Cardio Flashcards
Infections of the cardiovascular system: myocarditis, pericarditis, endocarditis
Ok
Myocarditis
Inflammation of the myocardium that results in myocardial injury via cytoplasmic effect or secondary to immune system response
Myopericarditis
Extension of myocarditis into the pericardium
Clinical features myocarditis
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
Differential diagnosis myocarditis
Acute MI v acute and/or chronic heart failure v. Atypical chest pain v pericarditis v cardiomyopathies v valvular disease
*not all encompassing
PE myocarditis
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
Work up myocarditis
EKG
Cxr
Ekg myocarditis
Assess for arrhythmia (sinus tachycardia most common), transient ST-T wave abnormalities. Findings nonspecific
CXR myocarditis
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
Echocardiogram
Assessment of ventricular function and structure. Evaluation of ejection fraction, left ventricular size, wall option abnormalities
PCR
Detection of viral genome
Labs
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)
___ biopsy can aid in a definitive diagnosis
Endomyocardial
Complications myocarditis
Dilated cardiomyopathy
Myopericarditis
Sudden cardiac death (20%)
Treat myocarditis
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
Infection etiologies myocarditis
Coxsackie B, trypanosome cruzi, trichinella spiralis
Cocksackie B (picornaviridae, enterovirus) myocarditis
+ SsRNA, small, naked, icosahedral
Peak incidence summer and fall
Fecal oral transmission
Manifestations coxsackie B
URI, pleurodynia (devils grip-severe intercostal pain and fever), myocarditis (most common infectious etiology), aseptic meningitis
How get trypanosome Cruzi
Reduvviid, animal
Where is trypanosome cruzi
Southern US, Mexico, SA
What is trypanosome cruzi
Intracellular Protozoa (hemoflagellate)
Phases of chagas
Acute-1 month
Intermediate
Chronic-years-decades to develop
Diagnose trypanosome cruzi
Peripheral smear for trypmastigotes, xenodiagnosis
Acute chagas
Chagoma, romana sign
Fever, malaise, LAD
CV-myocarditis
CNS-severe meningoencephalitis (young patients)
Intermediate chagas
Asymptomatic
Chronic chagas
CV: dilated cardiomyopathy, arrhythmias
Megacolon, achlasia
Trichinella spiralis
Invasive nematode
How get trichinella spiralis
Ingestionof cysts from raw pork (boars or even horses)
Humans are dead end host
Trichinella in human
Larvae develop in gut->mate->larvae disseminate hematogenous lh->penetrate muscle tissue
Skeletal muscle, heart brain
Invasive cycle trichinella spiralis
With heavy infection can be lethal
Symptoms trichinella spiralis
Abdominal pain, diarrhea, fever (while in small intestine)
Muscle invasion: muscle aches, other sx dictated by location of larvae invasion
When consider trichinella spiralis diagnosis
Periorbital edema, myositis, eosinophilis
Diagnostics for trichinella spiralis
Serologic (ELISA) or latex agglutination, CPK levels, muscle biopsy
Pericarditis
Inflammation of the pericardium
Infectious agents of pericarditis
Viruses, bacteria, TB (caseating pericarditis), fungi, parasites
Presentation pericarditis
Chest pain (sharp, often positional and pleuritic in nature, relieved by leaning forward), fever, palpations
DDx considerations
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
PE pericarditis
Friction rub upon cardiac auscultation, rapid or irregular pulse. Secondary to extensive differential considerations, complete cardiac and pulmonary exams are essential
Work up pericarditis
EKG
CXR
Echo
Labs
EKG
Diffuse ST elevations with reciprocal depressions in leads aVR and V1 with PR depression
CXR
Majority of CXR with pericarditis show minimal abnormalities
Exception-pericardial effusion>250 mL will cause a symmetrically enlarged cardiac silhouette. Water bottle sign
CXR
Pericardial effusion (visible) with water bottle sign. Notice flattening of the diaphragms to compensate for the weight of the effusion
Echo pericarditis
Pericardial effusion (visible) with water bottle sign . Notice flattening of the diaphragms to compensate for the weight of the effusion
Echo pericarditis
Assess for pericardial effusion and/or tamponade. More sensitive than a CXR
Labs pericarditis
Cardiac enzymes (serial), CBC with differential, ESR, CRP, blood cultures if temp over 38@
Complciations pericardiis
Cardiac tamponade-treated with pericardiocentesis
*counsel about activity restrictions
Treat pericarditis
High dose asprin TID (ibuprofen, indomethacin) and colchicine
What is contraindicated in pericarditis
Anticoagulants
Infectious agents pericarditis
Cocksackis B (serous pericarditis), mycobacterium TB (caseous pericarditis)
Cocksackis B
Picornaviridae, enterovirus
+SsRNA, small naked icosahedral
Transmission cocksackis B
Fecal oral
Manifestations cocksackie B
URI, pleurodynia (devils grip-severe intercostal pain and fever), myocarditis(mostcommon infectious etiology), aseptic meningitis
Mycobacterium tuberculosis
Acid fast (weakly G+), obligate aerobes, facultative intracellular (macrophages)
AFB secondary to mycotic acid cell wall composition (highly resistant to desiccation including NaOH)
Virluence mycobacterium Tb
Facultative intracellular, sulfatides, cord factor, surface protein can cause a deflated hypersensitivity and cell mediated immunity reaction (utilized for PPD skin testing ) wax d
Stains mycobacterium BT
Acid fast (ziehl-neelsen, Kenyon)-red rods
Auramine-rhodamine staining-fluorescent apple green color
Manifestation mycobacterium Tb
Pulmonary tuberculosis
CAN cause a caseating pericarditis through direct lymphatic of hematogenous dissemination of the bacteria
Infective endocarditis
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
Risk factors IE
Age>60 M>F, poor dentition, IV drug abuse, structural heart disease, congenital heart disease, valvular heart disease, provalve replacemnt, rheumatic heart disease
Clinical manifestion IE
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
Acute IE
Rapid and life threatening progression of symptoms and cardiac damage
High fever, chills, weakness, SOB, pleuritic chest pain
Subacute IE
Slow, indolent course
Low grade fever, weight loss over time, fatigue, arthralgias/myalgia
Complciations IE
CHF, abscess formation, hematogenous spread, embolism, systemic immune reaction , death
Cardiac manifestations IE
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
Diagnostic work up IE
Blood culture x3 (always prior to abx!!!!), CBC with diff, CMP
EKG, ESR, CRP, UA (assess for hematuria
Transesophageal echocardiogram, CXR
Major criteria for IE duke
Blood culture + with consistent microorganisms from 2 separate blood cultures
At least two positive >12 hr apart or lll of the three or
Definite diagnosis
2 major criteria or 1 major and 3 minor criteria or 5 minor criteria
Treat IE
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
Give high risk patients prophylactic before dental or respiratoy procedures
Able to take PO-amoxicillin
IV-ampicillin or cefazolin or ceftriaxone
Allergic to penicillin -desensitize, cephalexin, clindamycin, azithromycin
Common infectious agents of IE
S aureus, s epidermis, s viridans, enterococcus(D strep)
HÁČEK, coxiella burnetti, brucellosis , s agalactiae0rare
S aureus
G+ cocci, clusters, coagulate and catalase positive, facultative anaerobes
Normal flora on skin (can breach) and colonize nasopharyngeal
Virluence s aureus
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
Invasion of tissue and blood stream s aureus
Hyaluronic ASD-breaks down CT
Staphylokinase-lyse s formed clots
Lipase-breaks down fat
Toxin mediated manifestations
Food poisoning, scalded skin syndrome, toxic shock syndrome
Local manifestations of s aureus
