Transcript 042308 Cardiac Assess, L&RVF, MI, PE,Cor

Cardiac Patient Assessment &
Treatment
1
Review:

Cardiac Output
– 5000-6000 ml/min.
HR or SV = CO
 Sympathetic effects:

– HR and SV

Parasympathetic:
– Slows HR
– Little effect on SV
2
Review:

SV = pressure in ventricle
– Frank Starling effect

Peripheral vascular constriction
increases venous return
– = Increased RV output.

Vasodilation of arteries decreases PVR
and diastolic pressure
– = Increased CO.
3
Vital Signs

Normal B/P is 120/70 mmHg
– Increases with age
– General:
• Systolic – 100 + age up to 140
– At age 50: usually 140 mmHg
– Increases 1 mmHg/yr after 50.
4
Abnormal Cardiac Function
 Dispatched
as:
– Man down
– Chest pain
– Heart attack
– SOB
– Fainted
– Dizzy
– Passed out
– Choking
– Stroke
– DFO
– DRT
5
Initial Assessment:

Brief History
– Onset
– Provoking factors
– Quality
– Radiation
– Severity
– Time
– BP changes
6
Initial Assessment
– Meds
– Cardiac rhythm
– Abnormal breathing
– Edema
– Rales
– Changes in skin color and moisture
7
Acquired heart diseases
(Not Congenital)
– Angina Pectoris
– Myocardial Ischemia
– Myocardial Infarction
– Cardiogenic Shock
– Cor Pulmonale
– Hypertension
8
Angina Pectoris

Physiology:
– Myocardial Demands not met

Stable
– Onset with exertion
– Subsides with rest within 5 minutes
– If onset with stress, pain may last 15 min.
9
Angina Pectoris
 S/S:
– Heavy squeezing pressure with
radiation
– Anxious
– Diaphoretic
– Clammy
– SOB
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Angina Pectoris

Unstable
– In patients with previously stable angina
• Frequency, Severity & Duration
Pain with less activity or at rest.
 More resistant to relief with NTG.

11
Myocardial Ischemia

Physiology:
– Similar but worse

Occurs anytime
– Can last 30-60 minutes
– Not permanent damage
• May fail acutely or fibrillate
12
Myocardial Ischemia

S/S
– Tachycardia
– Elevated systolic BP
– Transient (Brief) ST depression
– Possible T wave inversion
– Precursor to …
13
Myocardial Infarction


Physiology: Coronary Thrombus
Arteriosclerosis / Atherosclerosis
History: (**)
–
–
–
–
–
–
CP
Possible Radiation
Sweating
Nausea
SOB
Pallor
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AMI - Another Rhythm?

Circadian rhythm
– 3x more likely in AM
– Usually 3-4 hrs. after awakening.

CP awakened from sleep
15
AMI
 Note:
– Elders & Diabetics often have no pain
 History:
– General Malaise
– Burning
– Syncope
– Dizziness
16
AMI History
– Nausea
– Diaphoresis
– Weakness, unknown fatigue
– Hot flash
– Nonspecific chest discomfort
– CHF; rales
17
AMI History
– Intermittent sx
– Seasonal - fall and winter
– MI at rest - no precipitating factors
18
AMI HUGE Risk Factors
2x more likely to die in 1st year post MI
 Increased stroke risk
 1/2 > 75 y/o
 PMHx: HTN, Diabetes

19
AMI Little Known Fact
-Cliff Claven

Socialization key clue (Females)
– Significantly less likely to be referred to
cardiac cath lab, thrombolytics, or
angioplasty

** Increase index of suspicion
20
Treatment of AMI
 Treatments,
as always, are based
on Symptoms
– Ectopy
– Pain
– Coronary Perfusion
– Container Problem
– Fluid (mis)placement problem
21
Hospital Assessment of AMI

Cardiac Enzymes
– Qualitative CPK (Creatine phosphokinase)
• CK-MB: :0 – 4
– PEAK 12-24 H
• Troponin: 0 – 0.1
– ONSET 1 – 4 H
– PEAK 12-24 H
– Significant ECG Changes
– Symptoms within 24 hours
– History (Surgeries)

Candidate for Thrombolytics?
22
Acute Left Ventricular Failure

Acute LVF from heart disease:
– #1 cause of heart failure.
– Assume the worst, hope for best

Pt. with CAD w/ hx of MI (new or old)
– May develop LVF.

Frequently LVF is only manifestation of
AMI.
23
LVF

Common causes
– Systemic HTN
• Afterload
– Coronary artery disease
• Arteriosclerosis/atherosclerosis
– Ischemia
• Local/temporary occlusion
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LVF

Common Causes
– Infarction
• Permanent, necrosis
• Significant Sized Infarct
– Decrease effective wall motion
– Decreased stroke volume
– Cardiomyopathy
• Diseased heart muscle tissue
– ETOH
– Enlargement
25
LVF

Causes
– Volume overload
• Bag of Potato Chips
– Severe anemia
• Hypoxemia
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LVF and Pulmonary Edema
Incidence of CHF doubles per decade
of life
 CO falls and pulmonary capillary
pressure rises.

