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Cardio Flashcards

1
Q

Infections of the cardiovascular system: myocarditis, pericarditis, endocarditis

A

Ok

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2
Q

Myocarditis

A

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

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3
Q

Myopericarditis

A

Extension of myocarditis into the pericardium

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4
Q

Clinical features myocarditis

A

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

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5
Q

Differential diagnosis myocarditis

A

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

*not all encompassing

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6
Q

PE myocarditis

A

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

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7
Q

Work up myocarditis

A

EKG

Cxr

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8
Q

Ekg myocarditis

A

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

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9
Q

CXR myocarditis

A

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

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10
Q

Echocardiogram

A

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

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11
Q

PCR

A

Detection of viral genome

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12
Q

Labs

A

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)

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13
Q

___ biopsy can aid in a definitive diagnosis

A

Endomyocardial

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14
Q

Complications myocarditis

A

Dilated cardiomyopathy
Myopericarditis

Sudden cardiac death (20%)

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15
Q

Treat myocarditis

A

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

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16
Q

Infection etiologies myocarditis

A

Coxsackie B, trypanosome cruzi, trichinella spiralis

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17
Q

Cocksackie B (picornaviridae, enterovirus) myocarditis

A

+ SsRNA, small, naked, icosahedral

Peak incidence summer and fall

Fecal oral transmission

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18
Q

Manifestations coxsackie B

A

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

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19
Q

How get trypanosome Cruzi

A

Reduvviid, animal

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20
Q

Where is trypanosome cruzi

A

Southern US, Mexico, SA

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21
Q

What is trypanosome cruzi

A

Intracellular Protozoa (hemoflagellate)

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22
Q

Phases of chagas

A

Acute-1 month

Intermediate

Chronic-years-decades to develop

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23
Q

Diagnose trypanosome cruzi

A

Peripheral smear for trypmastigotes, xenodiagnosis

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24
Q

Acute chagas

A

Chagoma, romana sign

Fever, malaise, LAD

CV-myocarditis

CNS-severe meningoencephalitis (young patients)

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25
Q

Intermediate chagas

A

Asymptomatic

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26
Q

Chronic chagas

A

CV: dilated cardiomyopathy, arrhythmias

Megacolon, achlasia

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27
Q

Trichinella spiralis

A

Invasive nematode

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28
Q

How get trichinella spiralis

A

Ingestionof cysts from raw pork (boars or even horses)

Humans are dead end host

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29
Q

Trichinella in human

A

Larvae develop in gut->mate->larvae disseminate hematogenous lh->penetrate muscle tissue

Skeletal muscle, heart brain

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30
Q

Invasive cycle trichinella spiralis

A

With heavy infection can be lethal

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31
Q

Symptoms trichinella spiralis

A

Abdominal pain, diarrhea, fever (while in small intestine)

Muscle invasion: muscle aches, other sx dictated by location of larvae invasion

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32
Q

When consider trichinella spiralis diagnosis

A

Periorbital edema, myositis, eosinophilis

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33
Q

Diagnostics for trichinella spiralis

A

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

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34
Q

Pericarditis

A

Inflammation of the pericardium

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35
Q

Infectious agents of pericarditis

A

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

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36
Q

Presentation pericarditis

A

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

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37
Q

DDx considerations

A

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

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38
Q

PE pericarditis

A

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

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39
Q

Work up pericarditis

A

EKG

CXR

Echo

Labs

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40
Q

EKG

A

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

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41
Q

CXR

A

Majority of CXR with pericarditis show minimal abnormalities

Exception-pericardial effusion>250 mL will cause a symmetrically enlarged cardiac silhouette. Water bottle sign

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42
Q

CXR

A

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

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43
Q

Echo pericarditis

A

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

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44
Q

Echo pericarditis

A

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

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45
Q

Labs pericarditis

A

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

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46
Q

Complciations pericardiis

A

Cardiac tamponade-treated with pericardiocentesis

*counsel about activity restrictions

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47
Q

Treat pericarditis

A

High dose asprin TID (ibuprofen, indomethacin) and colchicine

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48
Q

What is contraindicated in pericarditis

A

Anticoagulants

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49
Q

Infectious agents pericarditis

A

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

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50
Q

Cocksackis B

A

Picornaviridae, enterovirus

+SsRNA, small naked icosahedral

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51
Q

Transmission cocksackis B

A

Fecal oral

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52
Q

Manifestations cocksackie B

A

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

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53
Q

Mycobacterium tuberculosis

A

Acid fast (weakly G+), obligate aerobes, facultative intracellular (macrophages)

AFB secondary to mycotic acid cell wall composition (highly resistant to desiccation including NaOH)

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54
Q

Virluence mycobacterium Tb

A

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

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55
Q

Stains mycobacterium BT

A

Acid fast (ziehl-neelsen, Kenyon)-red rods

Auramine-rhodamine staining-fluorescent apple green color

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56
Q

Manifestation mycobacterium Tb

A

Pulmonary tuberculosis

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

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57
Q

Infective endocarditis

A

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

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58
Q

Risk factors IE

A

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

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59
Q

Clinical manifestion IE

A

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

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60
Q

Acute IE

A

Rapid and life threatening progression of symptoms and cardiac damage

High fever, chills, weakness, SOB, pleuritic chest pain

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61
Q

Subacute IE

A

Slow, indolent course

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

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62
Q

Complciations IE

A

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

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63
Q

Cardiac manifestations IE

A

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

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64
Q

Diagnostic work up IE

A

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

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65
Q

Major criteria for IE duke

A

Blood culture + with consistent microorganisms from 2 separate blood cultures

At least two positive >12 hr apart or lll of the three or

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66
Q

Definite diagnosis

A

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

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67
Q

Treat IE

A

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

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68
Q

Give high risk patients prophylactic before dental or respiratoy procedures

A

Able to take PO-amoxicillin

IV-ampicillin or cefazolin or ceftriaxone

Allergic to penicillin -desensitize, cephalexin, clindamycin, azithromycin

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69
Q

Common infectious agents of IE

A

S aureus, s epidermis, s viridans, enterococcus(D strep)

HÁČEK, coxiella burnetti, brucellosis , s agalactiae0rare

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70
Q

S aureus

A

G+ cocci, clusters, coagulate and catalase positive, facultative anaerobes

Normal flora on skin (can breach) and colonize nasopharyngeal

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71
Q

Virluence s aureus

A

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

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72
Q

Invasion of tissue and blood stream s aureus

A

Hyaluronic ASD-breaks down CT

Staphylokinase-lyse s formed clots

Lipase-breaks down fat

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73
Q

Toxin mediated manifestations

A

Food poisoning, scalded skin syndrome, toxic shock syndrome

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74
Q

Local manifestations of s aureus

A

Skin-impetigo, cellulitis, folliculitis, furuncles, carbuncles

Respiratory-pneumonia

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75
Q

Systemic manifestations s aureus

A

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

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76
Q

Thx s aureus

A

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

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77
Q

Signs of acute endocarditis from s aureus

A

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

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78
Q

Streptococcus viridans

A

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

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79
Q

Manifestations strep viridans

A

Dental caries, subacute endocarditis

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80
Q

Treat strep viridans

A

Penicillin

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81
Q

Staph epidermidis

A

Coagulate negative staph CoNS

G_ coccci, clusters, coagulate negative, catalase positive, novobicin sensitive, facultative anaerobes

