 4 chambers.
Ventricular tracing = rapidly decent (will see a "square root sign"
Rx: Surgical resection of the pericardium
3rd degree HEART BLOCK
NO conduction of atrial impulses to ventrcles, no correspondence between P waves and QRS complexes
ventricular pacemaker (escape rhythm) maintains rate of ~25-40 bpm but #1 = AV dissociation
Medical therapy for stable angina or CAD
ASA - all patients with CAD; decreased morbidity and risk of MI
BB - blocks symp system on heart (dec CO dec HR dec SVR)
Nitrates - generalized vasodilation (decreases preload)
CCB - causes coronary vasodilation and afterload reduction (amylodipine)
What are the physical findings of aortic insufficiency
De musset sign = headbobbing
Muller's sign = uvula bobs
Duroziez's sign = pistol shot sound at the femoral arteries
What is BNP?
Brain natriuretic peptide that is released from the venctricles in resposne to elevated ventricular volume/volume expansion and pressure overload
BNP > 100 = decompensated CHF. Deciphers whether the CHF due to COPD or HF
HOW is hypertrophic CM diagnosed and treated if asymptomatic versus symptomatic?
Diagnosis of HCM is by that of ECHO, clinical, family history
1. Asymptomatic: no Rx, avoid vigorous exercise - BB #1 choice, then CCB
a. BB - reduces symptoms by improving diastolic filling (HR dec, duration in diastole increases) and decrease mycontracting and O2 consumption.
b. CCB (verapamil)
d. Afibb - treat with BB
e. Surgery - myomectomy, MV replacement
Hypotention despite fluids --> hypoperfusion --> organ failure --> death
Causes: pneumonia, pyelonephritic, meningitis, cholangitis, cellulitis, peritonitis
Timeline: SIRS --> Sepsis --> Shock --> MODS
Pathophysiology: Decreased SVR secondary to peripheral vasodilation, increased CO (maintains SV/tachy); EF decreases secondary to decreased contract.
Which Rx can be helpful adjuvant in USA, especially if undergoing PTCA or stenting?
Symptoms of LEFTSIDED heart FAILURE
1. SOB - dyspnea secondary to pulmonary congestions on exersion
2. Orthopnea - diffculty breathing supine
3. PND - awakening 1-2 hrs of sleep with difficulture of SO
4. Nocturnal cough - nonproductive, worse supine
5. Confusion/memory loss - decreased brain perfusion
6. Diaphoresis and cool
Sinus tachycardia post MI
Caused by pain and anxiety, fever, caffeine, pericarditis, medications
-worsens ischemia (increased myocardial O2 consumption)
-treat underlying cause (analgesics for pain ASA for fever)
Pharmacologic Rx of PSVT
1. IV adenosine due to SA-duration of action (~15 seconds and terminates STs by decreasing SA node and AV)
2. IV verapamil (CCB) OR IV esmolol --> use digoxin in patients with LV function
Prevent with = digoxin, verapamil, radiofrequency ABLATION of AV/accessory loop
Patients with PVD should be evaluated with:
1. CV system (HTN, CAROTID BRUITS MURMUR, and AAA)
2. Assess arterial pulses
3. Inspect the lower pulses, color change, ulcers, atrophy, hair loss, thick toenails
4. Do a ECG, CBC, RFT, coagulation profile (Factor V leiden, AT3, PC and PS)
Holosystolic murmur that starts at S1 and continues to S2 at the apex, radiating to back and clavicular area depending upon the leaflet wound
Early beat that fires on own from a focus in ventricle and spreads to other ventricle. Doesnt occur through normal contraction but through muscle and is much slower so QRS is slow and WIDE
Couplet: two successive PVCs
Bigeminal = sinus followed PVC
Trigeminal = sinus followed by two PVCs
MV Stenosis murmur:
Diastolic murmur: S2 with an opening snap with a low pitch diastolic rumble and is followed by S1 that is LOUD.
LOUD S1 is the most prominent and GETS WORSE in the LL decubitus position
Diagnosis of AAA
US = #1choice to evaluate location and size of AAA; 100% sensitive
CTscan = 100% sensitive to detect AAA takes longer than CXR/US; use in hemodynamically STABLE pts only
Abdominal radiographs = shows calcification of dilated segment
New heart murmor with unexplained fever?
1. Diagnostic: Dukes clinical criteria (2 major/1major+2minor)
2. Parenteral AB based on culture results (4-6 weeks)
-if culture negative, treat empirically with VANCOMYCIN or penicillin + AG
When heart doesnt generate CO sufficient to maintain tissue perfusion with systolic BP < 90 with urine output < 20 mL/hr and adequate LVFP
Causes: acute MI = #1 cause, tamponade, tension pneumothorax, arrhythmias, massive PE --> RVF, CM, Myocarditis
Dx: ECG; ECHO; Swan ganz cath
Rx: ABC; Rx udnerlying pressors (DA, dobutamine, NE), IABP
Rx for RESTRICTIVE CM
Due to: hemochromatosis (deferoxiamine and phlebotomy)
Amyloidosis (NO rx) - can usually give digoxin if sys dys unless patient + for amyloid, so if were to adminster would cause tox)
If pulm edem/peripheral edema --> Diuretics (loops, thiazine, spironolactone)/vasodilators like clonidine/hydralazine for perpheral edema
Coarctation of the aorta
Increased in L ventricle afterload due to obstruction bt proximal and distal aorta; common in Turners patients
Features: HTN in upper extremities and HYPO tension in lower. Well developed upper body, poorly developed lower body. Headache; cold extremities, clausication with exercise.
