-
Class I Heart Failure
No limitation of physical activity, ordinary physical activity does not cause undue fatigue, dyspnea, or anginal pain
-
Class II Heart Failure
Slight limitation of physical activity; ordinary physical activity results in sx
-
Class III Heart Failure
Marked limitation of physical activity; comfortable at rest, but less than ordinary activity causes sx
-
Class IV Heart Failure
Unable to engage in physical activity without discomfort, sx may be present even at rest
-
Shock
severe CV failure caused by poor blood flow or inadequate distribution of flow. Inadequate oxygen delivery to body tissues results in shock, which lead to organ failure and death
-
Hypovolemic shock causes
- hemorrhage, loss of plasma, loss of fluid and electrolytes, resulting in decreased intravascular volume.
- This may be caused by obvious loss of by third-spacing
-
Cardiogenic shock causes
MI, dysrhythmias, HF, defects in the valves or septum, cardiac contusion, rupture of ventricular septum, or cardiomyopathies
-
Obstructive shock causes
tension ptx, pericardial tamponade, obstructive valvular disease, pulmonary problems, PE
-
Distributive shock causes
sepsis, SIRS, anaphylaxis, neurogenic shock
-
Causes of neurogenic shock
spinal cord injury or adverse effects of spinal or epidural anesthetic
-
S/Sx of shock
LBP, orthostatic changes, tachycardia, peripheral hypoperfusion, AMS, oliguria or anuria, insulin resistance, and metabolic acidosis
-
End organ hypoperfusion s/sx
Cool or mottled extremities, weak/thready or abset peripheral pulses
-
Tx of shock
- ABCs
- Tx cause
- Trendelenberg or supine position with legs elevated maximizes blood flow to the brain
- good urine output
- continuous cardiac monitoring (CVP or capillary wedge pressure)
- Pressures (dopamine, etc) will increase GFR, contractility, and heart rate
-
Urine output goal in shock
0.5mL/kg/hr or more
-
Causes of postural hypotension
decreased cardiac output, paroxysmal cardiac dysrhythmias, low blood volume, medications, and various endocrine and metabolic disorders
-
Postural hypotension
Greater than 20 mm Hg drop in SBP between supine and sitting and/or standing measurements
-
How do you know that decreased blood volume is the cause of postural hypotension?
- increase in pulse by 15 bpm
- if no increase in pulse, consider meds, CNS disease (Parkinsons, Shy-Drager), or peripheral neuropathies
-
Metabolic syndrome
truncal obesity, hyperinsulinemia and insulin resistance, hypertriglyercidemia, HTN)
-
Secondary causes of HTN
sleep apnea, estrogen use, pheochromocytoma, coarctation of the aorta, pseudotumor cerebri, parenechymal renal diesase, renal artery stenosis, chronic steroid therapy, Cushing's syndrome, thyroid and parathyroid disease, primary hyperaldosteronism, and pregnancy
-
stage 1 HTN
140-159/90-99
-
-
How soon must HTN emergencies be reduced?
