Cardio

Question 1

Infections of the cardiovascular system: myocarditis, pericarditis, endocarditis

Answer 1

Ok

Question 2

Myocarditis

Answer 2

Inflammation of the myocardium that results in myocardial injury via cytoplasmic effect or secondary to immune system response

Question 3

Myopericarditis

Answer 3

Extension of myocarditis into the pericardium

Question 4

Clinical features myocarditis

Answer 4

Excessive fatigue or exercise intolerance

Chest pain

Unexplained sinus tachycardia

S3, s4, or summation gallop

Abnormal ecg and echo

New cardiomegaly on chest radiograph

Atrial or ventricular arrhymia

Partial or complete heart block, new onset bundle branch block

New onset or worsening heart failure

Acute pericarditis

Cardiogenic shock

Sudden cardiac death

Respiratoy distress/tachypnea

Hepatomegaly

Question 5

Differential diagnosis myocarditis

Answer 5

Acute MI v acute and/or chronic heart failure v. Atypical chest pain v pericarditis v cardiomyopathies v valvular disease

*not all encompassing

Question 6

PE myocarditis

Answer 6

Soft s3/s4 (impaired ventricular function), new murmur (secondary to valvular insuffiency-variable), pericardial friction rub (if there is extension into pericardium)
*think systolic CHF (decreased contractility )-orthopnea, dyspnea on exertion, crackles, dyspnea, paroxysmal nocturnal dyspnea

Question 7

Work up myocarditis

Answer 7

EKG

Cxr

Question 8

Ekg myocarditis

Answer 8

Assess for arrhythmia (sinus tachycardia most common), transient ST-T wave abnormalities. Findings nonspecific

Question 9

CXR myocarditis

Answer 9

Patient is presenting with chest pain and.or symptoms of heart failure-must consider all etiologies espicially: pulmonary disease, heart failure, dissection. Assess for cardiomegaly

Question 10

Echocardiogram

Answer 10

Assessment of ventricular function and structure. Evaluation of ejection fraction, left ventricular size, wall option abnormalities

Question 11

PCR

Answer 11

Detection of viral genome

Question 12

Labs

Answer 12

CBC (possible leukocytosis), cardiac enzymes (likely elevated secondaryocyte damage), BNP (signs and sx of heart failrue), CPK (assessing muscle damage), (ESR and CRP (acute phase reactants)

Question 13

___ biopsy can aid in a definitive diagnosis

Answer 13

Endomyocardial

Question 14

Complications myocarditis

Answer 14

Dilated cardiomyopathy
Myopericarditis

Sudden cardiac death (20%)

Question 15

Treat myocarditis

Answer 15

Heart failure therapy (depending on clinical presentation), therapy for arrhythmias

• beta blocker, ACEI, diuretics are feasible options
• avoid NSAIDS, EtOH, exercise (restricted)

Prognosis is dependent upon clinicopatholigc types of myocarditis

Question 16

Infection etiologies myocarditis

Answer 16

Coxsackie B, trypanosome cruzi, trichinella spiralis

Question 17

Cocksackie B (picornaviridae, enterovirus) myocarditis

Answer 17

+ SsRNA, small, naked, icosahedral

Peak incidence summer and fall

Fecal oral transmission

Question 18

Manifestations coxsackie B

Answer 18

URI, pleurodynia (devils grip-severe intercostal pain and fever), myocarditis (most common infectious etiology), aseptic meningitis

Question 19

How get trypanosome Cruzi

Answer 19

Reduvviid, animal

Question 20

Where is trypanosome cruzi

Answer 20

Southern US, Mexico, SA

Question 21

What is trypanosome cruzi

Answer 21

Intracellular Protozoa (hemoflagellate)

Question 22

Phases of chagas

Answer 22

Acute-1 month

Intermediate

Chronic-years-decades to develop

Question 23

Diagnose trypanosome cruzi

Answer 23

Peripheral smear for trypmastigotes, xenodiagnosis

Question 24

Acute chagas

Answer 24

Chagoma, romana sign

Fever, malaise, LAD

CV-myocarditis

CNS-severe meningoencephalitis (young patients)

Question 25

Intermediate chagas

Answer 25

Asymptomatic

Question 26

Chronic chagas

Answer 26

CV: dilated cardiomyopathy, arrhythmias Megacolon, achlasia

Question 27

Trichinella spiralis

Answer 27

Invasive nematode

Question 28

How get trichinella spiralis

Answer 28

Ingestionof cysts from raw pork (boars or even horses) | Humans are dead end host

Question 29

Trichinella in human

Answer 29

Larvae develop in gut->mate->larvae disseminate hematogenous lh->penetrate muscle tissue Skeletal muscle, heart brain

Question 30

Invasive cycle trichinella spiralis

Answer 30

With heavy infection can be lethal

Question 31

Symptoms trichinella spiralis

Answer 31

Abdominal pain, diarrhea, fever (while in small intestine) | Muscle invasion: muscle aches, other sx dictated by location of larvae invasion

Question 32

When consider trichinella spiralis diagnosis

Answer 32

Periorbital edema, myositis, eosinophilis

Question 33

Diagnostics for trichinella spiralis

Answer 33

Serologic (ELISA) or latex agglutination, CPK levels, muscle biopsy

Question 34

Pericarditis

Answer 34

Inflammation of the pericardium

Question 35

Infectious agents of pericarditis

Answer 35

Viruses, bacteria, TB (caseating pericarditis), fungi, parasites

Question 36

Presentation pericarditis

Answer 36

Chest pain (sharp, often positional and pleuritic in nature, relieved by leaning forward), fever, palpations

Question 37

DDx considerations

Answer 37

Acute coronary syndrome (STEMI v NSTEMI v unstable angina) v ischemic heart disease v aortic dissection v pulmonary embolism v pneumothorax c cardiac tamponade v mediastinitis v gerd v gastric/duodenal ulcer v musculoskeletal (rib fix muscle spasm, costochondritis) v psychiatric (panic attack, anxiety) v cocaine induced vasospasm

Question 38

PE pericarditis

Answer 38

Friction rub upon cardiac auscultation, rapid or irregular pulse. Secondary to extensive differential considerations, complete cardiac and pulmonary exams are essential

Question 39

Work up pericarditis

Answer 39

EKG CXR Echo Labs

Question 40

EKG

Answer 40

Diffuse ST elevations with reciprocal depressions in leads aVR and V1 with PR depression

Question 41

CXR

Answer 41

Majority of CXR with pericarditis show minimal abnormalities Exception-pericardial effusion>250 mL will cause a symmetrically enlarged cardiac silhouette. Water bottle sign

Question 42

CXR

Answer 42

Pericardial effusion (visible) with water bottle sign. Notice flattening of the diaphragms to compensate for the weight of the effusion

Question 43

Echo pericarditis

Answer 43

Pericardial effusion (visible) with water bottle sign . Notice flattening of the diaphragms to compensate for the weight of the effusion

Question 44

Echo pericarditis

Answer 44

Assess for pericardial effusion and/or tamponade. More sensitive than a CXR

Question 45

Labs pericarditis

Answer 45

Cardiac enzymes (serial), CBC with differential, ESR, CRP, blood cultures if temp over 38@

Question 46

Complciations pericardiis

Answer 46

Cardiac tamponade-treated with pericardiocentesis | *counsel about activity restrictions

Question 47

Treat pericarditis

Answer 47

High dose asprin TID (ibuprofen, indomethacin) and colchicine

Question 48

What is contraindicated in pericarditis

Answer 48

Anticoagulants

Question 49

Infectious agents pericarditis

Answer 49

Cocksackis B (serous pericarditis), mycobacterium TB (caseous pericarditis)

Question 50

Cocksackis B

Answer 50

Picornaviridae, enterovirus | +SsRNA, small naked icosahedral

Question 51

Transmission cocksackis B

Answer 51

Fecal oral

Question 52

Manifestations cocksackie B

Answer 52

URI, pleurodynia (devils grip-severe intercostal pain and fever), myocarditis(mostcommon infectious etiology), aseptic meningitis

Question 53

Mycobacterium tuberculosis

Answer 53

Acid fast (weakly G+), obligate aerobes, facultative intracellular (macrophages) AFB secondary to mycotic acid cell wall composition (highly resistant to desiccation including NaOH)

Question 54

Virluence mycobacterium Tb

Answer 54

Facultative intracellular, sulfatides, cord factor, surface protein can cause a deflated hypersensitivity and cell mediated immunity reaction (utilized for PPD skin testing ) wax d

Question 55

Stains mycobacterium BT

Answer 55

Acid fast (ziehl-neelsen, Kenyon)-red rods Auramine-rhodamine staining-fluorescent apple green color

Question 56

Manifestation mycobacterium Tb

Answer 56

Pulmonary tuberculosis | CAN cause a caseating pericarditis through direct lymphatic of hematogenous dissemination of the bacteria

Question 57

Infective endocarditis

Answer 57

Infection of the cardiac valves or endocardium that leads to development of vegetations and destruction of underlying cardiac tissues. The majority of IE cases are bacterial in nature and are further subdivided into acute v subacute presentations

Question 58

Risk factors IE

Answer 58

Age>60 M>F, poor dentition, IV drug abuse, structural heart disease, congenital heart disease, valvular heart disease, provalve replacemnt, rheumatic heart disease

Question 59

Clinical manifestion IE

Answer 59

Manifestation can be variable and generally dependent on the virluence of the organism involved Constitutional symptoms: onset of symptoms can be nonspecific in nature and then progress towards fever, chills, weight loss, new/worsening murmur, fatigue, arthralgias and myalgia

Question 60

Acute IE

Answer 60

Rapid and life threatening progression of symptoms and cardiac damage High fever, chills, weakness, SOB, pleuritic chest pain

Question 61

Subacute IE

Answer 61

Slow, indolent course Low grade fever, weight loss over time, fatigue, arthralgias/myalgia

Question 62

Complciations IE

Answer 62

CHF, abscess formation, hematogenous spread, embolism, systemic immune reaction , death

Question 63

Cardiac manifestations IE

Answer 63

Heart murmurs-new or worsening Acute IE-R side of heart> left side of heart (Tricuspid>aortic, espicially with s aureus involvement) Subacute IE-L side of heart> R side of heart

Question 64

Diagnostic work up IE

Answer 64

Blood culture x3 (always prior to abx!!!!), CBC with diff, CMP EKG, ESR, CRP, UA (assess for hematuria Transesophageal echocardiogram, CXR

Question 65

Major criteria for IE duke

Answer 65

Blood culture + with consistent microorganisms from 2 separate blood cultures At least two positive >12 hr apart or lll of the three or

Question 66

Definite diagnosis

Answer 66

2 major criteria or 1 major and 3 minor criteria or 5 minor criteria

Question 67

Treat IE

Answer 67

Cardiogenic shock-surgery Toxic0start empiric abx Obtain BCx first and foremost then initiate empiric ABx *vancomycin with or without gentamicin Culture and sensitivities will determine how to tailor treatment-may not be necessary to initiate empiric antibiotic therapy for subacute infective endocarditis Can be best to wait for culture and sensitivities to target specific organisms

Question 68

Give high risk patients prophylactic before dental or respiratoy procedures

Answer 68

Able to take PO-amoxicillin IV-ampicillin or cefazolin or ceftriaxone Allergic to penicillin -desensitize, cephalexin, clindamycin, azithromycin

Question 69

Common infectious agents of IE

Answer 69

S aureus, s epidermis, s viridans, enterococcus(D strep) HÁČEK, coxiella burnetti, brucellosis , s agalactiae0rare

Question 70

S aureus

Answer 70

G+ cocci, clusters, coagulate and catalase positive, facultative anaerobes Normal flora on skin (can breach) and colonize nasopharyngeal

Question 71

Virluence s aureus

Answer 71

Host cell invasion! Protein A-prevents opsonization by binding Fc or IgG Coagulate-forms fibrin clot around organism Catalase-breaks down H2O2 Hemolysis-destroy RBC Leukocydins-destroy WBC

Question 72

Invasion of tissue and blood stream s aureus

Answer 72

Hyaluronic ASD-breaks down CT Staphylokinase-lyse s formed clots Lipase-breaks down fat

Question 73

Toxin mediated manifestations

Answer 73

Food poisoning, scalded skin syndrome, toxic shock syndrome

Question 74

Local manifestations of s aureus

Answer 74

Skin-impetigo, cellulitis, folliculitis, furuncles, carbuncles Respiratory-pneumonia

Question 75

Systemic manifestations s aureus

Answer 75

Acute-endocarditis, meningitis, osteomyelitis (#1 cause in adults and children), septic arthritis

Question 76

Thx s aureus

Answer 76

Will vary based off of clinical presentation. For systemic disease, vancomycin is an exceptional choice. For MSSA-nafcillin is a great stating point

Question 77

Signs of acute endocarditis from s aureus

Answer 77

Fatigue, chills, fever, night sweats, dyspnea, CHF,

Question 78

Streptococcus viridans

Answer 78

G_ cocci in chains, a hemolytic (green zone), catalase negative, facultative anaerobes, optochin resitstant, normal oral flora, nasopharynx, GI tract Extracellular dextran binds heart valves

Question 79

Manifestations strep viridans

Answer 79

Dental caries, subacute endocarditis

Question 80

Treat strep viridans

Answer 80

Penicillin

Question 81

Staph epidermidis

Answer 81

Coagulate negative staph CoNS G_ coccci, clusters, coagulate negative, catalase positive, novobicin sensitive, facultative anaerobes Normals skin flora

Question 82

Virluence staph epidermidis

Answer 82

Adhesion polysaccharide capsule-adherence to prosthetic devices, indwelling catheters Biofilm formation

Question 83

Manifestations s epidermidis

Answer 83

Subacute endocarditis, infection bacteria in neutrophil patients (susceptible)

Question 84

Treat staph epidermidis

Answer 84

Vancomycin (very antibiotic resistant)