Dx: ECG shows LVH and CXR should notching of ribs with "fig 3" appearance of aorta
Treatment if patient has moderate cardiac disease:
1. Normal EF
2. Moderate angina
3. 2 vessel disease
1. Nitrates (nitroprusside, nitroglycerine)
2. BB (metaprolol)
3. CCB if BB are not effective
4. consider PTCA or cabg if above combo doesnt work
What is acute arterial occlusion and how does it differ from PVD
AAO clinically: pallor, pain, pulselessness, paresthesias, paralysis, polar (cold)
PVD clinically: claudication, rest pain, decreased pulses, ischemic ulcers
Rx: for PVD
Treatment for claudication (conservative therapy)
Treatment for rest pain (surgery)
Rx: for AAO
Rx: anticoagulation; emergent surgery
Which maneuvers increase the MVP sound?
Standing, valsalva, leg raise increases this heart murmur along with that of handgripping. Why? because decreased LV chamber size, less to fill up due to lower venous return on standing.
Those which decrease the MVP murmor: squatting (increases the chamber size and thus delays click
Treatment of ventricular tachycardia
1. Sustained VTACH if stable: mild symp + SBP >90 admin amiodarone, procainamide, sotalol (ALL IV)
2. Sustained VTACH if unstable: Seroconvert dc immediatiately. Follow with amiodarone IV, placement of ICD will be required unless EF > 50%.
1. NONsustained VTACH: if no underlying heart disease, do not treat. If heart disease, consider a ICD placement.
What complications arise with that of AV stenosis, how does the hearts mechanical ability change?
With AV stenosis, this decreases the LV output due to increased resistence across ths valve, therefore the heart must increase stroke volume by either increasing CO or HR to maintain certain level of arterial pressure. That being said, LVH will occur due to attempted compensation. WHen AV area < 0.7cm2, dec CO and increased exertional angina. THis progressive LV dys can further pull on the MV annulus causing mitral regurgitiation hence why AVS with secondary MVR can be seen.
Treatment of chronic venous stasis disease (CVI)
1. Leg elevation
2. Avoid long periods of sitting/standing
3. Elastic stockings
4. Ulcers = "wet-to-dry" dressings
5. Unna venous boot = change every week --> 10 days
How is PDA diagnosed?
Echo - patent ductus with turbulent blood flow
Rx: if PVD not present then LIGATE; if pulm HTN or R to L shunt is present then do not correct.
Unstable angina pectoris
O2 demand unchanged but decreased coronary flow at rest thus indicates a STENOSIS with enlarged d/t thrombosis
Increased and worsening chest pain that is severe AT REST.
**CHEST PAIN AT REST = USA
Coronary artery disease presents with which of the following
Sudden Cardiac Death
What is Dresslers syndrome?
Occurs post MI, presents within WEEKS to MONTHS with:
Imaging/method of obtaining a culture in patients with endocarditis that is infective:
Transesophaeal echo > than a transthoracic echo
Local tenderness, erythema along course of superficial vein
Rx: analgesics (ASA); monitor; continue activity if pain and cellulitis (rest with warm compression)
What is Beck's TRIAD for CARDIAC TAMPONADE?
2. muffled heart sounds
3. JVD ***MOST COMMON FINDING; prominant waveforms (x descent) with absent y descent
What is sick sinus syndrome (now called sinus node dysfunction-SND)
Characterized by a sinus block: syncope, confusion, fatigue, CHF
Rx: Atropine if unstable; pacemaker for LT
Recurrent infarction post MI
Extension of existing infarction/reinfarction of new area
1. Cardiac enzymes will already be elecated from the initial infarct. Troponin levels remian elevated for one week and reutrns to normal faster. re-evaluation of CKMB 26-48 hours later can indicates recurrent infarct.
2. Repeat ST segment levations of EKG on first 24 hours post infarction
Complications of ASD:
Treatment of ASD
1. Pulmonary HTN (<20YO) but common if > 40YO
2. Eisenmengers disease (late comp; irreversible pulm HTN leads to reversal shunt from L --> R) back to R --> L causing HF and cyanosis
3. RHF, AFIBB, STROKE/CVA
Surgical repair if pulmonary:systemic flow > 1.5:1 or 2:1 or symptomatic
Constrictive pericarditis differs from acute pericarditis by what mechanism?
Fibrous scarring of PERICARDIUM leads to thickening and oliteration of the pericardial cavity. This will not only restrict diastolic filling of heart, but it will resulting in an early UNimpeded ventricular filling during diastole because intracardial volume has not yet reached limit defined by stiff pericardium.
LATE diastole WILL BE IMPEDED and halts filling due to (usually) calcifications along the pericardium that can form.