By one hour to prvent progression of end-organ damage or death
-
Malignant HTN
elevated BP associated with papiledema and either encephalopathy or nephropathy; if untx, progressive renal failure occurs
-
End organ damage in untx HTN
HF, renal failure, stroke, dementia, aortic dissection, atherosclerosis, and retinal hemorrhage
-
HTN urgency
>220/125 with no end organ damage
-
HTN emergency
>220/130 with papilledema
-
Complications of HTN emergency
HTN encephalopathy, nephropathy, intracranial hemorrhage, aortic dissection, preeclampsia or eclampsia, pulmonary edema, unstable angina, MI
-
EKG findings in HTN
LVH or HF, strain failure indicates advanced disease and a poorer prognosis
-
Diurectic MOA
Reduce plasma volume and chronically reduce peripheral resistance
-
Initial therapy for essential HTN
thiazide diuretics; loops in those with renal dysfunction and when close electrolyte monitoring is assured
-
ACE-I MOA
inhibit bradykinin degradation and stimulate synthesis of vasodilating prostaglandins
-
ARB MOA
- block the itneraction of angiogensin II on receptors
- Do not increase bradykinins, therefore do not cause cough
-
CCB MOA
peripheral vasodilation, good in AA and elderly
-
A-adrenergic MOA
lower peripheral resistance
-
aldosterone receptor antagonist role in HTN
refractoy HTN in addition to other HTN
-
Tx of HTN emergency
- sodium nitroprusside
- nitro or BB if ischemia is present
-
Tx of aortic dissection
Nitroprusside and BB (usually labetaolol or esmolol) and urgent surgery
-
CHF effect on cardiac function
adversely affects left atrial pressure and cardiac output
-
-
cardiac signs of heart failure
parasternal lift, enlarged apical impulse, diminished first heart sound, S3 gallop
-
Initial therapy in CHF
loop diuretic and an ACE-I
-
Role of CCBs in CHF
associated angina or HTN
-
Metabolic syndrome values
- 3 or more of the following:
- abdominal obesity, TG > 150, HDL <40 for men and <50 for women, FBP > 110, and HTN
-
Prinzmetal's angina
vasopasm at rest
-
Unstable angina
increasing pattern of pain in previously stable pts; less responsive to medication, lasts longer, and occurs with rest or with less exertion
-
Angina > 30 mins
unstable angina, MI, or another dx
-
angina time frame
should be <3m
-
Most sensitive clinical sign of angina
horizontal or downsloping ST-segment depression on an EKG
-
First line therapy for chronic angina
BB
-
CCB role in angina
third line therapy
-
m/c cause of MI
thrombus formation on a preexisting atherosclerotic plaque
-
Populations most likely to have uncommon presentation of MI
women, diabetics, elderly
-
MI pain occurs most often when?
early in the morning
-
Inferior MI EKG
II, III, aVF
-
-
Anteroseptal MI EKG
V1, V2
-
Anterior MI EKG
V1, V2, V3
-
Anterolateral MI EKG
V4, V5, V6
-
Cardiac exam in MI
nl, or JVD, soft heart sounds, mitral regurg, and S4 gallop
-
Dressler's syndrome
- Post-MI syndrome, usually 1-2 weeks
- Pericarditis, fever, leukocytosis, pericardial or pleural effusion
-
When should CK-MG be drawn?
3 times, 12 hours apart
-
When should troponin I be drawn?
12 hours after onset of CP
-
When should troponin T be drawn?
12 hours after onset of CP
-
When should LDH be drawn in an MI?
Once, at least 24 hours after onset of CP
-
When does LDH peak?
24-48 hours
-
When does LDH return to nl?
10-14 days
-
When does CK-MB peak?
24 hours
-
When does CK-MB return to nl?
48-72 hours
-
When does troponin I peak?
24 hours
-
When does troponin I return to nl?
5-10 days
-
When does troponin T peak?
12-48 hours
-
When does troponin T return to nl?
5-14 days
-
What is myoglobin's timing in MI?
- Initially elevates in 1-4 hours
- Peaks in 6-7h
- Returns to nl in 24 hours
-
When do the troponins appear?
3-12 hours after onset of MI
-
When does Ck-MB appear?