Question 85

Enterococcus (group D strep) | Enterococcus faecalis

Answer 85

Gram + cocci, catalase negative, facultative anaerobes, variable hemolytic nature (alpha or gamma) Normal human bowel

Question 86

Virluence factor enterococcus

Answer 86

Extracellular dextran helps bind heart valves

Question 87

Manifestations enterococcus

Answer 87

Subacute bacterial endocarditis, UTI, biliary tract infections

Question 88

Media requirements enterococci

Answer 88

Can grow 40% bile AND 6.5% NaCl , blood agar

Question 89

Treat enterococcus

Answer 89

Vancomycin resistant forms on the rise

Question 90

Non enterococci group D strep

Answer 90

Strep Boris -associated with colonic ancer and IBD) G+ cocci in chains, catalase negative, facultative anaerobes, variable hemolytic nature (a or y)normal flora in human bowel

Question 91

Virluence non enterococci group d strep

Answer 91

Extracellular dextran helps bind heart valves

Question 92

Manifestations non enterococci

Answer 92

Biliary tract infections, UTI, subacute bacterial endocarditis

Question 93

Media non enterococci

Answer 93

40% bile , blood agar

Question 94

HÁČEK

Answer 94

Gram - group of bacilli, fastidious, suspected cause of culture negative endocarditis Part of normal flora

Question 95

Media HACEK

Answer 95

Chocolate agar

Question 96

HACEK

Answer 96

Haemophilus (H parainfluenza most likel to cause endocarditis) Aggregatibacter sp Cardiobacterium sp Eikenella corrodens Kinde;Lola sp

Question 97

Manifestation HACEK

Answer 97

Subacute endocarditis rare

Question 98

Recall Haemophilus sp have the ability to be grown on ____ (contains factors v and x, aka NAD and Hemin). Haemophilus sp cant grow on ___ (exception-will show stellate growth on blood agar if placed on same place as s aureus. Why? S aureus has the virluence factor hemolysis-lyse s RBC)

Answer 98

Chocolate agar Blood agar

Question 99

Coxiella burnetti

Answer 99

G- pleomorphic, obligate intracellular, aerobic, zoonotic, aerosol transmission

Question 100

Symptoms coxiella burnetti

Answer 100

Q fever is a flu like sickness caused by the germ coxiella burnetti. Goats, sheep, cows and other animals carry it It is inside cell Animals spread the germ when they give birth. People who help animals give birth such as farmers and vets have higher chance of getting Q fever Wind can carry barnyard dust mixed with Q fever germs for miles. You may get sick when breath it in even if not near animals

Question 101

Cardiac rhythm disturbances (atrial, junctional, ventricular)

Answer 101

Ok

Question 102

Principles

Answer 102

Treat patient no ECG Establish urgency of treatment and treat reversible causes Access hemodynamically stability (LOC< BP< HR) Antiarrhythmic/electrical therapy

Question 103

Arrhythmias

Answer 103

Symptoms, palpitations-skin, pounds, irregular Lightheadness-faint-like Syncope (near syncope), chest pain, dyspnea, sudden death

Question 104

Etiology arrhythmias

Answer 104

Stress Ischemia (CAD), MI, HF Hypoxia , PE, COPD Metabolic acidosis Infection-endocarditis, RF Inflammation-myocarditis, pericarditis Cardiomyopathy/alcohol’ chemo Electrolytic imbalance 9low, k mg ca) Drugs -caffeine, nicotine, thyroid, aminophylline, otc, cocaine, HTN

Question 105

Sinus tachycardia

Answer 105

Physiologic/pathological process Look for the cause Emotion, anxiety, fear, drugs, hyperthyroid Fever, pregnancy, anemia, CHF Hypovolemia Rx-underlying cause

Question 106

Sinus node

Answer 106

Normally, the dominant cardiac pacemaker bc ofits intrinsic discharge rate is the highest of all potential cardiac pacemakers Bradycardia<60 bpm

Question 107

Medical conditions situations associated with bradycardia

Answer 107

Normal ppl Healthy athlete-well trained, good endurance Physiologic component to sleep, fright, carotid sinus massage, carotid hypersensitivity, avoid tight collars, shave neck lightly, massage or ocular pressure (glaucoma), mental control-yoga training Obstructive jaundice-effect of bile salts on SAN Sliding hiatal hernia Valsava maneuver-lifting heavy objects, straining bowels Disease of the atrium or SAN-CAD(inflammation, neoplasm, cardiomyopathy, muscular dystrophy, amyloidosis) Drugs and electrolytes(digitalis, quinidine, hyperkalemia, drugs used for HTN mech is to inhibit sympathetic tone like clonidine, methyldopa, reserpine. Also beta blockers propranolol metoprolol Acute inferior MI (increased vagal tone, NV Ischemia Decrease O2, increase CO2, decrease pH, increase BP, SSS, convalescence from god toxicity

Question 108

Causes of bradycardia

Answer 108

Sinus bradycardia Non conducted atrial bigeminy Sino atrial block AV block-incompete or complete - sinus rhythm with 2:1 - sinus tach with 3:1 - sinus rhythm or tach with complete block - a flutter with complete block - a fib with complete block Sinus arrhythmia-SAN forms impulses irregularly - waxes/wanes with phases of respiration - HR increase with inspiration - HR decrease with expiration - sinus arrhythmia is a normal finding

Question 109

EKG of sinus bradycardia

Answer 109

P wave represents formation of sinus impulses, each atrial impulse is followed by a ventricular beat - rate <60 min - p wave of sinus origin (Norma axis) - constraint and normal PR interval (.12-.2 - constant P wave confirugation in each lead - regular or slightly irregular PP cycle or RR Yale

Question 110

EKG SSS-tachy-Brady

Answer 110

EKG SB S arrest SA block -slow junctional rhythm seen in ischemic, sclerotic, inflammatory changes in SAN may cause syncope, dizziness, fatigue, heart failrue

Question 111

Treat sinus bradycardia

Answer 111

Depends on clinical setting and cause -may not need to be treated Depends on hemodynamics/impaired Depends on circulation - maybe no or a few symptoms-no RX - if hemodynamically compromised may get combination of-low BP - low CO, SV, renal perfusion-oliguria - SOB, decreased cerebral profusion-confusion - CP, cool, clammy, diaphoresis - syncope, dizziness - fatigue Commonly see SB in acute inferior MI-espicially in the 1st few hours. This is related to SN ischemica or to a vagal reflex initiated int he ischemic area RX is HR <45-50 with hemodynamic compromise/unstable acute situations

Question 112

What treat sinus bradycardia with

Answer 112

Atropine Epinephrine Isoproterenol Pacemaker

Question 113

Atropine

Answer 113

2 mg IV for SB and repeat 10 min Use caution in glaucoma can increase IOP-narrow angle AE-urinary retention, and distention, transient

Question 114

Epinephrine for SB

Answer 114

2-10 ug.min

Question 115

Isoproterenol for SB

Answer 115

1 mg in 500 cc D5Q-1-4 ug/min IV

Question 116

What is automaticity

Answer 116

Idk

Question 117

Atrial arrhythmias

Answer 117

Premature atrial contraction (PAC) also APC Seen in absence of significant heart disease; associated with stress, alcohol, tobacco, coffee, COPD, and CAD

Question 118

Premature beat of atrial arrhythmia

Answer 118

An irritable focus spontaneously fires a single stimulus - premature atrial beat - premature junctional beat - premature ventricular beat

Question 119

SA node resets in step with __

Answer 119

Premature atrial beat

Question 120

Premature atrial beat with aberrant ventricular conduction

Answer 120

Wide QRS

Question 121

Non conducted premature atrial beat

Answer 121

No QRS

Question 122

PAC

Answer 122

A single complex occurs earlier than the next expected sinus complex After the PAC, sinus rhythm usually resumes

Question 123

Rhythm PAC

Answer 123

Irregular

Question 124

P wave PAC

Answer 124

Present, may have different shape

Question 125

normal in PAC

Answer 125

PR -varies or normaland WRS

Question 126

Clinical PAC

Answer 126

In patients with heart disease, frequent PAC ma precede paroxysmal supraventricular tachycardia, a fib or a flutter

Question 127

Treat PAC

Answer 127

If symptomatic - reverse causes - beta adrenergic antagonist (BB) - metoprolol 25-50mg BID-TID

Question 128

Paroxysmal atrial tachycardia

Answer 128

Sudden heart rate greater than 100 | -rate irritable focus P wave

Question 129

PAT with block (AV block)

Answer 129

Greater than one P/QRS complex; 2 p waves for each QRS Suspect digitalis toxicity Rapid rate, spiked P waves 2:1 ratio of P: QRS

Question 130

Multifocal atrial tachycardia

Answer 130

3 or more different p waves PR interval varies Irregular ventricular rhythm Atrial rate>100 Associated with lung disease (COPD, pneumonia, ventilator, theophylline, beta agonist, electrolyte abnormalities (decreased K, decrease MG( digitalis toxicity, sepsis Irregular rhythm -P wave shape varies, atrial rate excessds 100, irregular ventricular rhythm

Question 131

Mat treat

Answer 131

DC theophylline IV MG SO4 2 grams in 50 cc saline over 1 min, then 6 grams in 500 cc saline 6 hours IV verampamil

Question 132

Treat MAT-focus on underlying cause

Answer 132

CCD-nondihydropyridine-to control vent rate and dec. ectopic atrial impulses Dilitazem 20 mg IV then 5-15 mg/hr drip Verampamil 2-10 mg IV (avoid if EF<40%) MgSO4 2 grams IV over 1 min, then 1-2 grams/hr, amiodarone.adenosine. Cautions ith bb (pulmonary problems). Digitalis isn’t helpful and DC cardioversion isn’t effective

Question 133

ECG a fib

Answer 133

Atrial rate>350-600/min -multiple foci discharging rapidly Undulating baseline No p wave Irregular RR interval Irregularly irregular ventricular rhythm Irregular continuous chaotic atrial spikes Irregular ventricular rhythm

Question 134

Atrial flutter

Answer 134

Saw tooth appearance Leads II, III, AVF< V often best leads 250-350/min

Question 135

Identifying a flutter may require

Answer 135

Inverting the tracing Or employing a vagal maneuver

Question 136

Junctional (nodal) rhythma

Answer 136

Paroxysmal junctional tachycardia 150-250 /min P wave may be lost , inverted before or after each QRD Sudden, irritable junctional focus paces rapidly

Question 137

Junctional foci inherent rate

Answer 137

40-60 min

Question 138

Premature ventricular contractions (PVC VPC) etiology

Answer 138

Normal heart CAD, MI, HF, myocardial ischemia, hypoxia Valvular heart disease, congenital heart disease Cardiomyopathy, electrolyte abnormalities Acid base imbalance Hyperthyroid Drugs

Question 139

Premature ventricular contractions ECG

Answer 139

Premature, wide, bizarre QRS No preceding p wave; may produce a retrograde o wave in ST segment ST-T wave moves in opposite direction of QRS Usually full compensatory

Question 140

Principles of treatment ventricular rhythm disturbances: causes

Answer 140

Consider the setting -normal, stress, hypoxia Drugs -nicotine , caffeine, thyroid, aminophylline, digitalis, intonation Heart failure Acute MI Ischemic hear disease Cardiomyopathy Electrolyte disorder -hypokalemia, hyperkalemia, hypomagnesemia

Question 141

Treat PVC

Answer 141

If stable no RX: if symptomatic or in setting of ACS-metoprolol 2.5-10 mg IV If unstable-amiodarone, lidocaine (1-1.5 mg/kg up to 3 mg/kg), procainamide

Question 142

Ventricular tachycardia

Answer 142

3 or more consecutive bizarre QRS complexes Ventricular rate 120-200 (100-250) Usually regular, wide QRS (>.12 sec) P wave often lost; if seen no relationship to QRS (AV dissociation) Lasts longer than 30 seconds (sustained) Fusion beats (dressler) Capture beats

Question 143

V fibrillation

Answer 143

Disorganized depolarization Not effective pump Clinical setting-AMI, HF< K disturbance (low or high)

Question 144

V flutter

Answer 144

250-350 per minute Sine waves Leads to v fib

Question 145

Torsades de pointes

Answer 145

Twisting of the points QRS swings from positive to negative direction May be inherited (prolonged QT) or acquired (class I, II, antiarrhythmatias, alchol, TCA, electrolyte imbalance-K, Ca, Mg)

Question 146

Treat tdp

Answer 146

MgSO4, 1-2 grams IV bolus Overdrive pacing Isoproternol

Question 147

Electrolyte disturbances (K, Ca, Mg)

Answer 147

Altered milieu

Question 148

K disturbance

Answer 148

Low; lowers resting membrane potential Enhances automaticity High; raises resting membrane potential, slows conduction, widens QRS

Question 149

Calcium disturbances

Answer 149

Low; prolongs QT (torsades) High: shortens QT Acidosis Reduces threshold for VF Sensitized myocardium to re entrainment arrhythmias

Question 150

Hypokalemia

Answer 150

Very common in hospital or office From diuretics, metabolic alkalosis (transcellular shift of K into cell), high aldosterone (conns Cushing), beta agonist overdose, diarrhea, renal loss

Question 151

ECG hypokalemia

Answer 151

U waves, inc QT interval, flat or inverted T wave

Question 152

Hyperkalemia etiology

Answer 152

Renal failure (insuffiency), metabolic acidosis, DKA, cell breakdown (hemolysis, rhamdomyolysis) ECG -peaked T wave, wide QRS, inc PR interval, loss of P wave

Question 153

Hypocalcemia

Answer 153

Chronic renal failure, vitamin D defiency, hypoparathyroidism, acute pancreatitis, hypomagnesium ECG-prolongation of QT interval (QTc corrected for rate)

Question 154

Hypercalcemia

Answer 154

Hyperparathyroidism, malignancy, granulomatous disorders (TB sarcoidosis), endocrine disorders (adrenal insuffiency, hyperthyroid) ECG-short QT, short ST