Skin-impetigo, cellulitis, folliculitis, furuncles, carbuncles
Respiratory-pneumonia
Systemic manifestations s aureus
Acute-endocarditis, meningitis, osteomyelitis (#1 cause in adults and children), septic arthritis
Thx s aureus
Will vary based off of clinical presentation. For systemic disease, vancomycin is an exceptional choice. For MSSA-nafcillin is a great stating point
Signs of acute endocarditis from s aureus
Fatigue, chills, fever, night sweats, dyspnea, CHF,
Streptococcus viridans
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
Manifestations strep viridans
Dental caries, subacute endocarditis
Treat strep viridans
Penicillin
Staph epidermidis
Coagulate negative staph CoNS
G_ coccci, clusters, coagulate negative, catalase positive, novobicin sensitive, facultative anaerobes
Normals skin flora
Virluence staph epidermidis
Adhesion polysaccharide capsule-adherence to prosthetic devices, indwelling catheters
Biofilm formation
Manifestations s epidermidis
Subacute endocarditis, infection bacteria in neutrophil patients (susceptible)
Treat staph epidermidis
Vancomycin (very antibiotic resistant)
Enterococcus (group D strep)
Enterococcus faecalis
Gram + cocci, catalase negative, facultative anaerobes, variable hemolytic nature (alpha or gamma)
Normal human bowel
Virluence factor enterococcus
Extracellular dextran helps bind heart valves
Manifestations enterococcus
Subacute bacterial endocarditis, UTI, biliary tract infections
Media requirements enterococci
Can grow 40% bile AND 6.5% NaCl , blood agar
Treat enterococcus
Vancomycin resistant forms on the rise
Non enterococci group D strep
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
Virluence non enterococci group d strep
Extracellular dextran helps bind heart valves
Manifestations non enterococci
Biliary tract infections, UTI, subacute bacterial endocarditis
Media non enterococci
40% bile , blood agar
HÁČEK
Gram - group of bacilli, fastidious, suspected cause of culture negative endocarditis
Part of normal flora
Media HACEK
Chocolate agar
HACEK
Haemophilus (H parainfluenza most likel to cause endocarditis)
Aggregatibacter sp
Cardiobacterium sp
Eikenella corrodens
Kinde;Lola sp
Manifestation HACEK
Subacute endocarditis rare
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)
Chocolate agar
Blood agar
Coxiella burnetti
G- pleomorphic, obligate intracellular, aerobic, zoonotic, aerosol transmission
Symptoms coxiella burnetti
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
Cardiac rhythm disturbances (atrial, junctional, ventricular)
Ok
Principles
Treat patient no ECG
Establish urgency of treatment and treat reversible causes
Access hemodynamically stability (LOC< BP< HR)
Antiarrhythmic/electrical therapy
Arrhythmias
Symptoms, palpitations-skin, pounds, irregular
Lightheadness-faint-like
Syncope (near syncope), chest pain, dyspnea, sudden death
Etiology arrhythmias
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
Sinus tachycardia
Physiologic/pathological process
Look for the cause
Emotion, anxiety, fear, drugs, hyperthyroid
Fever, pregnancy, anemia, CHF
Hypovolemia
Rx-underlying cause
Sinus node
Normally, the dominant cardiac pacemaker bc ofits intrinsic discharge rate is the highest of all potential cardiac pacemakers
Bradycardia<60 bpm
Medical conditions situations associated with bradycardia
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
Causes of bradycardia
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
EKG of sinus bradycardia
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
EKG SSS-tachy-Brady
EKG SB
S arrest
SA block
-slow junctional rhythm seen in ischemic, sclerotic, inflammatory changes in SAN may cause syncope, dizziness, fatigue, heart failrue
Treat sinus bradycardia
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
What treat sinus bradycardia with
Atropine
Epinephrine
Isoproterenol
Pacemaker
Atropine
2 mg IV for SB and repeat 10 min
Use caution in glaucoma can increase IOP-narrow angle
AE-urinary retention, and distention, transient
Epinephrine for SB
2-10 ug.min
Isoproterenol for SB
1 mg in 500 cc D5Q-1-4 ug/min IV
What is automaticity
Idk
Atrial arrhythmias
Premature atrial contraction (PAC) also APC
Seen in absence of significant heart disease; associated with stress, alcohol, tobacco, coffee, COPD, and CAD
Premature beat of atrial arrhythmia
An irritable focus spontaneously fires a single stimulus
- premature atrial beat
- premature junctional beat
- premature ventricular beat
SA node resets in step with __
Premature atrial beat
Premature atrial beat with aberrant ventricular conduction
Wide QRS
Non conducted premature atrial beat
No QRS
PAC
A single complex occurs earlier than the next expected sinus complex
After the PAC, sinus rhythm usually resumes
Rhythm PAC
Irregular
P wave PAC
Present, may have different shape
normal in PAC
PR -varies or normaland WRS
Clinical PAC
In patients with heart disease, frequent PAC ma precede paroxysmal supraventricular tachycardia, a fib or a flutter
Treat PAC
If symptomatic
- reverse causes
- beta adrenergic antagonist (BB)
- metoprolol 25-50mg BID-TID
Paroxysmal atrial tachycardia
Sudden heart rate greater than 100
-rate irritable focus P wave
PAT with block (AV block)
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
Multifocal atrial tachycardia
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
Mat treat
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
Treat MAT-focus on underlying cause
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
ECG a fib
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
Atrial flutter
Saw tooth appearance
Leads II, III, AVF< V often best leads
250-350/min
Identifying a flutter may require
Inverting the tracing
Or employing a vagal maneuver
Junctional (nodal) rhythma
Paroxysmal junctional tachycardia
150-250 /min
P wave may be lost , inverted before or after each QRD
Sudden, irritable junctional focus paces rapidly
Junctional foci inherent rate
40-60 min
Premature ventricular contractions (PVC VPC) etiology
Normal heart
CAD, MI, HF, myocardial ischemia, hypoxia
Valvular heart disease, congenital heart disease
Cardiomyopathy, electrolyte abnormalities
Acid base imbalance
Hyperthyroid
Drugs
Premature ventricular contractions ECG
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
Principles of treatment ventricular rhythm disturbances: causes
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
Treat PVC
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
Ventricular tachycardia
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
V fibrillation
Disorganized depolarization
Not effective pump
Clinical setting-AMI, HF< K disturbance (low or high)
V flutter
250-350 per minute
Sine waves
Leads to v fib
Torsades de pointes
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)
Treat tdp
MgSO4, 1-2 grams IV bolus
Overdrive pacing
Isoproternol
Electrolyte disturbances (K, Ca, Mg)
Altered milieu
K disturbance
Low; lowers resting membrane potential
Enhances automaticity
High; raises resting membrane potential, slows conduction, widens QRS
Calcium disturbances
Low; prolongs QT (torsades)
High: shortens QT
Acidosis
Reduces threshold for VF
Sensitized myocardium to re entrainment arrhythmias
Hypokalemia
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
ECG hypokalemia
U waves, inc QT interval, flat or inverted T wave
Hyperkalemia etiology
Renal failure (insuffiency), metabolic acidosis, DKA, cell breakdown (hemolysis, rhamdomyolysis)
ECG
-peaked T wave, wide QRS, inc PR interval, loss of P wave
Hypocalcemia
Chronic renal failure, vitamin D defiency, hypoparathyroidism, acute pancreatitis, hypomagnesium
ECG-prolongation of QT interval (QTc corrected for rate)
Hypercalcemia