Normals skin flora

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82
Q

Virluence staph epidermidis

A

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

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83
Q

Manifestations s epidermidis

A

Subacute endocarditis, infection bacteria in neutrophil patients (susceptible)

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84
Q

Treat staph epidermidis

A

Vancomycin (very antibiotic resistant)

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85
Q

Enterococcus (group D strep)

Enterococcus faecalis

A

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

Normal human bowel

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86
Q

Virluence factor enterococcus

A

Extracellular dextran helps bind heart valves

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87
Q

Manifestations enterococcus

A

Subacute bacterial endocarditis, UTI, biliary tract infections

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88
Q

Media requirements enterococci

A

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

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89
Q

Treat enterococcus

A

Vancomycin resistant forms on the rise

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90
Q

Non enterococci group D strep

A

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

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91
Q

Virluence non enterococci group d strep

A

Extracellular dextran helps bind heart valves

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92
Q

Manifestations non enterococci

A

Biliary tract infections, UTI, subacute bacterial endocarditis

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93
Q

Media non enterococci

A

40% bile , blood agar

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94
Q

HÁČEK

A

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

Part of normal flora

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95
Q

Media HACEK

A

Chocolate agar

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96
Q

HACEK

A

Haemophilus (H parainfluenza most likel to cause endocarditis)

Aggregatibacter sp

Cardiobacterium sp

Eikenella corrodens

Kinde;Lola sp

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97
Q

Manifestation HACEK

A

Subacute endocarditis rare

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98
Q

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)

A

Chocolate agar

Blood agar

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99
Q

Coxiella burnetti

A

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

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100
Q

Symptoms coxiella burnetti

A

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

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101
Q

Cardiac rhythm disturbances (atrial, junctional, ventricular)

A

Ok

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102
Q

Principles

A

Treat patient no ECG
Establish urgency of treatment and treat reversible causes

Access hemodynamically stability (LOC< BP< HR)

Antiarrhythmic/electrical therapy

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103
Q

Arrhythmias

A

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

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104
Q

Etiology arrhythmias

A

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

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105
Q

Sinus tachycardia

A

Physiologic/pathological process

Look for the cause

Emotion, anxiety, fear, drugs, hyperthyroid

Fever, pregnancy, anemia, CHF

Hypovolemia
Rx-underlying cause

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106
Q

Sinus node

A

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

Bradycardia<60 bpm

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107
Q

Medical conditions situations associated with bradycardia

A

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

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108
Q

Causes of bradycardia

A

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
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109
Q

EKG of sinus bradycardia

A

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
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110
Q

EKG SSS-tachy-Brady

A

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

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111
Q

Treat sinus bradycardia

A

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

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112
Q

What treat sinus bradycardia with

A

Atropine

Epinephrine

Isoproterenol

Pacemaker

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113
Q

Atropine

A

2 mg IV for SB and repeat 10 min

Use caution in glaucoma can increase IOP-narrow angle

AE-urinary retention, and distention, transient

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114
Q

Epinephrine for SB

A

2-10 ug.min

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115
Q

Isoproterenol for SB

A

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

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116
Q

What is automaticity

A

Idk

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117
Q

Atrial arrhythmias

A

Premature atrial contraction (PAC) also APC

Seen in absence of significant heart disease; associated with stress, alcohol, tobacco, coffee, COPD, and CAD

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118
Q

Premature beat of atrial arrhythmia

A

An irritable focus spontaneously fires a single stimulus

  • premature atrial beat
  • premature junctional beat
  • premature ventricular beat
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119
Q

SA node resets in step with __

A

Premature atrial beat

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120
Q

Premature atrial beat with aberrant ventricular conduction

A

Wide QRS

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121
Q

Non conducted premature atrial beat

A

No QRS

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122
Q

PAC

A

A single complex occurs earlier than the next expected sinus complex

After the PAC, sinus rhythm usually resumes

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123
Q

Rhythm PAC

A

Irregular

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124
Q

P wave PAC

A

Present, may have different shape

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125
Q

normal in PAC

A

PR -varies or normaland WRS

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126
Q

Clinical PAC

A

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

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127
Q

Treat PAC

A

If symptomatic

  • reverse causes
  • beta adrenergic antagonist (BB)
  • metoprolol 25-50mg BID-TID
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128
Q

Paroxysmal atrial tachycardia

A

Sudden heart rate greater than 100

-rate irritable focus P wave

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129
Q

PAT with block (AV block)

A

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

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130
Q

Multifocal atrial tachycardia

A

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

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131
Q

Mat treat

A

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

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132
Q

Treat MAT-focus on underlying cause

A

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

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133
Q

ECG a fib

A

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

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134
Q

Atrial flutter

A

Saw tooth appearance

Leads II, III, AVF< V often best leads

250-350/min

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135
Q

Identifying a flutter may require

A

Inverting the tracing

Or employing a vagal maneuver

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136
Q

Junctional (nodal) rhythma

A

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

Sudden, irritable junctional focus paces rapidly

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137
Q

Junctional foci inherent rate

A

40-60 min

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138
Q

Premature ventricular contractions (PVC VPC) etiology

A

Normal heart

CAD, MI, HF, myocardial ischemia, hypoxia

Valvular heart disease, congenital heart disease

Cardiomyopathy, electrolyte abnormalities

Acid base imbalance

Hyperthyroid

Drugs

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139
Q

Premature ventricular contractions ECG

A

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

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140
Q

Principles of treatment ventricular rhythm disturbances: causes

A

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

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141
Q

Treat PVC

A

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

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142
Q

Ventricular tachycardia

A

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

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143
Q

V fibrillation

A

Disorganized depolarization

Not effective pump

Clinical setting-AMI, HF< K disturbance (low or high)

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144
Q

V flutter

A

250-350 per minute

Sine waves

Leads to v fib

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145
Q

Torsades de pointes

A

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)

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146
Q

Treat tdp

A

MgSO4, 1-2 grams IV bolus

Overdrive pacing

Isoproternol

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147
Q

Electrolyte disturbances (K, Ca, Mg)

A

Altered milieu

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148
Q

K disturbance

A

Low; lowers resting membrane potential

Enhances automaticity

High; raises resting membrane potential, slows conduction, widens QRS

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149
Q

Calcium disturbances

A

Low; prolongs QT (torsades)
High: shortens QT

Acidosis

Reduces threshold for VF

Sensitized myocardium to re entrainment arrhythmias

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150
Q

Hypokalemia

A

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

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151
Q

ECG hypokalemia

A

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

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152
Q

Hyperkalemia etiology

A

Renal failure (insuffiency), metabolic acidosis, DKA, cell breakdown (hemolysis, rhamdomyolysis)