3-12 hours after onset of MI
-
TX of STEMI
- MONA
- Antiplt (ASA, clopidogrel) and anticoag (unfractionated hep, enoxaparin, fondoparinux, or bivalirudin therapy)
-
CI to BB in ACS
CHF, bradycardia, heart block
-
role of CCBs in STEMI
only in pts who can't take nitrates and BB or in those with CI to these drugs
-
Reperfusion therapy in ACS
- coronary angiography and primary percutaneous coronary intervention are superior to thrombolysis in high-volume centers
- Thrombolytic therapy within 3 hours reduces mortality and limits size of the infarction
- Statin therapy within days of ACS
-
M/c thrombolytic agents
alteplase, reteplase, tenecteplase
-
Absolute CI to thrombolytic therapy
- Previous hemorrhagic stroke
- any stroke within the past year
- known brain mass
- active internal bleeding
- suspected aortic dissection
-
Relative CI to thrombolytic therapy
- Known bleeding diathesis
- trauma within the past 2-4 weeks
- major surgery within the past 3 weeks
- prolonged or traumatic cardiopulmonary resuscitation
- recent internal bleeding
- noncompressible vascular puncture
- active diabetic retinopathy
- pregnancy
- active PUD
- current use of anticoag
- BP >180/110
-
Cyanotic heart defect
right to left shunt
-
Types of cyanotic heart defects
- ToF
- Pulmonary atresia
- Hypoplastic left heart syndrome
- Transposition of the great vessels
-
Noncyanotic heart defect causes
- ASD
- VSD
- AV septal defect
- PDA
- Coarctation of the aorta
-
ToF
- Subaortic septal defect
- right ventricular outflow obstruction
- overriding aorta
- RVH
-
Pulmonary atresia
closed pulmonary valve, atrial-septal opening and PDA are present
-
Hypoplastic left heart syndrome
Group of defects with a small left ventricle and nl placed great vessels
-
Transposition of the great vessels
M/C a complete transposition of the aorta and pulmonary artery
-
-
ASD
opening between right and left atria
-
AV septal defect
incomplete fusion of the endocardial cushions, common in Down
-
PDA
failure to close or a delay in closure of the channel bypassing the lungs, which allows placental gas exchange during the fetal state
-
Coarctation of the aorta
narrowing in proximal thoracic aorta
-
ToF murmur
crescendo-descresndo, holosystolic at LSB, radiating to back
-
Cardiac findings in toF
Murmur, cyanosis, clubbing, increased RV impulse at LLSB, loud S2
-
TET spells
- Medical emergency
- extreme cyanosis, hyperpnea, agitation
-
M/C sign of transposition of great vessels
cyanosis in newborn
-
-
m/c cause of mitral valve disorder
congenital defect
-
m/c cause of aortic valve disorder
congenital defect
-
widened pulse pressure
aortic insufficiency
-
murmur that is loud with a thrill
aortic stenosis
-
Aids to hearing aortic stenosis better
sitting and leaning forward
-
aids to hearing aortic regurg better
sitting and leadnign forward, full exhalation
-
Aids to hearing mitral stenosis better
LLD, full exhalation
-
Pulses large and bounding (murmur)
aortic insufficiency
-
aids to haering tricupid regurg better
inspiration
-
Tx of heart murmurs
- surgical repair, replacement of valve, balloon valvuloplasty
- pts with good exercise tolerance may be tx with diuretics and vasodilators for pulm congestion and with dig or BB for dysrhythmias
- anticoag therapy for prevention of throboemboli, particularly if afib occurs
-
Difference in age presentation in the murmurs
- triscuspid and pulmonic: usually present in infancy or childhood
- mitral and aortic: usually present in adults
-
Tricuspid and pulmonic valve murmurs may lead to what?