Hyperparathyroidism, malignancy, granulomatous disorders (TB sarcoidosis), endocrine disorders (adrenal insuffiency, hyperthyroid)
ECG-short QT, short ST
HypoMg
Poor nutrition, alcoholism, dec absorption, renal magnesium loss, diuretics
ECG-long Pr, wide QRS, long QT, dec T wave
Hypermg
Renal failure, magnesia containing drugs
Hyperkalemia
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
Hypokalemia
ST depression
T flattening
Hypercalcemia
Shortened QT interval due to a shortened st segment
Hypocalcemia
Prolonged QT interval due to a prolonged ST segment. T wave duration normal
Digitalis
ST depression
T wave flattening on inversion
Shortened QT interval, increased U wave amplitude
Quinidine -procainamide
Disopyramide
Phenothiazines
Tricyclic antidepressants
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
Hypothermia
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
Pulmonary embolus
Sudden dyspnea+clear lung+x ray=PE
Tachycardia
Nonspecific ST-T changes
ECG- S1, Q3, T3
T wave inversion V1-V4
Transient RBBB
Cerebral hemorrhage
Impressive ST T changes
Hypothyroidism
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
Wolf parkinson
Short PR interval
Slurred upstroke (delta wave) of QRS complex
Accessory AV conduction pathway (bundle of Kent)
Valvular heart disease Dr. Khalid
Ok
Recognize the etiologies, of valvular heart disease
Discuss auscultation findings associated with VHD
Discuss the valvular causes of systolic, diastolic and continuous murmurs
Valvular heart disease
20 million in USA
Age dependent 3-6% of those>65
Symptoms -dyspnea on exertion (most common) -angina -syncope -palpitations Fatigue, edema, ascites
Most common conditions encountered today
Degenerative (calcification)
Myxomatosis degeneration (MVP)
Congenital (bicuspid aortic valve)
Decline in incidence of rheumatic valvular disease*huge decline just in immigrant or visitors
Valves affect by pressure or volume overload. Or by disease process. Like what..often multiple valves
Heart failur, endocarditis, rheumatic fever
Stenosis
Impedes forward flow
Stenosis, sclerosis, fibrosis, calcification
Leads to pressure overload; hypertrophy and heart failure
As and MS
Regurgitation
Failure to close adequately (leaks)
Reversal of flow
Insufficiency, incompetitence
Leas to volume overload; dilates
AI and MR
Types of VHD
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
Rheumatic heart disease
Due to RH
Females 4:1
Caused by group A strep infection (pharyngitis) virtually only cause of acquired MS(can be congenital)
Jones criteria
Rheumatic
Example: myocarditis, pericarditis
Carditis-inflammation of heart muscle
- fever
- arthralgia
- increased seed rate of CRP
- Leukocytosis
- Prolonged PR internal
- Elevated ASO titer
Symptoms RHD
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
Diagnose RHD (CRP not specific for inflammation lots have)
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????
Mitral stenosis
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
Mitral stenosis
4th decade, fatigue associated with decreased CO
DOE, cough orthopnea, PND, pulmonary edema, hemoptysis, arterial emboli, a fib
PHT with RHF-edema
Ortner syndrome
Hoarseness d/+ compression of left recurrent laryngeal nerve
PE mitral stenosis
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.
How hear mitral stenosis
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
Why could th patient develop progressive symptoms to RVF
Malar face rash kid
Ok
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
*smoker is distactor its not COPD
MS
ECG-a fib and left atrial enlargement
Mitral stenosis treat
Anticoagulation if in a fib-prevent stroke
Percutaneous balloon valvuloplasty MVR (replacement)
Progressive symptoms-possible RVF
RVFfailure-see ascites low extremity edema
RVF symptoms progressive from MS
Patients get increase LA pressure, pulmonary HTN, pulmonary edema, hepatomegale, ascites, peripheral edema
Blood back!
A fib ecg
No p wave
QRS to QRS is different
Irregularly irregular rhythm
Left atrial enlargement
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
Right atrial enlargement
V2 lead 2?
Atria hypertrophy?
Not really always dilates bc so thin
Vent hypertrophy and dilate
Either
Did diagnosis for case
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
Look at left border of heart if see straightening
Left atrial enlargement
Do we anticoagulatns this patient
Yes they have a fib bc of risk of emboli
Treat MS
Anticoagulant if in a fib;risk emboli
Percutaneous balloon valvuloplasty (mitral commissions); success rate 95% MVR (replacement)
Progressive symptoms-possible RV
Chronic mitral regurgitation
MVP-most common etiology/myxomatous or degenerative MV
MAC (mitral annular calcification
Acute Mitral regurgitation
Rupture of chordal tendineae
Rupture of papillary msucle
Ischemic papillary muscle dysfunction-(CAD/MI: next most common cause of MR)
IE; valve perforation
Chest x ray mitral regurgitation
Pulmonary edema
Acute MR
Inc. LA pressure abruptly; pulmonary edema, LVF
Chronic MR
Generally well compensated
ECG-LAE
MAC
2% pop
Symptoms mitral regurgitation
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
PE mitral regurgitation
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
Treat mitral regurgitaiton
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
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
Ok
Loud systolic murmur at apex
Mitral regurgitation
S3 gallop
Heart failure
Differential
CAD
Murmur of mitral regurgitaiton
Chest pain
MI
Acute MI complicated by acute LVF
Ischemic papilalry msucle dysfunction causing acute MR
What test
Ecg, MR
Chest x ray
Cardiac enxymes up
MR turbulent flow one chamber to another
Regurgitaiton
ECG inferior MI
ST elevation on II III AVF
RCA supplies papillary muscle causing mitral regurgitaiton
Cardiac enzymes MI
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
MVP
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
Symptoms MVP
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
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
Differential
Palpitations SVT, TC, PVC< MVP R/O hyperthyroid, R/O collagen abnormalities
Echo ecg, holter,TSH, free T4, CXR
Treat MVP and thyroid disorder
MVP with mitral regurg
B blocker for hyper state
Regulate thyroid meds
Aortic stenosis
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)
Pathophysiology AS
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
Symptoms AS
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
PE AS
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)
How see LVH on ecg
V5 v6 high
Will happen in aortic stenosis
LVH in aortic stenosis
Ok
Treat AS don’t work just temporary relief
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%
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
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
Treat severe symptomatic AS
Valve replacement
No med can give
Aortic regurgitaiton
Due to leaflet abnormalities (bicuspid AoV, IE)
Due to aortic root abnormalities (marfan syndome, aortic dissection, aging, HTN)
What causes acute AR
IE, aortic dissection, BAV, chest trauma, balloon valvuloplasty
Causes of chronic AR
Syphilis, ankylosis spondylitis, ascending aortic dilation, BAV, calcfic degeneration, rheumatic, chest radiation
Pathophysiology regurgitation
Volume overload can increase LVEDV, LVH, left sided HF; SOB fatigue , angina
Symptoms aortic regurgitaiton
Depends on rapidity of onset-due to compensatory mechanism onset
Acute aortic regurgitaiton
IE, aortic dissection/acute pulmonary edema, cardiogenic shock
Chronic aortic regurgitation
Develops over time/dyspnea, orthopnea, PND, chest pain
PE aortic regurgitaiton
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
Crescendo decrescendo-AS?