ECG
-peaked T wave, wide QRS, inc PR interval, loss of P wave

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153
Q

Hypocalcemia

A

Chronic renal failure, vitamin D defiency, hypoparathyroidism, acute pancreatitis, hypomagnesium

ECG-prolongation of QT interval (QTc corrected for rate)

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154
Q

Hypercalcemia

A

Hyperparathyroidism, malignancy, granulomatous disorders (TB sarcoidosis), endocrine disorders (adrenal insuffiency, hyperthyroid)

ECG-short QT, short ST

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155
Q

HypoMg

A

Poor nutrition, alcoholism, dec absorption, renal magnesium loss, diuretics

ECG-long Pr, wide QRS, long QT, dec T wave

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156
Q

Hypermg

A

Renal failure, magnesia containing drugs

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157
Q

Hyperkalemia

A

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

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158
Q

Hypokalemia

A

ST depression

T flattening

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159
Q

Hypercalcemia

A

Shortened QT interval due to a shortened st segment

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160
Q

Hypocalcemia

A

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

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161
Q

Digitalis

A

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

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162
Q

Quinidine -procainamide
Disopyramide
Phenothiazines
Tricyclic antidepressants

A

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

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163
Q

Hypothermia

A

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

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164
Q

Pulmonary embolus

A

Sudden dyspnea+clear lung+x ray=PE

Tachycardia

Nonspecific ST-T changes

ECG- S1, Q3, T3
T wave inversion V1-V4
Transient RBBB

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165
Q

Cerebral hemorrhage

A

Impressive ST T changes

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166
Q

Hypothyroidism

A

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

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167
Q

Wolf parkinson

A

Short PR interval

Slurred upstroke (delta wave) of QRS complex

Accessory AV conduction pathway (bundle of Kent)

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168
Q

Valvular heart disease Dr. Khalid

A

Ok

Recognize the etiologies, of valvular heart disease

Discuss auscultation findings associated with VHD

Discuss the valvular causes of systolic, diastolic and continuous murmurs

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169
Q

Valvular heart disease

A

20 million in USA

Age dependent 3-6% of those>65

Symptoms 
-dyspnea on exertion (most common)
-angina
-syncope
-palpitations
Fatigue, edema, ascites
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170
Q

Most common conditions encountered today

A

Degenerative (calcification)
Myxomatosis degeneration (MVP)
Congenital (bicuspid aortic valve)

Decline in incidence of rheumatic valvular disease*huge decline just in immigrant or visitors

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171
Q

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

A

Heart failur, endocarditis, rheumatic fever

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172
Q

Stenosis

A

Impedes forward flow

Stenosis, sclerosis, fibrosis, calcification

Leads to pressure overload; hypertrophy and heart failure

As and MS

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173
Q

Regurgitation

A

Failure to close adequately (leaks)

Reversal of flow

Insufficiency, incompetitence

Leas to volume overload; dilates

AI and MR

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174
Q

Types of VHD

A

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

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175
Q

Rheumatic heart disease

A

Due to RH
Females 4:1

Caused by group A strep infection (pharyngitis) virtually only cause of acquired MS(can be congenital)

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176
Q

Jones criteria

A

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
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177
Q

Symptoms RHD

A

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

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178
Q

Diagnose RHD (CRP not specific for inflammation lots have)

A

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????

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179
Q

Mitral stenosis

A

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

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180
Q

Mitral stenosis

A

4th decade, fatigue associated with decreased CO

DOE, cough orthopnea, PND, pulmonary edema, hemoptysis, arterial emboli, a fib

PHT with RHF-edema

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181
Q

Ortner syndrome

A

Hoarseness d/+ compression of left recurrent laryngeal nerve

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182
Q

PE mitral stenosis

A

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.

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183
Q

How hear mitral stenosis

A

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

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184
Q

Why could th patient develop progressive symptoms to RVF

Malar face rash kid

A

Ok

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185
Q

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

A

*smoker is distactor its not COPD

MS

ECG-a fib and left atrial enlargement

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186
Q

Mitral stenosis treat

A

Anticoagulation if in a fib-prevent stroke

Percutaneous balloon valvuloplasty MVR (replacement)

Progressive symptoms-possible RVF

RVFfailure-see ascites low extremity edema

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187
Q

RVF symptoms progressive from MS

A

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

Blood back!

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188
Q

A fib ecg

A

No p wave

QRS to QRS is different

Irregularly irregular rhythm

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189
Q

Left atrial enlargement

A

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

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190
Q

Right atrial enlargement

A

V2 lead 2?

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191
Q

Atria hypertrophy?

A

Not really always dilates bc so thin

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192
Q

Vent hypertrophy and dilate

A

Either

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193
Q

Did diagnosis for case

A

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

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194
Q

Look at left border of heart if see straightening

A

Left atrial enlargement

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195
Q

Do we anticoagulatns this patient

A

Yes they have a fib bc of risk of emboli

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196
Q

Treat MS

A

Anticoagulant if in a fib;risk emboli

Percutaneous balloon valvuloplasty (mitral commissions); success rate 95% MVR (replacement)
Progressive symptoms-possible RV

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197
Q

Chronic mitral regurgitation

A

MVP-most common etiology/myxomatous or degenerative MV

MAC (mitral annular calcification

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198
Q

Acute Mitral regurgitation

A

Rupture of chordal tendineae
Rupture of papillary msucle

Ischemic papillary muscle dysfunction-(CAD/MI: next most common cause of MR)

IE; valve perforation

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199
Q

Chest x ray mitral regurgitation

A

Pulmonary edema

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200
Q

Acute MR

A

Inc. LA pressure abruptly; pulmonary edema, LVF

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201
Q

Chronic MR

A

Generally well compensated

ECG-LAE

MAC
2% pop

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202
Q

Symptoms mitral regurgitation

A

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

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203
Q

PE mitral regurgitation

A

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

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204
Q

Treat mitral regurgitaiton

A

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

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205
Q

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

A

Ok

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206
Q

Loud systolic murmur at apex

A

Mitral regurgitation

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207
Q

S3 gallop

A

Heart failure

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208
Q

Differential

A

CAD
Murmur of mitral regurgitaiton

Chest pain

MI

Acute MI complicated by acute LVF

Ischemic papilalry msucle dysfunction causing acute MR

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209
Q

What test

A

Ecg, MR

Chest x ray

Cardiac enxymes up

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210
Q

MR turbulent flow one chamber to another

A

Regurgitaiton

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211
Q

ECG inferior MI

A

ST elevation on II III AVF

RCA supplies papillary muscle causing mitral regurgitaiton

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212
Q

Cardiac enzymes MI

A

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

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213
Q

MVP

A

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

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214
Q

Symptoms MVP

A

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

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215
Q

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

A

Differential
Palpitations SVT, TC, PVC< MVP R/O hyperthyroid, R/O collagen abnormalities