Question 155

HypoMg

Answer 155

Poor nutrition, alcoholism, dec absorption, renal magnesium loss, diuretics ECG-long Pr, wide QRS, long QT, dec T wave

Question 156

Hypermg

Answer 156

Renal failure, magnesia containing drugs

Question 157

Hyperkalemia

Answer 157

Mild to moderate (K 5-7) Tall, symmetrically peaked T waves with a narrow base More severe (K=8-11 ) QRS widens, PR segment prolongs , P waves disappears; ECG resembles a sine wave in severe cases

Question 158

Hypokalemia

Answer 158

ST depression T flattening

Question 159

Hypercalcemia

Answer 159

Shortened QT interval due to a shortened st segment

Question 160

Hypocalcemia

Answer 160

Prolonged QT interval due to a prolonged ST segment. T wave duration normal

Question 161

Digitalis

Answer 161

ST depression T wave flattening on inversion Shortened QT interval, increased U wave amplitude

Question 162

Quinidine -procainamide Disopyramide Phenothiazines Tricyclic antidepressants

Answer 162

Long QT , mainly due to prolonged T wave duration With flattening or inversion QRS prolongation Increased U wave amplitude Diffuse, wide, deeply inverted T waves with prolonged QT

Question 163

Hypothermia

Answer 163

Temp <35 C Slow heart rate (bradycardia) J wave (Osborne wave) J point elevationwith a characteristic of an early ST segment. Slow rhythm, baseline artifact due to shivering often present

Question 164

Pulmonary embolus

Answer 164

Sudden dyspnea+clear lung+x ray=PE Tachycardia Nonspecific ST-T changes ECG- S1, Q3, T3 T wave inversion V1-V4 Transient RBBB

Question 165

Cerebral hemorrhage

Answer 165

Impressive ST T changes

Question 166

Hypothyroidism

Answer 166

Whenever you see widespread flattening or mild inversion of T waves without associated ST segment displacement, always think of hypothyroidism about 50% of the time, the hunch will be correct Other most constant ECG finding in myxedema is low voltage of the QRS complex. Sinus bradycardia, though often mentioned is less often seen

Question 167

Wolf parkinson

Answer 167

Short PR interval Slurred upstroke (delta wave) of QRS complex Accessory AV conduction pathway (bundle of Kent)

Question 168

Valvular heart disease Dr. Khalid

Answer 168

Ok Recognize the etiologies, of valvular heart disease Discuss auscultation findings associated with VHD Discuss the valvular causes of systolic, diastolic and continuous murmurs

Question 169

Valvular heart disease

Answer 169

20 million in USA Age dependent 3-6% of those>65 ``` Symptoms -dyspnea on exertion (most common) -angina -syncope -palpitations Fatigue, edema, ascites ```

Question 170

Most common conditions encountered today

Answer 170

Degenerative (calcification) Myxomatosis degeneration (MVP) Congenital (bicuspid aortic valve) Decline in incidence of rheumatic valvular disease*huge decline just in immigrant or visitors

Question 171

Valves affect by pressure or volume overload. Or by disease process. Like what..often multiple valves

Answer 171

Heart failur, endocarditis, rheumatic fever

Question 172

Stenosis

Answer 172

Impedes forward flow Stenosis, sclerosis, fibrosis, calcification Leads to pressure overload; hypertrophy and heart failure As and MS

Question 173

Regurgitation

Answer 173

Failure to close adequately (leaks) Reversal of flow Insufficiency, incompetitence Leas to volume overload; dilates AI and MR

Question 174

Types of VHD

Answer 174

Congenital Acquired/calcification of mitral annulus Valvular dysfunction depends on tempo of disease onset (acute/chronic *** how disease presents atria size?) Example: IE-aortic cusp destruction; acute AI Example: RHD complications develop over years; compensatory mechanism

Question 175

Rheumatic heart disease

Answer 175

Due to RH Females 4:1 Caused by group A strep infection (pharyngitis) virtually only cause of acquired MS(can be congenital)

Question 176

Jones criteria

Answer 176

Rheumatic Example: myocarditis, pericarditis Carditis-inflammation of heart muscle 1. fever 2. arthralgia 3. increased seed rate of CRP 4. Leukocytosis 5. Prolonged PR internal 6. Elevated ASO titer

Question 177

Symptoms RHD

Answer 177

Migratory olyarthritis (large joints like knees hips) Subcutaneous nodules-painless , over bone and tendon Sydenham’s chorea (st virus dance)-rapid purposeless movement of face and arms Arythema marginatum

Question 178

Diagnose RHD (CRP not specific for inflammation lots have)

Answer 178

Two major criteria or one major and two minor criteria Minor 1. Fever, arthralgia, increased seed rate or CRP, leukocytosis, ECG prolonged PR, elevated ASO or antiDNASEb Major . Carditis, migratory polyarthritis, subcutaneous nodules, chorea, erythema marginatum Myocarditis, pericarditis, carditis-inflammation of heart msucle????

Question 179

Mitral stenosis

Answer 179

Normal MV orifice 4-6cm^2 Fusion of mitral commissures leads to narrowing; MVA of 1-1.5 cm^2 or less equals severe MS that leases to pulmonary HTN, RVF Narrowing leads to increased left AV pressure gradient ; LAE (a fib , pul vascular changes, RVH) MAC, chest radiation

Question 180

Mitral stenosis

Answer 180

4th decade, fatigue associated with decreased CO DOE, cough orthopnea, PND, pulmonary edema, hemoptysis, arterial emboli, a fib PHT with RHF-edema

Question 181

Ortner syndrome

Answer 181

Hoarseness d/+ compression of left recurrent laryngeal nerve

Question 182

PE mitral stenosis

Answer 182

Malar rash-ruddy cheeks (pulm color-red) or blue facies(CO2 retention assoicated with PHT; vasodilation effect) Increased Lou’s S1, increase s2 (P2 if PHT is present) Opening snap after S2 (if leaflet is mobile) S2-OS interval is short if severe MS Diastolic, low pitch, decrescendo, rumbling murmur.

Question 183

How hear mitral stenosis

Answer 183

Use bell Diastolic, low pitch, decrescendo, rumbling murmur. Best heard at apex with patient in left lateral decubitus position Best heard at apex Low rumble

Question 184

Why could th patient develop progressive symptoms to RVF Malar face rash kid

Answer 184

Ok

Question 185

Case: 48 yo female with fatigue, exertional dyspnea, hoarseness, orthopnea and hemoptysis. Progression of symptoms over past 3 months. Smoker x 20 years Told she has a heart murmur since adolescence. Also remembers that she had arthritis as a pre teenager PE hoarseness noted with a raspy voice. Coughed often during exam with streaks of blood in sputum Mild JVD at 45 degrees(from right ventricle, increased right heart volume) while lying down Heart irregularly irregular rhythm (MEANS A FIB), rate 90 bpm Increase S1 S2 Loud P2-pulmonary HTN Diastolic murmur Increase S1 P2 Lungs-basilar crackles (has to be left (MS aortic stenosis) heart if think lungs involved) Mild moderate peripheral edema of lower hepatomegaly

Answer 185

*smoker is distactor its not COPD MS ECG-a fib and left atrial enlargement

Question 186

Mitral stenosis treat

Answer 186

Anticoagulation if in a fib-prevent stroke Percutaneous balloon valvuloplasty MVR (replacement) Progressive symptoms-possible RVF RVFfailure-see ascites low extremity edema

Question 187

RVF symptoms progressive from MS

Answer 187

Patients get increase LA pressure, pulmonary HTN, pulmonary edema, hepatomegale, ascites, peripheral edema Blood back!

Question 188

A fib ecg

Answer 188

No p wave QRS to QRS is different Irregularly irregular rhythm

Question 189

Left atrial enlargement

Answer 189

Look at V1 first part in normal person is most predominate and biphasic is small If see negative portion larger than 1 small square Biphasic and f

Question 190

Right atrial enlargement

Answer 190

V2 lead 2?

Question 191

Atria hypertrophy?

Answer 191

Not really always dilates bc so thin

Question 192

Vent hypertrophy and dilate

Answer 192

Either

Question 193

Did diagnosis for case

Answer 193

MS (diastolic rumble), a fib, hoarseness, ortner syndrome, RF-arthritis A fib-left atrial enlargement cause which is secondary to MS Ortner Possible pulmonary disease from smoking

Question 194

Look at left border of heart if see straightening

Answer 194

Left atrial enlargement

Question 195

Do we anticoagulatns this patient

Answer 195

Yes they have a fib bc of risk of emboli

Question 196

Treat MS

Answer 196

Anticoagulant if in a fib;risk emboli Percutaneous balloon valvuloplasty (mitral commissions); success rate 95% MVR (replacement) Progressive symptoms-possible RV

Question 197

Chronic mitral regurgitation

Answer 197

MVP-most common etiology/myxomatous or degenerative MV | MAC (mitral annular calcification

Question 198

Acute Mitral regurgitation

Answer 198

Rupture of chordal tendineae Rupture of papillary msucle Ischemic papillary muscle dysfunction-(CAD/MI: next most common cause of MR) IE; valve perforation

Question 199

Chest x ray mitral regurgitation

Answer 199

Pulmonary edema

Question 200

Acute MR

Answer 200

Inc. LA pressure abruptly; pulmonary edema, LVF

Question 201

Chronic MR

Answer 201

Generally well compensated ECG-LAE MAC 2% pop

Question 202

Symptoms mitral regurgitation

Answer 202

Asymptomatic years-> fatigue, DOE Acute; volume overload add LV dilation, LA HTN, PHT, RVF/orthopnea, PND, RHF/LHF Acute MR can present with cardiogenic shock

Question 203

PE mitral regurgitation

Answer 203

Systolic murmur(blowing, holosystolic; may be mid late systolic best heard at apex, use diaphragm Radiated into left axilla Loudness of murmur correlates with severity Decreased S1 or normal; may have a systolic click if due to MVP Valsava moves click and murmur closer to S1 , murmur increases with hand grip

Question 204

Treat mitral regurgitaiton

Answer 204

Vasodilator-afterload reduction (nitroprusside) Decrease resistance to flow (decrease aortic impedance and MR to improve CO) ACE inhibitors-chronic MR IABP-decreases afterload; helps to perfuse coronary arteries Surgery for acute severe MR

Question 205

Case: 54 SOB hyperlipidemia, HTN, diabetes, comes in chest pain , oethopnea, one episode PND, hard breathing, tachycardia, irregular pulse, RR high, JVD 45% O2 84%, loud systolic murmur at apex S3 gallop

Answer 205

Ok

Question 206

Loud systolic murmur at apex

Answer 206

Mitral regurgitation

Question 207

S3 gallop

Answer 207

Heart failure

Question 208

Differential

Answer 208

CAD Murmur of mitral regurgitaiton Chest pain MI Acute MI complicated by acute LVF Ischemic papilalry msucle dysfunction causing acute MR

Question 209

What test

Answer 209

Ecg, MR Chest x ray Cardiac enxymes up

Question 210

MR turbulent flow one chamber to another

Answer 210

Regurgitaiton

Question 211

ECG inferior MI

Answer 211

ST elevation on II III AVF RCA supplies papillary muscle causing mitral regurgitaiton

Question 212

Cardiac enzymes MI

Answer 212

Markers for MI Troponin T and I; more sensitive and specific than CK-MB Elevated in 4-6 hours; peak 8-12 hours Elevated for 5-7 days Creatinine phosphokinase-rise 4-8 hours; peak 24 hours. Return to normal 48-72 hours CKMB isoenzymes more specific for MI; also elevate in myocarditis, cardioversion and CKD

Question 213

MVP

Answer 213

One or both mitral leaflets will prolapse into LA during systole to cause MR/redundant tissue/myxedematous degeneration: elongated chordate 7:1 female Associated with marfans/skeletal changes

Question 214

Symptoms MVP

Answer 214

Asymptomatic to arrhythmias (SVT, PVC, VT), chest pain , syncope Systolic murmur; may have systolic click RX-if hyper adrenergic state (anxious, palpitations), consider beta blocker Valve repair favored over replacement

Question 215

Case 24 yo palpitations, chest pain, murmurs ith click, hypothyroid, tachycardia, RR high, restless, high arched palate, brownish pigmented mole R side of neck, heart systolic murmur (grade 2-3/6) at apex with radiation into L axilla. (THIS IS MITRAL REGURGITATION with MVP) S2 normal Lung clear Long arms and legs High arched palate Straight back

Answer 215

Differential Palpitations SVT, TC, PVC< MVP R/O hyperthyroid, R/O collagen abnormalities Echo ecg, holter,TSH, free T4, CXR

Question 216

Treat MVP and thyroid disorder | MVP with mitral regurg

Answer 216

B blocker for hyper state | Regulate thyroid meds

Question 217

Aortic stenosis

Answer 217

Normal AoV area is 4 cm^2 Degeneration of valve (calcific or senile) most common/aging 3% persons >65 Congenital or acquired bicuspid aortic valve (BAV)/1% population; 75% develop AS/2-10% AI Rheumatic, post inflammatory scarring (radiation)

Question 218

Pathophysiology AS

Answer 218

Obstruction leads to pressure overload: LVH increase LVED pressure, diastolic dysfunction, systolic heart failure Gradient across valve >40 mmHg Different pressures Severe AS if AoV>1cm^2 LV! Not in mitral stenosis

Question 219

Symptoms AS

Answer 219

6th decade-exertional dyspnea, angina, syncope, heart failure (If before 60 bicuspid) Without treatment prognosis is poor Without treatment most will die within three years of developing syncope and within two years of onset of HF Die 5 years angina 3 syncope 2 CHF