Blowing murmur
Ok
Treat aortic regurgitation
ARB-decrease afterload to decrease regurgitation volume
Surgery AoVR (replace or repair ) when symptomatic or EF<50-55%
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
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
Valvular heart disease treatment
Reserved for when symptomatic
Tricuspid stenosis
Associated with MS, TR, and RHD
Can be associated with carcinoid, ergot agents (cabergoline)
Pathophysiology tricuspid stenosis
Prominent A wave in JVP ascites, hepatomegalia (may pulsate)
Hear tricuspid stenosis
Diastolic, low pitch, decrescendo, murmur LSB; increase with inspiration (Corvallis sign) and decrease with expiration and valsava
Diastolic murmur apex
MS
Diastolic murmur left sternal border
Tricuspid stenosis
Every right valve disease
Intensity increase with inspiration due to increase intrathoracic pressure, increased venous return so murmur increase on right side
Tricuspid regurgitation
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
A wave JVP
Tricuspid stenosis
V wave-tricuspid regurgitation during systolic
Pulmonary stenosis
Atresia, congenital, can cause angina, syncope,
Auscultation pulmonary stenosis
Systolic crescendo-decrescendo murmur, ejection click
2nd 3rd ICS, LSB/radiated toward left shoulder clavicle and increases on inspiration/RVH
Association pulm stenosis
TOF TGA
Treat pulmonary stenosis
Balloon commissural to my if pressure gradient>50mmHg
Cause pulmonic regurgitation
Most due to pulmonary HTN
Sound pulmonic regurgitaiton
Diastolic, decrescendo blowing murmur 2nd LSB
Increase P2 if PHT
Systolic murmu
MR (MVP), TR
- AS, PS
- VSD
Autopulmonary shunts murmur
Early mid late, holosystolic/pansystolic
Diastolic murmur
AR, PR
-MS, TS
Atrial myxoma
Murmur plop
Continuous murmur
PDA-machinery*
AV fistula
ASD with high LA pressure
Coarctation
AV blocks
Ok
What is an AV block
In the cardiac conduction system that causes a disruption of atrial-to-ventricular electrical conduction
What are the types of AV blocks and fasciculus blocks
First degree Av
Second degree AV
Third degree AV
Fasciculus blocks (hemiblocks)
Left anterior hemiblock
Left posterior hemiblock
Primary AV block
Prolongs AV node conduction
PR interval more than .2 sec.
ECG 1st degree block
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
Etiology of 1st degree AV block
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
How calculate regular rhythm
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
2nd degree block types
Mobitz I
Mobitz II
Second degree av block
Progressive PR-Interval
Prolongation prior to dropped QRS
Grouped beats
Mobitz I
Progressive lengthening results from earlier arrival in relative refractory period AV conduction
Implies impairment of AV conduction (AV node)
Transient
Etiology mobitz I
All those things that cause 1st degree AV block
Digitalis toxicity
Ischemic events (MI inferior)
Myocarditis
2nd degree AV block -mobitz
May be seen with inferior AMI
Level of block is at level of AV node
Narrow QRS complex
Etiology 2nd degree AV block-mobitz type II
Ischemic heart disease
May be seen with acute anterior myocardial infarction
Degeneration of conduction system
2nd degree AV block, mobitz type II mobitz
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
Features of high AV block
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
Low AV block
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
Third degree heart block (complete heart block)
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
Etiology 3rd degree heart block
Ischemic
Infiltrating diseases
Cardiac surgery
- by pass, valve replacement
- myocarditis
- degenerative
How do you treat 3rd degree block
Pacemaker
What check on every ECG
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
R
As impulse travels toward the electrode +
S
As impulse travels away from the electrode - deflection
In normal ventricular conduction, what is the origin of a small q wave in V5 and V6
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
The septum is activated from _ to _
L to R
L septal surface activated .1 s before R septal surface
Why normal ventricular muscle activated L to R
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
Intrinsic deflection
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
What is intrinsic deflection for V1 and V2
V1 .02 s
V2 .04 s
What does it mean if it takes longer for the ID to start downward,
The impulse is late in reaching the pericardial surface
Late ID in: a. BBB b. Hypertrophy/dilated
Common features of BBB
Wide QRS complex (.12 s or greater)
ST segment -T waves slope off in opposite direction to QRS
Which side of the septum is activated first in RBBB
Left
In RBBB is there an S wave in V6?