Echo ecg, holter,TSH, free T4, CXR

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216
Q

Treat MVP and thyroid disorder

MVP with mitral regurg

A

B blocker for hyper state

Regulate thyroid meds

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217
Q

Aortic stenosis

A

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)

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218
Q

Pathophysiology AS

A

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

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219
Q

Symptoms AS

A

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

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220
Q

PE AS

A

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)

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221
Q

How see LVH on ecg

A

V5 v6 high

Will happen in aortic stenosis

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222
Q

LVH in aortic stenosis

A

Ok

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223
Q

Treat AS don’t work just temporary relief

A

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%

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224
Q

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

A

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

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225
Q

Treat severe symptomatic AS

A

Valve replacement

No med can give

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226
Q

Aortic regurgitaiton

A

Due to leaflet abnormalities (bicuspid AoV, IE)

Due to aortic root abnormalities (marfan syndome, aortic dissection, aging, HTN)

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227
Q

What causes acute AR

A

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

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228
Q

Causes of chronic AR

A

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

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229
Q

Pathophysiology regurgitation

A

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

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230
Q

Symptoms aortic regurgitaiton

A

Depends on rapidity of onset-due to compensatory mechanism onset

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231
Q

Acute aortic regurgitaiton

A

IE, aortic dissection/acute pulmonary edema, cardiogenic shock

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232
Q

Chronic aortic regurgitation

A

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

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233
Q

PE aortic regurgitaiton

A

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

234
Q

Crescendo decrescendo-AS?

Blowing murmur

235
Q

Treat aortic regurgitation

A

ARB-decrease afterload to decrease regurgitation volume

Surgery AoVR (replace or repair ) when symptomatic or EF<50-55%

236
Q

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

A

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

237
Q

Valvular heart disease treatment

A

Reserved for when symptomatic

238
Q

Tricuspid stenosis

A

Associated with MS, TR, and RHD

Can be associated with carcinoid, ergot agents (cabergoline)

239
Q

Pathophysiology tricuspid stenosis

A

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

240
Q

Hear tricuspid stenosis

A

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

241
Q

Diastolic murmur apex

242
Q

Diastolic murmur left sternal border

A

Tricuspid stenosis

243
Q

Every right valve disease

A

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

244
Q

Tricuspid regurgitation

A

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

245
Q

A wave JVP

A

Tricuspid stenosis

V wave-tricuspid regurgitation during systolic

246
Q

Pulmonary stenosis

A

Atresia, congenital, can cause angina, syncope,

247
Q

Auscultation pulmonary stenosis

A

Systolic crescendo-decrescendo murmur, ejection click

2nd 3rd ICS, LSB/radiated toward left shoulder clavicle and increases on inspiration/RVH

248
Q

Association pulm stenosis

249
Q

Treat pulmonary stenosis

A

Balloon commissural to my if pressure gradient>50mmHg

250
Q

Cause pulmonic regurgitation

A

Most due to pulmonary HTN

251
Q

Sound pulmonic regurgitaiton

A

Diastolic, decrescendo blowing murmur 2nd LSB

Increase P2 if PHT

252
Q

Systolic murmu

A

MR (MVP), TR

  • AS, PS
  • VSD
253
Q

Autopulmonary shunts murmur

A

Early mid late, holosystolic/pansystolic

254
Q

Diastolic murmur

A

AR, PR

-MS, TS

255
Q

Atrial myxoma

A

Murmur plop

256
Q

Continuous murmur

A

PDA-machinery*

AV fistula

ASD with high LA pressure

Coarctation

257
Q

AV blocks

258
Q

What is an AV block

A

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

259
Q

What are the types of AV blocks and fasciculus blocks

A

First degree Av
Second degree AV
Third degree AV

Fasciculus blocks (hemiblocks)
Left anterior hemiblock
Left posterior hemiblock

260
Q

Primary AV block

A

Prolongs AV node conduction

PR interval more than .2 sec.

261
Q

ECG 1st degree block

A

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

262
Q

Etiology of 1st degree AV block

A

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

263
Q

How calculate regular rhythm

A

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

264
Q

2nd degree block types

A

Mobitz I

Mobitz II

265
Q

Second degree av block

A

Progressive PR-Interval
Prolongation prior to dropped QRS

Grouped beats

266
Q

Mobitz I

A

Progressive lengthening results from earlier arrival in relative refractory period AV conduction

Implies impairment of AV conduction (AV node)

Transient

267
Q

Etiology mobitz I

A

All those things that cause 1st degree AV block

Digitalis toxicity

Ischemic events (MI inferior)

Myocarditis

268
Q

2nd degree AV block -mobitz

A

May be seen with inferior AMI

Level of block is at level of AV node

Narrow QRS complex

269
Q

Etiology 2nd degree AV block-mobitz type II

A

Ischemic heart disease

May be seen with acute anterior myocardial infarction

Degeneration of conduction system

270
Q

2nd degree AV block, mobitz type II mobitz

A 
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

271
Q

Features of high AV block

A

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

272
Q

Low AV block

A

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

273
Q

Third degree heart block (complete heart block)

A

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

274
Q

Etiology 3rd degree heart block

A

Ischemic

Infiltrating diseases

Cardiac surgery

  • by pass, valve replacement
  • myocarditis
  • degenerative
275
Q

How do you treat 3rd degree block

276
Q

What check on every ECG

A

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
277
Q

R

A

As impulse travels toward the electrode +

278
Q

S

A

As impulse travels away from the electrode - deflection

279
Q

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

A

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

280
Q

The septum is activated from _ to _

A

L to R

L septal surface activated .1 s before R septal surface

281
Q

Why normal ventricular muscle activated L to R

A

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

282
Q

Intrinsic deflection

A

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

283
Q

What is intrinsic deflection for V1 and V2

A

V1 .02 s

V2 .04 s

284
Q

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

A

The impulse is late in reaching the pericardial surface

Late ID in: a. BBB b. Hypertrophy/dilated

285
Q

Common features of BBB

A

Wide QRS complex (.12 s or greater)

ST segment -T waves slope off in opposite direction to QRS

286
Q

Which side of the septum is activated first in RBBB

287
Q

In RBBB is there an S wave in V6?