RHF
-
m/c presentation of pulmonic or tricuspid murmurs
exercise intolerance
-
Tx of tricuspid and pulmonic murmurs
- sodium restriction, diuretics
- tx pulm HTN with arterial vasodilators or positive inotropic agents
- definitive: surgery, valvuloplasty, repacement
-
Causes of sinus tach
- fever
- exercise
- pain
- emotion
- shock
- thyrotoxicosis
- anemia
- HF
- drugs
-
m/c paroxysmal tachycardia
PSVT
-
Class Ia antiarrythmatics MOA
Na channel blockers, depress phase 0 depolarization, slow conduction, prolong repolarization
-
quinidine
Ia antiarrhythmatic
-
procainamide
Ia antiarrythmatic
-
disopyramide
Ia antiarrythmatic
-
Uses for Class Ia
- Supraventricular tachycardia
- V tach
- prevention of V fib
- sxmatic PVCs
-
Class Ib antiarrythmatics MOA
shorten repolarization
-
Class Ib antiarrythmatics indications
- V tach
- prevention of V fib
- sxmatic PVCs
-
lidocaine
Class Ib antiarrythmatics
-
class Ic antiarrythmatics
depress phase 0 repolarization, slow conduction
-
Indications for Ic antiarrythmatics
- Life-threatening vtach or vfib
- refractory SVT
-
flecainide
Ib antiarrythmatic
-
Propafenone
Class Ic antiarrythmatic
-
Class II antiarrythmatics MOA
beta blockers, slow AV conduction
-
Class III antiarrythmatics MOA
prolong action potential
-
Class III antiarrythmatics indications
refractory vtach, SCT
-
amiodarone
Class III antiarrythmatic
-
sotalol
class III antiarrythmatic
-
dofetilide
Class III antiarrythmatic
-
ibutilide
Class III antiarrythmatic
-
Class IV antiarrythmatics MOA
slow CCBs
-
Inidcations for class IV antiarrythmatic
SVT
-
Class V antiarrythmatics MOA
- Adenosine: slows conduction time through AV node, interrupts rentry pathways
- digoxin: direct action on cardiac muscle and indirect action on CV system via ANS
-
Indications for Class V antiarrythmatics
SVT
-
adenosine
Class V antiarrythmatic
-
digoxin
Class V antiarrythmatic
-
Causes of atrial flutter
- COPD
- CHF
- ASD
- CAD
- Mitral valve disorders
-
Causes of junctional rhythms
pts with nl hearts, those with myocarditis, cAD, digitalis toxicity
-
Mechanical tx of PSVT
- valsalva
- coughing
- breath holding
- stretching
- putting head b/w knees
- applying cold water to face
- U/L carotid sinus massage
-
Nonpharm intervention of PSVT
- surgery or ablation
- Cardioversion
- electrical pacing
-
Meds for PSVT
- IV adenosine or PO verapmil eliminates most episdoes of PSVT
- Prevention with diltiazem and/or verapamil or BB
-
Tx of atrial flutter
Ibutilide or electric cardioversion
-
Tx of chronic atrial flutter
Amiodarone or dofetilide
-
V tach def
three or more consecutive PVCs
-
Causes of Torsades
- Hypokalemia
- Hypomagnesemia
- drugs that prolong QT interval
-
Brugada's syndrome
- Genetic disorder
- M/c in asians and men
- causes syncope, v fib, and sudden death
-
tx of PVCs
BB is pt is sxmatic, class I and III with caution
-
acute v tach tx
- lidocaine
- amidoarone
- procainamide
- empiric mag may help
-
-
Tx of torsades
BB, Mg, temporary atrial or ventricular pacing
-
Sick sinus syndrome causes
- digitalis, CCB, BB, smpatholytic agents, and antiarrhythmatic drugs
- underlying collagen vascular disorder or metastatic disease, surgical injury, or rarely coronar disease
-
m/c type of cardiomyopathies
DCM
-
causes of DCM
- excessive alcohol
- postpartum
- chemo toxicity
- endocrinopathies
- myocarditis
- idiopathic
-
Restrictive cardiomyopathy causes
- amyloidosis m/c
- fibrosis, infiltration of ventricular wall d/t collagen defect diseases
- radiation
- post op changes
- diabetes
- endomyocardial fibrosis
-
m/c presentation of DCM
dyspnea
-
Cardiac findings in DCM
S3 gallop, rales, increased jugular venous pressure
-
M/c presentation of HCM
dyspnea and angina
-
Cardiac findings of HCM
- sustained PMI or triple apical impulse
- loud S4 gallop
- variable systolic murmur
- bisferiens carotid pulse
- JVP with prominent a wave
-
Tx of DCM
- abstain from alcohol
- tx underly dz
- supportive tx for CHF
-
Tx of HCM
- BB or CCB, disopyramide for negative inotropic effects