Ok
Sequence of ventricular activation in RBBB
After septal activation, then activation begins in LV free wall
RsR’ variants in V1-V2
Normal
Pertussis or straight back
RV diastolic volume overload
WPW syndrome
RVH
Du henna dystrophy
In lead V1 why is there a small r wave morphology in RBBB
Ok
Sequence of ventricular activation in LBBB
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
LBB more apt to occur with
HTN
Ischemia
Aortic stenosis
Cardiomyopathy
LBBB with LAD
More myocardial dysfunction
More disease in conduction system
Maybe higher mortality
LBB with RAD
Think congestive cardiomyopathy
Limb leads in BBB
I and AVL usually have features of V6
T wave in BBB
Polarity is opposite QRS direction
What causes secondary T wave changes T wave in BBB
Disturbance in depolrepol
If t wave polarity is in the same direction of the QRS complex, it is called __ t wave change, usually due to ____
Primary
Ischemia
In LBBB which ventricle is activated first
Right
Hemiblock/fasciculus block
Term for blockage of one of two main divisions of left bundle branch
Left bundle branch
Anterior division (superior)
Posterior division (inferior)
Hemiblocks
Left anterior hemiblock (LAH)-more common
Left posterior hemiblock (LPH)
Etiology of LHA
Disease in conduction system
Often associated with MI (left anterior descending-LAD occlusion)
Criteria for LAH
Left axis deviation (usually >minus 60 degrees; others> minute 45 degrees)
ECG LAH
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)
Anterior hemiblock
LAD-usually associated with MI (or other heart disease
Normal or slightly widened QRS
Q1S3
Etiology of left posterior hemiblock -less common
Disease in conduction system
Criteria of left posterior hemiblock
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
What causes atrial enlargement
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
P wave
Depolarization of atria
Doesn’t exceed 3 mm
Increased amplitude-hypertrophy, HTN, AV valve disease, Cor pulmonale, congenital
P of RAE
Tall, pointed; taller in III than in I
P-pulmonale
P of LAE
Wide, notched; taller in I than in III
P-mitrale
2nd half of p wave negative in V1 of III
RAE
Associated with TV disease or pul HTN
COPD , PE, MS, or MR are causes of pul HTN
Right atrial enlargement (RAE)
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
LAE
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
Causes LAE
MS MR
Ventricular hypertrophy (enlargement)
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
Left ventricular hypertrophy
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
ECG pattern LVH
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
Criteria for LVH
Lack sensitivity (low 40-50%) but are specific (high 90%)
Romhilt estes scoring system for LVH
5 LVH
4. Probable LVH
- 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 - (1)Any ST shift (without digitalis
Typical strain STT(with digitalis) - (2)LAD 30 or more
- (1)QRS interval .09 sec or more
- (1)ID in V5-V6 .04 sec or more
- (3) P terminal force in V1 with more than .03 sec in duration >1 mm in depth
Sokolow lyon criteria
R in I and S in III>25 mm
R in AVL >11
R in V6>26 mm
Right ventricular hypertrophy cause
Cause-COPD
RVOT obstruction, VSD
Congenital-TOF< pulmonic stenosis, transposition of great vessels
Mitral stenosis, tricuspid regurgitaiton
ECG RVH
R waves assume prominence in right precordal leads and deep S waves develop in left precordial leads
R:S ration>1
Clues to RVH
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)
Causes of dominant r waves in V1
RVH
Posterior or lateral MI
WPW
Hypertrophic cardiomyopathy
Muscular dystrophy
Normal variant
CAD general comments
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
What happens with atherosclerotic coronary arteries from plaques
Can undergo…
Fissuring or erosion
Triggers thrombus formation to cause ischemia to myocardium
Risk factors for atherosclerosis
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
Metabolic syndrome
Insulin resistant-increased glucose
HTN
High TG, low HDL
Hyperuricemia
Hyper coagulation
Obese BMI>30-central obesity
Desireable : BMI 21-24
BMI=weughtx705/height
Angina pectoris
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_
Supply angina
Decreased oxygen delivery to tissue leads to ischemia
Example supply angina
Coronary vasoconstriction, stenosis, platelets release serotonin and thromboxane A2
Demand angina
Increased myocardial oxygen requirements and workload can lead to ischemia
Examples of demand angina
Exercise, stress, emotion, fever, thyrotoxicosis
LVH due to As
Anemia (low oxygen carrying capacity)
Effects of ischemia
Mechanical consequences
Biochemical consequences
Electrical consequences
Mechanical consequences ischemia
Angina, is ischemia is prolonged or develop coronary occlusion, may lead to myocardial necrosis
Segmental akinetic bulging (dyskinesia)
Biochemical consequences ischemia
Fatty acids can’t be oxidized
Increased lactate production
Reduced pH with metabolic acidosis
Electoral consequences ischemia
Inversion fo T wave
Transient displacement of ST segment
Depression-subendocardial
-elevation-subepicardial
Electrical instability instability; VT, VF
LAD MI
Anterior wall infarction
Leads V1-V7
RCA MI
Inferior wall infarction (RV infarction)
Leads II, III, AVF
Circumflex artery MI
Lateral wall
Leads I, AVL
Posterior descending artery
Posterior wall infarction
V1-V3
CV causes of chest pain
Ischemic heart disease (angina , UA, ACS, MI), VHD, pericarditis, myocarditis, cardiomyopathies
Non cardiac cause of chest pain
Pleuritis/pneumonia/PE
Pulmonary infarction, pneumothorax, GI
GI disease: GERD, PUD, gallstones, esophageal motility disorder chest wall syndromes
Lung cancer
Aortic aneurysm
Non chest pain symptoms of chronic ischemic heart disease
Dyspnea, non chest locations of discomfort (((exertional or rest)
Mid epigastric or abdominal
Diaphoresis
Excessive fatigue and weakness
Dizziness and syncope
Anginapectoris why exercise effect it
Fixed CA stenosis/fixed O2 supply; produces ischemia bc of increased oxygen demand
Angina equivalent
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
Signs or risk factors for angina
Xanthelasma
Xanthomas
Diabetic skin lesion
Nicotine stains
Pale
Absent peripheral pulses
Angina
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
What can mimic angina in absence of CAD***
AS, AI, pulmonary HTN, hypertrophic cardiomyopathy, heart failure
Unstable angina
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
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
NSTEMI
Both UA and NSTEMI are called NSTEMI ACS or NSTE ACS
1.2 million US hospitalized a ACS 2/3 have NSTE ACS
Pathology UA and NSTEMI
Most subjects with ACS have an atherosclerotic plaque rupture or erosion; platelet aggregation and thrombus leading to partial occlusion of artery
Stable angina ecg
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
ECG unstable angina/NSTE ACS
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
Differential diagnosis of NSTE ACS
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
Lab CAD
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
Diagnostic testing for atherosclerosis
Functional and/or anatomical information for CAD
Functional diagnostic testing for atherosclerotic CAD
Exercise ECG, single photon emission CT (SPECT, PET)
Coronary flow (PET, fractional flow reserve)
Wall motion abnormalities (echo, cardiac magnetic imaging CMRI)
Anatomical diagnostic testing for atherosclerotic CAD
Invasive angiography, coronary CT angio (CTA)