288
Q

Sequence of ventricular activation in RBBB

A

After septal activation, then activation begins in LV free wall

289
Q

RsR’ variants in V1-V2

A

Normal

Pertussis or straight back

RV diastolic volume overload

WPW syndrome

RVH

Du henna dystrophy

290
Q

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

291
Q

Sequence of ventricular activation in LBBB

A

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

292
Q

LBB more apt to occur with

A

HTN
Ischemia
Aortic stenosis
Cardiomyopathy

293
Q

LBBB with LAD

A

More myocardial dysfunction

More disease in conduction system

Maybe higher mortality

294
Q

LBB with RAD

A

Think congestive cardiomyopathy

295
Q

Limb leads in BBB

A

I and AVL usually have features of V6

296
Q

T wave in BBB

A

Polarity is opposite QRS direction

297
Q

What causes secondary T wave changes T wave in BBB

A

Disturbance in depolrepol

298
Q

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

A

Primary

Ischemia

299
Q

In LBBB which ventricle is activated first

300
Q

Hemiblock/fasciculus block

A

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

301
Q

Left bundle branch

A

Anterior division (superior)

Posterior division (inferior)

302
Q

Hemiblocks

A

Left anterior hemiblock (LAH)-more common

Left posterior hemiblock (LPH)

303
Q

Etiology of LHA

A

Disease in conduction system

Often associated with MI (left anterior descending-LAD occlusion)

304
Q

Criteria for LAH

A

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

305
Q

ECG LAH

A

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)

306
Q

Anterior hemiblock

A

LAD-usually associated with MI (or other heart disease

Normal or slightly widened QRS

Q1S3

307
Q

Etiology of left posterior hemiblock -less common

A

Disease in conduction system

308
Q

Criteria of left posterior hemiblock

A

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

309
Q

What causes atrial enlargement

A

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

310
Q

P wave

A

Depolarization of atria

Doesn’t exceed 3 mm

Increased amplitude-hypertrophy, HTN, AV valve disease, Cor pulmonale, congenital

311
Q

P of RAE

A

Tall, pointed; taller in III than in I

P-pulmonale

312
Q

P of LAE

A

Wide, notched; taller in I than in III

P-mitrale

2nd half of p wave negative in V1 of III

313
Q

RAE

A

Associated with TV disease or pul HTN

COPD , PE, MS, or MR are causes of pul HTN

314
Q

Right atrial enlargement (RAE)

A

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

315
Q

LAE

A

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

316
Q

Causes LAE

317
Q

Ventricular hypertrophy (enlargement)

A

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

318
Q

Left ventricular hypertrophy

A

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

319
Q

ECG pattern LVH

A

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

320
Q

Criteria for LVH

A

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

321
Q

Romhilt estes scoring system for LVH

A

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
322
Q

Sokolow lyon criteria

A

R in I and S in III>25 mm

R in AVL >11

R in V6>26 mm

323
Q

Right ventricular hypertrophy cause

A

Cause-COPD

RVOT obstruction, VSD

Congenital-TOF< pulmonic stenosis, transposition of great vessels

Mitral stenosis, tricuspid regurgitaiton

324
Q

ECG RVH

A

R waves assume prominence in right precordal leads and deep S waves develop in left precordial leads

R:S ration>1

325
Q

Clues to RVH

A

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)

326
Q

Causes of dominant r waves in V1

A

RVH

Posterior or lateral MI

WPW

Hypertrophic cardiomyopathy

Muscular dystrophy

Normal variant

327
Q

CAD general comments

A

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

328
Q

What happens with atherosclerotic coronary arteries from plaques

A

Can undergo…
Fissuring or erosion

Triggers thrombus formation to cause ischemia to myocardium

329
Q

Risk factors for atherosclerosis

A

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

330
Q

Metabolic syndrome

A

Insulin resistant-increased glucose

HTN

High TG, low HDL

Hyperuricemia

Hyper coagulation

Obese BMI>30-central obesity

Desireable : BMI 21-24

BMI=weughtx705/height

331
Q

Angina pectoris

A 
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_

332
Q

Supply angina

A

Decreased oxygen delivery to tissue leads to ischemia

333
Q

Example supply angina

A

Coronary vasoconstriction, stenosis, platelets release serotonin and thromboxane A2

334
Q

Demand angina

A

Increased myocardial oxygen requirements and workload can lead to ischemia

335
Q

Examples of demand angina

A

Exercise, stress, emotion, fever, thyrotoxicosis

LVH due to As

Anemia (low oxygen carrying capacity)

336
Q

Effects of ischemia

A

Mechanical consequences

Biochemical consequences

Electrical consequences

337
Q

Mechanical consequences ischemia

A

Angina, is ischemia is prolonged or develop coronary occlusion, may lead to myocardial necrosis

Segmental akinetic bulging (dyskinesia)

338
Q

Biochemical consequences ischemia

A

Fatty acids can’t be oxidized

Increased lactate production

Reduced pH with metabolic acidosis

339
Q

Electoral consequences ischemia

A

Inversion fo T wave

Transient displacement of ST segment

Depression-subendocardial

-elevation-subepicardial

Electrical instability instability; VT, VF

340
Q

LAD MI

A

Anterior wall infarction

Leads V1-V7

341
Q

RCA MI

A

Inferior wall infarction (RV infarction)

Leads II, III, AVF

342
Q

Circumflex artery MI

A

Lateral wall

Leads I, AVL

343
Q

Posterior descending artery

A

Posterior wall infarction

V1-V3

344
Q

CV causes of chest pain

A

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

345
Q

Non cardiac cause of chest pain

A

Pleuritis/pneumonia/PE

Pulmonary infarction, pneumothorax, GI

GI disease: GERD, PUD, gallstones, esophageal motility disorder chest wall syndromes

Lung cancer

Aortic aneurysm

346
Q

Non chest pain symptoms of chronic ischemic heart disease

A

Dyspnea, non chest locations of discomfort (((exertional or rest)

Mid epigastric or abdominal

Diaphoresis

Excessive fatigue and weakness

Dizziness and syncope

347
Q

Anginapectoris why exercise effect it

A

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

348
Q

Angina equivalent

A

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

349
Q

Signs or risk factors for angina

A

Xanthelasma

Xanthomas

Diabetic skin lesion

Nicotine stains

Pale

Absent peripheral pulses

350
Q

Angina

A

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

351
Q

What can mimic angina in absence of CAD***

A

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

352
Q

Unstable angina

A

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

353
Q

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

354
Q

Both UA and NSTEMI are called NSTEMI ACS or NSTE ACS

A

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

355
Q

Pathology UA and NSTEMI

A

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

356
Q

Stable angina ecg

A

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

357
Q

ECG unstable angina/NSTE ACS

A

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

358
Q

Differential diagnosis of NSTE ACS

A

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

359
Q

Lab CAD

A

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

360
Q

Diagnostic testing for atherosclerosis

A

Functional and/or anatomical information for CAD

361
Q

Functional diagnostic testing for atherosclerotic CAD

A

Exercise ECG, single photon emission CT (SPECT, PET)

Coronary flow (PET, fractional flow reserve)

Wall motion abnormalities (echo, cardiac magnetic imaging CMRI)

362
Q

Anatomical diagnostic testing for atherosclerotic CAD

A

Invasive angiography, coronary CT angio (CTA)

