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Clinical Cardiopulmonary
Risk Factors for Heart Disease
Metabolic Syndrome
1. Hyperlipidemia
2. Obesity
3. Diabetes mellitus/ Glucose intolerance
4. Hypertension
• Genetic predisposition
• Cigarette smoking
• Sedentary life-style
• Excessive alcohol consumption
• Higher risk for males than premenopausal
women
• Stress
Hypotension
• Orthostatic hypotension – temporary low BP and
dizziness when suddenly rising from a sitting or reclining
position
– Common side effect of BP medication.
• Chronic hypotension –
– poor nutrition. Low protein = low albumin = reduced
osmotic gradient for Venus return.
– Addison’s disease= ↓ ACTH= ↓ Aldosterone
• Acute hypotension – important sign of circulatory shock
– Threat to patients undergoing surgery and those in
intensive care units
Hypertension
• Hypertension maybe transient or persistent
• Primary or essential hypertension – risk
factors in primary hypertension include
– diet, obesity, age, race, heredity, stress, and
smoking
• Secondary hypertension – due to identifiable
disorders, including excessive renin
secretion, arteriosclerosis, and endocrine
disorders
Antihypertensive Therapy
– Beta Blockers :Block sympathetic stimulation to Beta-1
receptors located on cardiac muscle. This lowers the heart
rate and contractility reducing myocardial demand.
Increases time in diastole which increases the perfusion
time of the heart. Reduces cardiac afterload.
– Diuretics increase electrolytes elimination such as sodium
in the urine. This reduces the blood volume which reduces
blood returning to the heart. The result is a reduction in
preload.
– Ca+ channel blockers: decrease the amount of
intracellular Ca2+. The reduction in intracellular Ca2+
promotes relaxation of the myocardium and muscles
within the artery walls. The result is decreased ventricular
contractility, SV and arterial blood pressure. This will
reduce the afterload thus reducing cardiac workload.
– Nitroglycerin: promotes rapid vasodilation which can
reduce both preload and afterload. This is the drug of
choice if someone is complaining of chest pain.
Development of Arteriosclerosis
• LDL has a long half life allowing more time for oxidation from sugar,
cigarette smoking ,heavy metals and reactive oxygen species(ROS).
• HTN damages the lining allowing the oxidized cholesterol in.
• HDL remove cholesterol from macrophages reducing likelihood of
becoming foam cells.
Progression of Arteriosclerosis
Inflammation
• Inflammation is a non specific, localized response
by the immune system to cellular injury.
• Classification of inflammation:
– Acute inflammation: bacterial inflections or injury
to tissue
– Chronic inflammation: viral infections, persistent
foreign agent, overactive immune system
• Controllable risk factors:
– Diet
– Environment
– Lifestyle modifications
21-11
Cardiovascular
Diseases
Visceral Fat
• .
• Metabolic syndrome: constellation of
disorders that predispose you to many
chronic diseases
– Visceral obesity:
• promotes insulin resistance and inflammatory
chemicals:
• Adipose release IL-6 resulting in increased proinflammatory PGE2 and CRP.
– Diabetes: hyperglycemia and endothelial
dysfunction
– Hypertension and dyslipidemia
– Heart disease
• Chronic stress = elevated cortisol levels.
– Cortisol elevates triglycerides levels.
• visceral fat has more cortisol receptors.
– High cortisol levels suppress satiety hormones insulin and
leptin.
• Crave high energy food!
– Cortisol: is a vasoconstrictor. HTN increases inflammation
to the endothelium.
• Sleep deprivation:
– This is a stress that raises cortisol, BP and risk of all
chronic diseases.
– Increases in ghrelin increases appetite.
• High calorie diets= oxidative stress from free
radicals.
• Inactivity + weight gain:
• Dietary contributions:
– Hormone response to food
• High insulin levels increases fat
deposition.
– Immune response to food: Leaky gut
syndrome
– Modulated by fatty acid profile.
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Saturated fatty acid
(Stearic acid)
O
C
CH2
(CH2)5
CH2
CH
CH
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Double bonds deform
the linear chain and give
the fatty acid a kinked 3dimensional structure.
Unsaturated fatty acid
(Linoleic acid)
CH
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CH2
(CH2)15
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Fatty Acid Composition In Food
Cell Membrane
Free radicals
phospholipase A2
Inflammatory Cytokines
Arachidonic Acid
1. Anything that damages the cell membrane such as free radicals, glycation (sugar bonds to
proteins), microbial infestation, smoking, heavy metals, trans fats, and emotional stress
can activate inflammatory cascade.