Diagnosis of AORTIC dissection
Widened mediastinum (>8mm on AP view)
1. Transesophageal echocardiogram (TEE) has a very high sensitivity and specificity; noninvasive and done at bedside
2. CT scan/MRI highly accurate
3. Aortic angiography - determines the extent of dissection for surgery
Anterior infarction shows changes in the ECG by?
Anterior leads V1, V2, V3, V4 (ST SEGMENT ELEVATION)
Anterior leads V1, V2, V3, V4 (Q Waves show late change)
General characteristics = failure of sympathetic nervous system to maintain adequate vascular tone.
Causes = SC injury/head injury/pharmacologic symptoms/peripheral vasodilation with decreased SVR
Features: warm; well perfused skin, URINE output low, brady cardia/HYPOtn (CO normal, SVR lo, PCWP lo)
Rx: FLUIDS, VASOCONTRICTIONS BUT CAUTIOUS, WATCH TEMP
What is the treatment of acute pericarditis?
1. Most are self-limited in viral etiology (2-6) weeks
2. NSAIDS good for symptomatic treatment and for pain.
3. Glucocorticoids if NSAIDs do not work
Rapid repetitive firing of 3 or greater PVCs in a row @ rate of 100-250 bpm. AV dissociation (sinus P wave cycle) originates @ the bundle of HIS
Arrhythmias post MI: Premature ventricular contractions (PVCs)
Conservative treatment (observe indicated); no need for antiarrhythmic agents
How is cardiac tamponade diagnosed?
Clinically: look for BECKs triad: hypotension, JVD, muffled heart sounds
1. ECHO - most sensitive and noninvasive
2. CXR - enlargement of cardiac silouette by >250mL
3. ECG - electrical alterans (alt beat variation in direction of ECG waveform) due to swinging of heart with in pericadial space.
4. Cardiac CATH - equal pressures (4 chambers) - loss of y decent
What are the causes of diastolic dysfunction dut to restrictive CM?
Amyloidosis, sarcoidosis, hemachromatosis
Prognostic indicators of CAD
1. Left ventricular function (EF)
2. Vessels occluded
EF: normal > 50%; if EF < 50%, associated with increased mortality
1. LMain Coronary Artery = poor prognosis because covers ~2/3 heart
2. 2nd or 3 vessel CAD - worse prognosis
General characteristics of AAA:
Abnormal localized dilitation of aorta occurs between renal arteries and iliac bifurcation; incidence increases with age (AAA < 50 rare) - 65-70 YO common M>F
1. Atherosclerotic weakening of aortic wall (trauma, HTN, vasculitis, smoking, + family Hx)
2. Syphilis and connective tissue abnormalities; Marfans, ehler-danlos syndrome, osteogenesis imperfecta
Infiltrations of the myocardium resulting in impaired diastolic ventricular filling due to decreased compliance of ventricles.
Cause: amyloid, sarcoid, hemochromatosis, scleroderma, carcinoid syndrome
Paroxysmal SVT (PSVT
#1 cause: reentry by AV node; one fast and one slow within AV node so the reentrant circuit occurs within AV. This results in a narrow QRS with no visible P waves because within that of the QRS. Due to short circuit and rapid conduction so both the atria and ventricles are activated simultaneously.
#2 cause: Orthodromic AV reentrant tachycardia
Small, discrete areas of tissue ischemia, resulting in blue/black toes, renal insufficiency and or abdominal pain/bleeding --> intestinal hypoperfusion
Cholesterol Embolization Syndrome
AV block (bradyarrhythmias)
1. PR interval is prolonged (>0.20 sec)
2. A QRS complex follows every P wave, so its normal
3. Delay is in the AV node
4. Benign - no RX
What is the most accurate method of identifying presense and severity of CAD?
Coronary arteriography (angiography)
1. Standard test to delineated coronary artery
2. Purpose is to determine whether revascularization is needed
3. Coronary artery stenosis >70% produces angina
1. Causes of chronic versus acute:
Acute causes of AVR: Trauma, Infective endocarditis (Staph), Aortic Dissection
Chronic causes of AVR:
1. Primary valvular: RF; bicuspid AV valve; MARFANS; EHLORS-DANLOS; ANK SPA; SLE
2. Aortic root disease: Syphilis in tertiary, osteogenesis imperfecta (collagen dz); AD; Reiters syndrome
Post surgical methods of prophylaxis after surgery
a. Leg elevation, compression socks, ambulation
b. Pneumatic compression boots
a. Heparin or LMWH = UFHep or LMWH post op until ambulation
Cardiac catherderization with coronary angiography is used for what purpose?
1. Determines specific cardiac dx (gives hemodynamic, intracardiac pressure, CO, O2 saturdation)
2. Coronary angiography alwyas performed to visualize coronary arteries
3. When to perform cardiac cathederization
-post positive stress test
-patient with angina and noninvasive test are nondiagnostic, angina +/- therapy
-if patient symptomatic + need diag
-evaluate for valvular disease
What is the treatment for systolic dysfunction or (CHF)
1. Restriction of sodium (<4g/day)
2. Diuretics (loops - ferusemide - post potenti)
3. ACEi - venous and arterial dilation (dec preload and afterload) - best in renal failure patients as well
5. BB - good if post mI CHF
If a patient present with severe
2. Markedly elevated BP
What should next step be?