-coronary artery calcium scoring (CAC) (note, CAC doesn’t provide data on coronary luminal narrowing

363
Q

Signs of high risk for coronary event

A

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

364
Q

Stress testing: exercise ECG

A

Exercise electrocardiography (preferred if patient is suspected to have angina)

Safe… only 1 death or MI per 2500 tests

365
Q

Contradictions exercise ECG

A

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

366
Q

Sensitivity and specificity exercise ECG

A

70% and 75% specific

367
Q

Stress echocardiography

A

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

368
Q

Nuclear myocardial perfusion imaging

A

SPECT (single photon emission computer tomography)

Useful in LBBB, LVH, digitalis effect

Technetium 99

369
Q

Pharmacological stress test

A

Patient unable to exercise/abnormal ECG LBBB, LVH

Use: vasodilator nuclear perfusion

  • adenosine/regadenosine/dipyridamole
  • vasodilators increase HR
370
Q

When use dobutamine echocardiogram

A

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

371
Q

Coronary angiography

A

Cardiac cath

Provides anatomic diagnosis of severity of CAD

Percutaneous revascularization can be performed after study

Exposed to radio contrast (kidney dysfunction

372
Q

Use of coronary angiography

A

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

373
Q

Coronary CT angiography

A

Ability to quantify lesion severity can be limited by significant calcification

374
Q

CXR

A

Usually normal unless history of mi, HF< VHD

Cardiomegalia in HTN< VHD, cardiomyopathy, pericardial effusion

375
Q

Treatment of patients with stable angina non pharm

A

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

376
Q

Pharm treat to prevent MI/death/reduce symptoms

A

Asprin

Beta blocker

ACEI

Statins

Nitro/nitrates

CCB

377
Q

Identify aggravating conditions

A

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

378
Q

Pharm treatment ASA

A

ASA:cyclooxygenase inhibitors of platelet activation

Inhibit thromboxane production

Clopidogrel blockers in ADP induced platelet aggregation

379
Q

Bb

A

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

380
Q

Contraindication bb

A

Decompensated HF, hypotension, advanced AV block

381
Q

ACEI

A

Blocks conversion of A1 to A11

Decrease CV mortality

Useful in diabetic (renal protection) and patients with LV systolic dysfunction

382
Q

Nitrates

A

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

383
Q

What not take nitrate with

A

Phosphodiesterase inhibitor

384
Q

CCB

A

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

385
Q

Myocardial revascularization

A

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

386
Q

Treat prinzmetal

A

Relieved by nitro

Dihydropyridine CCB (amlodipine)

387
Q

Manage los risk patient

A

Antianginal - BB, nitro, CCB
Statin

Antiplatelet-ASA/clopidogrel

Anticoagulant-UF heparin

Cath:revascularization if appropriate

388
Q

High risk patient (US or NSTEMI) manag

A

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

389
Q

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

A

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

390
Q

Statins for hyperlipidemia

A 
ASA
Nitrates
B blocker
ACE
Ranexa inhibit late phase of inward Na current during repolarization; decrease angina occurrence
391
Q

Diet for CAD/angina to protect against atherosclerosis

A

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

392
Q

Shock

A

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

393
Q

Pathophysiology shock

A

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

394
Q

Skinextremities shock

A

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)

395
Q

Neck veins shock

A

Distended (HF, PE, tamponade)

Flare (hypovolemia)

396
Q

HR shock

A

Fast (sensitive indicator of shock); occasionally LO

397
Q

BP shock

A

Systolic low diastolic low

398
Q

Respiration shoc

A

Tachypnea, bronchospasm, respiratory failure

399
Q

Renal shock

A

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

400
Q

Heart shock

A

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

401
Q

Categories of shock

A

Hypovolemia shock

Distributive shock

Cardiogenic shock

Extracardiac obstructive shock

402
Q

Hypovolemia shock hemorrhagic

A

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

403
Q

Non hemorrhagic hypovolemia shock

A

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

404
Q

DKA hypovolemia shock

A

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

405
Q

Most common cause of hypovolemia shock

A

Hemorrhagic shock

406
Q

Treatment issues of volume loss

A

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

407
Q

Fluid change

A

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

408
Q

Shock class I

A

Lose 750 ml or up to 15% blood

Normal bp
Increased pulse pressure

Give crystalloid

409
Q

Class II hemorrhagic shock

A

Lose 750-1500 ml of 15-30% blooc
Bp normal

Pulse pressure decreased

Give crystalloid

410
Q

Class II hemorrhagic shock

A

Lose 1500-2000 ml blood

Decrease bp
Decrease pulse pressure

Give crystalloid and blood

411
Q

Clas IV hemorrhagic shock

A

Over 2000
Decreased bp
Decreased pulse pressure

412
Q

Distributive shock types

A

Septic or non septic (vasodilation)

Most commoncause of non cardiogenic shock

230000 patients yearly

30-40% mortality

413
Q

Sepsis signs/symptoms

A

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

414
Q

Common sources of infection distributive shock

A

Pulmonary-pneumonia, emphysema

Ab-peritonitis, cholangitis

GU-pyelonephritis, abscess

CNS-meningitis

Skin-cellulitis, necrotizing fasciitis

415
Q

Septic shock

A

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

416
Q

Pathophysiology distributive shock

A

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

417
Q

Signs and symptoms of distributive shock

A

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

418
Q

Vasodilators effects of septic shock

A

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%
419
Q

Anaphylactic shock diagnosis

A

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)

420
Q

Life threatening/danger signals of anaphylactic shock

A

Rapid progression of symptoms

421
Q

Respiratory distress of anaphylactic shock

A

Strider, persistent cough, wheezing, hypotension

422
Q

Pathophysiology anaphylactic shock

A

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

423
Q

Distributive hemodynamic profile of anaphylactic shock

A

PCWP (PAOP) N(early or decrease late

CO decrease or increase

SVR decrease

Tissue perfusion (mixed venous oxyhemoglobin sate) >65%

424
Q

Cardiogenic shock

A

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
425
Q

Cardiogenic shock definition

A

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%

426
Q

Types of cardiogenic shock

A

Cardiomyopathies

Arrhythmogenic

Mechanical

427
Q

Cardiomyopathic cardiogenic shock

A

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

428
Q

Arrhythmogenic cardiogenic shock

A

Tach ( a fib, a flutter , re entrant tach), VT, VF

-Brady: complete heart block, mobitz II)

429
Q

Mechanical cardiogenic shock

A

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

430
Q

Diagnose cardiogenic shock

A

Decrease BP, decrease UO, mental status changes

Cool, mottled extremities

Distended neck veins

Pul edema

Document myocardial dysfunction-echocardiogram-cath

431
Q

Etiology cardiogenic shock

A

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)

432
Q

Pathophysiology cardiogenic shock

A

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

433
Q

Comments on cardiogenic shock

A

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)
434
Q

Treat

A

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

435
Q

Treat STEMI

A 
PCI-preferred
CABG
Fibrinolytic
ASA
Heparin
NSTEMI-glycoprotein IIb/IIIa inhibitors
P-pressers-norepinephrine
-CS inotropy
436
Q