-coronary artery calcium scoring (CAC) (note, CAC doesn’t provide data on coronary luminal narrowing
Signs of high risk for coronary event
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
Stress testing: exercise ECG
Exercise electrocardiography (preferred if patient is suspected to have angina)
Safe… only 1 death or MI per 2500 tests
Contradictions exercise ECG
Recent MI or acute MI, unstable arrhythmias, acute PE, aortic dissection, unstable angina, severe AS, decompensated HF, endocarditis, DVT
Sensitivity and specificity exercise ECG
70% and 75% specific
Stress echocardiography
Recommended when baseline ECG findings are abnormal or when area of myocardium is at risk with exercise or when patients can’t exercise
Nuclear myocardial perfusion imaging
SPECT (single photon emission computer tomography)
Useful in LBBB, LVH, digitalis effect
Technetium 99
Pharmacological stress test
Patient unable to exercise/abnormal ECG LBBB, LVH
Use: vasodilator nuclear perfusion
- adenosine/regadenosine/dipyridamole
- vasodilators increase HR
When use dobutamine echocardiogram
When patient cant exercise or when area of myocardium is at risk
Coronary angiography
Cardiac cath
Provides anatomic diagnosis of severity of CAD
Percutaneous revascularization can be performed after study
Exposed to radio contrast (kidney dysfunction
Use of coronary angiography
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
Coronary CT angiography
Ability to quantify lesion severity can be limited by significant calcification
CXR
Usually normal unless history of mi, HF< VHD
Cardiomegalia in HTN< VHD, cardiomyopathy, pericardial effusion
Treatment of patients with stable angina non pharm
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
Pharm treat to prevent MI/death/reduce symptoms
Asprin
Beta blocker
ACEI
Statins
Nitro/nitrates
CCB
Identify aggravating conditions
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
Pharm treatment ASA
ASA:cyclooxygenase inhibitors of platelet activation
Inhibit thromboxane production
Clopidogrel blockers in ADP induced platelet aggregation
Bb
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
Contraindication bb
Decompensated HF, hypotension, advanced AV block
ACEI
Blocks conversion of A1 to A11
Decrease CV mortality
Useful in diabetic (renal protection) and patients with LV systolic dysfunction
Nitrates
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
What not take nitrate with
Phosphodiesterase inhibitor
CCB
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
Myocardial revascularization
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
Treat prinzmetal
Relieved by nitro
Dihydropyridine CCB (amlodipine)
Manage los risk patient
Antianginal - BB, nitro, CCB
Statin
Antiplatelet-ASA/clopidogrel
Anticoagulant-UF heparin
Cath:revascularization if appropriate
High risk patient (US or NSTEMI) manag
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
Hyperlipidemia adult treatment panel (NCEP guideline III stricter target lipid levels)
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
Statins for hyperlipidemia
ASA Nitrates B blocker ACE Ranexa inhibit late phase of inward Na current during repolarization; decrease angina occurrence
Diet for CAD/angina to protect against atherosclerosis
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
Shock
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
Pathophysiology shock
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
Skinextremities shock
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)
Neck veins shock
Distended (HF, PE, tamponade)
Flare (hypovolemia)
HR shock
Fast (sensitive indicator of shock); occasionally LO
BP shock
Systolic low diastolic low
Respiration shoc
Tachypnea, bronchospasm, respiratory failure
Renal shock
Receives 20% CO; oliguria associated with vomiting, diarrhea, hemorrhage
Heart shock
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
Categories of shock
Hypovolemia shock
Distributive shock
Cardiogenic shock
Extracardiac obstructive shock
Hypovolemia shock hemorrhagic
Hemorrhagic: GI bleeding(varice ulcer diverticula), pelvic bleeding (post partum hemorrhage, vaginal hemorrhage), hemorrhagic pancreatitis, AVM
Non hemorrhagic hypovolemia shock
GI losses (vomiting diarrhea), skin losses (burns, heart strokes)
DKA hypovolemia shock
Renal losses (salt washing, osmotic diuresis) hypoaldosteronism, adrenal insuffiency, third space loss (pancreatitis, bowel obstruction (sequesteration of fluids), systemic inflammation
Most common cause of hypovolemia shock
Hemorrhagic shock
Treatment issues of volume loss
Depends on the circulating integrity (shock)-over zealous or too rapid correction
-rate of replacement composition of replacement
Fluid change
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
Shock class I
Lose 750 ml or up to 15% blood
Normal bp
Increased pulse pressure
Give crystalloid
Class II hemorrhagic shock
Lose 750-1500 ml of 15-30% blooc
Bp normal
Pulse pressure decreased
Give crystalloid
Class II hemorrhagic shock
Lose 1500-2000 ml blood
Decrease bp
Decrease pulse pressure
Give crystalloid and blood
Clas IV hemorrhagic shock
Over 2000
Decreased bp
Decreased pulse pressure
Distributive shock types
Septic or non septic (vasodilation)
Most commoncause of non cardiogenic shock
230000 patients yearly
30-40% mortality
Sepsis signs/symptoms
Fever, tachycardia (>90), tachypnea(>20 breaths), increase WBC 12000
Common sources of infection distributive shock
Pulmonary-pneumonia, emphysema
Ab-peritonitis, cholangitis
GU-pyelonephritis, abscess
CNS-meningitis
Skin-cellulitis, necrotizing fasciitis
Septic shock
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
Pathophysiology distributive shock
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
Signs and symptoms of distributive shock
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
Vasodilators effects of septic shock
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%
Anaphylactic shock diagnosis
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)
Life threatening/danger signals of anaphylactic shock
Rapid progression of symptoms
Respiratory distress of anaphylactic shock
Strider, persistent cough, wheezing, hypotension
Pathophysiology anaphylactic shock
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
Distributive hemodynamic profile of anaphylactic shock
PCWP (PAOP) N(early or decrease late
CO decrease or increase
SVR decrease
Tissue perfusion (mixed venous oxyhemoglobin sate) >65%
Cardiogenic shock
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
Cardiogenic shock definition
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%
Types of cardiogenic shock
Cardiomyopathies
Arrhythmogenic
Mechanical
Cardiomyopathic cardiogenic shock
MI(>40% LV or extensive ischemia) severe RVMI, stunned myocardium, severe septic shock (depressed EF), myocarditis, cardiomyopathy-exacerbation of severe HF
Arrhythmogenic cardiogenic shock
Tach ( a fib, a flutter , re entrant tach), VT, VF
-Brady: complete heart block, mobitz II)
Mechanical cardiogenic shock
Severe AI or MR; acute valvular rupture (papillary or chordate tendinae rupture , abscess); critical AS, VSD, ruptured vent wall aneurysm, atrial myxoma
Diagnose cardiogenic shock
Decrease BP, decrease UO, mental status changes
Cool, mottled extremities
Distended neck veins
Pul edema
Document myocardial dysfunction-echocardiogram-cath
Etiology cardiogenic shock
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)
Pathophysiology cardiogenic shock
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