Question 220

PE AS

Answer 220

Narrow pulse pressure; decreased SV and systolic pressure Delayed pulses - parvis (weak, decreased amplitude due to decreased CO) - tarsus (late, delayed, dec carotid upstroke) Dec A2, SYSTOLIC MURMUR HARSH 2nd INTERCOSTAL SPACE ON RIGHT SIDE (hear bettter here bc pulmonary artery and aorta criss cross), radiated into Supra sternal notch/carotids Gallavardin phenomenon-murmur radiated to apex (like MR)

Question 221

How see LVH on ecg

Answer 221

V5 v6 high Will happen in aortic stenosis

Question 222

LVH in aortic stenosis

Answer 222

Ok

Question 223

Treat AS don’t work just temporary relief

Answer 223

Balloon valvuloplasty-bridge therapy to TARV or surgery (surgical valve replacement is gold standard) TARC (transcatheter aortic valve replacement -for symptomatic , trileaflet AoV sclerosis with high surgical risk. No AI Surgery and TARV operative mortality 1-3%

Question 224

60 yo male DOE, substernal discomfort related to activity. The chest discomfort is usually relieved by rest; one time he took a nitroglycerin and he obtained relief PMH HTN, hyper lipid, peripheral vascular disease, smoker HCTZ statin, circulation pill for legs, albuterol MDI, prn, dyspnea Bp up, RR high, O290%(not good) JVP. Bit raised 30 degrees, Decreased carotid upstroke bilaterally (AS) PMI 5th 6th on left side (VH) Palpable thrill and heave, loud murmur, raspy Systolic murmur 4-6 with 3nd ICS radiated into substernal notch and carotids systolic murmur (AS) Expirations wheezes-COPD smoker

Answer 224

Concerns-CAD, diabetes, Need-PE, ecg, echo, chest x ray Differential=AS, angina, HTN, hyperlipidemia, probable COPD Wheezes-can get from COPD of heart failure, all wheezing is not COPD can also be heart failure, but not all heart failure wheezes Tests-ekg, echo, CXR, cardiac enzymes, Echo AoV-1cm^2 (normal is 4 cm, anything 1 or below is severe AS) Diagnosis severe AS

Question 225

Treat severe symptomatic AS

Answer 225

Valve replacement No med can give

Question 226

Aortic regurgitaiton

Answer 226

Due to leaflet abnormalities (bicuspid AoV, IE) Due to aortic root abnormalities (marfan syndome, aortic dissection, aging, HTN)

Question 227

What causes acute AR

Answer 227

IE, aortic dissection, BAV, chest trauma, balloon valvuloplasty

Question 228

Causes of chronic AR

Answer 228

Syphilis, ankylosis spondylitis, ascending aortic dilation, BAV, calcfic degeneration, rheumatic, chest radiation

Question 229

Pathophysiology regurgitation

Answer 229

Volume overload can increase LVEDV, LVH, left sided HF; SOB fatigue , angina

Question 230

Symptoms aortic regurgitaiton

Answer 230

Depends on rapidity of onset-due to compensatory mechanism onset

Question 231

Acute aortic regurgitaiton

Answer 231

IE, aortic dissection/acute pulmonary edema, cardiogenic shock

Question 232

Chronic aortic regurgitation

Answer 232

Develops over time/dyspnea, orthopnea, PND, chest pain

Question 233

PE aortic regurgitaiton

Answer 233

Wide pule(diastolic low systolic high) De musket sign Corrigans pulse Quince pulse Trouble sign Durozrey sign Hills sign Bisferious pulse Diastolic, decrescendo murmur 3rd ICS LSB Systolic murmur usually present, soft Austin flint murmur; can mimic MS

Question 234

Crescendo decrescendo-AS? Blowing murmur

Answer 234

Ok

Question 235

Treat aortic regurgitation

Answer 235

ARB-decrease afterload to decrease regurgitation volume Surgery AoVR (replace or repair ) when symptomatic or EF<50-55%

Question 236

Cause 72 yo male ankylosis spondylotis Started over right SI pint with pain at rest, which originally improved on ambulation. Over time progressively developed thoracic kyphosis and stiffness of lumbar spine. You have not appreciated any cardiac problems when he firs became your patient Past 12 moths complained of fatigue, exertional dyspnea, two pillow orthopnea and one to two episodes of PND in the past 30 days(developing symptoms) BP high, O2 sat 90% Slight rhythmical movement of the head with the heart bears Systolic and diastolic murmur over a partially compressed peripheral artery (from wide puls pressure) Heart-grade 2/6 diastolic, blowing murmur over 2nd -3rd ICS LSB no s3 or s4 gallop S1 normal s2 dismissed(comes from aortic valve closure if regurg will be soft) Lung-decreased breast sound Kyphosis and decreased flexion, SB and extension of lumbar spine

Answer 236

Concern-heart failure? Progressive ankylosis sponyltois with aortic regurgitaiton Aortic regurg De mussel-head bob Durozrey-to and fro murmur over artery Echo CT of chest-why for ankylosis spondylitis and aortic regurg to look for disections want to see aortic root

Question 237

Valvular heart disease treatment

Answer 237

Reserved for when symptomatic

Question 238

Tricuspid stenosis

Answer 238

Associated with MS, TR, and RHD Can be associated with carcinoid, ergot agents (cabergoline)

Question 239

Pathophysiology tricuspid stenosis

Answer 239

Prominent A wave in JVP ascites, hepatomegalia (may pulsate)

Question 240

Hear tricuspid stenosis

Answer 240

Diastolic, low pitch, decrescendo, murmur LSB; increase with inspiration (Corvallis sign) and decrease with expiration and valsava

Question 241

Diastolic murmur apex

Answer 241

MS

Question 242

Diastolic murmur left sternal border

Answer 242

Tricuspid stenosis

Question 243

Every right valve disease

Answer 243

Intensity increase with inspiration due to increase intrathoracic pressure, increased venous return so murmur increase on right side

Question 244

Tricuspid regurgitation

Answer 244

Common, functional, asymptomatic Associated with pulmonary HTN (COPD , Cor pulmonale, RVF), RV infarction, inferior MI, pacemaker, endocarditis, congenital trauma V wave in JVP, palpable RV lift , pulsating liver Blowing holosystolic murmur LSB, 4th ICS, increase with inspiration (Corvallis sign) due to increase venous return

Question 245

A wave JVP

Answer 245

Tricuspid stenosis V wave-tricuspid regurgitation during systolic

Question 246

Pulmonary stenosis

Answer 246

Atresia, congenital, can cause angina, syncope,

Question 247

Auscultation pulmonary stenosis

Answer 247

Systolic crescendo-decrescendo murmur, ejection click 2nd 3rd ICS, LSB/radiated toward left shoulder clavicle and increases on inspiration/RVH

Question 248

Association pulm stenosis

Answer 248

TOF TGA

Question 249

Treat pulmonary stenosis

Answer 249

Balloon commissural to my if pressure gradient>50mmHg

Question 250

Cause pulmonic regurgitation

Answer 250

Most due to pulmonary HTN

Question 251

Sound pulmonic regurgitaiton

Answer 251

Diastolic, decrescendo blowing murmur 2nd LSB Increase P2 if PHT

Question 252

Systolic murmu

Answer 252

MR (MVP), TR - AS, PS - VSD

Question 253

Autopulmonary shunts murmur

Answer 253

Early mid late, holosystolic/pansystolic

Question 254

Diastolic murmur

Answer 254

AR, PR | -MS, TS

Question 255

Atrial myxoma

Answer 255

Murmur plop

Question 256

Continuous murmur

Answer 256

PDA-machinery* AV fistula ASD with high LA pressure Coarctation

Question 257

AV blocks

Answer 257

Ok

Question 258

What is an AV block

Answer 258

In the cardiac conduction system that causes a disruption of atrial-to-ventricular electrical conduction

Question 259

What are the types of AV blocks and fasciculus blocks

Answer 259

First degree Av Second degree AV Third degree AV Fasciculus blocks (hemiblocks) Left anterior hemiblock Left posterior hemiblock

Question 260

Primary AV block

Answer 260

Prolongs AV node conduction | PR interval more than .2 sec.

Question 261

ECG 1st degree block

Answer 261

P wave precedes QRS complex PR interval >.2 s (>5 small boxes) Normal PR interval (.12-.2 s) Minor AV conduction defect with delay at or below AV node

Question 262

Etiology of 1st degree AV block

Answer 262

Presence of atherosclerosis, HTN, diabetes enhances chances Degeneration of conduction system/fibrosis congenital heart disease CAD-ischemia Drugs-BB, CCB, digitalis, antiarrhythmias (class I and III) Endocrine-hypothyroid, hyperthyroid, adrenal insuffiency Inflammatory-RF, SLE, MCTD, myocarditis Infiltrating-amyloidosis, sarcoidosis, hemochromatosis Valvular calcification-mitral, aortic

Question 263

How calculate regular rhythm

Answer 263

Count the number of large boxes between P waves (atrial rate), R waves (ventricular rate), or pacer spikes (pacemaker rate) BPM=300 divided by the number of large boxes

Question 264

2nd degree block types

Answer 264

Mobitz I Mobitz II

Question 265

Second degree av block

Answer 265

Progressive PR-Interval Prolongation prior to dropped QRS Grouped beats

Question 266

Mobitz I

Answer 266

Progressive lengthening results from earlier arrival in relative refractory period AV conduction Implies impairment of AV conduction (AV node) Transient

Question 267

Etiology mobitz I

Answer 267

All those things that cause 1st degree AV block Digitalis toxicity Ischemic events (MI inferior) Myocarditis

Question 268

2nd degree AV block -mobitz

Answer 268

May be seen with inferior AMI Level of block is at level of AV node Narrow QRS complex

Question 269

Etiology 2nd degree AV block-mobitz type II

Answer 269

Ischemic heart disease May be seen with acute anterior myocardial infarction Degeneration of conduction system