– Fluid move (interstitial & alveolar)
– Lymphatic system fails to remove/filter.
27
CHF

Acute CHF
– Rapid

Chronic CHF
– Slow
– Midnight shoppers
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Pulmonary edema results from:
– CVA
– Pulmonary embolism
– Infection - Sepsis
– Allergy
– Inhalation of fumes
– Narcotic abuse
• Especially Inhaled (Heroin)
– Altitude sickness.
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Pulmonary Edema – S/S





Generalized
weakness
Fatigue
Dyspnea
Cyanosis
Tachycardia





JVD – Indirect
Increase B/P &
Pulse
Chest pain
Agitation
Anxiety
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Pulmonary Edema – S/S
Tachypnea
 Orthopnea
 Paroxysmal Nocturnal Dyspnea

– Elevation of pulmonary venous & cap
pressures
– Wakening from sleep
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Pulmonary Edema – S/S



Noisy Labored
Breathing
Rales
Wheezes


Coughing
Blood Tinged
Sputum
– Pink Frothy
– Reflex airway spasm
– “Cardiac asthma”

Rhonchi (larger
airways)
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Cardiogenic Shock
LV function compromised and CO falls
 S/S - Decompensating

– Systolic BP < 80 mmHg
– Usually semiconscious
– Cold, clammy skin
– Mild to moderate cyanosis of lips and nail
beds.
– EKG usually sinus tach
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Cardiogenic Shock

Note: If pt appears dehydrated
– (neck veins flat)
– Suspect hypovolemia.

Fluid Resuscitation? Or Not?
– Hmmmmmmmmm.
36
Right Ventricle Failure

Leading Cause
– LVF
– MI’s & HTN mostly affect LV

Isolated RVF
– Pulmonary HTN & Cor Pulmonale
– RA / RV Infarct (Rare)
– Pulmonary and Mitral valve stenosis
– Pulmonary vascular HTN
37
RVF – Physiology
Preload High
 RV cannot keep up
 Increased pressure in Big Veins

– Max stretch & density reached
Backflow in systemic circulation
 Fluid forced to interstitial spaces

38
RVF – S/S

Neck Veins
– Semi-fowlers position (45 Degrees)

Peripheral Edema
– Dependent edema
– Pitting edema
– Sacral (bedridden)

Fluid Collection
– Ascites
– Pleural Effusion
– Pericardial Effusion
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RVF – S/S

Clubbing of fingers
– Chronic Hypoxia with RHF






Most of the other LVF S/S also
Cor Pulmonale
SOB
Tachypnea
Anxiety
Etc…
40
RVF – S/S

Liver Engorgement
– Big Belly (uneven to the right) – Suspect

Hx of MI
– Lasix
– Digoxin
– “Enlarged Heart”
– “Weak Heart”
– “Bum Ticker”
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Cor Pulmonale

Hypertrophy of RV 2nd to Resp Disorder
– Acute PE 2nd to clot (R Heart)

Clot / Occlusion
– Increase in pulmonary vascular resistance

COPD Patients
– (High Right Heart Workload, High Risk)
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Cor Pulmonale S/S
–
–
–
–
–
–
–
–
–
Sudden onset unexplained SOB
Difficulty breathing
HR elevated
Chest pain with cough
Dyspnea not aggravated by lying flat
Cold
Diaphoretic
Cyanotic
Neck veins may be distended
43
Cor Pulmonale – Case
58 yo male
 Hx of chronic bronchitis or emphysema

– Typical S/S of bronchitis

Progression
– Deterioration of pulmonary capillaries
– Alveolar fibrosis
– Chronic hypoxemia
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Cor Pulmonale – Case

Progression
– Increase in pulmonary artery pressures
– Result RV afterload increase
• RV ill equipped
– RV Enlarges (Hypertrophy)
– Chronic RH HTN leads to RVF
45
Cor Pulmonale – Case

Patient displays all signs of:
– RVF
– Initial cause was pulmonary condition
46
Hypertension

Defined as BP > 150/90 mmHg.

Precise cause unknown for 90% pt.

Acute Life-threatening Hypertension
47
S/S – Hypertensive Crisis
– Recent onset of H/A
– Altered mental status
– Signs of CHF
– BP usually > 200/120
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So, What to do?
Decide – Sick/NotSick?
 Vitals
 Look

– Skin – wet/dry, color, temp
– JVD
– Peripheral edema
– Subtle signs
49

Listen
– Breath sounds
– Bruit
– Pulse x 6
– Skin
50
Treatment

OMI
– Oxygen, Monitor, IV

MONA - if appropriate
– Morphine, Oxygen, Nitro, ASA (Not in that
order)
Don’t let patient walk!
 Position of comfort
 Reassure

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Treatment (cont.)