1st step is to lower BP with antiHTN agent
2nd step is to order CT scan of head to rule out intracranial bleeding (SAH is DDx for headache) - ischemic stroke shows up 24-48 hours
If CT scan is negative; flu with lumbar puncture
Diagnosis of ARF (Acute Rheumatic Fever)
Require 2 major or one major and 2 minor symptoms/signs:
1. Joint - migrating polyangitis
2. New murmor - CHF
3. N-nodules that are subQ
4. Erythema marginatum
5. Syndynems chorea
2. Elevated ESR
4. Prolongs PR
5. Evidence of GAS infection
Causes and diagnosis of hypovolemic shock:
1. Hemorrhagic = trauma, GI bleeding, retroperitoneal
2. Nonhemorrhagic = vomiting, diarrhea, dehydration, burns
Dx: central venous line or pulmonary artery cateder gives invaluble information; cvp/PCWP decreases, decrease CO, increases SVR
Treatment for unstable angina
1. IV access
2. 4L o2 by NC
3. Control pain with nitrates and morphine
How does DVT causes CV stasis disease
1. Destruction of venous valves in deep venous system. Valvular in comp causes gravitational pressure of blood column to ankles
2. Valves in perforation veins damage secondary to chronic increases deep venous pressure inhibitory transmission of super --> deep
Inherited as autodominant but can be spontaneous
Pathophysiology: Diastolic dys due to stiff, hypertrophic ventricle with an elevated LVEDV and LVEDP
Clinically: Pressures in LV increase during exercise or increase with HR/CO activity or dec LV filling (VALSALVA MANEUVER, OUTFLOW OBSTRUCTION OBS d/t hypertrophy of IVS)
Causes of PSVT?
Digitoxin toxicity (2:1) block most common
AV node reentry
Aflutter with rapid ventricular response
AV reciprocating tachycardia excessive caffeine/alcohol
If cardioversion is successful post VFIBB and DC synchronization
Continue IV infusions of the effective antiarrhythmic agent (IV amio has een shown to be most effective)
Implantable defibrillater/LT amio for LT treatment
How might WOMEN (DM, elderly, post-operative) patients with heart ischemia d/t MI present?
Asymptomatic - painless infarcts or atypical presentation
Treatment of MVR medically v. treatment performed surgically
afterload decreases with
Vasodilaters like hydralazine and a-methyldopa, clonidine
Decreased salt reduction
chronic antigoagulation if AFIBB present
IABP as bridge to surgery for acute MVR
Surgical: MVR/replacement; done b4 LVFcn severe
Intermittent claudication v. Rest pain (continuous)
Cramping leg pain thats reliably reproduced by same walking distance; relieved by rest. = intermittent claudication
Worse prognosis felt over distal metatarsel, prominent at night awakens pt from sleep, frank gangrene.
Tachyarrhythmias: Atrial fibrillation
Multiple foci in atria firing continuously: total irregularly rapid ventricular rate
Atria are not contracting but instead they are quivering
Atrial rate > 400 bpm but most are blocked at the AV node therefore the ventricular rate will be between 75-175
How might MV stenosis be diagnosed:
CXR: LA enlargement
ECHO: Most important test to confirm (LA thickness); thick calcified MV, narrow fishmouth shaped; RVF
Infective endocarditis - infection of the endocardium that involves the cusps of the valves
1. Acute endocarditis (S. aureus) - occurs on normal hearts but is fatal in < 6wks without treatment. VIRULENT
2. Subacute endocarditis (S. viridans, enterococcus) - occurs on damaged valves and is not as acutely fatal > 6wks.
Use of IABP improves survival in patient with cardiogenic shock decrease CO, increase SVR, increased PCWP
Intraaortic balloon pump
1. Decreases afterload
2. Increases CO
3. Myo O2 demand
1. Fluid accumulation:
1. 200 mL fluid that develops rapidly can cause cardiac tamponade
2. 2L of fluid may accumulate slowly before cardiac tamponade occurs. When it occurs slowly, the pericardium has opportunity to stretch and adapt to the increased volume
Pathophysiology of pericardial effusion: it impairs the ability for diastolic filling thus leads to elevation and equalization of intracardial pressures such that all RA, RV, LA, LV are equal in pressure. Pulm artery and pericardium are also equali in pressure and thus during diastole there is difficulty in properly filling ventricles due to little change in pressure.
WHen/what maneuvers increase with HCM?