Question 270

2nd degree AV block, mobitz type II mobitz

Answer 270

``` PR interval uniform Dropped beat (QRS) -P wave fails to conduct ``` This block occurs at level of - bundle of HIS - both bundle branches - fasciculus branches Progressive/irreversible *may be seen with anterior AMI bc block is distal to AV; worse prognosis

Question 271

Features of high AV block

Answer 271

Crest of AV node blocker Junctional escape rhythm narrow QRS, adequate rate (40-55) Right coronary artery disease, diaphragmatic infarction, edema around AV node Preceded by mobitz I second degree AV

Question 272

Low AV block

Answer 272

Bundle of His, bilateral bundle branch , or trifascicular Ventricular escape rhythm Wide QRS Inadequate rate (20-40) Danger of asystole or ventricular tachycardia Left anterior descending coronary artery disease, large large anteromedial infarction, or chronic degeneration of conduction system Mobitz II second degree

Question 273

Third degree heart block (complete heart block)

Answer 273

P waves never related to QRS complexes Two independent rhythms -AV dissociation-no P waves conduct to the ventricle Can occur above or below Av node Above-junctional rhythm, narrow QRS (rate 40-55_ Bellow-ventricular pacemaker wide QRS (rate 20-40

Question 274

Etiology 3rd degree heart block

Answer 274

Ischemic Infiltrating diseases Cardiac surgery - by pass, valve replacement - myocarditis - degenerative

Question 275

How do you treat 3rd degree block

Answer 275

Pacemaker

Question 276

What check on every ECG

Answer 276

PR interval - increased consistently in primary AV block - progressively increases in each series of cycles with wenckenbach - totally variable in third degree block - decreased in WPW and LGL syndromes P without QRS response - weckebach and mobitz 2 AV blocks - third AV block-independent

Question 277

R

Answer 277

As impulse travels toward the electrode +

Question 278

S

Answer 278

As impulse travels away from the electrode - deflection

Question 279

In normal ventricular conduction, what is the origin of a small q wave in V5 and V6

Answer 279

Q wave is first downward deflection after the p wave and the first element in the QRS complex. Negative deflection of QRS complex It is the net direction of early ventricular depolarization projects toward the negative pole of the lead axis in question

Question 280

The septum is activated from _ to _

Answer 280

L to R L septal surface activated .1 s before R septal surface

Question 281

Why normal ventricular muscle activated L to R

Answer 281

Right wall is thinner than L wall, therefore the impulse activates the epicardium of the RV before the LV The LV pericardial surface is activated from apex to base

Question 282

Intrinsic deflection

Answer 282

Time lapse from beginning of the QRS to the peak of the R wave The time that lapses from the beginning to the QRS complex to the peak of the R wave is measured horizontally Measure time when impulse reaches the pericardial surface of ventricle

Question 283

What is intrinsic deflection for V1 and V2

Answer 283

V1 .02 s V2 .04 s

Question 284

What does it mean if it takes longer for the ID to start downward,

Answer 284

The impulse is late in reaching the pericardial surface Late ID in: a. BBB b. Hypertrophy/dilated

Question 285

Common features of BBB

Answer 285

Wide QRS complex (.12 s or greater) ST segment -T waves slope off in opposite direction to QRS

Question 286

Which side of the septum is activated first in RBBB

Answer 286

Left

Question 287

In RBBB is there an S wave in V6?

Answer 287

Ok

Question 288

Sequence of ventricular activation in RBBB

Answer 288

After septal activation, then activation begins in LV free wall

Question 289

RsR’ variants in V1-V2

Answer 289

Normal Pertussis or straight back RV diastolic volume overload WPW syndrome RVH Du henna dystrophy

Question 290

In lead V1 why is there a small r wave morphology in RBBB

Answer 290

Ok

Question 291

Sequence of ventricular activation in LBBB

Answer 291

Septum activated from R side, nearly same time as RV is activated Strong septal forces, therefore neg. deflection in V1 (QS) Positive deflection V6-monophonic R

Question 292

LBB more apt to occur with

Answer 292

HTN Ischemia Aortic stenosis Cardiomyopathy

Question 293

LBBB with LAD

Answer 293

More myocardial dysfunction More disease in conduction system Maybe higher mortality

Question 294

LBB with RAD

Answer 294

Think congestive cardiomyopathy

Question 295

Limb leads in BBB

Answer 295

I and AVL usually have features of V6

Question 296

T wave in BBB

Answer 296

Polarity is opposite QRS direction

Question 297

What causes secondary T wave changes T wave in BBB

Answer 297

Disturbance in depolrepol

Question 298

If t wave polarity is in the same direction of the QRS complex, it is called __ t wave change, usually due to ____

Answer 298

Primary Ischemia

Question 299

In LBBB which ventricle is activated first

Answer 299

Right

Question 300

Hemiblock/fasciculus block

Answer 300

Term for blockage of one of two main divisions of left bundle branch

Question 301

Left bundle branch

Answer 301

Anterior division (superior) Posterior division (inferior)

Question 302

Hemiblocks

Answer 302

Left anterior hemiblock (LAH)-more common Left posterior hemiblock (LPH)

Question 303

Etiology of LHA

Answer 303

Disease in conduction system Often associated with MI (left anterior descending-LAD occlusion)

Question 304

Criteria for LAH

Answer 304

Left axis deviation (usually >minus 60 degrees; others> minute 45 degrees)

Question 305

ECG LAH

Answer 305

Small Q in leads I and AVL Small R in leads II, III and AVF Usually normal QRS duration or slightly widened Q1S3 (Q in I and S in III)

Question 306

Anterior hemiblock

Answer 306

LAD-usually associated with MI (or other heart disease Normal or slightly widened QRS Q1S3

Question 307

Etiology of left posterior hemiblock -less common

Answer 307

Disease in conduction system

Question 308

Criteria of left posterior hemiblock

Answer 308

RAD >120 degrees Small R in leads I and AVL Small Q in leads II, III, AVF S1Q3 (S in I and Q in III) No evidence of RVH

Question 309

What causes atrial enlargement

Answer 309

Increase in volume of blood int he chamber or Increase in resistance to blood flow out of chamber Volume overload or diastolic overload-dilation Pressure overload or systolic overload-causes hypertrophy Good leads I II III V1 RA activated first LA actiavated later

Question 310

P wave

Answer 310

Depolarization of atria Doesn’t exceed 3 mm Increased amplitude-hypertrophy, HTN, AV valve disease, Cor pulmonale, congenital

Question 311

P of RAE

Answer 311

Tall, pointed; taller in III than in I | P-pulmonale

Question 312

P of LAE

Answer 312

Wide, notched; taller in I than in III P-mitrale 2nd half of p wave negative in V1 of III

Question 313

RAE

Answer 313

Associated with TV disease or pul HTN COPD , PE, MS, or MR are causes of pul HTN

Question 314

Right atrial enlargement (RAE)

Answer 314

P-pulmonale peaked p wave with amplitude greater than .25 mv (2.5 mm) in leads II, III AVF and greater than .1 mv in leads V1 and V2

Question 315

LAE

Answer 315

Left atrial enlargement , P mitral M signs to P wave , broad, notched P wave duration .11 sec and amplitude of terminal negatively directed portion in V1 to greater than .1 mv or 1 mm deep and .04 sec wide with slight acid of o wave

Question 316

Causes LAE

Answer 316

MS MR

Question 317

Ventricular hypertrophy (enlargement)

Answer 317

Ventricles dilate in response to receiving excess volume of loot during diastole and become hypertrophied INR esponse to exerting pressure in ejecting the blood during systol

Question 318

Left ventricular hypertrophy

Answer 318

Most common cause is HTN. Other causes include AS, AI, hypertrophic cardiomyopathy and coarctation of aorta Wall of LV is thicker so impulse will take longer to transverse it and arrive at pericardial surface Voltage and interval of QRS complex will increase, producing deeper S waves over RV and taller R waves over LV

Question 319

ECG pattern LVH

Answer 319

Fails to distinguish between concentric hypertrophy and dilated chamber; use the term ventricular enlargement. It is the total muscle mass of the ventricle that mainly determines the QRS voltage

Question 320

Criteria for LVH

Answer 320

Lack sensitivity (low 40-50%) but are specific (high 90%)

Question 321

Romhilt estes scoring system for LVH

Answer 321

5 LVH 4. Probable LVH 1. 3)R or S in limb lead 20 mm or more S in V1 V2 or V3 25 mm or more R in V5 V6 30 mm or more 2. (1)Any ST shift (without digitalis Typical strain STT(with digitalis) 3. (2)LAD 30 or more 4. (1)QRS interval .09 sec or more 5. (1)ID in V5-V6 .04 sec or more 6. (3) P terminal force in V1 with more than .03 sec in duration >1 mm in depth

Question 322

Sokolow lyon criteria

Answer 322

R in I and S in III>25 mm R in AVL >11 R in V6>26 mm

Question 323

Right ventricular hypertrophy cause

Answer 323

Cause-COPD RVOT obstruction, VSD Congenital-TOF< pulmonic stenosis, transposition of great vessels Mitral stenosis, tricuspid regurgitaiton

Question 324

ECG RVH

Answer 324

R waves assume prominence in right precordal leads and deep S waves develop in left precordial leads R:S ration>1

Question 325

Clues to RVH

Answer 325

RAD +90 degree or more R in V1 7 mm or more R in V1 +S in V6 10 mm or more R/S ration in V1>1 mm or more S/R ration in V6>1 or more Late intrinsicoid deflection in V1 (.03 of more) Incomplete RBBB ST-T strain pattern in II, III, AVF P pulmonale S1 S2 S3 pattern (kids)

Question 326

Causes of dominant r waves in V1

Answer 326

RVH Posterior or lateral MI WPW Hypertrophic cardiomyopathy Muscular dystrophy Normal variant

Question 327

CAD general comments

Answer 327

Heart disease remains the leading cause of mortality int he USA Ischemia heart disease is now the leading cause of death worldwide 1.5 million Americans currently have CAD 25% with CAD die suddenly ; no previous manifestations Atherosclerosis is underlying cause of CAD and 90% of cases of MI and most of heart failrue

Question 328

What happens with atherosclerotic coronary arteries from plaques

Answer 328

Can undergo... Fissuring or erosion Triggers thrombus formation to cause ischemia to myocardium

Question 329

Risk factors for atherosclerosis

Answer 329

Hyperlipidemia-high LDL, low HDL, high TG, high lipoprotein ; 1% decrease LDL decreases risk of CAD by 1-.1% increase HDL decreases risk of CAD by 2-3% -31 million have total cholesterol greater than 240 mg/dl Smoking-benefit decreases risk of being non smoker afte 10 years Diabetes mellitus-AHA/major risk factor; increased CVD risk 2-4 times/CVD risk equivalent HTN Family history of coronary heart disease, ischemic stroke or peripheral vascular disease -ethnicity increased risk in Alaska natives, American Indians and Pacific Islanders Obesity Physical inactivity (need 10-60 min med intensity 4-7 days/week Stress Sleep problems Age and gender (male>55 female >65

Question 330

Metabolic syndrome

Answer 330

Insulin resistant-increased glucose HTN High TG, low HDL Hyperuricemia Hyper coagulation Obese BMI>30-central obesity Desireable : BMI 21-24 BMI=weughtx705/height

Question 331

Angina pectoris

Answer 331

``` Chest discomfort (chest pain) Term angina (Latin origin; Angkor animifear of life being extinguished from the breast) ``` Most frequent expression of myocardial ischemia Chronic stable angina: is a consequence of imbalance between oxygen supply demand Low risk of plaque rupture (small lipid core and thick fibrous cap_

Question 332

Supply angina

Answer 332

Decreased oxygen delivery to tissue leads to ischemia

Question 333

Example supply angina

Answer 333

Coronary vasoconstriction, stenosis, platelets release serotonin and thromboxane A2

Question 334

Demand angina

Answer 334

Increased myocardial oxygen requirements and workload can lead to ischemia

Question 335

Examples of demand angina

Answer 335

Exercise, stress, emotion, fever, thyrotoxicosis LVH due to As Anemia (low oxygen carrying capacity)

Question 336

Effects of ischemia

Answer 336

Mechanical consequences Biochemical consequences Electrical consequences

Question 337

Mechanical consequences ischemia

Answer 337

Angina, is ischemia is prolonged or develop coronary occlusion, may lead to myocardial necrosis Segmental akinetic bulging (dyskinesia)

Question 338

Biochemical consequences ischemia

Answer 338

Fatty acids can’t be oxidized Increased lactate production Reduced pH with metabolic acidosis

Question 339

Electoral consequences ischemia

Answer 339

Inversion fo T wave Transient displacement of ST segment Depression-subendocardial -elevation-subepicardial Electrical instability instability; VT, VF

Question 340

LAD MI

Answer 340

Anterior wall infarction Leads V1-V7

Question 341

RCA MI

Answer 341

Inferior wall infarction (RV infarction) Leads II, III, AVF

Question 342

Circumflex artery MI

Answer 342

Lateral wall Leads I, AVL

Question 343

Posterior descending artery

Answer 343

Posterior wall infarction | V1-V3

Question 344

CV causes of chest pain

Answer 344

Ischemic heart disease (angina , UA, ACS, MI), VHD, pericarditis, myocarditis, cardiomyopathies

Question 345

Non cardiac cause of chest pain

Answer 345

Pleuritis/pneumonia/PE Pulmonary infarction, pneumothorax, GI GI disease: GERD, PUD, gallstones, esophageal motility disorder chest wall syndromes Lung cancer Aortic aneurysm

Question 346

Non chest pain symptoms of chronic ischemic heart disease

Answer 346

Dyspnea, non chest locations of discomfort (((exertional or rest) Mid epigastric or abdominal Diaphoresis Excessive fatigue and weakness Dizziness and syncope

Question 347

Anginapectoris why exercise effect it

Answer 347

Fixed CA stenosis/fixed O2 supply; produces ischemia bc of increased oxygen demand

Question 348

Angina equivalent

Answer 348

Due to ischemia, but described as dyspnea, fatigue, faintness and gastric educations (belching) Pathogenesis-schematic causing an elevated LV filling pressure that leads to pulmonary edema-diabetic , elderly, women

Question 349

Signs or risk factors for angina

Answer 349

Xanthelasma Xanthomas Diabetic skin lesion Nicotine stains Pale Absent peripheral pulses

Question 350

Angina

Answer 350

Abnormal cardiac impulse (LV dyskinesia) Bruits-carotid, abdominal area, femoral Gallop -S3, S4, both Systolic murmur of MR if papillary msucle is dysfunctional; associated with inferior or inferior posterior ischemia due to right coronary artery disease

Question 351

What can mimic angina in absence of CAD***

Answer 351

AS, AI, pulmonary HTN, hypertrophic cardiomyopathy, heart failure

Question 352

Unstable angina

Answer 352

New or worsening chest pain Tempo has changed, more severe, prolonged, more frequent; may occur at rest , awaken from sleep. Pain lasting longer than 20 minutes Using more medication for relief Less effort to provoke symptoms No evidence of myocyte necrosis (no elevation of tropI or CK-MB). Enzymes are normal

Question 353

Chest pain with elevation of cardiac enzymes (trop I or CK-MB) and without ST elevation is said to have a non st elevation myocardial infarction

Answer 353

NSTEMI

Question 354

Both UA and NSTEMI are called NSTEMI ACS or NSTE ACS

Answer 354

1.2 million US hospitalized a ACS 2/3 have NSTE ACS

Question 355

Pathology UA and NSTEMI

Answer 355

Most subjects with ACS have an atherosclerotic plaque rupture or erosion; platelet aggregation and thrombus leading to partial occlusion of artery

Question 356

Stable angina ecg

Answer 356

Normal in 50% (resting During angina attack may have displaced st segment; most common change is ST depression (subendocardial injury ischemia) May show old MI

Question 357

ECG unstable angina/NSTE ACS

Answer 357

Magnitude of st segment depression correlated with prognosis If ST segment depressed I mm or greater in 2 or more leads-almost 4x as likel yto die within 1 year If 2 mm or greater st segment depression-almost 6x likely to die within a year If St depression is 2 mm or greater in more than one region of ecg, mortality is 10 fold

Question 358

Differential diagnosis of NSTE ACS

Answer 358

PE-ecg changes, elevated troponin Aortic dissection VHD (AS, AI, hypertrophic cardiomyopathy) Myocarditis-pericarditis Stress cardiomyopathy (takostubo syndrome/broken heart syndrome) deeply inverted T wave

Question 359

Lab CAD

Answer 359

Cardiac enzymes-troponin I; detected in 2-4 hours in NSTEMI Increase CK-mB (3-6 hours) BNP-increase in BNP associated with increase mortality in NSTE ACS CRP-inflammatory biomarker CMP BUN, creatinine, liver panel, electrolytes, CBC, FLP

Question 360

Diagnostic testing for atherosclerosis

Answer 360

Functional and/or anatomical information for CAD

Question 361

Functional diagnostic testing for atherosclerotic CAD

Answer 361

Exercise ECG, single photon emission CT (SPECT, PET) Coronary flow (PET, fractional flow reserve) Wall motion abnormalities (echo, cardiac magnetic imaging CMRI)

Question 362

Anatomical diagnostic testing for atherosclerotic CAD

Answer 362

Invasive angiography, coronary CT angio (CTA) | -coronary artery calcium scoring (CAC) (note, CAC doesn’t provide data on coronary luminal narrowing

Question 363

Signs of high risk for coronary event

Answer 363

Positive stress test at low work load St depression greater than 5 minutes after completion of test Decrease in BP-syst fall>10 mmHg during exercise VT during exercise Reduced EF during exercise (stress echo

Question 364

Stress testing: exercise ECG

Answer 364

Exercise electrocardiography (preferred if patient is suspected to have angina) Safe... only 1 death or MI per 2500 tests

Question 365

Contradictions exercise ECG

Answer 365

Recent MI or acute MI, unstable arrhythmias, acute PE, aortic dissection, unstable angina, severe AS, decompensated HF, endocarditis, DVT