- surgical or nonsurgical ablation of hypertrophic septum may be required
- dual-chamber pacing, implantable defibrillators, mitral valve replacement
-
Tx of restrictive cardiomyopathy
diuretics
-
Causes of pericarditis
- viral or bacterial infection
- autoimmune or connective tissue disease
- neoplasms
- radiation therapy
- chemotherapy or other drug toxicity
- cardiac surgery
- myxedema
- tuberculosis
-
causes of pericardial effusions
secondary to pericarditis, uremia, or cardiac trauma
-
cardiac tamponade
fluid compresses cardiac filling and impairs cardiac output
-
Class presenation of pericarditis
- pleuritic substernal radiating CP relived by sitting updright and leaning forward
- friction rub
-
Typical presentation of cardiac tamponade
- tachycardia
- tachypnea
- narrow pulse pressure
- pulsus paradoxus
-
Electrical alternans
patho for effusion
-
Tx of pericarditis
- if hemodynamic compromise, pericardiocentesis
- steroids or NSAIDs
-
M/c causes of infectious endocarditis
- staph aureus
- Group D strep
- enterococci
- HACEK
-
m/c cause of infectious endocarditis in drug users
staph
-
m/c valve infected in infectious endocarditis in drug users
tricuspid
-
M/c cause of prosthetic valve endocarditis
staph
-
Classic presentation of infectious endocarditis
- palatal, conjunctival, or subungual petechiae
- splinter hemorrhages
- osler nodes
- janeway lesions
- roth spots
-
Roth spots
exudative lesions on the retina (infectious endocarditis)
-
Janeway lesions
painless red lesions on the palms or soles (infectious endocarditis)
-
Osler nodes
Painful, violaceous, raised lesions of the fingers, toes, or feet (infectious endocarditis)
-
infectious endocarditis workup
- three sets of blood cultures at least 1 hour apart before starting abx
- TEE
- CXR
-
Duke criteria
- Infectious endocarditis
- 1 major/1 major, 1 minor/three minor
- Major: two positive blood cultures, evidence of endocardial involvement on echo, development of new regurgitant murmur
- Minor: predisposing factor, fever >38.8C (100.4), vascular phenomena, immunologic phenomena, positive blood culture not meeting major criteria
-
Tx of infectious endocarditis
- Empiric abx at first (vanco plus ceftriaxone)
- abx prophylaxis
-
Rheumatic fever
systemic immune response occuring usually 2-3 weeks following strep pharyngitis
-
Age group m/c implicated in rheumatic fever
5-15 yo
-
Typical lesion of valve in rheumatic fever
Pervascular granuloma with vasculitis
-
M/c valve involved in rheumatic fever
Mitral, followed by aortic
-
Jones criteria
- rheumatic fever
- Two major or one major and two minor
- Major: carditis, erythema marginatum, subcutaneous nodules, choera, polyarthritis
- Minor: fever, polyarthalgias, reversible prolongation of PR interval, rapid ESR, CRP
-
Tx of rheumatic fever
- Strict bed rest until stable
- ASA for fever and joint problems
- Corticosteroids for joint sx
- IM PCN for documented strep infection (erythromycin if PCN allergic)
-
Prevention of recurrence of rheumatic fever
benzathine PCN q4w
-
m/c pattern of PAD
- Type 3
- affects aorta, iliac, femoral, popliteal and tibial arteries
-
First sx of PAD
loewr leg pain with exercise that is relieved with rest (intermittent claudication)
-
leriche's syndrome
ED in the presence of iliac artery disease
-
Acute arterial occlusion of lower extremities
- pain
- pallor
- pulselessness
- paresthesias
- poikiloterhmia
- paralysis
-
Lab findings in PAD
ABI < 0.9 indicates significant disease
-
Tx of PAD
- Progressive exercise
- Lipid loewring meds
- Pletal is main tx (Cilostazol)
- Antiplatelet therapy in all pts without CI
- Tx ED
- Thromboendarterectomy, embolectomy, thrombolytic therapy,
-
m/c vein affected in varicose veins
long saphenous
-
Tx of varicose veins
- Graduated elastic stockings
- Leg elevation and regular exercise
- Tx of ulcers
- radiogrquency or laser ablation, compression sclerotherapy, surgical stripping of vein
-
Thrombophlebitis