2. membrane rigidity is increased with excessive saturated fatty acid consumption.
3. To much omega -6 fatty acids can result in increased production of arachidonic acid.
Cell Membrane
Free radicals
phospholipase A2
inflammatory Cytokines
Arachidonic Acid
cyclooxygenase 1-
PGI 1: (COX1): Homeostasis of the GI, renal(tissue repair) and platelet aggregation
Cell Membrane
Free radicals
phospholipase A2
inflammatory Cytokines
Arachidonic Acid
cyclooxygenase 2
PGE2
Thromboxane A2
PGE2:(COX2) : vasodilation, platelet aggregation, Inflammation and cell proliferation.
Thromboxane A2 : promote platelet aggregation and vasoconstriction
Cell Membrane
Free radicals
phospholipase A2
inflammatory Cytokines
Cortisol , quercetin & Turmeric
Arachidonic Acid
cyclooxygenase 1-2
PGE2
Thromboxane A2
PGE 1: (COX1): Homeostasis of the GI, renal and platelet aggregation
PGE2:(COX2) vasodilation, platelet aggregation, Inflammation and cell proliferation.
Thromboxane A2 : promote platelet aggregation and vasoconstriction
Cell Membrane
Free radicals
phospholipase A2
inflammatory Cytokines
NSAIDS
Ginger &Turmeric
Quercetin
Cortisol , quercetin & Turmeric
Arachidonic Acid
cyclooxygenase 1-2
PGE2
Thromboxane A2
NSAIDS
PGE 1: (COX1): Homeostasis of the GI, renal and platelet aggregation
PGE2:(COX2) vasodilation, platelet aggregation, Inflammation and cell proliferation.
Thromboxane A2 : promote platelet aggregation and vasoconstriction
Cell Membrane
Free radicals
phospholipase A2
inflammatory Cytokines
Arachidonic Acid
Lipooxygenase
Luekotrienes
Luekotrienes: bronchoconstriction, increased mucous production, and inflammation.
They also contribute to vasodilatation and mucosal swelling, which results in the
congestion associated with conditions such as allergic rhinitis.
Cell Membrane
Free radicals
phospholipase A2
inflammatory Cytokines
NSAIDS
Cortisol , quercetin & Turmeric
Arachidonic Acid
cyclooxygenase 1-2
Lipooxygenase
quercetin & Turmeric
Ginger &Turmeric
Quercetin
PGE2
Thromboxane A2
Luekotrienes
NSAIDS
PGE 1: (COX1): Homeostasis of the GI, renal and platelet aggregation
PGE2:(COX2) vasodilation, platelet aggregation, Inflammation and cell proliferation.
Thromboxane A2 : promote platelet aggregation and vasoconstriction
Luekotrienes: bronchoconstriction, increased mucous production, and inflammation. They also contribute to
vasodilatation and mucosal swelling, which results in the congestion associated with conditions such as allergic
• Blood work:
• Vertical Auto Profile (VAP)
• TG/HDL ratio
– Not all LDL is created equal.
• High sensitivity-C-reactive protein: synthesized in
the liver in response to inflammation
• Omega 3 blood test.
– Omega 3 ratio to omega 6
– AA/EPA ratio
• Antibody tests
– ANA profile: identifies abnormal antibodies associated
with autoimmunity
Dietary and Lifestyle
Recommendation
• Contributors:
– Trans fats, smoking, excessive alcohol, excessive
exercise and high glycemic foods
• Reduce inflammation by:
– Omega 3 fatty acids, Low glycemic foods, dietary
fiber, exercise, arginine rich foods such as nuts
and seeds
– Manage stress!
Myocardial Ischemia
• Not enough oxygen is being delivered or meet myocardial
metabolic demands.
– Anaerobic metabolism takes over resulting in a buildup of lactic acid.
» Lactic acid decreases strength of contractions
– Electrolyte imbalances interfere with normal cardiac
conduction.
– Typically present with angina
• Silent Ischemia: totally asymptomatic
– May be due to secondary to neuropathy
• Very common in diabetic patients
Myocardial Infarction
• Progression of coronary artery
disease
• Thrombus breaks of and
becomes an embolism.