Mechanical support

A

IABD
LVAD
ECMO

437
Q

IABD

A

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

438
Q

LVAD

A

Bridge for transplant, tandem heart/impels

439
Q

ECMO

A

When O2 is severely impaired

440
Q

Arginase

A

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

441
Q

Pressure

A

Norepi

Dopamine

Inotropy s

442
Q

Norepi

A

Preferred-alpha I, B1 B2 agonist

Vasopressin-vasoconstrictor/use in vasodilators shock

443
Q

Dopamine

A

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

444
Q

Inotropes

A

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

445
Q

Treat RV infarct

A

Fluids for high filling pressure

446
Q

PAC

A

Useful when despite adequate fluids given, but not favored

447
Q

Indices of tissue perfusion

A

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

448
Q

What avoid

A

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

449
Q

Oasis

A

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

450
Q

Acute obstruction to flow in circulation

A

Extracardiac obstructive shock

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

451
Q

Pulmonary vascular extracardiac obstructive chock

A

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

452
Q

Mechanical extracardiac obstructed shock

A

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

453
Q

Extra obstructive cardiac shock pearls

A

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

454
Q

Presentation extracardiac obstructive shock tension pneumothorax

A

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

455
Q

RX extracardiogenic tension pneumothorax

A

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

456
Q

Pericardial tamponade signs

A

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

457
Q

Echo pericardial tamponade

A

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

458
Q

RX pericardial tamp

A

Echo/US to guide pericardialcentesis

459
Q

Symptoms of hemodynamically significant pulmonary embolus

A

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

460
Q

Risk factors for hemodynamically significant pulmonary embolus

A

VTE in leges, pelvis, arms-most common,

Non thrombotic material (fat, air , tumor cells, amniotic cancer, hypercoagulabiltiy (factor V ) previous VTE?PE, pregnancy

461
Q

Pathophysiology hemodynamically significant pulmonary embolus

A

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

462
Q

PE hemodynamicaly significant pulmonary embolus

A

Increase JVD, increase P2 or widely split P2-due to delayed emptying of RV

R>20/min, increase HR

463
Q

Obstructive hemodynamic profile

A

Decrease

Increase HR

Increase JVD

Extremities cool

Lungs dry

Co-N decrease

PCWP PAOP N or decrease

SVR increase

464
Q

CTPA imaging

A

Computer tomography pulmonary angiography

Permits visualization of thrombi in pul arteries

Preferred over ventilationperfusion lung V/Q

465
Q

V/Q scan

A

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

466
Q

D dimer

A

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

467
Q

ECG

468
Q

Echocardiogram

A

RV dilation, TR

469
Q

hemodynamically significant pulmonary embolus BNP and trop

A

BNP and troponin elevated

470
Q

CXR pulmonary embolism

A

Atelectasis RLL, otherwise normal

471
Q

ECG pulmonary embolism

A

Sinus tach, incomplete RBBB, PAC, st changes

472
Q

ABG pulmonary embolism

A

PH 7.5 pCO2 29, PO2 58 HCO3 26

473
Q

CBC CMP pulmonary embolism

474
Q

Venous Doppler

A

R leg DVT femoral vein

475
Q

CTPA pulmonary embolism

A

Large thrombus in PA

476
Q

D dimer pulmonary embolism

477
Q

Echo pulmonary embolism

478
Q

Heart failure

A

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

479
Q

What percent of adults will develop HF

A

10, 10% of people over 53 have this

480
Q

Mortality rate HF

A

1 year 10-20% 5 year 50%

481
Q

Etiology HF

A

60-75% CAD-ISD

18% idiopathic
12% valvular

10% hypertensive

*most common cause of LV systolic dysfunction is from ischemic heart disease

482
Q

Basic cause of HF

A

Restriction/obstruction to ventricular filling

  • RV infarct
  • constrictive pericarditis
  • MS
  • atrial myxoma
483
Q

State A HF

A

HF risk factors no heart disease no symtpoms

484
Q

Stage B HF

A

Heart disease no symptoms

Asymptomatic LV dysfunction

485
Q

State C HF

A

Prior or current HF symptoms

486
Q

Stage C heart failrue

A

Refractory symptoms

487
Q

Stage A ACC/AHA

A

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)

488
Q

Stage B ACC/AHA

A

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

489
Q

Stage C ACC?AHA

A

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

490
Q

Stage D ACC AHA stages

A

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

491
Q

Class I NYHA

A

No limitation of physical activity

No symptoms. With ordinary exertion

One year mortality 5-10%

Asymptomatic

492
Q

Class II NYHA

A

Slight limitation on physical activity

Ordinary activity causes symtpoms

One year mortality 15-30%

No rest sx
Exertional sx with ordainary activity

493
Q

Class III NYHA

A

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

494
Q

Class IV NYHA

A

Inability to carry out physical activity without discomfort
Symptoms at rest

One year mortality 50-60%

Rest sx

495
Q

Pathogenesis of HF

A

Impaired systolic function

Impaired diastolic function

Mechanical abnormalities

Disorders of rate/rhythm

Pulmonary heart disease

High output states

496
Q

Echo can see what specific causes of heart failrue

A 
Hypertensive heart disease
Ischemic heart disease
Hypertrophic heart disease
Infiltrating heart disease
Primary valvular heart disease
497
Q

What is echo necessary to distinguish

A

Necessary to distinguish systolic heart failure from diastolic heart failrue

498
Q

Types of heart failure

A

Systolic/diastolic

High/low

Acute/chronic

Right/left

Forward/backward

499
Q

Acute HF

A

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

500
Q

Chronic HF

A

Multivalvular disease of dilated cardiomyopathy

Progresses slow

Edema, weight gain

501
Q

Systolic HF (HFrEF-reduced)

A

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

502
Q

Diastolic HF-normal EF (HFpEF-preserved)

A

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

503
Q

High output

A

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

504
Q

Low output

A

Ischemic heart disease, HTN

-dilated cardiomyopathy, valvular and pericardial disease

505
Q

Right sided HF

A

Affects RV

Pulmonary HTN due to pulmonary embolus

Edema, hepatomegalia, venous distention

506
Q

Left sided HF

A

LV is overloaded

AS, MI

Dyspnea, orthopnea, due to pul congestion

507
Q

Neurohormonal compensation response of HF

A 
SNS
RAAS
Cytokines activation
Altered renal physiology
LV remodeling
508
Q

RAAS

A

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

509
Q

Arginine vasopressin

A

AVP or ADH

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

510
Q

Precipitating causes of HF

A

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
511
Q

Signs and symptoms of HF

A

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

512
Q

Heart and HF

A

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

513
Q

RV failrue

A

Peripheral/sacral edema

Hepatomegalia

Ascites

Increased JVD, HJR

514
Q

Where is the JVD Seen

A

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

515
Q

How measure JVD

A

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,

516
Q

What is a venous pressure above normal

A

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

517
Q

Diagnostic test for HF

A

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

518
Q

CXR HF

A

Cardiomegalia

Pulmonary edema with central peripheral infiltrates

Increased size of vessels in upper portion of lungs

Pleural effusions

519
Q

Echo HF

A

Practical useful, mobile, bedside/ICU/ED

Chamber size, clots, tumors
Wall motion muscle thickness
Pericardial effusions
Valvular disease

