Step Up to Medicine: Chapter 01 Diseases of the Cardiovascular System

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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
Short PR
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

5. Psychiatric

6. Cocaine

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

Immediate therapy
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

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

Ventricular fibrillation

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


Decreased and delayed upstrokes of carotid artery seen in AV stenosis

Treatment of DVT

1. Anticoagulation
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?

Orthostatic hypotension


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
SUDDEN death

For treatment in hypovolemic shock


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
2. Pregnancy
3. Hyperthyroid
4. AV fistula
5. Wet beriberi
6. Paget's disease of the bone
7. MVR
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
-RV infarction
-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)
4. Hyper/hypothyroid
5. Sepsis
6. Stress
7. Alcohol
8. Sick sinus syndrome (sinus node dysfunction -SND)
9. Pheochromocytoma

Chronic stable angina verusus USA


ECG + cardiac enzymes
Give ASA
Begin IV heparin

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
4. Uremia
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

Leading cause of death in patients with PDA

Heart failure

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

BB (metoprolol)
Nitrates (SL)

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
6. Vasculitis
7. Alcohol withdrawal
8. Pheochromocytoma
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

(-) Cardiac enzymes + ST segment depression

Unstable angina

What are the causes of chest wall pain?

Muscle strain
Rib fracture
Herpes zoster
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)
2 Oliguria
3. Tachycardia
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

Lateral infarction with ECG changes

Will show change in leads aVL, I, II in Q wave

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)

Patients with a positive echo or stress ECG should undergo ____ ___.

Cardiac catheterization

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

Ventricular fibrillation as a complication post MI:

Immediate unsynchronized defibrillation and CPR

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

Systolic click with midsystolic rumble when standing/valsalva and decreases with squatting:


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

Triad of AAA

-Abdominal pain
-Palpable pulsatile abdominal mass

Emergent laparatomy

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)

Atrial myxoma

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

Inferior infarction with ECG changes?

Leads II, III, aVF will show pathologic Q waves

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
2. Symptomatic:
a. BB - reduces symptoms by improving diastolic filling (HR dec, duration in diastole increases) and decrease mycontracting and O2 consumption.
b. CCB (verapamil)
c. Diuretics
d. Afibb - treat with BB
e. Surgery - myomectomy, MV replacement
f. Pacemaker

Septic shock

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?

1. Abiximab
2. Tirofiban

Glycoprotein IIb/IIIa

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:

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


Preventricular Contraction

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

Cardiogenic shock

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


Due to: hemochromatosis (deferoxiamine and phlebotomy)
sarcoidosis (corticosteroids/glucocorticoids)
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
Diagnosis: arteriogram
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 decreases frequency of cardiovascular events


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

% of patients who improve from medical regimen of (nitrates, enoxparin, BB, ASA) +/- PTCA/CABG?


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.


Coronary artery disease presents with which of the following

Stable angina
Sudden Cardiac Death

What is Dresslers syndrome?

Occurs post MI, presents within WEEKS to MONTHS with:

1. Fever
2. Malaise
3. Pericarditis
4. Leukocytosis
5. Pleuritis


Imaging/method of obtaining a culture in patients with endocarditis that is infective:

Transesophaeal echo > than a transthoracic echo

2 forms of revascularization of MI

1. Thrombolysis
2. PTCA (if one vessel - CABG if more) *

Superficial thrombophlebitis
Diagnosis: Rx:

Local tenderness, erythema along course of superficial vein

Dx: clinical

Rx: analgesics (ASA); monitor; continue activity if pain and cellulitis (rest with warm compression)


1. hypotension
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

Surgical repair if pulmonary:systemic flow > 1.5:1 or 2:1 or symptomatic

If patient has QRS tachy with wide (>0.12) seconds, then:


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)

Neurogenic shock

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)


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

Ventricular tachycardias

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
Diagnostic tests:
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

Vessels involved:
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

Restrictive cardiomyopathy
1. Characteristics
2. Causes

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

MI is associated with ___% mortality rate, where 1/2 deaths are pre-hospital


AV block (bradyarrhythmias)

1st degree:

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

AV Regurgitation:

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

1. Mechanical
a. Leg elevation, compression socks, ambulation
b. Pneumatic compression boots
2. Pharmacologic
a. Heparin or LMWH = UFHep or LMWH post op until ambulation

Cardiac catherderization with coronary angiography is used for what purpose?

Cardiac cath:
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

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