Standing, valsalva, leg raise = increase HCM murmur and S3 S4 sounds
Complications of coarctation of the AORTA and Rx:
Ruptured aneuryms within the cerebrum
Rx: Surgically decompress; percutaneous balloon aortoplasty is common
Management for intermittent claudication
1. Stop smoking
4. Atherosclerotic risk factor reduction control of hyperlipidemia/HTN/weight/DM and so on
5. Avoid cold temperatures
7. Trental (pentoxiphylline) decreases blood viscosity
Clinical features of TVR
1. RVF (ascites, hepatomeg, edema, JVD)
2. Pulsatile liver
3. V waves in JVP
4. Inspiratory S3 in LLSB
5. Blowing holosystolic murmur
Dx: ECHO (quantifies the amount of TVR) and identifies prolapse/flail TVL and pulmonary pressures
EKG: RA/RV enlargement
Diagnosis of Vtach
ECG: Wide and bizarre QRS
QRS: Monophasic VT = QRS complex identical
Polyphasic VT = QRS complexes differ
If SEVERE CAD: Decreased EF <50%, severe angina, 3 vessel disease + LAD
1. Coronary angiography
2. Consider CABG
When is revascularization preferred in patients with CAD
HIGH risk patients (very low EF or LAD/3 vessel occlusion)
Do not decrease incidence of MI but instead dec symptoms
Causes: Bicuspid aortic valve; tricuspic aortic valve in elderly; congenital unileaflet valve; rheumatic fever (although dominant in MV stenosis)
Course: Patients asymp for years (40s) until middle ages despite severe obstruction (bicuspid). Development of angina, syncope, HF, poooooor prognosis
Dx: CXR - calcification of AV caused ^ in LA and LV
EKG = LVH/LA abnormality
ECHO = DIAGNOSTIC FOR AVS
SIGNS of LSHF v. SIGNS of RSHF
LSHF: displaced MI; pathologic S3 heard post S2 into a noncompliant ventricular chamber; heart at the APEX. Pathological S4 in atrial systole into noncompliant LV chamber at L sternal border preceededS1. CRACKLES AND RALES HEARD AT BASES OF THE LUNGS SECONDARY TO INCREASED FLUID INTO THE ALVEOLI DUE TO PULMONARY EDEMA. Dullness to percussion over lung bases due to effusion. Increase intensity of pulmonary component of 2nd heart sound.(P2)
RSHF: Peripheral pitting edema; pedal edema (in elderly due to venous insufficiency); nocturia due to increased VR with elevation of legs; JVD; hepatomegaly; ascites
AV block post MI
1st degree: prolonged PR interval without dropped QRS
2nd degree Type I: Wenkebach (progressive elongated PR interval with a dropped QRS 2:1)
2nd degree Type II: Anterior MI, disregulated randomly dropped QRS
3rd degree: Unrelated p wave and QRS. REQUIRES pacemaker
Clinical features of DVT
1. Lower extremity pain and swelling (worse with walking; better with elevation)
2. Homans sign (calf pain on dorsiflex)
3. Palpabale cord
DVT --> CVI --> ambulatory venous HTN
-Interstitial fluid accumulation = edema
-Extravasation of plasma proteins and RBC into subQ tissue resulting in browny black color
PDA = communication between the _____ and the ______ artery that persists post birth
Pulmonary and Aortic
PGE and low O2 fetally mantain the ductus arteriosis. Blood shunting from nonfcning lungs = normally closes within days post birth.
1. Becomes L-R shunt in life outside of womb if patients (aorta --> pulm)
2. Seen in congenital rubella, HIGH altitude, prematurity
Causes of Atrial FLUTTER
1. Irritable automaticity focus in the atria fires ~250-350 bpm giving rise to regular atrial contractions
2. Atrial rate = 250-350 bpm
3. Ventricular rate = 1/3 - 1/2 atrial rate
Causes: COPD, CHF, Rheumatic fever, CAD, ASD
____ ______ is impaired during _______ in cardiac tamponade leading to decreased filling, decreased SV, and decreased CO
SInus rate < 60 bpm
Clinical significant if < 45 bpm
Ischemia, dec vagal tone antiarrhymic drugs (symp: fatigue, no exercise, angina, syncope)
Treatment for hypertensive emergency
Decrease MAP by 25% within 2hrs
-do not immediately acheive normal BP, but get pt out of danger then reduce BP gradually.
-If diastole > 130 or HTN encephalopathy, IV nitroprusside, labetolol, nitroglycerin used
Posterior infarction with ecg changes?
Large R wave in V1 and V2
ST segment depression in V1, V2
Upright T waves in V1 and V2
primary tumors of heart are rare
-mets from primary tumors more common (75%) via the lung, breast, skin, kidney, lymphoma, kaposi's sarcoma in patients with aids
What cardiac enzymes are the golden standard for diagnosing myocardial injury?
CK-MB - creatinine kinase: ^ 4-8 hours and returns to normal 2-3days and peaks in 1 day. If measure betwenn 24-36 hours, then peaks Levels of total CK and CK-MG is measured on admission and every 8 hours for 24 hours (therefore 3x total)
Troponins (troponin I and T) are the most important test to order (enzymes)
Cardinal manifestations of acute pericarditis:
1. Chest pain (pleuritic, retrosternal to ridge/neck) pain is positional and relived by sitting up and forward
2. Pericardial friction rub *viscera and parietal precodial surgaces" Scratching/high pitched sounds
3. ECG changes = ST elevation or PR depression; ST turns normal but T wave with invert then return to normal
Causes of ventricular tachycardia?
1. CAD with prior MI = #1 cause ~2-3 days post M
2. Active inschemia/hypotension
4. Congenital defects
5. Prolonged QT syndrome
6. Drug toxicity
Post MI Arrhythmia Ventricular Tachycardia (VT)
Sustained Vtach needs to be treated
1. If unstable: electrical cardioversion required
2. If stable: antiarrhythmia therapy (amiodarone IV)
What tests should be ordered to diagnose that of CHEST PAIN
1. Ancillary tests:
-Cardiac enzymes *troponin and CKMB
-Workup of PE
MVR pathophysiology (acute v. chronic)
1. ACUTE MVR: abrupt increase in L atrial pressure in normal sized LA and compliance, causing backflow into pulmonary circulation with pulmonary edema. Decreased cardiac output because decreased forward flow so HYPOTENSION and shock results from severe case of MVR.