Comments on cardiogenic shock
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)
Treat
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
Treat STEMI
PCI-preferred CABG Fibrinolytic ASA Heparin NSTEMI-glycoprotein IIb/IIIa inhibitors P-pressers-norepinephrine -CS inotropy
Mechanical support
IABD
LVAD
ECMO
IABD
Decreases afterload, deflated during systole; inflates during diastole-coronary perfusion use for mechanical complication
LVAD
Bridge for transplant, tandem heart/impels
ECMO
When O2 is severely impaired
Arginase
Inhibitor enzyme for endothelial NOS; ROSC-restore spontaneous circulation; EECP-early enhanced contour pulsation
Pressure
Norepi
Dopamine
Inotropy s
Norepi
Preferred-alpha I, B1 B2 agonist
Vasopressin-vasoconstrictor/use in vasodilators shock
Dopamine
Alpha B1 agonist
High dose vasoconstrictor-alpha stimulation+inotrope low dose 2 microg/kr vasodilator; phenylephrine peripheral alpha antagonist
Inotropes
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
Treat RV infarct
Fluids for high filling pressure
PAC
Useful when despite adequate fluids given, but not favored
Indices of tissue perfusion
Goal increase BP, increase UO, incrase mental status, incrase skin color
What avoid
NTG or nitroprusside bc decrease BP=vasodilators-decrease preload, decrease afterload
Oasis
Blocks Na K CL transport and increase urinary excretion of Na and Cl to decrease pul edema
Acute obstruction to flow in circulation
Extracardiac obstructive shock
-obstruction of RV output (massive PE air embolus) impaired diastolic filling of RV (SVC syndrome); cardiac tamponade; constrictive pericarditis; severe hypertension
Pulmonary vascular extracardiac obstructive chock
Hemodynamically significant , pulmonary embolus, severe pulmonary HTN, severe or acute obstruction of pulmonary or tricuspid valve
Mechanical extracardiac obstructed shock
Tension pneumothorax (trauma, ventilator induces, iatrogenic), pericardial tamponade, constrictive pericarditis, restrictive cardiomyopathy
Extra obstructive cardiac shock pearls
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
Presentation extracardiac obstructive shock tension pneumothorax
SOB, unilateral pleuritic chest pain and decreased breath sounds, neck vein distention
TRACHEAL DEVIATION AWAY FROM AFFECTED SIDE
RX extracardiogenic tension pneumothorax
IV catheter in 2nd, 3rd ICS, MCL followed by chest tube or emergent tube thoracotomy in 5th
Pericardial tamponade signs
Dyspnea, tachycardia, decrease BP, increase JVD< muffles heart, pulsus paradoxus, ECG, electrical alternana
Echo pericardial tamponade
RA collapse (highly sensitive sign; RV collapse; IVC dilation
RX pericardial tamp
Echo/US to guide pericardialcentesis
Symptoms of hemodynamically significant pulmonary embolus
Dyspnea, hypoxia, hypotension (sudden), tachypnea, tachycardia, cough, pleuritic chest pain, syncope, sudden death
Risk factors for hemodynamically significant pulmonary embolus
VTE in leges, pelvis, arms-most common,
Non thrombotic material (fat, air , tumor cells, amniotic cancer, hypercoagulabiltiy (factor V ) previous VTE?PE, pregnancy
Pathophysiology hemodynamically significant pulmonary embolus
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
PE hemodynamicaly significant pulmonary embolus
Increase JVD, increase P2 or widely split P2-due to delayed emptying of RV
R>20/min, increase HR
Obstructive hemodynamic profile
Decrease
Increase HR
Increase JVD
Extremities cool
Lungs dry
Co-N decrease
PCWP PAOP N or decrease
SVR increase
CTPA imaging
Computer tomography pulmonary angiography
Permits visualization of thrombi in pul arteries
Preferred over ventilationperfusion lung V/Q
V/Q scan
Used if Agilent is allergic to contrast agents (used for CTPA), renal insuffiency , women <40 yo decreased radiation and preg
D dimer
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
ECG
S1 Q3 T3
Echocardiogram
RV dilation, TR
hemodynamically significant pulmonary embolus BNP and trop
BNP and troponin elevated
CXR pulmonary embolism
Atelectasis RLL, otherwise normal
ECG pulmonary embolism
Sinus tach, incomplete RBBB, PAC, st changes
ABG pulmonary embolism
PH 7.5 pCO2 29, PO2 58 HCO3 26
CBC CMP pulmonary embolism
Normal
Venous Doppler
R leg DVT femoral vein
CTPA pulmonary embolism
Large thrombus in PA
D dimer pulmonary embolism
Positive
Echo pulmonary embolism
Normal
Heart failure
Inability of the heart to meet the metabolic demands of the body
What percent of adults will develop HF
10, 10% of people over 53 have this
Mortality rate HF
1 year 10-20% 5 year 50%
Etiology HF
60-75% CAD-ISD
18% idiopathic
12% valvular
10% hypertensive
*most common cause of LV systolic dysfunction is from ischemic heart disease
Basic cause of HF
Restriction/obstruction to ventricular filling
- RV infarct
- constrictive pericarditis
- MS
- atrial myxoma
State A HF
HF risk factors no heart disease no symtpoms
Stage B HF
Heart disease no symptoms
Asymptomatic LV dysfunction
State C HF
Prior or current HF symptoms
Stage C heart failrue
Refractory symptoms
Stage A ACC/AHA
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)
Stage B ACC/AHA
Asymptomatic patients has LVH and/or impaired LV function (low EF) previous MI, valvular disease, structural heart disease; hemodynamically stable. One year mortality 50%
Stage C ACC?AHA
Patient with current or past symtpoms of HF with structural heart disease; SOB , fatigue, reduced exercise tolerance; one year mortality 15-30%
Stage D ACC AHA stages
Refractory HFl eligible for specialized treatment (mechanical support , transplants) one years mortality 50-60%
Class I NYHA
No limitation of physical activity
No symptoms. With ordinary exertion
One year mortality 5-10%
Asymptomatic
Class II NYHA
Slight limitation on physical activity
Ordinary activity causes symtpoms
One year mortality 15-30%
No rest sx
Exertional sx with ordainary activity
Class III NYHA
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
Class IV NYHA
Inability to carry out physical activity without discomfort
Symptoms at rest
One year mortality 50-60%
Rest sx
Pathogenesis of HF
Impaired systolic function
Impaired diastolic function
Mechanical abnormalities
Disorders of rate/rhythm
Pulmonary heart disease
High output states
Echo can see what specific causes of heart failrue
Hypertensive heart disease Ischemic heart disease Hypertrophic heart disease Infiltrating heart disease Primary valvular heart disease
What is echo necessary to distinguish
Necessary to distinguish systolic heart failure from diastolic heart failrue
Types of heart failure
Systolic/diastolic
High/low
Acute/chronic
Right/left
Forward/backward
Acute HF
Heart failure due to acute MI, ruptured papillary msucle , MR, AI, toxins
Chronic HF
Multivalvular disease of dilated cardiomyopathy
Progresses slow
Edema, weight gain
Systolic HF (HFrEF-reduced)
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
Diastolic HF-normal EF (HFpEF-preserved)
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
High output
Hyperthyroidism, anemia, pregnancy, AV fistula, beriberi, paget
High CO but low EF
Low output
Ischemic heart disease, HTN
-dilated cardiomyopathy, valvular and pericardial disease
Right sided HF
Affects RV
Pulmonary HTN due to pulmonary embolus
Edema, hepatomegalia, venous distention
Left sided HF
LV is overloaded
AS, MI
Dyspnea, orthopnea, due to pul congestion
Neurohormonal compensation response of HF
SNS RAAS Cytokines activation Altered renal physiology LV remodeling
RAAS
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
Arginine vasopressin
AVP or ADH