Question 366

Sensitivity and specificity exercise ECG

Answer 366

70% and 75% specific

Question 367

Stress echocardiography

Answer 367

Recommended when baseline ECG findings are abnormal or when area of myocardium is at risk with exercise or when patients can’t exercise

Question 368

Nuclear myocardial perfusion imaging

Answer 368

SPECT (single photon emission computer tomography) Useful in LBBB, LVH, digitalis effect Technetium 99

Question 369

Pharmacological stress test

Answer 369

Patient unable to exercise/abnormal ECG LBBB, LVH Use: vasodilator nuclear perfusion - adenosine/regadenosine/dipyridamole - vasodilators increase HR

Question 370

When use dobutamine echocardiogram

Answer 370

When patient cant exercise or when area of myocardium is at risk

Question 371

Coronary angiography

Answer 371

Cardiac cath Provides anatomic diagnosis of severity of CAD Percutaneous revascularization can be performed after study Exposed to radio contrast (kidney dysfunction

Question 372

Use of coronary angiography

Answer 372

Gold standard for anatomic definition of CAD Patients being considered by revascularization (CABG or PCI) PCI-90% successful; stent insertion CABG-for L main disease or 3 vessel disease

Question 373

Coronary CT angiography

Answer 373

Ability to quantify lesion severity can be limited by significant calcification

Question 374

CXR

Answer 374

Usually normal unless history of mi, HF< VHD Cardiomegalia in HTN< VHD, cardiomyopathy, pericardial effusion

Question 375

Treatment of patients with stable angina non pharm

Answer 375

Rule out and control aggravating conditions - associated noncardiac diseases - associated cardiac disease - use of drugs aggravating angina Smoking cessation Dietary counseling for body weight and lipid control Exercise prescription Treat to targets -HTN Lipids Diabetes

Question 376

Pharm treat to prevent MI/death/reduce symptoms

Answer 376

Asprin Beta blocker ACEI Statins Nitro/nitrates CCB

Question 377

Identify aggravating conditions

Answer 377

Obesity-weight loss consult dietitian HTN-treat to goal Hyperthyroid-meds, RAI Anemia-find cause and treat Smoking-cease Hyperlipidemia-statins Diabetes-ADA diet, oral agents, insulin

Question 378

Pharm treatment ASA

Answer 378

ASA:cyclooxygenase inhibitors of platelet activation Inhibit thromboxane production Clopidogrel blockers in ADP induced platelet aggregation

Question 379

Bb

Answer 379

Block binding of catecholamines to beta receptor Decrease HR, workload, contractibility, decreased BP and myocardial O2 consumption and demand, Decrease ischemia and symptoms Decrease CV mortliaty Prior MI

Question 380

Contraindication bb

Answer 380

Decompensated HF, hypotension, advanced AV block

Question 381

ACEI

Answer 381

Blocks conversion of A1 to A11 Decrease CV mortality Useful in diabetic (renal protection) and patients with LV systolic dysfunction

Question 382

Nitrates

Answer 382

Vasodilator of vascular smooth msucle; metabolized to NO to relax smooth muscle and coronaries Relieves ischemia and angina due to vasoconstriction Decrease preload and ventricular wall stress Nitrate intolerance; need 8-12 nitrate free interval

Question 383

What not take nitrate with

Answer 383

Phosphodiesterase inhibitor

Question 384

CCB

Answer 384

Doesn’t decrease mortality but Vasodilators; decrease workload, O2 demand, coronary vasospasm and reduced affected non dihydropyridines (verapamil and dilitazem) Decrease HR; verampamil negative inotropy effect Ranolazine-inhibits inward Na current and decrease intracellular calcium

Question 385

Myocardial revascularization

Answer 385

CABG for L main or 3 vessel CAD multivessel with LVEF<50% Decreases angina, MI, complications from revascularization procedures; improves survival PCI-1 or 2 vessel disease -stents

Question 386

Treat prinzmetal

Answer 386

Relieved by nitro Dihydropyridine CCB (amlodipine)

Question 387

Manage los risk patient

Answer 387

Antianginal - BB, nitro, CCB Statin Antiplatelet-ASA/clopidogrel Anticoagulant-UF heparin Cath:revascularization if appropriate

Question 388

High risk patient (US or NSTEMI) manag

Answer 388

Antianginal-BB, nitro, CCB Statin-plague stabilization Restore: endothelial function Antiplatelet-ASA/clopidogrel or prasugrel or ticagrelor glycoprotein inhibitor-11b/111a Time of catheter or PCI; blocks above platelet inhibitors tha impairs fibrinogen binding and inhibits platelet aggregation Anticoagulant-UFH or enoxaparin or bivalirudin or fondaparinux Cath: revascularization if appropriate

Question 389

Hyperlipidemia adult treatment panel (NCEP guideline III stricter target lipid levels)

Answer 389

For all patients with proper events, a CHD risk equivalent or a 10 year risk of 20% or greater the goals are: LDLc less than 70mg/dl HDLc greater than 60. If less than 40 do lipid analysis TG high is 120 mg/dl Total chol less than 200 mg/dl-A1% decrease in TC yields a 3% decrease in risk of CAD

Question 390

Statins for hyperlipidemia

Answer 390

``` ASA Nitrates B blocker ACE Ranexa inhibit late phase of inward Na current during repolarization; decrease angina occurrence ```

Question 391

Diet for CAD/angina to protect against atherosclerosis

Answer 391

Reduce calories with goal of ideal BMI Low saturated fat Low cholesterol High fibers Fish oil or fish Antioxidants-vit c 2 g na and reduce alcohol

Question 392

Shock

Answer 392

Tissue hypo perfusion and cellular hypoxia caused by Decreased O2 Decreased O2 utilization Increase O2 consumption Hypotension <80-90mmHg systolic Decrease systolic BP 40 mmHg below baseline MAP <60-65 mmHg

Question 393

Pathophysiology shock

Answer 393

Failure to deliver and utilize O2-anaerobic metabolism Increase O2 consumption (tissue demand) also anaerobic metabolism Anaerobic glycolysis leads to lactate Non compensatory response-pathologic results Vasodilators shock-unregulated NOS, interstitial fluid, cellular edema, impaired O2 diffusion, increase lactate->acidosis accompanies shock Lactate levels are reflection of tissue hypoxia If Do2 (systemic O2 delivery) failrue to meet O3 demand, develop O2 debt. Cellular inflammation and injury; irreversible/decompensated shock

Question 394

Skinextremities shock

Answer 394

Cool, clammy, cyanosis, mottled distally, decrease perfusion/vasoconstriction, dry mucous membranes, decrease skin turgor-seen in hypovolemia, cardiogenic, obstructive shock Warm and pink-associated with vasodilation of distributive/dissociative shock (cyanide poisoning)

Question 395

Neck veins shock

Answer 395

Distended (HF, PE, tamponade) Flare (hypovolemia)

Question 396

HR shock

Answer 396

Fast (sensitive indicator of shock); occasionally LO

Question 397

BP shock

Answer 397

Systolic low diastolic low

Question 398

Respiration shoc

Answer 398

Tachypnea, bronchospasm, respiratory failure

Question 399

Renal shock

Answer 399

Receives 20% CO; oliguria associated with vomiting, diarrhea, hemorrhage

Question 400

Heart shock

Answer 400

Pain: decrease coronary perfusion, ischemia, increase LVDP; mental status changes- decrease cerebral perfusion, confused, restless, agitated, delirious, stupor, coma -metabolic: respiratory alk (decrease pco2 breathing fast), followed by met acidosis (Na-(Cl=hCO3); frequently increased lactate-think shock; higher lactate=higher mortality

Question 401

Categories of shock

Answer 401

Hypovolemia shock Distributive shock Cardiogenic shock Extracardiac obstructive shock

Question 402

Hypovolemia shock hemorrhagic

Answer 402

Hemorrhagic: GI bleeding(varice ulcer diverticula), pelvic bleeding (post partum hemorrhage, vaginal hemorrhage), hemorrhagic pancreatitis, AVM

Question 403

Non hemorrhagic hypovolemia shock

Answer 403

GI losses (vomiting diarrhea), skin losses (burns, heart strokes)

Question 404

DKA hypovolemia shock

Answer 404

Renal losses (salt washing, osmotic diuresis) hypoaldosteronism, adrenal insuffiency, third space loss (pancreatitis, bowel obstruction (sequesteration of fluids), systemic inflammation

Question 405

Most common cause of hypovolemia shock

Answer 405

Hemorrhagic shock

Question 406

Treatment issues of volume loss

Answer 406

Depends on the circulating integrity (shock)-over zealous or too rapid correction -rate of replacement composition of replacement

Question 407

Fluid change

Answer 407

If in shock, rx fluids fast-monitor BP and tissue perfusion Crystalloids-Na (main cation) NS useful in hypovolemia from renal, GI, sweat, burns, hemorrhage D5-W equivalent to free water Packed RBC-for hemorrhage function is erythrocytes O2 carriage with delivery

Question 408

Shock class I

Answer 408

Lose 750 ml or up to 15% blood Normal bp Increased pulse pressure Give crystalloid

Question 409

Class II hemorrhagic shock

Answer 409

Lose 750-1500 ml of 15-30% blooc Bp normal Pulse pressure decreased Give crystalloid

Question 410

Class II hemorrhagic shock

Answer 410

Lose 1500-2000 ml blood Decrease bp Decrease pulse pressure Give crystalloid and blood

Question 411

Clas IV hemorrhagic shock

Answer 411

Over 2000 Decreased bp Decreased pulse pressure

Question 412

Distributive shock types

Answer 412

Septic or non septic (vasodilation) Most commoncause of non cardiogenic shock 230000 patients yearly 30-40% mortality

Question 413

Sepsis signs/symptoms

Answer 413

Fever, tachycardia (>90), tachypnea(>20 breaths), increase WBC 12000

Question 414

Common sources of infection distributive shock

Answer 414

Pulmonary-pneumonia, emphysema Ab-peritonitis, cholangitis GU-pyelonephritis, abscess CNS-meningitis Skin-cellulitis, necrotizing fasciitis

Question 415

Septic shock

Answer 415

Severe sepsis and dysfunction of organ systems (decrease O2, decrease UO, increase lactate, decrease platelets, decrease sensorium) -decrease BP <90 for systolic or >40 despite fluids

Question 416

Pathophysiology distributive shock

Answer 416

Tissue hypoxia activates inflammation Endothelial injury-release NO potent vasodilator Mediators of sepsis-endotoxin - cytokines (IL6, TNFa) - NO Microorganisms activate innate, adaptive, and endothelial immune responses and coagulation Endothelial injury-becomes permeable to leak fluids into tissue (lung, intestine, capillary leak) release NO2, potent vasodilator decrease preload Distributive-abnormal distribution of systemic blood flow In addition to vasodilation/microvascular vasoconstrictive tissue hypoxia->increase lactate

Question 417

Signs and symptoms of distributive shock

Answer 417

Extremities/skin-warm flushed(vasodilation) HR fast, 10-30% have myocardial depression BP low <90 for systolic Neck veins flat Mental status changes Renal Hypovolemia, vasodilation, impaired tissue O2 use dissociative shock

Question 418

Vasodilators effects of septic shock

Answer 418

Decrease BP, decrease JVP, creased CVP, decrease SVR Increase HR, N decrease CO increase, PAP-N, N, or decrease in PCWP POAP-pulmonary artery occlusive pressure Extremities-warm, CI>4.2 ``` Lungs-dry Tissue perfusion(mixed venous SVO2 oxyhemoglobin sat)>65% ```

Question 419

Anaphylactic shock diagnosis

Answer 419

CLINCIALLY Signs and symptoms are cutaneous (urticaria, oral facial angioedema, hives, flushing, pruritus), respiratory (dyspnea, cough, wheezing, strider), abdominal (cramping pain), vascular (decrease BP, chest pain and arrhthmias)

Question 420

Life threatening/danger signals of anaphylactic shock

Answer 420

Rapid progression of symptoms

Question 421

Respiratory distress of anaphylactic shock

Answer 421

Strider, persistent cough, wheezing, hypotension

Question 422

Pathophysiology anaphylactic shock

Answer 422

Type I IGE mediated hypersensitivity reaction allergens activate mast cells to release mediators (cytokines, histamine, tryptase) that causes vasodilation, vascular permeability, visceral smooth muscle contraction, tissue inflammation Allergens : drugs, insect bite, foos, latex

Question 423

Distributive hemodynamic profile of anaphylactic shock

Answer 423

PCWP (PAOP) N(early or decrease late CO decrease or increase SVR decrease Tissue perfusion (mixed venous oxyhemoglobin sate) >65%

Question 424

Cardiogenic shock

Answer 424

Decrease in systemic oxygen delivery (DO2) caused by deterioration of cardiac function due to myocardial, valvular, structural, toxic or infectious causes Inadequate cardiac pumping leads to: - decrease BP(<90 or >30 mmHg below baseline) - decrease CO leads to decrease UO (<20 cc/hr) - MSDs(multisystem disorder) - peripheral vasoconstriction

Question 425

Cardiogenic shock definition

Answer 425

CI<22 L/min/m2 Increase PCWP Decrease EF Increase PCWP (PAOP0.18 mmHg SVR (to compensate for decreased BP Decreased tissue perfusion-mixed venous oxyhemoglobin <65%

Question 426

Types of cardiogenic shock

Answer 426

Cardiomyopathies Arrhythmogenic Mechanical

Question 427

Cardiomyopathic cardiogenic shock

Answer 427

MI(>40% LV or extensive ischemia) severe RVMI, stunned myocardium, severe septic shock (depressed EF), myocarditis, cardiomyopathy-exacerbation of severe HF

Question 428

Arrhythmogenic cardiogenic shock

Answer 428

Tach ( a fib, a flutter , re entrant tach), VT, VF | -Brady: complete heart block, mobitz II)

Question 429

Mechanical cardiogenic shock

Answer 429

Severe AI or MR; acute valvular rupture (papillary or chordate tendinae rupture , abscess); critical AS, VSD, ruptured vent wall aneurysm, atrial myxoma

Question 430

Diagnose cardiogenic shock

Answer 430

Decrease BP, decrease UO, mental status changes Cool, mottled extremities Distended neck veins Pul edema Document myocardial dysfunction-echocardiogram-cath

Question 431

Etiology cardiogenic shock

Answer 431

Most common-LV failure due to AMI. Other causes of CS are Acute MR - papillary muscle dysfunction/rupture - chordate tendinae rupture - seen in inferior/posterior MI VSD - ruptures IVS (L to R) - seen in anterior MI RV infarction (RV shock) Vent wall rupture (tamponade)

Question 432

Pathophysiology cardiogenic shock

Answer 432

Failure to pump-decrease myocardial contractility, decrease CO-tissue hypoperfusion, decrease coronary perfusion-pul congestion-pul edema 9increase PCWP-PAOP_ Decrease SV and CI-decrease BO, decrease pO2, incrase alctate, myocardial depression, compensatory vasoconstriction, increase SVR-cool extremities; systemic inflammatory state similar to sepsis AMI associated with increased cytokines-NOW-increase NO-vasodilation-decrease coronary perfusion-incrase ischemia-further myocardial dysfunction

Question 433

Comments on cardiogenic shock

Answer 433

Mortality CS approximately 40-50% Average time to develop CS is 7-10 hours after STEMI CS due to LAD often associated with anterior wall STEMI CS associate with inferior wall STEMI often associated with mechanical complications RV infarction - associated with inferior MI - elevated st segments V4R - distended neck veins, clear lungs, decrease BP - RX -IV fluids (preload sensitive)

Question 434

Treat

Answer 434

Cardiac cath If left main or triple vessel disease, consider surgery If no cath lab, give thrombolytic therapy and transfer to tertiary facility If patients does not want to transfer to another hospital, begin thrombolytic therapy if no contraindication AMI reperfusion

Question 435

Treat STEMI

Answer 435