2. Chronic MVR: gradual change in LA pressure in setting of DILATED LA and LV *unlike that of acute. Increase of LA compliants. Pulmonary HTN (>35 mm Hg on exertion and > 25mm Hg at rest) can result from CHRONIC backflow.
How is atrial fibrillation on EKG treated?
Irregularly irregular rhythm (RR intervals and small erratic spikes without P waves on EKG)
If UNstable: immediately cardioversion to sinus rhythm
If stable: (1) control rate: if AFIBB but pulse >60-100 then use CCB like amlodipine. If L ventricle- use amiodarone/dig. (2) Cardiovert to sinus rhythm (begin anticoagulation prevention if afib > 48hrs. Then get a tracheoesophageal echo (TEE) of the L atrium to check for thrombosis.
As preload increases or (RV pressure or LVEDV/LVEDP) the CO should also INCREASE as contracitility and stroke volume increases. Preload represents the ability to which the heart is stretched (taut) at steady state. When preload is low, difference in performance between normal and failing heart is minimal
IF systolic dysfunction, there is NOT elevation in CO and EF < 50%
ASD = congenital heart defect
Ostium secundum (80%)
1. O2 blood passes from the LA into the RA and increases the R-Heart OUTPUT and thus increases pulm flow.
2. Increases shunt; increases RA; increases RV, and with pulm to systemic flow ratios of 1.5-1.0 --> pulm htn results
3. Benign until 40YO like that of AV stenosis
Heart sounds: midsystolic murmor in pulmonic area secondary to increased pulmonary blood flow. Wide, fixed S2.
Dx: TEE is diagnostic; CXR: large PArteries; ECG: RBBB, RA deviation
For patients with normal resting ECG in diagnosis of CAD, what test should be performed next?
1. Exercise stress if patient can do so
2. Stress ECG records before, during, after treadmill exercise at 85% max HR
3. Exercise indiced ischemia results in SE ischeia and thus ST depression
4. + Test = HF, V. arrhythmia, hypotension
5. Stress echo records b4 and after exercise
6. Exercise induced ischemia with wall abnormalities (akinesis/dyskines) not present at rest.
7. Favored over ECG because assess LV size and function
How might AAA present? Diagnosis?
Asymptomatic until abdominal exam or CXR for another reason (incidental diagnosis)
2. Pulsatile abdominal mass in hypogastrium and lower back-throbbing character
3. "Grey Turners" sign = ecchymosis on back and flanks
4. "Cullen sign" = ecchymosis around umbilicus
Causes of shock and INITAL STEPS TO APPROACH
1. Fever + site of infection ~~ septic
2. Trauma.GI bleed.Vomiting. Diarrhea = hypovolemia
3. History of MI/CHF/Angina ~~cardiogenic
4. JVD ~~cardiogenic
5. SC injury/neuro change ~~ neurogenic
1. Establish 2 large venous catheders, central line, arterial line
2. FLuid bolus (1500-1000 mL saline)
3. Draw blood (CBC/RFT/PT/PTT)
5. Pulse ox
How is Atrial flutter diagnosed?
Sawtooth baseline QRS complex appearing post every 2nd-3rd "tooth" P wave. These are usually seen in leads II, III, and aVF (inferior leads)
Treatment is similar to that of AFIB:
1. Rate control: BB/CCB
2. Cardiovert if unstable to get normal sinus rhythm
3. Anticoagulation therapy starting with ASA if low risk or going WARFARIN if serious complications
Ventricular aneursym can occur post MI by?
-increase ventricular tacharrythmias
-medical management maybe protective
of patient with severe VSD:
ECG: Biventricular hypertrophy if PVR high because shunt was l to R causing RVH (HIGH P to low P) then once PVR>SVR, shunt was R to L causing LVH
CXR: ^ Pulmonary artery
^ Cardiac silhouette; as pvr ^ (L-R shunt decreases), heart size decreasesm pulmonary artery size increases and R to L shunt increases
ECHO: shows septal defect
Clinical features of ______ _______ include:
1. No BP
2. No heart sounds
3. Patient unconscious
4. If untreated, eventual SUDDEN CARDIAC DEATH
Resulting from damage to aortic wall secondary to infection
Blood cultures (+)
Rx: IV AB and excision
SYMPTOMS: Cough, Exertional dyspnea, orthopenia
SIGNS: JVD, kussmauls sign, pericardial knock, ascites, dependent edema
What/how can ("PRINZMETAL'S") ANGINA can be definitively test for?
How is prinzmetals Rx?
IV Ergonovine (provokes chest pain)
Vasodilators = CCB, nitrates
Treatment for CAD/CHD
#1 - Smoking cessation cuts by 50% post 1 year
#2 - HTN
#3 - Hyperlipidemia - decrease serum LDL with statins
#4 - DM - strict glycemic control
#5 - Obesity - wt loss modifiers (DM, HTN)
#6 - Exercise - decreases emotional stress and promotes weight loss
#7 - diet
#8 - hyperhomocysthemia
What are the clinical features of AVR?