• Platelets aggregate blocking
additional blood flow. (ACS)
– (acute coronary syndrome).
• Embolism travels through the
artery until it blocks the flow of
blood distal to the clot.
• Lack of blood=lack of O2
(hypoxia)=myocardial muscle
death
Congestive Heart Failure (CHF)
• Congestive heart failure (CHF) is caused by:
– Coronary atherosclerosis, high blood
pressure, multiple myocardial infarcts
– Look at the anatomy to figure out why you
have the symptoms and what part of your
heart is involved.
– Can be:
• Right sided
• Left sided
• Biventricular
Left Sided Heart Failure
• Left ventricle is not able to pump the blood out
as fast as it returns. This results in the blood
backing up to the lungs.
– Presents as fatigue and SOB with minimal exertion.
– Paroxysmal Nocturnal Dyspnea (episodes of sudden
dyspnea and orthopnea that waken a pt from sleep.
– Orthopnea (need to be upright)
– Crackles in the lung bases
– Tachycardia, fatigue and muscle weakness.
– Cyanosis ( blue lips, and nail beds)
Right Sided Heart Failure
• When the right side is pump blood out as fast as
it returns it will back up in both vena cavas.
Clinically you will see :
– Organomegoly: (Enlargement) Palpate the liver and
spleen
– Abdominal ascites and weight gain
– Pitting Edema usually in the both legs.
– Distention of jugular vein
Drugs and Ventricular Contractility
What type of cardiac medication will do the following.
Prevent the binding of epinephrine to the b-adrenergic receptors
– Blocking sympathetic input to the heart decreasing ventricular
contractility, SV and arterial blood pressure
Hypoxia
• Causes:
– hypoxemic hypoxia - usually due to inadequate
pulmonary gas exchange
• high altitudes, drowning, aspiration, respiratory arrest,
degenerative lung diseases, CO poisoning
– ischemic hypoxia - inadequate circulation
– anemic hypoxia - anemia
– histotoxic hypoxia - metabolic poison (cyanide)
• Signs: cyanosis - blueness of skin, finger nail
clubbing
• Primary effect: tissue necrosis,
Signs of Cyanosis
Chronic Obstructive Pulmonary
Disease
• Asthma
– Chemical irritants cause the release of
release of histamine which activates the PNS.
This leads to intense bronchoconstriction
(blocks air flow)
• Treatment is Epinephrine. Why?
Chronic Obstructive Pulmonary
Disease (COPD)
• Exemplified by chronic bronchitis and obstructive
emphysema
• Patients have a history of:
– Smoking
– Dyspnea, where labored breathing occurs and
gets progressively worse
– Coughing and frequent pulmonary infections
• COPD victims develop respiratory failure
accompanied by hypoxemia, carbon dioxide
retention, and respiratory acidosis
Effects of COPD
•  pulmonary compliance and vital capacity
• Hypoxemia, hypercapnia, respiratory
acidosis
– hypoxemia stimulates erythropoietin release
and leads to polycythemia
• cor pulmonale
– hypertrophy and potential failure of right heart
due to obstruction of pulmonary circulation
Chronic Obstructive Pulmonary
Disease
• Emphysema
– alveolar walls break down reducing the area
gas exchange
– healthy lungs are like a sponge; in emphysema, lungs
are more like a rigid balloon
– lungs fibrotic and less elastic
– air passages collapse with exhalation trapping
CO2 in lungs.
Figure 22.21a
Cardiac /Pulmonary Evaluation
Important Patient Intake
•
•
•
•
Diagnosis
Symptoms
Medical history
Medications
• Occupation
• Risk factors
• Social Hx
Previous Patient Workup
• Procedures
• ABGs (Arterial blood gases)
• Vitals – BP, pulses, RR, pain, PO2 and temp
• Lab data
– EKG
– HDL/LDL level (ratio),
– Chest X-ray (size of heart) large = failure
• Special tests
– Echo-cardiography
– Coronary angiography
– stress test
Physical Examination
• Inspection
– Configuration of thorax
– Excessive bruising
– Color and breaks in skin
– Lye at 30 degrees an look for JVD with pen
light.