``` PCI-preferred CABG Fibrinolytic ASA Heparin NSTEMI-glycoprotein IIb/IIIa inhibitors P-pressers-norepinephrine -CS inotropy ```

Question 436

Mechanical support

Answer 436

IABD LVAD ECMO

Question 437

IABD

Answer 437

Decreases afterload, deflated during systole; inflates during diastole-coronary perfusion use for mechanical complication

Question 438

LVAD

Answer 438

Bridge for transplant, tandem heart/impels

Question 439

ECMO

Answer 439

When O2 is severely impaired

Question 440

Arginase

Answer 440

Inhibitor enzyme for endothelial NOS; ROSC-restore spontaneous circulation; EECP-early enhanced contour pulsation

Question 441

Pressure

Answer 441

Norepi Dopamine Inotropy s

Question 442

Norepi

Answer 442

Preferred-alpha I, B1 B2 agonist Vasopressin-vasoconstrictor/use in vasodilators shock

Question 443

Dopamine

Answer 443

Alpha B1 agonist High dose vasoconstrictor-alpha stimulation+inotrope low dose 2 microg/kr vasodilator; phenylephrine peripheral alpha antagonist

Question 444

Inotropes

Answer 444

Dobutamine-B1 agonist; peripheral alpha 1 and b2 agonist. Can vasodilator used with norepi Milrinone-phosphodiesterases inhibit prevents degradation of cAMP. Increase HR, SV and CO

Question 445

Treat RV infarct

Answer 445

Fluids for high filling pressure

Question 446

PAC

Answer 446

Useful when despite adequate fluids given, but not favored

Question 447

Indices of tissue perfusion

Answer 447

Goal increase BP, increase UO, incrase mental status, incrase skin color

Question 448

What avoid

Answer 448

NTG or nitroprusside bc decrease BP=vasodilators-decrease preload, decrease afterload

Question 449

Oasis

Answer 449

Blocks Na K CL transport and increase urinary excretion of Na and Cl to decrease pul edema

Question 450

Acute obstruction to flow in circulation

Answer 450

Extracardiac obstructive shock -obstruction of RV output (massive PE air embolus) impaired diastolic filling of RV (SVC syndrome); cardiac tamponade; constrictive pericarditis; severe hypertension

Question 451

Pulmonary vascular extracardiac obstructive chock

Answer 451

Hemodynamically significant , pulmonary embolus, severe pulmonary HTN, severe or acute obstruction of pulmonary or tricuspid valve

Question 452

Mechanical extracardiac obstructed shock

Answer 452

Tension pneumothorax (trauma, ventilator induces, iatrogenic), pericardial tamponade, constrictive pericarditis, restrictive cardiomyopathy

Question 453

Extra obstructive cardiac shock pearls

Answer 453

Pleuritic chest pain and dyspnea-PE Chronic dyspnea, increased P2=PHT Chest pain, tracheal deviation (away from affected side), decreased unilateral breath sounds-tension pneumothorax Distended neck veins, muffles heart sounds, pulsus paradoxus dilated IVC=cardiac tamponade Equalization of pressures (RA, RVEDP, PCWPP)=think tamponade, constrictive pericardial disease, restrictive cardiomyopathy0

Question 454

Presentation extracardiac obstructive shock tension pneumothorax

Answer 454

SOB, unilateral pleuritic chest pain and decreased breath sounds, neck vein distention TRACHEAL DEVIATION AWAY FROM AFFECTED SIDE

Question 455

RX extracardiogenic tension pneumothorax

Answer 455

IV catheter in 2nd, 3rd ICS, MCL followed by chest tube or emergent tube thoracotomy in 5th

Question 456

Pericardial tamponade signs

Answer 456

Dyspnea, tachycardia, decrease BP, increase JVD< muffles heart, pulsus paradoxus, ECG, electrical alternana

Question 457

Echo pericardial tamponade

Answer 457

RA collapse (highly sensitive sign; RV collapse; IVC dilation

Question 458

RX pericardial tamp

Answer 458

Echo/US to guide pericardialcentesis

Question 459

Symptoms of hemodynamically significant pulmonary embolus

Answer 459

Dyspnea, hypoxia, hypotension (sudden), tachypnea, tachycardia, cough, pleuritic chest pain, syncope, sudden death

Question 460

Risk factors for hemodynamically significant pulmonary embolus

Answer 460

VTE in leges, pelvis, arms-most common, Non thrombotic material (fat, air , tumor cells, amniotic cancer, hypercoagulabiltiy (factor V ) previous VTE?PE, pregnancy

Question 461

Pathophysiology hemodynamically significant pulmonary embolus

Answer 461

Clots embolize; large clot may lodge in main PA or branches, smaller clots peripherally; may cause PE infarction; vent> perfusion (V/Q mismatch) increase pul vascular resistance, incrase PASBP, increase RV afterload, increase RVEDP, increase RAP increase TR

Question 462

PE hemodynamicaly significant pulmonary embolus

Answer 462

Increase JVD, increase P2 or widely split P2-due to delayed emptying of RV R>20/min, increase HR

Question 463

Obstructive hemodynamic profile

Answer 463

Decrease Increase HR Increase JVD Extremities cool Lungs dry Co-N decrease PCWP PAOP N or decrease SVR increase

Question 464

CTPA imaging

Answer 464

Computer tomography pulmonary angiography Permits visualization of thrombi in pul arteries Preferred over ventilationperfusion lung V/Q

Question 465

V/Q scan

Answer 465

Used if Agilent is allergic to contrast agents (used for CTPA), renal insuffiency , women <40 yo decreased radiation and preg

Question 466

D dimer

Answer 466

Degradation product of fibrin; indirect index of clotting. High sensitivity , low specificity. If negative, PE not likely diagnosis. Venous Doppler of legs/pelvis /arms-looking for VTE

Question 467

ECG

Answer 467

S1 Q3 T3

Question 468

Echocardiogram

Answer 468

RV dilation, TR

Question 469

hemodynamically significant pulmonary embolus BNP and trop

Answer 469

BNP and troponin elevated

Question 470

CXR pulmonary embolism

Answer 470

Atelectasis RLL, otherwise normal

Question 471

ECG pulmonary embolism

Answer 471

Sinus tach, incomplete RBBB, PAC, st changes

Question 472

ABG pulmonary embolism

Answer 472

PH 7.5 pCO2 29, PO2 58 HCO3 26

Question 473

CBC CMP pulmonary embolism

Answer 473

Normal

Question 474

Venous Doppler

Answer 474

R leg DVT femoral vein

Question 475

CTPA pulmonary embolism

Answer 475

Large thrombus in PA

Question 476

D dimer pulmonary embolism

Answer 476

Positive

Question 477

Echo pulmonary embolism

Answer 477

Normal

Question 478

Heart failure

Answer 478

Inability of the heart to meet the metabolic demands of the body

Question 479

What percent of adults will develop HF

Answer 479

10, 10% of people over 53 have this

Question 480

Mortality rate HF

Answer 480

1 year 10-20% 5 year 50%

Question 481

Etiology HF

Answer 481

60-75% CAD-ISD 18% idiopathic 12% valvular 10% hypertensive *most common cause of LV systolic dysfunction is from ischemic heart disease

Question 482

Basic cause of HF

Answer 482

Restriction/obstruction to ventricular filling - RV infarct - constrictive pericarditis - MS - atrial myxoma

Question 483

State A HF

Answer 483

HF risk factors no heart disease no symtpoms

Question 484

Stage B HF

Answer 484

Heart disease no symptoms Asymptomatic LV dysfunction

Question 485

State C HF

Answer 485

Prior or current HF symptoms

Question 486

Stage C heart failrue

Answer 486

Refractory symptoms

Question 487

Stage A ACC/AHA

Answer 487

CAD (ischemis, atherosclerotic), HT, DM< obesity, metabolic syndrome, excess alcohol; who do not demonstrate structural heart disease or symptoms. One year mortality (about 5-10% using cardiotoxins/family history of cardiomyopathy) (associated with any existing co-morbid conditions)

Question 488

Stage B ACC/AHA

Answer 488

Asymptomatic patients has LVH and/or impaired LV function (low EF) previous MI, valvular disease, structural heart disease; hemodynamically stable. One year mortality 50%

Question 489

Stage C ACC?AHA

Answer 489

Patient with current or past symtpoms of HF with structural heart disease; SOB , fatigue, reduced exercise tolerance; one year mortality 15-30%

Question 490

Stage D ACC AHA stages

Answer 490

Refractory HFl eligible for specialized treatment (mechanical support , transplants) one years mortality 50-60%

Question 491

Class I NYHA

Answer 491

No limitation of physical activity No symptoms. With ordinary exertion One year mortality 5-10% Asymptomatic

Question 492

Class II NYHA

Answer 492

Slight limitation on physical activity Ordinary activity causes symtpoms One year mortality 15-30% No rest sx Exertional sx with ordainary activity

Question 493

Class III NYHA

Answer 493

Marked limitation of physical activity Less that ordinary activity causes symptoms Asymptomatic at rest One year mortality 15-30% No rest sx Sx with minimal activity

Question 494

Class IV NYHA

Answer 494

Inability to carry out physical activity without discomfort Symptoms at rest One year mortality 50-60% Rest sx

Question 495

Pathogenesis of HF

Answer 495

Impaired systolic function Impaired diastolic function Mechanical abnormalities Disorders of rate/rhythm Pulmonary heart disease High output states

Question 496

Echo can see what specific causes of heart failrue

Answer 496

``` Hypertensive heart disease Ischemic heart disease Hypertrophic heart disease Infiltrating heart disease Primary valvular heart disease ```

Question 497

What is echo necessary to distinguish

Answer 497

Necessary to distinguish systolic heart failure from diastolic heart failrue

Question 498

Types of heart failure

Answer 498

Systolic/diastolic High/low Acute/chronic Right/left Forward/backward

Question 499

Acute HF

Answer 499

Heart failure due to acute MI, ruptured papillary msucle , MR, AI, toxins

Question 500

Chronic HF

Answer 500

Multivalvular disease of dilated cardiomyopathy Progresses slow Edema, weight gain

Question 501

Systolic HF (HFrEF-reduced)

Answer 501

At least 50% of cases: decrease SV, increase vent filling pressure EF less than 40%, hypoperfuion with impaired ventricular emptying Weak, fatigues, reduced exercise tolerance DOE, orthopnea, PND LVEF=SV/EDV Associated with CAD, VHD, HT, myocarditis

Question 502

Diastolic HF-normal EF (HFpEF-preserved)

Answer 502

SOB, DOE, pulmonary edema Inability of LV to relax/fill; increased resistance to vent filling; decreased compliance or increased stiffness Decreased vent diastolic capacity to relax Ex. Restrictive/constrictive pericarditis, HTN, hypertrophic, cardiomyopathy Impaired vent relax- - acute ischemia - myocardial fibrosis - amyloidosis Associated with HT, obesity, DM, CAD< aging

Question 503

High output

Answer 503

Hyperthyroidism, anemia, pregnancy, AV fistula, beriberi, paget High CO but low EF

Question 504

Low output

Answer 504

Ischemic heart disease, HTN | -dilated cardiomyopathy, valvular and pericardial disease

Question 505

Right sided HF

Answer 505

Affects RV Pulmonary HTN due to pulmonary embolus Edema, hepatomegalia, venous distention

Question 506

Left sided HF

Answer 506

LV is overloaded AS, MI Dyspnea, orthopnea, due to pul congestion

Question 507

Neurohormonal compensation response of HF

Answer 507

``` SNS RAAS Cytokines activation Altered renal physiology LV remodeling ```

Question 508

RAAS

Answer 508

Decreased renal perfusion Increased renin, angiotensinogen, A1 A1 ACE increases BP by vasoconstriction; stimulates adrenal gland release aldosterone . Na and H2O retention (increase preload, congestive symtpoms and volume expansion) A11-vasoconstrictor increases PVR (increase afterload