4. WIdened pulse pressures (elevated systolic and decreased diastolic)
5. Corrigans pulse: water hammer pulse is one in which collapse suddenly as arterial pressures decrease rapidly in late systole and diastole
6. Austin flint murmor
3 complications post DVT
1. Pulmonary embolism
2. Postthrombotic syndrome (CV insufficiency)
3. Phlegmasis cerulea DOLENS
-major venous obstruction, leg edema, compromises arterial supply therefore decreased nerve and decreased sensory motor function.
If the patient with STABLE ANGINA, normal resting ECG and cannot exercise to perform stress test, what Rx should be performed?
Pharmacologic stress test:
1. IV adenosine, dipyramidole, dobutamine --> cardiac stress increases c/out exercise
2. Can be combined with ECG, echo, IV nuclear perfusion
3. Adenosine dypyramidole = coronary vasodilation
4. Dobutamine increases myocardial O2 demand, increases HR, increases CO, increases SVR (BP).
How is heart failure diagnosed?
CXR = Kerley B lines with prominent interstitial markings and pleural effusion.
ECHO = initail chest of choice to determine estimates of the EF both sys/dys
ECG = nonspecific
Diagnosis and treatment of MVP
Dx: echo most useful
Rx: Reassurance if asymptomatic; BB if chest pain occurs;
**administer AB prophylaxis for dental procedures to prevent endocarditis
Aggressive management for patients with Unstable Angina
3. LMWH (IV) or UFH for 2 days (PTT at 2-2.5x normal if UFH)
4. Enoxaparin > LMWH because has better coverage with factor X
5. Nitrates = 1st line!!!
6. Glycoprotein IIb/IIIa
DO NOT _____ FOR ASYSTOLE. Try ____ or transcutaneous pacing.
Defibrillate (not for asystole, or PEA)
Atheromatous occlusion of distal aorta just above the bifurcation causing bilateral claudication, importence, absent/diminished pulses
RIGHT ventricular infarction will present with what clinical changes and EKG changes?
Inferior ECG changes (II, III, aVF)
Premature atrial complexes as a type of arrhythmia
1. Early in atria, fires on own
-srugs, alcohol, tobacco, electrolyte imbalances, ischemia, infection
Signs on EKG:
1. Early P waves that differ from others (not normal sinue rhythm)
2. QRS complex is normal
3. Found 50% of normal adults with holter monitoring
4. Causes palpitations or PSVTs
TREATMENT: BB - metoprolol
What are the causes of MVR: *Acute and Chronic
Causes of acute: Endocarditis, Papillary m. rupture, infarction or dysfcn, higher mortality
Causes of chronic: RF, Marfans, Cardiomyopathy
Almost all causes are secondary to:
Mitrial valve stenosis: #1 cause due to Rheumatic Heart Disease/Fever
1. Scarring/narrowing of the MV oriface - increase LA pressure and PV press
2. Asymptomatic until MV area < 1.5cm2 normal is (4-5cm2)
Clinical features: Exertional dyspnea, orthopnea, PND; Palpitations, chest pain; hemoptysis (because as there is an increase in LA pressure, this ruptures anastomosis of small bronchial veins and thus causes coughing up of blood). Thromboembolism can occur
SIGNS: (MV Stenosis murmur) Heart during diastole between that of S2 and S1 at the apex of the heart. Will be heard best on EXPIRATION because L side heart. Diastolic following S2 with an opening snap.
Native heart valve is most commonly affected by: _____________
Prosthetic heart valve is most commonly affected by : _____________
Endocarditis of IV drug users: _______________
1. S. Viridans most common native valve endocarditis organism but is SUBACUTE
-Staphylococcus (aureus > epi)
-HACEK group = Haemophilus, actinobacillus, cardiobacterium, Eikenella, Kingella
2. Staph epi > aureaus within 60 days of surgery. Streptococcus later onset > 60 days.
3. Right sided; S. Aureus = #1 cause/candida/entero/Pseudo
Treatment of shock
1. Cardiogenic (dec CO inc SVR inc PCWP)
2. Hypovolemic (dec CO, inc SVR dec PCWP)
3. Neurogenic (dec CO dec SVR dec PCWP)
4. Septic (inc CO, dec SVR, dec PCWP)
1. Airways, breathing, circulation
Characteritistics: Any cause of acute pericarditis leading to exudative fluid into the pericardial space -- can occur with ascites, pleural effusion in sodium and water retention states like CHF, cirrhosis, nephrotic syndrome.
Clinical findings: Muffled heart sounds, soft PMI, dullness at L lung base, pericardial fricition rub
Dx: ECHO - most sensitive and specific for effusion (shows 20mL fluid)
CXR - enlargement of the silouette > 250mL fluid
EKG - low QRS, low T wave = ELECTRICAL ALTERANS
#1 type of CM
Cause: CAD (with prior MI) - most common; toxin (alcohol, doxorubicin, adriamycin); metabolic (thiamine/selenium deficiency); infectious (coxsackieBvirus/chagas/lyme/HIV), peripartum; CVD; SLE; COCAINE: idiopathic
Features: LCHF (pulm HTN, pleural effusion, SOB, crackles and rales at lung bases, pulm edema, S3/S4). RCHF (peripheral edema, RVH, JVD, ascites, nocturia)
Acute pericarditis post MI?