Partial or complete occlusion of vein and inflammatory changes
-
superficial thrombophlebitis causes
- spontaneous or following trauma
- frequently at PICC sites
-
M/c location of DVT
lower extremities and pelvis
-
Presentation of superficial thrombophlebitis
- dull pain, erythema, tenderness, and induraction of involved vein
- no sx
-
m/c location for superficial thrombophlebitis
long saphenous vein
-
Classic presentatio of DVT
swelling of involved area with heat and redness over site
-
Preferred study for DVT
- duplex US
- d-dimer...if neg, no need for US
-
most accurate method for definitive dx of DVT
venography, but it has increased risk and is rarely needed
-
Tx of superficial thrombophlebitis
bed rest, local heat, elevation of extremity, and NSAIDs
-
Tx of DVT
LMWH, or hep followed by warfarin
-
Chronic venous insufficiency
Loss of wall tension in veins, which results in stasis of venous blood
-
Common comorbidities with chronic venous insufficiency
- DVT
- leg injury
- varicose vein
-
Presentation of chronic venous insufficiency
- Progressive edema starting at the ankle
- itching, dull pain with standing and pain with ulceration
- skin is shiny, thin, atrophic with dark pigmentary changes and subcutaneuos induration
-
Tx of chronic venous insufficiency
elevate legs, avoiding sitting or standing for long periods of time
-
Tx of stasis dermatitis
- wet compresses and hydrocortisone cream
- if chronic, add zinc ocide with ichthammol and an antifungal cream
-
GCA
inflammatory condition involving medium and alrge vessels
-
Lab findings in GCA
- high ESR and CRP
- normochromic normocytic anemia and thrombocytosis
- some have elevated alk phos
-
M/c cause of aortic aneurysm
atherosclerosis
-
Causes of aortic aneursym
- atherosclerosis
- congenital
- syphilis
- GCA
- vasculitis
- trama
- Marfans/Ehler-Danlos
-
M/C location for aneursym
Abdominal
-
Most effective medication for converting atrial tachycardia to NSR
Ibutilide
-
Mitral stenosis often occurs with what cardiac problem in pts with a hx of rheumatic heart disease?
Tricuspid stenosis
-
Side effects of CCBs
HA and peripheral edema
-
First degree AV block tx
None, just monitor
-
Best HL drug in pregnancy
Welchol (Coleselvem)
-
When should ASA and antiplt medicines be stopped in the event of a major surgery?
D/C 5-7 days prior to surgery
-
m/c EKG findings of ASD
RAD
-
radiation of aortic insufficiency murmur
LLSB, apex
-
Pulsus paradoxus
- decrease in systolic arterial pressure of greater than 10 mmHg.
- accentuation of the normal decrease in systolic arterial pressure of less then 10mm Hg that normally accompanies inspiration
-
How to better hear MVP
have pt stand
-
causes of high output heart failure
- Beriberi
- severe IDA
- Thyrotoxicosis
- AV shunting
-
-
What is the most common clinical cardiac abnormality that is associated with acute rheumatic heart disease?
Carditis
-
tx of chronic SVT
flecanide
-
management of WPW syndrome
flecanide
-
According to the most recent American College of Cardiology/American Heart Association Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation MI recommendations, an EKG should be performed on patients with a clinical suspicion for acute coronary syndrome within how many minutes of their arrival to the emergency department?
10 mins
-
Prinzmetal's angina is common with what comorbidities?
migraine cephalgia and Raynaud's phenomenon
-
causes of bigeminy
thiazide diuretic use leading to hypokalemia
-
In MI pts, how soon should they have PCI?
Within 90 mins of sx
-
Classic presentation of ASD
fixed and widely split S2, a right ventricular heave, and a systolic ejection murmur present.
-
How do you increase HDL in low risk pt?
exercise
-
Two electrolyte disorders that can inflict a ventricular tachycardia?
Hypomagnesia and hypokalemia
-
tx of new onset aflutter in pts with hx of mitral disease
wafarin plus cardioversion
-
-
tx of prinzmetals angina
CCB and long term nitrate therapy
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