IV Ntg, Nitroprusside if BP >100 mmHG

Dobutamine 2-10 g /kg/min if BP <100

Positive Pressure Ventilations

Thrombolytics

Dig if A-fib

Angioplasty

Bypass
52
Treatment of RVF & LVF
CHF a circumstance not a Dx
 Treatment objectives

– Decrease myocardial:
• Workload
• Oxygen demand
– Increase force & efficiency of contraction
– Reduce fluid retention
53
Treatment

Decrease Workload
– No Physical activity
– Sitting upright
– Oxygen
• Pt may tolerate BVM
– CPAP
– BiPAP
54
Treatment

Vasodilatory Therapy (Nitrates)
• AMI reperfusion
• Container expansion reduces preload
Morphine 
 Reduce Fluid Retention

– Diuretics
• Lasix
• Bumex
55
Treatment

Increase Contractility
– Shock algorithm directs
• Dopamine
• Dobutamine
• Norepinephrine
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Acute Pulmonary Embolism
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Acute Pulmonary Embolism
58
Defined

Blockage in pulmonary artery
– Blocks pulmonary artery flow
– Supplied area ceases to function
– Decreased gas exchange
– V/Q mismatch
59
Defined
 Typically
a clot forms in deep veins
of thighs
 Can
also be fat or air
60
History
 Anticoagulation
therapy
– Heparin – 1930s
– Streptokinase – 1930
– Urokinase – 1951
– 1960s – Large study of clot resolution
– Recently TPA
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Incidence

Unknown, range from 50,000100,000/yr

Higher than diagnosed, most
diagnosed postmortem

8% death rate with heparin tx

1/3 will die within 1 hour
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Risk Factors

Deep vein thrombosis

Prolonged immobilization

Surgery

Trauma
– Pelvic or femur fractures

Late pregnancy
63
Risk Factors

Thrombophlebitis

Certain meds
– Oral contraceptives

Atrial fibrillation

Smoking

Unknown
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Increasing Frequency
 Older
population
– Malignancies
– More sedentary
– Heart failure
– COPD
– Surgical procedures
65
Presentation
 Variable
and Non-specific
– Dyspnea
– Pleuritic chest pain
– Syncope
– Hemoptysis
– RHF
– Tachycardia
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Presentation
 No
physical findings significantly
accurate
 Deep venous thrombosis in
proximal lower ext. helpful for Dx
– Only about ½ source known
67
Why doesn’t lung tissue die from
emboli like heart muscle?
 Lung
has two blood
supplies
– Pulmonary and
Bronchial
– Share capillary beds
68
Pre-hospital Treatment

Good Physical Exam and History

Index of suspicion

Airway

High flow O2

IV

Rapid Transport
69
Treatment ???
Heparin
 Thrombolytic agents

– Streptokinase
– TPA
Catheter fragmentation
 Catheter embolectomy
 Open-chest embolectomy

70
Definitive Diagnosis
????
 Angiographic
 V/Q
scan (venous/perfusion mismatch)
 Operative
 Multiple
sources of evidence
71
Differential Diagnosis












Pneumonia
Herpes Zoster
Pleurisy
COPD
Rib fracture
Asthma
Angina
MI
Pneumothorax
Pancreatitis
Hepatitis
Salicylate OD











Bronchitis
Hyperventilation
Lung carcinoma
Sepsis
TB
Muscle pain
Costochondritis
CA
Pericarditis
CHF
Percardial tamponade
72
Watch Out
 Extraordinarily
difficult to
diagnose
 Watch
out for hyperventilation
 Young
women
73
GENERAL TREATMENT
PLAN
74
Fix any Volume Problem
 Fluid
challenge
– 250-500 cc
 Any
 Go
Change?
to Meds
75
Fix BP next
<70mmHg - Dopamine
 70-100 mmHg - Dopamine, if D >20 g,
BP 90 can start Dobutamine
 70-100 mmHg no shock sx, 250-500 cc
then Dopamine
 >100 mmHg & in Pulmonary Edema,
Ntg or Nitroprusside

76
Fix Pulmonary Edema last

Sit up

High Flow O2, Intubation if needed

Ntg, Ntg, Ntg

MS

Lasix, 0.5-1.0 mg/kg
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78
Summary






AMI
Pulmonary Edema
LVF
RVF
Hypertensive
What a mess!!!
– This is going to be confusing

Differential Diagnosis is the key
– Treat/assume the worst & hope for the best
79