ASA is Rx for acute pericardial inflammation = do not administer NSAIDs or CORTICOSTEROIDS because hinders the mycardial scar formation.
Which maneuvers diminish the intensity of ALL murmurs but will increase those of MVP and HCM?
Squatting increases the intensity of all murmose but ___ that of MVP and HCM
Squatting will dec intensity of MVP and HCM
Standing, Valsalva, Leg raise - all decrease murmurs except for MVP and HCM
This is because these all dec the LV volume by decreasing venous return. Thus, HCM is caused by diastolic dys; no change in size, and decreased filling of venticle will result in a increase of sound.
Thus MVP/HCM gets louder with standing, valsava and leg raise. Gets diminished with squatting because inc LV volume, inc filling and thus decreased the murmor.
Complications of VSD and Rx:
Progressive AORTIC regurgitiation
Pulm HTN/shunt reversal
Rx: Prophylaxis if endocarditis (vanc and amoxicillin and aminoglycosides)
Surgical repair if PVR to SVR flow is >1.5:1 or 2:1
Patients with: Mild disease (CAD)
1. Normal EF (>55%)
2. MILD Angina
3. Single vessel disease
1. Nitrates (symptoms as prophylaxis)
2. BB (metoprolol)
-use CCB if symptoms continue
Which rapid polymorphic VT leads to Vfibb, associates with prolonged AT syndromes, TCAs, anti-ACh and can be treated with IV Mg2+
Torsades de pointes
#1 cause death in ICU =
Rx: IV AB
surgical drainage if necessary
fluid to maintain BP
pressors (DA, dobutamine, NE)
Signs of Left sided HF
Displaced PMI due to cardiomegaly
S3 ventricular gallop
1. Rapid filling into noncomplaint LV, normal in children; adults = CHF
2. Difficult to hear but MOST specific in CHF pateints heard at the apex by following SV
Sinus bradycardia post MI
Common occurance in EARLY stages of acute MI; may be protective mechanism by reducing myocardial O2 consumption. NO treatment (OBSERVE) if mild; if gets severe, administer ATROPINE to increase HR
Bundle of Kent accessory pathway from atria to ventricles causing a premature ventricular excitation because lacks the delay seen in teh AV node. Can result in PSCTs of orthodromic reciprocating tachy (anterograde limb, depolarizing ventricles, then goes back with accessory pathway, retrograde and redepoarizing atria). No hange in wave because conduction retrograde. SVT (afib/flutter) usually AV node only allows certain impulses to vent, but with accessory, all/most get to the ventricles
Treatment of AAA
Consider age as a factor in AAA patients that are assymptomatic
Managment depends on aneurysm size > 5cm in diameter or symptomatic
Surgical resection with synthetic graft placement recommended
What did the HOPE trial show regarding drugs that dec mortality, stroke, AND renal disease in patients with vascular disease?
ACEi = ramipril
Three drugs needed for A fibb:
1. Rate control - CCB
2. Restore normal sinus rhythm (cardiovert)
3. Start coag therapy to avoid clot formation (anticoag therapy)
Myocarditis is caused by _______ which leads to inflammation of the myocardium
Viruses (coxsackie B virus); bacteria (GAS in RF, LYME Dz, MYOCOPLASMA)
Dx: Look for increased ^CK-MB/TROPONIN; Elevated ESR
Main goal of someone with AAO?
1. Assess viability of tissues to salvage the limb
2. Skeletal muscle tolerates 6 horus of ischemia
3. Amputation necessary
4. IV heparinas anticoagulation
5. Embolectomy indicated via cutdown and fogarty balloon. Bypass reserved for embolectomy failure.
Treatment of sinus bradycardia?
1. Atropine (blocks vagal stimulation) - mad as hat blind as bat
2. Pacemaker if persist
Categories of infarcts include:
1. ST Segment elevation infarct = transmural (involving entire thickness of the wall); tends to be larger; seen in prinzmetals angina as well
2. Non-ST segment elevation infarct: subendocardial involving inner 1/3 of wall; tend to be smaller and presentation of such similar to USA. THus both nonSTEMI and USA have elevated ST only nSTEMI has increased cardiac enzymes
Signs of _____ ______ include:
1. Harsh crescendo-descendo sys murmur
2. Heard in secondary right intercostal space
3. Radiates to the carotid arteries
Characteristics: longstanding HTN (70%);trauma; CTD (Marfans/Ehlers danlos) syndrome; biscuspid valve; coarctation of the aorta; 3rd trimester pregnancy
Type A: proximal involving AA with retrograde extension from descending aorta
Type B: Distal and limited to descending aorta
Treatment of patients with diagnosed MI
Admit patient to CCU and establish IV access
Admin O2 and analgesics (nitrates; morphine)
Medical therapy that dec mortality
2. BB - stimulation HR and contractility, decreases afterload; dec mortality
3. ACEi - initiate within hours of hospitalization