-stimulation of thirst leads to increase TBW and hyponatremia (dilutional). Increases preload (salt and water retention)
Precipitating causes of HF
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
Signs and symptoms of HF
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
Heart and HF
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
RV failrue
Peripheral/sacral edema
Hepatomegalia
Ascites
Increased JVD, HJR
Where is the JVD Seen
As crosses the sternocleidomastoid muscle into the posterior triangle of the neck and disappears beneath the clavicle to join the brachiocephalic vein
How measure JVD
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,
What is a venous pressure above normal
At >3m above the sternal angle, or more than 8 cm or 9 cm in total distance above the right atrium
Diagnostic test for HF
No single diagnostic test for HF; it is largely a clinical diagnosis checked on a careful HP
CXR HF
Cardiomegalia
Pulmonary edema with central peripheral infiltrates
Increased size of vessels in upper portion of lungs
Pleural effusions
Echo HF
Practical useful, mobile, bedside/ICU/ED
Chamber size, clots, tumors
Wall motion muscle thickness
Pericardial effusions
Valvular disease
Systolic.diastolic HF-ejection fraction
ECG HF
May have ischemia, infarction, hypertrophy
Rhythm disturbances (atrial, junctional, ventricular )
Tachycardia/bradycardia/blocks
Troponin T and I
Released from myocytes when damaged
- increase 3-12 hours from onset of chest pain
- peak 24-48 hours; return to baseline 5-14 days
CK-MB
Increases 3-12 hours from onset of chest pain
Peak 24 hours; baseline 1-3 days
Sensitivity
CBC HF
Anemia secondary to chronic disease
Anemia may aggravate HF
CMP HF
Electrolyte imbalance-low Na, K
Pre renal azotemia-high BUN to creatine
UA HF
Protein in urine
Thyroid labs HF
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
BNP
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
Differential diagnosis of HF
Pulmonary problems
- PE
- asthma
- pneumonia
Cirrhosis
- ascites
- edema
Renal-edema
Venous insuffiency-edema
Five basic principles of HF
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
Indications for admission to hospital for management of HF
Acute MI Severe respiratory distress Hypoxia Hypotension Cardiogenic shock Anascara Syncope Heart failure refractory to oral medications
Non pharm treatment of HF
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
How counsel patient HF before discharge of hospital
Diet-patient with spouse/other sodium restriction, Carl our restriction if overweight stimulants
Education
Rehab exercise
Medes: ACE/ARB, bb, ASA, statin, nitro prn
CO
SVxHR
Stoke volume is modulated by what
Preload
Afterload
Contractility
Conventional treatments of HF
Diuretics
-reduce fluid volume
Vasodilators
-decrease preload and/or afterload
Inotropes
-augment contractility
Class I
Evidence and/or agreement that therapy/procedure is beneficial, useful and/or effective; beneficial, useful and/or effective; benefit 3+ risk
Class II
Conflicting evidence and/or divergence of opinion
IIa-weight of evidence .opinion infavor -benefit 2+ risk
IIb-less established evidence/opinion-benefit 1+ risk
Class III
Evidence and/or agreement that therapy/procedure is not effective; may be harmful
-no benefit
A level evidence
Data from meta analysis or multiple randomized clinical trials; multiple populations evaluated
B level evidence
Data from single randomized trial or non randomized studies; limited population evaluated
Level C evidence
Only consensus opinion of experts , case studies, or standard of care, very limited populations
Pharm treatment of HF
ACE I or ARB
BB
Diuretic
Spironolactone
Digitalis
IV inotropes
Hydralazine
Nitrates
CCB
Sacubitril-Vallarta’s ivabradine
ACE I
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
When use ACE cautiously
Use cautiously with renal insuffiency or K greater than 5 mEq/l
Contraindication ACE I
Angioedema
Pregnancy
AE ACE I
Bilateral RAS(renal artery stenosis)
Cough
List ACE I
Lisinopril Enalapril Captopril Benazepril Ramipril Quinapril
ARB
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
ACE
Block angiotensin I to angiotensin II
Improve LV relax and contraction
Veno and vasodilation
ARB action
Increases myocardial fibrosis
Increases NE
Increases vasoconstriction
Increases endothelin1
Why get cough from ACE
Bradykinin accumulated
ARB vs ACE
Comparable but neither more effective
Don’t give ARB to patient that got angioedema from ACE
Name ARBS
Losartan Vallarta’s Candesartan Telmisartan Irbesartan Entresto; sacubitril is the neprilysin inhibitor and Vallarta’s is AII receptor blocker
BB
Survival benefit in chronic syst HF and dilated cardiomyopathy
Slow progression of disease and decrease hospitalization
Improve cardiac performance and symptoms of HF
Hemodynamics of BB
Decrease heart rate
Antiarrhythmic properties
Antiischemic
Blunts SNS effects of NE
Reverse remodeling
BB good
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
Who don’t give BB
Unstable class IV
Who give BB
All stable patients with symptoms of HF, reduced EF, unless contraindicated. Level of evidence: A
Patients with class II and II NYHA
Diuretics for HF
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
AL or LOH diuretics
Lasix (furosemide)
Bumex (bumetanide)
Demanded (torsemide)
DT
Thiazide
Zaroxolyn (metolazone)
Late DT
Spironolactone (aldactone)
How give furosemide
10 mg IV.he or 40 mg IV every 8-12 hours
Watch K Mg, Na, BUN, creatinine
Digitalis
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
Why use digitalis
HFrEF and a fib for ventricular rate control
MOA digitalis
Inhibits Na/K/ATPase; affect to increase contractile state by increasing intracellular calcium conc. Useful in atrial fibrillation to slow ventricular rate
Spironolactone
Antagonizes effects of aldosterone
Use in addition to standard care (ACE, BB, diuretic, dig)
RALES
Randomized aldactone evil study (aldactone-spironolactone) 12.5-25 mg/day; class III-IV patients -30% reduction in mortality
How watch spironolactone
Watch K closely if GFR is less than 30 cc/min or creatinine is greater than 1.6 mg/dl
Level of evidence of spironolactone
B-decreased mortality, decreased HF hospitalization s
Eplerenone
New watch K
Inotropes
Increases contractility
Dobutamine
-stimulating beta1 and beta2 receptors
Milrinone
- inotropic vasodilator
- inhibits phosphodiesterase
Dopamine
Stimulates beta 1 receptor
2-10 ug/kg/min
Higher doses stimulate alpha receptors
Useful short term
Hydralazine plus isosorbide dinitrate
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
Isosorbide dinitrate
Isosorbide mononitrate
Better response to hydralazine and isosorbide in african Americans that in whites; use if intolerant to ACE/ARB
Nitroprusside
Vasodilator monitor BP closely
Nitrates hemodynamic effects
- Venous vasodilation
Decrease preload leads to pulmonary congestion, decrease ventricular size, decrease vent wall stress, decrease MVO - Coronary vasodilation
- increase myocardial perfusion - Arterial vasodilation
- decrease afterload leads to decreased CO, BP
CCB
Class III
No benefit
Not recommended as routine
Treatment for patients with HF associated with reduced ejection fraction
Role of OMM if HF lymph treatment
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
Effleuragepetrissage-distal to proximal stroking of extremities
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
Conclusion HF
Make the right diagnosis
Look for the precipitating causes and underlying etiology
Provide treatment based on solid evidence based recommendations.