Systolic.diastolic HF-ejection fraction

520
Q

ECG HF

A

May have ischemia, infarction, hypertrophy

Rhythm disturbances (atrial, junctional, ventricular )

Tachycardia/bradycardia/blocks

521
Q

Troponin T and I

A

Released from myocytes when damaged

  • increase 3-12 hours from onset of chest pain
  • peak 24-48 hours; return to baseline 5-14 days
522
Q

CK-MB

A

Increases 3-12 hours from onset of chest pain

Peak 24 hours; baseline 1-3 days

Sensitivity

523
Q

CBC HF

A

Anemia secondary to chronic disease

Anemia may aggravate HF

524
Q

CMP HF

A

Electrolyte imbalance-low Na, K

Pre renal azotemia-high BUN to creatine

525
Q

UA HF

A

Protein in urine

526
Q

Thyroid labs HF

A

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

527
Q

BNP

A

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

528
Q

Differential diagnosis of HF

A

Pulmonary problems

  • PE
  • asthma
  • pneumonia

Cirrhosis

  • ascites
  • edema

Renal-edema

Venous insuffiency-edema

529
Q

Five basic principles of HF

A

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

530
Q

Indications for admission to hospital for management of HF

A 
Acute MI
Severe respiratory distress
Hypoxia
Hypotension
Cardiogenic shock
Anascara
Syncope
Heart failure refractory to oral medications
531
Q

Non pharm treatment of HF

A

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

532
Q

How counsel patient HF before discharge of hospital

A

Diet-patient with spouse/other sodium restriction, Carl our restriction if overweight stimulants

Education

Rehab exercise

Medes: ACE/ARB, bb, ASA, statin, nitro prn

533
Q

CO

534
Q

Stoke volume is modulated by what

A

Preload

Afterload

Contractility

535
Q

Conventional treatments of HF

A

Diuretics
-reduce fluid volume

Vasodilators
-decrease preload and/or afterload

Inotropes
-augment contractility

536
Q

Class I

A

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

537
Q

Class II

A

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

IIb-less established evidence/opinion-benefit 1+ risk

538
Q

Class III

A

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

539
Q

A level evidence

A

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

540
Q

B level evidence

A

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

541
Q

Level C evidence

A

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

542
Q

Pharm treatment of HF

A

ACE I or ARB

BB
Diuretic

Spironolactone
Digitalis

IV inotropes

Hydralazine

Nitrates

CCB
Sacubitril-Vallarta’s ivabradine

543
Q

ACE I

A

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

544
Q

When use ACE cautiously

A

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

545
Q

Contraindication ACE I

A

Angioedema

Pregnancy

546
Q

AE ACE I

A

Bilateral RAS(renal artery stenosis)

Cough

547
Q

List ACE I

A 
Lisinopril
Enalapril
Captopril
Benazepril
Ramipril
Quinapril
548
Q

ARB

A

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

549
Q

ACE

A

Block angiotensin I to angiotensin II

Improve LV relax and contraction

Veno and vasodilation

550
Q

ARB action

A

Increases myocardial fibrosis
Increases NE
Increases vasoconstriction
Increases endothelin1

551
Q

Why get cough from ACE

A

Bradykinin accumulated

552
Q

ARB vs ACE

A

Comparable but neither more effective

Don’t give ARB to patient that got angioedema from ACE

553
Q

Name ARBS

A 
Losartan 
Vallarta’s
Candesartan
Telmisartan
Irbesartan
Entresto; sacubitril is the neprilysin inhibitor and Vallarta’s is AII receptor blocker
554
Q

BB

A

Survival benefit in chronic syst HF and dilated cardiomyopathy

Slow progression of disease and decrease hospitalization

Improve cardiac performance and symptoms of HF

555
Q

Hemodynamics of BB

A

Decrease heart rate

Antiarrhythmic properties

Antiischemic

Blunts SNS effects of NE

Reverse remodeling

556
Q

BB good

A

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
557
Q

Who don’t give BB

A

Unstable class IV

558
Q

Who give BB

A

All stable patients with symptoms of HF, reduced EF, unless contraindicated. Level of evidence: A

Patients with class II and II NYHA

559
Q

Diuretics for HF

A

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

560
Q

AL or LOH diuretics

A

Lasix (furosemide)

Bumex (bumetanide)
Demanded (torsemide)

561
Q

DT

A

Thiazide

Zaroxolyn (metolazone)

562
Q

Late DT

A

Spironolactone (aldactone)

563
Q

How give furosemide

A

10 mg IV.he or 40 mg IV every 8-12 hours

Watch K Mg, Na, BUN, creatinine

564
Q

Digitalis

A

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

565
Q

Why use digitalis

A

HFrEF and a fib for ventricular rate control

566
Q

MOA digitalis

A

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

567
Q

Spironolactone

A

Antagonizes effects of aldosterone

Use in addition to standard care (ACE, BB, diuretic, dig)

568
Q

RALES

A 
Randomized aldactone evil study (aldactone-spironolactone) 
12.5-25 mg/day; class III-IV patients -30% reduction in mortality
569
Q

How watch spironolactone

A

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

570
Q

Level of evidence of spironolactone

A

B-decreased mortality, decreased HF hospitalization s

571
Q

Eplerenone

A

New watch K

572
Q

Inotropes

A

Increases contractility

Dobutamine
-stimulating beta1 and beta2 receptors

Milrinone

  • inotropic vasodilator
  • inhibits phosphodiesterase
573
Q

Dopamine

A

Stimulates beta 1 receptor

2-10 ug/kg/min

Higher doses stimulate alpha receptors

Useful short term

574
Q

Hydralazine plus isosorbide dinitrate

A

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

575
Q

Isosorbide dinitrate

Isosorbide mononitrate

A

Better response to hydralazine and isosorbide in african Americans that in whites; use if intolerant to ACE/ARB

Nitroprusside
Vasodilator monitor BP closely

576
Q

Nitrates hemodynamic effects

A
  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
577
Q

CCB

A

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

578
Q

Role of OMM if HF lymph treatment

A

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

579
Q

Effleuragepetrissage-distal to proximal stroking of extremities

A

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

580
Q

Conclusion HF

A

Make the right diagnosis

Look for the precipitating causes and underlying etiology

Provide treatment based on solid evidence based recommendations.

► Med Notes (62 decks)

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