• Auscultation
• Palpation
• Current activity level
Diagnostic Tests
•
•
•
•
Electrocardiogram (EKG)
Clinical Lab Values ( blood work)
64-Slice CT
Percutaneous Transluminal Coronary Angioplasty
– (stent placement)
•
•
•
•
•
Coronary Artery Bypass Graph
Exercise Stress Test
Nuclear Stress Test
Stress Echocardiography
Holter Monitor
Why Get an EKG
• Unexplained chest pain, or reduced blood flow
to the heart (ischemia), shortness of breath,
dizziness, fainting, or rapid and irregular
heartbeats (palpitations).
• Identify ventricle hypertrophy and other changes
of the myocardium.
• Check how well mechanical devices, such as
pacemakers or defibrillators implanted in the
heart, are working to control a normal heartbeat.
Normal Sinus Rhythm
• The heart is being paced by the SA node. There is a degree of
regularity between all components of EKG
• Normal heart rate ranges between 60-100bpm.
– 75bpm( average) dependent on activity.
• Find a QRS that falls on a solid black line.
• Then count 300-150-100-75-60-50-43 for each successive black
line. Distance between QRS complexes are 5 black lines =60 Beats
per minute
Sinus Bradycardia
(SB) is defined as a sinus rhythm with a rate below 60 bpm.
• Normally found in well trained persons and during sleep.
• May also be found in patients post myocardial infarction
• Beta Blockers reduce sympathetic input to the heart
reducing both cardiac workload and blood pressure.
– If on this medication heart rate is not a valid measure of exertion.
– Must use the Borg Preserved Exertion Scale
Tachycardia
• This is a perfectly normal rhythm if you are exercising.
• Heart beats faster under the influence of the SNS in
order to meet the bodies increased demand of oxygen.
• Stress, anxiety, or underline pathology may result in an
elevated HR.
– Context is important.
Atrial Fibrillation
• Multiple ectopic foci fire chaotically in the atrium
• This diminished the atriums ability to contract and results
in pooling in the atrium.
– (High risk of blood clot formation =need blood thinners)
– Loss of atrial kick = reduced SV
– May lead to a more severe arrhythmia.
Premature Ventricular Contraction
(PVC)
Ventricles contract before the atria in a cardiac
cycle
The SA node is not pacing the heart here.
– typically caused by emotional stress, lack of sleep,
smoking or stimulants (caffeine) which initiate an AP
in the ventricles
Ventricular Tachycardia( V-Tach)
• Heart rate greater then 150 that originates from an irritable foci in
the ventricle.
• It is a regular rhythm but is hemo-dynamically inefficient. The heart
CO will be very poor due to reduced ventricular filling.
• Reduced CO leads to poor coronary perfusion.
• Will lead to Ventricular Fibrillation
Ventricular Fibrillation( V-FIB)
• This is the most dangerous rhythm. There is no discernable pattern.
• Multiple areas of the ventricles are initiating impulses at the same
time resulting in a quivering heart instead of a contracting heart.
• The heart will not efficiently fill up with blood.
– Oxygen will not be delivered to the tissues.
– Toe tag is eminent unless a defibrillator ( AED) is near.
Implantable Cardioverter Defibrillator
• For patients at risk for recurrent, sustained ventricular tachycardia or
fibrillation.
– EF ≤ 30%
• The device is connected to leads positioned inside the heart or on its
surface.
• These leads are used to deliver electrical shocks, sense the cardiac
rhythm and sometimes pace the heart, as needed.
Exercise Stress Test
• Use of treadmill or stationary
bike.
• Every 2 or 3 minutes, your
doctor will increase the
speed and incline of the
treadmill or stationary bike,
• Monitor heart by12 lead
EKG, blood pressure and
patient tolerance.
• Goal is to reach 85% of age
related Maximum target
heart rate
Bruce Protocol
Percutaneous Transluminal
Coronary Angioplasty –
• Aka. PTCA is performed by threading a
slender balloon-tipped tube – a catheter –
from the femoral artery to a occluded spot
in a coronary artery.
• The balloon is then inflated, compressing
the plaque in the narrowed coronary artery
restoring blood flow.
• This is often accompanied by inserting an
expandable stent.
Cardiac Catheterization &
Angioplasty
Before
Preprocedure
Source: HCRI EIII 9 month (IVUS 8 months
After PTCA
Postprocedure
Coronary Artery Bypass Graph
• Coronary artery
bypass graft: aka
CABG. Creates new
routes around narrowed
and blocked coronary
arteries.
• The bypass graft for a
CABG can be a vein
from the leg or an artery
in the chest wall or wrist.