Question 509

Arginine vasopressin

Answer 509

AVP or ADH | -stimulation of thirst leads to increase TBW and hyponatremia (dilutional). Increases preload (salt and water retention)

Question 510

Precipitating causes of HF

Answer 510

Sometimes decompensation of HF relates to underlying progression of heart disease Non compliance with diet - too much Na - too many calories - too many stimulants Non compliance with meds - too costly - side effects Medes that worsen HF-CCB, BB, NSAIDS< antiarrhythmias Infection Anemia - increased oxygen needs of tissues - increased CO Thyrotoxicosis/pregnancy -high CO state Arrhythmias - tachyarrhythmias-decrease diastolic filling time, leading to ischemia - bradycardia

Question 511

Signs and symptoms of HF

Answer 511

Decreased arterial perfusion to organs and venous congestion leads to dyspnea-most common Exercise intolerance, orthopnea, PND< nocturnal angina-due to pul congestion and increased LA pressure PND increases the likelihood of HF Weakness, fatigue not specific Pulmonary edema-crackles , transsudation of fluid from pulmonary capillaries into alveolar spaces and interstitium. Wheeze, frothy pink fluid, possible cyanosis and acidosis Hepatomegalia-passive congestion with increased LFT altered coagulation studies, ascites, increased abdominal girth, peripheral and sacral edema JVD-CVP can be elevated in volume overload; prominent in cardiac tamponade and COPD

Question 512

Heart and HF

Answer 512

S3 gallop increases likely hood of HF 11 fold S4 LV failure Orthopnea, PND Tachypnea, wheezing, crackles, decreased breath sounds Dullness to percussion over pleural effusions

Question 513

RV failrue

Answer 513

Peripheral/sacral edema Hepatomegalia Ascites Increased JVD, HJR

Question 514

Where is the JVD Seen

Answer 514

As crosses the sternocleidomastoid muscle into the posterior triangle of the neck and disappears beneath the clavicle to join the brachiocephalic vein

Question 515

How measure JVD

Answer 515

Raise head slightly of f pillow to relax sternocleidomastoid Raise the head of bed 30 degrees turn head slightly away fromt he side you are inspecting Use tangential lighting and examine both sides of the neck. Find internal jugular venous pulsation If necessary, raise or lower head of bed till see oscillation point of internal jugular venous pulsation in the lower half Focus on right internal jugular vein. Look for pulsation int he suprasternal notch, between the attachments of the sternomastoid muscle on the sternum and clavicle or just posterior to sternomastoic Identify highest point of pulsation in the right jugular vein-extend a long rectangular object or card horizontally from this point and a centimeter ruler vertically from the sternal angle, making an exact right angle. Measure the vertical distance in centimeters above the sternal angle where the horizontal object crosses the ruler and add to this distance 4 cm,

Question 516

What is a venous pressure above normal

Answer 516

At >3m above the sternal angle, or more than 8 cm or 9 cm in total distance above the right atrium

Question 517

Diagnostic test for HF

Answer 517

No single diagnostic test for HF; it is largely a clinical diagnosis checked on a careful HP

Question 518

CXR HF

Answer 518

Cardiomegalia Pulmonary edema with central peripheral infiltrates Increased size of vessels in upper portion of lungs Pleural effusions

Question 519

Echo HF

Answer 519

Practical useful, mobile, bedside/ICU/ED Chamber size, clots, tumors Wall motion muscle thickness Pericardial effusions Valvular disease Systolic.diastolic HF-ejection fraction

Question 520

ECG HF

Answer 520

May have ischemia, infarction, hypertrophy Rhythm disturbances (atrial, junctional, ventricular ) Tachycardia/bradycardia/blocks

Question 521

Troponin T and I

Answer 521

Released from myocytes when damaged - increase 3-12 hours from onset of chest pain - peak 24-48 hours; return to baseline 5-14 days

Question 522

CK-MB

Answer 522

Increases 3-12 hours from onset of chest pain Peak 24 hours; baseline 1-3 days Sensitivity

Question 523

CBC HF

Answer 523

Anemia secondary to chronic disease Anemia may aggravate HF

Question 524

CMP HF

Answer 524

Electrolyte imbalance-low Na, K | Pre renal azotemia-high BUN to creatine

Question 525

UA HF

Answer 525

Protein in urine

Question 526

Thyroid labs HF

Answer 526

If patient is in HF, greater that 65 years old with a fib, check the thyroid Free t4, TSH ABG-may have hypoxia, metabolic acidosis from lactic acidosis

Question 527

BNP

Answer 527

Brain natiuretic peptide Neurohormonal, made in ventricles Sensitive to ventricle stretching and volume overload. Preload/afterload are stimuli Lower EF, high BNP If value is less than 100pg/ml, there is a 97% chance of no HF Increased BNP in heart failure, AMI, PE, renal failure, old age

Question 528

Differential diagnosis of HF

Answer 528

Pulmonary problems - PE - asthma - pneumonia Cirrhosis - ascites - edema Renal-edema Venous insuffiency-edema

Question 529

Five basic principles of HF

Answer 529

Make correct diagnosis-exclude mimics of HF Determine etiology of heart disease Determine precipitating factors Understand pathophysiology of HF Understand mechanism of action of pharmacological therapy

Question 530

Indications for admission to hospital for management of HF

Answer 530

``` Acute MI Severe respiratory distress Hypoxia Hypotension Cardiogenic shock Anascara Syncope Heart failure refractory to oral medications ```

Question 531

Non pharm treatment of HF

Answer 531

Quit smoking Lower weight AHA diet, 2 gram Na diet Fluid restriction <2 L a day Avoid isometric activity-increase SVR and afterload Encourage isotonic activity-walking, hiking, golf Stool softened Subcut levenox Oxygen Avoid alcohol Treat HTN, hyperlipidemia, diabetes

Question 532

How counsel patient HF before discharge of hospital

Answer 532

Diet-patient with spouse/other sodium restriction, Carl our restriction if overweight stimulants Education Rehab exercise Medes: ACE/ARB, bb, ASA, statin, nitro prn

Question 533

CO

Answer 533

SVxHR

Question 534

Stoke volume is modulated by what

Answer 534

Preload Afterload Contractility

Question 535

Conventional treatments of HF

Answer 535

Diuretics -reduce fluid volume Vasodilators -decrease preload and/or afterload Inotropes -augment contractility

Question 536

Class I

Answer 536

Evidence and/or agreement that therapy/procedure is beneficial, useful and/or effective; beneficial, useful and/or effective; benefit 3+ risk

Question 537

Class II

Answer 537

Conflicting evidence and/or divergence of opinion IIa-weight of evidence .opinion infavor -benefit 2+ risk IIb-less established evidence/opinion-benefit 1+ risk

Question 538

Class III

Answer 538

Evidence and/or agreement that therapy/procedure is not effective; may be harmful -no benefit

Question 539

A level evidence

Answer 539

Data from meta analysis or multiple randomized clinical trials; multiple populations evaluated

Question 540

B level evidence

Answer 540

Data from single randomized trial or non randomized studies; limited population evaluated

Question 541

Level C evidence

Answer 541

Only consensus opinion of experts , case studies, or standard of care, very limited populations

Question 542

Pharm treatment of HF

Answer 542

ACE I or ARB BB Diuretic Spironolactone Digitalis IV inotropes Hydralazine Nitrates CCB Sacubitril-Vallarta’s ivabradine

Question 543

ACE I

Answer 543

Block conversion of angiotensin I to angiotensin II -useful for all NYHA functional classifications with systolic heart failrue Lower mortality and morbidity by 20% supported by several good drug trials Useful in preventing HF in high risk patients (ASHD, MI, HT) level of evidence A Recommended in patients with symptoms of HF, reduced EF, unless contraindicated: L or E: A

Question 544

When use ACE cautiously

Answer 544

Use cautiously with renal insuffiency or K greater than 5 mEq/l

Question 545

Contraindication ACE I

Answer 545

Angioedema | Pregnancy

Question 546

AE ACE I

Answer 546

Bilateral RAS(renal artery stenosis) Cough

Question 547

List ACE I

Answer 547

``` Lisinopril Enalapril Captopril Benazepril Ramipril Quinapril ```

Question 548

ARB

Answer 548

Block AT1 and AT2 receptor for angioteensin Blocker A11 at receptor without inhibiting kininase Don’t get cough that is due to accumulation of kinins

Question 549

ACE

Answer 549

Block angiotensin I to angiotensin II Improve LV relax and contraction Veno and vasodilation

Question 550

ARB action

Answer 550

Increases myocardial fibrosis Increases NE Increases vasoconstriction Increases endothelin1

Question 551

Why get cough from ACE

Answer 551

Bradykinin accumulated

Question 552

ARB vs ACE

Answer 552

Comparable but neither more effective Don’t give ARB to patient that got angioedema from ACE

Question 553

Name ARBS

Answer 553

``` Losartan Vallarta’s Candesartan Telmisartan Irbesartan Entresto; sacubitril is the neprilysin inhibitor and Vallarta’s is AII receptor blocker ```

Question 554

BB

Answer 554

Survival benefit in chronic syst HF and dilated cardiomyopathy Slow progression of disease and decrease hospitalization Improve cardiac performance and symptoms of HF

Question 555

Hemodynamics of BB

Answer 555

Decrease heart rate Antiarrhythmic properties Antiischemic Blunts SNS effects of NE Reverse remodeling

Question 556

BB good

Answer 556

Clinical trials reveal decrease mortality -CIBIS II US carvedilol HF program - improve LVEF and well being - Corey, alpha1, beta1, beta2 receptor, with vasodilator property and antioxidant

Question 557

Who don’t give BB

Answer 557

Unstable class IV

Question 558

Who give BB

Answer 558

All stable patients with symptoms of HF, reduced EF, unless contraindicated. Level of evidence: A Patients with class II and II NYHA

Question 559

Diuretics for HF

Answer 559

Relieve congestion(pulmonary) symtpoms by reducing preload Increase cardiac function Promote natiuretic, urinalysis Na excretion Inhibits NaCl resorption from AL or LOH Increase risk of arrhythmia deaths without K sparing

Question 560

AL or LOH diuretics

Answer 560

Lasix (furosemide) Bumex (bumetanide) Demanded (torsemide)

Question 561

DT

Answer 561

Thiazide Zaroxolyn (metolazone)

Question 562

Late DT

Answer 562

Spironolactone (aldactone)

Question 563

How give furosemide

Answer 563

10 mg IV.he or 40 mg IV every 8-12 hours Watch K Mg, Na, BUN, creatinine

Question 564

Digitalis

Answer 564

Inotropes agent DIG Improves the quality of life associated with HF but no demonstrable effect on survival Useful in HFrEF and a fib for ventricular rate control

Question 565

Why use digitalis

Answer 565

HFrEF and a fib for ventricular rate control

Question 566

MOA digitalis

Answer 566

Inhibits Na/K/ATPase; affect to increase contractile state by increasing intracellular calcium conc. Useful in atrial fibrillation to slow ventricular rate

Question 567

Spironolactone

Answer 567

Antagonizes effects of aldosterone Use in addition to standard care (ACE, BB, diuretic, dig)

Question 568

RALES

Answer 568

``` Randomized aldactone evil study (aldactone-spironolactone) 12.5-25 mg/day; class III-IV patients -30% reduction in mortality ```

Question 569

How watch spironolactone

Answer 569

Watch K closely if GFR is less than 30 cc/min or creatinine is greater than 1.6 mg/dl

Question 570

Level of evidence of spironolactone

Answer 570

B-decreased mortality, decreased HF hospitalization s

Question 571

Eplerenone

Answer 571

New watch K

Question 572

Inotropes

Answer 572

Increases contractility Dobutamine -stimulating beta1 and beta2 receptors Milrinone - inotropic vasodilator - inhibits phosphodiesterase

Question 573

Dopamine

Answer 573

Stimulates beta 1 receptor 2-10 ug/kg/min Higher doses stimulate alpha receptors Useful short term

Question 574

Hydralazine plus isosorbide dinitrate

Answer 574

Hydralazine -arterial vasodilator, reduces afterload and SVR Nitrates -vasodilator to reduce preload or reduce venous return to increase CO When H+ N are added to diuretics and dig, may: Reduce mortality Increase EF Increase exercise tolerance

Question 575

Isosorbide dinitrate | Isosorbide mononitrate

Answer 575

Better response to hydralazine and isosorbide in african Americans that in whites; use if intolerant to ACE/ARB Nitroprusside Vasodilator monitor BP closely

Question 576

Nitrates hemodynamic effects

Answer 576

1. Venous vasodilation Decrease preload leads to pulmonary congestion, decrease ventricular size, decrease vent wall stress, decrease MVO 2. Coronary vasodilation - increase myocardial perfusion 3. Arterial vasodilation - decrease afterload leads to decreased CO, BP

Question 577

CCB

Answer 577

Class III No benefit Not recommended as routine Treatment for patients with HF associated with reduced ejection fraction

Question 578

Role of OMM if HF lymph treatment

Answer 578

Open thoracic inlet to decrease flow fascial restriction, to allow between lymphatic flow in thoracic duct - if blocked, will not have optimal fluid drainage. - always do this before and after lymph treatment so moblized fluids has a place in drain. Rib raising-dec. hyperactive sympathetic tone -helps open chest cage for more optimal breathing effort, rib excursion. Mobilizes fluid Diaphragm abd doming -as effective as LE exercise for fluid movement

Question 579

Effleuragepetrissage-distal to proximal stroking of extremities

Answer 579

Can reduce edema of extremities by helping move fluid centrally Cervical stroking (opposite of myofascial release, push toward chest from head Open thoracic duct again Ensure fluid has a place to drain

Question 580

Conclusion HF

Answer 580

Make the right diagnosis Look for the precipitating causes and underlying etiology Provide treatment based on solid evidence based recommendations.